FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Green, KA
   Zarek, SM
   Catherino, WH
AF Green, Katherine A.
   Zarek, Shvetha M.
   Catherino, William H.
TI Gynecologic health and disease in relation to the microbiome of the
   female reproductive tract
SO FERTILITY AND STERILITY
LA English
DT Review
DE Microbiome; lactobacilli; bacterial vaginosis; sexually transmitted
   infection
ID IMMUNODEFICIENCY-VIRUS TYPE-1; PELVIC-INFLAMMATORY-DISEASE;
   BACTERIAL-VAGINOSIS; VAGINAL MICROBIOME; GENITAL-TRACT; GRAM STAIN;
   NONSPECIFIC VAGINITIS; MENSTRUAL-CYCLE; RISK-FACTORS;
   LACTOBACILLUS-ACIDOPHILUS
AB It is well established that the vagina is colonized by bacteria that serve important roles in homeostasis. Imbalances in the proportion of bacteria may lead to a predisposition to infection or reproductive complications. Molecular-based approaches demonstrated a greater degree of microbial diversity both within and between women than previously recognized. The vaginal microbiome may fluctuate during various states of health, such as during the menstrual cycle or after menopause, and there may be differences in the vaginal microbiome between women of different ethnicities. Furthermore, the specific composition of the vaginal microbiome may influence the predisposition to dysbiosis and the transmission of sexually transmitted infections. An understanding of the diversity of the vaginal microbial environment during states of health is essential for the identification of risk factors for disease and the development of appropriate treatment. (C) 2015 by American Society for Reproductive Medicine.
C1 [Green, Katherine A.; Zarek, Shvetha M.; Catherino, William H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
   [Catherino, William H.] Uniformed Serv Univ Hlth Sci, Dept Obstet & Gynecol, Bldg A,Room 3078,4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
RP Catherino, WH (reprint author), Uniformed Serv Univ Hlth Sci, Dept Obstet & Gynecol, Bldg A,Room 3078,4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM william.catherino@usuhs.edu
FU American Society for Reproductive Medicine; Bayer Schering Pharma;
   Abbvie Pharmaceuticals; American Board of Obstetrics and Gynecology;
   Kantar Health; Intramural Research Program of the Eunice Kennedy Shriver
   National Institute of Child Health and Human Development, National
   Institutes of Health, Bethesda, Maryland
FX W.H.C. reports personal fees from American Society for Reproductive
   Medicine, grants from Bayer Schering Pharma, personal fees from Abbvie
   Pharmaceuticals, personal fees from American Board of Obstetrics and
   Gynecology, personal fees from Kantar Health, personal fees from Grand
   Rounds Speaker, multiple sites, outside the submitted work; and reports
   that his wife is an employee of Recombine (genetic testing, not related
   to leiomyomas or gonadal hormones). K.A.G. has nothing to disclose.
   S.M.Z. has nothing to disclose.; This study was funded, in part, by the
   Intramural Research Program of the Eunice Kennedy Shriver National
   Institute of Child Health and Human Development, National Institutes of
   Health, Bethesda, Maryland.
NR 89
TC 5
Z9 6
U1 7
U2 15
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD DEC
PY 2015
VL 104
IS 6
BP 1351
EP 1357
DI 10.1016/j.fertnstert.2015.10.010
PG 7
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA DC4DC
UT WOS:000369169300004
PM 26597627
ER

PT J
AU Steiner, AZ
   Diamond, MP
   Legro, RS
   Schlaff, WD
   Barnhart, KT
   Casson, PR
   Christman, GM
   Alvero, R
   Hansen, KR
   Geisler, WM
   Thomas, T
   Santoro, N
   Zhang, HP
   Eisenberg, E
AF Steiner, Anne Z.
   Diamond, Michael P.
   Legro, Richard S.
   Schlaff, William D.
   Barnhart, Kurt T.
   Casson, Peter R.
   Christman, Gregory M.
   Alvero, Ruben
   Hansen, Karl R.
   Geisler, William M.
   Thomas, Tracey
   Santoro, Nanette
   Zhang, Heping
   Eisenberg, Esther
CA Reprod Med Network
TI Chlamydia trachomatis immunoglobulin G3 seropositivity is a predictor of
   reproductive outcomes in infertile women with patent fallopian tubes
SO FERTILITY AND STERILITY
LA English
DT Article
DE Chlamydia trachomatis; infertility; pregnancy; ectopic pregnancy
ID SUBFERTILE WOMEN; TUBAL PATHOLOGY; ANTIBODIES; METAANALYSIS; INFECTION;
   PREGNANCY; SEROLOGY; HISTORY; RATES; MODEL
AB Objective: To determine if Chlamydia trachomatis (C. trachomatis) seropositivity, as detected by the C. trachomatis elementary body (EB)-based enzyme-linked immunosorbent assay [EB ELISA] predicts pregnancy and pregnancy outcome among infertile women with documented tubal patency.
   Design: Cohort study.
   Setting: Outpatient clinics.
   Patient(s): In all, 1,250 infertile women with documented tubal patency enrolled in 1 of 2 randomized controlled trials: Pregnancy in Polycystic Ovary Syndrome II; and the Assessment of Multiple Intrauterine Gestations From Ovarian Stimulation.
   Intervention(s): Sera were analyzed for anti-C. trachomatis immunoglobulin G (IgG) 1 and IgG3 antibodies, using a research C. trachomatis EB ELISA. The optical density (OD)(405) readings of >= 0.35 and >= 0.1 were considered positive for IgG1 and IgG3, respectively.
   Main Outcome Measure(s): Primary outcomes included pregnancy, live birth, and ectopic pregnancy. Log-linear regression was used to determine the relative risk after adjusting for age, race, treatment medication, smoking status, and current alcohol use.
   Result(s): A total of 243 (19%) women were seropositive for anti-C. trachomatis IgG3. They tended to be nonwhite and smokers. AntiC. trachomatis IgG3 seropositive women were significantly less likely to conceive (risk ratio [RR] 0.65, 95% confidence interval [CI] 0.52-0.83) or to have a live birth (RR 0.59, 95% CI 0.43-0.80); these associations were weakened after adjusting for number of hysterosalpingography-documented patent tubes (RR 0.73, 95% CI 0.56-0.97) and (RR 0.73, 95% CI 0.50-1.04), respectively. AntiC. trachomatis IgG3 seropositive women who conceived had a x2.7 risk (95% CI 1.40-5.34) of ectopic pregnancy.
   Conclusion(s): Even in the presence of tubal patency, anti-C. trachomatis IgG3 seropositivity is associated with a lower likelihood of pregnancy. Anti-C. trachomatis IgG3 seropositive women have as high as 3 times the risk of ectopic pregnancy. (C) 2015 by American Society for Reproductive Medicine.
C1 [Steiner, Anne Z.] Univ N Carolina, Dept Obstet & Gynecol, Chapel Hill, NC 27599 USA.
   [Diamond, Michael P.] Wayne State Univ, Dept Obstet & Gynecol, Detroit, MI USA.
   [Diamond, Michael P.] Georgia Regents Univ, Dept Obstet & Gynecol, Augusta, GA USA.
   [Legro, Richard S.] Penn State Univ, Dept Obstet & Gynecol, Hershey, PA USA.
   [Schlaff, William D.; Alvero, Ruben; Santoro, Nanette] Univ Colorado, Dept Obstet & Gynecol, Aurora, CO USA.
   [Barnhart, Kurt T.] Univ Penn, Dept Obstet & Gynecol, Philadelphia, PA 19104 USA.
   [Casson, Peter R.] Univ Vermont, Dept Obstet & Gynecol, Burlington, VT USA.
   [Christman, Gregory M.] Univ Michigan, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA.
   [Hansen, Karl R.] Univ Oklahoma, Dept Obstet & Gynecol, Oklahoma City, OK USA.
   [Geisler, William M.] Univ Alabama Birmingham, Dept Med, Birmingham, AL 35294 USA.
   [Thomas, Tracey; Zhang, Heping] Yale Univ, Dept Biostat, New Haven, CT USA.
   [Eisenberg, Esther] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
RP Steiner, AZ (reprint author), Univ N Carolina, Sch Med, Dept Obstet & Gynecol, CB 7570,Old Clin Bldg, Chapel Hill, NC 27599 USA.
EM asteiner@med.unc.edu
OI Diamond, Michael/0000-0001-6353-4489
FU Ferring; Astra Zeneca; Euroscreen; Clarus Therapeutics; Takeda; AbbVie
   Pharmaceuticals; Bayer Pharmaceuticals; Yale University/Reproductive
   Medicine Network/NICHD; Ferring International Pharmascience Center US;
   Roche Diagnostics; NICHD; NIH; National Institutes of Health
   (NIH)/Eunice Kennedy Shriver National Institute of Child Health and
   Human Development (NICHD) [U10HD077844, U10 HD39005, U10 HD38992, U10
   HD27049, U10 HD38998, U10 HD055942, HD055944, U10 HD055936, U10HD055925,
   U10 U54-HD29834]; NIH [UL1 TR000127]
FX A.Z.S. has nothing to disclose. M.P.D. has nothing to disclose. R.S.L.
   reports a grant from Ferring; and personal fees from Ferring, Astra
   Zeneca, Euroscreen, Clarus Therapeutics, and Takeda. W.D.S. reports
   research support grants from AbbVie Pharmaceuticals. K.T.B. has nothing
   to disclose. P.R.C. has nothing to disclose. G.M.C. is on the advisory
   board of Bayer Pharmaceuticals; received grants from Bayer
   Pharmaceuticals and Abbvie Pharmaceuticals; received honoraria from
   Abbvie Pharmaceuticals. R.A. has nothing to disclose. K.R.H.
   subcontracted with Yale University/Reproductive Medicine Network/NICHD
   for salary support and patient care costs; and has received grants from
   Ferring International Pharmascience Center US and Roche Diagnostics.
   W.M.G. was contracted by Yale University (a research center of the
   Reproductive Medicine Network) to perform the chlamydia serology for the
   study; contract funds were research funds that went to University of
   Alabama. T.T. reports an Reproductive Medicine Network grant from NICHD.
   N.S. has nothing to disclose. H.Z. reports an NIH grant. E.E. has
   nothing to disclose.; This work was supported by National Institutes of
   Health (NIH)/Eunice Kennedy Shriver National Institute of Child Health
   and Human Development (NICHD) grants U10HD077844 (to A.Z.S.), U10
   HD39005 (to M.P.D.), U10 HD38992 (to R.S.L.), U10 HD27049 (to K.T.B.),
   U10 HD38998 (to R.A. and W.D.S), U10 HD055942, HD055944 (to P.R.C.), U10
   HD055936 (to G.M.C.), U10HD055925 (to H.Z.); U10 U54-HD29834 (to the
   University of Virginia Center for Research in Reproduction Ligand Assay
   and Analysis Core of the Specialized Cooperative Centers Program in
   Reproduction and Infertility Research); and an NIH grant UL1 TR000127
   (to Pennsylvania State University).
NR 21
TC 2
Z9 2
U1 1
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD DEC
PY 2015
VL 104
IS 6
BP 1522
EP 1526
DI 10.1016/j.fertnstert.2015.08.022
PG 5
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA DC4DC
UT WOS:000369169300031
PM 26413816
ER

PT J
AU Fagoonee, S
   Singh, SR
   Altruda, F
   Pellicano, R
AF Fagoonee, S.
   Singh, S. R.
   Altruda, F.
   Pellicano, R.
TI Surface markers of gastric cancer stem cells
SO MINERVA BIOTECNOLOGICA
LA English
DT Review
DE Stomach neoplasms; Neoplastic stem cells; Helicobacter; Bone marrow
   cells
ID MARROW-DERIVED CELLS; HELICOBACTER-PYLORI INFECTION; LYMPH-NODE
   METASTASIS; BONE-MARROW; EPITHELIAL-CELLS; PROGENITOR CELLS; MOUSE
   STOMACH; SELF-RENEWAL; IN-VITRO; CD44
AB The integrity of the gastric epithelium is maintained by the gastric stem cells, which proliferate and self-renew, giving rise to transient amplifying cells that replace the constantly renewing epithelium. Since in rapidly renewing organs like the stomach, stem cells live long enough to accumulate the multiple genetic changes required for transformation, it is postulated that resident stem cells may, in a chronically inflamed environment, accumulate a series of genetic and epigenetic changes over time that lead to the emergence of gastric cancer stem cells. Alternatively, the setting of chronic inflammatory stress may lead to loss of the indigenous gastric stem cells from their niches, followed by recruitment and engraftment of bone marrow derived stem cells into the gastric epithelium, thus contributing to gastric cancer. Recently, gastric stem cell responses after Helicobacter pylori (H. pylori) infection and recruitment of bone marrow derived stem cells to the inflammatory site have been reported. Despite the tremendous efforts made to identify markers to isolate gastric cancer stem cells, hitherto, only two molecules have been shown to be promising as marker progenitors: villin and Lgr5. This review highlights the advances in the identification of surface markers of gastric cancer stem cells, with emphasis on the effect of H. pylori infection on the stem cell compartment.
C1 [Fagoonee, S.] Univ Turin, Ctr Mol Biotechnol, Inst Biostruct & Bioimages CNR, Turin, Italy.
   [Singh, S. R.] Natl Canc Inst, Basic Res Lab, Frederick, MD USA.
   [Altruda, F.] Univ Turin, Mol Biotechnol Ctr, Turin, Italy.
   [Pellicano, R.] Molinette Mauriziano Hosp, Dept Gastroenterol & Hepatol, Turin, Italy.
RP Pellicano, R (reprint author), Molinette Hosp SGAS, Dept Gastroenterol & Hepatol, Via Cavour 31, I-10126 Turin, Italy.
EM rinaldo_pellican@hotmail.com
RI Singh, Shree Ram/B-7614-2008
OI Singh, Shree Ram/0000-0001-6545-583X
NR 75
TC 0
Z9 0
U1 3
U2 8
PU EDIZIONI MINERVA MEDICA
PI TURIN
PA CORSO BRAMANTE 83-85 INT JOURNALS DEPT., 10126 TURIN, ITALY
SN 1120-4826
EI 1827-160X
J9 MINERVA BIOTECNOL
JI Minerva Biotechnol.
PD DEC
PY 2015
VL 27
IS 4
BP 225
EP 233
PG 9
WC Biotechnology & Applied Microbiology
SC Biotechnology & Applied Microbiology
GA DC4SO
UT WOS:000369210800010
ER

PT J
AU Captur, G
   Zemrak, F
   Muthurangu, V
   Petersen, SE
   Li, CM
   Bassett, P
   Kawel-Boehm, N
   McKenna, WJ
   Elliott, PM
   Lima, JAC
   Bluemke, DA
   Moon, JC
AF Captur, Gabriella
   Zemrak, Filip
   Muthurangu, Vivek
   Petersen, Steffen E.
   Li, Chunming
   Bassett, Paul
   Kawel-Boehm, Nadine
   McKenna, William J.
   Elliott, Perry M.
   Lima, Joao A. C.
   Bluemke, David A.
   Moon, James C.
TI Fractal Analysis of Myocardial Trabeculations in 2547 Study
   Participants: Multi-Ethnic Study of Atherosclerosis
SO RADIOLOGY
LA English
DT Article
ID LEFT-VENTRICULAR NONCOMPACTION; MAGNETIC-RESONANCE; NON-COMPACTION;
   CARDIOMYOPATHY; DIAGNOSIS; MRI
AB Purpose: To quantitatively determine the population variation and relationship of left ventricular (LV) trabeculation to LV function, structure, and clinical variables.
   Materials and Methods: This HIPAA-compliant multicenter study was approved by institutional review boards of participating centers. All participants provided written informed consent. Participants from the Multi-Ethnic Study of Atherosclerosis with cardiac magnetic resonance (MR) data were evaluated to quantify LV trabeculation as a fractal dimension (FD). Entire cohort participants free of cardiac disease, hypertrophy, hypertension, and diabetes were stratified by body mass index (BMI) into three reference groups (BMI <25 kg/m(2); BMI >= 25 kg/m(2) to <30 kg/m(2); and BMI >= 30 kg/m(2)) to explore maximal apical FD (FDMaxApical). Multivariable linear regression models determined the relationship between FD and other parameters.
   Results: Included were 2547 participants (mean age, 68.7 years +/- 9.1 [standard deviation]; 1211 men). FDMaxApical are in arbitrary units. FDMaxApical reference ranges for BMI 30 kg/m(2) or greater (n = 163), 25 kg/m(2) or greater to less than 30 kg/m(2) (n = 206), and less than 25 kg/m(2) (n = 235) were 1.203 +/- 0.06 (95% confidence interval: 1.194, 1.212), 1.194 +/- 0.06 (95% confidence interval: 1.186, 1.202), and 1.169 +/- 0.05 (95% confidence interval: 1.162, 1.176), respectively. In the entire cohort, adjusted for anthropometrics, trabeculation was higher in African American participants (standardized beta [s beta] = 0.09; P <= .001) and Hispanic participants (s beta = 0.05; P = .013) compared with white participants and was also higher in African American participants compared with Chinese American participants (s beta = 0.08; P = .01), and this persisted after adjustment for hypertension and LV size. Hypertension (s beta = 0.07; P < .001), LV mass (s beta = 0.22; P < .001), and wall thickness (s beta = 0.27; P < .001) were positively associated with FDMaxApical even after adjustment. In the group with BMIs less than 25 kg/m(2), Chinese American participants had less trabeculation than white participants (s beta = 20.15; P = .032).
   Conclusion: Fractal analysis of cardiac MR imaging data measures endocardial complexity, which helps to differentiate normal from abnormal trabecular patterns in healthy versus diseased hearts. Trabeculation is influenced by race and/or ethnicity and, more importantly, by cardiac loading conditions and comorbidities. Clinicians who interpret cine MR imaging data should expect slightly less endocardial complexity in Chinese American patients and more in African American patients, Hispanic patients, hypertensive patients, and those with hypertrophy. (C) RSNA, 2015
C1 [Captur, Gabriella; Bassett, Paul; McKenna, William J.; Elliott, Perry M.; Moon, James C.] Heart Hosp, Div Cardiovasc Imaging & Biostat, 16-18 Westmoreland St, London W1G 8PH, England.
   [Captur, Gabriella; Muthurangu, Vivek; McKenna, William J.; Elliott, Perry M.; Moon, James C.] UCL, UCL Inst Cardiovasc Sci, London, England.
   [Zemrak, Filip; Petersen, Steffen E.] Queen Mary Univ London, Barts & London Sch Med & Dent, Cardiovasc Biomed Res Unit, London, England.
   [Zemrak, Filip; Petersen, Steffen E.] London Chest Hosp, Div Cardiovasc Imaging, London E2 9JX, England.
   [Muthurangu, Vivek] UCL, Ctr Cardiovasc Imaging, London, England.
   [Muthurangu, Vivek] Great Ormond St Hosp Sick Children, London, England.
   [Li, Chunming] Univ Penn, Dept Radiol, Philadelphia, PA 19104 USA.
   [Kawel-Boehm, Nadine] Hosp Graubuenden, Dept Radiol, Loestrasse, Switzerland.
   [Lima, Joao A. C.; Bluemke, David A.] NIH, Dept Radiol & Imaging Sci, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA.
   [Bluemke, David A.] Johns Hopkins Univ Hosp, Dept Cardiovasc Imaging, Baltimore, MD 21287 USA.
RP Moon, JC (reprint author), Heart Hosp, Div Cardiovasc Imaging & Biostat, 16-18 Westmoreland St, London W1G 8PH, England.; Moon, JC (reprint author), UCL, UCL Inst Cardiovasc Sci, London, England.
EM j.moon@ucl.ac.uk
RI Petersen, Steffen/A-8389-2011; 
OI Petersen, Steffen/0000-0003-4622-5160; moon, james/0000-0001-8071-1491
FU National Institutes of Health [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 95168, CL090019, EB000072]
FX This research was supported by the National Institutes of Health (grants
   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 95168, CL090019, and
   EB000072).
NR 22
TC 6
Z9 6
U1 1
U2 3
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD DEC
PY 2015
VL 277
IS 3
BP 707
EP 715
DI 10.1148/radiol.2015142948
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA DC9EY
UT WOS:000369525100010
PM 26069924
ER

PT J
AU Muller, BG
   Shih, JH
   Sankineni, S
   Marko, J
   Rais-Bahrami, S
   George, AK
   de la Rosette, JJMCH
   Merino, MJ
   Wood, BJ
   Pinto, P
   Choyke, PL
   Turkbey, B
AF Muller, Berrend G.
   Shih, Joanna H.
   Sankineni, Sandeep
   Marko, Jamie
   Rais-Bahrami, Soroush
   George, Arvin Koruthu
   de la Rosette, Jean J. M. C. H.
   Merino, Maria J.
   Wood, Bradford J.
   Pinto, Peter
   Choyke, Peter L.
   Turkbey, Baris
TI Prostate Cancer: Interobserver Agreement and Accuracy with the Revised
   Prostate Imaging Reporting and Data System at Multiparametric MR Imaging
SO RADIOLOGY
LA English
DT Article
ID TRANSRECTAL ULTRASOUND BIOPSY; RADS SCORING SYSTEM; IN-BORE BIOPSY;
   FUSION; VALIDATION; DIAGNOSIS
AB Purpose: To evaluate accuracy and interobserver variability with the use of the Prostate Imaging Reporting and Data System (PI-RADS) version 2.0 for detection of prostate cancer at multiparametric magnetic resonance (MR) imaging in a biopsy-naive patient population.
   Materials and Methods: This retrospective HIPAA-compliant study was approved by the local ethics committee, and written informed consent was obtained from all patients for use of their imaging and histopathologic data in future research studies. In 101 biopsy-naive patients with elevated prostate-specific antigen levels who underwent multiparametric MR imaging of the prostate and subsequent transrectal ultrasonography (US)-MR imaging fusion-guided biopsy, suspicious lesions detected at multiparametric MR imaging were scored by five readers who were blinded to pathologic results by using to the newly revised PI-RADS and the scoring system developed in-house. Interobserver agreement was evaluated by using k statistics, and the correlation of pathologic results with each of the two scoring systems was evaluated by using the Kendall T correlation coefficient.
   Results: Specimens of 162 lesions in 94 patients were sampled by means of transrectal US-MR imaging fusion biopsy. Results for 87 (54%) lesions were positive for prostate cancer. Kendall T values with the PI-RADS and the in-house-developed scoring system, respectively, at T2-weighted MR imaging in the peripheral zone were 0.51 and 0.17 and in the transitional zone, 0.45 and 20.11; at diffusion-weighted MR imaging, 0.42 and 0.28; at dynamic contrast material-enhanced MR imaging, 0.23 and 0.24, and overall suspicion scores were 0.42 and 0.49. Median k scores among all possible pairs of readers for PI-RADS and the in-house-developed scoring system, respectively, for T2-weighted MR images in the peripheral zone were 0.47 and 0.15; transitional zone, 0.37 and 0.07; diffusion-weighted MR imaging, 0.41 and 0.57; dynamic contrast-enhanced MR imaging, 0.48 and 0.41; and overall suspicion scores, 0.46 and 0.55.
   Conclusion: Use of the revised PI-RADS provides moderately reproducible MR imaging scores for detection of clinically relevant disease. (C) RSNA, 2015
C1 [Muller, Berrend G.; Sankineni, Sandeep; Choyke, Peter L.; Turkbey, Baris] NCI, Mol Imaging Program, NIH, 10 Ctr Dr,MSC 1182,Bldg 10,Room B3B85, Bethesda, MD 20892 USA.
   [Shih, Joanna H.] NCI, Biometr Res Branch, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
   [Rais-Bahrami, Soroush; George, Arvin Koruthu; Pinto, Peter] NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
   [Merino, Maria J.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
   [Wood, Bradford J.] NCI, Ctr Intervent Oncol, NIH, Bethesda, MD 20892 USA.
   [Muller, Berrend G.; de la Rosette, Jean J. M. C. H.] AMC Univ Hosp, Dept Urol, Amsterdam, Netherlands.
   [Marko, Jamie] Uniformed Serv Univ Hlth Sci, Dept Radiol & Radiol Sci, Edward Hebert Sch Med, Bethesda, MD 20814 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
NR 29
TC 35
Z9 38
U1 2
U2 5
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD DEC
PY 2015
VL 277
IS 3
BP 741
EP 750
DI 10.1148/radiol.2015142818
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA DC9EY
UT WOS:000369525100014
PM 26098458
ER

PT J
AU Sullivan, DC
   Obuchowski, NA
   Kessler, LG
   Raunig, DL
   Gatsonis, C
   Huang, EP
   Kondratovich, M
   McShane, LM
   Reeves, AP
   Barboriak, DP
   Guimaraes, AR
   Wahl, RL
AF Sullivan, Daniel C.
   Obuchowski, Nancy A.
   Kessler, Larry G.
   Raunig, David L.
   Gatsonis, Constantine
   Huang, Erich P.
   Kondratovich, Marina
   McShane, Lisa M.
   Reeves, Anthony P.
   Barboriak, Daniel P.
   Guimaraes, Alexander R.
   Wahl, Richard L.
CA RSNA-QIBA Metrol Working Grp
TI Metrology Standards for Quantitative Imaging Biomarkers
SO RADIOLOGY
LA English
DT Article
ID STATISTICAL-METHODS; TECHNICAL PERFORMANCE; GOLD STANDARD; LUNG-CANCER;
   REPRODUCIBILITY; AGREEMENT; PET; ISSUES
AB Although investigators in the imaging community have been active in developing and evaluating quantitative imaging biomarkers (QIBs), the development and implementation of QIBs have been hampered by the inconsistent or incorrect use of terminology or methods for technical performance and statistical concepts. Technical performance is an assessment of how a test performs in reference objects or subjects under controlled conditions. In this article, some of the relevant statistical concepts are reviewed, methods that can be used for evaluating and comparing QIBs are described, and some of the technical performance issues related to imaging biomarkers are discussed. More consistent and correct use of terminology and study design principles will improve clinical research, advance regulatory science, and foster better care for patients who undergo imaging studies. (C)RSNA, 2015
C1 [Sullivan, Daniel C.; Barboriak, Daniel P.] Duke Univ, Med Ctr, Dept Radiol, Box 2715, Durham, NC 27710 USA.
   [Obuchowski, Nancy A.] Cleveland Clin Fdn, Dept Quantitat Hlth Sci, Cleveland, OH 44195 USA.
   [Kessler, Larry G.] Univ Washington, Dept Publ Hlth, Seattle, WA 98195 USA.
   [Raunig, David L.] ICON Med, Dept Informat, Washington, PA USA.
   [Gatsonis, Constantine] Brown Univ, Ctr Stat Sci, Providence, RI 02912 USA.
   [Huang, Erich P.; McShane, Lisa M.] NCI, Bethesda, MD 20892 USA.
   [Kondratovich, Marina] US FDA, Ctr Devices & Radiol Hlth, White Oak, MD USA.
   [Reeves, Anthony P.] Cornell Univ, Dept Elect & Comp Engn, Ithaca, NY USA.
   [Guimaraes, Alexander R.] Oregon Hlth & Sci Univ, Dept Radiol, Portland, OR 97201 USA.
   [Wahl, Richard L.] Washington Univ, Sch Med, Mallinckrodt Inst Radiol, St Louis, MO USA.
RP Sullivan, DC (reprint author), Duke Univ, Med Ctr, Dept Radiol, Box 2715, Durham, NC 27710 USA.
EM daniel.sullivan@duke.edu
FU National Institutes of Health [HHSN268201000050C]
FX This research was supported by the National Institutes of Health (grant
   no. HHSN268201000050C).
NR 31
TC 19
Z9 19
U1 3
U2 8
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD DEC
PY 2015
VL 277
IS 3
BP 813
EP 825
DI 10.1148/radiol.2015142202
PG 13
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA DC9EY
UT WOS:000369525100021
PM 26267831
ER

PT J
AU Lee, KS
   Burke, TR
   Park, JE
   Bang, JK
   Lee, E
AF Lee, Kyung S.
   Burke, Terrence R., Jr.
   Park, Jung-Eun
   Bang, Jeong K.
   Lee, Eunhye
TI Recent Advances and New Strategies in Targeting Plk1 for Anticancer
   Therapy
SO TRENDS IN PHARMACOLOGICAL SCIENCES
LA English
DT Review
ID POLO-LIKE-KINASE; ACUTE MYELOID-LEUKEMIA; HUMAN CANCER-CELLS;
   PROTEIN-PROTEIN INTERACTIONS; ACUTE MYELOGENOUS LEUKEMIA; SMALL-MOLECULE
   INHIBITORS; BOX DOMAIN; ANTITUMOR-ACTIVITY; FLUORESCENCE POLARIZATION;
   HEMATOLOGIC MALIGNANCIES
AB Polo-like kinase 1 (Plk1) plays key roles in regulating mitotic processes that are crucial for cellular proliferation. Overexpression of Plk1 is tightly associated with the development of particular cancers in humans, and a large body of evidence suggests that Plk1 is an attractive target for anticancer therapeutic development. Drugs targeting Plk1 can potentially be directed at two distinct sites: the N-terminal catalytic kinase domain (KD), which phosphorylates substrates, and the C-terminal polo-box domain (PBD) which is essential for protein-protein interactions. In this review we summarize recent advances and new challenges in the development of Plk1 inhibitors targeting these two domains. We also discuss novel strategies for designing and developing next-generation inhibitors to effectively treat Plk1-associated human disorders.
C1 [Lee, Kyung S.; Park, Jung-Eun; Lee, Eunhye] NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Burke, Terrence R., Jr.] Natl Canc Inst Frederick, Chem Biol Lab, Ctr Canc Res, Frederick, MD 21702 USA.
   [Bang, Jeong K.] Korea Basic Sci Inst, Div Magnet Resonance, Chungbuk 363883, Cheongwon, South Korea.
RP Lee, KS (reprint author), NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM kyunglee@gmail.nih.gov
FU National Institutes of Health (NIH) National Cancer Institute (NCI);
   Korea Basic Science Institute [T35418]; Korean Biomedical Scientist
   Fellowship from the KRIBB Research Initiative Program, Korea Research
   Institute of Bioscience and Biotechnology, Republic of Korea
FX We would like to thank Klaus Strebhardt for critical reading of the
   manuscript and many colleagues for generously sharing their views and
   insights. We apologize to all authors whose work could not be cited
   owing to space limitations. This research was supported in part by the
   Intramural Research Program of the National Institutes of Health (NIH)
   National Cancer Institute (NCI) (K.S.L. and T.R.B), Korea Basic Science
   Institute grant T35418 (J.K.B.), and a Korean Biomedical Scientist
   Fellowship from the KRIBB Research Initiative Program, Korea Research
   Institute of Bioscience and Biotechnology, Republic of Korea.
NR 153
TC 10
Z9 10
U1 7
U2 22
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0165-6147
J9 TRENDS PHARMACOL SCI
JI Trends Pharmacol. Sci.
PD DEC
PY 2015
VL 36
IS 12
BP 858
EP 877
DI 10.1016/j.tips.2015.08.013
PG 20
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA DC6RV
UT WOS:000369348200005
PM 26478211
ER

PT J
AU Chandler, RK
   Kahana, SY
   Fletcher, B
   Jones, D
   Finger, MS
   Aklin, WM
   Hamill, K
   Webb, C
AF Chandler, Redonna K.
   Kahana, Shoshana Y.
   Fletcher, Bennett
   Jones, Dionne
   Finger, Matthew S.
   Aklin, Will M.
   Hamill, Kathleen
   Webb, Candace
TI Data Collection and Harmonization in HIV Research: The Seek, Test,
   Treat, and Retain Initiative at the National Institute on Drug Abuse
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Editorial Material
ID CHRONIC MENTAL-ILLNESS; ANTIRETROVIRAL THERAPY; PREVENTION; ADHERENCE;
   PEOPLE; CARE; COVERAGE; DISORDERS; INFECTION; HIV/AIDS
AB Large-scale, multisite data sets offer the potential for exploring the public health benefits of biomedical interventions. Data harmonization is an emerging strategy to increase the comparability of research data collected across independent studies, enabling research questions to be addressed beyond the capacity of any individual study.
   The National Institute on Drug Abuse recently implemented this novel strategy to prospectively collect and harmonize data across 22 independent research studies developing and empirically testing interventions to effectively deliver an HIV continuum of care to diverse drug-abusing populations.
   We describe this data collection and harmonization effort, collectively known as the Seek, Test, Treat, and Retain Data Collection and Harmonization Initiative, which can serve as a model applicable to other research endeavors.
C1 [Chandler, Redonna K.; Kahana, Shoshana Y.; Fletcher, Bennett; Jones, Dionne; Finger, Matthew S.; Aklin, Will M.; Hamill, Kathleen] NIDA, NIH, Bethesda, MD 20892 USA.
   [Webb, Candace] HIV AIDS Bur, Hlth Resources & Serv Adm, Rockville, MD USA.
RP Chandler, RK (reprint author), NIH, 6701 Democracy Blvd,Off 934, Bethesda, MD 20892 USA.
EM redonna.chandler@nih.gov
NR 28
TC 5
Z9 5
U1 0
U2 2
PU AMER PUBLIC HEALTH ASSOC INC
PI WASHINGTON
PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA
SN 0090-0036
EI 1541-0048
J9 AM J PUBLIC HEALTH
JI Am. J. Public Health
PD DEC
PY 2015
VL 105
IS 12
BP 2416
EP 2422
DI 10.2105/AJPH.2015.302788
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA DC4BB
UT WOS:000369163600020
PM 26469642
ER

PT J
AU Dawber, TR
   Moore, FE
   Mann, GV
AF Dawber, Thomas R.
   Moore, Felix E.
   Mann, George V.
TI II. Coronary Heart Disease in the Framingham Study (Reprinted from AM J
   Public Health, vol 47, pg 4-24, 1957)
SO INTERNATIONAL JOURNAL OF EPIDEMIOLOGY
LA English
DT Reprint
C1 [Dawber, Thomas R.; Moore, Felix E.; Mann, George V.] NIH, Natl Heart Inst, Publ Hlth Serv, Bldg 10, Bethesda, MD 20892 USA.
RP Dawber, TR (reprint author), NIH, Natl Heart Inst, Publ Hlth Serv, Bldg 10, Bethesda, MD 20892 USA.
NR 17
TC 1
Z9 1
U1 3
U2 7
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0300-5771
EI 1464-3685
J9 INT J EPIDEMIOL
JI Int. J. Epidemiol.
PD DEC
PY 2015
VL 44
IS 6
BP 1767
EP 1780
DI 10.1093/ije/dyv346
PG 14
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA DC0NW
UT WOS:000368915400003
PM 26705414
ER

PT J
AU Hung, GCL
   Hahn, J
   Alamiri, B
   Buka, SL
   Goldstein, JM
   Laird, N
   Nelson, CA
   Smoller, W
   Gilman, SE
AF Hung, Galen Chin-Lun
   Hahn, Jill
   Alamiri, Bibi
   Buka, Stephen L.
   Goldstein, Jill M.
   Laird, Nan
   Nelson, Charles A.
   Smoller, Jordan W.
   Gilman, Stephen E.
TI Socioeconomic disadvantage and neural development from infancy through
   early childhood
SO INTERNATIONAL JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE Neural development; soft signs; neurological abnormality; socioeconomic
   status
ID NEUROLOGICAL SOFT SIGNS; COLLABORATIVE PERINATAL PROJECT; 1ST-EPISODE
   SCHIZOPHRENIA; BIPOLAR DISORDER; SEX-DIFFERENCES; BIRTH COHORT;
   CHILDREN; STRESS; NEURODEVELOPMENT; OUTCOMES
AB Background: Early social experiences are believed to shape neurodevelopment, with potentially lifelong consequences. Yet minimal evidence exists regarding the role of the social environment on children's neural functioning, a core domain of neurodevelopment.
   Methods: We analysed data from 36 443 participants in the United States Collaborative Perinatal Project, a socioeconomically diverse pregnancy cohort conducted between 1959 and 1974. Study outcomes included: physician (neurologist or paediatrician)-rated neurological abnormality neonatally and thereafter at 4 months and 1 and 7 years; indicators of neurological hard signs and soft signs; and indicators of autonomic nervous system function.
   Results: Children born to socioeconomically disadvantaged parents were more likely to exhibit neurological abnormalities at 4 months [odds ratio (OR) = 1.20; 95% confidence interval (CI) = 1.06, 1.37], 1 year (OR = 1.35; CI = 1.17, 1.56), and 7 years (OR = 1.67; CI = 1.48, 1.89), and more likely to exhibit neurological hard signs (OR = 1.39; CI = 1.10, 1.76), soft signs (OR = 1.26; CI = 1.09, 1.45) and autonomic nervous system dysfunctions at 7 years. Pregnancy and delivery complications, themselves associated with socioeconomic disadvantage, did not account for the higher risks of neurological abnormalities among disadvantaged children.
   Conclusions: Parental socioeconomic disadvantage was, independently from pregnancy and delivery complications, associated with abnormal child neural development during the first 7 years of life. These findings reinforce the importance of the early environment for neurodevelopment generally, and expand knowledge regarding the domains of neurodevelopment affected by environmental conditions. Further work is needed to determine the mechanisms linking socioeconomic disadvantage with children's neural functioning, the timing of such mechanisms and their potential reversibility.
C1 [Hung, Galen Chin-Lun] Taipei City Hosp, Taipei City Psychiat Ctr, Dept Gen Psychiat, Taipei, Taiwan.
   [Hung, Galen Chin-Lun] Natl Yang Ming Univ, Sch Med, Dept Publ Hlth, Taipei 112, Taiwan.
   [Hahn, Jill; Gilman, Stephen E.] Harvard Univ, Sch Publ Hlth, Dept Social & Behav Sci, Boston, MA USA.
   [Alamiri, Bibi] Lahey Hosp & Med Ctr, Sect Child & Adolescent Psychiat, Burlington, MA USA.
   [Alamiri, Bibi; Gilman, Stephen E.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
   [Buka, Stephen L.] Brown Univ, Sch Publ Hlth, Dept Epidemiol, Providence, RI 02912 USA.
   [Goldstein, Jill M.] Brigham & Womens Hosp, Dept Psychiat, Boston, MA USA.
   [Goldstein, Jill M.] Brigham & Womens Hosp, Dept Med, Boston, MA USA.
   [Laird, Nan] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
   [Nelson, Charles A.] Harvard Univ, Sch Med, Boston Childrens Hosp, Dept Pediat, Boston, MA USA.
   [Smoller, Jordan W.] Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, Boston, MA 02114 USA.
   [Smoller, Jordan W.; Gilman, Stephen E.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
   [Smoller, Jordan W.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
   [Gilman, Stephen E.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, Rockville, MD USA.
RP Gilman, SE (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, 6100 Execut Blvd,Room 7B13M, Rockville, MD 20852 USA.
EM stephen.gilman@nih.gov
OI Gilman, Stephen/0000-0002-8331-6419
FU National Institutes of Health [RO1MH087544, P50MH082679]; Intramural
   Research Program of the Eunice Kennedy Shriver National Institute of
   Child Health and Human Development
FX This work was supported in part by grants from the National Institutes
   of Health [RO1MH087544 to S.E.G. and P50MH082679 to J.M.G.] and the
   Intramural Research Program of the Eunice Kennedy Shriver National
   Institute of Child Health and Human Development.
NR 79
TC 5
Z9 5
U1 1
U2 9
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0300-5771
EI 1464-3685
J9 INT J EPIDEMIOL
JI Int. J. Epidemiol.
PD DEC
PY 2015
VL 44
IS 6
BP 1889
EP 1899
DI 10.1093/ije/dyv303
PG 11
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA DC0NW
UT WOS:000368915400019
ER

PT J
AU Stirratt, MJ
   Dunbar-Jacob, J
   Crane, HM
   Simoni, JM
   Czajkowski, S
   Hilliard, ME
   Aikens, JE
   Hunter, CM
   Velligan, DI
   Huntley, K
   Ogedegbe, G
   Rand, CS
   Schron, E
   Nilsen, WJ
AF Stirratt, Michael J.
   Dunbar-Jacob, Jacqueline
   Crane, Heidi M.
   Simoni, Jane M.
   Czajkowski, Susan
   Hilliard, Marisa E.
   Aikens, James E.
   Hunter, Christine M.
   Velligan, Dawn I.
   Huntley, Kristen
   Ogedegbe, Gbenga
   Rand, Cynthia S.
   Schron, Eleanor
   Nilsen, Wendy J.
TI Self-report measures of medication adherence behavior: recommendations
   on optimal use
SO TRANSLATIONAL BEHAVIORAL MEDICINE
LA English
DT Article
DE Adherence; Compliance; Self-management; Medication; Self-report
ID FACE-TO-FACE; COMBINATION ANTIRETROVIRAL THERAPY; VIROLOGICAL TREATMENT
   RESPONSE; DIABETES TREATMENT ADHERENCE; RANDOMIZED CONTROLLED-TRIAL;
   SEVERE MENTAL-ILLNESS; INJECTING DRUG-USERS; VISUAL ANALOG SCALE;
   QUALITY-OF-LIFE; PSYCHOMETRIC PROPERTIES
AB Medication adherence plays an important role in optimizing the outcomes of many treatment and preventive regimens in chronic illness. Self-report is the most common method for assessing adherence behavior in research and clinical care, but there are questions about its validity and precision. The NIH Adherence Network assembled a panel of adherence research experts working across various chronic illnesses to review self-report medication adherence measures and research on their validity. Self-report medication adherence measures vary substantially in their question phrasing, recall periods, and response items. Self-reports tend to overestimate adherence behavior compared with other assessment methods and generally have high specificity but low sensitivity. Most evidence indicates that self-report adherence measures show moderate correspondence to other adherence measures and can significantly predict clinical outcomes. The quality of self-report adherence measures may be enhanced through efforts to use validated scales, assess the proper construct, improve estimation, facilitate recall, reduce social desirability bias, and employ technologic delivery. Self-report medication adherence measures can provide actionable information despite their limitations. They are preferred when speed, efficiency, and low-cost measures are required, as is often the case in clinical care.
C1 [Stirratt, Michael J.] NIMH, Div AIDS Res, NIH, Bethesda, MD 20892 USA.
   [Dunbar-Jacob, Jacqueline] Univ Pittsburgh, Sch Nursing, Pittsburgh, PA 15261 USA.
   [Crane, Heidi M.] Univ Washington, Div Infect Dis, Seattle, WA 98195 USA.
   [Simoni, Jane M.] Univ Washington, Dept Psychol, Seattle, WA 98195 USA.
   [Czajkowski, Susan] NHLBI, NIH, Bethesda, MD 20892 USA.
   [Hilliard, Marisa E.] Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA.
   [Aikens, James E.] Univ Michigan, Dept Family Med, Ann Arbor, MI 48109 USA.
   [Hunter, Christine M.] NIDDK, NIH, Bethesda, MD 20892 USA.
   [Velligan, Dawn I.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
   [Huntley, Kristen] NIDA, NIH, Bethesda, MD 20892 USA.
   [Ogedegbe, Gbenga] NYU, Sch Med, New York, NY USA.
   [Rand, Cynthia S.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
   [Schron, Eleanor] NEI, NIH, Bethesda, MD 20892 USA.
   [Nilsen, Wendy J.] Natl Sci Fdn, Arlington, VA 22230 USA.
RP Stirratt, MJ (reprint author), NIMH, Div AIDS Res, NIH, Bethesda, MD 20892 USA.
EM stirrattm@mail.nih.gov
OI Simoni, Jane/0000-0002-8711-1576
FU NIH Office of Behavioral and Social Sciences (OBSSR)
FX The paper is based in part on an NIH Adherence Network meeting on
   "Advancing the Science of Adherence Assessment: A Working Meeting on
   Self-Report Measures," sponsored by the NIH Office of Behavioral and
   Social Sciences (OBSSR) and held 17 October 2011. We are grateful to
   Shoshana Kahana for her contributions, to Janet de Moor, Martha Hare,
   Donna McCloskey, and Anne Trontell for their paper feedback, and to all
   members of the NIH Adherence Network for their support.
NR 135
TC 17
Z9 17
U1 8
U2 18
PU SPRINGER INTERNATIONAL PUBLISHING AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 1869-6716
EI 1613-9860
J9 TRANSL BEHAV MED
JI Transl. Behav. Med.
PD DEC
PY 2015
VL 5
IS 4
BP 470
EP 482
DI 10.1007/s13142-015-0315-2
PG 13
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA DC0LV
UT WOS:000368909700011
PM 26622919
ER

PT J
AU Riddle, M
AF Riddle, Melissa
CA Sci Behav Change Working Grp
TI News from the NIH: using an experimental medicine approach to facilitate
   translational research
SO TRANSLATIONAL BEHAVIORAL MEDICINE
LA English
DT News Item
C1 [Riddle, Melissa; Sci Behav Change Working Grp] NIH, Bldg 10, Bethesda, MD 20892 USA.
RP Riddle, M (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
EM riddleme@mail.nih.gov
NR 4
TC 2
Z9 2
U1 3
U2 3
PU SPRINGER INTERNATIONAL PUBLISHING AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 1869-6716
EI 1613-9860
J9 TRANSL BEHAV MED
JI Transl. Behav. Med.
PD DEC
PY 2015
VL 5
IS 4
BP 486
EP 488
DI 10.1007/s13142-015-0333-0
PG 3
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA DC0LV
UT WOS:000368909700013
PM 26622921
ER

PT J
AU Tang, H
   Fan, XQ
   Xing, JY
   Liu, ZY
   Jiang, B
   Dou, Y
   Gorospe, M
   Wang, WG
AF Tang, Hao
   Fan, Xiuqin
   Xing, Junyue
   Liu, Zhenyun
   Jiang, Bin
   Dou, Yali
   Gorospe, Myriam
   Wang, Wengong
TI NSun2 delays replicative senescence by repressing p27 (KIP1) translation
   and elevating CDK1 translation
SO AGING-US
LA English
DT Article
DE NSun2; p27KIP1; mRNA methylation; translational regulation; replicative
   senescence
ID HUMAN-DIPLOID FIBROBLASTS; RIBOSOMAL-RNA METHYLATIONS; CYCLIN-DEPENDENT
   KINASES; P27(KIP1) MESSENGER-RNA; CELL-CYCLE; ESCHERICHIA-COLI; REDUCED
   EXPRESSION; CANCER; PROLIFERATION; INHIBITORS
AB A rise in the levels of the cyclin-dependent kinase (CDK) inhibitor p27(KIP1) is important for the growth arrest of senescent cells, but the mechanisms responsible for this increase are poorly understood. Here, we show that the tRNA methyltransferase NSun2 represses the expression of p27 in replicative senescence. NSun2 methylated the 5'-untranslated region (UTR) of p27 mRNA at cytosine C64 in vitro and in cells, thereby repressing the translation of p27. During replicative senescence, increased p27 protein levels were accompanied by decreased NSun2 protein levels. Knockdown of NSun2 in human diploid fibroblasts (HDFs) elevated p27 levels and reduced the expression of CDK1 (encoded by CDK1 mRNA, a previously reported target of NSun2), which in turn further repressed cell proliferation and accelerated replicative senescence, while overexpression of NSun2 exerted the opposite effect. Ectopic overexpression of the p27 5'UTR fragment rescued the effect of NSun2 overexpression in lowering p27, increasing CDK1, promoting cell proliferation, and delaying replicative senescence. Our findings indicate that NSun2-mediated mRNA methylation regulates p27 and CDK1 levels during replicative senescence.
C1 [Tang, Hao; Fan, Xiuqin; Xing, Junyue; Liu, Zhenyun; Jiang, Bin; Wang, Wengong] Peking Univ, Hlth Sci Ctr, Beijing Key Lab Prot Posttranslat Modificat & Cel, Dept Biochem & Mol Biol,Sch Basic Med Sci, Beijing 100191, Peoples R China.
   [Dou, Yali] Univ Michigan, Dept Pathol & Biol Chem, MSI 5215A, Ann Arbor, MI 48105 USA.
   [Gorospe, Myriam] NIA, Genet Lab, NIH, Baltimore, MD 21224 USA.
RP Wang, WG (reprint author), Peking Univ, Hlth Sci Ctr, Beijing Key Lab Prot Posttranslat Modificat & Cel, Dept Biochem & Mol Biol,Sch Basic Med Sci, Beijing 100191, Peoples R China.
EM wwg@bjmu.edu.cn
FU National Science Foundation of China [81230008, 81420108016, 91339114];
   Ministry of Education of People's Republic of China [B07001]; NIA-IRP,
   NIH
FX This work was supported by Grants 81230008, 81420108016, and 91339114
   from the National Science Foundation of China; Grant B07001 (111
   project) from the Ministry of Education of People's Republic of China.
   M.G. was supported by the NIA-IRP, NIH.
NR 42
TC 5
Z9 5
U1 0
U2 0
PU IMPACT JOURNALS LLC
PI ALBANY
PA 6211 TIPTON HOUSE, STE 6, ALBANY, NY 12203 USA
SN 1945-4589
J9 AGING-US
JI Aging-US
PD DEC
PY 2015
VL 7
IS 12
BP 1143
EP 1158
PG 16
WC Cell Biology
SC Cell Biology
GA DB5BU
UT WOS:000368528900013
PM 26687548
ER

PT J
AU Roman, TS
   Marvelle, AF
   Fogarty, MP
   Vadlamudi, S
   Gonzalez, AJ
   Buchkovich, ML
   Huyghe, JR
   Fuchsberger, C
   Jackson, AU
   Wu, Y
   Civelek, M
   Lusis, AJ
   Gaulton, KJ
   Sethupathy, P
   Kangas, AJ
   Soininen, P
   Ala-Korpela, M
   Kuusisto, J
   Collins, FS
   Laakso, M
   Boehnke, M
   Mohlke, KL
AF Roman, Tamara S.
   Marvelle, Amanda F.
   Fogarty, Marie P.
   Vadlamudi, Swarooparani
   Gonzalez, Arlene J.
   Buchkovich, Martin L.
   Huyghe, Jeroen R.
   Fuchsberger, Christian
   Jackson, Anne U.
   Wu, Ying
   Civelek, Mete
   Lusis, Aldons J.
   Gaulton, Kyle J.
   Sethupathy, Praveen
   Kangas, Antti J.
   Soininen, Pasi
   Ala-Korpela, Mika
   Kuusisto, Johanna
   Collins, Francis S.
   Laakso, Markku
   Boehnke, Michael
   Mohlke, Karen L.
TI Multiple Hepatic Regulatory Variants at the GALNT2 GWAS Locus Associated
   with High-Density Lipoprotein Cholesterol
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; POLYPEPTIDE N-ACETYLGALACTOSAMINYLTRANSFERASE;
   UPSTREAM STIMULATORY FACTOR; ALPHA-D-GALACTOSAMINE; C/EBP-BETA; LIPID
   CONCENTRATIONS; ENDOTHELIAL LIPASE; O-GLYCOSYLATION; GENOTYPE DATA; CDNA
   CLONING
AB Genome-wide association studies (GWASs) have identified more than 150 loci associated with blood lipid and cholesterol levels; however, the functional and molecular mechanisms for many associations are unknown. We examined the functional regulatory effects of candidate variants at the GALNT2 locus associated with high-density lipoprotein cholesterol (HDL-C). Fine-mapping and conditional analyses in the METSIM study identified a single locus harboring 25 noncoding variants (r(2) > 0.7 with the lead GWAS variants) strongly associated with total cholesterol in medium-sized HDL (e.g., rs17315646, p = 3.5 x 10(-12)). We used luciferase reporter assays in HepG2 cells to test all 25 variants for allelic differences in regulatory enhancer activity. rs2281721 showed allelic differences in transcriptional activity (75-fold [T] versus 27-fold [C] more than the empty-vector control), as did a separate 780-bp segment containing rs4846913, rs2144300, and rs6143660 (49-fold [AT(-) haplotype] versus 16-fold [CC+ haplotype] more). Using electrophoretic mobility shift assays, we observed differential CEBPB binding to rs4846913, and we confirmed this binding in a native chromatin context by performing chromatin-immunoprecipitation (ChIP) assays in HepG2 and Huh-7 cell lines of differing genotypes. Additionally, sequence reads in HepG2 DNase-I-hypersensitivity and CEBPB ChIP-seq signals spanning rs4846913 showed significant allelic imbalance. Allelic-expression-imbalance assays performed with RNA from primary human hepatocyte samples and expression-quantitative-trait-locus (eQTL) data in human subcutaneous adipose tissue samples confirmed that alleles associated with increased HDL-C are associated with a modest increase in GALNT2 expression. Together, these data suggest that at least rs4846913 and rs2281721 play key roles in influencing GALNT2 expression at this HDL-C locus.
C1 [Roman, Tamara S.; Marvelle, Amanda F.; Fogarty, Marie P.; Vadlamudi, Swarooparani; Gonzalez, Arlene J.; Buchkovich, Martin L.; Wu, Ying; Gaulton, Kyle J.; Sethupathy, Praveen; Mohlke, Karen L.] Univ N Carolina, Dept Genet, Chapel Hill, NC 27599 USA.
   [Roman, Tamara S.] Univ N Carolina, Curriculum Genet & Mol Biol, Chapel Hill, NC 27599 USA.
   [Huyghe, Jeroen R.; Fuchsberger, Christian; Jackson, Anne U.; Boehnke, Michael] Univ Michigan, Sch Publ Hlth, Dept Biostat, Ann Arbor, MI 48109 USA.
   [Huyghe, Jeroen R.; Fuchsberger, Christian; Jackson, Anne U.; Boehnke, Michael] Univ Michigan, Sch Publ Hlth, Ctr Stat Genet, Ann Arbor, MI 48109 USA.
   [Civelek, Mete; Lusis, Aldons J.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA.
   [Civelek, Mete] Univ Virginia, Ctr Publ Hlth Genom, Dept Biomed Engn, Charlottesville, VA 22908 USA.
   [Lusis, Aldons J.] Univ Calif Los Angeles, David Geffen Sch Med, Deparment Microbiol Immunol & Mol Genet, Los Angeles, CA 90095 USA.
   [Lusis, Aldons J.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Human Genet, Los Angeles, CA 90095 USA.
   [Gaulton, Kyle J.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England.
   [Kangas, Antti J.; Soininen, Pasi; Ala-Korpela, Mika] Univ Oulu, Inst Hlth Sci, Computat Med, Oulu 90014, Finland.
   [Soininen, Pasi; Ala-Korpela, Mika] Univ Eastern Finland, Sch Pharm, Nucl Magnet Resonance Metabol Lab, Kuopio 70211, Finland.
   [Ala-Korpela, Mika] Oulu Univ Hosp, Oulu 90220, Finland.
   [Ala-Korpela, Mika] Univ Bristol, Sch Social & Community Med, Computat Med, Bristol BS8 2BN, Avon, England.
   [Ala-Korpela, Mika] Univ Bristol, MRC, Integrat Epidemiol Unit, Bristol BS8 2BN, Avon, England.
   [Kuusisto, Johanna; Laakso, Markku] Univ Eastern Finland, Dept Med, Kuopio 70210, Finland.
   [Kuusisto, Johanna; Laakso, Markku] Kuopio Univ Hosp, SF-70210 Kuopio, Finland.
   [Collins, Francis S.] NHGRI, NIH, Bethesda, MD 20892 USA.
RP Mohlke, KL (reprint author), Univ N Carolina, Dept Genet, Chapel Hill, NC 27599 USA.
EM mohlke@med.unc.edu
OI Fuchsberger, Christian/0000-0002-5918-8947; Civelek,
   Mete/0000-0002-8141-0284
FU NIH [T32HL069768, T32GM007092, R01DK072193, R21DA027040, R01DK093757,
   T32GM067553, R01DK062370, K99HL121172, P01HL28481]; National Human
   Genome Research Institute Division of Intramural Research [Z01HG000024];
   American Heart Association [13PRE16930025]; Academy of Finland [77299,
   124243]; Finnish Heart Foundation; Finnish Diabetes Foundation; Finnish
   Funding Agency for Technology and Innovation (TEKES) [1510/31/06];
   Commission of the European Community [HEALTH-F2-2007-201681]; University
   of Oulu; British Heart Foundation; Wellcome Trust; Medical Research
   Council
FX This study was supported by NIH grants T32HL069768 (T.S.R.), T32GM007092
   (T.S.R.), R01DK072193 (K.L.M.), R21DA027040 (K.L.M.), R01DK093757
   (K.L.M.), T32GM067553 (M.L.B), R01DK062370 (M.B.), K99HL121172 (M.C.),
   and P01HL28481 (A.J.L.) and National Human Genome Research Institute
   Division of Intramural Research project number Z01HG000024 (F.S.C.);
   American Heart Association Predoctoral Fellowship 13PRE16930025
   (M.L.B.); Academy of Finland grants 77299 and 124243 (M.L.); the Finnish
   Heart Foundation (M.L.); the Finnish Diabetes Foundation (M.L.); Finnish
   Funding Agency for Technology and Innovation (TEKES) contract 1510/31/06
   (M.L.); and Commission of the European Community HEALTH-F2-2007-201681
   (M.L.). Applications and development of the quantitative-serum
   nuclear-magnetic-resonance (NMR) metabolomics platform are supported by
   the Academy of Finland, TEKES, Sigrid Juselius Foundation, Novo Nordisk
   Foundation, and Finnish Diabetes Research Foundation. A.J.K., P.S., and
   M.A.-K. are supported by the University of Oulu, British Heart
   Foundation, Wellcome Trust, and Medical Research Council. Bristol Myers
   Squibb supported the generation of METSIM microarray data. The authors
   acknowledge the GoT2D Consortium for access to the reference panel used
   for imputation; human organ donors whose liver samples were used in this
   study; the ENCODE and NIH Roadmap Epigenomics Consortia, Data Analysis
   and Coordination Centers, and production laboratories that generated the
   chromatin, histone-modification, and chromatin-immunoprecipitation
   (ChIP) sequencing data used for variant annotation. We thank Terry Furey
   and Greg Crawford for interpretating ENCODE data, Jennifer Kulzer for
   editing the manuscript, Yun Li and Qing Duan for providing 1000 Genomes
   linkage-disequilibrium data, Scott Bultman and Dallas Donohoe for
   providing advice on ChIP experiments, and Sumeet Khetarpal and Daniel
   Rader for sharing unpublished results.
NR 64
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Z9 7
U1 0
U2 5
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0002-9297
EI 1537-6605
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD DEC
PY 2015
VL 97
IS 6
BP 801
EP 815
DI 10.1016/j.ajhg.2015.10.016
PG 15
WC Genetics & Heredity
SC Genetics & Heredity
GA DB3UM
UT WOS:000368437900003
PM 26637976
ER

PT J
AU O'Rawe, JA
   Wu, YY
   Dorfel, MJ
   Rope, AF
   Au, PYB
   Parboosingh, JS
   Moon, S
   Kousi, M
   Kosma, K
   Smith, CS
   Tzetis, M
   Schuette, JL
   Hufnagel, RB
   Prada, CE
   Martinez, F
   Orellana, C
   Crain, J
   Caro-Llopis, A
   Oltra, S
   Monfort, S
   Jimenez-Barron, LT
   Swensen, J
   Ellingwood, S
   Smith, R
   Fang, H
   Ospina, S
   Stegmann, S
   Den Hollander, N
   Mittelman, D
   Highnam, G
   Robison, R
   Yang, E
   Faivre, L
   Roubertie, A
   Riviere, JB
   Monaghan, KG
   Wang, K
   Davis, EE
   Katsanis, N
   Kalscheuer, VM
   Wang, EH
   Metcalfe, K
   Kleefstra, T
   Innes, AM
   Kitsiou-Tzeli, S
   Rosello, M
   Keegan, CE
   Lyon, GJ
AF O'Rawe, Jason A.
   Wu, Yiyang
   Doerfel, Max J.
   Rope, Alan F.
   Au, P. Y. Billie
   Parboosingh, Jillian S.
   Moon, Sungjin
   Kousi, Maria
   Kosma, Konstantina
   Smith, Christopher S.
   Tzetis, Maria
   Schuette, Jane L.
   Hufnagel, Robert B.
   Prada, Carlos E.
   Martinez, Francisco
   Orellana, Carmen
   Crain, Jonathan
   Caro-Llopis, Alfonso
   Oltra, Silvestre
   Monfort, Sandra
   Jimenez-Barron, Laura T.
   Swensen, Jeffrey
   Ellingwood, Sara
   Smith, Rosemarie
   Fang, Han
   Ospina, Sandra
   Stegmann, Sander
   Den Hollander, Nicolette
   Mittelman, David
   Highnam, Gareth
   Robison, Reid
   Yang, Edward
   Faivre, Laurence
   Roubertie, Agathe
   Riviere, Jean-Baptiste
   Monaghan, Kristin G.
   Wang, Kai
   Davis, Erica E.
   Katsanis, Nicholas
   Kalscheuer, Vera M.
   Wang, Edith H.
   Metcalfe, Kay
   Kleefstra, Tjitske
   Innes, A. Micheil
   Kitsiou-Tzeli, Sophia
   Rosello, Monica
   Keegan, Catherine E.
   Lyon, Gholson J.
TI TAF1 Variants Are Associated with Dysmorphic Features, Intellectual
   Disability, and Neurological Manifestations
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID LINKED DYSTONIA-PARKINSONISM; DE-LANGE-SYNDROME; NEURON-SPECIFIC
   ISOFORM; ACETYLTRANSFERASE ACTIVITY; TRANSCRIPTION; GENE; COMPLEX;
   EXPRESSION; CORNELIA; DISEASE
AB We describe an X-linked genetic syndrome associated with mutations in TAF1 and manifesting with global developmental delay, intellectual disability (ID), characteristic facial dysmorphology, generalized hypotonia, and variable neurologic features, all in male individuals. Simultaneous studies using diverse strategies led to the identification of nine families with overlapping clinical presentations and affected by de novo or maternally inherited single-nucleotide changes. Two additional families harboring large duplications involving TAF1 were also found to share phenotypic overlap with the probands harboring single-nucleotide changes, but they also demonstrated a severe neurodegeneration phenotype. Functional analysis with RNA-seq for one of the families suggested that the phenotype is associated with downregulation of a set of genes notably enriched with genes regulated by E-box proteins. In addition, knockdown and mutant studies of this gene in zebrafish have shown a quantifiable, albeit small, effect on a neuronal phenotype. Our results suggest that mutations in TAF1 play a critical role in the development of this X-linked ID syndrome.
C1 [O'Rawe, Jason A.; Wu, Yiyang; Doerfel, Max J.; Crain, Jonathan; Jimenez-Barron, Laura T.; Fang, Han; Lyon, Gholson J.] Cold Spring Harbor Lab, Stanley Inst Cognit Genom, POB 100, Cold Spring Harbor, NY 11724 USA.
   [O'Rawe, Jason A.; Wu, Yiyang; Lyon, Gholson J.] SUNY Stony Brook, Grad Program Genet, Stony Brook, NY 11794 USA.
   [Rope, Alan F.] Northwest Kaiser Permanente, Dept Med Genet, Portland, OR 97227 USA.
   [Au, P. Y. Billie; Parboosingh, Jillian S.; Smith, Christopher S.; Innes, A. Micheil] Univ Calgary, Dept Med Genet, Calgary, AB T3B 6A8, Canada.
   [Au, P. Y. Billie; Parboosingh, Jillian S.; Smith, Christopher S.; Innes, A. Micheil] Univ Calgary, Alberta Childrens Hosp, Res Inst, Cumming Sch Med, Calgary, AB T3B 6A8, Canada.
   [Moon, Sungjin; Kousi, Maria; Davis, Erica E.; Katsanis, Nicholas] Duke Univ, Ctr Human Dis Modeling, Durham, NC 27708 USA.
   [Kosma, Konstantina; Tzetis, Maria; Kitsiou-Tzeli, Sophia] Univ Athens, Sch Med, Dept Med Genet, Athens 11527, Greece.
   [Kosma, Konstantina; Tzetis, Maria] Childrens Hosp, Res Inst Study Genet & Malignant Disorders Childh, Aghia Sophia, Athens 11527, Greece.
   [Schuette, Jane L.] Univ Michigan, Dept Pediat, Div Genet, Ann Arbor, MI 48109 USA.
   [Schuette, Jane L.; Keegan, Catherine E.] Univ Michigan, Dept Human Genet, Ann Arbor, MI 48109 USA.
   [Hufnagel, Robert B.; Prada, Carlos E.] Cincinnati Childrens Hosp, Div Human Genet, Cincinnati, OH 45229 USA.
   [Hufnagel, Robert B.] NEI, Unit Pediat Dev & Genet Ophthalmol, Ophthalm Genet & Visual Funct Branch, NIH, Bethesda, MD 20892 USA.
   [Prada, Carlos E.] Fdn Cardiovasc Colombia, Ctr Med Genom & Metab, Santander 681004, Colombia.
   [Martinez, Francisco; Orellana, Carmen; Caro-Llopis, Alfonso; Oltra, Silvestre; Monfort, Sandra; Rosello, Monica] Hosp Univ & Politecn La Fe, Unidad Genet, Valencia 46026, Spain.
   [Jimenez-Barron, Laura T.] Univ Nacl Autonoma Mexico, Ctr Ciencias Genom, Cuernavaca 62210, Morelos, Mexico.
   [Swensen, Jeffrey] Caris Life Sci, Phoenix, AZ 85040 USA.
   [Ellingwood, Sara] Maine Med Partners, Pediat Specialty Care, Div Genet, Portland, ME 04102 USA.
   [Smith, Rosemarie] Barbara Bush Childrens Hosp, Maine Med Ctr, Dept Pediat, Div Genet, Portland, ME 04102 USA.
   [Ospina, Sandra] Fdn Cardioinfantil, Bogota 681004, Colombia.
   [Ospina, Sandra] Univ Rosario, Bogota 681004, Colombia.
   [Stegmann, Sander] Dept Clin Genet, NL-6202 AZ Maastricht, Netherlands.
   [Den Hollander, Nicolette] Leiden Univ, Med Ctr, Dept Clin Genet, NL-2300 RC Leiden, Netherlands.
   [Mittelman, David; Highnam, Gareth] Gene Gene Ltd, Houston, TX 77008 USA.
   [Robison, Reid; Lyon, Gholson J.] Utah Fdn Biomed Res, Salt Lake City, UT 84107 USA.
   [Robison, Reid] Tute Genom, Provo, UT 84601 USA.
   [Yang, Edward] Boston Childrens Hosp, Dept Radiol, Boston, MA 02115 USA.
   [Faivre, Laurence; Riviere, Jean-Baptiste] Univ Bourgogne Franche Comte, Genet Anomalies Dev EA4271, F-21000 Dijon, France.
   [Faivre, Laurence] CHU Dijon, Ctr Reference Malad Rares Anomalies Dev & Syndrom, Ctr Genet, F-21000 Dijon, France.
   [Roubertie, Agathe] Univ Montpellier, Inst Neurosci Montpellier, F-34950 Montpellier 5, France.
   [Roubertie, Agathe] CHU Gui de Chauliac, Serv Neuropediat, F-34000 Montpellier, France.
   [Monaghan, Kristin G.] GeneDx, Gaithersburg, MD 20877 USA.
   [Wang, Kai] Univ So Calif, Zilkha Neurogenet Inst, Dept Psychiat & Prevent Med, Los Angeles, CA 90089 USA.
   [Kalscheuer, Vera M.] Max Planck Inst Mol Genet, Res Grp Dev & Dis, D-14195 Berlin, Germany.
   [Wang, Edith H.] Univ Washington, Dept Pharmacol, Seattle, WA 98195 USA.
   [Metcalfe, Kay] Cent Manchester Univ Hosp NHS Fdn Trust, St Marys Hosp, Manchester Ctr Genom Med, Clin Genet Serv, Manchester M13 9WL, Lancs, England.
   [Kleefstra, Tjitske] Radboud Univ Nijmegen, Med Ctr, Dept Human Genet, NL-6500 HB Nijmegen, Netherlands.
RP Lyon, GJ (reprint author), Cold Spring Harbor Lab, Stanley Inst Cognit Genom, POB 100, Cold Spring Harbor, NY 11724 USA.
EM gholsonjlyon@gmail.com
RI Oltra, Silvestre/A-2697-2009; innes, allan micheil/A-9955-2017;
   Martinez, Francisco/A-2543-2009
OI Oltra, Silvestre/0000-0001-6863-4382; Martinez,
   Francisco/0000-0002-0589-2584
FU Stanley Institute for Cognitive Genomics at Cold Spring Harbor
   Laboratory; NIH [HG006465]; Alberta Children's Hospital Foundation;
   Instituto de Salud Carlos III Accion Estrategica en Salud [PI14/00350];
   Netherlands Organization for Health Research and Development, ZonMw
   [907-00-365]; Cincinnati Children's Hospital
FX G.J.L. is supported by funds from the Stanley Institute for Cognitive
   Genomics at Cold Spring Harbor Laboratory. K.W. is supported by NIH
   grant HG006465. The sequencing by Complete Genomics was provided by a
   data-analysis grant to K.W. We would like to thank Megan Cho for
   facilitating discovery of affected individuals through GeneDx. Margaret
   Yoon and David Tegay assisted with Human Phenotype Ontology annotation.
   A.M.I. and J.S.P. were supported by a grant from the Alberta Children's
   Hospital Foundation and would like to thank Francois Bernier and Ryan
   Lamont for helpful discussions and contributions. F.M., M.R., and
   colleagues are supported by grant PI14/00350 (Instituto de Salud Carlos
   III Accion Estrategica en Salud 2013-2016; Fondo Europeo de Desarrollo
   Regional). This work was supported in part by funding from grants from
   the Netherlands Organization for Health Research and Development, ZonMw
   (grant 907-00-365 to T.K.), and an institutional award from Cincinnati
   Children's Hospital (R.B.H.). N.K. is a distinguished George W. Brumley
   Professor. The authors would like to thank the Exome Aggregation
   Consortium and the groups that provided exome variant data for
   comparison. A full list of contributing groups can be found at
   http://exac.broadinstitute.org/about.
NR 56
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Z9 7
U1 1
U2 7
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0002-9297
EI 1537-6605
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD DEC
PY 2015
VL 97
IS 6
BP 922
EP 932
DI 10.1016/j.ajhg.2015.11.005
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA DB3UM
UT WOS:000368437900015
PM 26637982
ER

PT J
AU Corren, J
   Togias, A
AF Corren, Jonathan
   Togias, Alkis
TI Remodeling in Allergic Rhinitis Adding New Data to an Old Debate
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Editorial Material
ID ASTHMA; AIRWAYS
C1 [Corren, Jonathan] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA.
   [Togias, Alkis] NIAID, Div Allergy Immunol & Transplantat, Bethesda, MD 20892 USA.
RP Corren, J (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA.
NR 13
TC 0
Z9 0
U1 1
U2 1
PU AMER THORACIC SOC
PI NEW YORK
PA 25 BROADWAY, 18 FL, NEW YORK, NY 10004 USA
SN 1073-449X
EI 1535-4970
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD DEC
PY 2015
VL 192
IS 12
BP 1403
EP 1404
PG 2
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA DB3RT
UT WOS:000368429700002
PM 26669466
ER

PT J
AU Lam, S
   Szabo, E
AF Lam, Stephen
   Szabo, Eva
TI Preinvasive Endobronchial Lesions: Lung Cancer Precursors and Risk
   Markers?
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Editorial Material
ID AUTOFLUORESCENCE BRONCHOSCOPY; BRONCHIAL EPITHELIUM; DYSPLASIA;
   CARCINOMA; SMOKERS
C1 [Lam, Stephen] British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada.
   Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
   NCI, NIH, Rockville, MD USA.
RP Lam, S (reprint author), British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada.
NR 20
TC 3
Z9 3
U1 0
U2 0
PU AMER THORACIC SOC
PI NEW YORK
PA 25 BROADWAY, 18 FL, NEW YORK, NY 10004 USA
SN 1073-449X
EI 1535-4970
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD DEC
PY 2015
VL 192
IS 12
BP 1411
EP 1413
PG 4
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA DB3RT
UT WOS:000368429700007
PM 26669471
ER

PT J
AU Boyer, PL
   Das, K
   Arnold, E
   Hughes, SH
AF Boyer, Paul L.
   Das, Kalyan
   Arnold, Eddy
   Hughes, Stephen H.
TI Analysis of the Zidovudine Resistance Mutations T215Y, M41L, and L210W
   in HIV-1 Reverse Transcriptase
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; HIGH-LEVEL RESISTANCE; DRUG-RESISTANCE;
   T-LYMPHOCYTES; MOLECULAR-MECHANISMS; SELECTIVE EXCISION; AZT RESISTANCE;
   DE-NOVO; INHIBITORS; ASSOCIATION
AB Although anti-human immunodeficiency virus type 1 (HIV-1) therapies have become more sophisticated and more effective, drug resistance continues to be a major problem. Zidovudine (azidothymidine; AZT) was the first nucleoside reverse transcriptase (RT) inhibitor (NRTI) approved for the treatment of HIV-1 infections and is still being used, particularly in the developing world. This drug targets the conversion of single-stranded RNA to double-stranded DNA by HIV-1 RT. However, resistance to the drug quickly appeared both in viruses replicating in cells in culture and in patients undergoing AZT monotherapy. The primary resistance pathway selects for mutations of T215 that change the threonine to either a tyrosine or a phenylalanine (T215Y/F); this resistance pathway involves an ATP-dependent excision mechanism. The pseudo-sugar ring of AZT lacks a 3' OH; RT incorporates AZT monophosphate (AZTMP), which blocks the end of the viral DNA primer. AZT-resistant forms of HIV-1 RT use ATP in an excision reaction to unblock the 3' end of the primer strand, allowing its extension by RT. The T215Y AZT resistance mutation is often accompanied by two other mutations, M41L and L210W. In this study, the roles of these mutations, in combination with T215Y, were examined to determine whether they affect polymerization and excision by HIV-1 RT. The M41L mutation appears to help restore the DNA polymerization activity of RT containing the T215Y mutation and also enhances AZTMP excision. The L210W mutation plays a similar role, but it enhances excision by RTs that carry the T215Y mutation when ATP is present at a low concentration.
C1 [Boyer, Paul L.; Hughes, Stephen H.] NCI, HIV Dynam & Replicat Program, NIH, Frederick, MD 21701 USA.
   [Das, Kalyan; Arnold, Eddy] Rutgers State Univ, Ctr Adv Biotechnol & Med, Piscataway, NJ 08854 USA.
   [Das, Kalyan; Arnold, Eddy] Rutgers State Univ, Dept Chem & Chem Biol, Piscataway, NJ USA.
RP Hughes, SH (reprint author), NCI, HIV Dynam & Replicat Program, NIH, Frederick, MD 21701 USA.
EM hughesst@mail.nih.gov
FU Intramural Research Program of the NIH, NCI-Frederick; NIH [R37
   AI027690]
FX This research was supported by the Intramural Research Program of the
   NIH, NCI-Frederick. E.A. is grateful to NIH merit award R37 AI027690 for
   support.
NR 34
TC 1
Z9 1
U1 0
U2 10
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
EI 1098-6596
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD DEC
PY 2015
VL 59
IS 12
BP 7184
EP 7196
DI 10.1128/AAC.05069-14
PG 13
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA DB2KO
UT WOS:000368337300004
PM 26324274
ER

PT J
AU Levendosky, K
   Mizenina, O
   Martinelli, E
   Jean-Pierre, N
   Kizima, L
   Rodriguez, A
   Kleinbeck, K
   Bonnaire, T
   Robbiani, M
   Zydowsky, TM
   O'Keefe, BR
   Fernandez-Romero, JA
AF Levendosky, Keith
   Mizenina, Olga
   Martinelli, Elena
   Jean-Pierre, Ninochka
   Kizima, Larisa
   Rodriguez, Aixa
   Kleinbeck, Kyle
   Bonnaire, Thierry
   Robbiani, Melissa
   Zydowsky, Thomas M.
   O'Keefe, Barry R.
   Fernandez-Romero, Jose A.
TI Griffithsin and Carrageenan Combination To Target Herpes Simplex Virus 2
   and Human Papillomavirus
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID ENTRY INHIBITOR GRIFFITHSIN; TO-CELL SPREAD; GLYCOPROTEIN-D; IN-VITRO;
   VAGINAL MICROBICIDE; SOUTH-AFRICA; INFECTION; RECEPTOR; VIVO;
   IDENTIFICATION
AB Extensive preclinical evaluation of griffithsin (GRFT) has identified this lectin to be a promising broad-spectrum microbicide. We set out to explore the antiviral properties of a GRFT and carrageenan (CG) combination product against herpes simplex virus 2 (HSV-2) and human papillomavirus (HPV) as well as determine the mechanism of action (MOA) of GRFT against both viruses. We performed the experiments in different cell lines, using time-of-addition and temperature dependence experiments to differentiate inhibition of viral attachment from entry and viral receptor internalization. Surface plasmon resonance (SPR) was used to assess GRFT binding to viral glycoproteins, and immunoprecipitation and immunohistochemistry were used to identify the specific glycoprotein involved. We determined the antiviral activity of GRFT against HSV-2 to be a 50% effective concentration (EC50) of 230 nM and provide the first evidence that GRFT has moderate anti-HPV activity (EC50 = 0.429 to 1.39 mu M). GRFT blocks the entry of HSV-2 and HPV into target cells but not the adsorption of HSV-2 and HPV onto target cells. The results of the SPR, immunoprecipitation, and immunohistochemistry analyses of HSV-2 combined suggest that GRFT may block viral entry by binding to HSV-2 glycoprotein D. Cell-based assays suggest anti-HPV activity through alpha(6) integrin internalization. The GRFT-CG combination product but not GRFT or CG alone reduced HSV-2 vaginal infection in mice when given an hour before challenge (P = 0.0352). While GRFT significantly protected mice against vaginal HPV infection when dosed during and after HPV16 pseudovirus challenge (P < 0.026), greater CG-mediated protection was afforded by the GRFT-CG combination for up to 8 h (P < 0.0022). These findings support the development of the GRFT-CG combination as a broad-spectrum microbicide.
C1 [Levendosky, Keith; Mizenina, Olga; Martinelli, Elena; Jean-Pierre, Ninochka; Kizima, Larisa; Rodriguez, Aixa; Kleinbeck, Kyle; Bonnaire, Thierry; Robbiani, Melissa; Zydowsky, Thomas M.; Fernandez-Romero, Jose A.] Populat Council, Ctr Biomed Res, New York, NY 10021 USA.
   [O'Keefe, Barry R.] NCI, Mol Targets Lab, Ctr Canc Res, Frederick, MD 21701 USA.
RP Fernandez-Romero, JA (reprint author), Populat Council, Ctr Biomed Res, 1230 York Ave, New York, NY 10021 USA.
EM jromero@popcouncil.org
FU U.S. Agency for International Development (USAID) [GPO A 00 04 00019
   00]; NIH, National Cancer Institute, Center for Cancer Research
FX This research has been supported by the President's Emergency Plan for
   AIDS Relief (PEPFAR) through the U.S. Agency for International
   Development (USAID) under the terms of GPO A 00 04 00019 00. This
   research was also supported by the Intramural Research Program of the
   NIH, National Cancer Institute, Center for Cancer Research (to B.R.O.).
NR 46
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Z9 4
U1 3
U2 6
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
EI 1098-6596
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD DEC
PY 2015
VL 59
IS 12
BP 7290
EP 7298
DI 10.1128/AAC.01816-15
PG 9
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA DB2KO
UT WOS:000368337300016
PM 26369967
ER

PT J
AU Yaniv, Y
   Lakatta, EG
AF Yaniv, Yael
   Lakatta, Edward G.
TI The end effector of circadian heart rate variation: the sinoatrial node
   pacemaker cell
SO BMB REPORTS
LA English
DT Review
DE Cardiac denervation; Coupled-clock pacemaker system; Fractal-like
   behavior; Heart rate variability; Ultradian rhythm of the heart rate
ID CARDIOMYOCYTE MOLECULAR CLOCK; POWER-LAW BEHAVIOR; RATE-VARIABILITY;
   SUPRACHIASMATIC NUCLEUS; ARRHYTHMIA SUSCEPTIBILITY;
   CARDIOVASCULAR-DISEASE; BLOOD-PRESSURE; RHYTHMS; MODULATION; MECHANISMS
AB Cardiovascular function is regulated by the rhythmicity of circadian, infradian and ultradian clocks. Specific time scales of different cell types drive their functions: circadian gene regulation at hours scale, activation-inactivation cycles of ion channels at millisecond scales, the heart's beating rate at hundreds of millisecond scales, and low frequency autonomic signaling at cycles of tens of seconds. Heart rate and rhythm are modulated by a hierarchical clock system: autonomic signaling from the brain releases neurotransmitters from the vagus and sympathetic nerves to the heart's pacemaker cells and activate receptors on the cell. These receptors activating ultradian clock functions embedded within pacemaker cells include sarcoplasmic reticulum rhythmic spontaneous Ca2+ cycling, rhythmic ion channel current activation and inactivation, and rhythmic oscillatory mitochondria ATP production. Here we summarize the evidence that intrinsic pacemaker cell mechanisms are the end effector of the hierarchical brain-heart circadian clock system.
C1 [Yaniv, Yael] Technion Israel Inst Technol, Biomed Engn Fac, Haifa, Israel.
   [Lakatta, Edward G.] NIA, Cardiovasc Sci Lab, Biomed Res Ctr, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
RP Yaniv, Y (reprint author), Technion Israel Inst Technol, Biomed Engn Fac, Haifa, Israel.
EM yaely@bm.technion.ac.il; lakattae@grc.nia.nih.gov
FU Intramural Research Program of the NIH, National Institute on Aging;
   Technion V.P.R Fund-Krbling Biomedical Engineering Research Fund
FX This research was partially supported by the Intramural Research Program
   of the NIH, National Institute on Aging and by Technion V.P.R
   Fund-Krbling Biomedical Engineering Research Fund (Y.Y).
NR 69
TC 2
Z9 2
U1 7
U2 14
PU KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
PI SEOUL
PA KOREA SCIENCE & TECHNOLOGY CENTER, # 801,  635-4 , YEOKSAM-DONG,
   KANGNAM-KU, SEOUL, 135-703, SOUTH KOREA
SN 1976-6696
EI 1976-670X
J9 BMB REP
JI BMB Rep.
PD DEC
PY 2015
VL 48
IS 12
BP 677
EP 684
DI 10.5483/BMBRep.2015.48.12.061
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA DB4VE
UT WOS:000368510900006
PM 25999176
ER

PT J
AU Fox, A
   Jeffrey, B
   Hasni, S
   Nussenblatt, R
   Sen, HN
AF Fox, Austin
   Jeffrey, Brett
   Hasni, Sarfaraz
   Nussenblatt, Robert
   Sen, H. Nida
TI Rituximab treatment for nonparaneoplastic autoimmune retinopathy
SO CANADIAN JOURNAL OF OPHTHALMOLOGY-JOURNAL CANADIEN D OPHTALMOLOGIE
LA English
DT Letter
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; RETINAL VASCULITIS; EFFICACY; SAFETY
C1 [Fox, Austin; Jeffrey, Brett; Nussenblatt, Robert; Sen, H. Nida] NEI, NIH, Bethesda, MD 20892 USA.
   [Hasni, Sarfaraz; Nussenblatt, Robert; Sen, H. Nida] NIAMSD, NIH, Bethesda, MD 20892 USA.
RP Sen, HN (reprint author), NEI, NIH, Bethesda, MD 20892 USA.
EM senh@nei.nih.gov
FU Howard Hughes Medical Institute; Intramural NIH HHS
NR 14
TC 1
Z9 1
U1 0
U2 0
PU CANADIAN OPHTHAL SOC
PI OTTAWA
PA 1525 CARLING AVE SUITE 610, OTTAWA, ONTARIO K1Z 8R9, CANADA
SN 0008-4182
EI 1715-3360
J9 CAN J OPHTHALMOL
JI Can. J. Opthalmol.-J. Can. Opthalmol.
PD DEC
PY 2015
VL 50
IS 6
BP E101
EP E104
DI 10.1016/j.jcjo.2015.08.009
PG 4
WC Ophthalmology
SC Ophthalmology
GA DB2RA
UT WOS:000368355500001
PM 26651312
ER

PT J
AU Sotillo, E
   Barrett, DM
   Black, KL
   Bagashev, A
   Oldridge, D
   Wu, G
   Sussman, R
   Lanauze, C
   Ruella, M
   Gazzara, MR
   Martinez, NM
   Harrington, CT
   Chung, EY
   Perazzelli, J
   Hofmann, TJ
   Maude, SL
   Raman, P
   Barrera, A
   Gill, S
   Lacey, SF
   Melenhorst, JJ
   Allman, D
   Jacoby, E
   Fry, T
   Mackall, C
   Barash, Y
   Lynch, KW
   Maris, JM
   Grupp, SA
   Thomas-Tikhonenko, A
AF Sotillo, Elena
   Barrett, David M.
   Black, Kathryn L.
   Bagashev, Asen
   Oldridge, Derek
   Wu, Glendon
   Sussman, Robyn
   Lanauze, Claudia
   Ruella, Marco
   Gazzara, Matthew R.
   Martinez, Nicole M.
   Harrington, Colleen T.
   Chung, Elaine Y.
   Perazzelli, Jessica
   Hofmann, Ted J.
   Maude, Shannon L.
   Raman, Pichai
   Barrera, Alejandro
   Gill, Saar
   Lacey, Simon F.
   Melenhorst, Jan J.
   Allman, David
   Jacoby, Elad
   Fry, Terry
   Mackall, Crystal
   Barash, Yoseph
   Lynch, Kristen W.
   Maris, John M.
   Grupp, Stephan A.
   Thomas-Tikhonenko, Andrei
TI Convergence of Acquired Mutations and Alternative Splicing of CD19
   Enables Resistance to CART-19 Immunotherapy
SO CANCER DISCOVERY
LA English
DT Article
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; B-CELL DEVELOPMENT; PRE-MESSENGER-RNA;
   MODIFIED T-CELLS; MYC; CHROMATIN; PROTEINS; PATHWAY; BINDING; WEB
AB The CD19 antigen, expressed on most B-cell acute lymphoblastic leukemias (B-ALL), can be targeted with chimeric antigen receptor-armed T cells (CART-19), but relapses with epitope loss occur in 10% to 20% of pediatric responders. We detected hemizygous deletions spanning the CD19 locus and de novo frameshift and missense mutations in exon 2 of CD19 in some relapse samples. However, we also discovered alternatively spliced CD19 mRNA species, including one lacking exon 2. Pull-down/siRNA experiments identified SRSF3 as a splicing factor involved in exon 2 retention, and its levels were lower in relapsed B-ALL. Using genome editing, we demonstrated that exon 2 skipping bypasses exon 2 mutations in B-ALL cells and allows expression of the N-terminally truncated CD19 variant, which fails to trigger killing by CART-19 but partly rescues defects associated with CD19 loss. Thus, this mechanism of resistance is based on a combination of deleterious mutations and ensuing selection for alternatively spliced RNA isoforms.
   SIGNIFICANCE: CART-19 yield 70% response rates in patients with B-ALL, but also produce escape variants. We discovered that the underlying mechanism is the selection for preexisting alternatively spliced CD19 isoforms with the compromised CART-19 epitope. This mechanism suggests a possibility of targeting alternative CD19 ectodomains, which could improve survival of patients with B-cell neoplasms. (C) 2015 AACR.
C1 [Sotillo, Elena; Black, Kathryn L.; Bagashev, Asen; Wu, Glendon; Lanauze, Claudia; Harrington, Colleen T.; Chung, Elaine Y.; Raman, Pichai; Thomas-Tikhonenko, Andrei] Childrens Hosp Philadelphia, Div Canc Pathobiol, Philadelphia, PA 19104 USA.
   [Barrett, David M.; Oldridge, Derek; Sussman, Robyn; Perazzelli, Jessica; Hofmann, Ted J.; Maude, Shannon L.; Raman, Pichai; Maris, John M.; Grupp, Stephan A.] Childrens Hosp Philadelphia, Div Oncol, Philadelphia, PA 19104 USA.
   [Wu, Glendon; Thomas-Tikhonenko, Andrei] Univ Penn, Perelman Sch Med, Immunol Grad Grp, Philadelphia, PA 19104 USA.
   [Lanauze, Claudia; Harrington, Colleen T.; Thomas-Tikhonenko, Andrei] Univ Penn, Perelman Sch Med, Cell & Mol Biol Grad Grp, Philadelphia, PA 19104 USA.
   [Ruella, Marco; Gill, Saar] Univ Penn, Perelman Sch Med, Ctr Cellular Immunotherapies, Philadelphia, PA 19104 USA.
   [Gazzara, Matthew R.; Barrera, Alejandro; Barash, Yoseph] Univ Penn, Perelman Sch Med, Dept Genet, Philadelphia, PA 19104 USA.
   [Gazzara, Matthew R.; Martinez, Nicole M.; Lynch, Kristen W.] Univ Penn, Perelman Sch Med, Dept Biochem & Biophys, Philadelphia, PA 19104 USA.
   [Gill, Saar; Lacey, Simon F.; Melenhorst, Jan J.] Univ Penn, Perelman Sch Med, Dept Med, Philadelphia, PA 19104 USA.
   [Allman, David; Thomas-Tikhonenko, Andrei] Univ Penn, Perelman Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
   [Jacoby, Elad; Fry, Terry; Mackall, Crystal] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
RP Thomas-Tikhonenko, A (reprint author), Univ Penn, Childrens Hosp Philadelphia, 4056 Colket Translat Res Bldg,3501 Civ Ctr Blvd, Philadelphia, PA 19104 USA.
EM andreit@mail.med.upenn.edu
RI Thomas-Tikhonenko, Andrei/E-5329-2011
OI Thomas-Tikhonenko, Andrei/0000-0002-2739-2206
FU V Foundation for Cancer Research; William Lawrence and Blanche Hughes
   Foundation; Leukemia & Lymphoma Society; Alex's Lemonade Stand
   Foundation; NIH [R01 CA102709, T32 GM007229, T32 HL007439]; Stand Up To
   Cancer St. Baldrick's Pediatric Dream Team Translational Research Grant
   [SU2C-AACR-DT1113]
FX This work was supported by the V Foundation for Cancer Research, the
   William Lawrence and Blanche Hughes Foundation, the Leukemia & Lymphoma
   Society, the Alex's Lemonade Stand Foundation, the NIH (grants R01
   CA102709, T32 GM007229 "Training Program in Cell and Molecular Biology,"
   and T32 HL007439 "Hematology Clinical Research Training Program"), and
   Stand Up To Cancer St. Baldrick's Pediatric Dream Team Translational
   Research Grant SU2C-AACR-DT1113. Stand Up To Cancer is a program of the
   Entertainment Industry Foundation administered by the American
   Association for Cancer Research.
NR 49
TC 45
Z9 46
U1 2
U2 15
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
EI 2159-8290
J9 CANCER DISCOV
JI Cancer Discov.
PD DEC
PY 2015
VL 5
IS 12
BP 1282
EP 1295
DI 10.1158/2159-8290.CD-15-1020
PG 14
WC Oncology
SC Oncology
GA DB5TW
UT WOS:000368577500024
PM 26516065
ER

PT J
AU Joe, AK
   Schnoll-Sussman, F
   Bresalier, RS
   Abrams, JA
   Hibshoosh, H
   Cheung, K
   Friedman, RA
   Yang, CS
   Milne, GL
   Liu, DD
   Lee, JJ
   Abdul, K
   Bigg, M
   Foreman, J
   Su, T
   Wang, XM
   Ahmed, A
   Neugut, AI
   Akpa, E
   Lippman, SM
   Perloff, M
   Brown, PH
   Lightdale, CJ
AF Joe, Andrew K.
   Schnoll-Sussman, Felice
   Bresalier, Robert S.
   Abrams, Julian A.
   Hibshoosh, Hanina
   Cheung, Ken
   Friedman, Richard A.
   Yang, Chung S.
   Milne, Ginger L.
   Liu, Diane D.
   Lee, J. Jack
   Abdul, Kazeem
   Bigg, Michelle
   Foreman, Jessica
   Su, Tao
   Wang, Xiaomei
   Ahmed, Aqeel
   Neugut, Alfred I.
   Akpa, Esther
   Lippman, Scott M.
   Perloff, Marjorie
   Brown, Powel H.
   Lightdale, Charles J.
TI Phase Ib Randomized, Double-Blinded, Placebo-Controlled, Dose Escalation
   Study of Polyphenon E in Patients with Barrett's Esophagus
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID MAJOR URINARY METABOLITE; GREEN TEA EXTRACTS; INTRAEPITHELIAL NEOPLASIA;
   CONTROLLED TRIAL; PROSTATE-CANCER; BREAST-CANCER; PGE-M; PROSTAGLANDIN;
   PHARMACOKINETICS; CARCINOGENESIS
AB This study was conducted to determine the safety and efficacy of the green tea-derived Polyphenon E (Poly E) in patients with Barrett's Esophagus (BE). Subjects were randomized to a 6-month, twice daily (BID) oral treatment of placebo or Poly E (200, 400, or 600 mg). Endoscopic evaluation, including biopsies, was performed before and after treatment. The primary objective was to demonstrate safety; secondary objectives investigated catechin accumulation and effects in clinical specimens. Of the 44 enrolled subjects, 11 received placebo, and 33 received Poly E. No dose-limiting toxicities were encountered, and a maximum tolerated dose (MTD) was not reached. The recommended phase II dose was 600 mg twice daily. The most common treatment-related adverse events (AE) in Poly E-treated subjects were grade I and II nausea, grade I belching, and grade I lactate dehydrogenase (LDH) elevation. No treatment-related AEs were reported in placebo-treated subjects, aside from grade I laboratory abnormalities. Pill counts and subject diaries were not consistently collected, and compliance was difficult to determine. However, on the basis of an intention-to-treat analysis, there was a significant relationship between Poly E dose and esophageal EGCG level-mean changes (pmol/g) of 0.79 (placebo), 6.06 (200 mg), 35.67 (400 mg), and 34.95 (600 mg); P = 0.005. There was a possible relationship between Poly E dose and urine PGE-M concentration. In conclusion, Poly E was well-tolerated, and treatment with Poly E (400 and 600 mg) but not Poly E (200 mg) or placebo resulted in clinically relevant and detectable EGCG accumulation in the target organ, esophageal mucosa. (C) 2015 AACR.
C1 [Joe, Andrew K.; Abrams, Julian A.; Neugut, Alfred I.; Lightdale, Charles J.] Columbia Univ, Med Ctr, Dept Med, New York, NY 10032 USA.
   [Schnoll-Sussman, Felice; Bigg, Michelle] Weill Cornell Med Ctr, Dept Med, New York, NY USA.
   [Bresalier, Robert S.; Foreman, Jessica] Univ Texas MD Anderson Canc Ctr, Gastroenterol Hepatol & Nutr, Houston, TX 77030 USA.
   [Hibshoosh, Hanina] Columbia Univ, Med Ctr, Dept Pathol & Cell Biol, New York, NY 10032 USA.
   [Cheung, Ken; Friedman, Richard A.; Abdul, Kazeem; Su, Tao; Wang, Xiaomei; Ahmed, Aqeel] Columbia Univ, Med Ctr, Herbert Irving Comprehens Canc Ctr, New York, NY 10032 USA.
   [Yang, Chung S.] Rutgers State Univ, Dept Chem Biol, Piscataway, NJ USA.
   [Milne, Ginger L.] Vanderbilt Univ, Div Clin Pharmacol, Brentwood, TN USA.
   [Liu, Diane D.; Lee, J. Jack] Univ Texas MD Anderson Canc Ctr, Dept Biostat, Houston, TX 77030 USA.
   [Akpa, Esther; Brown, Powel H.] Univ Texas MD Anderson Canc Ctr, Dept Clin Canc Prevent, Houston, TX 77030 USA.
   [Lippman, Scott M.] Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA.
   [Perloff, Marjorie] NCI, Canc Prevent Div, Rockville, MD USA.
RP Joe, AK (reprint author), Columbia Univ, Coll Phys & Surg, Dept Med, 177 Ft Washington Ave, New York, NY 10032 USA.
EM akj3@cumc.columbia.edu
RI Milne, Ginger/D-7648-2014
OI Milne, Ginger/0000-0003-3890-151X
FU National Cancer Institute Division of Cancer Prevention NCI, DCP
   Contract [N01 CN 035159]
FX This trial was supported by the National Cancer Institute Division of
   Cancer Prevention NCI, DCP Contract N01 CN 035159 to the UTMD Anderson
   Early Phase Chemoprevention Consortium.
NR 27
TC 4
Z9 4
U1 1
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
EI 1940-6215
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD DEC
PY 2015
VL 8
IS 12
BP 1131
EP 1137
DI 10.1158/1940-6207.CAPR-14-0274-T
PG 7
WC Oncology
SC Oncology
GA DB5BS
UT WOS:000368528700001
PM 26471236
ER

PT J
AU Fabian, CJ
   Kimler, BF
   Zalles, CM
   Phillips, TA
   Metheny, T
   Petroff, BK
   Havighurst, TC
   Kim, K
   Bailey, HH
   Heckman-Stoddard, BM
AF Fabian, Carol J.
   Kimler, Bruce F.
   Zalles, Carola M.
   Phillips, Teresa A.
   Metheny, Trina
   Petroff, Brian K.
   Havighurst, Thomas C.
   Kim, KyungMann
   Bailey, Howard H.
   Heckman-Stoddard, Brandy M.
TI Clinical Trial of Acolbifene in Premenopausal Women at High Risk for
   Breast Cancer
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID ESTROGEN-RECEPTOR MODULATORS; FINE-NEEDLE-ASPIRATION; LOW-DOSE
   TAMOXIFEN; QUALITY-OF-LIFE; POSTMENOPAUSAL WOMEN; MAMMARY-GLAND;
   ANTIESTROGEN EM-800; OVARIAN CYSTS; TREATED WOMEN; PURE SERM
AB The purpose of this study was to assess the feasibility of using the selective estrogen receptor modulator (SERM) acolbifene as a breast cancer prevention agent in premenopausal women. To do so, we assessed change in proliferation in benign breast tissue sampled by randomperiareolar fine-needle aspiration (RPFNA) as a primary endpoint, along with changes in other risk biomarkers and objective and subjective side effects as secondary endpoints. Twenty-five women with cytologic hyperplasia +/- atypia and >= 2% of breast epithelial cells staining positive for Ki-67, received 20 mg acolbifene daily for 6-8months, and then had benign breast tissue and blood risk biomarkers reassessed. Ki-67 decreased from a median of 4.6% [ interquartile range (IQR), 3.1%-8.5%] at baseline to 1.4% (IQR, 0.6%-3.5%) after acolbifene (P < 0.001; Wilcoxon signed-rank test), despite increases in bioavailable estra-diol. There were also significant decreases in expression (RT-qPCR) of estrogen-inducible genes that code for pS2, ERa, and progesterone receptor (P <= 0.026). There was no significant change in serumIGF1, IGFBP3, IGF1: IGFBP3 ratio, ormammographic breast density. Subjective side effects were minimal with no significant increase in hot flashes, muscle cramps, arthralgias, or fatigue. Objective measures showed a clinically insignificant decrease in lumbar spinebone density (DEXA) and an increase in ovarian cysts but no change in endometrial thickness (sonography). In summary, acolbifene was associated with favorable changes in benign breast epithelial cell proliferation and estrogen-inducible gene expression but minimal side effects, suggesting a phase IIB placebo- controlled trial evaluating it further for breast cancer prevention. (C) 2015 AACR.
C1 [Fabian, Carol J.; Phillips, Teresa A.; Metheny, Trina; Petroff, Brian K.] Univ Kansas, Med Ctr, Dept Internal Med, Kansas City, KS 66160 USA.
   [Kimler, Bruce F.] Univ Kansas, Med Ctr, Dept Radiat Oncol, Kansas City, KS 66160 USA.
   [Zalles, Carola M.] Mercy Hosp, Miami, FL USA.
   [Havighurst, Thomas C.; Kim, KyungMann] Univ Wisconsin, Dept Biostat & Med Informat, Madison, WI USA.
   [Bailey, Howard H.] Univ Wisconsin, Carbone Canc Ctr, Madison, WI USA.
   [Heckman-Stoddard, Brandy M.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Kimler, BF (reprint author), Univ Kansas, Med Ctr, 3901 Rainbow Blvd, Kansas City, KS 66160 USA.
EM bkimler@kumc.edu
FU University of Wisconsin Cancer Consortium for "Phase I and Phase II
   Clinical Trials of Cancer Chemopreventive Agents" [938N232]; NCI, NIH
   [NO1-CN-35153]
FX This study was supported by Subcontract 938N232 from the University of
   Wisconsin Cancer Consortium for "Phase I and Phase II Clinical Trials of
   Cancer Chemopreventive Agents" (PI: H.H. Bailey, MD) and NO1-CN-35153,
   NCI, NIH.
NR 59
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
EI 1940-6215
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD DEC
PY 2015
VL 8
IS 12
BP 1146
EP 1155
DI 10.1158/1940-6207.CAPR-15-0109
PG 10
WC Oncology
SC Oncology
GA DB5BS
UT WOS:000368528700003
PM 26391916
ER

PT J
AU Petrick, JL
   Sahasrabuddhe, VV
   Chan, AT
   Alavanja, MC
   Beane-Freeman, LE
   Buring, JE
   Chen, J
   Chong, DQ
   Freedman, ND
   Fuchs, CS
   Gaziano, JM
   Giovannucci, E
   Graubard, BI
   Hollenbeck, AR
   Hou, LF
   Jacobs, EJ
   King, LY
   Koshiol, J
   Lee, IM
   Linet, MS
   Palmer, JR
   Purdue, MP
   Rosenberg, L
   Schairer, C
   Sesso, HD
   Sigurdson, AJ
   Wactawski-Wende, J
   Zeleniuch-Jacquotte, A
   Campbell, PT
   McGlynn, KA
AF Petrick, Jessica L.
   Sahasrabuddhe, Vikrant V.
   Chan, Andrew T.
   Alavanja, Michael C.
   Beane-Freeman, Laura E.
   Buring, Julie E.
   Chen, Jie
   Chong, Dawn Q.
   Freedman, Neal D.
   Fuchs, Charles S.
   Michael Gaziano, John
   Giovannucci, Edward
   Graubard, Barry I.
   Hollenbeck, Albert R.
   Hou, Lifang
   Jacobs, Eric J.
   King, Lindsay Y.
   Koshiol, Jill
   Lee, I-Min
   Linet, Martha S.
   Palmer, Julie R.
   Purdue, Mark P.
   Rosenberg, Lynn
   Schairer, Catherine
   Sesso, Howard D.
   Sigurdson, Alice J.
   Wactawski-Wende, Jean
   Zeleniuch-Jacquotte, Anne
   Campbell, Peter T.
   McGlynn, Katherine A.
TI NSAID Use and Risk of Hepatocellular Carcinoma and Intrahepatic
   Cholangiocarcinoma: The Liver Cancer Pooling Project
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; COLORECTAL-CANCER; UNITED-STATES;
   CELL-GROWTH; ASPIRIN; CYCLOOXYGENASE-2; INHIBITORS; PREVENTION;
   APOPTOSIS; SURVIVAL
AB Chronic inflammation plays a pivotal role in the pathogenesis of hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC), the two most common types of liver cancer. A number of prior experimental studies have suggested that nonsteroidal antiinflammatory drugs (NSAIDs), including aspirin and ibuprofen, may potentially protect against liver cancer. However, no observational study has examined the associationbetween aspirin duration and dose or other over-the-counter non-aspirin NSAIDs, such as ibuprofen, and liver cancer incidence. Furthermore, the association between NSAID use and risk of ICC is unclear. As part of the Liver Cancer Pooling Project, we harmonized data on 1,084,133 individuals (HCC = 679, ICC = 225) from 10 U.S.-based prospective cohort studies. Cox proportional hazards regression models were used to evaluate multivariable-adjusted HRs and 95% confidence intervals (CI). Current aspirin use, versus nonuse, was inversely associated with HCC (HR, 0.68; 95% CI, 0.57-0.81), which persisted when restricted to individuals not using non-aspirin NSAIDs and in a 5-and 10-year lag analysis. The association between aspirin use and HCC risk was stronger for users who reported daily use, longer duration use, and lower dosage. Ibuprofen use was not associated with HCC risk. Aspirin usewas associated with a reduced ICC risk in men (HR, 0.64; 95% CI, 0.42-0.98) but not women (HR, 1.34; 95% CI, 0.89-2.01; P-interaction = 0.01). The observed inverse association between aspirin use and liver cancer in our study, together with previous data, suggests the merit of future intervention studies of aspirin and other agents that affect chronic inflammatory pathways for HCC and possibly ICC. (C) 2015 AACR.
C1 [Petrick, Jessica L.; Sahasrabuddhe, Vikrant V.; Alavanja, Michael C.; Beane-Freeman, Laura E.; Chen, Jie; Freedman, Neal D.; Graubard, Barry I.; Koshiol, Jill; Linet, Martha S.; Purdue, Mark P.; Schairer, Catherine; Sigurdson, Alice J.; McGlynn, Katherine A.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Sahasrabuddhe, Vikrant V.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
   [Sahasrabuddhe, Vikrant V.] Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37212 USA.
   [Sahasrabuddhe, Vikrant V.] Brigham & Womens Hosp, Dept Med, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA.
   [Chan, Andrew T.; Chong, Dawn Q.; King, Lindsay Y.] Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02114 USA.
   [Chan, Andrew T.; Chong, Dawn Q.; Fuchs, Charles S.; King, Lindsay Y.] Harvard Univ, Sch Med, Boston, MA USA.
   [Buring, Julie E.; Giovannucci, Edward; Lee, I-Min; Sesso, Howard D.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
   [Chong, Dawn Q.] Natl Canc Ctr Singapore, Div Med Oncol, Singapore, Singapore.
   [Fuchs, Charles S.] Dana Farber Canc Inst, Dept Med, Boston, MA 02115 USA.
   [Michael Gaziano, John] VA Boston Healthcare Syst, Brockton, MA USA.
   [Hollenbeck, Albert R.] AARP, Washington, DC USA.
   [Hou, Lifang] Northwestern Univ, Dept Prevent Med, Chicago, IL 60611 USA.
   [Jacobs, Eric J.; Campbell, Peter T.] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
   [Palmer, Julie R.; Rosenberg, Lynn] Boston Univ, Slone Epidemiol Ctr, Boston, MA 02215 USA.
   [Wactawski-Wende, Jean] SUNY Buffalo, Dept Epidemiol & Environm Hlth, Buffalo, NY 14260 USA.
   [Zeleniuch-Jacquotte, Anne] NYU, Sch Med, Dept Populat Hlth, New York, NY USA.
RP Petrick, JL (reprint author), NCI, 9609 Med Ctr Dr,7E-232, Bethesda, MD 20892 USA.
EM jessica.petrick@nih.gov
RI Purdue, Mark/C-9228-2016; Beane Freeman, Laura/C-4468-2015; 
OI Purdue, Mark/0000-0003-1177-3108; Beane Freeman,
   Laura/0000-0003-1294-4124; Zeleniuch-Jacquotte, Anne/0000-0001-9350-1303
FU NIH Intramural Research Program, National Cancer Institute; National
   Cancer Institute [CA047988, HL043851, HL080467, HL099355, DK098311,
   CA186107, CA87969, CA167552]
FX The study was supported by NIH Intramural Research Program, National
   Cancer Institute (J.L. Petrick, V.V. Sahasrabuddhe, M.C. Alavanja, L.
   Beane-Freeman, J. Chen, N.D. Freedman, B.I. Graubard, J. Koshiol, M.S.
   Linet, C. Schairer, A.J. Sigurdson, K.A. McGlynn). National Cancer
   Institute Grants CA047988 (I. Lee, J.E. Buring), HL043851 (I. Lee, J.E.
   Buring), HL080467 (I. Lee, J.E. Buring), HL099355 (I. Lee, J. E.
   Buring), DK098311 (A.T. Chan), CA186107 (A.T. Chan), CA87969 (A.T.
   Chan), and CA167552 (A.T. Chan).
NR 46
TC 1
Z9 1
U1 1
U2 7
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
EI 1940-6215
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD DEC
PY 2015
VL 8
IS 12
BP 1156
EP 1162
DI 10.1158/1940-6207.CAPR-15-0126
PG 7
WC Oncology
SC Oncology
GA DB5BS
UT WOS:000368528700004
PM 26391917
ER

PT J
AU Pretzel, SM
   Andrews, TS
   Broski, K
   Childs, JC
   Gren, LH
   Ogden, SL
   Mabie, J
   Thomas, B
   Rozjabek, HM
   Marcus, PM
AF Pretzel, Shannon M.
   Andrews, Tara S.
   Broski, Karen
   Childs, Jeffery C.
   Gren, Lisa H.
   Ogden, Sheryl L.
   Mabie, Jerome
   Thomas, Brett
   Rozjabek, Heather M.
   Marcus, Pamela M.
TI Participants' Views of Retention Materials Used in the PLCO Cancer
   Screening Trial
SO CLINICAL MEDICINE & RESEARCH
LA English
DT Article
DE Randomized controlled trial as subject; Mass screening; Patient
   compliance; Cancer; USA; Internet usage
ID MORTALITY; PROSTATE; LUNG
AB Objective: To obtain information from participants in the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial regarding their perception of the retention materials employed by the screening centers. Also, to determine the viability of using email or the internet as a data collection tool with an older population.
   Design: Three of ten PLCO screening centers queried participants towards the end of the study (2010) as to their opinions of the various retention materials and whether they would have been willing to use electronic communication for study activities, had the option been available. Setting: The questionnaires were administered by mail, and responses were returned to the originating screening center.
   Participants: The participants in this study consisted of all the active participants at three PLCO screening centers: the University of Colorado Anschutz Medical Campus, the University of Utah, and Henry Ford Health System.
   Methods: A short, self-administered questionnaire was mailed to all active participants at three PLCO centers (n= 41,482). This was a one-time mailing with no follow-up, as the responses were designed to be anonymous in order to obtain the most honest responses. Results: The response rate was 62%. Of respondents, 97% reported their PLCO experience was good or excellent. Nearly 50% of respondents indicated that receipt of an annual newsletter made them more likely to participate; newsletter features they reported as most important were those that conveyed information on cancer, study findings, and how their data were being used.
   Results did not support study coordinators' suppositions that receipt of a token gift or birthday card by participants was important for retention. Fewer than 30% of respondents indicated that they would have been unwilling to use a secure website to complete study forms.
   Conclusion: These data indicate the importance of querying participants rather than relying on impressions of study staff, and also indicate that the internet will be a viable means of data collection in future prevention studies that include older Americans.
C1 [Pretzel, Shannon M.; Ogden, Sheryl L.] Univ Colorado, Ctr Canc, Anschutz Med Campus,13001 E 17th Pl,Mail Stop C31, Aurora, CO 80045 USA.
   [Andrews, Tara S.; Broski, Karen] Henry Ford Hlth Syst, Dept Publ Hlth Sci, Detroit, MI USA.
   [Childs, Jeffery C.] Univ Utah, Div Oncol, Salt Lake City, UT USA.
   [Gren, Lisa H.] Univ Utah, Dept Family & Prevent Med, Salt Lake City, UT USA.
   [Mabie, Jerome; Thomas, Brett] Informat Management Syst, Rockville, MD USA.
   [Rozjabek, Heather M.; Marcus, Pamela M.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
   [Rozjabek, Heather M.] Drexel Univ, Sch Publ Hlth, Philadelphia, PA 19104 USA.
RP Pretzel, SM (reprint author), Univ Colorado, Anschutz Med Campus,13001 E 17th Pl,Mail Stop C31, Aurora, CO 80045 USA.
EM Shannon.pretzel@ucdenver.edu
OI Broski, Karen/0000-0003-1503-8768
FU NCI NIH HHS [N01-CN-25524, N01 CN25514, N01-CN-25512, N01 CN25524, N01
   CN25512, N01-CN-25514, N02-CN-35001-45, N01 CN25476, N01-CN-25476,
   N02-CN-55023-76]
NR 9
TC 0
Z9 0
U1 0
U2 0
PU MARSHFIELD CLINIC
PI MARSHFIELD
PA 1000 N OAK AVE, MAILSTOP ML7, MARSHFIELD, WI 54449 USA
SN 1539-4182
EI 1554-6179
J9 CLIN MED RES
JI Clin. Med. Res.
PD DEC 1
PY 2015
VL 13
IS 3-4
BP 139
EP 146
DI 10.3121/cmr.2015.1274
PG 8
WC Medicine, General & Internal
SC General & Internal Medicine
GA DB5UW
UT WOS:000368580100004
PM 26387707
ER

PT J
AU Mayer-Barber, KD
   Barber, DL
AF Mayer-Barber, Katrin D.
   Barber, Daniel L.
TI Innate and Adaptive Cellular Immune Responses to Mycobacterium
   tuberculosis Infection
SO COLD SPRING HARBOR PERSPECTIVES IN MEDICINE
LA English
DT Article
ID CD4(+) T-CELLS; IMMUNODEFICIENCY-VIRUS-INFECTION; RECONSTITUTION
   INFLAMMATORY SYNDROME; NITRIC-OXIDE SYNTHASE;
   PNEUMOCYSTIS-CARINII-PNEUMONIA; LUNG DENDRITIC CELLS; W-BEIJING STRAINS;
   IN-VIVO DEPLETION; PULMONARY TUBERCULOSIS; INTERFERON-GAMMA
AB Host resistance to Mycobacterium tuberculosis (Mtb) infection requires the coordinated efforts of innate and adaptive immune cells. Diverse pulmonary myeloid cell populations respond to Mtb with unique contributions to both host-protective and potentially detrimental inflammation. Although multiple cell types of the adaptive immune system respond to Mtb infection, CD4 T cells are the principal antigen-specific cells responsible for containment of Mtb infection, but they can also be major contributors to disease during Mtb infection in several different settings. Here, we will discuss the role of different myeloid populations as well as the dual nature of CD4 T cells in Mtb infection with a primary focus on data generated using in vivo cellular immunological studies in experimental animal models and in humans when available.
C1 [Mayer-Barber, Katrin D.] NIAID, Immunobiol Sect, Parasit Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
   [Barber, Daniel L.] NIAID, Lymphocyte Biol Unit T, Parasit Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
RP Mayer-Barber, KD (reprint author), NIAID, Immunobiol Sect, Parasit Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM barberd@niaid.nih.gov
NR 169
TC 0
Z9 0
U1 3
U2 5
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 2157-1422
J9 CSH PERSPECT MED
JI Cold Spring Harb. Perspect. Med.
PD DEC
PY 2015
VL 5
IS 12
AR a018424
DI 10.1101/cshperspect.a018424
PG 19
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA DB6CA
UT WOS:000368599500008
ER

PT J
AU Garfinkel, BP
   Arad, S
   Le, PT
   Bustin, M
   Rosen, CJ
   Gabet, Y
   Orly, J
AF Garfinkel, Benjamin P.
   Arad, Shiri
   Le, Phuong T.
   Bustin, Michael
   Rosen, Clifford J.
   Gabet, Yankel
   Orly, Joseph
TI Proportionate Dwarfism in Mice Lacking Heterochromatin Protein 1 Binding
   Protein 3 (HP1BP3) Is Associated With Alterations in the Endocrine IGF-1
   Pathway
SO ENDOCRINOLOGY
LA English
DT Article
ID GROWTH-FACTOR-I; BONE-MINERAL DENSITY; TRANSGENIC MICE;
   POSTNATAL-GROWTH; HORMONE RECEPTOR; TARGETED DISRUPTION;
   GENETIC-EVIDENCE; SKELETAL GROWTH; SERUM IGF-1; AGING MEN
AB Heterochromatin protein 1 binding protein 3 (HP1BP3) is a recently described histone H1-related protein with roles in chromatin structure and transcriptional regulation. To explore the potential physiological role of HP1BP3, we have previously described an Hp1bp3(-/-) mouse model with reduced postnatal viability and growth. We now find that these mice are proportionate dwarfs, with reduction in body weight, body length, and organ weight. In addition to their small size, microcomputed tomography analysis showed that Hp1bp3(-/-) mice present a dramatic impairment of their bone development and structure. By 3 weeks of age, mice of both sexes have severely impaired cortical and trabecular bone, and these defects persist into adulthood and beyond. Primary cultures of both osteoblasts and osteoclasts from Hp1bp3(-/-) bone marrow and splenocytes, respectively, showed normal differentiation and function, strongly suggesting that the impaired bone accrual is due to noncell autonomous systemic cues in vivo. One major endocrine pathway regulating both body growth and bone acquisition is the IGF regulatory system, composed of IGF-1, the IGF receptors, and the IGF-binding proteins (IGFBPs). At 3 weeks of age, Hp1bp3(-/-) mice exhibited a 60% reduction in circulating IGF-1 and a 4-fold increase in the levels of IGFBP-1 and IGFBP-2. These alterations were reflected in similar changes in the hepatic transcripts of the Igf1, Igfbp1, and Igfbp2 genes. Collectively, these results suggest that HP1BP3 plays a key role in normal growth and bone development by regulating transcription of endocrine IGF-1 components.
C1 [Garfinkel, Benjamin P.; Arad, Shiri; Orly, Joseph] Hebrew Univ Jerusalem, Alexander Silberman Inst Life Sci, Dept Biol Chem, IL-91904 Jerusalem, Israel.
   [Le, Phuong T.; Rosen, Clifford J.] Maine Med Ctr Res Inst, Ctr Clin & Translat Res, Scarborough, ME 04074 USA.
   [Bustin, Michael] NCI, Prot Sect, Lab Metab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
   [Gabet, Yankel] Tel Aviv Univ, Sackler Fac Med, Dept Anat & Anthropol, IL-64239 Tel Aviv, Israel.
RP Orly, J (reprint author), Hebrew Univ Jerusalem, Alexander Silberman Inst Life Sci, Dept Biol Chem, IL-91904 Jerusalem, Israel.
EM benny.garfinkel@mail.huji.ac.il; orly@vms.huji.ac.il
RI Bustin, Michael/G-6155-2015
FU United States-Israel Binational Science Foundation Grants [2009326,
   2013194]
FX This work was supported by The United States-Israel Binational Science
   Foundation Grants 2009326 (to J.O. and M.B.) and 2013194 (to C.J.R. and
   J.O.).
NR 57
TC 3
Z9 3
U1 0
U2 5
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0013-7227
EI 1945-7170
J9 ENDOCRINOLOGY
JI Endocrinology
PD DEC
PY 2015
VL 156
IS 12
BP 4558
EP 4570
DI 10.1210/en.2015-1668
PG 13
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA DB3KT
UT WOS:000368410900017
PM 26402843
ER

PT J
AU Varki, A
   Cummings, RD
   Aebi, M
   Packer, NH
   Seeberger, PH
   Esko, JD
   Stanley, P
   Hart, G
   Darvill, A
   Kinoshita, T
   Prestegard, JJ
   Schnaar, RL
   Freeze, HH
   Marth, JD
   Bertozzi, CR
   Etzler, ME
   Frank, M
   Vliegenthart, JFG
   Lutteke, T
   Perez, S
   Bolton, E
   Rudd, P
   Paulson, J
   Kanehisa, M
   Toukach, P
   Aoki-Kinoshita, KF
   Dell, A
   Narimatsu, H
   York, W
   Taniguchi, N
   Kornfeld, S
AF Varki, Ajit
   Cummings, Richard D.
   Aebi, Markus
   Packer, Nicole H.
   Seeberger, Peter H.
   Esko, Jeffrey D.
   Stanley, Pamela
   Hart, Gerald
   Darvill, Alan
   Kinoshita, Taroh
   Prestegard, James J.
   Schnaar, Ronald L.
   Freeze, Hudson H.
   Marth, Jamey D.
   Bertozzi, Carolyn R.
   Etzler, Marilynn E.
   Frank, Martin
   Vliegenthart, Johannes F. G.
   Luetteke, Thomas
   Perez, Serge
   Bolton, Evan
   Rudd, Pauline
   Paulson, James
   Kanehisa, Minoru
   Toukach, Philip
   Aoki-Kinoshita, Kiyoko F.
   Dell, Anne
   Narimatsu, Hisashi
   York, William
   Taniguchi, Naoyuki
   Kornfeld, Stuart
TI Symbol Nomenclature for Graphical Representations of Glycans
SO GLYCOBIOLOGY
LA English
DT Editorial Material
C1 [Varki, Ajit; Esko, Jeffrey D.] Univ Calif San Diego, La Jolla, CA 92093 USA.
   [Cummings, Richard D.] Consortium Funct Glycom, London, England.
   [Cummings, Richard D.] Harvard Univ, Sch Med, Boston, MA USA.
   [Aebi, Markus] ETH, Zurich, Switzerland.
   [Packer, Nicole H.] Macquarie Univ, Sydney, NSW 2109, Australia.
   [Seeberger, Peter H.] Max Planck Inst, Potsdam, Germany.
   [Stanley, Pamela] Albert Einstein Coll Med, New York, NY USA.
   [Hart, Gerald; Schnaar, Ronald L.] Johns Hopkins Univ, Baltimore, MD USA.
   [Darvill, Alan; Prestegard, James J.; York, William] Univ Georgia, Athens, GA 30602 USA.
   [Kinoshita, Taroh] Osaka Univ, Osaka, Japan.
   [Freeze, Hudson H.] Sanford Burnham Prebys Med Discovery Inst, La Jolla, CA USA.
   [Marth, Jamey D.] Univ Calif Santa Barbara, Santa Barbara, CA 93106 USA.
   [Bertozzi, Carolyn R.] Stanford Univ, Stanford, CA 94305 USA.
   [Etzler, Marilynn E.] Univ Calif Davis, Davis, CA 95616 USA.
   [Frank, Martin; Vliegenthart, Johannes F. G.; Luetteke, Thomas] IUPAC Carbohydrate Nomenclature Comm, Gothenburg, Sweden.
   [Frank, Martin] Biognos AB, Gothenburg, Sweden.
   [Vliegenthart, Johannes F. G.] Univ Utrecht, Utrecht, Netherlands.
   [Luetteke, Thomas] MonosaccharideDB, Giessen, Germany.
   [Luetteke, Thomas] Univ Giessen, Giessen, Germany.
   [Perez, Serge] Glycopedia, St Martin Dheres, France.
   [Perez, Serge] Univ Grenoble Alpes, CNRS, St Martin Dheres, France.
   [Bolton, Evan] Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
   [Bolton, Evan] Natl Lib Med, Bethesda, MD USA.
   [Rudd, Pauline] Oxford Glycobiol Inst, Dublin, Ireland.
   [Rudd, Pauline] Natl Inst Bioproc Res & Training, Dublin, Ireland.
   [Paulson, James] Consortium Funct Glyc, La Jolla, CA USA.
   [Paulson, James] Scripps Res Inst, La Jolla, CA 92037 USA.
   [Kanehisa, Minoru] KEGG Database, Kyoto, Japan.
   [Kanehisa, Minoru] Kyoto Univ, Kyoto, Japan.
   [Toukach, Philip] Carbohydrate Struct Database CSDB, Moscow, Russia.
   [Toukach, Philip] Zelinsky Inst Organ Chem, Moscow, Russia.
   [Aoki-Kinoshita, Kiyoko F.] GlyTouCan Database, Tokyo, Japan.
   [Aoki-Kinoshita, Kiyoko F.] Soka Univ, Tokyo, Japan.
   [Dell, Anne] Univ London Imperial Coll Sci Technol & Med, London, England.
   [Narimatsu, Hisashi] Natl Inst Adv Ind Sci & Technol, Tsukuba, Ibaraki, Japan.
   [Taniguchi, Naoyuki] RIKEN, Saitama, Japan.
   [Kornfeld, Stuart] Washington Univ, Sch Med, St Louis, MO USA.
RP Varki, A (reprint author), Univ Calif San Diego, La Jolla, CA 92093 USA.
RI Aoki-Kinoshita, Kiyoko/I-2696-2016; Schnaar, Ronald/S-8967-2016; 
OI Aoki-Kinoshita, Kiyoko/0000-0002-6662-8015; Schnaar,
   Ronald/0000-0002-7701-5484; Freeze, Hudson/0000-0001-6316-0501; Lutteke,
   Thomas/0000-0002-7140-9933; Toukach, Philip/0000-0001-9887-8919
FU NHLBI NIH HHS [P01 HL107151, R01 HL125352]; NIDDK NIH HHS [R01
   DK099551]; NIGMS NIH HHS [R01 GM105399]
NR 8
TC 36
Z9 36
U1 8
U2 28
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0959-6658
EI 1460-2423
J9 GLYCOBIOLOGY
JI Glycobiology
PD DEC
PY 2015
VL 25
IS 12
BP 1323
EP 1324
DI 10.1093/glycob/cwv091
PG 2
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA DB3WL
UT WOS:000368443700002
PM 26543186
ER

PT J
AU Kun-Rodrigues, C
   Ganos, C
   Guerreiro, R
   Schneider, SA
   Schulte, C
   Lesage, S
   Darwent, L
   Holmans, P
   Singleton, A
   Bhatia, K
   Bras, J
AF Kun-Rodrigues, Celia
   Ganos, Christos
   Guerreiro, Rita
   Schneider, Susanne A.
   Schulte, Claudia
   Lesage, Suzanne
   Darwent, Lee
   Holmans, Peter
   Singleton, Andrew
   Bhatia, Kailash
   Bras, Jose
CA Int Parkinson's Dis Genomics
TI A systematic screening to identify de novo mutations causing sporadic
   early-onset Parkinson's disease
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID AMYOTROPHIC-LATERAL-SCLEROSIS; AUTISM SPECTRUM DISORDERS; SYNUCLEIN GENE
   DUPLICATION; PTEN TUMOR-SUPPRESSOR; PRESENILIN-1 GENE; VAPB; GERMLINE;
   NEURONS; ALS; DELETION
AB Despite the many advances in our understanding of the genetic basis of Mendelian forms of Parkinson's disease (PD), a large number of early-onset cases still remain to be explained. Many of these cases, present with a form of disease that is identical to that underlined by genetic causes, but do not have mutations in any of the currently known disease-causing genes. Here, we hypothesized that de novo mutations may account for a proportion of these early-onset, sporadic cases. We performed exome sequencing in full parent-child trios where the proband presents with typical PD to unequivocally identify de novo mutations. This approach allows us to test all genes in the genome in an unbiased manner. We have identified and confirmed 20 coding de novo mutations in 21 trios. We have used publicly available population genetic data to compare variant frequencies and our independent in-house dataset of exome sequencing in PD (with over 1200 cases) to identify additional variants in the same genes. Of the genes identified to carry de novo mutations, PTEN, VAPB and ASNA1 are supported by various sources of data to be involved in PD. We show that these genes are reported to be within a protein-protein interaction network with PD genes and that they contain additional rare, case-specific, mutations in our independent cohort of PD cases. Our results support the involvement of these three genes in PD and suggest that testing for de novo mutations in sporadic disease may aid in the identification of novel disease-causing genes.
C1 [Kun-Rodrigues, Celia; Guerreiro, Rita; Darwent, Lee; Bras, Jose] UCL Inst Neurol, Dept Mol Neurosci, London WC1N 3AR, England.
   [Ganos, Christos] Univ Med Ctr Hamburg Eppendorf UKE, Dept Neurol, D-20246 Hamburg, Germany.
   [Ganos, Christos; Bhatia, Kailash] UCL, UCL Inst Neurol, Sobell Dept Motor Neurosci & Movement Disorders, London WC1N 3BG, England.
   [Schneider, Susanne A.] Univ Hosp Schleswig Holstein, Dept Neurol, D-24105 Kiel, Germany.
   [Schulte, Claudia] German Ctr Neurodegenerat Dis, Tubingen, Germany.
   [Schulte, Claudia] Univ Tubingen, Hertie Inst Clin Brain Res, Dept Neurodegenerat Dis, D-72076 Tubingen, Germany.
   [Lesage, Suzanne] Hop La Pitie Salpetriere, Brain & Spinal Cord Inst ICM, INSERM, U M27, F-75013 Paris, France.
   [Holmans, Peter] Cardiff Univ, Inst Psychol Med & Clin Neurosci, Med Res Council, Ctr Neuropsychiat Genet & Gen, Cardiff CF24 4HQ, S Glam, Wales.
   [Singleton, Andrew] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
RP Bras, J (reprint author), UCL, Inst Neurol, Dept Mol Neurosci, DRC, 8-11 Queen Sq,Box 16, London WC1N 3AR, England.
EM j.bras@ucl.ac.uk
RI Singleton, Andrew/C-3010-2009; 
OI Bras, Jose/0000-0001-8186-0333; Holmans, Peter/0000-0003-0870-9412
FU Wellcome Trust; Medical Research Council
FX Funding to pay the Open Access publication charges for this article was
   provided by the Wellcome Trust and the Medical Research Council.
NR 64
TC 3
Z9 3
U1 2
U2 11
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
EI 1460-2083
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD DEC 1
PY 2015
VL 24
IS 23
BP 6711
EP 6720
DI 10.1093/hmg/ddv376
PG 10
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA DB2WP
UT WOS:000368371600013
PM 26362251
ER

PT J
AU Gharib, SA
   Loth, DW
   Artigas, MS
   Birkland, TP
   Wilk, JB
   Wain, LV
   Brody, JA
   Obeidat, M
   Hancock, DB
   Tang, WB
   Rawal, R
   Boezen, HM
   Imboden, M
   Huffman, JE
   Lahousse, L
   Alves, AC
   Manichaikul, A
   Hui, J
   Morrison, AC
   Ramasamy, A
   Smith, AV
   Gudnason, V
   Surakka, I
   Vitart, V
   Evans, DM
   Strachan, DP
   Deary, IJ
   Hofman, A
   Glaser, S
   Wilson, JF
   North, KE
   Zhao, JH
   Heckbert, SR
   Jarvis, DL
   Probst-Hensch, N
   Schulz, H
   Barr, RG
   Jarvelin, MR
   O'Connor, GT
   Kahonen, M
   Cassano, PA
   Hysi, PG
   Dupuis, J
   Hayward, C
   Psaty, BM
   Hall, IP
   Parks, WC
   Tobin, MD
   London, SJ
AF Gharib, Sina A.
   Loth, Daan W.
   Artigas, Maria Soler
   Birkland, Timothy P.
   Wilk, Jemma B.
   Wain, Louise V.
   Brody, Jennifer A.
   Obeidat, Ma'en
   Hancock, Dana B.
   Tang, Wenbo
   Rawal, Rajesh
   Boezen, H. Marike
   Imboden, Medea
   Huffman, Jennifer E.
   Lahousse, Lies
   Alves, Alexessander C.
   Manichaikul, Ani
   Hui, Jennie
   Morrison, Alanna C.
   Ramasamy, Adaikalavan
   Smith, Albert Vernon
   Gudnason, Vilmundur
   Surakka, Ida
   Vitart, Veronique
   Evans, David M.
   Strachan, David P.
   Deary, Ian J.
   Hofman, Albert
   Glaeser, Sven
   Wilson, James F.
   North, Kari E.
   Zhao, Jing Hua
   Heckbert, Susan R.
   Jarvis, Deborah L.
   Probst-Hensch, Nicole
   Schulz, Holger
   Barr, R. Graham
   Jarvelin, Marjo-Riitta
   O'Connor, George T.
   Kahonen, Mika
   Cassano, Patricia A.
   Hysi, Pirro G.
   Dupuis, Josee
   Hayward, Caroline
   Psaty, Bruce M.
   Hall, Ian P.
   Parks, William C.
   Tobin, Martin D.
   London, Stephanie J.
CA CHARGE Consortium
   SpiroMeta Consortium
TI Integrative pathway genomics of lung function and airflow obstruction
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID SET ENRICHMENT ANALYSIS; WIDE ASSOCIATION; PULMONARY-DISEASE; MATRIX
   METALLOPROTEINASES; GENOMEWIDE ASSOCIATION; EXPRESSION; RISK;
   IDENTIFICATION; INFLAMMATION; METAANALYSIS
AB Chronic respiratory disorders are important contributors to the global burden of disease. Genome-wide association studies (GWASs) of lung function measures have identified several trait-associated loci, but explain only a modest portion of the phenotypic variability. We postulated that integrating pathway-based methods with GWASs of pulmonary function and airflow obstruction would identify a broader repertoire of genes and processes influencing these traits. We performed two independent GWASs of lung function and applied gene set enrichment analysis to one of the studies and validated the results using the second GWAS. We identified 131 significantly enriched gene sets associated with lung function and clustered them into larger biological modules involved in diverse processes including development, immunity, cell signaling, proliferation and arachidonic acid. We found that enrichment of gene sets was not driven by GWAS-significant variants or loci, but instead by those with less stringent association P-values. Next, we applied pathway enrichment analysis to a meta-analyzed GWAS of airflow obstruction. We identified several biologic modules that functionally overlapped with those associated with pulmonary function. However, differences were also noted, including enrichment of extracellular matrix (ECM) processes specifically in the airflow obstruction study. Network analysis of the ECM module implicated a candidate gene, matrix metalloproteinase 10 (MMP10), as a putative disease target. We used a knockout mouse model to functionally validate MMP10' s role in influencing lung's susceptibility to cigarette smoke-induced emphysema. By integrating pathway analysis with population-based genomics, we unraveled biologic processes underlying pulmonary function traits and identified a candidate gene for obstructive lung disease.
C1 [Gharib, Sina A.; Birkland, Timothy P.] Univ Washington, Ctr Lung Biol, Computat Med Core, Seattle, WA 98195 USA.
   [Gharib, Sina A.; Psaty, Bruce M.] Univ Washington, Dept Med, Seattle, WA USA.
   [Brody, Jennifer A.; Heckbert, Susan R.; Psaty, Bruce M.] Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
   [Heckbert, Susan R.; Psaty, Bruce M.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
   [Psaty, Bruce M.] Univ Washington, Dept Hlth Serv, Seattle, WA 98195 USA.
   [Loth, Daan W.; Lahousse, Lies; Hofman, Albert] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
   [Artigas, Maria Soler; Wain, Louise V.; Tobin, Martin D.] Univ Leicester, Dept Hlth Sci, Genet Epidemiol Grp, Leicester, Leics, England.
   [Artigas, Maria Soler; Wain, Louise V.; Tobin, Martin D.] Glenfield Hosp, Leicester Resp Biomed Res Unit, NIHR, Leicester, Leics, England.
   [Wilk, Jemma B.] Pfizer Global Res & Dev, Human Genet & Computat Biomed, Cambridge, MA USA.
   [Obeidat, Ma'en] Univ British Columbia, Ctr Heart Lung Innovat, Vancouver, BC V5Z 1M9, Canada.
   [Hancock, Dana B.] Res Triangle Inst RTI Int, Behav Hlth & Criminal Justice Div, Behav & Urban Hlth Program, Res Triangle Pk, NC USA.
   [Tang, Wenbo; Cassano, Patricia A.] Cornell Univ, Div Nutr Sci, Ithaca, NY 14853 USA.
   [Rawal, Rajesh] German Res Ctr Environm Hlth, Inst Genet Epidemiol, Helmholtz Zentrum Munchen, Neuherberg, Germany.
   [Schulz, Holger] German Res Ctr Environm Hlth, Inst Epidemiol 1, Helmholtz Zentrum Munchen, Neuherberg, Germany.
   [Boezen, H. Marike] Univ Groningen, Univ Med Ctr Groningen, Dept Epidemiol, Groningen, Netherlands.
   [Boezen, H. Marike] Univ Groningen, Univ Med Ctr Groningen, GRIAC Res Inst, Groningen, Netherlands.
   [Imboden, Medea; Probst-Hensch, Nicole] Swiss Trop & Publ Hlth Inst, Basel, Switzerland.
   [Imboden, Medea; Probst-Hensch, Nicole] Univ Basel, Basel, Switzerland.
   [Huffman, Jennifer E.; Vitart, Veronique; Hayward, Caroline] Univ Edinburgh, MRC IGMM, MRC Human Genet Unit, Edinburgh, Midlothian, Scotland.
   [Deary, Ian J.] Univ Edinburgh, Ctr Cognit Ageing & Cognit Epidemiol, Edinburgh, Midlothian, Scotland.
   [Wilson, James F.] Univ Edinburgh, Usher Inst Populat Hlth Sci & Informat, Edinburgh, Midlothian, Scotland.
   [Lahousse, Lies] Ghent Univ Hosp, Dept Resp Med, Ghent, Belgium.
   [Alves, Alexessander C.] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, London, England.
   [Jarvis, Deborah L.] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Resp Epidemiol & Publ Hlth Grp, London, England.
   [Jarvelin, Marjo-Riitta] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, Ctr Environm & Hlth, Dept Epidemiol & Biostat,MRC Hlth Protect Agcy HP, London, England.
   [Manichaikul, Ani] Univ Virginia, Ctr Publ Hlth Genom, Charlottesville, VA USA.
   [Manichaikul, Ani] Univ Virginia, Dept Publ Hlth Sci, Div Biostat & Epidemiol, Charlottesville, VA USA.
   [Hui, Jennie] PathWest Lab Med WA, Nedlands, WA, Australia.
   [Hui, Jennie] Univ Western Australia, Sch Populat Hlth, Sch Pathol & Lab Med, Nedlands, WA 6009, Australia.
   [Morrison, Alanna C.] Univ Texas Hlth Sci Ctr Houston, Sch Publ Hlth, Human Genet Ctr, Houston, TX 77030 USA.
   [Ramasamy, Adaikalavan] Kings Coll London, Dept Med & Mol Genet, London WC2R 2LS, England.
   [Hysi, Pirro G.] Kings Coll London, Dept Twins Res & Genet Epidemiol, London WC2R 2LS, England.
   [Smith, Albert Vernon; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
   [Smith, Albert Vernon; Gudnason, Vilmundur] Univ Iceland, Reykjavik, Iceland.
   [Surakka, Ida] Natl Inst Hlth & Welf THL, Dept Chron Dis Prevent, Publ Hlth Genom Unit, Helsinki, Finland.
   [Evans, David M.] Univ Queensland, Diamantina Inst, Translat Res Inst, Woolloongabba, Qld 4102, Australia.
   [Evans, David M.] MRC Integrat Epidemiol Unit, Bristol BS8 2BN, Avon, England.
   [Strachan, David P.] Univ London, Populat Hlth Res Inst, London, England.
   [Hofman, Albert] NGI, Consortium Healthy Aging NCHA, Rotterdam, Netherlands.
   [Glaeser, Sven] Univ Hosp Greifswald, Dept Internal Med Pneumol Cardiol Intens Care &, Greifswald, Germany.
   [Zhao, Jing Hua] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
   [Zhao, Jing Hua] Addenbrookes Hosp, Inst Metab Sci, MRC Epidemiol Unit, Cambridge, England.
   [Heckbert, Susan R.] Grp Hlth Cooperat Puget Sound, Grp Hlth Res Inst, Seattle, WA USA.
   [Barr, R. Graham] Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY USA.
   [Jarvelin, Marjo-Riitta] Univ Oulu, Inst Hlth Sci, Oulu, Finland.
   [Jarvelin, Marjo-Riitta] Univ Oulu, Bioctr Oulu, Oulu, Finland.
   [Jarvelin, Marjo-Riitta] Oulu Univ Hosp, Unit Primary Care, Oulu, Finland.
   [Jarvelin, Marjo-Riitta] Natl Inst Hlth & Welfare, Dept Children & Young People & Families, Oulu, Finland.
   [O'Connor, George T.] Boston Univ, Sch Med, Pulmonary Ctr, Boston, MA 02118 USA.
   [O'Connor, George T.; Dupuis, Josee] NHLBI, Framingham Heart Study, Framingham, MA USA.
   [Kahonen, Mika] Univ Tampere, Dept Clin Physiol, FIN-33101 Tampere, Finland.
   [Kahonen, Mika] Tampere Univ Hosp, Tampere, Finland.
   [Cassano, Patricia A.] Weill Cornell Med Coll, Div Biostat & Epidemiol, Dept Healthcare Policy & Res, New York, NY USA.
   [Dupuis, Josee] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
   [Hall, Ian P.] Univ Nottingham Hosp, Div Resp Med, Nottingham NG7 2UH, England.
   [Parks, William C.] Cedars Sinai Med Ctr, Dept Med, Los Angeles, CA 90048 USA.
   [London, Stephanie J.] NIEHS, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
RP Gharib, SA (reprint author), 850 Republ St,POB 358052, Seattle, WA 98109 USA.
EM sagharib@u.washington.edu
RI Soler Artigas, Maria/L-6529-2013; Smith, Albert Vernon/K-5150-2015; 
OI Soler Artigas, Maria/0000-0002-3213-1107; Smith, Albert
   Vernon/0000-0003-1942-5845; Manichaikul, Ani/0000-0002-5998-795X; Evans,
   David/0000-0003-0663-4621; Lahousse, Lies/0000-0002-3494-4363; London,
   Stephanie/0000-0003-4911-5290; Wain, Louise/0000-0003-4951-1867
FU Biotechnology and Biological Sciences Research Council [BB/F019394/1];
   Chief Scientist Office [CZB/4/505, ETM/55]; MRC [G0902313, G1000861,
   G1001799, MC_PC_12010, MC_PC_U127561128, MC_UU_12013/4, MR/K026992/1,
   MR/N01104X/1]
NR 62
TC 3
Z9 3
U1 0
U2 8
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
EI 1460-2083
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD DEC 1
PY 2015
VL 24
IS 23
BP 6836
EP 6848
DI 10.1093/hmg/ddv378
PG 13
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA DB2WP
UT WOS:000368371600022
PM 26395457
ER

PT J
AU Hagg, S
   Ganna, A
   Van der Laan, SW
   Esko, T
   Pers, TH
   Locke, AE
   Berndt, SI
   Justice, AE
   Kahali, B
   Siemelink, MA
   Pasterkamp, G
   Strachan, DP
   Speliotes, EK
   North, KE
   Loos, RJF
   Hirschhorn, JN
   Pawitan, Y
   Ingelsson, E
AF Hagg, Sara
   Ganna, Andrea
   Van der Laan, Sander W.
   Esko, Tonu
   Pers, Tune H.
   Locke, Adam E.
   Berndt, Sonja I.
   Justice, Anne E.
   Kahali, Bratati
   Siemelink, Marten A.
   Pasterkamp, Gerard
   Strachan, David P.
   Speliotes, Elizabeth K.
   North, Kari E.
   Loos, Ruth J. F.
   Hirschhorn, Joel N.
   Pawitan, Yudi
   Ingelsson, Erik
CA GIANT Consortium
TI Gene-based meta-analysis of genome-wide association studies implicates
   new loci involved in obesity
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID ACTIN-INTERACTING PROTEIN; BODY-MASS INDEX; MITOCHONDRIAL TRNA(ILE);
   MISSING HERITABILITY; DATABASE; VARIANTS; TISSUE; CELLS; KRAP; MICE
AB To date, genome-wide association studies (GWASs) have identified > 100 loci with single variants associated with body mass index (BMI). This approach may miss loci with high allelic heterogeneity; therefore, the aim of the present study was to use gene-based meta-analysis to identify regions with high allelic heterogeneity to discover additional obesity susceptibility loci. We included GWAS data from 123 865 individuals of European descent from 46 cohorts in Stage 1 and Metabochip data from additional 103 046 individuals from 43 cohorts in Stage 2, all within the Genetic Investigation of AN thropometric Traits (GIANT) consortium. Each cohort was tested for association between similar to 2.4million (Stage 1) or similar to 200 000 (Stage 2) imputed or genotyped single variants and BMI, and summary statistics were subsequently meta-analyzed in 17 941 genes. We used the 'VErsatile Gene-based Association Study' (VEGAS) approach to assign variants to genes and to calculate gene-based P-values based on simulations. The VEGAS method was applied to each cohort separately before a gene-based meta-analysis was performed. In Stage 1, two known (FTO and TMEM18) and six novel (PEX2, MTFR2, SSFA2, IARS2, CEP295 and TXNDC12) loci were associated with BMI (P < 2.8x10(-6) for 17 941 gene tests). We confirmed all loci, and six of them were gene-wide significant in Stage 2 alone. We provide biological support for the loci by pathway, expression and methylation analyses. Our results indicate that gene-based meta-analysis of GWAS provides a useful strategy to find loci of interest that were not identified in standard single-marker analyses due to high allelic heterogeneity.
C1 [Hagg, Sara; Pawitan, Yudi] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
   [Hagg, Sara; Ingelsson, Erik] Uppsala Univ, Dept Med Sci, Mol Epidemiol & Sci Life Lab, SE-75141 Uppsala, Sweden.
   [Ganna, Andrea] Broad Inst MIT & Harvard, Program Med & Populat Genet, Cambridge, MA USA.
   [Ganna, Andrea] Massachusetts Gen Hosp, Dept Med, Analyt & Translat Genet Unit, Boston, MA 02114 USA.
   [Ganna, Andrea] Harvard Univ, Sch Med, Boston, MA USA.
   [Van der Laan, Sander W.; Siemelink, Marten A.; Pasterkamp, Gerard] Univ Med Ctr Utrecht, Div Heart & Lungs, Lab Expt Cardiol, NL-3584 CX Utrecht, Netherlands.
   [Esko, Tonu; Pers, Tune H.; Hirschhorn, Joel N.] Boston Childrens Hosp, Div Endocrinol & Genet, Boston, MA 02115 USA.
   [Esko, Tonu; Pers, Tune H.; Hirschhorn, Joel N.] Boston Childrens Hosp, Ctr Basic & Translat Obes Res, Boston, MA 02115 USA.
   [Esko, Tonu; Pers, Tune H.; Hirschhorn, Joel N.] Broad Inst Massachusetts Inst Technol & Harvard U, Cambridge, MA 02142 USA.
   [Esko, Tonu; Pers, Tune H.; Hirschhorn, Joel N.] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA.
   [Esko, Tonu] Univ Tartu, Estonian Genome Ctr, EE-51010 Tartu, Estonia.
   [Pers, Tune H.] Statens Serum Inst, Dept Epidemiol Res, DK-2300 Copenhagen, Denmark.
   [Pers, Tune H.] Univ Copenhagen, Novo Nordisk Fdn Ctr Basic Metab Res, Copenhagen, Denmark.
   [Locke, Adam E.] Univ Michigan, Ctr Stat Genet, Dept Biostat, Ann Arbor, MI 48109 USA.
   [Kahali, Bratati; Speliotes, Elizabeth K.] Univ Michigan, Dept Internal Med, Div Gastroenterol, Ann Arbor, MI 48109 USA.
   [Kahali, Bratati; Speliotes, Elizabeth K.] Univ Michigan, Dept Computat Med & Bioinformat, Ann Arbor, MI 48109 USA.
   [Berndt, Sonja I.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Justice, Anne E.; North, Kari E.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC 27599 USA.
   [North, Kari E.] Univ N Carolina, Carolina Ctr Genome Sci, Chapel Hill, NC 27599 USA.
   [Pasterkamp, Gerard] UMC Utrecht, Lab Clin Chem & Hematol, Div Labs & Pharm, Utrecht, Netherlands.
   [Strachan, David P.] Univ London, London SW17 0RE, England.
   [Loos, Ruth J. F.] Univ Cambridge, Addenbrookes Hosp, MRC Epidemiol Unit, Inst Metab Sci, Cambridge CB2 0QQ, England.
   [Loos, Ruth J. F.] Icahn Sch Med Mt Sinai, Charles Bronfman Inst Personalized Med, New York, NY 10029 USA.
   [Loos, Ruth J. F.] Univ Oxford, Genet Obes & Related Metab Traits Program, Oxford, England.
   [Loos, Ruth J. F.] Univ Oxford, Mindich Child Hlth & Dev Inst, Oxford, England.
   [Ingelsson, Erik] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
   [Ingelsson, Erik] Stanford Univ, Sch Med, Div Cardiovasc Med, Dept Med, Stanford, CA 94305 USA.
RP Ingelsson, E (reprint author), Uppsala Univ, Dept Med Sci, Mol Epidemiol & Sci Life Lab, SE-75141 Uppsala, Sweden.
EM erik.ingelsson@medsci.uu.se
OI Locke, Adam/0000-0001-6227-198X; Ganna, Andrea/0000-0002-8147-240X
FU Foundation for Geriatric Diseases, Karolinska Institutet
FX The study was supported by the Foundation for Geriatric Diseases,
   Karolinska Institutet.
NR 43
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Z9 6
U1 2
U2 10
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
EI 1460-2083
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD DEC 1
PY 2015
VL 24
IS 23
BP 6849
EP 6860
DI 10.1093/hmg/ddv379
PG 12
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA DB2WP
UT WOS:000368371600023
PM 26376864
ER

PT J
AU Baird, DD
   Saldana, TM
   Shore, DL
   Hill, MC
   Schectman, JM
AF Baird, D. D.
   Saldana, T. M.
   Shore, D. L.
   Hill, M. C.
   Schectman, J. M.
TI A single baseline ultrasound assessment of fibroid presence and size is
   strongly predictive of future uterine procedure: 8-year follow-up of
   randomly sampled premenopausal women aged 35-49 years
SO HUMAN REPRODUCTION
LA English
DT Article
DE uterine leiomyoma; ultrasonography; disease progression; hysterectomy;
   heath disparity
ID ULIPRISTAL ACETATE; NATURAL-HISTORY; WHITE WOMEN; LEIOMYOMATA;
   HYSTERECTOMY; GROWTH; EPIDEMIOLOGY; MANAGEMENT; DIAGNOSIS
AB STUDY QUESTION: How well can a single baseline ultrasound assessment of fibroid burden (presence or absence of fibroids and size of largest, if present) predict future probability of having a major uterine procedure?
   SUMMARY ANSWER: During an 8-year follow-up period, the risk of having a major uterine procedure was 2% for those without fibroids and increased with fibroid size for those with fibroids, reaching >= 7% for those with fibroids >= 4 cm in diameter at baseline.
   WHAT IS KNOWN ALREADY: Uterine fibroids are a leading indication for hysterectomy. However, when fibroids are found, there are few available data to help clinicians advise patients about disease progression.
   STUDY DESIGN, SIZE, DURATION: Women who were 35-49 years old were randomly selected from the membership of a large urban health plan; 80% of those determined to be eligible were enrolled and screened with ultrasound for fibroids >= 0.5 cm in diameter. African-American and white premenopausal participants who responded to at least one follow-up interview (N = 964, 85% of those eligible) constituted the study cohort. During follow-up (5822 person-years), participants self-reported any major uterine procedure (67% hysterectomies). Life-table analyses and Cox regression (with censoring for menopause) were used to estimate the risk of having a uterine procedure for women with no fibroids, small (<2 cm in diameter), medium (2-3.9 cm), and large fibroids (>= 4 cm). Differences between African-American and white women, importance of a clinical diagnosis of fibroids prior to study enrollment, and the impact of submucosal fibroids on risk were investigated.
   PARTICIPANTS/MATERIALS, SETTING, METHODS: There was a greater loss to follow-up for African-Americans than whites (19 versus 11%). For those with follow-up data, 64% had fibroids at baseline, 33% of whom had had a prior diagnosis. Of those with fibroids, 27% had small fibroids (<2 cm in diameter), 46% had medium (largest fibroid 2-3.9 cm in diameter), and 27% had large fibroids (largest >= 4 cm in diameter). Twenty-one percent had at least one submucosal fibroid.
   MAIN RESULTS AND THE ROLE OF CHANCE: Major uterine procedures were reported by 115 women during follow-up. The estimated risk of having a procedure in any given year of follow-up for those with fibroids compared with those without fibroids increased markedly with fibroid-size category (from 4-fold, confidence interval (CI) (1.4-11.1) for the small fibroids to 10-fold, CI (4.4-24.8) for the medium fibroids, to 27-fold, CI (11.5-65.2) for the large fibroids). This influence of fibroid size on risk did not differ between African-Americans and whites (P-value for interaction = 0.88). Once fibroid size at enrollment was accounted for, having a prior diagnosis at the time of ultrasound screening was not predictive of having a procedure. Exclusion of women with a submucosal fibroid had little influence on the results. The 8-year risk of a procedure based on lifetable analyses was 2% for women with no fibroids, 8, 23, and 47%, respectively, for women who had small, medium or large fibroids at enrollment. Given the strong association of fibroid size with subsequent risk of a procedure, these findings are unlikely to be due to chance.
   LIMITATIONS, REASONS FOR CAUTION: Despite a large sample size, the number of women having procedures during follow-up was relatively small. Thus, covariates such as BMI, which were not important in our analyses, may have associations that were too small to detect with our sample size. Another limitation is that the medical procedures were self-reported. However, we attempted to retrieve medical records when participants agreed, and 77% of the total procedures reported were verified. Our findings are likely to be generalizable to other African-American and white premenopausal women in their late 30s and 40s, but other ethnic groups have not been studied.
   WIDER IMPLICATIONS OF THE FINDINGS: Though further studies are needed to confirm and extend the results, our findings provide an initial estimate of disease progression that will be helpful to clinicians and their patients.
C1 [Baird, D. D.] NIEHS, Epidemiol Branch, POB 12233, Res Triangle Pk, NC 27709 USA.
   [Saldana, T. M.] Social & Sci Syst Inc, Durham, NC 27703 USA.
   [Shore, D. L.] Westat Corp, Durham, NC 27703 USA.
   [Hill, M. C.] George Washington Univ, Med Ctr, Dept Radiol, Washington, DC 20037 USA.
   [Schectman, J. M.] Univ Virginia Hlth Syst, Dept Med, Charlottesville, VA 22903 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 National Institute of Environmental Health Sciences; Office of Research
   on Minority Health, National Institutes of Health, Health and Human
   Services (IRB) [OH95-E-N048]
FX Funding came from the Intramural Research Program of the National
   Institute of Environmental Health Sciences and the Office of Research on
   Minority Health, National Institutes of Health, Health and Human
   Services (IRB #OH95-E-N048).
NR 32
TC 2
Z9 2
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0268-1161
EI 1460-2350
J9 HUM REPROD
JI Hum. Reprod.
PD DEC
PY 2015
VL 30
IS 12
BP 2936
EP 2944
DI 10.1093/humrep/dev235
PG 9
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA DB3UI
UT WOS:000368437300027
PM 26409013
ER

PT J
AU Ringeisen, H
   Aldworth, J
   Colpe, LJ
   Pringle, B
   Simile, C
AF Ringeisen, Heather
   Aldworth, Jeremy
   Colpe, Lisa J.
   Pringle, Beverly
   Simile, Catherine
TI Estimating the prevalence of any impairing childhood mental disorder in
   the national health interview survey
SO INTERNATIONAL JOURNAL OF METHODS IN PSYCHIATRIC RESEARCH
LA English
DT Article
DE children; adolescents; epidemiology; estimation; methods
ID PSYCHIATRIC-ASSESSMENT CAPA; TEST-RETEST RELIABILITY; DIFFICULTIES
   QUESTIONNAIRE; PSYCHOMETRIC PROPERTIES; CALIBRATION; POPULATION;
   DIAGNOSES; STRENGTHS; CHILDREN; VERSION
AB This study investigates whether the six-item Strengths and Difficulties Questionnaire SDQ (five symptoms and one impact item) included in the National Health Interview Survey (NHIS) can be used to construct models that accurately estimate the prevalence of any impairing mental disorder among children 4-17 years old as measured by a shortened Child/Adolescent or Preschool Age Psychiatric Assessment (CAPA or PAPA). A subsample of 217 NHIS respondents completed a follow-up CAPA or PAPA interview. Logistic regression models were developed to model presence of any child mental disorder with impairment (MDI) or with severe impairment (MDSI). Models containing only the SDQ impact item exhibited highly biased prevalence estimates. The best-performing model included information from both the five symptom SDQ items and the impact item, where absolute bias was reduced and sensitivity and concordance were increased. This study illustrates the importance of using all available information from the six-item SDQ to accurately estimate the prevalence of any impairing childhood mental disorder from the NHIS. Copyright (C) 2015 John Wiley & Sons, Ltd.
C1 [Ringeisen, Heather; Aldworth, Jeremy] RTI Int, Res Triangle Pk, NC USA.
   [Colpe, Lisa J.; Pringle, Beverly] NIMH, Bethesda, MD 20892 USA.
   [Simile, Catherine] Ctr Dis Control & Prevent, Natl Ctr Hlth Stat, Hyattsville, MD 20782 USA.
RP Ringeisen, H (reprint author), RTI Int, Survey Res Div, POB 12194, Res Triangle Pk, NC 27709 USA.
EM hringeisen@rti.org
FU National Institute of Mental Health [200-2009-F-32679]; NCHS within the
   Centers for Disease Control and Prevention
FX The views expressed in this manuscript do not necessarily represent the
   views of the National Institutes of Health, the National Center for
   Health Statistics (NCHS) or the Federal Government. This research was
   supported by National Institute of Mental Health through contract
   200-2009-F-32679 with the NCHS within the Centers for Disease Control
   and Prevention. The authors acknowledge reviews by Joe Gfroerer, Jonaki
   Bose, and Sarra Hedden from the Substance Abuse and Mental Health
   Services Administration and Patricia Pastor, Marcie Cynamon, Stephen
   Blumberg, and Jennifer Madans from the National Center for Health
   Statistics. At RTI International, Anne Gering and Judith Cannada
   provided editorial assistance and report production. The statistical
   expert was Jeremy Aldworth.
NR 21
TC 0
Z9 0
U1 2
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1049-8931
EI 1557-0657
J9 INT J METH PSYCH RES
JI Int. J. Methods Psychiatr. Res.
PD DEC
PY 2015
VL 24
IS 4
BP 266
EP 274
DI 10.1002/mpr.1471
PG 9
WC Psychiatry
SC Psychiatry
GA DB3NY
UT WOS:000368419600003
PM 26202997
ER

PT J
AU Coffman, MC
   Trubanova, A
   Richey, JA
   White, SW
   Kim-Spoon, J
   Ollendick, TH
   Pine, DS
AF Coffman, Marika C.
   Trubanova, Andrea
   Richey, J. Anthony
   White, Susan W.
   Kim-Spoon, Jungmeen
   Ollendick, Thomas H.
   Pine, Daniel S.
TI Validation of the NIMH-ChEFS adolescent face stimulus set in an
   adolescent, parent, and health professional sample
SO INTERNATIONAL JOURNAL OF METHODS IN PSYCHIATRIC RESEARCH
LA English
DT Article
DE adolescent development; face processing; methodology; emotion
   perception; face stimulus set
ID FACIAL EXPRESSIONS; PROCESSING BIASES; EMOTIONAL FACES; SOCIAL PHOBIA;
   VISUAL-SEARCH; CHILDREN; ANXIETY; ADULTS; RECOGNITION; DEPRESSION
AB Attention to faces is a fundamental psychological process in humans, with atypical attention to faces noted across several clinical disorders. Although many clinical disorders onset in adolescence, there is a lack of well-validated stimulus sets containing adolescent faces available for experimental use. Further, the images comprising most available sets are not controlled for high-and low-level visual properties. Here, we present a cross-site validation of the National Institute of Mental Health Child Emotional Faces Picture Set (NIMH-ChEFS), comprised of 257 photographs of adolescent faces displaying angry, fearful, happy, sad, and neutral expressions. All of the direct facial images from the NIMH-ChEFS set were adjusted in terms of location of facial features and standardized for luminance, size, and smoothness. Although overall agreement between raters in this study and the original development-site raters was high (89.52%), this differed by group such that agreement was lower for adolescents relative to mental health professionals in the current study. These results suggest that future research using this face set or others of adolescent/child faces should base comparisons on similarly-aged validation data. Copyright (C) 2015 John Wiley & Sons, Ltd.
C1 [Coffman, Marika C.; Trubanova, Andrea; Richey, J. Anthony; White, Susan W.; Kim-Spoon, Jungmeen; Ollendick, Thomas H.] Virginia Polytech Inst & State Univ, Dept Psychol, Blacksburg, VA 24061 USA.
   [Pine, Daniel S.] NIMH, Sect Dev & Affect Neurosci, Mood Program, Intramural Res Program, Bethesda, MD 20892 USA.
   [Pine, Daniel S.] NIMH, Sect Dev & Affect Neurosci, Anxiety Program, Intramural Res Program, Bethesda, MD 20892 USA.
RP Coffman, MC (reprint author), Virginia Polytech Inst & State Univ, Dept Psychol, Blacksburg, VA 24061 USA.
EM marika@vt.edu
FU National Institute of Mental Health (NIMH) [R34 MH096915]; NIMH
FX This work was supported in part by the National Institute of Mental
   Health (NIMH) Grant # R34 MH096915 awarded to Thomas H. Ollendick. The
   authors gratefully acknowledge the NIMH for its support and the many
   colleagues who assisted them with various aspects of the present
   research, including Kathleen Driscoll who helped create the surveys.
   Finally, the authors thank the parents, teenagers, and colleagues who
   participated in the validation ratings.
NR 43
TC 3
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U1 3
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1049-8931
EI 1557-0657
J9 INT J METH PSYCH RES
JI Int. J. Methods Psychiatr. Res.
PD DEC
PY 2015
VL 24
IS 4
BP 275
EP 286
DI 10.1002/mpr.1490
PG 12
WC Psychiatry
SC Psychiatry
GA DB3NY
UT WOS:000368419600004
PM 26359940
ER

PT J
AU Lee, L
   Igarashi, H
   Fujimori, N
   Hijioka, M
   Kawabe, K
   Oda, Y
   Jensen, RT
   Ito, T
AF Lee, Lingaku
   Igarashi, Hisato
   Fujimori, Nao
   Hijioka, Masayuki
   Kawabe, Ken
   Oda, Yoshinao
   Jensen, Robert T.
   Ito, Tetsuhide
TI Long-term outcomes and prognostic factors in 78 Japanese patients with
   advanced pancreatic neuroendocrine neoplasms: a single-center
   retrospective study
SO JAPANESE JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
DE pancreatic neuroendocrine neoplasms; pancreatic neuroendocrine tumor;
   pancreatic neuroendocrine carcinoma; Ki-67 index; prognostic factor
ID FACTORS INFLUENCING SURVIVAL; ZOLLINGER-ELLISON-SYNDROME; ISLET-CELL
   CARCINOMA; ENDOCRINE TUMORS; MITOTIC COUNT; KI-67 INDEX; PHASE-II;
   EPIDEMIOLOGY; METASTASES; SYSTEM
AB Objective: Despite an increase in the number of Japanese patients with pancreatic neuroendocrine neoplasms, long-term outcomes and prognostic factors, especially for those with advanced disease, remain unclear.
   Methods: We retrospectively reviewed the medical records of 78 patients with unresectable pancreatic neuroendocrine neoplasms treated at our hospital from January 1987 to March 2015. Survival analyses were performed using Kaplan-Meier methods. Prognostic significance of several clinicopathological factors were analyzed by univariate and multivariate analyses using a Cox regression model.
   Results: Median overall survivals of pancreatic neuroendocrine tumor (n = 64) and pancreatic neuroendocrine carcinoma (n = 14) were 83.7 and 9.1 months, respectively (hazard ratio: 0.02, 95% confidence interval: 0.01-0.08, P < 0.001). Although no significant differences were observed using a Ki-67 cut-off value of 2% (hazard ratio: 0.46, 95% confidence interval: 0.16-1.13, P = 0.0989), a Ki-67 cut-off of 10% was a significant predictor in patients with pancreatic neuroendocrine tumor (hazard ratio: 9.95, 95% confidence interval, 3.01-32.97, P < 0.001). Treatment after the advent of targeted therapy (hazard ratio: 0.07, 95% confidence interval: 0.03-0.19, P < 0.001) and the presence of bone metastases (hazard ratio: 4.38, 95% confidence interval: 1.42-11.29, P = 0.013) were significant prognostic factors in patients with pancreatic neuroendocrine tumor evaluated by univariate analysis. Multivariate analysis also revealed that a Ki-67 index = 10% (hazard ratio: 38.8, 95% confidence interval: 8.42-226.62, P < 0.001), approval of targeted therapy (hazard ratio: 0.02, 95% confidence interval: 0.00-0.11, P < 0.001) and bone metastases (hazard ratio: 5.56, 95% confidence interval: 1.10-24.00, P = 0.039) were independent prognostic factors.
   Conclusions: We elucidated the long-term outcomes and prognostic factors in Japanese patients with advanced pancreatic neuroendocrine neoplasms.
C1 [Lee, Lingaku; Igarashi, Hisato; Fujimori, Nao; Hijioka, Masayuki; Kawabe, Ken; Ito, Tetsuhide] Kyushu Univ, Grad Sch Med Sci, Dept Med & Bioregulatory Sci, Fukuoka 8128582, Japan.
   [Oda, Yoshinao] Kyushu Univ, Grad Sch Med Sci, Dept Anat Pathol, Fukuoka 8128582, Japan.
   [Jensen, Robert T.] NIDDK, Digest Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Ito, T (reprint author), Kyushu Univ, Grad Sch Med Sci, Dept Med & Bioregulatory Sci, Higashi Ku, 3-1-1 Maidashi, Fukuoka 8128582, Japan.
EM itopapa@intmed3.med.kyushu-u.ac.jp
RI U-ID, Kyushu/C-5291-2016
FU Research Committee of Intractable Pancreatic Disease by Ministry of
   Health, Labour and Welfare of Japan
FX This study was supported in part by the Research Committee of
   Intractable Pancreatic Disease (Principal Investigator: Yoshifumi
   Takeyama) provided by the Ministry of Health, Labour and Welfare of
   Japan.
NR 56
TC 3
Z9 3
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0368-2811
EI 1465-3621
J9 JPN J CLIN ONCOL
JI Jpn. J. Clin. Oncol.
PD DEC
PY 2015
VL 45
IS 12
BP 1131
EP 1138
DI 10.1093/jjco/hyv143
PG 8
WC Oncology
SC Oncology
GA DB3JB
UT WOS:000368405900006
PM 26378090
ER

PT J
AU Chon, B
   Tokumasu, F
   Lee, JY
   Allen, DW
   Rice, JP
   Hwang, J
AF Chon, Bonghwan
   Tokumasu, Fuyuki
   Lee, Ji Youn
   Allen, David W.
   Rice, Joseph P.
   Hwang, Jeeseong
TI Digital phantoms generated by spectral and spatial light modulators
SO JOURNAL OF BIOMEDICAL OPTICS
LA English
DT Article
DE hyperspectral imaging; optical imaging standard; digital phantom; single
   cell molecular imaging; scatter imaging; spatial light modulator
ID PLASMODIUM-FALCIPARUM; MALARIA PIGMENT; HEMOZOIN; SYSTEM
AB A hyperspectral image projector (HIP) based on liquid crystal on silicon spatial light modulators is explained and demonstrated to generate data cubes. The HIP-constructed data cubes are three-dimensional images of the spatial distribution of spectrally resolved abundances of intracellular light-absorbing oxyhemoglobin molecules in single erythrocytes. Spectrally and spatially resolved image data indistinguishable from the real scene may be used as standard data cubes, so-called digital phantoms, to calibrate image sensors and validate image analysis algorithms for their measurement quality, performance consistency, and interlaboratory comparisons for quantitative biomedical imaging applications. (C) 2015 Society of Photo-Optical Instrumentation Engineers (SPIE)
C1 [Chon, Bonghwan; Lee, Ji Youn; Hwang, Jeeseong] NIST, Quantum Elect & Photon Div, Boulder, CO 80305 USA.
   [Tokumasu, Fuyuki] NIH, Lab Malaria & Vector Res, Bethesda, MD 20892 USA.
   [Allen, David W.; Rice, Joseph P.] NIST, Sensor Sci Div, Gaithersburg, MD 20899 USA.
RP Hwang, J (reprint author), NIST, Quantum Elect & Photon Div, 325 Broadway St, Boulder, CO 80305 USA.
EM jch@nist.gov
FU NIST Innovations in Measurement Science Program on Optical Medical
   Imaging for Clinical Applications and the Intramural Research Program of
   the NIAID, NIH; NIST and the Intramural Program of the National
   Institute for Biomedical Imaging and Bioengineering of the NIH
FX Certain commercial equipments, instruments, or materials are identified
   in this paper. Such identification does not imply recommendation or
   endorsement by the National Institute of Standards and Technology, nor
   does it imply that the materials or equipment identified are necessarily
   the best available for the purpose. This research was supported by the
   NIST Innovations in Measurement Science Program on Optical Medical
   Imaging for Clinical Applications and the Intramural Research Program of
   the NIAID, NIH. This research was performed while J.L. held a National
   Research Council Research Associateship Award at NIH (NIBIB)/NIST.
   Funding for this award was provided by the NIST and the Intramural
   Program of the National Institute for Biomedical Imaging and
   Bioengineering of the NIH. Authors would like to thank to Dr. Kimberly
   Briggman, Dr. Maritoni Litorja, and Dr. Eric Shirley at NIST, Do-Hyun
   Kim at USFDA, and Stephen Kanick at Dartmouth College for valuable
   discussions.
NR 31
TC 0
Z9 0
U1 2
U2 2
PU SPIE-SOC PHOTO-OPTICAL INSTRUMENTATION ENGINEERS
PI BELLINGHAM
PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98225 USA
SN 1083-3668
EI 1560-2281
J9 J BIOMED OPT
JI J. Biomed. Opt.
PD DEC
PY 2015
VL 20
IS 12
AR 121309
DI 10.1117/1.JBO.20.12.121309
PG 8
WC Biochemical Research Methods; Optics; Radiology, Nuclear Medicine &
   Medical Imaging
SC Biochemistry & Molecular Biology; Optics; Radiology, Nuclear Medicine &
   Medical Imaging
GA DB3VG
UT WOS:000368440300012
PM 26502383
ER

PT J
AU Ghassemi, P
   Wang, JT
   Melchiorri, AJ
   Ramella-Roman, JC
   Mathews, SA
   Coburn, JC
   Sorg, BS
   Chen, Y
   Pfefer, TJ
AF Ghassemi, Pejhman
   Wang, Jianting
   Melchiorri, Anthony J.
   Ramella-Roman, Jessica C.
   Mathews, Scott A.
   Coburn, James C.
   Sorg, Brian S.
   Chen, Yu
   Pfefer, T. Joshua
TI Rapid prototyping of biomimetic vascular phantoms for hyperspectral
   reflectance imaging
SO JOURNAL OF BIOMEDICAL OPTICS
LA English
DT Article
DE three-dimensional printing; tissue phantoms; hyperspectral reflectance
   imaging; oximetry
ID TISSUE OPTICAL-PROPERTIES; TURBID MEDIA; IN-VITRO; SATURATION
AB The emerging technique of rapid prototyping with three-dimensional (3-D) printers provides a simple yet revolutionary method for fabricating objects with arbitrary geometry. The use of 3-D printing for generating morphologically biomimetic tissue phantoms based on medical images represents a potentially major advance over existing phantom approaches. Toward the goal of image-defined phantoms, we converted a segmented fundus image of the human retina into a matrix format and edited it to achieve a geometry suitable for printing. Phantoms with vessel-simulating channels were then printed using a photoreactive resin providing biologically relevant turbidity, as determined by spectrophotometry. The morphology of printed vessels was validated by x-ray microcomputed tomography. Channels were filled with hemoglobin (Hb) solutions undergoing desaturation, and phantoms were imaged with a near-infrared hyperspectral reflectance imaging system. Additionally, a phantom was printed incorporating two disjoint vascular networks at different depths, each filled with Hb solutions at different saturation levels. Light propagation effects noted during these measurements-including the influence of vessel density and depth on Hb concentration and saturation estimates, and the effect of wavelength on vessel visualization depth-were evaluated. Overall, our findings indicated that 3-D-printed biomimetic phantoms hold significant potential as realistic and practical tools for elucidating light-tissue interactions and characterizing biophotonic system performance. (C) The Authors. Published by SPIE under a Creative Commons Attribution 3.0 Unported License.
C1 [Ghassemi, Pejhman; Wang, Jianting; Coburn, James C.; Pfefer, T. Joshua] US FDA, Ctr Devices & Radiol Hlth, Silver Spring, MD 20993 USA.
   [Wang, Jianting; Melchiorri, Anthony J.; Chen, Yu] Univ Maryland, Fischell Dept Bioengn, College Pk, MD 20742 USA.
   [Ramella-Roman, Jessica C.] Florida Int Univ, Dept Biomed Engn, Miami, FL 33174 USA.
   [Ramella-Roman, Jessica C.] Florida Int Univ, Herbert Wertheim Coll Med, Miami, FL 33174 USA.
   [Mathews, Scott A.] Catholic Univ Amer, Dept Elect Engn & Comp Sci, Washington, DC 20064 USA.
   [Sorg, Brian S.] NCI, NIH, Rockville, MD 20852 USA.
RP Pfefer, TJ (reprint author), US FDA, Ctr Devices & Radiol Hlth, 10903 New Hampshire Ave, Silver Spring, MD 20993 USA.
EM Joshua.Pfefer@fda.hhs.gov
FU Food and Drug Administration (FDA) Critical Path Initiative; National
   Science Foundation's FDA Scholar-in-Residence program (NSF)
   [CBET-1238407]; University of Maryland's Center for Excellence in
   Regulatory Science and Innovation
FX The authors would like to thank Dr. Srinidhi Nagaraja, Dr. Maureen
   Dreher, and Dr. Maria Iacono for their help with mu-CT imaging and 3-D
   visualization. The authors gratefully acknowledge funding support from
   the Food and Drug Administration (FDA) Critical Path Initiative, the
   National Science Foundation's FDA Scholar-in-Residence program (NSF,
   CBET-1238407), and the University of Maryland's Center for Excellence in
   Regulatory Science and Innovation.
NR 29
TC 2
Z9 2
U1 1
U2 5
PU SPIE-SOC PHOTO-OPTICAL INSTRUMENTATION ENGINEERS
PI BELLINGHAM
PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98225 USA
SN 1083-3668
EI 1560-2281
J9 J BIOMED OPT
JI J. Biomed. Opt.
PD DEC
PY 2015
VL 20
IS 12
AR 121312
DI 10.1117/1.JBO.20.12.121312
PG 10
WC Biochemical Research Methods; Optics; Radiology, Nuclear Medicine &
   Medical Imaging
SC Biochemistry & Molecular Biology; Optics; Radiology, Nuclear Medicine &
   Medical Imaging
GA DB3VG
UT WOS:000368440300015
PM 26662064
ER

PT J
AU Aufforth, RD
   Ramakant, P
   Sadowski, SM
   Mehta, A
   Trebska-McGowan, K
   Nilubol, N
   Pacak, K
   Kebebew, E
AF Aufforth, Rachel D.
   Ramakant, Pooja
   Sadowski, Samira M.
   Mehta, Amit
   Trebska-McGowan, Katarzyna
   Nilubol, Naris
   Pacak, Karel
   Kebebew, Electron
TI Pheochromocytoma Screening Initiation and Frequency in von Hippel-Lindau
   Syndrome
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID DISEASE; NORMETANEPHRINE; METANEPHRINE
AB Context: Patients with von Hippel-Lindau (VHL) syndrome have a 25-30% chance of developing pheochromocytoma. Although practice guidelines recommend biochemical and radiological screening every 1-2 years for pheochromocytoma in patients with VHL, there are limited data on the optimal age and frequency for screening.
   Objective: Our objective was to determine the earliest age of onset and frequency of contralateral and recurrent pheochromocytomas in patients with VHL syndrome.
   Methods: This is a retrospective analysis of a prospective cohort of patients with VHL enrolled in a natural history study.
   Results: A total of 273 patients diagnosed with VHL were enrolled in a natural history clinical study. Thirty-one percent (84) were diagnosed with pheochromocytoma. The mean age of diagnosis was 28.8 +/- 13.9 years. The earliest age at diagnosis was 5.5 years. Median follow-up for the cohort was 116.6 months (range, 0.1-613.2). Ninety-nine percent (83) of patients underwent adrenalectomy. Fifty-eight and 32% of patients had metanephrines and/or catecholamines elevated more than two times and more than four times the upper limit of normal, respectively. Twenty-five percent (21) of pheochromocytomas were diagnosed in pediatric patients younger than 19 years of age, and 86% and 57% of pediatric patients had an elevation more than two times and more than four times upper limit of normal, respectively. Eight patients had a total of nine recurrences. The median age at recurrence was 33.5 years (range, 8.8-51.9). Recurrences occurred as short as 0.5 years and as long as 39.7 years after the initial operation.
   Conclusions: Our findings among VHL pediatric patients supports the need for biochemical screening starting at age 5 with annual lifelong screening.
C1 [Aufforth, Rachel D.; Sadowski, Samira M.; Nilubol, Naris; Kebebew, Electron] NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
   [Ramakant, Pooja] Christian Med Coll & Hosp, Dept Endocrine Surg, Vellore, Tamil Nadu, India.
   [Mehta, Amit] Geisel Sch Med, Hanover, NH USA.
   [Trebska-McGowan, Katarzyna] NCI, Thorac & Gastrointestinal Oncol Branch, Bethesda, MD 20892 USA.
   [Pacak, Karel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
RP Kebebew, E (reprint author), NCI, Endocrine Oncol Branch, Bethesda, MD 20892 USA.
EM kebebewe@mail.nih.gov
FU intramural research programs of the Center for Cancer Research, National
   Cancer Institute, National Institutes of Health
FX This research was supported by the intramural research programs of the
   Center for Cancer Research, National Cancer Institute, National
   Institutes of Health.
NR 21
TC 2
Z9 2
U1 0
U2 4
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0021-972X
EI 1945-7197
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD DEC
PY 2015
VL 100
IS 12
BP 4498
EP 4504
DI 10.1210/jc.2015-3045
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA DB3RI
UT WOS:000368428600030
PM 26451910
ER

PT J
AU Rampling, T
   Ewer, K
   Bowyer, G
   Wright, D
   Venkatraman, N
   Payne, R
   Nicosia, A
   Sullivan, N
   Graham, B
   Pollard, A
   Draper, S
   Ballou, R
   Lawrie, A
   Gilbert, S
   Hill, A
AF Rampling, Tommy
   Ewer, Katie
   Bowyer, Georgina
   Wright, Danny
   Venkatraman, Navin
   Payne, Ruth
   Nicosia, Alfredo
   Sullivan, Nancy
   Graham, Barney
   Pollard, Andrew
   Draper, Simon
   Ballou, Ripley
   Lawrie, Alison
   Gilbert, Sarah
   Hill, Adrian
TI SAFETY AND IMMUNOGENICITY OF THE HETEROLOGOUS PRIME-BOOST EBOLAVIRUS
   VACCINE REGIMEN CHAD3-EBO Z AND MVA-BN (R) FILO IN HEALTHY UK ADULTS
SO JOURNAL OF INFECTION
LA English
DT Meeting Abstract
C1 [Rampling, Tommy; Ewer, Katie; Bowyer, Georgina; Wright, Danny; Venkatraman, Navin; Payne, Ruth; Pollard, Andrew; Draper, Simon; Lawrie, Alison; Gilbert, Sarah; Hill, Adrian] Univ Oxford, Oxford, England.
   [Sullivan, Nancy; Graham, Barney] NIAID, Rockville, MD USA.
   [Ballou, Ripley] GlaxoSmithkline, Rixensart, Belgium.
   [Nicosia, Alfredo] ReiThera, Rome, Italy.
RI Ewer, Katie/B-4328-2011
OI Ewer, Katie/0000-0001-9827-9836
NR 0
TC 0
Z9 0
U1 0
U2 1
PU W B SAUNDERS CO LTD
PI LONDON
PA 32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND
SN 0163-4453
EI 1532-2742
J9 J INFECTION
JI J. Infect.
PD DEC
PY 2015
VL 71
IS 6
BP 688
EP 688
DI 10.1016/j.jinf.2015.09.031
PG 1
WC Infectious Diseases
SC Infectious Diseases
GA DB4JZ
UT WOS:000368480600022
ER

PT J
AU Peng, YH
   Shen, DG
   Liao, S
   Turkbey, B
   Rais-Bahrami, S
   Wood, B
   Karademir, I
   Antic, T
   Yousef, A
   Jiang, YL
   Pinto, PA
   Choyke, PL
   Oto, A
AF Peng, Yahui
   Shen, Dinggang
   Liao, Shu
   Turkbey, Baris
   Rais-Bahrami, Soroush
   Wood, Bradford
   Karademir, Ibrahim
   Antic, Tatjana
   Yousef, Ambereen
   Jiang, Yulei
   Pinto, Peter A.
   Choyke, Peter L.
   Oto, Aytekin
TI MRI-Based Prostate Volume-Adjusted Prostate-Specific Antigen in the
   Diagnosis of Prostate Cancer
SO JOURNAL OF MAGNETIC RESONANCE IMAGING
LA English
DT Article
ID TRANSITION ZONE VOLUME; RADICAL PROSTATECTOMY; TRANSRECTAL ULTRASOUND;
   SPECIMEN VOLUMES; GLEASON SCORE; PSA DENSITY; HYPERPLASIA; MEN; TRIAL;
   NG/ML
AB Purpose: To determine whether prostate-specific antigen (PSA) levels adjusted by prostate and zonal volumes estimated from magnetic resonance imaging (MRI) improve the diagnosis of prostate cancer (PCa) and differentiation between patients who harbor high-Gleason-sum PCa and those without PCa.
   Materials and Methods: This retrospective study was Health Insurance Portability and Accountability Act (HIPAA)-compliant and approved by the Institutional Review Board of participating medical institutions. T-2-weighted MR images were acquired for 61 PCa patients and 100 patients with elevated PSA but without PCa. Computer methods were used to segment prostate and zonal structures and to estimate the total prostate and central-gland (CG) volumes, which were then used to calculate CG volume fraction, PSA density, and PSA density adjusted by CG volume. These quantities were used to differentiate patients with and without PCa. Area under the receiver operating characteristic curve (AUC) was used as the figure of merit.
   Results: The total prostate and CG volumes, CG volume fraction, and PSA density adjusted by the total prostate and CG volumes were statistically significantly different between patients with PCa and patients without PCa (P <= 0.007). AUC values for the total prostate and CG volumes, and PSA density adjusted by CG volume, were 0.68 +/- 0.04, 0.68 +/- 0.04, and 0.66 +/- 0.04, respectively, and were significantly better than that of PSA (P< 0.02), for differentiation of PCa patients from patients without PCa.
   Conclusion: The total prostate and CG volumes estimated from T-2-weighted MR images and PSA density adjusted by these volumes can improve the effectiveness of PSA for the diagnosis of PCa and differentiation of high-Gleason-sum PCa patients from patients without PCa.
C1 [Peng, Yahui] Beijing Jiaotong Univ, Sch Elect & Informat Engn, Beijing 100044, Peoples R China.
   [Peng, Yahui; Karademir, Ibrahim; Yousef, Ambereen; Jiang, Yulei; Oto, Aytekin] Univ Chicago, Dept Radiol, Chicago, IL 60637 USA.
   [Shen, Dinggang; Liao, Shu] Univ N Carolina, Dept Radiol, Chapel Hill, NC USA.
   [Turkbey, Baris] Natl Canc Inst, NIH, Mol Imaging Program, Bethesda, MD USA.
   [Rais-Bahrami, Soroush; Wood, Bradford; Pinto, Peter A.] Natl Canc Inst, NIH, Urol Oncol Branch, Bethesda, MD USA.
   [Antic, Tatjana] Univ Chicago, Dept Pathol, Chicago, IL 60637 USA.
   [Choyke, Peter L.] NIH, Dept Diagnost Radiol, Bethesda, MD 20892 USA.
RP Peng, YH (reprint author), Beijing Jiaotong Univ, Sch Elect & Informat Engn, 3 Shangyuancun, Beijing 100044, Peoples R China.
EM yhpeng@bjtu.edu.cn
OI Rais-Bahrami, Soroush/0000-0001-9466-9925
FU US Army Medical Research and Materiel Command Prostate Cancer Research
   Program; Idea Development Award [PC093485]; Beijing Jiaotong University
   Talent Fund [2014RC044]
FX Contract grant sponsor: US Army Medical Research and Materiel Command
   Prostate Cancer Research Program; Contract grant number: Idea
   Development Award PC093485; Contract grant sponsor: Beijing Jiaotong
   University Talent Fund; Contract grant number: 2014RC044.
NR 41
TC 3
Z9 3
U1 2
U2 4
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 DEC
PY 2015
VL 42
IS 6
BP 1733
EP 1739
DI 10.1002/jmri.24944
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA DB1HD
UT WOS:000368258100030
PM 25946664
ER

PT J
AU Siglinsky, E
   Krueger, D
   Ward, RE
   Caserotti, P
   Strotmeyer, ES
   Harris, TB
   Binkley, N
   Buehring, B
AF Siglinsky, E.
   Krueger, D.
   Ward, R. E.
   Caserotti, P.
   Strotmeyer, E. S.
   Harris, T. B.
   Binkley, N.
   Buehring, B.
TI Effect of age and sex on jumping mechanography and other measures of
   muscle mass and function
SO JOURNAL OF MUSCULOSKELETAL & NEURONAL INTERACTIONS
LA English
DT Article
DE Aging; Skeletal Muscle; Sarcopenia; Jumping Mechanography; Muscle
   Function Tests
ID LOWER-EXTREMITY FUNCTION; PHYSICAL PERFORMANCE BATTERY; X-RAY
   ABSORPTIOMETRY; OLDER-ADULTS; BODY-COMPOSITION; SUBSEQUENT DISABILITY;
   WALKING SPEED; GAIT SPEED; SARCOPENIA; POWER
AB Objectives: Sarcopenia increases falls and fracture risk. Sarcopenia clinical trials require robust quantitative tools to evaluate muscle function; jumping mechanography (JM) is likely one such tool. However, US data comparing JM with traditional tests across the lifespan is limited. This study evaluated the effect of age and sex on JM compared with traditional function tests and lean mass. Methods: US adults (213 women/119 men; mean age 65.4 years, range 27-96) performed functional tests including JM, Short Physical Performance Battery (SPPB) and grip strength (GS). Appendicular lean mass (ALM) was measured using DXA. Results: Men had higher relative jump power [mean (SD) 28.5 (10.52) vs. 21.9 (7.11) W/kg], GS [35.5 (9.84) vs. 22.7 (6.98) kg] and ALM/ht(2) [8.25 (1.35) vs. 6.99 (1.38) kg/m(2)] (all p< 0.0001); no difference was observed for SPPB components. JM parameters were more strongly correlated with age than traditional tests (R-2= 0.38-0.61 vs. R-2= 0.01-0.28) and weakly with GS and chair rise time (R-2= 0.30-0.36). Conclusion: JM parameters are correlated with GS and chair rise time and demonstrate stronger correlations with age. JM shows promise as a valuable tool to evaluate and monitor interventions for sarcopenia as it could potentially detect change in muscle function more precisely than existing tools.
C1 [Siglinsky, E.; Krueger, D.; Binkley, N.; Buehring, B.] Univ Wisconsin, Osteoporosis Clin Res Program, Madison, WI 53705 USA.
   [Ward, R. E.] Spaulding Rehabil Hosp, Cambridge, MA USA.
   [Ward, R. E.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
   [Caserotti, P.] Univ Southern Denmark, Odense, Denmark.
   [Strotmeyer, E. S.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Ctr Aging & Populat Hlth, Pittsburgh, PA USA.
   [Harris, T. B.] NIA, Bethesda, MA USA.
   [Buehring, B.] William S Middleton Mem Vet Adm Med Ctr, Madison, WI USA.
RP Buehring, B (reprint author), Univ Wisconsin, Osteoporosis Clin Res Program, 2870 Univ Ave,Suite 100, Madison, WI 53705 USA.
EM bbuehring@medicine.wisc.edu
RI Buehring, Bjoern/L-5581-2013; 
OI Buehring, Bjoern/0000-0003-3841-624X; Strotmeyer,
   Elsa/0000-0002-4093-6036
FU National Institute on Aging [P01-AG020166]; General Clinical Research
   Centers Program; National Center for Advancing Translational Sciences
   (NCATS), National Institutes of Health [UL1TR000427]; Merck Co., Inc.
FX The MIDUS research is supported by a grant from the National Institute
   on Aging (P01-AG020166). The research was further supported by the
   General Clinical Research Centers Program and UL1TR000427 (UW) from the
   National Center for Advancing Translational Sciences (NCATS), National
   Institutes of Health". Jump Validation and Vitamin D studies at the
   University of Wisconsin sponsored by an investigator initiated research
   grant from Merck & Co., Inc.
NR 43
TC 3
Z9 3
U1 2
U2 7
PU JMNI
PI NAFPLION
PA 7 SPILIADOU SQ, NAFPLION, 21 100, GREECE
SN 1108-7161
J9 J MUSCULOSKEL NEURON
JI J. Musculoskelet. Neuronal Interact.
PD DEC
PY 2015
VL 15
IS 4
BP 301
EP 308
PG 8
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA DB1CF
UT WOS:000368244900001
PM 26636275
ER

PT J
AU Sorond, FA
   Cruz-Almeida, Y
   Clark, DJ
   Viswanathan, A
   Scherzer, CR
   De Jager, P
   Csiszar, A
   Laurienti, PJ
   Hausdorff, JM
   Chen, WG
   Ferrucci, L
   Rosano, C
   Studenski, SA
   Black, SE
   Lipsitz, LA
AF Sorond, Farzaneh A.
   Cruz-Almeida, Yenisel
   Clark, David J.
   Viswanathan, Anand
   Scherzer, Clemens R.
   De Jager, Philip
   Csiszar, Anna
   Laurienti, Paul J.
   Hausdorff, Jeffery M.
   Chen, Wen G.
   Ferrucci, Luiggi
   Rosano, Caterina
   Studenski, Stephanie A.
   Black, Sandra E.
   Lipsitz, Lewis A.
TI Aging, the Central Nervous System, and Mobility in Older Adults: Neural
   Mechanisms of Mobility Impairment
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
   SCIENCES
LA English
DT Article
DE CNS; Aging; Mobility; Imaging
ID SMALL VESSEL DISEASE; VASCULAR COGNITIVE IMPAIRMENT; WHITE-MATTER
   LESIONS; CEREBROVASCULAR HEMODYNAMICS; ISCHEMIC-STROKE; GAIT SPEED;
   CADASIL; ASSOCIATION; PLASTICITY; WALKING
AB Background. Mobility is crucial for successful aging and is impaired in many older adults. We know very little about the subtle, subclinical age-related changes in the central nervous system (CNS) that mediate mobility impairment.
   Methods. A conference series focused on aging, the CNS, and mobility was launched. The second conference addressed major age-associated mechanisms of CNS-mediated mobility impairment. Speakers and conference attendees recommended key areas for future research, identified barriers to progress, and proposed strategies to overcome them.
   Results. Priorities identified for future research include (a) studying interactions among different mechanisms; (b) examining effects of interventions targeting these mechanisms; (c) evaluating the effect of genetic polymorphisms on risks and course of age-related mobility impairment; and (d) examining the effect of age on CNS repair processes, neuroplasticity, and neuronal compensatory mechanisms. Key strategies to promote research include (a) establish standard measures of mobility across species; (b) evaluate the effect of aging in the absence of disease on CNS and mobility; and (c) use advanced computational methods to better evaluate the interactions between CNS and other systems involved in mobility.
   Conclusions. CNS is a major player in the process, leading to mobility decline with aging. Future research in this area has the potential to prolong independence in older persons. Better interactions among disciplines and shared research paradigms are needed to make progress. Research priorities include the development of innovative approaches to integrate research on aging, cognition, and movement with attention to neurovascular function, neuroplasticity, and neurophysiological reserve.
C1 [Sorond, Farzaneh A.] Brigham & Womens Hosp, Stroke Div, Dept Neurol, Boston, MA 02115 USA.
   [Cruz-Almeida, Yenisel] Univ Florida, Coll Med, Dept Aging & Geriatr Res, Inst Aging, Gainesville, FL USA.
   [Clark, David J.] Univ Florida, Dept Aging & Geriatr Res, North Florida South Georgia Vet Hlth Syst, Brain Rehabil Res Ctr, Gainesville, FL USA.
   [Viswanathan, Anand] Harvard Univ, Sch Med, Dept Neurol, Stroke Div,Massachusetts Gen Hosp, Boston, MA 02115 USA.
   [Scherzer, Clemens R.; De Jager, Philip] Harvard Univ, Brigham & Womens Hosp, Dept Neurol, Sch Med, Boston, MA 02115 USA.
   [Csiszar, Anna] Univ Oklahoma, Hlth Sci Center, Reynolds Oklahoma Ctr Aging, Dept Geriatr Med, Norman, OK 73019 USA.
   [Laurienti, Paul J.] Wake Forest Sch Med, Dept Radiol, Winston Salem, NC USA.
   [Hausdorff, Jeffery M.] Tel Aviv Univ, Tel Aviv Sourasky Med Ctr, Dept Med, IL-69978 Tel Aviv, Israel.
   [Chen, Wen G.] NIA, Sensory & Motor Disorders Aging, Bethesda, MD 20892 USA.
   [Ferrucci, Luiggi] NIA, Longitudinal Studies Sect, Bethesda, MD 20892 USA.
   [Rosano, Caterina] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15260 USA.
   [Studenski, Stephanie A.] Pittsburgh Healthcare Syst, Div Geriatr Med, Dept Med, Pittsburgh, PA USA.
   [Black, Sandra E.] Univ Toronto, Sunnybrook Res Inst, Dept Neurol, Toronto, ON M5S 1A1, Canada.
   [Lipsitz, Lewis A.] Harvard Univ, Sch Med, Hebrew Senior Life, Inst Aging Res,Res, Boston, MA USA.
RP Sorond, FA (reprint author), Brigham & Womens Hosp, Stroke Div, Dept Neurol, 75 Francis St, Boston, MA 02115 USA.
EM fsorond@partners.org
OI Rosano, Caterina/0000-0002-0909-1506; Rosano,
   Caterina/0000-0002-4271-6010
FU National Institute on Aging [U13-AG-041613-01, T32-AG-000181];
   University of Pittsburgh Claude D. Pepper Older Americans Independence
   Center (National Institute on Aging) [P30-AG-024827];  [RO1-NS-085002]
FX This work was supported by a cooperative conference grant (National
   Institute on Aging, U13-AG-041613-01), the University of Pittsburgh
   Claude D. Pepper Older Americans Independence Center (National Institute
   on Aging, P30-AG-024827), a postdoctoral training grant (National
   Institute on Aging, T32-AG-000181), and RO1-NS-085002.
NR 45
TC 6
Z9 6
U1 2
U2 8
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD DEC
PY 2015
VL 70
IS 12
BP 1526
EP 1532
DI 10.1093/gerona/glv130
PG 7
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA DB2UB
UT WOS:000368364100009
PM 26386013
ER

PT J
AU Marcum, ZA
   Perera, S
   Newman, AB
   Thorpe, JM
   Switzer, GE
   Gray, SL
   Simonsick, EM
   Shorr, RI
   Bauer, DC
   Castle, NG
   Studenski, SA
   Hanlon, JT
AF Marcum, Zachary A.
   Perera, Subashan
   Newman, Anne B.
   Thorpe, Joshua M.
   Switzer, Galen E.
   Gray, Shelly L.
   Simonsick, Eleanor M.
   Shorr, Ronald I.
   Bauer, Douglas C.
   Castle, Nicholas G.
   Studenski, Stephanie A.
   Hanlon, Joseph T.
CA Hlth ABC Study
TI Antihypertensive Use and Recurrent Falls in Community-Dwelling Older
   Adults: Findings From the Health ABC Study
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
   SCIENCES
LA English
DT Article
DE Falls; Medication; Epidemiology; Drug related
ID BODY-COMPOSITION; DRUG-USE; HYPERTENSION; MEDICATIONS; RISK; PREDICTORS;
   FRACTURES; PEOPLE; ELDERS; AGE
AB Background. Despite wide-spread use of antihypertensives in older adults, the literature is unclear about their association with incident recurrent falls over time.
   Methods. Health, Aging and Body Composition study participants (n = 2,948) who were well functioning at baseline (1997) were followed to Year 7 (2004). The main outcome was recurrent falls (>= 2) in the ensuing 12 months. Antihypertensive use was examined as: (a) any versus none, (b) long-versus short-term (<= 2 vs <2 years), and by (c) summated standardized daily dose (SDD; 1 = maximum recommended daily dose for one antihypertensive), and (d) subclass.
   Results. Controlling for potential demographic, health status/behavior and access to care confounders, we found no increase in risk of recurrent falls in antihypertensive users compared to nonusers (adjusted odds ratio [AOR] = 1.13; 95% CI = 0.88-1.46), or those taking higher SDDs or for longer durations. Only those using a loop diuretic were found to have a modest increased risk of recurrent falls (AOR = 1.50; 95% CI = 1.11-2.03).
   Conclusions. Antihypertensive use overall was not statistically significantly associated with recurrent falls after adjusting for important confounders. Loop diuretic use may be associated with recurrent falls and needs further study.
C1 [Marcum, Zachary A.; Perera, Subashan; Newman, Anne B.; Hanlon, Joseph T.; Hlth ABC Study] Univ Pittsburgh, Dept Geriatr Med, Pittsburgh, PA 15260 USA.
   [Perera, Subashan; Hanlon, Joseph T.] Univ Pittsburgh, Dept Biostat, Pittsburgh, PA 15260 USA.
   [Newman, Anne B.; Hanlon, Joseph T.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15260 USA.
   [Thorpe, Joshua M.; Hanlon, Joseph T.] Univ Pittsburgh, Dept Pharm & Therapeut, Pittsburgh, PA 15260 USA.
   [Thorpe, Joshua M.; Switzer, Galen E.] Vet Affairs Pittsburgh Healthcare Syst, Ctr Hlth Equity Res, Pittsburgh, PA USA.
   [Switzer, Galen E.] Univ Pittsburgh, Dept Med Gen Internal, Pittsburgh, PA 15260 USA.
   [Switzer, Galen E.] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15260 USA.
   [Gray, Shelly L.] Univ Washington, Sch Pharm, Seattle, WA 98195 USA.
   [Simonsick, Eleanor M.] NIA, Intramural Res Program, Baltimore, MD 21224 USA.
   [Shorr, Ronald I.] North Florida South Georgia Vet Hlth Syst GRECC, Gainesville, FL USA.
   [Bauer, Douglas C.] Univ Calif San Francisco, Div Gen Internal Med, San Francisco, CA 94143 USA.
   [Castle, Nicholas G.] Univ Pittsburgh, Dept Hlth Policy & Management, Pittsburgh, PA 15260 USA.
   [Hanlon, Joseph T.] Vet Affairs Pittsburgh Healthcare Syst, GRECC, Pittsburgh, PA USA.
RP Marcum, ZA (reprint author), Univ Washington, Sch Pharm, Dept Pharm, 1959 NE Pacific St,Box 357630, Seattle, WA 98195 USA.
EM zmarcum@uw.edu
RI Newman, Anne B./C-6408-2013
OI Newman, Anne B./0000-0002-0106-1150
FU National Institute on Aging (NIA) [R01AG027017, P30AG024827,
   T32AG021885, K07AG033174]; Intramural Research program of the National
   Institutes of Health [N01AG62101, N01AG62103, N01AG62106, R01AG028050];
   National Institute of Nursing Research grant [R01NR012459]
FX This work was supported by National Institute on Aging (NIA) grants
   (R01AG027017, P30AG024827, T32AG021885, and K07AG033174). This work was
   also supported in part by the Intramural Research program of the
   National Institutes of Health (N01AG62101, N01AG62103, N01AG62106, and
   R01AG028050) and a National Institute of Nursing Research grant
   (R01NR012459).
NR 33
TC 0
Z9 0
U1 2
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD DEC
PY 2015
VL 70
IS 12
BP 1562
EP 1568
DI 10.1093/gerona/glv095
PG 7
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA DB2UB
UT WOS:000368364100014
PM 26265732
ER

PT J
AU Patel, AV
   Johansson, G
   Colbert, MC
   Dasgupta, B
   Ratner, N
AF Patel, Ami V.
   Johansson, Gunnar
   Colbert, Melissa C.
   Dasgupta, Biplab
   Ratner, Nancy
TI Fatty acid synthase is a metabolic oncogene targetable in malignant
   peripheral nerve sheath tumors
SO NEURO-ONCOLOGY
LA English
DT Article
DE C75; FASN; lipid droplet; MPNST; sarcoma
ID SCHWANN-CELL DEVELOPMENT; BREAST-CANCER CELLS; NEURAL CREST; THERAPEUTIC
   TARGET; INHIBITION; NEUROFIBROMATOSIS; C75; DIFFERENTIATION;
   MAINTENANCE; PROGRESSION
AB Background. Malignant peripheral nerve sheath tumors (MPNSTs) are soft tissue sarcomas with minimal therapeutic opportunities. We observed that lipid droplets (LDs) accumulate in human MPNST cell lines and in primary human tumor samples. The goal of this study was to investigate the relevance of lipid metabolism to MPNST survival and as a possible therapeutic target.
   Methods. Based on preliminary findings that MPNSTs accumulate LDs, we hypothesized that a deregulated lipid metabolism supports MPNST cell survival/proliferation rate. To test this, we examined respiration, role of fatty acid oxidation (FAO), and the enzyme fatty acid synthase involved in de novo fatty acid synthesis in MPNSTs using both genetic and pharmacological tools.
   Results. We demonstrate that LDs accumulate in MPNST cell lines, primary human and mouse MPNST tumors, and neural crest cells. LDs from MPNST cells disappear on lipid deprivation, indicating that LDs can be oxidized as a source of energy. Inhibition of FAO decreased oxygen consumption and reduced MPNST survival, indicating that MPNST cells likely metabolize LDs through active FAO. FAO inhibition reduced oxygen consumption and survival even in the absence of exogenous lipids, indicating that lipids synthesized de novo can also be oxidized. Consequently, inhibition of de novo fatty acid synthesis, which is overexpressed in human MPNST cell lines, effectively reduced MPNST survival and delayed induction of tumor growth in vivo.
   Conclusion. Our results show that MPNSTs depend on lipid metabolic pathways and suggest that disrupting lipid metabolism could be a potential new strategy for the development of MPNST therapeutics.
C1 [Patel, Ami V.; Ratner, Nancy] Childrens Hosp Med Ctr, Div Expt Hematol & Canc Biol, 3333 Burnet Ave,MLC 7013, Cincinnati, OH 45229 USA.
   [Dasgupta, Biplab] Cincinnati Childrens Hosp, Div Oncol, Cincinnati, OH USA.
   [Johansson, Gunnar] Umea Univ, Dept Radiat Sci, Oncol, Umea, Sweden.
   [Colbert, Melissa C.] Natl Inst Hlth, Compliance, Off Intramural Res, Bethesda, MD 20892 USA.
RP Ratner, N (reprint author), Childrens Hosp Med Ctr, Div Expt Hematol & Canc Biol, 3333 Burnet Ave,MLC 7013, Cincinnati, OH 45229 USA.
EM nancy.ratner@cchmc.org
FU Cancer Free Kids Grant [R01NS075291-01]; DAMD Program on
   Neurofibromatosis Postdoctoral Fellowship [W81XWH1110144]; Pelotonia
   Postdoctoral Award
FX This work was supported by a grant from Cancer Free Kids Grant for N.R.
   R01NS075291-01 to B.D. A.V.P. received funding from the DAMD Program on
   Neurofibromatosis Postdoctoral Fellowship W81XWH1110144 and a Pelotonia
   Postdoctoral Award.
NR 40
TC 4
Z9 4
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
EI 1523-5866
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD DEC
PY 2015
VL 17
IS 12
BP 1599
EP 1608
DI 10.1093/neuonc/nov076
PG 10
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA DB3ZO
UT WOS:000368452700008
PM 26116612
ER

PT J
AU Sharpe, MJ
   Wikenheiser, AM
   Niv, Y
   Schoenbaum, G
AF Sharpe, Melissa J.
   Wikenheiser, Andrew M.
   Niv, Yael
   Schoenbaum, Geoffrey
TI The State of the Orbitofrontal Cortex
SO NEURON
LA English
DT Editorial Material
ID BEHAVIOR; RATS
AB State representation is fundamental to behavior. However, identifying the true state of the world is challenging when explicit cues are ambiguous. Here, Bradfield and colleagues show that the medial OFC is critical for using associative information to discriminate ambiguous states.
C1 [Sharpe, Melissa J.; Wikenheiser, Andrew M.; Schoenbaum, Geoffrey] NIDA, Baltimore, MD 21224 USA.
   [Sharpe, Melissa J.; Niv, Yael] Princeton Univ, Princeton Neurosci Inst, Princeton, NJ 08544 USA.
   [Niv, Yael] Princeton Univ, Dept Psychol, Princeton, NJ 08544 USA.
   [Schoenbaum, Geoffrey] Univ Maryland, Sch Med, Dept Anat & Neurobiol, Baltimore, MD 21201 USA.
   [Schoenbaum, Geoffrey] Johns Hopkins Univ, Solomon H Snyder Dept Neurosci, Baltimore, MD 21218 USA.
RP Sharpe, MJ (reprint author), NIDA, Baltimore, MD 21224 USA.
EM melissa.sharpe@nih.gov; geoffrey.schoenbaum@nih.gov
NR 14
TC 2
Z9 2
U1 3
U2 8
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
EI 1097-4199
J9 NEURON
JI Neuron
PD DEC
PY 2015
VL 88
IS 6
BP 1075
EP 1077
DI 10.1016/j.neuron.2015.12.004
PG 4
WC Neurosciences
SC Neurosciences & Neurology
GA DB3WM
UT WOS:000368443900004
PM 26687216
ER

PT J
AU Gearhart, PJ
   Castiblanco, DP
   Knode, LMR
AF Gearhart, Patricia J.
   Castiblanco, Diana P.
   Knode, Lisa M. Russell
TI Exceptional Antibodies Produced by Successive Immunizations
SO PLOS BIOLOGY
LA English
DT Article
ID BROADLY NEUTRALIZING ANTIBODIES; SOMATIC HYPERMUTATION;
   MONOCLONAL-ANTIBODIES; VACCINE DEVELOPMENT; SEQUENCING REVEALS;
   IMMUNOGEN DESIGN; SUPER-ENHANCERS; VARIABLE GENES; HIV-1 VACCINE;
   B-CELLS
AB Antibodies stand between us and pathogens. Viruses mutate quickly to avoid detection, and antibodies mutate at similar rates to hunt them down. This death spiral is fueled by specialized proteins and error-prone polymerases that change DNA sequences. Here, we explore how B lymphocytes stay in the race by expressing activation-induced deaminase, which unleashes a tsunami of mutations in the immunoglobulin loci. This produces random DNA substitutions, followed by selection for the highest affinity antibodies. We may be able to manipulate the process to produce better antibodies by expanding the repertoire of specific B cells through successive vaccinations.
C1 [Gearhart, Patricia J.; Castiblanco, Diana P.; Knode, Lisa M. Russell] NIA, Lab Mol Biol & Immunol, NIH, Baltimore, MD 21224 USA.
RP Gearhart, PJ (reprint author), NIA, Lab Mol Biol & Immunol, NIH, Baltimore, MD 21224 USA.
EM gearhartp@mail.nih.gov
FU Intramural Research program of the NIH, National Institute on Aging
   [AG000714]
FX This work was supported entirely by the Intramural Research program of
   the NIH, National Institute on Aging, AG000714. The funders had no role
   in study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
NR 44
TC 0
Z9 0
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1545-7885
J9 PLOS BIOL
JI PLoS. Biol.
PD DEC
PY 2015
VL 13
IS 12
AR e1002321
DI 10.1371/journal.pbio.1002321
PG 7
WC Biochemistry & Molecular Biology; Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics
GA DB3WE
UT WOS:000368443000013
PM 26641938
ER

PT J
AU Hall, M
   Woolhouse, M
   Rambaut, A
AF Hall, Matthew
   Woolhouse, Mark
   Rambaut, Andrew
TI Epidemic Reconstruction in a Phylogenetics Framework: Transmission Trees
   as Partitions of the Node Set
SO PLOS COMPUTATIONAL BIOLOGY
LA English
DT Article
ID PATHOGENIC AVIAN INFLUENZA; HEPATITIS-C VIRUS; RELAXED PHYLOGENETICS;
   DISEASE TRANSMISSION; MITOCHONDRIAL-DNA; TIME-ESTIMATION; SEQUENCE DATA;
   GENETIC DATA; INFERENCE; OUTBREAKS
AB The use of genetic data to reconstruct the transmission tree of infectious disease epidemics and outbreaks has been the subject of an increasing number of studies, but previous approaches have usually either made assumptions that are not fully compatible with phylogenetic inference, or, where they have based inference on a phylogeny, have employed a procedure that requires this tree to be fixed. At the same time, the coalescent-based models of the pathogen population that are employed in the methods usually used for time-resolved phylogeny reconstruction are a considerable simplification of epidemic process, as they assume that pathogen lineages mix freely. Here, we contribute a new method that is simultaneously a phylogeny reconstruction method for isolates taken from an epidemic, and a procedure for transmission tree reconstruction. We observe that, if one or more samples is taken from each host in an epidemic or outbreak and these are used to build a phylogeny, a transmission tree is equivalent to a partition of the set of nodes of this phylogeny, such that each partition element is a set of nodes that is connected in the full tree and contains all the tips corresponding to samples taken from one and only one host. We then implement a Monte Carlo Markov Chain (MCMC) procedure for simultaneous sampling from the spaces of both trees, utilising a newly-designed set of phylogenetic tree proposals that also respect node partitions. We calculate the posterior probability of these partitioned trees based on a model that acknowledges the population structure of an epidemic by employing an individual-based disease transmission model and a coalescent process taking place within each host. We demonstrate our method, first using simulated data, and then with sequences taken from the H7N7 avian influenza outbreak that occurred in the Netherlands in 2003. We show that it is superior to established coalescent methods for reconstructing the topology and node heights of the phylogeny and performs well for transmission tree reconstruction when the phylogeny is well-resolved by the genetic data, but caution that this will often not be the case in practice and that existing genetic and epidemiological data should be used to configure such analyses whenever possible. This method is available for use by the research community as part of BEAST, one of the most widely-used packages for reconstruction of dated phylogenies.
C1 [Hall, Matthew; Woolhouse, Mark; Rambaut, Andrew] Univ Edinburgh, Inst Evolutionary Biol, Edinburgh, Midlothian, Scotland.
   [Hall, Matthew; Woolhouse, Mark; Rambaut, Andrew] Univ Edinburgh, Ctr Immun Infect & Evolut, Edinburgh, Midlothian, Scotland.
   [Rambaut, Andrew] NIH, Fogarty Int Ctr, Bldg 10, Bethesda, MD 20892 USA.
RP Hall, M (reprint author), Univ Edinburgh, Inst Evolutionary Biol, Edinburgh, Midlothian, Scotland.
EM m.d.hall@sms.ed.ac.uk
FU Scottish Government [EPIC II RA1651 544MWX]; European Research Council
   under the European Community [278433-PREDEMICS]; ERC [260864]
FX MH was supported by a Ph.D. studentship from the Scottish
   Government-funded EPIC (Epidemiology, Population Health and Infectious
   Disease Control) program under grant number EPIC II RA1651 544MWX
   (http://epicscotland.org/). AR has received funding from the European
   Research Council under the European Community's Seventh Framework
   Programme (FP7/2007-2013) under Grant Agreement no. 278433-PREDEMICS and
   ERC Grant agreement no. 260864
   (http://cordis.europa.eu/fp7/home_en.html). The funders had no role in
   study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
NR 54
TC 9
Z9 9
U1 1
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-734X
EI 1553-7358
J9 PLOS COMPUT BIOL
JI PLoS Comput. Biol.
PD DEC
PY 2015
VL 11
IS 12
AR e1004613
DI 10.1371/journal.pcbi.1004613
PG 36
WC Biochemical Research Methods; Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology
GA DB4ZJ
UT WOS:000368521900022
PM 26717515
ER

PT J
AU Arimbasseri, AG
   Blewett, NH
   Iben, JR
   Lamichhane, TN
   Cherkasova, V
   Hafner, M
   Maraia, RJ
AF Arimbasseri, Aneeshkumar G.
   Blewett, Nathan H.
   Iben, James R.
   Lamichhane, Tek N.
   Cherkasova, Vera
   Hafner, Markus
   Maraia, Richard J.
TI RNA Polymerase III Output Is Functionally Linked to tRNA Dimethyl-G26
   Modification
SO PLOS GENETICS
LA English
DT Article
ID SACCHAROMYCES-CEREVISIAE; SCHIZOSACCHAROMYCES-POMBE; NONSENSE
   SUPPRESSION; DIVERSE SIGNALS; GROWTH-CONTROL; FISSION YEAST; MAF1;
   TRANSCRIPTION; PROTEIN; TRANSLATION
AB Control of the differential abundance or activity of tRNAs can be important determinants of gene regulation. RNA polymerase (RNAP) III synthesizes all tRNAs in eukaryotes and it derepression is associated with cancer. Maf1 is a conserved general repressor of RNAP III under the control of the target of rapamycin (TOR) that acts to integrate transcriptional output and protein synthetic demand toward metabolic economy. Studies in budding yeast have indicated that the global tRNA gene activation that occurs with derepression of RNAP III via maf1-deletion is accompanied by a paradoxical loss of tRNA-mediated nonsense suppressor activity, manifested as an antisuppression phenotype, by an unknown mechanism. We show that maf1-antisuppression also occurs in the fission yeast S. pombe amidst general activation of RNAP III. We used tRNA-HydroSeq to document that little changes occurred in the relative levels of different tRNAs in maf1 Delta cells. By contrast, the efficiency of N2, N2-dimethyl G26 (m(2)(2)G26) modification on certain tRNAs was decreased in response to maf1-deletion and associated with antisuppression, and was validated by other methods. Over-expression of Trm1, which produces m(2)(2)G26, reversed maf1-antisuppression. A model that emerges is that competition by increased tRNA levels in maf1 Delta cells leads to m(2)(2)G26 hypomodification due to limiting Trm1, reducing the activity of suppressor-tRNASerUCA and accounting for antisuppression. Consistent with this, we show that RNAP III mutations associated with hypomyelinating leukodystrophy decrease tRNA transcription, increase m(2)(2)G26 efficiency and reverse antisuppression. Extending this more broadly, we show that a decrease in tRNA synthesis by treatment with rapamycin leads to increased m(2)(2)G26 modification and that this response is conserved among highly divergent yeasts and human cells.
C1 [Arimbasseri, Aneeshkumar G.; Blewett, Nathan H.; Iben, James R.; Lamichhane, Tek N.; Cherkasova, Vera] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Intramural Res Program, NIH, Bethesda, MD USA.
   [Hafner, Markus] NIAMSD, NIH, Bethesda, MD 20892 USA.
   [Maraia, Richard J.] US PHS, Commissioned Corps, Washington, DC USA.
RP Arimbasseri, AG (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Intramural Res Program, NIH, Bethesda, MD USA.
EM maraiar@mail.nih.gov
OI Arimbasseri, Gopalakrishnan Aneeshkumar/0000-0001-5266-2688
FU Intramural Research Programs of the Eunice Kennedy Shriver National
   Institute of Child Health and Human Development; National Institute of
   Arthritis and Musculoskeletal and Skin Diseases, NIH [HD000412-28]
FX This work was supported by the Intramural Research Programs of the
   Eunice Kennedy Shriver National Institute of Child Health and Human
   Development and the National Institute of Arthritis and Musculoskeletal
   and Skin Diseases, NIH. The Grant number is HD000412-28. The URL of
   funders website is
   http://data.nidb.nih.gov/reports/viewreports.taf?ipid=90327&ts=144061033
   6. The funders had no role in study design, data collection and
   analysis, decision to publish, or preparation of the manuscript.
NR 61
TC 8
Z9 8
U1 1
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7404
J9 PLOS GENET
JI PLoS Genet.
PD DEC
PY 2015
VL 11
IS 12
AR e1005671
DI 10.1371/journal.pgen.1005671
PG 22
WC Genetics & Heredity
SC Genetics & Heredity
GA DB4YB
UT WOS:000368518400014
PM 26720005
ER

PT J
AU Liu, Y
   Singh, SR
   Zeng, XK
   Zhao, JS
   Hou, SX
AF Liu, Ying
   Singh, Shree Ram
   Zeng, Xiankun
   Zhao, Jiangsha
   Hou, Steven X.
TI The Nuclear Matrix Protein Megator Regulates Stem Cell Asymmetric
   Division through the Mitotic Checkpoint Complex in Drosophila Testes
SO PLOS GENETICS
LA English
DT Article
ID SPINDLE ASSEMBLY CHECKPOINT; SOMATIC SUPPORT CELLS; SELF-RENEWAL;
   TRANSGENIC RNAI; PORE COMPLEX; GENE-EXPRESSION; GERM-CELLS; POLE BODY;
   NICHE; TPR
AB In adult Drosophila testis, asymmetric division of germline stem cells (GSCs) is specified by an oriented spindle and cortically localized adenomatous coli tumor suppressor homolog 2 (Apc2). However, the molecular mechanism underlying these events remains unclear. Here we identified Megator (Mtor), a nuclear matrix protein, which regulates GSC maintenance and asymmetric division through the spindle assembly checkpoint (SAC) complex. Loss of Mtor function results in Apc2 mis-localization, incorrect centrosome orientation, defective mitotic spindle formation, and abnormal chromosome segregation that lead to the eventual GSC loss. Expression of mitotic arrest-deficient-2 (Mad2) and monopolar spindle 1 (Mps1) of the SAC complex effectively rescued the GSC loss phenotype associated with loss of Mtor function. Collectively our results define a new role of the nuclear matrix-SAC axis in regulating stem cell maintenance and asymmetric division.
C1 [Liu, Ying; Singh, Shree Ram; Zeng, Xiankun; Zhao, Jiangsha; Hou, Steven X.] NCI, Basic Res Lab, NIH, Frederick, MD 21701 USA.
RP Liu, Y (reprint author), NCI, Basic Res Lab, NIH, Frederick, MD 21701 USA.
EM hous@mail.nih.gov
RI Singh, Shree Ram/B-7614-2008; Liu, Ying /K-8883-2016
OI Singh, Shree Ram/0000-0001-6545-583X; 
FU National Cancer Institute, National Institutes of Health
FX This research was supported by the Intramural Research Program of the
   National Cancer Institute, 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 60
TC 1
Z9 1
U1 3
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7404
J9 PLOS GENET
JI PLoS Genet.
PD DEC
PY 2015
VL 11
IS 12
AR e1005750
DI 10.1371/journal.pgen.1005750
PG 20
WC Genetics & Heredity
SC Genetics & Heredity
GA DB4YB
UT WOS:000368518400073
PM 26714316
ER

PT J
AU Pineda, S
   Real, FX
   Kogevinas, M
   Carrato, A
   Chanock, SJ
   Malats, N
   Van Steen, K
AF Pineda, Silvia
   Real, Francisco X.
   Kogevinas, Manolis
   Carrato, Alfredo
   Chanock, Stephen J.
   Malats, Nuria
   Van Steen, Kristel
TI Integration Analysis of Three Omics Data Using Penalized Regression
   Methods: An Application to Bladder Cancer
SO PLOS GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; GENE-EXPRESSION; DNA METHYLATION; ELASTIC-NET;
   LOCI; SELECTION; VARIANTS; PROTEINS; BIOLOGY; REVEAL
AB Omics data integration is becoming necessary to investigate the genomic mechanisms involved in complex diseases. During the integration process, many challenges arise such as data heterogeneity, the smaller number of individuals in comparison to the number of parameters, multicollinearity, and interpretation and validation of results due to their complexity and lack of knowledge about biological processes. To overcome some of these issues, innovative statistical approaches are being developed. In this work, we propose a permutation-based method to concomitantly assess significance and correct by multiple testing with the MaxT algorithm. This was applied with penalized regression methods (LASSO and ENET) when exploring relationships between common genetic variants, DNA methylation and gene expression measured in bladder tumor samples. The overall analysis flow consisted of three steps: (1) SNPs/CpGs were selected per each gene probe within 1Mb window upstream and downstream the gene; (2) LASSO and ENET were applied to assess the association between each expression probe and the selected SNPs/CpGs in three multivariable models (SNP, CPG, and Global models, the latter integrating SNPs and CPGs); and (3) the significance of each model was assessed using the permutation-based MaxT method. We identified 48 genes whose expression levels were significantly associated with both SNPs and CPGs. Importantly, 36 (75%) of them were replicated in an independent data set (TCGA) and the performance of the proposed method was checked with a simulation study. We further support our results with a biological interpretation based on an enrichment analysis. The approach we propose allows reducing computational time and is flexible and easy to implement when analyzing several types of omics data. Our results highlight the importance of integrating omics data by applying appropriate statistical strategies to discover new insights into the complex genetic mechanisms involved in disease conditions.
C1 [Pineda, Silvia; Malats, Nuria] Spanish Natl Canc Res Ctr CNIO, Genet & Mol Epidemiol Grp, Madrid, Spain.
   [Pineda, Silvia; Van Steen, Kristel] Univ Liege, Inst Montefiore, Syst & Modeling Unit, BIO3, B-4000 Liege, Belgium.
   [Real, Francisco X.] Spanish Natl Canc Res Ctr CNIO, Epithelial Carcinogenesis Grp, Madrid, Spain.
   [Real, Francisco X.] Univ Pompeu Fabra, Dept Ciencies Expt & Salut, Barcelona, Spain.
   [Kogevinas, Manolis] Ctr Res Environm Epidemiol CREAL, Barcelona, Spain.
   [Carrato, Alfredo] Hosp Univ Ramon & Cajal, Serv Oncol, Madrid, Spain.
   [Carrato, Alfredo] Hosp Univ Elche, Serv Oncol, Alicante, Spain.
   [Chanock, Stephen J.] NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
   [Van Steen, Kristel] GIGA R, Syst Biol & Chem Biol, Liege, Belgium.
RP Pineda, S (reprint author), Spanish Natl Canc Res Ctr CNIO, Genet & Mol Epidemiol Grp, Madrid, Spain.
EM nmalats@cnio.es; kristel.vansteen@ulg.ac.be
RI Kogevinas, Manolis/C-3918-2017; Real, Francisco X/H-5275-2015; 
OI Real, Francisco X/0000-0001-9501-498X; Malats, Nuria/0000-0003-2538-3784
FU Fondo de Investigaciones Sanitarias (FIS), Instituto de Salud Carlos
   III, Spain [PI06-1614, PI12-00815]; Red Tematica de Investigacion
   Cooperativa en Cancer, Spain [RD12/0036/0034, RD12/0036/0050];
   EU-FP7-HEALTH [F2-2008-201663-UROMOL, F2-2008-201333-DECanBio]; USA-NIH
   [RO1-CA089715, NO2-CP-11015]; European Cooperation in Science and
   Technology (COST Action) [BM1204: EU_Pancreas]; Obra Social Fundacion
   "la Caixa"
FX The work was partially supported by Fondo de Investigaciones Sanitarias
   (FIS), Instituto de Salud Carlos III, Spain (#PI06-1614 and
   #PI12-00815); Red Tematica de Investigacion Cooperativa en Cancer, Spain
   (#RD12/0036/0034 and #RD12/0036/0050); EU-FP7-HEALTH
   (F2-2008-201663-UROMOL and F2-2008-201333-DECanBio); USA-NIH
   (RO1-CA089715 and NO2-CP-11015); and European Cooperation in Science and
   Technology (COST Action #BM1204: EU_Pancreas). SP was funded by a Obra
   Social Fundacion "la Caixa". The funders had no role in study design,
   data collection and analysis, decision to publish, or preparation of the
   manuscript.
NR 47
TC 4
Z9 4
U1 1
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7404
J9 PLOS GENET
JI PLoS Genet.
PD DEC
PY 2015
VL 11
IS 12
AR e1005689
DI 10.1371/journal.pgen.1005689
PG 22
WC Genetics & Heredity
SC Genetics & Heredity
GA DB4YB
UT WOS:000368518400024
PM 26646822
ER

PT J
AU Yuen, CM
   Kurbatova, EV
   Tupasi, T
   Caoili, JC
   Van der Walt, M
   Kvasnovsky, C
   Yagui, M
   Bayona, J
   Contreras, C
   Leimane, V
   Ershova, J
   Via, LE
   Kim, H
   Akksilp, S
   Kazennyy, BY
   Volchenkov, GV
   Jou, R
   Kliiman, K
   Demikhova, OV
   Vasilyeva, IA
   Dalton, T
   Cegielski, JP
AF Yuen, Courtney M.
   Kurbatova, Ekaterina V.
   Tupasi, Thelma
   Caoili, Janice Campos
   Van der Walt, Martie
   Kvasnovsky, Charlotte
   Yagui, Martin
   Bayona, Jaime
   Contreras, Carmen
   Leimane, Vaira
   Ershova, Julia
   Via, Laura E.
   Kim, HeeJin
   Akksilp, Somsak
   Kazennyy, Boris Y.
   Volchenkov, Grigory V.
   Jou, Ruwen
   Kliiman, Kai
   Demikhova, Olga V.
   Vasilyeva, Irina A.
   Dalton, Tracy
   Cegielski, J. Peter
TI Association between Regimen Composition and Treatment Response in
   Patients with Multidrug-Resistant Tuberculosis: A Prospective Cohort
   Study
SO PLOS MEDICINE
LA English
DT Article
ID SPUTUM CULTURE CONVERSION; AGGRESSIVE REGIMENS; DRUG-RESISTANCE;
   2ND-LINE DRUGS; PREDICTORS; OUTCOMES; SUSCEPTIBILITY; PYRAZINAMIDE; 1ST
AB Background
   For treating multidrug-resistant tuberculosis (MDR TB), the World Health Organization (WHO) recommends a regimen of at least four second-line drugs that are likely to be effective as well as pyrazinamide. WHO guidelines indicate only marginal benefit for regimens based directly on drug susceptibility testing (DST) results. Recent evidence from isolated cohorts suggests that regimens containing more drugs may be beneficial, and that DST results are predictive of regimen effectiveness. The objective of our study was to gain insight into how regimen design affects treatment response by analyzing the association between time to sputum culture conversion and both the number of potentially effective drugs included in a regimen and the DST results of the drugs in the regimen.
   Methods and Findings
   We analyzed data from the Preserving Effective Tuberculosis Treatment Study (PETTS), a prospective observational study of 1,659 adults treated for MDR TB during 2005-2010 in nine countries: Estonia, Latvia, Peru, Philippines, Russian Federation, South Africa, South Korea, Thailand, and Taiwan. For all patients, monthly sputum samples were collected, and DST was performed on baseline isolates at the US Centers for Disease Control and Prevention. We included 1,137 patients in our analysis based on their having known baseline DST results for at least fluoroquinolones and second-line injectable drugs, and not having extensively drug-resistant TB. These patients were followed for a median of 20 mo (interquartile range 16-23 mo) after MDR TB treatment initiation. The primary outcome of interest was initial sputum culture conversion. We used Cox proportional hazards regression, stratifying by country to control for setting-associated confounders, and adjusting for the number of drugs to which patients' baseline isolates were resistant, baseline resistance pattern, previous treatment history, sputum smear result, and extent of disease on chest radiograph.
   In multivariable analysis, receiving an average of at least six potentially effective drugs (defined as drugs without a DST result indicating resistance) per day was associated with a 36% greater likelihood of sputum culture conversion than receiving an average of at least five but fewer than six potentially effective drugs per day (adjusted hazard ratio [aHR] 1.36, 95% CI 1.09-1.69). Inclusion of pyrazinamide (aHR 2.00, 95% CI 1.65-2.41) or more drugs to which baseline DST indicated susceptibility (aHR 1.65, 95% CI 1.48-1.84, per drug) in regimens was associated with greater increases in the likelihood of sputum culture conversion than including more drugs to which baseline DST indicated resistance (aHR 1.33, 95% CI 1.18-1.51, per drug). Including in the regimen more drugs for which DST was not performed was beneficial only if a minimum of three effective drugs was present in the regimen (aHR 1.39, 95% CI 1.09-1.76, per drug when three effective drugs present in regimen).
   The main limitation of this analysis is that it is based on observational data, not a randomized trial, and drug regimens varied across sites. However, PETTS was a uniquely large and rigorous observational study in terms of both the number of patients enrolled and the standardization of laboratory testing. Other limitations include the assumption of equivalent efficacy across drugs in a category, incomplete data on adherence, and the fact that the analysis considers only initial sputum culture conversion, not reversion or long-term relapse.
   Conclusions
   MDR TB regimens including more potentially effective drugs than the minimum of five currently recommended by WHO may encourage improved response to treatment in patients with MDR TB. Rapid access to high-quality DST results could facilitate the design of more effective individualized regimens. Randomized controlled trials are necessary to confirm whether individualized regimens with more than five drugs can indeed achieve better cure rates than current recommended regimens.
C1 [Yuen, Courtney M.; Kurbatova, Ekaterina V.; Caoili, Janice Campos; Kvasnovsky, Charlotte; Ershova, Julia; Dalton, Tracy; Cegielski, J. Peter] Ctr Dis Control & Prevent, Atlanta, GA USA.
   [Tupasi, Thelma; Caoili, Janice Campos] Trop Dis Fdn, Manila, Philippines.
   [Van der Walt, Martie; Kvasnovsky, Charlotte] MRC, Pretoria, South Africa.
   [Yagui, Martin] Natl Inst Hlth, Lima, Peru.
   [Bayona, Jaime] Partners Hlth, Boston, MA USA.
   [Contreras, Carmen] Socios Salud Sucursal, Lima, Peru.
   [Leimane, Vaira] Riga East Univ Hosp Ctr TB & Lung Dis, Riga, Latvia.
   [Via, Laura E.] NIAID, NIH, Bethesda, MD 20892 USA.
   [Kim, HeeJin] Korean Inst TB, Seoul, South Korea.
   [Akksilp, Somsak] Minist Publ Hlth, Dept Dis Control, Bangkok, Thailand.
   [Kazennyy, Boris Y.] Orel Oblast TB Dispensary, Oryol, Russia.
   [Volchenkov, Grigory V.] Vladimir Oblast TB Dispensary, Vladimir, Russia.
   [Jou, Ruwen] Taiwan Ctr Dis Control, Taipei, Taiwan.
   [Kliiman, Kai] Tartu Univ Hosp, Tartu, Estonia.
   [Demikhova, Olga V.; Vasilyeva, Irina A.] Russian Acad Med Sci, Cent TB Res Inst, Moscow, Russia.
RP Yuen, CM (reprint author), Ctr Dis Control & Prevent, Atlanta, GA USA.
EM gzc2@cdc.gov
FU U.S. Agency for International Development; U.S. Centers for Disease
   Control and Prevention (CDC); U.S. National Institutes of Health's
   Division of Intramural Research of the National Institute for Allergy
   and Infectious Diseases; Korean Ministry of Health and Welfare
FX This work was supported by the U.S. Agency for International
   Development, U.S. Centers for Disease Control and Prevention (CDC), U.S.
   National Institutes of Health's Division of Intramural Research of the
   National Institute for Allergy and Infectious Diseases, and the Korean
   Ministry of Health and Welfare. CDC Division of Tuberculosis Elimination
   led the study design, training for data collection and monitoring, data
   analysis, data interpretation, and writing of the report. Other sponsors
   had no roles in these activities. The views and opinions expressed in
   this article are those of the authors and do not necessarily represent
   an official position of the U.S. Centers for Disease Control and
   Prevention.
NR 21
TC 9
Z9 9
U1 4
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1549-1676
J9 PLOS MED
JI PLos Med.
PD DEC
PY 2015
VL 12
IS 12
AR e1001932
DI 10.1371/journal.pmed.1001932
PG 18
WC Medicine, General & Internal
SC General & Internal Medicine
GA DB3YZ
UT WOS:000368451100020
PM 26714320
ER

PT J
AU Al-Hamdan, NA
   Panackal, AA
   Al Bassam, TH
   Alrabea, A
   Al Hazmi, M
   Al Mazroa, Y
   Al Jefri, M
   Khan, AS
   Ksiazek, TG
AF Al-Hamdan, Nasser A.
   Panackal, Anil A.
   Al Bassam, Tami H.
   Alrabea, Abdullah
   Al Hazmi, Mohammed
   Al Mazroa, Yagoub
   Al Jefri, Mohammed
   Khan, Ali S.
   Ksiazek, Thomas G.
TI The Risk of Nosocomial Transmission of Rift Valley Fever
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID SAUDI-ARABIA; EBOLA; EPIDEMIC; VIRUS; EGYPT
AB In 2000, we investigated the Rift Valley fever (RVF) outbreak on the Arabian Peninsulathe first outside Africa-and the risk of nosocomial transmission. In a cross-sectional design, during the peak of the epidemic at its epicenter, we found four (0.6%) of 703 healthcare workers (HCWs) IgM seropositive but all with only community-associated exposures. Standard precautions are sufficient for HCWs exposed to known RVF patients, in contrast to other viral hemorrhagic fevers (VHF) such as Ebola virus disease (EVD) in which the route of transmission differs. Suspected VHF in which the etiology is uncertain should be initially managed with the most cautious infection control measures.
C1 [Al-Hamdan, Nasser A.] King Saud bin Abdulaziz Univ Hlth Sci, Fac Med, King Fahad Med City, Riyadh, Saudi Arabia.
   [Panackal, Anil A.] Ctr Dis Control & Prevent CDC, USPHS, Atlanta, GA USA.
   [Al Bassam, Tami H.] Hafr Albatin Hlth Reg, Hafr Albatin, Saudi Arabia.
   [Alrabea, Abdullah] Kahramanmaras Sutcu Imam Univ, Coll Med, Riyadh, Saudi Arabia.
   [Al Hazmi, Mohammed] King Fahad Cent Hosp, Jazan, Saudi Arabia.
   [Al Mazroa, Yagoub] Minist Hlth, Hlth Serv Council, Riyadh, Saudi Arabia.
   [Al Jefri, Mohammed] Minist Hlth, Dept Prevent Med, Riyadh, Saudi Arabia.
   [Khan, Ali S.] Univ Nebraska Med Ctr, Coll Publ Hlth, Omaha, NE USA.
   [Ksiazek, Thomas G.] Univ Texas Med Branch, Dept Pathol, Galveston Natl Lab, Galveston, TX 77555 USA.
RP Al-Hamdan, NA (reprint author), NIAID, LCID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM nalhamdan@kfmc.med.sa
FU NIH, NIAID; King Saud bin Abdulaziz University for Health Sciences,
   Riyadh, Kingdom of Saudi Arabia
FX This research was supported in part (decision to publish and preparation
   of manuscript) by the Intramural Research Program of the NIH, NIAID and
   King Saud bin Abdulaziz University for Health Sciences, Riyadh, Kingdom
   of Saudi Arabia; the funders had no role in study design or data
   collection and analysis.
NR 16
TC 0
Z9 1
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD DEC
PY 2015
VL 9
IS 12
AR e0004314
DI 10.1371/journal.pntd.0004314
PG 6
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA DB2NG
UT WOS:000368345100060
PM 26694834
ER

PT J
AU Cangalaya, C
   Zimic, M
   Marzal, M
   Gonzalez, AE
   Guerra-Giraldez, C
   Mahanty, S
   Nash, TE
   Garcia, HH
AF Cangalaya, Carla
   Zimic, Mirko
   Marzal, Miguel
   Gonzalez, Armando E.
   Guerra-Giraldez, Cristina
   Mahanty, Siddhartha
   Nash, Theodore E.
   Garcia, Hector H.
CA Cysticercosis Working Grp Peru
TI Inflammation Caused by Praziquantel Treatment Depends on the Location of
   the Taenia solium Cysticercus in Porcine Neurocysticercosis
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID BLOOD-BRAIN-BARRIER; JUNCTIONAL COMPLEX PROTEINS; MURINE
   NEUROCYSTICERCOSIS; SYMPTOMATIC NEUROCYSTICERCOSIS; DIFFERENTIAL
   CHANGES; COMPUTED-TOMOGRAPHY; HISTOPATHOLOGY; DISEASE; CNS
AB Background
   Neurocysticercosis (NCC), infection of the central nervous system by Taenia solium cysticerci, is a pleomorphic disease. Inflammation around cysticerci is the major cause of disease but is variably present. One factor modulating the inflammatory responses may be the location and characteristics of the brain tissue adjacent to cysticerci. We analyzed and compared the inflammatory responses to cysticerci located in the parenchyma to those in the meninges or cysticerci partially in contact with both the parenchyma and the meninges (corticomeningeal).
   Methodology/Principal Findings
   Histological specimens of brain cysticerci (n = 196) from 11 pigs naturally infected with Taenia solium cysticerci were used. Four pigs were sacrificed after 2 days and four after 5 days of a single dose of praziquantel; 3 pigs did not receive treatment. All pigs were intravenously injected with Evans Blue to assess disruption of the blood-brain barrier. The degree of inflammation was estimated by use of a histological score (ISC) based on the extent of the inflammation in the pericystic areas as assessed in an image composed of several photomicrographs taken at 40X amplification. Parenchymal cysticerci provoked a significantly greater level of pericystic inflammation (higher ISC) after antiparasitic treatment compared to meningeal and corticomeningeal cysticerci. ISC of meningeal cysticerci was not significantly affected by treatment. In corticomeningeal cysticerci, the increase in ISC score was correlated to the extent of the cysticercus adjacent to the brain parenchyma. Disruption of the blood-brain barrier was associated with treatment only in parenchymal tissue.
   Significance
   Inflammatory response to cysticerci located in the meninges was significantly decreased compared to parenchymal cysticerci. The suboptimal inflammatory response to cysticidal drugs may be the reason subarachnoid NCC is generally refractory to treatment compared to parenchymal NCC.
C1 [Cangalaya, Carla; Marzal, Miguel; Guerra-Giraldez, Cristina; Mahanty, Siddhartha; Nash, Theodore E.] Univ Peruana Cayetano Heredia, Fac Ciencias & Filosofia, Lab Inmunopatol Neurocisticercosis, Lima, Peru.
   [Zimic, Mirko] Univ Peruana Cayetano Heredia, Fac Ciencias & Filosofia, Lab Bioinformat & Biol Mol, Lima, Peru.
   [Zimic, Mirko; Guerra-Giraldez, Cristina; Garcia, Hector H.] Univ Peruana Cayetano Heredia, Fac Ciencias & Filosofia, Dept Ciencias Celulares & Mol, Lima, Peru.
   [Gonzalez, Armando E.] Univ Nacl Mayor San Marcos, Fac Med Vet, Lima 14, Peru.
   [Mahanty, Siddhartha; Nash, Theodore E.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
   [Garcia, Hector H.] Inst Nacl Ciencias Neurol, Unidad Cisticercosis, Lima, Peru.
RP Cangalaya, C (reprint author), Univ Peruana Cayetano Heredia, Fac Ciencias & Filosofia, Lab Inmunopatol Neurocisticercosis, Lima, Peru.
EM carla.cangalaya.l@upch.pe
OI Cangalaya, Carla/0000-0002-3525-8445; Guerra-Giraldez,
   Cristina/0000-0002-9287-9838; Mahanty, Siddhartha/0000-0003-1068-0524
FU Fogarty International Center, National Institutes of health, USA [D43
   TW001140, 2D43 TW007393]; Intramural Research Program of the National
   Institute of Allergy and Infectious Diseases
FX This work was partially supported by grants D43 TW001140 and 2D43
   TW007393 from the Fogarty International Center, National Institutes of
   health, USA, and by the Intramural Research Program of the National
   Institute of Allergy and Infectious Diseases. The funders had no role in
   study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
NR 32
TC 1
Z9 1
U1 1
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD DEC
PY 2015
VL 9
IS 12
AR e0004207
DI 10.1371/journal.pntd.0004207
PG 13
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA DB2NG
UT WOS:000368345100014
PM 26658257
ER

PT J
AU Hostetler, JB
   Sharma, S
   Bartholdson, SJ
   Wright, GJ
   Fairhurst, RM
   Rayner, JC
AF Hostetler, Jessica B.
   Sharma, Sumana
   Bartholdson, S. Josefin
   Wright, Gavin J.
   Fairhurst, Rick M.
   Rayner, Julian C.
TI A Library of Plasmodium vivax Recombinant Merozoite Proteins Reveals New
   Vaccine Candidates and Protein-Protein Interactions
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID DUFFY BINDING-PROTEIN; APICAL MEMBRANE ANTIGEN-1; DETERGENT-RESISTANT
   MICRODOMAINS; TRANSMISSION-BLOCKING VACCINE; NATURALLY ACQUIRED
   ANTIBODIES; HUMORAL IMMUNE-RESPONSES; MONTANIDE ISA 51; SURFACE
   PROTEIN-3; PROTECTIVE EFFICACY; MALARIA PARASITES
AB Background
   A vaccine targeting Plasmodium vivax will be an essential component of any comprehensive malaria elimination program, but major gaps in our understanding of P. vivax biology, including the protein-protein interactions that mediate merozoite invasion of reticulocytes, hinder the search for candidate antigens. Only one ligand-receptor interaction has been identified, that between P. vivax Duffy Binding Protein (PvDBP) and the erythrocyte Duffy Antigen Receptor for Chemokines (DARC), and strain-specific immune responses to PvDBP make it a complex vaccine target. To broaden the repertoire of potential P. vivax merozoite-stage vaccine targets, we exploited a recent breakthrough in expressing fulllength ectodomains of Plasmodium proteins in a functionally-active form in mammalian cells and initiated a large-scale study of P. vivax merozoite proteins that are potentially involved in reticulocyte binding and invasion.
   Methodology/Principal Findings
   We selected 39 P. vivax proteins that are predicted to localize to the merozoite surface or invasive secretory organelles, some of which show homology to P. falciparum vaccine candidates. Of these, we were able to express 37 full-length protein ectodomains in a mammalian expression system, which has been previously used to express P. falciparum invasion ligands such as PfRH5. To establish whether the expressed proteins were correctly folded, we assessed whether they were recognized by antibodies from Cambodian patients with acute vivax malaria. IgG from these samples showed at least a two-fold change in reactivity over naive controls in 27 of 34 antigens tested, and the majority showed heat-labile IgG immunoreactivity, suggesting the presence of conformation-sensitive epitopes and native tertiary protein structures. Using a method specifically designed to detect low-affinity, extracellular protein-protein interactions, we confirmed a predicted interaction between P. vivax 6-cysteine proteins P12 and P41, further suggesting that the proteins are natively folded and functional. This screen also identified two novel protein-protein interactions, between P12 and PVX_110945, and between MSP3.10 and MSP7.1, the latter of which was confirmed by surface plasmon resonance.
   Conclusions/Significance We produced a new library of recombinant full-length P. vivax ectodomains, established that the majority of them contain tertiary structure, and used them to identify predicted and novel protein-protein interactions. As well as identifying new interactions for further biological studies, this library will be useful in identifying P. vivax proteins with vaccine potential, and studying P. vivax malaria pathogenesis and immunity.
   Trial Registration
   ClinicalTrials.gov NCT00663546
C1 [Hostetler, Jessica B.; Fairhurst, Rick M.] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
   [Hostetler, Jessica B.; Sharma, Sumana; Bartholdson, S. Josefin; Wright, Gavin J.; Rayner, Julian C.] Wellcome Trust Sanger Inst, Malaria Programme, Cambridge, England.
   [Sharma, Sumana; Bartholdson, S. Josefin; Wright, Gavin J.] Wellcome Trust Sanger Inst, Cell Surface Signalling Lab, Cambridge, England.
RP Hostetler, JB (reprint author), NIAID, Lab Malaria & Vector Res, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM rfairhurst@niaid.nih.gov; jr9@sanger.ac.uk
OI Rayner, Julian/0000-0002-9835-1014
FU National Institute of Allergy and Infectious Diseases, National
   Institutes of Health; Wellcome Trust [090851]; UK Medical Research
   Council [MR/J002283/1]
FX This work was funded by the Intramural Research Program of the National
   Institute of Allergy and Infectious Diseases, National Institutes of
   Health, the Wellcome Trust (grant number 090851), and the UK Medical
   Research Council (grant number MR/J002283/1). The funders had no role in
   study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
NR 107
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PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD DEC
PY 2015
VL 9
IS 12
AR e0004264
DI 10.1371/journal.pntd.0004264
PG 24
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA DB2NG
UT WOS:000368345100039
PM 26701602
ER

PT J
AU Lord, JS
   Gurley, ES
   Pulliam, JRC
AF Lord, Jennifer S.
   Gurley, Emily S.
   Pulliam, Juliet R. C.
TI Rethinking Japanese Encephalitis Virus Transmission: A Framework for
   Implicating Host and Vector Species
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID WEST-NILE-VIRUS; CULEX-TRITAENIORHYNCHUS; INFECTION; CULICIDAE; DIPTERA;
   INDIA; HETEROGENEITY; BANGLADESH; EMERGENCE; MOSQUITOS
C1 [Lord, Jennifer S.] Univ Liverpool, Liverpool Sch Trop Med, Vector Grp, Liverpool L3 5QA, Merseyside, England.
   [Lord, Jennifer S.; Pulliam, Juliet R. C.] Univ Florida, Dept Biol, Gainesville, FL USA.
   [Gurley, Emily S.] Icddr B, Ctr Communicable Dis, Dhaka, Bangladesh.
   [Pulliam, Juliet R. C.] Univ Florida, Emerging Pathogens Inst, Gainesville, FL USA.
   [Pulliam, Juliet R. C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Lord, JS (reprint author), Univ Liverpool, Liverpool Sch Trop Med, Vector Grp, Liverpool L3 5QA, Merseyside, England.
EM jennifer.suzanne.lord@gmail.com
RI Pulliam, Juliet/A-6516-2008; Gurley, Emily/B-7903-2010
OI Pulliam, Juliet/0000-0003-3314-8223; Gurley, Emily/0000-0002-8648-9403
FU Emerging Pathogens Institute, University of Florida; Research and Policy
   for Infectious Disease Dynamics (RAPIDD) program; Research and Policy on
   Infectious Disease Dynamics (RAPIDD) Program of the Fogarty
   International Center, National Institutes of Health and Science and
   Technology Directorate, Department of Homeland Security
FX At the time of writing this manuscript JSL was a postdoctoral research
   associate in the Pulliam Lab at the University of Florida. We would like
   to acknowledge the Emerging Pathogens Institute, University of Florida
   for funding fieldwork, which contributed to the ideas within this
   manuscript. We would also like to acknowledge funding for a Japanese
   encephalitis workshop held in October 2012 by the Research and Policy
   for Infectious Disease Dynamics (RAPIDD) program. icddr,b is thankful to
   the Governments of Australia, Bangladesh, Canada, Sweden and the UK for
   providing core support. JRCP and ESG are supported by the Research and
   Policy on Infectious Disease Dynamics (RAPIDD) Program of the Fogarty
   International Center, National Institutes of Health and Science and
   Technology Directorate, Department of Homeland Security. The funders had
   no role in study design, data collection and analysis, decision to
   publish, or preparation of the manuscript.
NR 41
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U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD DEC
PY 2015
VL 9
IS 12
AR e0004074
DI 10.1371/journal.pntd.0004074
PG 7
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA DB2NG
UT WOS:000368345100003
PM 26657648
ER

PT J
AU Pajuelo, MJ
   Eguiluz, M
   Dahlstrom, E
   Requena, D
   Guzman, F
   Ramirez, M
   Sheen, P
   Frace, M
   Sammons, S
   Cama, V
   Anzick, S
   Bruno, D
   Mahanty, S
   Wilkins, P
   Nash, T
   Gonzalez, A
   Garcia, HH
   Gilman, RH
   Porcella, S
   Zimic, M
AF Pajuelo, Monica J.
   Eguiluz, Maria
   Dahlstrom, Eric
   Requena, David
   Guzman, Frank
   Ramirez, Manuel
   Sheen, Patricia
   Frace, Michael
   Sammons, Scott
   Cama, Vitaliano
   Anzick, Sarah
   Bruno, Dan
   Mahanty, Siddhartha
   Wilkins, Patricia
   Nash, Theodore
   Gonzalez, Armando
   Garcia, Hector H.
   Gilman, Robert H.
   Porcella, Steve
   Zimic, Mirko
CA Cysticercosis Working Grp Peru
TI Identification and Characterization of Microsatellite Markers Derived
   from the Whole Genome Analysis of Taenia solium
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID SIMPLE SEQUENCE REPEATS; GENETIC-VARIATION; POLYMORPHIC MICROSATELLITES;
   SCHISTOSOMA-JAPONICUM; EUKARYOTIC GENOMES; CODING DNA; INFECTIONS;
   CYSTICERCI; DIVERSITY; FREQUENCY
AB Background
   Infections with Taenia solium are the most common cause of adult acquired seizures worldwide, and are the leading cause of epilepsy in developing countries. A better understanding of the genetic diversity of T. solium will improve parasite diagnostics and transmission pathways in endemic areas thereby facilitating the design of future control measures and interventions. Microsatellite markers are useful genome features, which enable strain typing and identification in complex pathogen genomes. Here we describe microsatellite identification and characterization in T. solium, providing information that will assist in global efforts to control this important pathogen.
   Methods
   For genome sequencing, T. solium cysts and proglottids were collected from Huancayo and Puno in Peru, respectively. Using next generation sequencing (NGS) and de novo assembly, we assembled two draft genomes and one hybrid genome. Microsatellite sequences were identified and 36 of them were selected for further analysis. Twenty T. solium isolates were collected from Tumbes in the northern region, and twenty from Puno in the southern region of Peru. The size-polymorphism of the selected microsatellites was determined with multi-capillary electrophoresis. We analyzed the association between microsatellite polymorphism and the geographic origin of the samples.
   Results
   The predicted size of the hybrid (proglottid genome combined with cyst genome) T. solium genome was 111 MB with a GC content of 42.54%. A total of 7,979 contigs (>1,000 nt) were obtained. We identified 9,129 microsatellites in the Puno-proglottid genome and 9,936 in the Huancayo-cyst genome, with 5 or more repeats, ranging from mono-to hexa-nucleotide. Seven microsatellites were polymorphic and 29 were monomorphic within the analyzed isolates. T. solium tapeworms were classified into two genetic groups that correlated with the North/South geographic origin of the parasites.
   Conclusions/Significance
   The availability of draft genomes for T. solium represents a significant step towards the understanding the biology of the parasite. We report here a set of T. solium polymorphic microsatellite markers that appear promising for genetic epidemiology studies.
C1 [Pajuelo, Monica J.; Eguiluz, Maria; Requena, David; Guzman, Frank; Ramirez, Manuel; Sheen, Patricia; Zimic, Mirko] Univ Peruana Cayetano Heredia, Fac Ciencias & Filosofia, Lab Bioinformat & Biol Mol, Labs Invest & Desarrollo, Lima, Peru.
   [Dahlstrom, Eric; Anzick, Sarah; Bruno, Dan; Mahanty, Siddhartha; Nash, Theodore; Porcella, Steve] NIAID, Genom Unit, Res Technol Sect, Rocky Mt Labs,NIH, Hamilton, MT USA.
   [Frace, Michael; Sammons, Scott] Ctr Dis Control & Prevent, Biotechnol Core, Natl Ctr Emerging & Zoonot Infect Dis, Facil Branch, Atlanta, GA USA.
   [Cama, Vitaliano; Wilkins, Patricia] Ctr Dis Control & Prevent, Div Parasit Dis & Malaria, Ctr Global Hlth, Atlanta, GA USA.
   [Gonzalez, Armando] Univ Nacl Mayor San Marcos, Fac Med Vet, Lima 14, Peru.
   [Garcia, Hector H.] Univ Peruana Cayetano Heredia, Fac Ciencias & Filosofia, Dept Microbiol, Lima, Peru.
   [Garcia, Hector H.] Inst Nacl Ciencias Neurol, Lima, Peru.
   [Gilman, Robert H.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Int Hlth, Baltimore, MD USA.
RP Pajuelo, MJ (reprint author), Univ Peruana Cayetano Heredia, Fac Ciencias & Filosofia, Lab Bioinformat & Biol Mol, Labs Invest & Desarrollo, Lima, Peru.
EM Mirko.zimic@upch.pe
RI Guzman, Frank /H-1271-2014; 
OI Guzman, Frank /0000-0002-5048-4213; Mahanty,
   Siddhartha/0000-0003-1068-0524
FU Fogarty International Center/NIH [D43TW006581, D43TW001140]; Wellcome
   Trust Senior International Research Fellowship in Public Health and
   Tropical Medicine
FX This work was partially supported by the Fogarty International
   Center/NIH Training Grants D43TW001140 and D43TW006581. HHG. is
   supported by a Wellcome Trust Senior International Research Fellowship
   in Public Health and Tropical Medicine. The funders had no role in study
   design, data collection and analysis or interpretaion; in writing the
   report or in the decision to submit this manuscript for publication.
NR 43
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U1 1
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD DEC
PY 2015
VL 9
IS 12
AR e0004316
DI 10.1371/journal.pntd.0004316
PG 15
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA DB2NG
UT WOS:000368345100061
PM 26697878
ER

PT J
AU Fritz, R
   Kohan-Ghadr, HR
   Sacher, A
   Bolnick, AD
   Kilburn, BA
   Bolnick, JM
   Diamond, MP
   Drewlo, S
   Armant, DR
AF Fritz, Rani
   Kohan-Ghadr, Hamid Reza
   Sacher, Alex
   Bolnick, Alan D.
   Kilburn, Brian A.
   Bolnick, Jay M.
   Diamond, Michael P.
   Drewlo, Sascha
   Armant, D. Randall
TI Trophoblast retrieval and isolation from the cervix (TRIC) is unaffected
   by early gestational age or maternal obesity
SO PRENATAL DIAGNOSIS
LA English
DT Article
ID NONINVASIVE PRENATAL-DIAGNOSIS; CELL-FREE DNA; TRANSCERVICAL SAMPLES;
   FETAL CELLS; PREECLAMPSIA; ANEUPLOIDIES; PREGNANCY; SEQUENCES; PLASMA;
   MUCUS
AB Objective The objective of this study is to evaluate whether trophoblast yield obtained by trophoblast retrieval and isolation from the cervix (TRIC) is affected by pregnancy outcome, gestational age (GA) at retrieval, maternal body mass index (BMI), parity, or maternal age.
   Methods TRIC was performed on 224 ongoing pregnancies between 5 and 20 weeks of GA. Trophoblast cells were isolated from cervical cells using anti-human leukocyte antigen-G antibody coupled to magnetic nanoparticles. Purity was assessed by the percentage of isolated cells that express beta-hCG. Patient records were monitored until delivery, and pregnancy outcomes were determined. Trophoblast yield was compared with GA at time of collection, maternal BMI, parity, maternal age, and outcome of pregnancy, using linear regression.
   Results There was no effect of GA, maternal BMI, parity, and maternal age on trophoblast yield. Trophoblast yield decreased significantly with early pregnancy loss compared with uncomplicated pregnancies that delivered at term. Trophoblast yield with preeclampsia or intrauterine growth restriction was decreased compared with healthy term outcomes; however, they did not reach statistical significance.
   Conclusions If TRIC becomes available as a method for non-invasive prenatal testing, our data demonstrate that it is unaffected by BMI and is useful as early as 5 weeks of GA. (C) 2015 John Wiley & Sons, Ltd.
C1 [Fritz, Rani; Kohan-Ghadr, Hamid Reza; Sacher, Alex; Bolnick, Alan D.; Kilburn, Brian A.; Bolnick, Jay M.; Drewlo, Sascha; Armant, D. Randall] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA.
   [Diamond, Michael P.] Georgia Regents Univ, Dept Obstet & Gynecol, Augusta, GA USA.
   [Armant, D. Randall] NICHD, Program Reprod & Adult Endocrinol, NIH, DHHS, Bethesda, MD USA.
RP Armant, DR (reprint author), Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA.
EM D.Armant@Wayne.edu
OI Diamond, Michael/0000-0001-6353-4489; Armant, D.
   Randall/0000-0001-5904-9325
FU Intramural Research Program of the NICHD; NIH [HD071408, HL128628]; W.
   K. Kellogg Foundation; March of Dimes Foundation; Perkin Elmer, Inc.
FX This research was supported in part by the Intramural Research Program
   of the NICHD, grants from the NIH (HD071408 and HL128628), the W. K.
   Kellogg Foundation, the March of Dimes Foundation, and Perkin Elmer,
   Inc.
NR 31
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U1 3
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0197-3851
EI 1097-0223
J9 PRENATAL DIAG
JI Prenat. Diagn.
PD DEC
PY 2015
VL 35
IS 12
BP 1218
EP 1222
DI 10.1002/pd.4681
PG 5
WC Genetics & Heredity; Obstetrics & Gynecology
SC Genetics & Heredity; Obstetrics & Gynecology
GA DB3VV
UT WOS:000368442000010
PM 26288006
ER

PT J
AU Barile, JP
   Mitchell, SA
   Thompson, WW
   Zack, MM
   Reeve, BB
   Cella, D
   Smith, AW
AF Barile, John P.
   Mitchell, Sandra A.
   Thompson, William W.
   Zack, Matthew M.
   Reeve, Bryce B.
   Cella, David
   Smith, Ashley Wilder
TI Patterns of Chronic Conditions and Their Associations With Behaviors and
   Quality of Life, 2010
SO PREVENTING CHRONIC DISEASE
LA English
DT Article
ID MULTIPLE CHRONIC CONDITIONS; MENTAL-ILLNESS; IMPROVING HEALTH;
   MULTIMORBIDITY; ADULTS; OUTCOMES; OBESITY; SYSTEM; CARE
AB Introduction Co-occurring chronic health conditions elevate the risk of poor health outcomes such as death and disability, are associated with poor quality of life, and magnify the complexities of self-management, care coordination, and treatment planning. This study assessed patterns of both singular and multiple chronic conditions, behavioral risk factors, and quality of life in a population-based sample.
   Methods In a national survey, adults (n = 4,184) answered questions about the presence of 27 chronic conditions. We used latent class analysis to identify patterns of chronic conditions and to explore associations of latent class membership with sociodemographic characteristics, behavioral risk factors, and health.
   Results Latent class analyses indicated 4 morbidity profiles: a healthy class (class 1), a class with predominantly physical health conditions (class 2), a class with predominantly mental health conditions (class 3), and a class with both physical and mental health conditions (class 4). Class 4 respondents reported significantly worse physical health and well-being and more days of activity limitation than those in the other latent classes. Class 4 respondents were also more likely to be obese and sedentary, and those with predominantly mental health conditions were most likely to be current smokers.
   Conclusions Subgroups with distinct patterns of chronic conditions can provide direction for screening and surveillance, guideline development, and the delivery of complex care services.
C1 [Barile, John P.] Univ Hawaii Manoa, Dept Psychol, Honolulu, HI 96822 USA.
   [Mitchell, Sandra A.; Smith, Ashley Wilder] NCI, Rockville, MD USA.
   [Thompson, William W.; Zack, Matthew M.] Ctr Dis Control & Prevent, Atlanta, GA USA.
   [Reeve, Bryce B.] Univ N Carolina, Chapel Hill, NC USA.
   [Cella, David] Northwestern Univ, Chicago, IL 60611 USA.
RP Barile, JP (reprint author), Univ Hawaii Manoa, Dept Psychol, 2530 Dole St,Sakamaki C400, Honolulu, HI 96822 USA.
EM Barile@hawaii.edu
RI Barile, John/F-9456-2015
OI Barile, John/0000-0003-4098-0640
NR 31
TC 1
Z9 1
U1 1
U2 3
PU CENTERS  DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1545-1151
J9 PREV CHRONIC DIS
JI Prev. Chronic Dis.
PD DEC
PY 2015
VL 12
AR 150179
DI 10.5888/pcd12.150179
PG 11
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA DB7AC
UT WOS:000368665800012
ER

PT J
AU Kaufman, AR
   Land, S
   Parascandola, M
   Augustson, E
   Backinger, CL
AF Kaufman, Annette R.
   Land, Stephanie
   Parascandola, Mark
   Augustson, Erik
   Backinger, Cathy L.
TI Tobacco use transitions in the United States: The National Longitudinal
   Study of Adolescent Health
SO PREVENTIVE MEDICINE
LA English
DT Article
DE Adolescent; Tobacco; Smoking; Smokeless; Tobacco; National Longitudinal
   Study of Adolescent Health
ID HIGH-SCHOOL-STUDENTS; SMOKELESS TOBACCO; CIGARETTE-SMOKING; PRODUCT USE;
   POLYTOBACCO USE; RISK-FACTOR; PANEL-DATA; ADULTS; PREVALENCE; PREDICTORS
AB Objectives. The purpose of this study is to evaluate and describe transitions in cigarette and smokeless tobacco (ST) use, including dual use, prospectively from adolescence into young adulthood. Methods. The current study utilizes four waves of the National Longitudinal Study of Adolescent Health (Add Health) to examine patterns of cigarette and ST use (within 30 days of survey) over time among a cohort in the United States beginning in 7th-12th grade (1995) into young adulthood (2008-2009). Transition probabilities were estimated using Markov modeling. Results. Among the cohort (N = 20,774), 48.7% reported using cigarettes, 12.8% reported using ST, and 7.2% reported dual use (cigarettes and ST in the same wave) in at least one wave. In general, the risk for transitioning between cigarettes and ST was higher for males and those who were older. Dual users exhibited a high probability (81%) of continuing dual use over time. Conclusions. Findings suggest that adolescents who use multiple tobacco products are likely to continue such use as they move into young adulthood. When addressing tobacco use among adolescents and young adults, multiple forms of tobacco use should be considered. Published by Elsevier Inc.
C1 [Kaufman, Annette R.; Land, Stephanie; Parascandola, Mark; Augustson, Erik] NCI, Tobacco Control Res Branch, Rockville, MD 20850 USA.
   [Backinger, Cathy L.] US FDA, Ctr Tobacco Prod, Silver Spring, MD USA.
RP Kaufman, AR (reprint author), NCI, Tobacco Control Res Branch, Behav Res Program, Div Canc Control & Populat Sci,NIH, 9609 Med Ctr Dr,3-E-546, Rockville, MD 20850 USA.
EM kaufmana@mail.nih.gov
FU National Cancer Institute; Eunice Kennedy Shriver National Institute of
   Child Health and Human Development [P01-HD31921]
FX This work was supported by the National Cancer Institute. This research
   uses data from Add Health, a program project directed by Kathleen Mullan
   Harris and designed by J. Richard Udry, Peter S. Bearman, and Kathleen
   Mullan Harris at the University of North Carolina at Chapel Hill, and
   funded by grant P01-HD31921 from the Eunice Kennedy Shriver National
   Institute of Child Health and Human Development, with cooperative
   funding from 23 other federal agencies and foundations. Special
   acknowledgment is due Ronald R. Rindfuss and Barbara Entwisle for
   assistance in the original design. Information on how to obtain the Add
   Health data files is available on the Add Health website
   (http://www.cpc.unc.edu/addhealth). No direct support was received from
   grant P01-HD31921 for this analysis.
NR 45
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U1 1
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0091-7435
EI 1096-0260
J9 PREV MED
JI Prev. Med.
PD DEC
PY 2015
VL 81
BP 251
EP 257
DI 10.1016/j.ypmed.2015.08.026
PG 7
WC Public, Environmental & Occupational Health; Medicine, General &
   Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA DB3OP
UT WOS:000368421300038
PM 26361752
ER

PT J
AU Bellatorre, A
   Choi, K
   Bernat, D
AF Bellatorre, Anna
   Choi, Kelvin
   Bernat, Debra
TI The influence of the social environment on youth smoking status
SO PREVENTIVE MEDICINE
LA English
DT Article
DE Tobacco; Adolescent health; Peer influence
ID ADOLESCENT CIGARETTE-SMOKING; PEER INFLUENCE; PREDICTORS; INITIATION;
   IMPLICIT; BEHAVIOR; FRIENDS; ONSET
AB Objective. Youth smoking is complex with multilevel influences. While much is known about certain levels of influence on youth smoking, the lack of focus on institutional influences is notable. This study evaluated the effects of ambient smoking attitudes and behaviors in schools on individual youth smoking.
   Method. Data from the 2012 Florida Youth Tobacco Survey (n=67,460) were analyzed. Multinomial logistic regression was used to investigate individual and aggregated school-level factors that were associated with a youth being classified as a "susceptible nonsmoker" (SN) or " current smoker" (CS) relative to a " non-susceptible nonsmoker" (NN).
   Results. The aggregated percentage of regular smokers at a school, ambient school level positive smoking perceptions, and the standardized difference between individual and school-level positive smoking perceptions were statistically significant in the fully adjusted model. We also found an increased risk of being a SN relative to a NN for Hispanic youth. Moreover, our approach to modeling institutional-level factors raised the pseudo r-squared from 0.05 to 0.14.
   Conclusion. These findings suggest the importance of ambient smoking attitudes and behaviors on youth smoking. Prevention efforts affecting ambient smoking attitudes may be beneficial. Published by Elsevier Inc.
C1 [Bellatorre, Anna; Choi, Kelvin] Natl Inst Minor Hlth & Hlth Dispar, Bethesda, MD 20892 USA.
   [Bernat, Debra] Univ Maryland, College Pk, MD 20742 USA.
RP Choi, K (reprint author), Natl Inst Minor Hlth & Hlth Dispar, Bethesda, MD 20892 USA.
EM Kelvin.choi@nih.gov
FU Division of Intramural Research, National Institute on Minority Health
   and Health Disparities, National Institutes of Health; National Cancer
   Institute [R03 CA168411]
FX Dr. Bellatorre and Dr. Choi's effort on the study is funded by the
   Division of Intramural Research, National Institute on Minority Health
   and Health Disparities, National Institutes of Health. Dr. Bernat's
   effort is supported with a grant from the National Cancer Institute (R03
   CA168411; D. Bernat, Principal Investigator). The views presented in
   this paper don't necessarily reflect the views of the Florida Department
   of Health, the NIH, or the University of Maryland.
NR 31
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U2 8
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0091-7435
EI 1096-0260
J9 PREV MED
JI Prev. Med.
PD DEC
PY 2015
VL 81
BP 309
EP 313
DI 10.1016/j.ypmed.2015.09.017
PG 5
WC Public, Environmental & Occupational Health; Medicine, General &
   Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA DB3OP
UT WOS:000368421300048
PM 26449408
ER

PT J
AU Cherney, AR
   Marin, JR
   Brown, J
   Anise, A
   Krosnick, S
   Henriksen, K
   Lewis, RJ
   Mills, AM
AF Cherney, Alan R.
   Marin, Jennifer R.
   Brown, Jeremy
   Anise, Ayodola
   Krosnick, Steven
   Henriksen, Kerm
   Lewis, Roger J.
   Mills, Angela M.
TI Funding Research in Emergency Diagnostic Imaging: Summary of a Panel
   Discussion at the 2015 Academic Emergency Medicine Consensus Conference
SO ACADEMIC EMERGENCY MEDICINE
LA English
DT Article; Proceedings Paper
CT Academic-Emergency-Medicine (AEM) Consensus Conference
CY MAY 12, 2015
CL San Diego, CA
SP Acad Emergency Med
ID HEALTH-CARE RESEARCH; AGENCY
AB As part of the 2015 Academic Emergency Medicine consensus conference "Diagnostic Imaging in the Emergency Department: A Research Agenda to Optimize Utilization," a panel of representatives from the National Institute of Health's Office of Emergency Care Research, the National Institute of Biomedical Imaging and Bioengineering, the Agency for Healthcare Research and Quality, and the Patient-Centered Outcomes Research Institute was assembled to discuss future opportunities for funding research in this particular area of interest. Representatives from these agencies and organizations discussed their missions and priorities and how they distribute funding. They also addressed questions on mechanisms for new and established researchers to secure future funding. (C) 2015 by the Society for Academic Emergency Medicine
C1 [Cherney, Alan R.] Lehigh Valley Hlth Network, Dept Emergency Med, Allentown, PA USA.
   [Marin, Jennifer R.] Univ Pittsburgh, Sch Med, Dept Pediat, Pittsburgh, PA 15261 USA.
   [Marin, Jennifer R.] Univ Pittsburgh, Sch Med, Dept Emergency Med, Pittsburgh, PA USA.
   [Brown, Jeremy] Natl Inst Hlth Off Emergency Care Res, Bethesda, MD USA.
   [Anise, Ayodola] Patient Ctr Outcomes Res Inst, Addressing Dispar Program, Washington, DC USA.
   [Krosnick, Steven] Natl Inst Biomed Imaging & Bioengn, Bethesda, MD USA.
   [Henriksen, Kerm] Agcy Healthcare Res & Qual, Ctr Qual Improvement & Patient Safety, Human Factors Advisor Patient Safety, Rockville, MD USA.
   [Lewis, Roger J.] Harbor UCLA Med Ctr, Dept Emergency Med, Torrance, CA 90509 USA.
   [Mills, Angela M.] Univ Penn, Dept Emergency Med, Perelman Sch Med, Philadelphia, PA 19104 USA.
RP Mills, AM (reprint author), Univ Penn, Dept Emergency Med, Perelman Sch Med, Philadelphia, PA 19104 USA.
EM millsa@uphs.upenn.edu
FU Agency for Healthcare Research and Quality [R13HS023498-01]; Agency for
   Healthcare Research and Quality (AHRQ) [1R13HS023498-01]; National
   Institute of Biomedical Imaging and Bioengineering [1 R13 EB 019813-01]
FX Dr. Marin was supported by the Agency for Healthcare Research and
   Quality (R13HS023498-01); receives support as teaching faculty for 3rd
   Rock Ultrasound, LLC; and has served as a consultant for Venaxis, Inc.;
   Funding for this conference was made possible (in part) by grant number
   1R13HS023498-01 from the Agency for Healthcare Research and Quality
   (AHRQ) and grant number 1 R13 EB 019813-01 from the National Institute
   of Biomedical Imaging and Bioengineering. The views expressed in written
   conference materials or publications and by speakers and moderators do
   not necessarily reflect the official policies of the Department of
   Health and Human Services, nor does mention of trade names, commercial
   practices, or organizations imply endorsement by the U.S. Government.
NR 12
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U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1069-6563
EI 1553-2712
J9 ACAD EMERG MED
JI Acad. Emerg. Med.
PD DEC
PY 2015
VL 22
IS 12
SI SI
BP 1400
EP 1405
DI 10.1111/acem.12825
PG 6
WC Emergency Medicine
SC Emergency Medicine
GA DA5FP
UT WOS:000367828900006
PM 26567519
ER

PT J
AU Yang, K
   Lu, WJ
   Jiang, Q
   Yun, X
   Zhao, MM
   Jiang, HY
   Wang, J
AF Yang, Kai
   Lu, Wenju
   Jiang, Qian
   Yun, Xin
   Zhao, Mingming
   Jiang, Haiyang
   Wang, Jian
TI Peroxisome Proliferator-Activated Receptor gamma-Mediated Inhibition on
   Hypoxia-Triggered Store-Operated Calcium Entry A Caveolin-1-Dependent
   Mechanism
SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
LA English
DT Article
DE pulmonary hypertension; peroxisome proliferator-activated receptor
   gamma; caveolin-1; store-operated calcium entry; pulmonary arterial
   smooth muscle cells
ID ARTERIAL SMOOTH-MUSCLE; INDUCED PULMONARY-HYPERTENSION; UP-REGULATES
   CAVEOLIN-1; COLON-CANCER CELL; PPAR-GAMMA; ENDOTHELIAL-CELLS;
   INDEPENDENT PATHWAYS; TRPC EXPRESSION; KNOCKOUT MICE; CA2+ CHANNELS
AB Our previous publication demonstrated that peroxisome proliferator-activated receptor gamma (PPAR gamma) inhibits the pathogenesis of chronic hypoxia (CH)-induced pulmonary hypertension by targeting store-operated calcium entry (SOCE) in rat distal pulmonary arterial smooth muscle cells (PASMCs). In this study, we aim to determine the role of a membrane scaffolding protein, caveolin-1, during the suppressive process ofPPAR gamma on SOCE. Adult (6-8 weeks) male Wistar rats (200-250 g) were exposed to CH (10% O-2) for 21 days to establish CH-induced pulmonary hypertension. Primary cultured rat distal PASMCs were applied for the molecular biological experiments. First, hypoxic exposure led to 2.5-fold and 1-fold increases of caveolin-1 protein expression in the distal pulmonary arteries and PASMCs, respectively. Second, effective knockdown of caveolin-1 significantly reduced hypoxia-induced SOCE for 58.2% and 41.5%, measured by Mn2+ quenching and extracellular Ca2+ restoration experiments, respectively. These results suggested that caveolin-1 acts as a crucial regulator of SOCE, and hypoxia-up-regulated caveolin-1 largely accounts for hypoxia-elevated SOCE in PASMCs. Then, by using a high-potency PPAR gamma agonist, GW1929, we detected that PPAR gamma activation inhibited SOCE and caveolin-1 protein for 62.5% and 59.8% under hypoxia, respectively, suggesting that caveolin-1 also acts as a key target during the suppressive process of PPAR gamma on SOCE in PASMCs. Moreover, by using effective small interfering RNAs against PPAR gamma and caveolin-1, and PPAR gamma antagonist, T0070907, we observed that PPAR gamma plays an inhibitory role on caveolin-1 protein by promoting its lysosomal degradation, without affecting the messenger RNA level. PPAR gamma inhibits SOCE, at least partially, by suppressing cellular caveolin-1 protein in PASMCs.
C1 [Yang, Kai; Lu, Wenju; Jiang, Qian; Yun, Xin; Wang, Jian] Guangzhou Med Univ, Affiliated Hosp 1, Guangzhou Inst Resp Dis, State Key Lab Resp Dis, Guangzhou, Guangdong, Peoples R China.
   [Wang, Jian] Peoples Hosp Inner Mongolia, Div Pulm, Hohhot, Inner Mongolia, Peoples R China.
   [Yang, Kai; Lu, Wenju; Jiang, Qian; Yun, Xin; Jiang, Haiyang; Wang, Jian] Johns Hopkins Univ, Sch Med, Div Pulm & Crit Care Med, Baltimore, MD 21224 USA.
   [Zhao, Mingming] NIA, Lab Mol Biol & Immunol, Baltimore, MD 21224 USA.
RP Wang, J (reprint author), Johns Hopkins Univ, Sch Med, Div Pulm & Crit Care Med, 5501 Hopkins Bayview Circle,Room 4B30, Baltimore, MD 21224 USA.
EM jwang31@jhmi.edu
FU National Institutes of Health [R01-HL093020]; National Natural Science
   Foundation of China [81173112, 81470246, 81170052, 81220108001];
   Guangdong Natural Science Foundation [1035101200300000]; Guangzhou
   Department of Education Yangcheng Scholarship grant [12A001S]; Guangzhou
   Department of Natural Science grant [2014Y2-00167]; Guangdong Province
   Universities and Colleges Pearl River Scholar Funded Scheme, China;
   State Scholarship Fund; China Scholarship Council [201208440091]
FX This work was supported by National Institutes of Health grant
   R01-HL093020, National Natural Science Foundation of China grants
   81173112, 81470246, 81170052, and 81220108001, Guangdong Natural Science
   Foundation team grant 1035101200300000, Guangzhou Department of
   Education Yangcheng Scholarship grant 12A001S, Guangzhou Department of
   Natural Science grant 2014Y2-00167, and Guangdong Province Universities
   and Colleges Pearl River Scholar Funded Scheme 2014, China (W.L.). Also
   supported by an award from the State Scholarship Fund and China
   Scholarship Council grant 201208440091 (K.Y.).
NR 56
TC 6
Z9 6
U1 3
U2 7
PU AMER THORACIC SOC
PI NEW YORK
PA 25 BROADWAY, 18 FL, NEW YORK, NY 10004 USA
SN 1044-1549
EI 1535-4989
J9 AM J RESP CELL MOL
JI Am. J. Respir. Cell Mol. Biol.
PD DEC
PY 2015
VL 53
IS 6
BP 882
EP 892
DI 10.1165/rcmb.2015-0002OC
PG 11
WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
GA DB3NW
UT WOS:000368419400014
PM 26020612
ER

PT J
AU Clement, TM
   Inselman, AL
   Goulding, EH
   Willis, WD
   Eddy, EM
AF Clement, Tracy M.
   Inselman, Amy L.
   Goulding, Eugenia H.
   Willis, William D.
   Eddy, Edward M.
TI Disrupting Cyclin Dependent Kinase 1 in Spermatocytes Causes Late
   Meiotic Arrest and Infertility in Mice
SO BIOLOGY OF REPRODUCTION
LA English
DT Article
DE CDK1; cell cycle; chromosome condensation; male meiosis; meiotic arrest;
   metaphase-promoting factor; okadaic acid; synaptonemal complex
ID MOUSE OOCYTE MEIOSIS; SYNAPTONEMAL COMPLEX; METAPHASE-I; GERM-CELL;
   PACHYTENE SPERMATOCYTES; CROSSING-OVER; OKADAIC ACID; PROPHASE-I;
   SPERMATOGENESIS; DYNAMICS
AB While cyclin dependent kinase 1 (CDK1) has a critical role in controlling resumption of meiosis in oocytes, its role has not been investigated directly in spermatocytes. Unique aspects of male meiosis led us to hypothesize that its role is different in male meiosis than in female meiosis. We generated a conditional knockout (cKO) of the Cdk1 gene in mouse spermatocytes to test this hypothesis. We found that CDK1-null spermatocytes undergo synapsis, chiasmata formation, and desynapsis as is seen in oocytes. Additionally, CDK1-null spermatocytes relocalize SYCP3 to centromeric foci, express H3pSer10, and initiate chromosome condensation. However, CDK1-null spermatocytes fail to form condensed bivalent chromosomes in prophase of meiosis I and instead are arrested at prometaphase. Thus, CDK1 has an essential role in male meiosis that is consistent with what is known about the role of CDK1 in female meiosis, where it is required for formation of condensed bivalent metaphase chromosomes and progression to the first meiotic division. We found that cKO spermatocytes formed fully condensed bivalent chromosomes in the presence of okadaic acid, suggesting that cKO chromosomes are competent to condense, although they do not do so in vivo. Additionally, arrested cKO spermatocytes exhibited irregular cell shape, irregular large nuclei, and large distinctive nucleoli. These cells persist in the seminiferous epithelium through the next seminiferous epithelial cycle with a lack of stage XII checkpoint-associated cell death. This indicates that CDK1 is required upstream of a checkpoint-associated cell death as well as meiotic metaphase progression in mouse spermatocytes.
C1 [Clement, Tracy M.; Inselman, Amy L.; Goulding, Eugenia H.; Willis, William D.; Eddy, Edward M.] NIEHS, Gamete Biol Grp, Reprod & Dev Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Eddy, EM (reprint author), NIEHS, Gamete Biol Grp, Reprod & Dev Biol Lab, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM eddy@niehs.nih.gov
FU Intramural Research Program of the NIH, National Institute of
   Environmental Health Sciences
FX This work was supported by the Intramural Research Program of the NIH,
   National Institute of Environmental Health Sciences.
NR 77
TC 1
Z9 1
U1 0
U2 1
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1691 MONROE ST,SUITE # 3, MADISON, WI 53711-2021 USA
SN 0006-3363
EI 1529-7268
J9 BIOL REPROD
JI Biol. Reprod.
PD DEC 1
PY 2015
VL 93
IS 6
AR 137
DI 10.1095/biolreprod.115.134940
PG 12
WC Reproductive Biology
SC Reproductive Biology
GA DA8UL
UT WOS:000368081800001
PM 26490841
ER

PT J
AU Sabourin, JA
   Valdar, W
   Nobel, AB
AF Sabourin, Jeremy A.
   Valdar, William
   Nobel, Andrew B.
TI A Permutation Approach for Selecting the Penalty Parameter in Penalized
   Model Selection
SO BIOMETRICS
LA English
DT Article
DE LASSO; Penalized regression; Variable selection
ID REGRESSION SHRINKAGE; GENOME-WIDE; LASSO
AB We describe a simple, computationally efficient, permutation-based procedure for selecting the penalty parameter in LASSO-penalized regression. The procedure, permutation selection, is intended for applications where variable selection is the primary focus, and can be applied in a variety of structural settings, including that of generalized linear models. We briefly discuss connections between permutation selection and existing theory for the LASSO. In addition, we present a simulation study and an analysis of real biomedical data sets in which permutation selection is compared with selection based on the following: cross-validation (CV), the Bayesian information criterion (BIC), scaled sparse linear regression, and a selection method based on recently developed testing procedures for the LASSO.
C1 [Sabourin, Jeremy A.; Valdar, William] Univ N Carolina, Dept Genet, Chapel Hill, NC USA.
   [Sabourin, Jeremy A.] NHGRI, Genometr Sect, Computat & Stat Genom Branch, NIH, Baltimore, MD USA.
   [Nobel, Andrew B.] Univ N Carolina, Dept Stat & Operat Res, Chapel Hill, NC 27514 USA.
   [Valdar, William; Nobel, Andrew B.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
   [Nobel, Andrew B.] Univ N Carolina, Dept Biostat, Chapel Hill, NC USA.
RP Nobel, AB (reprint author), Univ N Carolina, Dept Stat & Operat Res, Chapel Hill, NC 27514 USA.
EM nobel@email.unc.edu
FU National Institute of General Medical Sciences of the National
   Institutes of Health (NIH) [R01GM104125]; National Institute of Mental
   Health of the NIH [R01MH101819]; National Science Foundation (NSF)
   [DMS-1310002]; University of North Carolina Lineberger Comprehensive
   Cancer Center; Division of Intramural Research at the National Human
   Genome Research Institute, NIH
FX The authors would like to thank Kai Zhang and Alexandre Belloni for
   helpful discussions concerning their work and the theoretical properties
   of the permutation selection procedure. Research reported in this
   manuscript was supported by the following: the National Institute of
   General Medical Sciences of the National Institutes of Health (NIH)
   under award number R01GM104125 (partial support for J. S. and W. V.);
   the National Institute of Mental Health of the NIH under award number
   R01MH101819 (A. N.); the National Science Foundation (NSF) under Grant
   number DMS-1310002 (A. N.); the University of North Carolina Lineberger
   Comprehensive Cancer Center (partial support for J. S. and W. V.); and
   by the Division of Intramural Research at the National Human Genome
   Research Institute, NIH (partial support for J. S.). The content is
   solely the responsibility of the authors and does not necessarily
   represent the official views of the NIH or NSF.
NR 22
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0006-341X
EI 1541-0420
J9 BIOMETRICS
JI Biometrics
PD DEC
PY 2015
VL 71
IS 4
BP 1185
EP 1194
DI 10.1111/biom.12359
PG 10
WC Biology; Mathematical & Computational Biology; Statistics & Probability
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
   Biology; Mathematics
GA DB0GT
UT WOS:000368187300035
PM 26243050
ER

PT J
AU Ribeiro-Gomes, FL
   Romano, A
   Lee, S
   Roffe, E
   Peters, NC
   Debrabant, A
   Sacks, D
AF Ribeiro-Gomes, F. L.
   Romano, A.
   Lee, S.
   Roffe, E.
   Peters, N. C.
   Debrabant, A.
   Sacks, D.
TI Apoptotic cell clearance of Leishmania major-infected neutrophils by
   dendritic cells inhibits CD8(+) T-cell priming in vitro by Mer tyrosine
   kinase-dependent signaling
SO CELL DEATH & DISEASE
LA English
DT Article
ID TOXOPLASMA-GONDII INFECTION; SAND FLIES; MACROPHAGES; ANTIGEN;
   PHAGOCYTOSIS; TUBERCULOSIS; ACTIVATION; PROTEIN; DEATH; MICE
AB Neutrophils are the predominant recruited and infected cells during the early stages of Leishmania major infection in the skin, and depletion of neutrophils promotes immunity to infection transmitted by sand fly bite. In order to better understand how the acute neutrophilic response suppresses immunity, we assessed the consequences of the interaction between neutrophils recovered from the skin-inoculation site and bone marrow-derived dendritic cells (DCs) in vitro. The capture of infected, apoptotic neutrophils by the DCs completely inhibited their cross-presentation function that was dependent on engagement of the receptor tyrosine kinase Mer on the DCs. The capture of uninfected neutrophils, or neutrophils infected with Toxoplasma gondii, had only slight immunomodulatory effects. These studies define the clearance of infected, apoptotic neutrophils by DCs and Mer receptor signaling as central to the early immune evasion strategies of L. major, with relevance to other vector-borne pathogens delivered by bite to the skin.
C1 [Ribeiro-Gomes, F. L.; Romano, A.; Lee, S.; Peters, N. C.; Sacks, D.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
   [Roffe, E.] NIAID, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
   [Debrabant, A.] US FDA, OBRR, CBER, Silver Spring, MD USA.
RP Sacks, D (reprint author), NIAID, Parasit Dis Lab, Bldg 4,Room B1-12,4 Ctr Dr,MSC 0425, Bethesda, MD 20892 USA.
EM dsacks@nih.gov
RI Roffe, Ester/H-4688-2012
FU Intramural Research Program of the National Institute of Allergy and
   Infectious Diseases, National Institutes of Health
FX We thank M Grigg and V Pzsenny for provision of the T. gondii strain,
   and C Rothlin and J Coligan for donation of the Mer<SUP>-/-</SUP> and
   CD300f<SUP>-/-</SUP> mice, respectively. We thank Kim Beacht for
   assistance with the animal studies. We thank T Moyer, C Henry, E
   Stregevsky and B Hague for cell sorting and S Ganesan for technical
   assistance with the confocal microscopy. This work was supported in part
   by the Intramural Research Program of the National Institute of Allergy
   and Infectious Diseases, National Institutes of Health.
NR 40
TC 7
Z9 7
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD DEC
PY 2015
VL 6
AR e2018
DI 10.1038/cddis.2015.351
PG 12
WC Cell Biology
SC Cell Biology
GA DB0BA
UT WOS:000368172400017
PM 26658192
ER

PT J
AU McShane, PJ
   Glassroth, J
AF McShane, Pamela J.
   Glassroth, Jeffrey
TI Pulmonary Disease Due to Nontuberculous Mycobacteria Current State and
   New Insights
SO CHEST
LA English
DT Article
ID COMPLEX LUNG-DISEASE; AVIUM COMPLEX; CYSTIC-FIBROSIS; HYPERSENSITIVITY
   PNEUMONITIS; CLINICAL-SIGNIFICANCE; RETROSPECTIVE COHORT;
   ANTIBIOTIC-THERAPY; PROGNOSTIC-FACTORS; NEGATIVE PATIENTS; UNITED-STATES
AB Since pulmonary nontuberculous mycobacteria (PNTM) lung disease was last reviewed in CHEST in 2008, new information has emerged spanning multiple domains, including epidemiology, transmission and pathogenesis, clinical presentation, diagnosis, and treatment. The overall prevalence of PNTM is increasing, and in the United States, areas of highest prevalence are clustered in distinct geographic locations with common environmental and socioeconomic factors. Although the accepted paradigm for transmission continues to be inhalation from the environment, provocative reports suggest that person-to-person transmission may occur. A panoply of host factors have been investigated in an effort to elucidate why infection from this bacteria develops in ostensibly immunocompetent patients, and there has been clarification that immunocompetent patients exhibit different histopathology from immunocompromised patients with nontuberculous mycobacteria infection. It is now evident that Mycobacterium abscessus, an increasingly prevalent cause of PNTM lung disease, can be classified into three separate subspecies with differing genetic susceptibility or resistance to macrolides. Recent publications also raise the possibility of improved control of PNTM through enhanced adherence to current treatment guidelines as well as new approaches to treatment and even prevention. These and other recent developments and insights that may inform our approach to PNTM lung disease are reviewed and discussed.
C1 [McShane, Pamela J.] NHLBI, NIH, Bethesda, MD 20892 USA.
   [Glassroth, Jeffrey] Univ Chicago, Div Biol Sci, Chicago, IL 60637 USA.
RP McShane, PJ (reprint author), NHLBI, NIH, Bldg 10,Room 6-3154, Bethesda, MD 20892 USA.
EM pamelamcshane@hotmail.com
NR 61
TC 7
Z9 7
U1 6
U2 11
PU AMER COLL CHEST PHYSICIANS
PI GLENVIEW
PA 2595 PATRIOT BLVD, GLENVIEW, IL 60026 USA
SN 0012-3692
J9 CHEST
JI Chest
PD DEC
PY 2015
VL 148
IS 6
BP 1517
EP 1527
DI 10.1378/chest.15-0458
PG 11
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA DB1NC
UT WOS:000368273900039
PM 26225805
ER

PT J
AU Xie, HH
   Xie, T
   Xu, JY
   Shen, CS
   Lai, ZJ
   Xu, NS
   Wang, SC
   Shan, JJ
AF Xie Hui-Hui
   Xie Tong
   Xu Jian-Ya
   Shen Cun-Si
   Lai Zi-Juan
   Xu Niu-Sheng
   Wang Shou-Chuan
   Shan Jin-Jun
TI Metabolomics Study of Aconitine and Benzoylaconine Induced Reproductive
   Toxicity in BeWo Cell
SO CHINESE JOURNAL OF ANALYTICAL CHEMISTRY
LA English
DT Article
DE Aconitine; Benzoylaconine; Gas chromatography-mass spectrometry;
   Metabolomics; BeWo cell; Fetal toxicity
ID METABONOMICS; METABOLISM; PLACENTA; RAT
AB An intracellular metabolomics method based on gas chromatography coupled with mass spectrometry (GC-MS) was established to explore the toxicity mechanism of aconitine and benzoylaconine. BeWo, a continuous cell lines originated from human placenta, was selected to establish in vitro placenta model. The intracellular metabolites were extracted after exposed to 5 mu g mL(-1) aconitine and benzoylaconine for 0, 6, 12, 24 and 36 h, respectively. The intracellular metabolic profiles were acquired by GC-MS. Orthogonal partial least squares discriminant analysis (OPLS-DA) score plot showed the time-dependent change of the metabolomic profiles between the control and intervention groups. After screening by variable influence on projection (VIP) value and one-way analysis of variance, and searching with NIST 2014 database, 11 metabolites were identified, including proline, glycine, threonine, glutamic acid, N-acetylglutamine, glutamine, lysine, histidine, succinic acid, glucose and galactose, which were mainly involved in the following pathways: (1) glutamine and glutamate metabolism; (2) glycine, serine and threonine metabolism; (3) alanine, aspartate and glutamate metabolism; (4) lysine degradation; (5) arginine and proline metabolism and (6) histidine metabolism. The results demonstrated that amino acid metabolism was the main metabolic pathway and responsible for the placental and fetal toxicity of aconitine and benzoylaconine.
C1 [Xie Hui-Hui; Xie Tong; Xu Jian-Ya; Shen Cun-Si; Wang Shou-Chuan; Shan Jin-Jun] Nanjing Univ Chinese Med, Inst Pediat Chinese Med, Jiangsu Key Lab Pediat Resp Dis, Nanjing 210023, Jiangsu, Peoples R China.
   [Lai Zi-Juan] Univ Calif Davis, Genome Ctr, NIH, West Coast Metabol Ctr, Davis, CA 95616 USA.
   [Xu Niu-Sheng] Thermo Fisher Sci, Shanghai 201206, Peoples R China.
RP Shan, JJ (reprint author), Nanjing Univ Chinese Med, Inst Pediat Chinese Med, Jiangsu Key Lab Pediat Resp Dis, Nanjing 210023, Jiangsu, Peoples R China.
EM jshan@njucm.edu.cn
FU Beijing Natural Science Foundation of China [81303299]
FX This work was supported by the Beijing Natural Science Foundation of
   China (No. 81303299).
NR 18
TC 0
Z9 0
U1 6
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0253-3820
EI 1872-2040
J9 CHINESE J ANAL CHEM
JI Chin. J. Anal. Chem.
PD DEC
PY 2015
VL 43
IS 12
BP 1808
EP 1812
DI 10.1016/S1872-2040(15)60881-7
PG 5
WC Chemistry, Analytical
SC Chemistry
GA DB0AZ
UT WOS:000368172300002
ER

PT J
AU Tuna, MM
   Dogant, BA
   Arduc, A
   Imga, NN
   Tutuncu, Y
   Berker, D
   Guler, S
AF Tuna, Mazhar M.
   Dogant, Bercem A.
   Arduc, Ayse
   Imga, Narin Nasiroglu
   Tutuncu, Yasemin
   Berker, Dilek
   Guler, Serdar
TI Impaired endothelial function in patients with mild primary
   hyperparathyroidism improves after parathyroidectomy
SO CLINICAL ENDOCRINOLOGY
LA English
DT Article
ID FLOW-MEDIATED VASODILATION; BRACHIAL-ARTERY REACTIVITY; RISK-FACTORS;
   CARDIOVASCULAR-DISEASE; PREDICTIVE-VALUE; AUDIT RESEARCH; HEART-DISEASE;
   D DEFICIENCY; VITAMIN-D; HORMONE
AB Background Primary hyperparathyroidism (PHPT) is associated with cardiovascular morbidity; however, data on the reversibility of cardiovascular disease in mild primary hyperparathyroidism are conflicting. The aim of this study was to assess endothelial function in patients with mild PHPT before and after parathyroidectomy (Ptx).
   Methods We prospectively evaluated 53 patients with mild PHPT (Group 1; 45 women, eight men; aged 52 +/- 3.1 years) and 46 healthy control subjects (Group 2; 38 women, eight men; aged 46 +/- 9.5 years). Endothelial function was measured as flow-mediated dilation (FMD) and carotid intima-media thickness (CIMT) using Doppler ultrasonography. Patients with diabetes mellitus, coronary heart disease, impaired renal function, hyperthyroidism, hypothyroidism and a history of smoking were excluded from the study. Patients were studied at baseline and 6-12 months after the first evaluation.
   Results There were no differences with respect to age, gender and BMI between the two groups. Hypertension prevalence was three times higher in group 1 than in controls. % FMD was lower in group 1 than in group 2 (2.6 +/- 1.2 vs 14.8 +/- 9.6, P < 0.001). CIMT was higher in patients with PHPT than controls (0.69 +/- 0.18 vs 0.61 +/- 0.12, P = 0.045). This significance remained when hypertensive patients were excluded from the analysis. While FMD and CIMT improved significantly after Ptx, there were no differences in mild PHPT patients who followed without parathyroidectomy.
   Conclusion FMD and CIMT are impaired in patients with mild PHPT compared to controls and improved significantly after a successful Ptx. Ptx improves endothelial function in patients with mild PHPT that may lead to decreased cardiovascular morbidity and mortality.
C1 [Tuna, Mazhar M.] Dicle Univ, Dept Metab, Med Fac Endocrinol, Diyarbakir, Turkey.
   [Dogant, Bercem A.; Imga, Narin Nasiroglu; Berker, Dilek] Ankara Numune Training & Res Hosp, Dept Endocrinol & Metab, Ankara, Turkey.
   [Arduc, Ayse] Natl Inst Hlth, Natl Inst Diabet & Digest & Kidney Dis, Diabet Endocrine & Obes Branch, Washington, DC USA.
   [Tutuncu, Yasemin] Haydarpasa Numune Training & Res Hosp, Dept Endocrinol & Metab, Istanbul, Turkey.
   [Guler, Serdar] Hitit Univ, Med Fac Endocrinol, Dept Metab, Corum, Turkey.
RP Tuna, MM (reprint author), Dicle Univ, Fac Med, Div Endocrinol & Metab, Diyarbakir, Turkey.
EM tunamazhar@gmail.com
NR 36
TC 3
Z9 3
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0300-0664
EI 1365-2265
J9 CLIN ENDOCRINOL
JI Clin. Endocrinol.
PD DEC
PY 2015
VL 83
IS 6
BP 951
EP 956
DI 10.1111/cen.12666
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA DB1TX
UT WOS:000368293000028
PM 25393455
ER

PT J
AU Jee, YH
   Celi, FS
   Sampson, M
   Sacks, DB
   Remaley, AT
   Kebebew, E
   Baron, J
AF Jee, Youn Hee
   Celi, Francesco S.
   Sampson, Maureen
   Sacks, David B.
   Remaley, Alan T.
   Kebebew, Electron
   Baron, Jeffrey
TI Midkine concentrations in fine-needle aspiration of benign and malignant
   thyroid nodules
SO CLINICAL ENDOCRINOLOGY
LA English
DT Article
ID ACID-RESPONSIVE GENE; MOUSE EMBRYOGENESIS; SERUM MIDKINE; EXPRESSION;
   CARCINOMA; DIAGNOSIS; PLEIOTROPHIN; BIOPSY; MK; DIFFERENTIATION
AB Context The primary preoperative method for distinguishing malignant from benign thyroid nodules is fine-needle aspiration (FNA) cytology, but it is frequently inconclusive. Midkine (MDK) is a heparin-binding growth factor, which is overexpressed in papillary thyroid carcinoma (PTC).
   Objective We measured MDK concentrations in FNA samples from benign and malignant thyroid nodules to explore the possibility that MDK measurement might aid in the evaluation of thyroid nodules.
   Design 35 subjects underwent preoperative FNA of 45 thyroid nodules, followed by thyroidectomy, providing a histological diagnosis. FNA needle contents were first expressed for cytology, and then, the needle was washed with buffer for immunoassay. In 46 subjects without preoperative FNA samples, FNA was performed ex vivo on 62 nodules within surgically excised thyroid tissue.
   Measurements MDK was measured using a high-sensitivity sandwich ELISA and normalized to thyroglobulin (Tg) concentration in the sample to adjust for tissue content in the aspirate.
   Results The MDK/Tg ratio was higher in 18 PTCs than in 87 benign nodules (204 +/- 106 vs 1.2 +/- 0.3 ng/mg, mean +/- SEM, P < 0.001). Using a threshold of 10 ng/mg, the sensitivity and specificity of the MDK/Tg ratio for diagnosis of PTC were 67% and 99%, respectively. All follicular variant PTCs had a MDK/Tg ratio < 10 ng/mg.
   Conclusions The findings indicate that, in FNA samples, the MDK/Tg ratio in PTC is greater than in benign thyroid nodules, raising the possibility that this approach might provide adjunctive diagnostic or prognostic information to complement existing approaches.
C1 [Jee, Youn Hee; Baron, Jeffrey] NIH, Sect Growth & Dev, Program Dev Endocrinol & Genet, Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA.
   [Celi, Francesco S.] Virginia Commonwealth Univ, Div Endocrinol & Metab, Bethesda, MD USA.
   [Sampson, Maureen; Sacks, David B.; Remaley, Alan T.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Kebebew, Electron] NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Baron, J (reprint author), NIH, Room 1-3330,10 Ctr Dr CRC,MSC 1103, Bethesda, MD 20892 USA.
EM jeffrey.baron@nih.gov
FU Intramural Research Programs of the Eunice Kennedy Shriver National
   Institute of Child Health and Human Development (NICHD); National
   Institute of Diabetes and Digestive and Kidney Diseases (NIDDK);
   National Cancer Institute (NCI); Clinical Center of the National
   Institutes of Health
FX This work was supported by the Intramural Research Programs of the
   Eunice Kennedy Shriver National Institute of Child Health and Human
   Development (NICHD), the National Institute of Diabetes and Digestive
   and Kidney Diseases (NIDDK), the National Cancer Institute (NCI) and the
   Clinical Center of the National Institutes of Health.
NR 31
TC 1
Z9 2
U1 1
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0300-0664
EI 1365-2265
J9 CLIN ENDOCRINOL
JI Clin. Endocrinol.
PD DEC
PY 2015
VL 83
IS 6
BP 977
EP 984
DI 10.1111/cen.12676
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA DB1TX
UT WOS:000368293000032
PM 25411136
ER

PT J
AU Pathak, A
   Stewart, DR
   Faucz, FR
   Xekouki, P
   Bass, S
   Vogt, A
   Zhang, XJ
   Boland, J
   Yeager, M
   Loud, JT
   Nathanson, KL
   McGlynn, KA
   Stratakis, CA
   Greene, MH
   Mirabello, L
AF Pathak, Anand
   Stewart, Douglas R.
   Faucz, Fabio R.
   Xekouki, Paraskevi
   Bass, Sara
   Vogt, Aurelie
   Zhang, Xijun
   Boland, Joseph
   Yeager, Meredith
   Loud, Jennifer T.
   Nathanson, Katherine L.
   McGlynn, Katherine A.
   Stratakis, Constantine A.
   Greene, Mark H.
   Mirabello, Lisa
TI Rare inactivating PDE11A variants associated with testicular germ cell
   tumors
SO ENDOCRINE-RELATED CANCER
LA English
DT Article
DE testicular cancer; PDE11A; rare variants; risk; cAMP
ID GENOME-WIDE ASSOCIATION; PHOSPHODIESTERASE 11A; SUSCEPTIBILITY LOCI;
   CANCER; MUTATIONS; RISK; IDENTIFICATION; INDIVIDUALS; HYPERPLASIA;
   POPULATION
AB Germline inactivating mutations of isoform 4 of phosphodiesterase (PDE) 11A (coded by the PDE11A gene) have been associated with familial adrenocortical tumors and familial testicular cancer. Testicular tissue is unique in expressing all four isoforms of PDE11A. In a prior candidate gene study of 94 familial testicular germ cell tumor (TGCT) subjects, we identified a significant association between the presence of functionally abnormal variants in PDE11A and familial TGCT risk. To validate this novel observation, we sequenced the PDE11A coding region in 259 additional TGCT patients (both familial and sporadic) and 363 controls. We identified 55 PDE11A variants: 20 missense, four splice-site, two nonsense, seven synonymous, and 22 intronic. Ten missense variants were novel; nine occurred in transcript variant 4 and one in transcript variant 3. Five rare mutations (p.F258Y, p.G291R, p.V820M, p.R545X, and p. K568R) were present only in cases and were significantly more common in cases vs controls (P=0.0037). The latter two novel variants were functionally characterized and shown to be functionally inactivating, resulting in reduced PDE activity and increased cAMP levels. In further analysis of this cohort, we focused on white participants only to minimize confounding due to population stratification. This study builds upon our prior reports implicating PDE11A variants in familial TGCT, provides the first independent validation of those findings, extends that work to sporadic testicular cancer, demonstrates that these variants are uncommonly but reproducibly associated with TGCT, and refines our understanding regarding which specific inactivating PDE11A variants are most likely to be associated with TGCT risk.
C1 [Pathak, Anand; Stewart, Douglas R.; Loud, Jennifer T.; Greene, Mark H.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Faucz, Fabio R.; Xekouki, Paraskevi; Stratakis, Constantine A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Dev Endocrinol & Genet, Bethesda, MD USA.
   [Bass, Sara; Vogt, Aurelie; Zhang, Xijun; Boland, Joseph; Yeager, Meredith] NCI, Canc Genom Res Lab, Div Canc Epidemiol & Genet, NIH, Rockville, MD USA.
   [Nathanson, Katherine L.] Univ Penn, Perelman Sch Med, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
   [Mirabello, Lisa] NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20850 USA.
   [McGlynn, Katherine A.] NCI, Hormonal & Reprod Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20850 USA.
RP Mirabello, L (reprint author), NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, 9609 Med Ctr Dr,Room 6E422, Rockville, MD 20850 USA.
EM mirabellol@mail.nih.gov
FU National Cancer Institute, National Institutes of Health; Division of
   Cancer Epidemiology and Genetics of the Intramural Research Program of
   the National Cancer Institute
FX This project has been funded in part with funds from the National Cancer
   Institute, National Institutes of Health. This work was supported by the
   Division of Cancer Epidemiology and Genetics of the Intramural Research
   Program of the National Cancer Institute (A Pathak, D R Stewart, S Bass,
   AVogt, MYeager, J T Loud, K A McGlynn, MH Greene, and LMirabello) and
   the Intramural Research Program of the Eunice Kennedy Shriver National
   Institute of Child Health and Human Development of the National
   Institute of Health (F R Faucz, P Xekouki, C A Stratakis).
NR 34
TC 1
Z9 1
U1 1
U2 4
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT,
   ENGLAND
SN 1351-0088
EI 1479-6821
J9 ENDOCR-RELAT CANCER
JI Endocr.-Relat. Cancer
PD DEC
PY 2015
VL 22
IS 6
BP 909
EP 917
DI 10.1530/ERC-15-0034
PG 9
WC Oncology; Endocrinology & Metabolism
SC Oncology; Endocrinology & Metabolism
GA DB0XB
UT WOS:000368230300016
PM 26459559
ER

PT J
AU Gharwan, H
   Bunch, KP
   Annunziata, CM
AF Gharwan, Helen
   Bunch, Kristen P.
   Annunziata, Christina M.
TI The role of reproductive hormones in epithelial ovarian carcinogenesis
SO ENDOCRINE-RELATED CANCER
LA English
DT Review
DE ovarian cancer; hormone action; reproductive; immune; endocrine
ID FOLLICLE-STIMULATING-HORMONE; NF-KAPPA-B; PROGESTERONE-RECEPTOR GENE;
   MESSENGER-RIBONUCLEIC-ACID; GYNECOLOGIC-ONCOLOGY-GROUP;
   EPIDERMAL-GROWTH-FACTOR; MULLERIAN-INHIBITING SUBSTANCE; BREAST-CANCER
   CELLS; PHASE-II TRIAL; FRAGMENT-LENGTH-POLYMORPHISM
AB Epithelial ovarian cancer comprises similar to 85% of all ovarian cancer cases. Despite acceptance regarding the influence of reproductive hormones on ovarian cancer risk and considerable advances in the understanding of epithelial ovarian carcinogenesis on a molecular level, complete understanding of the biologic processes underlying malignant transformation of ovarian surface epithelium is lacking. Various hypotheses have been proposed over the past several decades to explain the etiology of the disease. The role of reproductive hormones in epithelial ovarian carcinogenesis remains a key topic of research. Primary questions in the field of ovarian cancer biology center on its developmental cell of origin, the positive and negative effects of each class of hormones on ovarian cancer initiation and progression, and the role of the immune system in the ovarian cancer microenvironment. The development of the female reproductive tract is dictated by the hormonal milieu during embryogenesis. Intensive research efforts have revealed that ovarian cancer is a heterogenous disease that may develop from multiple extra-ovarian tissues, including both Mullerian (fallopian tubes, endometrium) and non-Mullerian structures (gastrointestinal tissue), contributing to its heterogeneity and distinct histologic subtypes. The mechanism underlying ovarian localization, however, remains unclear. Here, we discuss the role of reproductive hormones in influencing the immune system and tipping the balance against or in favor of developing ovarian cancer. We comment on animal models that are critical for experimentally validating existing hypotheses in key areas of endocrine research and useful for preclinical drug development. Finally, we address emerging therapeutic trends directed against ovarian cancer.
C1 [Gharwan, Helen] NCI, NIH, Bethesda, MD 20892 USA.
   [Bunch, Kristen P.; Annunziata, Christina M.] NCI, Womens Malignancies Branch, NIH, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Bunch, Kristen P.] Walter Reed Natl Mil Med Ctr, Dept Gynecol Oncol, Bethesda, MD USA.
RP Gharwan, H (reprint author), NCI, NIH, 10 Ctr Dr,Bldg 10, Bethesda, MD 20892 USA.
EM hgh7@hotmail.com
RI Annunziata, Christina/L-3219-2016
OI Annunziata, Christina/0000-0003-2033-6532
NR 305
TC 5
Z9 5
U1 3
U2 13
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT,
   ENGLAND
SN 1351-0088
EI 1479-6821
J9 ENDOCR-RELAT CANCER
JI Endocr.-Relat. Cancer
PD DEC
PY 2015
VL 22
IS 6
BP R339
EP R363
DI 10.1530/ERC-14-0550
PG 25
WC Oncology; Endocrinology & Metabolism
SC Oncology; Endocrinology & Metabolism
GA DB0XB
UT WOS:000368230300006
PM 26373571
ER

PT J
AU Gore, AC
   Chappell, VA
   Fenton, SE
   Flaws, JA
   Nadal, A
   Prins, GS
   Toppari, J
   Zoeller, RT
AF Gore, A. C.
   Chappell, V. A.
   Fenton, S. E.
   Flaws, J. A.
   Nadal, A.
   Prins, G. S.
   Toppari, J.
   Zoeller, R. T.
TI Executive Summary to EDC-2: The Endocrine Society's Second Scientific
   Statement on Endocrine-Disrupting Chemicals
SO ENDOCRINE REVIEWS
LA English
DT Review
ID XENOESTROGENS
AB This Executive Summary to the Endocrine Society's second Scientific Statement on environmental endocrine-disrupting chemicals (EDCs) provides a synthesis of the key points of the complete statement. The full Scientific Statement represents a comprehensive review of the literature on seven topics for which there is strong mechanistic, experimental, animal, and epidemiological evidence for endocrine disruption, namely: obesity and diabetes, female reproduction, male reproduction, hormone-sensitive cancers in females, prostate cancer, thyroid, and neurodevelopment and neuroendocrine systems. EDCs such as bisphenol A, phthalates, pesticides, persistent organic pollutants such as polychlorinated biphenyls, polybrominated diethyl ethers, and dioxins were emphasized because these chemicals had the greatest depth and breadth of available information. The Statement also included thorough coverage of studies of developmental exposures to EDCs, especially in the fetus and infant, because these are critical life stages during which perturbations of hormones can increase the probability of a disease or dysfunction later in life. A conclusion of the Statement is that publications over the past 5 years have led to a much fuller understanding of the endocrine principles by which EDCs act, including nonmonotonic dose-responses, low-dose effects, and developmental vulnerability. These findings will prove useful to researchers, physicians, and other healthcare providers in translating the science of endocrine disruption to improved public health. (Endocrine Reviews 36: 593-602, 2015)
C1 [Gore, A. C.] Univ Texas Austin, Coll Pharm, Pharmacol & Toxicol, Austin, TX 78734 USA.
   [Chappell, V. A.; Fenton, S. E.] NIEHS, Div Natl Toxicol Program, NIH, Res Triangle Pk, NC 27709 USA.
   [Flaws, J. A.] Univ Illinois, Dept Comparat Biosci, Urbana, IL 61802 USA.
   [Nadal, A.] Miguel Hernandez Univ Elche, Inst Bioengn, Alicante 03202, Spain.
   [Nadal, A.] Miguel Hernandez Univ Elche, CIBERDEM, Alicante 03202, Spain.
   [Prins, G. S.] Univ Illinois, Coll Med, Dept Urol, Chicago, IL 60612 USA.
   [Prins, G. S.] Univ Illinois, Coll Med, Dept Pathol, Chicago, IL 60612 USA.
   [Prins, G. S.] Univ Illinois, Coll Med, Dept Physiol & Biophys, Chicago, IL 60612 USA.
   [Toppari, J.] Univ Turku, Dept Physiol, FIN-20520 Turku, Finland.
   [Toppari, J.] Univ Turku, Dept Pediat, FIN-20520 Turku, Finland.
   Turku Univ Hosp, FIN-20520 Turku, Finland.
   [Zoeller, R. T.] Univ Massachusetts, Dept Biol, Amherst, MA 01003 USA.
RP Gore, AC (reprint author), Univ Texas Austin, 107 W Dean Keeton,C0875, Austin, TX 78712 USA.
EM andrea.gore@austin.utexas.edu
RI Nadal, Angel/G-6721-2014
OI Nadal, Angel/0000-0003-4178-2152
FU National Institutes of Health (NIH) [ES023254, ES020662]; NIH [ES019178,
   ES02207, ES020886, CA172220, ES010026, ES020908]; Ministerio de Economia
   y Competitividad [BFU2011-28358, SAF2014-58335-P]; Generalitat
   Valenciana [PROMETEO/2011/080, PROMETEO/2015/016]; Academy of Finland;
   EU FP7 Environment and Quality of Life; Sigrid Juselius Foundation;
   Turku University Hospital Special Research Fund
FX Grant support to authors included: National Institutes of Health (NIH)
   ES023254 and ES020662 (to A.C.G.); NIH ES019178 (to J.A.F.); Ministerio
   de Economia y Competitividad BFU2011-28358 and SAF2014-58335-P,
   Generalitat Valenciana PROMETEO/2011/080, and PROMETEO/2015/016 (to
   A.N.); NIH ES02207, ES020886, and CA172220 (to G.S.P.); Academy of
   Finland, EU FP7 Environment and Quality of Life, Sigrid Juselius
   Foundation, and Turku University Hospital Special Research Fund (to
   J.T.); and NIH ES010026, ES020908 (to R.T.Z.).
NR 7
TC 27
Z9 27
U1 2
U2 26
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0163-769X
EI 1945-7189
J9 ENDOCR REV
JI Endocr. Rev.
PD DEC
PY 2015
VL 36
IS 6
BP 593
EP 602
DI 10.1210/er.2015-1093
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA DB1OL
UT WOS:000368277700002
PM 26414233
ER

PT J
AU Gore, AC
   Chappell, VA
   Fenton, SE
   Flaws, JA
   Nadal, A
   Prins, GS
   Toppari, J
   Zoeller, RT
AF Gore, A. C.
   Chappell, V. A.
   Fenton, S. E.
   Flaws, J. A.
   Nadal, A.
   Prins, G. S.
   Toppari, J.
   Zoeller, R. T.
TI EDC-2: The Endocrine Society's Second Scientific Statement on
   Endocrine-Disrupting Chemicals
SO ENDOCRINE REVIEWS
LA English
DT Review
ID BISPHENOL-A EXPOSURE; IN-UTERO EXPOSURE; POLYBROMINATED DIPHENYL ETHERS;
   ESTROGEN-RECEPTOR-ALPHA; ARYL-HYDROCARBON RECEPTOR; SPRAGUE-DAWLEY RATS;
   PERSISTENT ORGANIC POLLUTANTS; MAMMARY-GLAND DEVELOPMENT; OVARIAN ANTRAL
   FOLLICLES; EPIGENETIC TRANSGENERATIONAL INHERITANCE
AB The Endocrine Society's first Scientific Statement in 2009 provided a wake-up call to the scientific community about how environmental endocrine-disrupting chemicals (EDCs) affect health and disease. Five years later, a substantially larger body of literature has solidified our understanding of plausible mechanisms underlying EDC actions and how exposures in animals and humans-especially during development-may lay the foundations for disease later in life. At this point in history, we have much stronger knowledge about how EDCs alter gene-environment interactions via physiological, cellular, molecular, andepigenetic changes, thereby producing effects in exposed individuals as well as their descendants. Causal links between exposure and manifestation of disease are substantiated by experimental animal models and are consistent with correlative epidemiological data in humans. There are several caveats because differences in how experimental animal work is conducted can lead to difficulties in drawing broad conclusions, and we must continue to be cautious about inferring causality in humans. In this second Scientific Statement, we reviewed the literature on a subset of topics for which the translational evidence is strongest: 1) obesity and diabetes; 2) female reproduction; 3) male reproduction; 4) hormone-sensitive cancers in females; 5) prostate; 6) thyroid; and 7) neurodevelopment and neuroendocrine systems. Our inclusion criteria for studies were those conducted predominantly in the past 5 years deemed to be of high quality based on appropriate negative and positive control groups or populations, adequate sample size and experimental design, and mammalian animal studies with exposure levels in arange that was relevant to humans. We also focused on studies using the developmental origins of health and disease model. No report was excluded based on a positive or negative effect of the EDC exposure. The bulk of the results across the board strengthen the evidence for endocrine health-related actions of EDCs. Based on this much more complete understanding of the endocrine principles by which EDCs act, including nonmonotonic dose-responses, low-dose effects, and developmental vulnerability, these findings can be much better translated to human health. Armed with this information, researchers, physicians, and other healthcare providers can guide regulators and policymakers as they make responsible decisions. (Endocrine Reviews 36: E1-E150, 2015)
C1 [Gore, A. C.] Univ Texas Austin, Coll Pharm, Pharmacol & Toxicol, Austin, TX 78734 USA.
   [Chappell, V. A.; Fenton, S. E.] NIEHS, Div Natl Toxicol Program, NIH, Res Triangle Pk, NC 27709 USA.
   [Flaws, J. A.] Univ Illinois, Dept Comparat Biosci, Urbana, IL 61802 USA.
   [Nadal, A.] Miguel Hernandez Univ Elche, Inst Bioengn, Alicante 03202, Spain.
   [Nadal, A.] Miguel Hernandez Univ Elche, CIBERDEM, Alicante 03202, Spain.
   [Prins, G. S.] Univ Illinois, Coll Med, Dept Urol, Chicago, IL 60612 USA.
   [Prins, G. S.] Univ Illinois, Coll Med, Dept Pathol, Chicago, IL 60612 USA.
   [Prins, G. S.] Univ Illinois, Coll Med, Dept Physiol & Biophys, Chicago, IL 60612 USA.
   [Toppari, J.] Univ Turku, Dept Physiol, FIN-20520 Turku, Finland.
   [Toppari, J.] Univ Turku, Dept Pediat, FIN-20520 Turku, Finland.
   Turku Univ Hosp, FIN-20520 Turku, Finland.
   [Zoeller, R. T.] Univ Massachusetts, Dept Biol, Amherst, MA 01003 USA.
RP Gore, AC (reprint author), Univ Texas Austin, 107 West Dean Keeton St,C0875, Austin, TX 78712 USA.
EM andrea.gore@austin.utexas.edu
RI Nadal, Angel/G-6721-2014
OI Nadal, Angel/0000-0003-4178-2152
FU National Institutes of Health (NIH) [ES023254, ES020662, ES019178];
   Ministerio de Economia y Competitividad [BFU2011-28358,
   SAF2014-58335-P]; Generalitat Valenciana [PROMETEO/2011/080,
   PROMETEO/2015/016]; NIH [ES02207, ES020886, CA172220, ES010026,
   ES020908]; Academy of Finland; EU FP7 Environment and Quality of Life;
   Sigrid Juselius Foundation; Turku University Hospital Special Research
   Fund
FX This work was supported by National Institutes of Health (NIH) Grants
   ES023254 and ES020662 (to A.C.G.) and ES019178 (to J.A.F.); Ministerio
   de Economia y Competitividad Grants BFU2011-28358 and SAF2014-58335-P
   (to A.N.); Generalitat Valenciana Grants PROMETEO/2011/080 and
   PROMETEO/2015/016 (to A.N.); NIH Grants ES02207, ES020886, and CA172220
   (to G.S.P.); the Academy of Finland, EU FP7 Environment and Quality of
   Life, the Sigrid Juselius Foundation, and Turku University Hospital
   Special Research Fund (to J.T.); and NIH Grants ES010026 and ES020908
   (to R.T.Z.).
NR 1290
TC 68
Z9 68
U1 31
U2 74
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0163-769X
EI 1945-7189
J9 ENDOCR REV
JI Endocr. Rev.
PD DEC
PY 2015
VL 36
IS 6
BP E1
EP E150
DI 10.1210/er.2015-1010
PG 150
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA DB1OL
UT WOS:000368277700001
PM 26544531
ER

PT J
AU Nicolaides, NC
   Lamprokostopoulou, A
   Polyzos, A
   Kino, T
   Katsantoni, E
   Triantafyllou, P
   Christophoridis, A
   Katzos, G
   Dracopoulou, M
   Sertedaki, A
   Chrousos, GP
   Charmandari, E
AF Nicolaides, Nicolas C.
   Lamprokostopoulou, Agaristi
   Polyzos, Alexandros
   Kino, Tomoshige
   Katsantoni, Eleni
   Triantafyllou, Panagiota
   Christophoridis, Athanasios
   Katzos, George
   Dracopoulou, Maria
   Sertedaki, Amalia
   Chrousos, George P.
   Charmandari, Evangelia
TI Transient generalized glucocorticoid hypersensitivity
SO EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
DE Glucocorticoid hypersensitivity; glucocorticoid receptor; glucocorticoid
   signalling; glucocorticoids; transcriptomics
ID CORTISOL HYPERREACTIVE SYNDROME; GENE-EXPRESSION; RECEPTOR GENE;
   RNA-SEQ; RESISTANCE; TRANSCRIPTS; DISORDERS; PATIENT; SYSTEMS
AB Background Transient generalized glucocorticoid hypersensitivity is a rare disorder characterized by increased tissue sensitivity to glucocorticoids and compensatory hypo-activation of the hypothalamic-pituitary-adrenal axis. The condition itself and the underlying molecular mechanisms have not been elucidated.
   Objective To present the clinical manifestations, endocrinologic evaluation and transcriptomic profile in a patient with transient generalized glucocorticoid hypersensitivity.
   Design and Results A 9-year-old girl presented with an 8-month history of clinical manifestations suggestive of Cushing syndrome. Endocrinologic evaluation revealed undetectable 08: 00 h ACTH (<1 pg/mL) and cortisol (0.025 mu g/dL) concentrations, which remained decreased throughout the 24-h period and did not respond to stimulation with ovine CRH. The disease gradually resolved spontaneously over the ensuing 3 months. Sequencing of the human glucocorticoid receptor gene revealed no mutations or polymorphisms. Western blot analysis in peripheral blood mononuclear cells revealed equal protein expression of hGR alpha of the patient in the disease and postresolution phases compared with a control subject. Transcriptomic analysis in peripheral blood mononuclear cells in the disease and postresolution phases identified 903 differentially expressed genes. Of these, 106 genes were up-regulated and 797 were down-regulated in the disease compared with the resolution phase. Bioinformatics analysis on the differentially expressed gene networks revealed Nuclear Factor-kappa B as the predominant transcription factor influencing the expression of the majority of differentially expressed genes.
   Conclusions Our findings indicate that a transient postreceptor defect, or a virus-or bacterium-encoded molecule, may have enhanced glucocorticoid signal transduction, leading to transient generalized glucocorticoid hypersensitivity and hypo-activation of the HPA axis.
C1 [Nicolaides, Nicolas C.; Dracopoulou, Maria; Sertedaki, Amalia; Chrousos, George P.; Charmandari, Evangelia] Acad Athens, Aghia Sophia Childrens Hosp, Sch Med, Dept Pediat 1,Div Endocrinol Metab & Diabet, Athens 11527, Greece.
   [Nicolaides, Nicolas C.; Lamprokostopoulou, Agaristi; Chrousos, George P.; Charmandari, Evangelia] Acad Athens, Biomed Res Fdn, Clin Res Ctr, Div Endocrinol & Metab, Athens 11527, Greece.
   [Polyzos, Alexandros] Acad Athens, Biomed Res Fdn, Inst Mol Biol Genet & Biotechnol, Athens 11527, Greece.
   [Kino, Tomoshige] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Unit Mol Hormone Act, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
   [Katsantoni, Eleni] Acad Athens, Biomed Res Fdn, Clin Res Ctr, Div Hematol, Athens 11527, Greece.
   [Triantafyllou, Panagiota; Christophoridis, Athanasios; Katzos, George] Aristotle Univ Thessaloniki, Sch Med, Dept Pediat 1, Thessaloniki, Greece.
   [Chrousos, George P.] King Abdulaziz Univ, King Fahd Med Res Ctr, Saudi Diabet Study Res Grp, Jeddah 21413, Saudi Arabia.
RP Nicolaides, NC (reprint author), Acad Athens, Biomed Res Fdn, Clin Res Ctr, Div Endocrinol & Metab, 4 Soranou Efessiou St, Athens 11527, Greece.
EM nnicolaides@bioacademy.gr
RI Charmandari, Evangelia/B-6701-2011
FU European Union (European Social Fund - ESF); Greek national funds
   through the Operational Program "Education and Lifelong Learning" of the
   National Strategic Reference Framework (NSRF) - Research Funding
   Program: THALIS -University of Athens (UOA), Athens, Greece
FX This work was supported by the European Union (European Social Fund -
   ESF) and Greek national funds through the Operational Program "Education
   and Lifelong Learning" of the National Strategic Reference Framework
   (NSRF) - Research Funding Program: THALIS -University of Athens (UOA),
   Athens, Greece.
NR 24
TC 0
Z9 0
U1 2
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2972
EI 1365-2362
J9 EUR J CLIN INVEST
JI Eur. J. Clin. Invest.
PD DEC
PY 2015
VL 45
IS 12
BP 1306
EP 1315
DI 10.1111/eci.12554
PG 10
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA DA6QH
UT WOS:000367929600010
PM 26479047
ER

PT J
AU Hoa, NN
   Akagawa, R
   Yamasaki, T
   Hirota, K
   Sasa, K
   Natsume, T
   Kobayashi, J
   Sakuma, T
   Yamamoto, T
   Komatsu, K
   Kanemaki, MT
   Pommier, Y
   Takeda, S
   Sasanuma, H
AF Nguyen Ngoc Hoa
   Akagawa, Remi
   Yamasaki, Tomomi
   Hirota, Kouji
   Sasa, Kentaro
   Natsume, Toyoaki
   Kobayashi, Junya
   Sakuma, Tetsushi
   Yamamoto, Takashi
   Komatsu, Kenshi
   Kanemaki, Masato T.
   Pommier, Yves
   Takeda, Shunichi
   Sasanuma, Hiroyuki
TI Relative contribution of four nucleases, CtIP, Dna2, Exo1 and Mre11, to
   the initial step of DNA double-strand break repair by homologous
   recombination in both the chicken DT40 and human TK6 cell lines
SO GENES TO CELLS
LA English
DT Article
ID RECQ FAMILY HELICASES; END-RESECTION; SACCHAROMYCES-CEREVISIAE;
   VERTEBRATE CELLS; ATM ACTIVATION; ENDONUCLEASE ACTIVITY; REPLICATION
   STRESS; DAMAGE RESPONSE; PATHWAY CHOICE; MRX COMPLEX
AB Homologous recombination (HR) is initiated by double-strand break (DSB) resection, during which DSBs are processed by nucleases to generate 30 single-strand DNA. DSB resection is initiated by CtIP and Mre11 followed by long-range resection by Dna2 and Exo1 in Saccharomyces cerevisiae. To analyze the relative contribution of four nucleases, CtIP, Mre11, Dna2 and Exo1, to DSB resection, we disrupted genes encoding these nucleases in chicken DT40 cells. CtIP and Dna2 are required for DSB resection, whereas Exo1 is dispensable even in the absence of Dna2, which observation agrees with no developmental defect in Exo1-deficient mice. Despite the critical role of Mre11 in DSB resection in S. cerevisiae, loss of Mre11 only modestly impairs DSB resection in DT40 cells. To further test the role of CtIP and Mre11 in other species, we conditionally disrupted CtIP and MRE11 genes in the human TK6 B cell line. As with DT40 cells, CtIP contributes to DSB resection considerably more significantly than Mre11 in TK6 cells. Considering the critical role of Mre11 in HR, this study suggests that Mre11 is involved in a mechanism other than DSB resection. In summary, CtIP and Dna2 are sufficient for DSB resection to ensure efficient DSB repair by HR.
C1 [Nguyen Ngoc Hoa; Akagawa, Remi; Yamasaki, Tomomi; Hirota, Kouji; Sasa, Kentaro; Takeda, Shunichi; Sasanuma, Hiroyuki] Kyoto Univ, Grad Sch Med, Dept Radiat Genet, Sakyo Ku, Kyoto 6068501, Japan.
   [Natsume, Toyoaki; Kanemaki, Masato T.] ROIS, Natl Inst Genet, Frontier Res Ctr, Mishima, Shizuoka 4118540, Japan.
   [Kobayashi, Junya; Komatsu, Kenshi] Kyoto Univ, Ctr Radiat Biol, Dept Genome Repair Dynam, Sakyo Ku, Kyoto 6068501, Japan.
   [Sakuma, Tetsushi; Yamamoto, Takashi] Hiroshima Univ, Grad Sch Sci, Dept Math & Life Sci, Higashihiroshima 7398526, Japan.
   [Kanemaki, Masato T.] SOKENDAI, Dept Genet, Mishima, Shizuoka 4118540, Japan.
   [Kanemaki, Masato T.] PREST, JST, Kawaguchi, Saitama 3320012, Japan.
   [Pommier, Yves] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Sasanuma, H (reprint author), Kyoto Univ, Grad Sch Med, Dept Radiat Genet, Sakyo Ku, Kyoto 6068501, Japan.
EM hiroysasa@rg.med.kyoto-u.ac.jp
RI Sakuma, Tetsushi/A-7615-2013
FU Ministry of Education, Science, Sport and Culture
FX We are grateful to P. Jeggo, J. Tainer, T. Paull and S. Gasser for his
   constructive comments on the manuscript. We also thank A. Noguchi and A.
   Kobayashi for their technical assistance and the laboratory members for
   their stimulating discussion. FACS analysis and DNA sequencing were
   carried out at the Medical Research Support Center, Graduate School of
   Medicine, Kyoto University. This work was supported by a Grant-in-Aid
   from the Ministry of Education, Science, Sport and Culture to J. K., K.
   K., T. N., M. K., S. T. and H. S.
NR 67
TC 4
Z9 4
U1 2
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1356-9597
EI 1365-2443
J9 GENES CELLS
JI Genes Cells
PD DEC
PY 2015
VL 20
IS 12
BP 1059
EP 1076
DI 10.1111/gtc.12310
PG 18
WC Cell Biology; Genetics & Heredity
SC Cell Biology; Genetics & Heredity
GA DB1HH
UT WOS:000368258600009
PM 26525166
ER

PT J
AU Berl, MM
   Walker, L
   Modi, P
   Irfanoglu, MO
   Sarlls, JE
   Nayak, A
   Pierpaoli, C
AF Berl, Madison M.
   Walker, Lindsay
   Modi, Pooja
   Irfanoglu, M. Okan
   Sarlls, Joelle E.
   Nayak, Amritha
   Pierpaoli, Carlo
TI Investigation of Vibration-Induced Artifact in Clinical
   Diffusion-Weighted Imaging of Pediatric Subjects
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE diffusion tensor imaging; weight; position; quality; regrowth
ID MINIMALLY CONSCIOUS STATE; TRAUMATIC BRAIN-INJURY; ROBUST ESTIMATION;
   QUALITY-CONTROL; LATE RECOVERY; TENSOR; MRI; RESTORE; TISSUES; IMPACT
AB It has been reported that mechanical vibrations of the magnetic resonance imaging scanner could produce spurious signal dropouts in diffusion-weighted images resulting in artifactual anisotropy in certain regions of the brain with red appearance in the Directionally Encoded Color maps. We performed a review of the frequency of this artifact across pediatric studies, noting differences by scanner manufacturer, acquisition protocol, as well as weight and position of the subject. We also evaluated the ability of automated and quantitative methods to detect this artifact. We found that the artifact may be present in over 50% of data in certain protocols and is not limited to one scanner manufacturer. While a specific scanner had the highest incidence, low body weight and positioning were also associated with appearance of the artifact for both scanner types evaluated, making children potentially more susceptible than adults. Visual inspection remains the best method for artifact identification. Software for automated detection showed very low sensitivity (10%). The artifact may present inconsistently in longitudinal studies. We discuss a published case report that has been widely cited and used as evidence to set policy about diagnostic criteria for determining vegetative state. That report attributed longitudinal changes in anisotropy to white matter plasticity without considering the possibility that the changes were caused by this artifact. Our study underscores the need to check for the presence of this artifact in clinical studies, analyzes circumstances for when it may be more likely to occur, and suggests simple strategies to identify and potentially avoid its effects. (C) 2015 Wiley Periodicals, Inc.
C1 [Berl, Madison M.] Div Pediat Neuropsychol, Washington, DC USA.
   [Berl, Madison M.] Childrens Natl Hlth Syst, Childrens Res Inst, Washington, DC USA.
   [Walker, Lindsay; Modi, Pooja; Irfanoglu, M. Okan; Nayak, Amritha; Pierpaoli, Carlo] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Pediat Imaging & Tissue Sci, Bethesda, MD USA.
   [Irfanoglu, M. Okan; Nayak, Amritha] Henry Jackson Fdn, Bethesda, MD USA.
   [Sarlls, Joelle E.] NINDS, NMRF, NIH, Bethesda, MD 20892 USA.
   [Pierpaoli, Carlo] Uniformed Serv Univ Hlth Sci, Ctr Neurosci & Regenerat Med, Bethesda, MD 20814 USA.
RP Berl, MM (reprint author), Childrens Natl Hlth Syst, Div Neuropsychol, 111 Michigan Ave NW, Washington, DC 20010 USA.
EM mberl@childrensnational.org
FU National Institutes of Health; Neurological Disorders and Stroke
   [K23NS065121- 01A2]; NICHD Intellectual and Developmental Disabilities
   Research Center; Children's National Medical Center [P30HD040677];
   Department of the Army [W81XWH-13-2-0019]
FX Contract grant sponsor: National Institutes of Health; Contract grant
   sponsor: Neurological Disorders and Stroke; Contract grant number:
   K23NS065121- 01A2 (to M.B.); Contract grant sponsor: NICHD Intellectual
   and Developmental Disabilities Research Center and Children's National
   Medical Center; Contract grant number: P30HD040677 (to M.B.); Contract
   grant sponsor: Department of the Army; Contract grant number:
   W81XWH-13-2-0019 (to A.N. and O.M.I.)
NR 41
TC 0
Z9 0
U1 2
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1065-9471
EI 1097-0193
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD DEC
PY 2015
VL 36
IS 12
BP 4745
EP 4757
DI 10.1002/hbm.22846
PG 13
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
   Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA DB1QF
UT WOS:000368283100001
PM 26350492
ER

PT J
AU Zhu, X
   Dutta, N
   Helton, SG
   Schwandt, M
   Yan, J
   Hodgkinson, CA
   Cortes, CR
   Kerich, M
   Hall, S
   Sun, H
   Phillips, M
   Momenan, R
   Lohoff, FW
AF Zhu, Xi
   Dutta, Nisha
   Helton, Sarah G.
   Schwandt, Melanie
   Yan, Jia
   Hodgkinson, Colin A.
   Cortes, Carlos R.
   Kerich, Mike
   Hall, Samuel
   Sun, Hui
   Phillips, Monte
   Momenan, Reza
   Lohoff, Falk W.
TI Resting-State Functional Connectivity and Presynaptic Monoamine
   Signaling in Alcohol Dependence
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE genetics; monoamine transporter; presynaptic; resting-state; mPFC;
   SLC18A1
ID INDEPENDENT COMPONENT ANALYSIS; EXECUTIVE CONTROL NETWORK;
   CENTRAL-NERVOUS-SYSTEM; 1 GENE VMAT1/SLC18A1; HUMAN BRAIN; SUBSEQUENT
   RELAPSE; CHROMOSOME 8P; ASSOCIATION; ROBUST; POLYMORPHISMS
AB Alcohol Dependence (AD) is a chronic relapsing disorder with high degrees of morbidity and mortality. While multiple neurotransmitter systems are involved in the complex symptomatology of AD, monoamine dysregulation and subsequent neuroadaptations have been long postulated to play an important role. Presynaptic monoamine transporters, such as the vesicular monoamine transporter 1 (VMAT1), are likely critical as they represent a key common entry point for monoamine regulation and may represent a shared pathway for susceptibility to AD. Excessive monoaminergic signaling as mediated by genetic variation in VMAT1 might affect functional brain connectivity in particular in alcoholics compared to controls. We conducted resting-state fMRI functional connectivity (FC) analysis using the independent component analysis (ICA) approach in 68 AD subjects and 72 controls. All subjects were genotyped for the Thr136Ile (rs1390938) variant in VMAT1. Functional connectivity analyses showed a significant increase of resting-state FC in 4 networks in alcoholics compared to controls (P<0.05, corrected). The FC was significantly positively correlated with Alcohol Dependence Scale (ADS). The hyperfunction allele 136Ile was associated with a significantly decreased FC in the Default Mode Network, Prefrontal Cortex Network, and Executive Control Network in alcohol dependent participants (P<0.05, corrected), but not in controls. Our data suggest that increased FC might represent a neuroadaptive mechanism relevant to AD that is furthermore mediated by genetic variation in VMAT1. The hyperfunction allele Thr136Ile might have a protective effect that is, in particular, relevant in AD by mechanism of increased monoamine transport into presynaptic storage vesicles. Published 2015.
C1 [Zhu, Xi; Cortes, Carlos R.; Kerich, Mike; Momenan, Reza] NIAAA, Sect Brain & Electrophysiol & Imaging, NIH, Bethesda, MD USA.
   [Dutta, Nisha; Helton, Sarah G.; Schwandt, Melanie; Hall, Samuel; Sun, Hui; Phillips, Monte; Lohoff, Falk W.] NIAAA, Sect Clin Genom & Expt Therapeut, NIH, Bethesda, MD USA.
   [Yan, Jia] NIAAA, Sect Human Psychopharmacol, NIH, Bethesda, MD USA.
   [Hodgkinson, Colin A.] NIAAA, Neurogenet Lab, NIH, Bethesda, MD USA.
RP Lohoff, FW (reprint author), NIAAA, Sect Clin Genom & Expt Therapeut CGET, Lasker Clin Res Scholar, LCTS,NIH, 10 Ctr Dr,10CRC-22352, Bethesda, MD 20892 USA.
EM falk.lohoff@nih.gov
RI Schwandt, Melanie/L-9866-2016; Lohoff, Falk/M-7951-2016
FU National Institute on Alcohol Abuse and Alcoholism
FX Contract grant sponsor: National Institute on Alcohol Abuse and
   Alcoholism.
NR 53
TC 5
Z9 5
U1 4
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1065-9471
EI 1097-0193
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD DEC
PY 2015
VL 36
IS 12
BP 4808
EP 4818
DI 10.1002/hbm.22951
PG 11
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
   Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA DB1QF
UT WOS:000368283100005
PM 26368063
ER

PT J
AU Ding, XY
   Yang, YH
   Stein, EA
   Ross, TJ
AF Ding, Xiaoyu
   Yang, Yihong
   Stein, Elliot A.
   Ross, Thomas J.
TI Multivariate Classification of Smokers and Nonsmokers Using SVM-RFE on
   Structural MRI Images
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE smoking addiction; structural MRI; voxel-based morphometry; support
   vector machine; recursive feature elimination; multivariate
   classification
ID SUPPORT VECTOR MACHINES; VOXEL-BASED MORPHOMETRY; STATE FUNCTIONAL
   CONNECTIVITY; GRAY-MATTER VOLUMES; SMOKING-CESSATION;
   SCHIZOPHRENIA-PATIENTS; ANATOMICAL NETWORKS; CIGARETTE-SMOKING; HEALTHY
   CONTROLS; BRAIN
AB Voxel-based morphometry (VBM) studies have revealed gray matter alterations in smokers, but this type of analysis has poor predictive value for individual cases, which limits its applicability in clinical diagnoses and treatment. A predictive model would essentially embody a complex biomarker that could be used to evaluate treatment efficacy. In this study, we applied VBM along with a multivariate classification method consisting of a support vector machine with recursive feature elimination to discriminate smokers from nonsmokers using their structural MRI data. Mean gray matter volumes in 1,024 cerebral cortical regions of interest created using a subparcellated version of the Automated Anatomical Labeling template were calculated from 60 smokers and 60 nonsmokers, and served as input features to the classification procedure. The classifier achieved the highest accuracy of 69.6% when taking the 139 highest ranked features via 10-fold cross-validation. Critically, these features were later validated on an independent testing set that consisted of 28 smokers and 28 nonsmokers, yielding a 64.04% accuracy level (binomial P = 0.01). Following classification, exploratory post hoc regression analyses were performed, which revealed that gray matter volumes in the putamen, hippocampus, prefrontal cortex, cingulate cortex, caudate, thalamus, pre-/post-central gyrus, precuneus, and the parahippocampal gyrus, were inversely related to smoking behavioral characteristics. These results not only indicate that smoking related gray matter alterations can provide predictive power for group membership, but also suggest that machine learning techniques can reveal underlying smoking-related neurobiology.
C1 [Ding, Xiaoyu; Yang, Yihong; Stein, Elliot A.; Ross, Thomas J.] NIDA, Neuroimaging Res Branch, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Ross, TJ (reprint author), NIDA, Neuroimaging Res Branch, Intramural Res Program, NIH, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM tross@mail.nih.gov
FU Intramural Research Program of the National Institute on Drug Abuse and
   FDA [NDA13001-001-00000]
FX Contract grant sponsor: Intramural Research Program of the National
   Institute on Drug Abuse and FDA (to E.A.S.); Contract grant number:
   NDA13001-001-00000.
NR 61
TC 2
Z9 2
U1 3
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1065-9471
EI 1097-0193
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD DEC
PY 2015
VL 36
IS 12
BP 4869
EP 4879
DI 10.1002/hbm.22956
PG 11
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
   Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA DB1QF
UT WOS:000368283100010
PM 26497657
ER

PT J
AU Kooragayala, K
   Gotoh, N
   Cogliati, T
   Nellissery, J
   Kaden, TR
   French, S
   Balaban, R
   Li, W
   Covian, R
   Swaroop, A
AF Kooragayala, Keshav
   Gotoh, Norimoto
   Cogliati, Tiziana
   Nellissery, Jacob
   Kaden, Talia R.
   French, Stephanie
   Balaban, Robert
   Li, Wei
   Covian, Raul
   Swaroop, Anand
TI Quantification of Oxygen Consumption in Retina Ex Vivo Demonstrates
   Limited Reserve Capacity of Photoreceptor Mitochondria
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
DE oxidative stress; neurodegeneration; photoreceptor homeostasis; retinal
   disease; mitochondrial function
ID OXIDATIVE STRESS; MOUSE MODELS; CELL-DEATH; DEGENERATION; ROD;
   PHOSPHORYLATION; DYSFUNCTION; OUTER; NRL; NEURODEGENERATION
AB PURPOSE. Cell death in neurodegeneration occurs at the convergence of diverse metabolic pathways. In the retina, a common underlying mechanism involves mitochondrial dysfunction since photoreceptor homeostasis and survival are highly susceptible to altered aerobic energy metabolism. We sought to develop an assay to directly measure oxygen consumption in intact retina with the goal of identifying alterations in respiration during photoreceptor dysfunction and degeneration.
   METHODS. Circular punches of freshly isolated mouse retina, adjacent to the optic nerve head, were used in the microplate-based Seahorse Extracellular Flux Analyzer to measure oxygen consumption. Tissue integrity was evaluated by propidium iodide staining and live imaging. Different substrates were tested for mitochondrial respiration. Basal and maximal respiration were expressed as oxygen consumption rate (OCR) and respectively measured in Ames' medium before and after the addition of mitochondrial uncoupler, BAM15.
   RESULTS. We show that glucose is an essential substrate for retinal mitochondria. At baseline, mitochondria respiration in the intact wild-type retina was close to maximal, with limited reserve capacity. Similar OCR and limited mitochondrial reserve capacity was also observed in cone-only Nrl(-/-) retina. However, the retina of Pde6brd1/rd1, Cep290rd16/rd16 and Rpgrip1(-/-) mice, all with dysfunctional or no photoreceptors, had reduced OCR and higher mitochondrial reserve capacity.
   CONCLUSIONS. We have optimized a method to directly measure oxygen consumption in acutely isolated, ex vivo mouse retina and demonstrate that photoreceptors have low mitochondrial reserve capacity. Our data provide a plausible explanation for the high vulnerability of photoreceptors to altered energy homeostasis caused by mutations or metabolic challenges.
C1 [Kooragayala, Keshav; Gotoh, Norimoto; Cogliati, Tiziana; Nellissery, Jacob; Swaroop, Anand] NEI, Neurobiol Neurodegenerat & Repair Lab, NIH, Bethesda, MD 20892 USA.
   [Kaden, Talia R.; Li, Wei] NEI, Retinal Neurobiol Sect, NIH, Bethesda, MD 20892 USA.
   [French, Stephanie; Balaban, Robert; Covian, Raul] NHLBI, Lab Cardiac Energet, NIH, Bethesda, MD 20892 USA.
RP Swaroop, A (reprint author), Bldg 6,Rm 338 MSC0610,6 Ctr Dr, Bethesda, MD 20892 USA.
EM raul.coviangarcia@nih.gov; swaroopa@nei.nih.gov
OI Swaroop, Anand/0000-0002-1975-1141
FU National Eye Institute, National Institutes of Health [EY000473,
   EY000474]
FX Supported by the Intramural Research Program of the National Eye
   Institute, National Institutes of Health (EY000473, EY000474). The
   authors alone are responsible for the content and writing of the paper.
NR 41
TC 3
Z9 3
U1 3
U2 4
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
EI 1552-5783
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD DEC
PY 2015
VL 56
IS 13
BP 8428
EP 8436
DI 10.1167/iovs.15-17901
PG 9
WC Ophthalmology
SC Ophthalmology
GA DB1BU
UT WOS:000368243800100
PM 26747773
ER

PT J
AU Babalonis, S
   Hampson, AJ
   Lofwall, MR
   Nuzzo, PA
   Walsh, SL
AF Babalonis, Shanna
   Hampson, Aidan J.
   Lofwall, Michelle R.
   Nuzzo, Paul A.
   Walsh, Sharon L.
TI Quinine as a Potential Tracer for Medication Adherence: A
   Pharmacokinetic and Pharmacodynamic Assessment of Quinine Alone and in
   Combination With Oxycodone in Humans
SO JOURNAL OF CLINICAL PHARMACOLOGY
LA English
DT Article
DE adherence; tracer; quinine; oxycodone; human; pharmacokinetic
ID TONIC WATER; DRUG; PHARMACOTHERAPY; HYDROCHLORIDE; RIBOFLAVIN;
   DEPENDENCE; LIABILITY; TOXICITY; HEROIN; CYP3A4
AB Effective strategies to monitor pharmacotherapy adherence are necessary, and sensitive biological markers are lacking. This study examined a subtherapeutic dose of quinine as a potential adherence tracer. Primary aims included examination of the plasma and urinary pharmacokinetic profile of once-daily quinine; secondary aims assessed pharmacokinetic/pharmacodynamic interactions with oxycodone (a CYP3A and CYP2D substrate). Healthy, nondependent opioid users (n = 9) were enrolled in this within-subject, double-blind, placebo-controlled inpatient study. Participants received the following oral doses: day 1, oxycodone (30 mg); days 2-4, quinine (80 mg); day 5, quinine and oxycodone (2 hours postquinine). Blood and 24-hour urine samples were collected throughout the study, and pharmacodynamic outcomes were assessed during experimental sessions (days 1, 4, 5). Quinine displayed a plasma T-max similar to 2 hours and t(1/2) similar to 10 hours. Oxycodone and noroxycodone parameters (T-max, C-max, t(1/2)) were similar with or without quinine present, although drug exposure (AUC) was slightly greater when combined with quinine. No pharmacodynamic interactions were detected, and doses were safely tolerated. During washout, quinine urinary concentrations steadily declined (elimination t(1/2) similar to 16 hours), with a 94% decrease observed 72 hours postdose. Overall, low-dose quinine appears to be a good candidate for a medication additive to monitor adherence for detection of missed medication.
C1 [Babalonis, Shanna; Lofwall, Michelle R.; Walsh, Sharon L.] Univ Kentucky, Coll Med, Dept Behav Sci, Lexington, KY 40508 USA.
   [Babalonis, Shanna; Lofwall, Michelle R.; Nuzzo, Paul A.; Walsh, Sharon L.] Univ Kentucky, Ctr Drug & Alcohol Res, Lexington, KY 40508 USA.
   [Hampson, Aidan J.] NIDA, Div Pharmacotherapies & Med Consequences, Rockville, MD USA.
   [Lofwall, Michelle R.; Walsh, Sharon L.] Univ Kentucky, Coll Med, Dept Psychiat, Lexington, KY 40508 USA.
   [Walsh, Sharon L.] Univ Kentucky, Coll Pharm, Dept Pharmaceut Sci, Lexington, KY 40508 USA.
   [Walsh, Sharon L.] Univ Kentucky, Coll Med, Dept Pharmacol, Lexington, KY 40508 USA.
RP Babalonis, S (reprint author), Univ Kentucky, Coll Med, Dept Behav Sci, Ctr Drug & Alcohol Res, 845 Angliana Ave, Lexington, KY 40508 USA.
EM babalonis@uky.edu
FU National Institute on Drug Abuse [R01DA016718-08S1]; National Center for
   Research Resources; National Center for Advancing of Translational
   Sciences (UK CTSA) [UL1TR000117-04]; National Center for Advancing of
   Translational Sciences [KL2TR000116-04]
FX Grants from the National Institute on Drug Abuse (R01DA016718-08S1
   [SLW]) and the National Center for Research Resources and National
   Center for Advancing of Translational Sciences (UL1TR000117-04 [UK
   CTSA]; KL2TR000116-04 [SB]) provided support for this research. We thank
   the staff at the University of Kentucky (UK) Center on Drug and Alcohol
   Research for research support: Stacy Conley, RN, Victoria Vessels, Tasia
   York, and John Beninato; Leta Hommel, Ken Westberry of the UK Center for
   Clinical and Translational Science (CCTS) Laboratory for assistance with
   specimens; the UK Investigational Pharmacy for preparing study
   medication, UK CCTS Inpatient Unit nursing staff for patient care,
   especially Lisa Chamblin, RN, for exceptional phlebotomy; and Dr.
   Samy-Claude Elayi (UK Department of Cardiology, Gill Heart Institute)
   for patient support. We also thank staff at the University of California
   San Francisco Drug Studies Unit for assay development and sample
   analyses: Dr. Young Huang, Winnie Gee, Shirley Yee, and Karen Kuncze;
   and Dr. Nora Chiang and Dr. Philip Krieter at the National Institute on
   Drug Abuse, Division of Pharmacotherapies and Medical Consequences of
   Drug Abuse, Chemistry and Pharmaceuticals Branch, for pharmacokinetic
   expertise and support.
NR 40
TC 3
Z9 3
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0091-2700
EI 1552-4604
J9 J CLIN PHARMACOL
JI J. Clin. Pharmacol.
PD DEC
PY 2015
VL 55
IS 12
BP 1332
EP 1343
DI 10.1002/jcph.557
PG 12
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA DA6ZH
UT WOS:000367953900002
PM 26032168
ER

PT J
AU Petruczynik, A
   Ciesla, LM
AF Petruczynik, Anna
   Ciesla, Lukasz M.
TI Thin-Layer Chromatography in the Analysis of Biologically Active Ionic
   and Ionizable Compounds
SO JPC-JOURNAL OF PLANAR CHROMATOGRAPHY-MODERN TLC
LA English
DT Review
DE Review; Ionic compounds; Weak electrolytes; Alkaloids; Phenolic acids
ID INDICATING HPTLC METHOD; PHARMACEUTICAL DOSAGE FORM; TLC-DENSITOMETRIC
   METHOD; MULTIDIMENSIONAL PLANAR CHROMATOGRAPHY; BONDED STATIONARY
   PHASES; DIODE-ARRAY DETECTION; QUANTITATIVE-ANALYSIS; HUMAN SERUM; BULK
   DRUG; BIOSYNTHETIC PRECURSORS
AB Ionic and ionizable solutes constitute a large group of compounds characterized with biological activity. Chromatographic analysis of these compounds is more difficult when compared to nonionic substances. This review focuses on different approaches used for the separation of basic and acidic substances by means of thin-layer chromatography. Biologically active basic compounds are more often used as prescribed drugs; therefore, chromatographic analysis of these substances was described in more detail when compared to acidic solutes.
   Direct stimulus to write this review was the 65th anniversary of Prof. Monika Waksmundzka-Hajnos' birthday. Prof. Hajnos is known for her great contributions to chromatographic analysis of ionic solutes.
C1 [Petruczynik, Anna; Ciesla, Lukasz M.] Med Univ Lublin, Dept Inorgan Chem, PL-20093 Lublin, Poland.
   [Ciesla, Lukasz M.] NIA, Lab Clin Invest, NIH, Baltimore, MD 21224 USA.
RP Petruczynik, A (reprint author), Med Univ Lublin, Dept Inorgan Chem, Chodzki 4a, PL-20093 Lublin, Poland.
EM anna.petruczynik@onet.pl; lukasz.ciesla@umlub.pl
NR 99
TC 1
Z9 1
U1 4
U2 12
PU AKADEMIAI KIADO RT
PI BUDAPEST
PA PRIELLE K U 19, PO BOX 245,, H-1117 BUDAPEST, HUNGARY
SN 0933-4173
EI 1789-0993
J9 JPC-J PLANAR CHROMAT
JI JPC-J. Planar Chromatogr.-Mod. TLC
PD DEC
PY 2015
VL 28
IS 6
BP 413
EP 425
DI 10.1556/1006.2015.28.6.1
PG 13
WC Chemistry, Analytical
SC Chemistry
GA DB0VU
UT WOS:000368226400001
ER

PT J
AU Miller, FG
   Kim, SYH
AF Miller, Franklin G.
   Kim, Scott Y. H.
TI Personal Care in Learning Health Care Systems
SO KENNEDY INSTITUTE OF ETHICS JOURNAL
LA English
DT Article
ID MAMMARY-ARTERY LIGATION; INFORMED-CONSENT; CONTROLLED-TRIALS;
   DISTINCTION; ETHICS
AB The idea of a "learning health care system" one that systematically integrates clinical research with medical care has received considerable attention recently. Some commentators argue that under certain conditions pragmatic comparative effectiveness randomized trials can be conducted ethically within the context of a learning health care system without the informed consent of patients for research participation. In this article, we challenge this perspective and contend that conducting randomized trials of individual treatment options without consent is neither necessary nor desirable to promote and sustain learning health care systems. Our argument draws on the normative conception of personal care developed by Charles Fried in a landmark 1974 book on the ethics of randomized controlled trials.
C1 [Miller, Franklin G.] Weill Cornell Med Coll, Med Eth Med, New York, NY 10065 USA.
   [Miller, Franklin G.] Hastings Ctr, New York, NY USA.
   [Kim, Scott Y. H.] NIH, Dept Bioeth, Bethesda, MD USA.
   [Kim, Scott Y. H.] Univ Michigan, Psychiat, Ann Arbor, MI 48109 USA.
   [Kim, Scott Y. H.] Univ Michigan, Ctr Bioeth & Behav Sci Med, Ann Arbor, MI 48109 USA.
RP Miller, FG (reprint author), Weill Cornell Med Coll, Med Eth Med, New York, NY 10065 USA.
FU Intramural Research Program of the Clinical Center, NIH
FX This research was supported by the Intramural Research Program of the
   Clinical Center, NIH.
NR 19
TC 0
Z9 0
U1 1
U2 2
PU JOHNS HOPKINS UNIV PRESS
PI BALTIMORE
PA JOURNALS PUBLISHING DIVISION, 2715 NORTH CHARLES ST, BALTIMORE, MD
   21218-4363 USA
SN 1054-6863
EI 1086-3249
J9 KENNEDY INST ETHIC J
JI Kennedy Inst. Ethics J.
PD DEC
PY 2015
VL 25
IS 4
BP 419
EP 435
PG 17
WC Ethics; Philosophy; Social Issues
SC Social Sciences - Other Topics; Philosophy; Social Issues
GA DB2BV
UT WOS:000368314200005
PM 26775880
ER

PT J
AU Capala, J
   Goetsch, SJ
   Orton, CG
AF Capala, Jacek
   Goetsch, Steven J.
   Orton, Colin G.
TI Medical use of all high activity sources should be eliminated for
   security concerns
SO MEDICAL PHYSICS
LA English
DT Editorial Material
C1 [Capala, Jacek] NCI, Div Canc Treatment & Diag, Bethesda, MD 20852 USA.
   [Goetsch, Steven J.] San Diego Gamma Knife Ctr, La Jolla, CA 92037 USA.
RP Capala, J (reprint author), NCI, Div Canc Treatment & Diag, Bethesda, MD 20852 USA.
EM capalaj@mail.nih.gov; stevegoetsch@sdgkc.com
NR 18
TC 0
Z9 0
U1 0
U2 4
PU AMER ASSOC PHYSICISTS MEDICINE AMER INST PHYSICS
PI MELVILLE
PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA
SN 0094-2405
EI 2473-4209
J9 MED PHYS
JI Med. Phys.
PD DEC
PY 2015
VL 42
IS 12
BP 6773
EP 6775
DI 10.1118/1.4934823
PG 3
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA DB1BX
UT WOS:000368244100001
PM 26632034
ER

PT J
AU Forest, A
   Amatulli, M
   Ludwig, DL
   Damoci, CB
   Wang, Y
   Burns, CA
   Donoho, GP
   Zanella, N
   Fiebig, HH
   Prewett, MC
   Surguladze, D
   DeLigio, JT
   Houghton, PJ
   Smith, MA
   Novosiadly, R
AF Forest, Amelie
   Amatulli, Michael
   Ludwig, Dale L.
   Damoci, Christopher B.
   Wang, Ying
   Burns, Colleen A.
   Donoho, Gregory P.
   Zanella, Nina
   Fiebig, Heinz H.
   Prewett, Marie C.
   Surguladze, David
   DeLigio, James T.
   Houghton, Peter J.
   Smith, Malcolm A.
   Novosiadly, Ruslan
TI Intrinsic Resistance to Cixutumumab Is Conferred by Distinct Isoforms of
   the Insulin Receptor
SO MOLECULAR CANCER RESEARCH
LA English
DT Article
ID GROWTH-FACTOR-I; ADVANCED SOLID TUMORS; MONOCLONAL-ANTIBODY; PHASE-2
   TRIAL; KINASE INHIBITORS; COLORECTAL-CANCER; TARGETED THERAPY;
   EWINGS-SARCOMA; LUNG-CANCER; OPEN-LABEL
AB Despite a recent shift away from anti-insulin-like growth factor I receptor (IGF-IR) therapy, this target has been identified as a key player in the resistance mechanisms to various conventional and targeted agents, emphasizing its value as a therapy, provided that it is used in the right patient population. Molecular markers predictive of antitumor activity of IGF-IR inhibitors remain largely unidentified. The aim of this study is to evaluate the impact of insulin receptor (IR) isoforms on the antitumor efficacy of cixutumumab, a humanized mAb against IGF-IR, and to correlate their expression with therapeutic outcome. The data demonstrate that expression of total IR rather than individual IR isoforms inversely correlates with single-agent cixutumumab efficacy in pediatric solid tumor models in vivo. Total IR, IR-A, and IR-B expression adversely affects the outcome of cixutumumab in combination with chemotherapy in patient-derived xenograft models of lung adenocarcinoma. IR-A overexpression in tumor cells confers complete resistance to cixutumumab in vitro and in vivo, whereas IR-B results in a partial resistance. Resistance in IR-B-overexpressing cells is fully reversed by anti-IGF-II antibodies, suggesting that IGF-II is a driver of cixutumumab resistance in this setting. The present study links IR isoforms, IGF-II, and cixutumumab efficacy mechanistically and identifies total IR as a biomarker predictive of intrinsic resistance to anti-IGF-IR antibody.
C1 [Forest, Amelie; Amatulli, Michael; Ludwig, Dale L.; Damoci, Christopher B.; Wang, Ying; Burns, Colleen A.; Prewett, Marie C.; Surguladze, David; DeLigio, James T.; Novosiadly, Ruslan] Eli Lilly & Co, New York, NY 10016 USA.
   [Donoho, Gregory P.] Eli Lilly & Co, Indianapolis, IN 46285 USA.
   [Zanella, Nina; Fiebig, Heinz H.] Oncotest, Freiburg, Germany.
   [Houghton, Peter J.] Nationwide Childrens Hosp, Columbus, OH USA.
   [Smith, Malcolm A.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Novosiadly, R (reprint author), Eli Lilly & Co, 450 East 29th St,11th Floor, New York, NY 10016 USA.
EM ruslan.novosiadly@lilly.com
FU NCI [NO1-CM-42216, CA165995]
FX This work was funded in part by the NCI grants (NO1-CM-42216 and
   CA165995).
NR 49
TC 1
Z9 1
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1541-7786
EI 1557-3125
J9 MOL CANCER RES
JI Mol. Cancer Res.
PD DEC
PY 2015
VL 13
IS 12
BP 1615
EP 1626
DI 10.1158/1541-7786.MCR-15-0279
PG 12
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA DB3UD
UT WOS:000368436500009
PM 26263910
ER

PT J
AU Drummond, RA
   Collar, AL
   Swamydas, M
   Rodriguez, CA
   Lim, JK
   Mendez, LM
   Fink, DL
   Hsu, AP
   Zhai, B
   Karauzum, H
   Mikelis, CM
   Rose, SR
   Ferre, EMN
   Yockey, L
   Lemberg, K
   Kuehn, HS
   Rosenzweig, SD
   Lin, X
   Chittiboina, P
   Datta, SK
   Belhorn, TH
   Weimer, ET
   Hernandez, ML
   Hohl, TM
   Kuhns, DB
   Lionakis, MS
AF Drummond, Rebecca A.
   Collar, Amanda L.
   Swamydas, Muthulekha
   Rodriguez, Carlos A.
   Lim, Jean K.
   Mendez, Laura M.
   Fink, Danielle L.
   Hsu, Amy P.
   Zhai, Bing
   Karauzum, Hatice
   Mikelis, Constantinos M.
   Rose, Stacey R.
   Ferre, Elise M. N.
   Yockey, Lynne
   Lemberg, Kimberly
   Kuehn, Hye Sun
   Rosenzweig, Sergio D.
   Lin, Xin
   Chittiboina, Prashant
   Datta, Sandip K.
   Belhorn, Thomas H.
   Weimer, Eric T.
   Hernandez, Michelle L.
   Hohl, Tobias M.
   Kuhns, Douglas B.
   Lionakis, Michail S.
TI CARD9-Dependent Neutrophil Recruitment Protects against Fungal Invasion
   of the Central Nervous System
SO PLOS PATHOGENS
LA English
DT Article
ID INHERITED CARD9 DEFICIENCY; ANTIFUNGAL IMMUNITY; CEREBROSPINAL-FLUID;
   CHEMOKINE RECEPTORS; MENINGITIS; MENINGOENCEPHALITIS; CANDIDIASIS;
   INFECTIONS; MUTATIONS; CHILDREN
AB Candida is the most common human fungal pathogen and causes systemic infections that require neutrophils for effective host defense. Humans deficient in the C-type lectin pathway adaptor protein CARD9 develop spontaneous fungal disease that targets the central nervous system (CNS). However, how CARD9 promotes protective antifungal immunity in the CNS remains unclear. Here, we show that a patient with CARD9 deficiency had impaired neutrophil accumulation and induction of neutrophil-recruiting CXC chemokines in the cerebrospinal fluid despite uncontrolled CNS Candida infection. We phenocopied the human susceptibility in Card9(-/-) mice, which develop uncontrolled brain candidiasis with diminished neutrophil accumulation. The induction of neutrophil-recruiting CXC chemokines is significantly impaired in infected Card9(-/-) brains, from both myeloid and resident glial cellular sources, whereas cell-intrinsic neutrophil chemotaxis is Card9-independent. Taken together, our data highlight the critical role of CARD9-dependent neutrophil trafficking into the CNS and provide novel insight into the CNS fungal susceptibility of CARD9-deficient humans.
C1 [Drummond, Rebecca A.; Collar, Amanda L.; Swamydas, Muthulekha; Rose, Stacey R.; Ferre, Elise M. N.; Yockey, Lynne] NIAID, Fungal Pathogenesis Unit, LCID, NIH, Bethesda, MD 20892 USA.
   [Rodriguez, Carlos A.; Lim, Jean K.] Icahn Sch Med Mt Sinai, Dept Microbiol, New York, NY 10029 USA.
   [Mendez, Laura M.; Fink, Danielle L.; Kuhns, Douglas B.] Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Neutrophil Monitoring Lab, Applied Dev Res Directorate, Frederick, MD USA.
   [Hsu, Amy P.] NIAID, Immunopathogenesis Sect, LCID, NIH, Bethesda, MD 20892 USA.
   [Zhai, Bing; Hohl, Tobias M.] Mem Sloan Kettering Canc Ctr, Infect Dis Serv, Dept Med, New York, NY 10021 USA.
   [Karauzum, Hatice; Datta, Sandip K.] NIAID, Bacterial Pathogenesis Unit, LCID, NIH, Bethesda, MD 20892 USA.
   [Mikelis, Constantinos M.] Texas Tech Univ, Dept Biomed Sci, Sch Pharm, Hlth Sci Ctr, Amarillo, TX USA.
   [Lemberg, Kimberly; Kuehn, Hye Sun; Rosenzweig, Sergio D.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Lin, Xin] Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol, Div Basic Sci Res, Houston, TX 77030 USA.
   [Chittiboina, Prashant] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
   [Belhorn, Thomas H.] Univ N Carolina, Dept Pediat, Chapel Hill, NC USA.
   [Weimer, Eric T.] Univ N Carolina, Dept Pathol & Lab Med, Chapel Hill, NC USA.
   [Hernandez, Michelle L.] Univ N Carolina, Ctr Environm Med Asthma & Lung Biol, Chapel Hill, NC USA.
RP Drummond, RA (reprint author), NIAID, Fungal Pathogenesis Unit, LCID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM lionakism@mail.nih.gov
OI Datta, Sandip/0000-0003-0243-7815; Drummond, Rebecca/0000-0001-5424-7074
FU Division of Intramural Research (DIR), NIAID, NIH; NIH [AI093808,
   AI105617]; Burroughs Wellcome Fund; National Cancer Institute, NIH
   [HHSN261200800001E]
FX This work was supported by the Division of Intramural Research (DIR),
   NIAID, NIH. TMH was supported by NIH grants AI093808 and AI105617, and
   by the Burroughs Wellcome Fund. LMM, DLF and DBK were funded by the
   National Cancer Institute, NIH, under Contract No. HHSN261200800001E.
   The funders had no role in study design, data collection and analysis,
   decision to publish, or preparation of the manuscript.
NR 43
TC 5
Z9 5
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7366
EI 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD DEC
PY 2015
VL 11
IS 12
AR e1005293
DI 10.1371/journal.ppat.1005293
PG 32
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA DB2IZ
UT WOS:000368332800021
PM 26679537
ER

PT J
AU Roche, J
   Louis, JM
   Bax, A
   Best, RB
AF Roche, Julien
   Louis, John M.
   Bax, Ad
   Best, Robert B.
TI Pressure-induced structural transition of mature HIV-1 protease from a
   combined NMR/MD simulation approach
SO PROTEINS-STRUCTURE FUNCTION AND BIOINFORMATICS
LA English
DT Article
DE protein folding and stability; high-pressure; packing defects;
   conformational fluctuations; cavities; ubiquitin
ID RESIDUAL DIPOLAR COUPLINGS; MOLECULAR-DYNAMICS SIMULATIONS; HIGH
   HYDROSTATIC-PRESSURE; CLINICAL INHIBITORS; PROTEINS; ALIGNMENT; WATER;
   PERTURBATION; FLUCTUATIONS; RELAXATION
AB We investigate the pressure-induced structural changes in the mature human immunodeficiency virus type 1 protease dimer, using residual dipolar coupling (RDC) measurements in a weakly oriented solution. D-1(NH) RDCs were measured under high-pressure conditions for an inhibitor-free PR and an inhibitor-bound complex, as well as for an inhibitor-free multidrug resistant protease bearing 20 mutations (PR20). While PR20 and the inhibitor-bound PR were little affected by pressure, inhibitor-free PR showed significant differences in the RDCs measured at 600 bar compared with 1 bar. The structural basis of such changes was investigated by MD simulations using the experimental RDC restraints, revealing substantial conformational perturbations, specifically a partial opening of the flaps and the penetration of water molecules into the hydrophobic core of the subunits at high pressure. This study highlights the exquisite sensitivity of RDCs to pressure-induced conformational changes and illustrates how RDCs combined with MD simulations can be used to determine the structural properties of metastable intermediate states on the folding energy landscape.
C1 [Roche, Julien; Louis, John M.; Bax, Ad; Best, Robert B.] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Best, RB (reprint author), NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
EM robertbe@helix.nih.gov
RI Best, Robert/H-7588-2016
OI Best, Robert/0000-0002-7893-3543
FU Intramural Research Program of the National Institute of Diabetes and
   Digestive and Kidney Diseases of the National Institutes of Health;
   Intramural AIDS Research Fellowship
FX Grant sponsor: Intramural Research Program of the National Institute of
   Diabetes and Digestive and Kidney Diseases of the National Institutes of
   Health; Grant sponsor: Intramural AIDS Research Fellowship.
NR 40
TC 3
Z9 3
U1 5
U2 17
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0887-3585
EI 1097-0134
J9 PROTEINS
JI Proteins
PD DEC
PY 2015
VL 83
IS 12
BP 2117
EP 2123
DI 10.1002/prot.24931
PG 7
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA DB2IE
UT WOS:000368330700001
PM 26385843
ER

PT J
AU Joo, K
   Joung, I
   Lee, J
   Lee, J
   Lee, W
   Brooks, B
   Lee, SJ
   Lee, J
AF Joo, Keehyoung
   Joung, Insuk
   Lee, Jinhyuk
   Lee, Jinwoo
   Lee, Weontae
   Brooks, Bernard
   Lee, Sung Jong
   Lee, Jooyoung
TI Protein structure determination by conformational space annealing using
   NMR geometric restraints
SO PROTEINS-STRUCTURE FUNCTION AND BIOINFORMATICS
LA English
DT Article
DE protein structure determination; NMR restraint; ambiguous distance
   correction; global optimization
ID GLOBAL OPTIMIZATION; STRUCTURE PREDICTION; CASP7 PREDICTIONS; DYNAMICS;
   CRYSTALLOGRAPHY; SPECTROSCOPY; MINIMIZATION; ALGORITHMS; FRAGMENT;
   PACKAGE
AB We have carried out numerical experiments to investigate the applicability of the global optimization method of conformational space annealing (CSA) to the enhanced NMR protein structure determination over existing PDB structures. The NMR protein structure determination is driven by the optimization of collective multiple restraints arising from experimental data and the basic stereochemical properties of a protein-like molecule. By rigorous and straightforward application of CSA to the identical NMR experimental data used to generate existing PDB structures, we redetermined 56 recent PDB protein structures starting from fully randomized structures. The quality of CSA-generated structures and existing PDB structures were assessed by multi-objective functions in terms of their consistencies with experimental data and the requirements of protein-like stereochemistry. In 54 out of 56 cases, CSA-generated structures were better than existing PDB structures in the Pareto-dominant manner, while in the remaining two cases, it was a tie with mixed results. As a whole, all structural features tested improved in a statistically meaningful manner. The most improved feature was the Ramachandran favored portion of backbone torsion angles with about 8.6% improvement from 88.9% to 97.5% (P-value <10(-17)). We show that by straightforward application of CSA to the efficient global optimization of an energy function, NMR structures will be of better quality than existing PDB structures. (C) 2015 Wiley Periodicals, Inc.
C1 [Joo, Keehyoung; Joung, Insuk; Lee, Sung Jong; Lee, Jooyoung] Korea Inst Adv Study, Ctr Sil Prot Sci, Seoul 130722, South Korea.
   [Joo, Keehyoung] Korea Inst Adv Study, Ctr Adv Computat, Seoul 130722, South Korea.
   [Joung, Insuk; Lee, Jooyoung] Korea Inst Adv Study, Sch Computat Sci, Seoul 130722, South Korea.
   [Lee, Jinhyuk] Korea Res Inst Biosci & Biotechnol, Korean Bioinformat Ctr KOBIC, Daejeon 305806, South Korea.
   [Lee, Jinhyuk] Univ Sci & Technol, Dept Nanobiotechnol & Bioinformat, Daejeon 305350, South Korea.
   [Lee, Jinwoo] Kwangwoon Univ, Dept Math, Seoul 139701, South Korea.
   [Lee, Weontae] Yonsei Univ, Dept Biochem, Seoul 120749, South Korea.
   [Brooks, Bernard] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20852 USA.
   [Lee, Sung Jong] Univ Suwon, Dept Phys, Hwaseong Si 445743, Gyeonggi Do, South Korea.
RP Lee, J (reprint author), Korea Inst Adv Study, Ctr Sil Prot Sci, Seoul 130722, South Korea.
EM jlee@kias.re.kr
FU Korea government (MEST) [2008-0061987]; Korea Research Institute of
   Bioscience and Biotechnology (KRIBB) Research Initiative Program;
   Research Grant of Kwangwoon University; MEST [NRF-2013R1A2A2A01068963]
FX Grant sponsor: Korea government (MEST); Grant number: 2008-0061987;
   Grant sponsors: Korea Research Institute of Bioscience and Biotechnology
   (KRIBB) Research Initiative Program (to JHL); Research Grant of
   Kwangwoon University (to JWL); and Mid-career Researcher Program (to
   WL); Grant sponsor: MEST; Grant number: NRF-2013R1A2A2A01068963.
NR 42
TC 0
Z9 0
U1 2
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0887-3585
EI 1097-0134
J9 PROTEINS
JI Proteins
PD DEC
PY 2015
VL 83
IS 12
BP 2251
EP 2262
DI 10.1002/prot.24941
PG 12
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA DB2IE
UT WOS:000368330700012
PM 26454251
ER

PT J
AU Stepanov, I
   Gupta, PC
   Dhumal, G
   Yershova, K
   Toscano, W
   Hatsukami, D
   Parascandola, M
AF Stepanov, Irina
   Gupta, Prakash C.
   Dhumal, Gauri
   Yershova, Katrina
   Toscano, William
   Hatsukami, Dorothy
   Parascandola, Mark
TI High levels of tobacco-specific N-nitrosamines and nicotine in Chaini
   Khaini, a product marketed as snus
SO TOBACCO CONTROL
LA English
DT Article
DE Carcinogens; Nicotine; Harm Reduction; Packaging and Labelling
ID SMOKELESS TOBACCO; MOIST SNUFF; PUBLIC-HEALTH; CANCER; INDIA;
   EPIDEMIOLOGY; SMOKING; MOUTH; RISK; PH
AB Introduction Recently, a tobacco product, Chaini Khaini, identified as snus appeared in India. The product marketing emphasises its discreet nature and explicitly claims safety by referring to the existing evidence on Swedish snus. We analysed tobacco-specific nitrosamines and nicotine in 12 samples of Chaini Khaini purchased in 2013 at open markets in India.
   Methods Samples were purchased twice: in March 2013 from Mumbai and in November 2013 from Mumbai and Ahmedabad. Chemical constituents were measured by our routine validated methods.
   Results Levels of carcinogenic nitrosamines NNN, NNK and NNAL averaged 22.9 (4.9), 2.6 (+/- 1.0) and 3.1 (+/- 1.5)mu g/g tobacco (wet weight), respectively. The levels of NAB, which is normally present in trace levels in tobacco products, ranged from 3.9 to 12.9 mu g/g tobacco. Total nicotine levels in all samples averaged 10.0mg/g tobacco and unprotonated nicotine accounted for an average 95.4% of the total nicotine content.
   Conclusions Chaini Khaini, which is labelled as snus and is marketed as a safe alternative to other tobacco products contains very high levels of carcinogenic nitrosamines and biologically available nicotine. Interventions are urgently needed to educate current and potential consumers of this product.
C1 [Stepanov, Irina; Yershova, Katrina; Hatsukami, Dorothy] Univ Minnesota, Masonic Canc Ctr, Minneapolis, MN 55455 USA.
   [Stepanov, Irina; Toscano, William] Univ Minnesota, Div Environm Hlth Sci, Minneapolis, MN 55455 USA.
   [Gupta, Prakash C.; Dhumal, Gauri] Healis Sekhsaria Inst Publ Hlth, Mumbai, Maharashtra, India.
   [Parascandola, Mark] Natl Canc Inst, Tobacco Control Res Branch, Bethesda, MD USA.
RP Stepanov, I (reprint author), Univ Minnesota, Masonic Canc Ctr, Canc & Cardiovasc Res Bldg,2231 6th St SE, Minneapolis, MN 55455 USA.
EM stepa011@umn.edu
OI Stepanov, Irina/0000-0001-5140-8944
FU National Cancer Institute [HHSN261201200392P]; Masonic Cancer Center,
   University of Minnesota via NCI [P30 CA077598]
FX This work was supported by the National Cancer Institute contract
   HHSN261201200392P and by startup funds to IS from the Masonic Cancer
   Center, University of Minnesota via NCI grant P30 CA077598.
NR 23
TC 3
Z9 3
U1 0
U2 2
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 DEC
PY 2015
VL 24
IS E4
BP E271
EP E274
DI 10.1136/tobaccocontrol-2014-051744
PG 4
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA DA5HQ
UT WOS:000367834300008
PM 25217658
ER

PT J
AU Custer, B
   Sheon, N
   Siedle-Khan, B
   Pollack, L
   Spencer, B
   Bialkowski, W
   D'Andrea, P
   Sullivan, M
   Glynn, S
   Williams, A
AF Custer, Brian
   Sheon, Nicolas
   Siedle-Khan, Bob
   Pollack, Lance
   Spencer, Bryan
   Bialkowski, Walter
   D'Andrea, Pam
   Sullivan, Marian
   Glynn, Simone
   Williams, Alan
CA NHLBI Recipient Epidemiology Donor
TI Blood donor deferral for men who have sex with men: the Blood Donation
   Rules Opinion Study (Blood DROPS)
SO TRANSFUSION
LA English
DT Article
ID TRANSFUSION-TRANSMITTED HIV; EVER HAD SEX; GAY MEN; RISK; POLICY;
   IMPACT; DISCRIMINATION; EXCLUSION; ENGLAND; WALES
AB BACKGROUND: In the United States, any man who discloses having had sex with another man (MSM) even once since 1977 is currently deferred from donating blood. A study was conducted to assess noncompliance with the policy at four geographically dispersed blood centers.
   STUDY DESIGN AND METHODS: Male donors 18+ years of age with e-mail addresses were randomly selected and invited to complete a confidential online survey between August and October 2013. No additional recruitment e-mails were sent. Survey content included demographics, sexual history, donation history, compliance with the policy, and opinions about current and modified policies.
   RESULTS: Response rate was 11.5% but varied by center (6.3% to 21.7%). Of 3183 completed surveys, 2.6% of respondents (95% confidence interval, 2.1%-3.2%) reported donation after male-male sex. Noncompliance was not statistically different among the centers (p=0.1), but was related to age with 5.7, 4.6, 2.5, and 1.0% of donors 18 to 24, 25 to 34, 35 to 54, and 50+ years of age, respectively, reporting noncompliance (p<0.001). Of all respondents, 6.8% reported at least six female and 0.3% reported at least six male sex partners in the past 5 years. Opinions about the current MSM policy were mixed with noncomplying donors more supportive of change than complying donors. Approximatey half of noncompliers indicated they would adhere to a 1-year deferral.
   CONCLUSION: Noncompliance with the MSM policy is evident and may be increasing compared to earlier data. Any change from the current policy will require close monitoring to determine whether it affects residual risk of HIV in the US blood supply.
C1 [Custer, Brian] UCSF, Blood Syst Res Inst, San Francisco, CA USA.
   [Custer, Brian] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA.
   [Sheon, Nicolas; Siedle-Khan, Bob; Pollack, Lance] UCSF, Ctr AIDS Prevent Studies, San Francisco, CA USA.
   [Spencer, Bryan] Amer Red Cross, Dedham, MA USA.
   [Bialkowski, Walter] BloodCtr Wisconsin, Milwaukee, WI USA.
   [D'Andrea, Pam] Inst Transfus Med, Pittsburgh, PA USA.
   [Sullivan, Marian] RTI Int, Rockville, MD USA.
   [Glynn, Simone] NHLBI, Bethesda, MD 20892 USA.
   [Williams, Alan] US FDA, Silver Spring, MD USA.
RP Custer, B (reprint author), Blood Syst Res Inst, 270 Mason Ave, San Francisco, CA 94118 USA.
EM bcuster@bloodsystems.org
FU US FDA; NHLBI REDS-III program
FX This study was funded by the US FDA and the NHLBI REDS-III program.
NR 34
TC 9
Z9 9
U1 1
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 DEC
PY 2015
VL 55
IS 12
BP 2826
EP 2834
DI 10.1111/trf.13247
PG 9
WC Hematology
SC Hematology
GA DA6YB
UT WOS:000367950600010
PM 26202349
ER

PT J
AU Mielke, MM
   Bandaru, VVR
   Han, DF
   An, Y
   Resnick, SM
   Ferrucci, L
   Haughey, NJ
AF Mielke, Michelle M.
   Bandaru, Veera Venkata Ratnam
   Han, Dingfen
   An, Yang
   Resnick, Susan M.
   Ferrucci, Luigi
   Haughey, Norman J.
TI Demographic and clinical variables affecting mid-to late-life
   trajectories of plasma ceramide and dihydroceramide species
SO AGING CELL
LA English
DT Article
DE aging; ceramide; dihydroceramide; human; longitudinal; sex differences
ID INSULIN-RESISTANCE; SPHINGOLIPID METABOLISM; MASS-SPECTROMETRY; DISEASE;
   SPAN; RISK; ALZHEIMERS; LIPIDOMICS; PROTEIN; STRESS
AB It has been increasingly recognized at the basic science level that perturbations in ceramide metabolism are associated with the development and progression of many age-related diseases. However, the translation of this work to the clinic has lagged behind. Understanding the factors longitudinally associated with plasma ceramides and dihydroceramides (DHCer) at the population level and how these lipid levels change with age, and by sex, is important for the clinical development of future therapeutics and biomarkers focused on ceramide metabolism. We, therefore, examined factors cross-sectionally and longitudinally associated with plasma concentrations of ceramides and DHCer among Baltimore Longitudinal Study of Aging participants (n = 992; 3960 total samples), aged 55 years and older, with plasma at a mean of 4.1 visits (range 2-6). Quantitative analyses were performed on a high-performance liquid chromatography-coupled electrospray ionization tandem mass spectrometer. Linear mixed models were used to assess the relationships between plasma ceramide and DHCer species and demographics, diseases, medications, and lifestyle factors. Women had higher plasma concentrations of most ceramide and DHCer species and showed steeper trajectories of age-related increases compared to men. Ceramides and DHCer were more associated with waist-hip ratio than body mass index. Plasma cholesterol and triglycerides, prediabetes, and diabetes were associated with ceramides and DHCer, but the relationship showed specificity to the acyl chain length and saturation. These results demonstrate the importance of examining the individual species of ceramides and DHCer, and of establishing whether intra-individual age- and sex-specific changes occur in synchrony to disease onset and progression.
C1 [Mielke, Michelle M.] Mayo Clin, Dept Hlth Sci Res, Rochester, MN 55905 USA.
   [Mielke, Michelle M.] Mayo Clin, Dept Neurol, Rochester, MN 55905 USA.
   [Bandaru, Veera Venkata Ratnam; Haughey, Norman J.] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21224 USA.
   [Han, Dingfen; Haughey, Norman J.] Johns Hopkins Univ, Sch Med, Psychiat, Baltimore, MD 21224 USA.
   [An, Yang; Resnick, Susan M.; Ferrucci, Luigi] NIA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Mielke, MM (reprint author), Mayo Clin, Dept Hlth Sci Res, Div Epidemiol, 200 First St SW, Rochester, MN 55905 USA.
EM mielke.michelle@mayo.edu
FU National Institutes of Health/National Institute on Aging [U01 AG37526]
FX This work was supported by a grant from the National Institutes of
   Health/National Institute on Aging (U01 AG37526) and by the Intramural
   Research Program of the National Institutes of Health/National Institute
   on Aging.
NR 45
TC 5
Z9 5
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1474-9718
EI 1474-9726
J9 AGING CELL
JI Aging Cell
PD DEC
PY 2015
VL 14
IS 6
BP 1014
EP 1023
DI 10.1111/acel.12369
PG 10
WC Cell Biology; Geriatrics & Gerontology
SC Cell Biology; Geriatrics & Gerontology
GA DA2XT
UT WOS:000367661200010
PM 26193443
ER

PT J
AU Li, Q
   Wang, SR
   Milot, E
   Bergeron, P
   Ferrucci, L
   Fried, LP
   Cohen, AA
AF Li, Qing
   Wang, Shengrui
   Milot, Emmanuel
   Bergeron, Patrick
   Ferrucci, Luigi
   Fried, Linda P.
   Cohen, Alan A.
TI Homeostatic dysregulation proceeds in parallel in multiple physiological
   systems
SO AGING CELL
LA English
DT Article
DE aging; biomarker; homeostasis; multi-system dysregulation; physiology;
   statistical distance
ID ALLOSTATIC LOAD; LONGEVITY; AGE; FRAILTY; HEALTH; TRAJECTORIES;
   POPULATION; MORTALITY; DECLINE
AB An increasing number of aging researchers believes that multisystem physiological dysregulation may be a key biological mechanism of aging, but evidence of this has been sparse. Here, we used biomarker data on nearly 33 000 individuals from four large datasets to test for the presence of multi-system dysregulation. We grouped 37 biomarkers into six a priori groupings representing physiological systems (lipids, immune, oxygen transport, liver function, vitamins, and electrolytes), then calculated dysregulation scores for each system in each individual using statistical distance. Correlations among dysregulation levels across systems were generally weak but significant. Comparison of these results to dysregulation in arbitrary 'systems' generated by random grouping of biomarkers showed that a priori knowledge effectively distinguished the true systems in which dysregulation proceeds most independently. In other words, correlations among dysregulation levels were higher using arbitrary systems, indicating that only a priori systems identified distinct dysregulation processes. Additionally, dysregulation of most systems increased with age and significantly predicted multiple health outcomes including mortality, frailty, diabetes, heart disease, and number of chronic diseases. The six systems differed in how well their dysregulation scores predicted health outcomes and age. These findings present the first unequivocal demonstration of integrated multi-system physiological dysregulation during aging, demonstrating that physiological dysregulation proceeds neither as a single global process nor as a completely independent process in different systems, but rather as a set of system-specific processes likely linked through weak feedback effects. These processes - probably many more than the six measured here - are implicated in aging.
C1 [Li, Qing; Milot, Emmanuel; Bergeron, Patrick; Cohen, Alan A.] Univ Sherbrooke, Dept Family Med, Grp Rech PRIMUS, Sherbrooke, PQ J1H 5N4, Canada.
   [Wang, Shengrui] Univ Sherbrooke, Dept Comp Sci, Sherbrooke, PQ J1K 2R1, Canada.
   [Ferrucci, Luigi] MedStar Harbor Hosp, Natl Inst Hlth, Natl Inst Aging, Translat Gerontol Branch,Longitudinal Studies Sec, Baltimore, MD 21225 USA.
   [Fried, Linda P.] Columbia Univ, Mailman Sch Publ Hlth, New York, NY 10032 USA.
RP Cohen, AA (reprint author), Univ Sherbrooke, Dept Family Med, Grp Rech PRIMUS, 3001 12E Ave N, Sherbrooke, PQ J1H 5N4, Canada.
EM alan.cohen@usherbrooke.ca
FU FRQ-S; CIHR [110789, 120305, 119485]; NSERC [402079-2011]; National
   Institute on Aging
FX AAC is a member of the FRQ-S-supported Centre de recherche sur le
   vieillissement and Centre de recherche du CHUS, and is a funded Research
   Scholar of the FRQ-S. This research was supported by CIHR grant #s
   110789, 120305, 119485 and by NSERC Discovery Grant # 402079-2011, as
   well as by the Intramural Research Program of the National Institute on
   Aging.
NR 43
TC 5
Z9 5
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1474-9718
EI 1474-9726
J9 AGING CELL
JI Aging Cell
PD DEC
PY 2015
VL 14
IS 6
BP 1103
EP 1112
DI 10.1111/acel.12402
PG 10
WC Cell Biology; Geriatrics & Gerontology
SC Cell Biology; Geriatrics & Gerontology
GA DA2XT
UT WOS:000367661200019
PM 26416593
ER

PT J
AU Hankins, JS
   McCarville, MB
   Rankine-Mullings, A
   Reid, ME
   Lobo, CLC
   Moura, PG
   Ali, S
   Soares, DP
   Aldred, K
   Jay, DW
   Aygun, B
   Bennett, J
   Kang, GL
   Goldsmith, JC
   Smeltzer, MP
   Boyett, JM
   Ware, RE
AF Hankins, Jane S.
   McCarville, Mary Beth
   Rankine-Mullings, Angela
   Reid, Marvin E.
   Lobo, Clarisse L. C.
   Moura, Patricia G.
   Ali, Susanna
   Soares, Deanne P.
   Aldred, Karen
   Jay, Dennis W.
   Aygun, Banu
   Bennett, John
   Kang, Guolian
   Goldsmith, Jonathan C.
   Smeltzer, Matthew P.
   Boyett, James M.
   Ware, Russell E.
TI Prevention of conversion to abnormal transcranial Doppler with
   hydroxyurea in sickle cell anemia: A Phase III international randomized
   clinical trial
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID FLOW VELOCITIES; YOUNG-CHILDREN; BABY HUG; DISEASE; STROKE; THERAPY;
   EVENTS; ULTRASONOGRAPHY; PERSPECTIVE; EXPERIENCE
AB Children with sickle cell anemia (SCA) and conditional transcranial Doppler (TCD) ultrasound velocities (170-199 cm/sec) may develop stroke. However, with limited available clinical data, the current standard of care for conditional TCD velocities is observation. The efficacy of hydroxyurea in preventing conversion from conditional to abnormal TCD (>= 200 cm/sec), which confers a higher stroke risk, has not been studied prospectively in a randomized trial. Sparing Conversion to Abnormal TCD Elevation (SCATE #NCT01531387) was a National Heart, Lung, and Blood Institute-funded Phase III multicenter international clinical trial comparing alternative therapy (hydroxyurea) to standard care (observation) to prevent conversion from conditional to abnormal TCD velocity in children with SCA. SCATE enrolled 38 children from the United States, Jamaica, and Brazil [HbSS (36), HbS beta(0)-thalassemia (1), and HbSD (1), median age=5.4 years (range, 2.7-9.8)]. Because of the slow patient accrual and administrative delays, SCATE was terminated early. In an intention-to-treat analysis, the cumulative incidence of abnormal conversion was 9% (95% CI=0-35%) in the hydroxyurea arm and 47% (95% CI=6-81%) in observation arm at 15 months (P=0.16). In post hoc analysis according to treatment received, significantly fewer children on hydroxyurea converted to abnormal TCD velocities when compared with observation (0% vs. 50%, P=0.02). After a mean of 10.1 months, a significant change in mean TCD velocity was observed with hydroxyurea treatment (-15.5 vs. +10.2 cm/sec, P=0.02). No stroke events occurred in either arm. Hydroxyurea reduces TCD velocities in children with SCA and conditional velocities. (C) 2015 Wiley Periodicals, Inc.
C1 [Hankins, Jane S.; McCarville, Mary Beth; Jay, Dennis W.; Kang, Guolian; Smeltzer, Matthew P.; Boyett, James M.] St Jude Childrens Res Hosp, Dept Hematol, Memphis, TN 38105 USA.
   [Rankine-Mullings, Angela; Reid, Marvin E.; Ali, Susanna; Soares, Deanne P.; Aldred, Karen] Univ W Indies, Res Inst Trop Med, Sickle Cell Unit, Kingston 7, Jamaica.
   [Lobo, Clarisse L. C.; Moura, Patricia G.] Inst De Hematol Arthur Siqueira Cavalcanti HEMORI, Rio De Janeiro, Brazil.
   [Aygun, Banu] Cohen Childrens Med Ctr New York, Div Pediat Hematol Oncol & Stem Cell Transplantat, New Hyde Pk, NY USA.
   [Bennett, John] Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA.
   [Goldsmith, Jonathan C.] NHLBI, Bethesda, MD 20892 USA.
   [Ware, Russell E.] Cincinnati Childrens Hosp Med Ctr, Div Hematol, Cincinnati, OH 45229 USA.
RP Hankins, JS (reprint author), St Jude Childrens Res Hosp, Dept Hematol, 262 Danny Thomas Pl,MS 800, Memphis, TN 38105 USA.
EM jane.hankins@stjude.org
OI Reid, Marvin/0000-0003-4005-9384
FU National Hearth Lung and Blood Institute [5R01HL098239]
FX Contract grant sponsor: National Hearth Lung and Blood Institute;
   Contract grant number: 5R01HL098239.
NR 36
TC 5
Z9 5
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0361-8609
EI 1096-8652
J9 AM J HEMATOL
JI Am. J. Hematol.
PD DEC
PY 2015
VL 90
IS 12
BP 1099
EP 1105
DI 10.1002/ajh.24198
PG 7
WC Hematology
SC Hematology
GA DA2ZS
UT WOS:000367666300013
PM 26414435
ER

PT J
AU Donkervoort, S
   Papadaki, M
   de Winter, JM
   Neu, MB
   Kirschner, J
   Bolduc, V
   Yang, ML
   Gibbons, MA
   Hu, Y
   Dastgir, J
   Leach, ME
   Rutkowski, A
   Foley, AR
   Kruger, M
   Wartchow, EP
   McNamara, E
   Ong, R
   Nowak, KJ
   Laing, NG
   Clarke, NF
   Ottenheijm, CAC
   Marston, SB
   Bonnemann, CG
AF Donkervoort, Sandra
   Papadaki, Maria
   de Winter, Josine M.
   Neu, Matthew B.
   Kirschner, Janbernd
   Bolduc, Veronique
   Yang, Michele L.
   Gibbons, Melissa A.
   Hu, Ying
   Dastgir, Jahannaz
   Leach, Meganne E.
   Rutkowski, Anne
   Foley, A. Reghan
   Krueger, Marcus
   Wartchow, Eric P.
   McNamara, Elyshia
   Ong, Royston
   Nowak, Kristen J.
   Laing, Nigel G.
   Clarke, Nigel F.
   Ottenheijm, Coen A. C.
   Marston, Steven B.
   Boennemann, Carsten G.
TI TPM3 Deletions Cause a Hypercontractile Congenital Muscle Stiffness
   Phenotype
SO ANNALS OF NEUROLOGY
LA English
DT Article
ID NEMALINE MYOPATHY PATIENTS; TROPONIN-I PHOSPHORYLATION;
   ALPHA-TROPOMYOSIN; THIN FILAMENT; F-ACTIN; ENERGY LANDSCAPES;
   HEART-FAILURE; CAUSE GAIN; MUTATIONS; SENSITIVITY
AB Objective: Mutations in TPM3, encoding Tpm3.12, cause a clinically and histopathologically diverse group of myopathies characterized by muscle weakness. We report two patients with novel de novo Tpm3.12 single glutamic acid deletions at positions Delta E218 and Delta E224, resulting in a significant hypercontractile phenotype with congenital muscle stiffness, rather than weakness, and respiratory failure in one patient.
   Methods: The effect of the Tpm3.12 deletions on the contractile properties in dissected patient myofibers was measured. We used quantitative in vitro motility assay to measure Ca2+ sensitivity of thin filaments reconstituted with recombinant Tpm3.12 Delta E218 and Delta E224.
   Results: Contractility studies on permeabilized myofibers demonstrated reduced maximal active tension from both patients with increased Ca2+ sensitivity and altered cross-bridge cycling kinetics in Delta DE224 fibers. In vitro motility studies showed a two-fold increase in Ca2+ sensitivity of the fraction of filaments motile and the filament sliding velocity concentrations for both mutations.
   Interpretation: These data indicate that Tpm3.12 deletions Delta E218 and Delta E224 result in increased Ca2+ sensitivity of the troponin-tropomyosin complex, resulting in abnormally active interaction of the actin and myosin complex. Both mutations are located in the charged motifs of the actin-binding residues of tropomyosin 3, thus disrupting the electrostatic interactions that facilitate accurate tropomyosin binding with actin necessary to prevent the on-state. The mutations destabilize the off-state and result in excessively sensitized excitation-contraction coupling of the contract-ile apparatus. This work expands the phenotypic spectrum of TPM3-related disease and provides insights into the pathophysiological mechanisms of the actin-tropomyosin complex.
C1 [Donkervoort, Sandra; Neu, Matthew B.; Bolduc, Veronique; Hu, Ying; Dastgir, Jahannaz; Leach, Meganne E.; Foley, A. Reghan; Boennemann, Carsten G.] NIH, Neuromuscular & Neurogenet Disorders Childhood Se, Bethesda, MD 20892 USA.
   [Papadaki, Maria; Marston, Steven B.] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London, England.
   [de Winter, Josine M.; Ottenheijm, Coen A. C.] Vrije Univ Amsterdam Med Ctr, Dept Physiol, Amsterdam, Netherlands.
   [Kirschner, Janbernd] Univ Med Ctr Freiburg, Dept Neuropediat & Muscle Disorders, Freiburg, Germany.
   [Yang, Michele L.] Univ Colorado, Sch Med, Sect Child Neurol, Dept Pediat & Neurol, Aurora, CO USA.
   [Gibbons, Melissa A.] Univ Colorado, Denver Sch Med, Aurora, CO USA.
   [Leach, Meganne E.] Childrens Natl Hlth Syst, Washington, DC USA.
   [Rutkowski, Anne] Kaiser Southern Calif Permanente Med Grp, Cure CMD, Olathe, KS USA.
   [Krueger, Marcus] Univ Med Ctr Freiburg, Dept Gen Pediat Adolescent Med & Neonatol, Freiburg, Germany.
   [Wartchow, Eric P.] Childrens Hosp Colorado, Dept Pathol, Aurora, CO USA.
   [McNamara, Elyshia; Ong, Royston; Nowak, Kristen J.; Laing, Nigel G.] Univ Western Australia, Neuromuscular Dis Lab, Med Res Ctr, Fac Med Dent & Hlth Sci, Crawley, WA, Australia.
   [McNamara, Elyshia; Ong, Royston; Nowak, Kristen J.; Laing, Nigel G.] Queen Elizabeth II Med Ctr, Harry Perkins Inst Med Res, Perth, WA, Australia.
   [Clarke, Nigel F.] Univ Sydney, Inst Neurosci & Muscle Res, Childrens Hosp Westmead, Sydney, NSW 2006, Australia.
RP Bonnemann, CG (reprint author), NIH, Porter Neurosci Res Ctr, 35 Convent Dr,Bldg 35,Room 2A-116, Bethesda, MD 20892 USA.
EM carsten.bonnemann@nih.gov
RI Kirschner, Janbernd/H-7418-2016
OI Kirschner, Janbernd/0000-0003-1618-7386
FU Australian National Health and Medical Research Council [APP1002147,
   APP1022707]; Australian Research Council [FT100100734]; British Heart
   Foundation [RG/11/20/29266, FS/12/24/29568]
FX This study was supported by an Australian National Health and Medical
   Research Council fellowship (APP1002147, N.G.L.) and project grant
   (APP1022707, E.M., R.O.); an Australian Research Council Future
   Fellowship (FT100100734, K.J.N.); and grants from the British Heart
   Foundation (RG/11/20/29266, FS/12/24/29568, S.B.M., M.K.).
NR 40
TC 3
Z9 3
U1 0
U2 1
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 DEC
PY 2015
VL 78
IS 6
BP 982
EP 994
DI 10.1002/ana.24535
PG 13
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DA3DY
UT WOS:000367678100014
PM 26418456
ER

PT J
AU Hu, GW
   McQuiston, T
   Bernard, A
   Park, YD
   Qiu, J
   Vural, A
   Zhang, NN
   Waterman, SR
   Blewett, NH
   Myers, TG
   Maraia, RJ
   Kehrl, JH
   Uzel, G
   Klionsky, DJ
   Williamson, PR
AF Hu, Guowu
   McQuiston, Travis
   Bernard, Amelie
   Park, Yoon-Dong
   Qiu, Jin
   Vural, Ali
   Zhang, Nannan
   Waterman, Scott R.
   Blewett, Nathan H.
   Myers, Timothy G.
   Maraia, Richard J.
   Kehrl, John H.
   Uzel, Gulbu
   Klionsky, Daniel J.
   Williamson, Peter R.
TI TOR-dependent post-transcriptional regulation of autophagy
SO AUTOPHAGY
LA English
DT Editorial Material
DE autoimmunity; autophagy; phosphorylation; TOR; translation
AB Regulation of autophagy is required to maintain cellular equilibrium and prevent disease. While extensive study of post-translational mechanisms has yielded important insights into autophagy induction, less is known about post-transcriptional mechanisms that could potentiate homeostatic control. In our study, we showed that the RNA-binding protein, Dhh1 in Saccharomyces cerevisiae and Vad1 in the pathogenic yeast Cryptococcusneoformans is involved in recruitment and degradation of key autophagy mRNAs. In addition, phosphorylation of the decapping protein Dcp2 by the target of rapamycin (TOR), facilitates decapping and degradation of autophagy-related mRNAs, resulting in repression of autophagy under nutrient-replete conditions. The post-transcriptional regulatory process is conserved in both mouse and human cells and plays a role in autophagy-related modulation of the inflammasome product IL1B. These results were then applied to provide mechanistic insight into autoimmunity of a patient with a PIK3CD/p110 gain-of-function mutation. These results thus identify an important new post-transcriptional mechanism of autophagy regulation that is highly conserved between yeast and mammals.
C1 [Hu, Guowu; McQuiston, Travis; Park, Yoon-Dong; Qiu, Jin; Zhang, Nannan; Waterman, Scott R.; Uzel, Gulbu; Williamson, Peter R.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
   [Bernard, Amelie; Klionsky, Daniel J.] Univ Michigan, Inst Life Sci, Ann Arbor, MI 48109 USA.
   [Vural, Ali; Kehrl, John H.] NIAID, Lab Immunoregulat, NIH, Bethesda, MD 20892 USA.
   [Blewett, Nathan H.; Maraia, Richard J.] NICHHD, Intramural Res Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
   [Myers, Timothy G.] NIAID, Genom Technol Sect, Res Technol Branch, NIH, Bethesda, MD 20892 USA.
RP Williamson, PR (reprint author), NIAID, Lab Clin Infect Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM williamsonpr@mail.nih.gov
FU NIGMS NIH HHS [R01 GM053396, GM053396]
NR 6
TC 1
Z9 1
U1 3
U2 7
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1554-8627
EI 1554-8635
J9 AUTOPHAGY
JI Autophagy
PD DEC
PY 2015
VL 11
IS 12
BP 2390
EP 2392
DI 10.1080/15548627.2015.1091142
PG 3
WC Cell Biology
SC Cell Biology
GA DA4XO
UT WOS:000367806300029
PM 26569496
ER

PT J
AU Lewis, DEA
   Adhya, S
AF Lewis, Dale E. A.
   Adhya, Sankar
TI Molecular Mechanisms of Transcription Initiation at gal Promoters and
   their Multi-Level Regulation by GalR, CRP and DNA Loop
SO BIOMOLECULES
LA English
DT Review
DE activation; repression; DNA looping; transcription; galactose operon
ID AMP RECEPTOR PROTEIN; COLI GALACTOSE OPERON; OPEN COMPLEX-FORMATION;
   POLYMERASE ALPHA-SUBUNIT; CAP-DEPENDENT PROMOTERS; GENE ACTIVATOR
   PROTEIN; HISTONE-LIKE PROTEINS; ESCHERICHIA-COLI; RNA-POLYMERASE;
   CYCLIC-AMP
AB Studying the regulation of transcription of the gal operon that encodes the amphibolic pathway of d-galactose metabolism in Escherichia coli discerned a plethora of principles that operate in prokaryotic gene regulatory processes. In this chapter, we have reviewed some of the more recent findings in gal that continues to reveal unexpected but important mechanistic details. Since the operon is transcribed from two overlapping promoters, P1 and P2, regulated by common regulatory factors, each genetic or biochemical experiment allowed simultaneous discernment of two promoters. Recent studies range from genetic, biochemical through biophysical experiments providing explanations at physiological, mechanistic and single molecule levels. The salient observations highlighted here are: the axiom of determining transcription start points, discovery of a new promoter element different from the known ones that influences promoter strength, occurrence of an intrinsic DNA sequence element that overrides the transcription elongation pause created by a DNA-bound protein roadblock, first observation of a DNA loop and determination its trajectory, and piggybacking proteins and delivering to their DNA target.
C1 [Lewis, Dale E. A.; Adhya, Sankar] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Lewis, DEA (reprint author), NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM lewisdal@mail.nih.gov; adhyas@mail.nih.gov
FU Intramural NIH HHS
NR 87
TC 1
Z9 1
U1 1
U2 3
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 2218-273X
J9 BIOMOLECULES
JI Biomolecules
PD DEC
PY 2015
VL 5
IS 4
BP 2782
EP 2807
DI 10.3390/biom5042782
PG 26
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA DA1DW
UT WOS:000367537500026
PM 26501343
ER

PT J
AU Gupta, S
   Yui, JC
   Xu, DH
   Fitzhugh, CD
   Clark, C
   Siddiqui, S
   Conrey, AK
   Kato, GJ
   Minniti, CP
AF Gupta, Sarthak
   Yui, Jennifer C.
   Xu, Dihua
   Fitzhugh, Courtney D.
   Clark, Caroline
   Siddiqui, Salahuddin
   Conrey, Anna K.
   Kato, Gregory J.
   Minniti, Caterina P.
TI Gout and sickle cell disease: not all pain is sickle cell pain
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Letter
DE inflammation; red blood cell disorders; sickle cell disease; gout;
   arthritis; pain
ID HYPERURICEMIA; ANEMIA
C1 [Gupta, Sarthak] NIAMSD, NIH, Bethesda, MD 20892 USA.
   [Yui, Jennifer C.; Xu, Dihua; Fitzhugh, Courtney D.; Clark, Caroline; Siddiqui, Salahuddin; Conrey, Anna K.; Minniti, Caterina P.] NHLBI, NIH, Bethesda, MD 20892 USA.
   [Kato, Gregory J.] Univ Pittsburg, Dept Med, Vasc Med Inst, Pittsburgh, PA USA.
RP Gupta, S (reprint author), NIAMSD, NIH, Bethesda, MD 20892 USA.
EM cminniti@montefiore.org
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
FU Intramural NIH HHS [Z99 HL999999]
NR 10
TC 2
Z9 2
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1048
EI 1365-2141
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD DEC
PY 2015
VL 171
IS 5
BP 872
EP 875
DI 10.1111/bjh.13433
PG 4
WC Hematology
SC Hematology
GA DA4AB
UT WOS:000367741400021
PM 25892648
ER

PT J
AU Cantor, D
AF Cantor, David
TI A History of Lung Cancer: The Recalcitrant Disease
SO BULLETIN OF THE HISTORY OF MEDICINE
LA English
DT Book Review
C1 [Cantor, David] NIH, Off Hist, Bethesda, MD 20892 USA.
RP Cantor, D (reprint author), NIH, Off Hist, Bldg 10, Bethesda, MD 20892 USA.
NR 1
TC 0
Z9 0
U1 1
U2 1
PU JOHNS HOPKINS UNIV PRESS
PI BALTIMORE
PA JOURNALS PUBLISHING DIVISION, 2715 NORTH CHARLES ST, BALTIMORE, MD
   21218-4363 USA
SN 0007-5140
EI 1086-3176
J9 B HIST MED
JI Bull. Hist. Med.
PD WIN
PY 2015
VL 89
IS 4
BP 836
EP 838
PG 3
WC Health Care Sciences & Services; History & Philosophy Of Science
SC Health Care Sciences & Services; History & Philosophy of Science
GA DA1LX
UT WOS:000367558400032
ER

PT J
AU Vedham, V
   Verma, M
   Mahabir, S
AF Vedham, Vidya
   Verma, Mukesh
   Mahabir, Somdat
TI Early-life exposures to infectious agents and later cancer development
SO CANCER MEDICINE
LA English
DT Review
DE Cancer; early life exposure; infectious agents; perinatal transmission
ID EPSTEIN-BARR-VIRUS; HEPATITIS-B VACCINATION; DNA-DAMAGE RESPONSE; HTLV-I
   INFECTION; MOTHER-TO-CHILD; HEPATOCELLULAR-CARCINOMA;
   HUMAN-PAPILLOMAVIRUS; NASOPHARYNGEAL CARCINOMA; BURKITTS-LYMPHOMA;
   IMMUNE-RESPONSES
AB There is a growing understanding that several infectious agents are acquired in early life and this is the reason why available vaccines target the new born, infants, and adolescents. Infectious agents are associated with cancer development and it is estimated that about 20% of the world's cancer burden is attributed to infectious agents. There is a growing evidence that certain infectious agents acquired in early life can give rise to cancer development, but estimates of the cancer burden from this early-life acquisition is unknown. In this article, we have selected five cancers (cervical, liver, Burkitt's lymphoma-leukemia, nasopharyngeal carcinoma, and adult T-cell leukemia-lymphoma) and examine their links to infectious agents (HPV, HBV, HCV, EBV, and HTLV-1) acquired in early life. For these agents, the acquisition in early life is from mother-to-child transmission, perinatal contact (with genital tract secretions, amniotic fluids, blood, and breast milk), saliva, sexual intercourse, and blood transfusion. We also discuss prevention strategies, address future directions, and propose mechanisms of action after a long latency period from the time of acquisition of the infectious agent in early life to cancer development.
C1 [Vedham, Vidya; Verma, Mukesh] NCI, Methods & Technol Branch, NIH, Rockville, MD 20850 USA.
   [Mahabir, Somdat] NCI, Environm Epidemiol Branch, Epidemiol & Genom Res Program, Div Canc Control & Populat Sci,NIH, Rockville, MD 20850 USA.
RP Mahabir, S (reprint author), NCI, Environm Epidemiol Branch, Epidemiol & Genom Res Program, Div Canc Control & Populat Sci,NIH, Room 4E112,9609 Med Ctr Dr, Rockville, MD 20850 USA.
EM mahabir@mail.nih.gov
NR 146
TC 3
Z9 4
U1 3
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD DEC
PY 2015
VL 4
IS 12
BP 1908
EP 1922
DI 10.1002/cam4.538
PG 15
WC Oncology
SC Oncology
GA DA5MI
UT WOS:000367846800014
PM 26377256
ER

PT J
AU Selker, HP
   Buse, JB
   Califf, RM
   Carter, R
   Cooper, DM
   Davis, J
   Ford, DE
   Galassetti, P
   Guay-Woodford, L
   Huggins, GS
   Kasper, A
   Kieburtz, K
   Kirby, A
   Klein, AK
   Kline, J
   Neill, RT
   Rape, M
   Reichgott, DJ
   Rojevsky, S
   Rosenthal, GE
   Rubinstein, EP
   Shepherd, A
   Stacy, M
   Terrin, N
   Wallace, M
   Welch, L
AF Selker, Harry P.
   Buse, John B.
   Califf, Robert M.
   Carter, Robert
   Cooper, Dan M.
   Davis, Jonathan
   Ford, Daniel E.
   Galassetti, Pietro
   Guay-Woodford, Lisa
   Huggins, Gordon S.
   Kasper, Amanda
   Kieburtz, Karl
   Kirby, Aaron
   Klein, Andreas K.
   Kline, Joel
   O' Neill, Robert T.
   Rape, Marie
   Reichgott, Douglas J.
   Rojevsky, Svetlana
   Rosenthal, Gary E.
   Rubinstein, Eric P.
   Shepherd, Amy
   Stacy, Mark
   Terrin, Norma
   Wallace, Mark
   Welch, Lisa
TI CTSA Consortium Consensus Scientific Review Committee (SRC) Working
   Group Report on the SRC Processes
SO CTS-CLINICAL AND TRANSLATIONAL SCIENCE
LA English
DT Article
DE translational research; clinical trials; outcomes research
AB Human research projects must have a scientifically valid study design, analytic plan, and be operationally feasible in order to be successfully completed and thus to have translational impact. To ensure this, institutions that conduct clinical research should have a scientific review process prior to submission to the Institutional Review Committee (IRB). This paper reports the Clinical and Translational Science Award (CTSA) Consortium Scientific Review Committee (SRC) Consensus Working Group's proposed framework for a SRC process. Recommendations are provided for institutional support and roles of CTSAs, multisite research, criteria for selection of protocols that should be reviewed, roles of committee members, application process, and committee process. Additionally, to support the SCR process effectively, and to ensure efficiency, the Working Group recommends information technology infrastructures and evaluation metrics to determine outcomes are provided.
C1 [Selker, Harry P.; Davis, Jonathan; Kirby, Aaron; Rojevsky, Svetlana; Shepherd, Amy; Terrin, Norma; Welch, Lisa] Tufts Med Ctr, Tufts Clin & Translat Sci Inst, Boston, MA 02111 USA.
   [Buse, John B.; Rape, Marie] Univ N Carolina, Translat & Clin Sci Inst, Chapel Hill, NC USA.
   [Califf, Robert M.; Stacy, Mark] Duke Univ, Duke Translat Med Inst, Durham, NC USA.
   [Carter, Robert] NIH, Bethesda, MD 20892 USA.
   [Cooper, Dan M.; Galassetti, Pietro] Univ Calif Irvine, Inst Clin & Translat Sci, Irvine, CA USA.
   [Ford, Daniel E.] Johns Hopkins Univ, Inst Clin & Translat Res, Baltimore, MD USA.
   [Guay-Woodford, Lisa; Kasper, Amanda] Clin & Translat Sci Inst Childrens Natl, Washington, DC USA.
   [Huggins, Gordon S.; Klein, Andreas K.; Reichgott, Douglas J.] Tufts Med Ctr, Boston, MA USA.
   [Kieburtz, Karl; Rubinstein, Eric P.] Univ Rochester, Med Ctr, Clin & Translat Sci Inst, Rochester, NY 14642 USA.
   [Kline, Joel; Rosenthal, Gary E.] Univ Iowa, Inst Clin & Translat Sci, Iowa City, IA USA.
   [O' Neill, Robert T.] US FDA, Silver Spring, MD USA.
   [Wallace, Mark] Univ Calif San Diego, Clin & Translat Res Inst, San Diego, CA 92103 USA.
RP Selker, HP (reprint author), Tufts Med Ctr, Tufts Clin & Translat Sci Inst, Boston, MA 02111 USA.
EM HSelker@tuftsmedicalcenter.org
FU National Institutes of Health Clinical and Translational Science Awards
   [UL1 TR001064]; University of North Carolina at Chapel Hill,
   Translational & Clinical Sciences Institute [1UL1TR001111]; Duke
   Translational Medicine Institute, Duke University, Institute for
   Clinical and Translational Science [UL1TR001117]; University of
   California, Irvine, Institute for Clinical and Translational Research
   [UL1TR000153]; Johns Hopkins University, Institute for Clinical &
   Translational Research [UL1TR001079]; Clinical and Translational Science
   Institute at Children's National Center for Translational Science
   [UL1TR000075]; University of Rochester Clinical and Translational
   Science Institute [UL1TR000042]; Institute for Clinical and
   Translational Science at the University of Iowa [U54TR001013]; Clinical
   and Translational Research Institute, University of California, San
   Diego [UL1TR000100]
FX This paper was supported by an administrative supplement award to the
   Tufts CTSI from the National Institutes of Health Clinical and
   Translational Science Awards (UL1 TR001064), with additional support
   from the Working Group's affiliated CTSAs. The affiliated CTSAs include:
   University of North Carolina at Chapel Hill, Translational & Clinical
   Sciences Institute (1UL1TR001111), Duke Translational Medicine
   Institute, Duke University, Institute for Clinical and Translational
   Science (UL1TR001117), University of California, Irvine, Institute for
   Clinical and Translational Research (UL1TR000153), Johns Hopkins
   University, Institute for Clinical & Translational Research
   (UL1TR001079), The Clinical and Translational Science Institute at
   Children's National Center for Translational Science (UL1TR000075),
   University of Rochester Clinical and Translational Science Institute
   (UL1TR000042), Institute for Clinical and Translational Science at the
   University of Iowa (U54TR001013), and Clinical and Translational
   Research Institute, University of California, San Diego (UL1TR000100).
NR 0
TC 0
Z9 0
U1 1
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1752-8054
EI 1752-8062
J9 CTS-CLIN TRANSL SCI
JI CTS-Clin. Transl. Sci.
PD DEC
PY 2015
VL 8
IS 6
BP 623
EP 631
DI 10.1111/cts.12306
PG 9
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA DA3DL
UT WOS:000367676600007
PM 26184433
ER

PT J
AU Begg, MD
   Bennett, LM
   Cicutto, L
   Gadlin, H
   Moss, M
   Tentler, J
   Schoenbaum, E
AF Begg, Melissa D.
   Bennett, L. Michelle
   Cicutto, Lisa
   Gadlin, Howard
   Moss, Marc
   Tentler, John
   Schoenbaum, Ellie
TI Graduate Education for the Future: New Models and Methods for the
   Clinical and Translational Workforce
SO CTS-CLINICAL AND TRANSLATIONAL SCIENCE
LA English
DT Article
DE clinical and translational research; education; pipeline; workforce;
   career development
ID INTERDISCIPLINARY RESEARCH; TEAM SCIENCE; SCHOLARS; COLLABORATION;
   FACULTY; MENTORS; SKILLS
AB This paper is the third in a five-part series on the clinical and translational science educational pipeline, and it focuses on strategies for enhancing graduate research education to improve skills for interdisciplinary team science. Although some of the most cutting edge science takes place at the borders between disciplines, it is widely perceived that advancements in clinical and translational science are hindered by the siloed efforts of researchers who are comfortable working in their separate domains, and reluctant to stray from their own discipline when conducting research. Without appropriate preparation for career success as members and leaders of interdisciplinary teams, talented scientists may choose to remain siloed or to leave careers in clinical and translational science all together, weakening the pipeline and depleting the future biomedical research workforce. To address this threat, it is critical to begin at what is perhaps the most formative moment for academics: graduate training. This paper focuses on designs for graduate education, and contrasts the methods and outcomes from traditional educational approaches with those skills perceived as essential for the workforce of the future, including the capacity for research collaboration that crosses disciplinary boundaries.
C1 [Begg, Melissa D.] Columbia Univ, Off Provost, New York, NY 10027 USA.
   [Bennett, L. Michelle] NCI, Ctr Res Strategy, Bethesda, MD 20892 USA.
   [Cicutto, Lisa] Univ Colorado, Clin Sci Program, Denver, CO 80202 USA.
   [Gadlin, Howard] NIH, Off Ombudsman, Bethesda, MD 20892 USA.
   [Moss, Marc] Univ Colorado, Colorado CTSI Educ Training & Career Dev Pillar, Aurora, CO USA.
   [Tentler, John] Univ Colorado, Colorado CTSI Educ Training & Career Dev Pillar, Program TL1, Aurora, CO USA.
   [Schoenbaum, Ellie] Albert Einstein Coll Med, Clin Res Training Program, Inst Clin & Translat Res, Bronx, NY 10467 USA.
RP Begg, MD (reprint author), Columbia Univ, Off Provost, New York, NY 10027 USA.
EM mdb3@columbia.edu
FU National Center for Advancing Translational Sciences, National
   Institutes of Health [UL1 TR000040, UL1 TR001073, UL1 TR001082]
FX This publication was supported in part by the National Center for
   Advancing Translational Sciences, National Institutes of Health, through
   Grant Numbers UL1 TR000040, UL1 TR001073, and UL1 TR001082.
NR 27
TC 0
Z9 0
U1 2
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1752-8054
EI 1752-8062
J9 CTS-CLIN TRANSL SCI
JI CTS-Clin. Transl. Sci.
PD DEC
PY 2015
VL 8
IS 6
BP 787
EP 792
DI 10.1111/cts.12359
PG 6
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA DA3DL
UT WOS:000367676600032
PM 26643714
ER

PT J
AU Telford, WG
AF Telford, William G.
TI Near-Ultraviolet Laser Diodes for Brilliant Ultraviolet Fluorophore
   Excitation
SO CYTOMETRY PART A
LA English
DT Article
DE flow cytometer; ultraviolet laser; near-ultraviolet laser diode; NUVLD;
   brilliant ultraviolet dye
ID HOECHST SIDE POPULATION; FLOW-CYTOMETRY; EXCITED FLUOROCHROMES; VIOLET
AB Although multiple lasers are now standard equipment on most modern flow cytometers, ultraviolet (UV) lasers (325-365 nm) remain an uncommon excitation source for cytometry. Nd:YVO4 frequency-tripled diode pumped solid-state lasers emitting at 355 nm are now the primary means of providing UV excitation on multilaser flow cytometers. Although a number of UV excited fluorochromes are available for flow cytometry, the cost of solid-state UV lasers remains prohibitively high, limiting their use to all but the most sophisticated multilaser instruments. The recent introduction of the brilliant ultraviolet (BUV) series of fluorochromes for cell surface marker detection and their importance in increasing the number of simultaneous parameters for high-dimensional analysis has increased the urgency of including UV sources in cytometer designs; however, these lasers remain expensive. Near-UV laser diodes (NUVLDs), a direct diode laser source emitting in the 370-380 nm range, have been previously validated for flow cytometric analysis of most UV-excited probes, including quantum nanocrystals, the Hoechst dyes, and 4',6-diamidino-2-phenylindole. However, they remain a little-used laser source for cytometry, despite their significantly lower cost. In this study, the ability of NUVLDs to excite the BUV dyes was assessed, along with their compatibility with simultaneous brilliant violet (BV) labeling. A NUVLD emitting at 375 nm was found to excite most of the available BUV dyes at least as well as a UV 355 nm source. This slightly longer wavelength did produce some unwanted excitation of BV dyes, but at sufficiently low levels to require minimal additional compensation. NUVLDs are compact, relatively inexpensive lasers that have higher power levels than the newest generation of small 355 nm lasers. They can, therefore, make a useful, cost-effective substitute for traditional UV lasers in multicolor analysis involving the BUV and BV dyes. Published 2015 Wiley Periodicals, Inc.
C1 [Telford, William G.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
RP Telford, WG (reprint author), NCI, Expt Transplantat & Immunol Branch, NIH, Bldg 10 CRC Room 3-3297 East,10 Ctr Dr, Bethesda, MD 20892 USA.
EM telfordw@mail.nih.gov
NR 16
TC 2
Z9 2
U1 1
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4922
EI 1552-4930
J9 CYTOM PART A
JI Cytom. Part A
PD DEC
PY 2015
VL 87A
IS 12
BP 1127
EP 1137
DI 10.1002/cyto.a.22686
PG 11
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA DA3BL
UT WOS:000367670800008
PM 25930008
ER

PT J
AU Smith-Trunova, S
   Prithviraj, R
   Spurrier, J
   Kuzina, I
   Gu, Q
   Giniger, E
AF Smith-Trunova, Svetlana
   Prithviraj, Ranjini
   Spurrier, Joshua
   Kuzina, Irina
   Gu, Qun
   Giniger, Edward
TI Cdk5 Regulates Developmental Remodeling of Mushroom Body Neurons in
   Drosophila
SO DEVELOPMENTAL DYNAMICS
LA English
DT Article
DE axon; dendrite; pruning; microtubules; proteasome; neurodegeneration
ID CYCLIN-DEPENDENT KINASE-5; UBIQUITIN-PROTEASOME SYSTEM; AXON
   DEGENERATION; WALLERIAN DEGENERATION; SYNAPTIC PLASTICITY; CENTRAL
   BRAIN; IN-VIVO; MECHANISMS; P35; DISTINCT
AB Background: During metamorphosis, axons and dendrites of the mushroom body (MB) in the Drosophila central brain are remodeled extensively to support the transition from larval to adult behaviors. Results: We show here that the neuronal cyclin-dependent kinase, Cdk5, regulates the timing and rate of mushroom body remodeling: reduced Cdk5 activity causes a delay in pruning of MB neurites, while hyperactivation accelerates it. We further show that Cdk5 cooperates with the ubiquitin-proteasome system in this process. Finally, we show that Cdk5 modulates the first overt step in neurite disassembly, dissolution of the neuronal tubulin cytoskeleton, and provide evidence that it also acts at additional steps of MB pruning. Conclusions: These data show that Cdk5 regulates the onset and extent of remodeling of the Drosophila MB. Given the wide phylogenetic conservation of Cdk5, we suggest that it is likely to play a role in developmental remodeling in other systems, as well. Moreover, we speculate that the well-established role of Cdk5 in neurodegeneration may involve some of the same cellular mechanisms that it uses during developmental remodeling. Developmental Dynamics 244:1550-1563, 2015. Published 2015. This article is a U.S. Government work and is in the public domain in the USA
C1 [Smith-Trunova, Svetlana; Prithviraj, Ranjini; Spurrier, Joshua; Kuzina, Irina; Gu, Qun; Giniger, Edward] NINDS, NIH, Bethesda, MD 20892 USA.
   [Spurrier, Joshua] Johns Hopkins Univ, NIH, Grad Partnership Program, Bethesda, MD USA.
RP Giniger, E (reprint author), NINDS, NIH, Bldg 35,Room 1C-1002,35 Convent Dr, Bethesda, MD 20892 USA.
EM ginigere@ninds.nih.gov
FU NIH/NINDS [Z01-NS003106]
FX Grant sponsor: NIH/NINDS; Grant number: Z01-NS003106
NR 45
TC 0
Z9 0
U1 2
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1058-8388
EI 1097-0177
J9 DEV DYNAM
JI Dev. Dyn.
PD DEC
PY 2015
VL 244
IS 12
BP 1550
EP 1563
DI 10.1002/DVDY.24350
PG 14
WC Anatomy & Morphology; Developmental Biology
SC Anatomy & Morphology; Developmental Biology
GA DA3FA
UT WOS:000367680900006
PM 26394609
ER

PT J
AU Damiano, D
AF Damiano, Diane
TI Muscle synergies: input or output variables for neural control?
SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY
LA English
DT Editorial Material
ID MOVEMENTS
C1 [Damiano, Diane] NIH, Dept Rehabil Med, Bethesda, MD 20892 USA.
RP Damiano, D (reprint author), NIH, Dept Rehabil Med, Bethesda, MD 20892 USA.
RI Damiano, Diane/B-3338-2010
OI Damiano, Diane/0000-0002-2770-5356
FU Intramural NIH HHS [Z99 CL999999]
NR 7
TC 1
Z9 1
U1 1
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0012-1622
EI 1469-8749
J9 DEV MED CHILD NEUROL
JI Dev. Med. Child Neurol.
PD DEC
PY 2015
VL 57
IS 12
BP 1091
EP 1092
DI 10.1111/dmcn.12843
PG 3
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA DA3GG
UT WOS:000367684600008
PM 26195185
ER

PT J
AU Gadalla, SM
   Andreotti, G
AF Gadalla, Shahinaz M.
   Andreotti, Gabriella
TI Polychlorinated Biphenyls and Cancer: Are Telomeres to Blame?
SO EBIOMEDICINE
LA English
DT Editorial Material
ID LENGTH
C1 [Gadalla, Shahinaz M.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Andreotti, Gabriella] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Gadalla, SM (reprint author), NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, NIH, 9609 Med Ctr Dr,Room 6E-534, Rockville, MD 20850 USA.
EM gadallas@mail.nih.gov
NR 10
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 2352-3964
J9 EBIOMEDICINE
JI EBioMedicine
PD DEC
PY 2015
VL 2
IS 12
BP 1856
EP 1857
DI 10.1016/j.ebiom.2015.12.011
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA DA1EC
UT WOS:000367538100012
PM 26844258
ER

PT J
AU Buckley, AW
   Scott, R
   Tyler, A
   Mahoney, JM
   Thurm, A
   Farmer, C
   Swedo, S
   Burroughs, SA
   Holmes, GL
AF Buckley, Ashura W.
   Scott, Rod
   Tyler, Anna
   Mahoney, J. Matthew
   Thurm, Audrey
   Farmer, Cristan
   Swedo, Susan
   Burroughs, Scott A.
   Holmes, Gregory L.
TI State-Dependent Differences in Functional Connectivity in Young Children
   With Autism Spectrum Disorder
SO EBIOMEDICINE
LA English
DT Article
DE Epilepsy; Power spectral analysis; Coherence; Pearson; Epileptiform; EEG
ID CORTICAL CONNECTIVITY; WORKING-MEMORY; EEG COHERENCE; BRAIN; SLEEP;
   RISK; FMRI; UNDERCONNECTIVITY; ADOLESCENTS; EPILEPSY
AB Background: While there is increasing evidence of altered brain connectivity in autism, the degree and direction of these alterations in connectivity and their uniqueness to autism has not been established. The aim of the present study was to compare connectivity in children with autism to that of typically developing controls and children with developmental delay without autism.
   Methods: We assessed EEG spectral power, coherence, phase lag, Pearson and partial correlations, and epileptiform activity during the awake, slow wave sleep, and REM sleep states in 137 children aged 2 to 6 years with autism (n=87), developmental delay without autism (n=21), or typical development (n=29).
   Findings: We found that brain connectivity, as measured by coherence, phase lag, and Pearson and partial correlations distinguished children with autism from both neurotypical and developmentally delayed children. In general, children with autism had increased coherence which was most prominent during slow wave sleep.
   Interpretation: Functional connectivity is distinctly different in children with autism compared to samples with typical development and developmental delay without autism. Differences in connectivity in autism are state and region related. In this study, children with autism were characterized by a dynamically evolving pattern of altered connectivity. Published by Elsevier B.V.
C1 [Buckley, Ashura W.; Thurm, Audrey; Farmer, Cristan; Swedo, Susan; Holmes, Gregory L.] NIMH, NIH, Bethesda, MD 20892 USA.
   [Scott, Rod; Tyler, Anna; Mahoney, J. Matthew; Burroughs, Scott A.] Univ Vermont, Coll Med, Dept Neurol Sci, Burlington, VT 05405 USA.
RP Buckley, AW (reprint author), NIMH, 10 Ctr Dr,Room 1C250, Bethesda, MD 20892 USA.
EM shu.buckley@nih.gov
FU Intramural NIH HHS
NR 55
TC 3
Z9 3
U1 5
U2 8
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 2352-3964
J9 EBIOMEDICINE
JI EBioMedicine
PD DEC
PY 2015
VL 2
IS 12
BP 1905
EP 1915
DI 10.1016/j.ebiom.2015.11.004
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA DA1EC
UT WOS:000367538100023
PM 26844269
ER

PT J
AU Petrovics, G
   Li, H
   Stumpel, T
   Tan, SH
   Young, D
   Katta, S
   Li, QY
   Ying, K
   Klocke, B
   Ravindranath, L
   Kohaar, I
   Chen, YM
   Ribli, D
   Grote, K
   Zou, H
   Cheng, J
   Dalgard, CL
   Zhang, SM
   Csabai, I
   Kagan, J
   Takeda, D
   Loda, M
   Srivastava, S
   Scherf, M
   Seifert, M
   Gaiser, T
   McLeod, DG
   Szallasi, Z
   Ebner, R
   Werner, T
   Sesterhenn, IA
   Freedman, M
   Dobi, A
   Srivastava, S
AF Petrovics, Gyorgy
   Li, Hua
   Stuempel, Tanja
   Tan, Shyh-Han
   Young, Denise
   Katta, Shilpa
   Li, Qiyuan
   Ying, Kai
   Klocke, Bernward
   Ravindranath, Lakshmi
   Kohaar, Indu
   Chen, Yongmei
   Ribli, Dezso
   Grote, Korbinian
   Zou, Hua
   Cheng, Joseph
   Dalgard, Clifton L.
   Zhang, Shimin
   Csabai, Istvan
   Kagan, Jacob
   Takeda, David
   Loda, Massimo
   Srivastava, Sudhir
   Scherf, Matthias
   Seifert, Martin
   Gaiser, Timo
   McLeod, David G.
   Szallasi, Zoltan
   Ebner, Reinhard
   Werner, Thomas
   Sesterhenn, Isabell A.
   Freedman, Matthew
   Dobi, Albert
   Srivastava, Shiv
TI A novel genomic alteration of LSAMP associates with aggressive prostate
   cancer in African American men
SO EBIOMEDICINE
LA English
DT Article
DE African American; Prostate cancer; Genome; LSAMP; ERG; PTEN
ID SOMATIC POINT MUTATIONS; ERG ONCOPROTEIN EXPRESSION; GENERATION
   SEQUENCING DATA; MOLECULAR DIFFERENCES; WIDE ASSOCIATION; COPY NUMBER;
   LANDSCAPE; CELLS; STRATIFICATION; CARCINOGENESIS
AB Evaluation of cancer genomes in global context is of great interest in light of changing ethnic distribution of the world population. We focused our study on men of African ancestry because of their disproportionately higher rate of prostate cancer (CaP) incidence and mortality. We present a systematic whole genome analyses, revealing alterations that differentiate African American (AA) and Caucasian American (CA) CaP genomes. We discovered a recurrent deletion on chromosome 3q13.31 centering on the LSAMP locus that was prevalent in tumors from AA men (cumulative analyses of 435 patients: whole genome sequence, 14; FISH evaluations, 101; and SNP array, 320 patients). Notably, carriers of this deletion experienced more rapid disease progression. In contrast, PTEN and ERG common driver alterations in CaP were significantly lower in AA prostate tumors compared to prostate tumors from CA. Moreover, the frequency of inter-chromosomal rearrangements was significantly higher in AA than CA tumors. These findings reveal differentially distributed somaticmutations in CaP across ancestral groups, which have implications for precision medicine strategies. (C) 2015 The Authors. Published by Elsevier B.V.
C1 [Petrovics, Gyorgy; Li, Hua; Tan, Shyh-Han; Young, Denise; Katta, Shilpa; Ying, Kai; Ravindranath, Lakshmi; Kohaar, Indu; Chen, Yongmei; McLeod, David G.; Dobi, Albert; Srivastava, Shiv] Uniformed Serv Univ Hlth Sci, Dept Surg, Ctr Prostate Dis Res, Bethesda, MD 20814 USA.
   [Petrovics, Gyorgy; Li, Hua; Tan, Shyh-Han; Young, Denise; Katta, Shilpa; Ying, Kai; Ravindranath, Lakshmi; Kohaar, Indu; Chen, Yongmei; McLeod, David G.; Dobi, Albert; Srivastava, Shiv] Walter Reed Natl Mil Med Ctr, Bethesda, MD 20814 USA.
   [Stuempel, Tanja; Klocke, Bernward; Grote, Korbinian; Scherf, Matthias; Seifert, Martin; Werner, Thomas] Genomatix Software GmbH, D-80335 Munchene, Germany.
   [Li, Qiyuan] Xiamen Univ, Coll Med, Xiamen 361102, Peoples R China.
   [Li, Qiyuan; Takeda, David; Loda, Massimo; Freedman, Matthew] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02215 USA.
   [Ribli, Dezso; Csabai, Istvan] Eotvos Lorand Univ, Dept Phys Complex Syst, H-1117 Budapest, Hungary.
   [Ribli, Dezso; Csabai, Istvan; Szallasi, Zoltan] Tech Univ Denmark, Dept Syst Biol, Ctr Biol Sequence Anal, DK-2800 Lyngby, Denmark.
   [Zou, Hua; Cheng, Joseph; Ebner, Reinhard] CytoTest Inc, Rockville, MD 20850 USA.
   [Dalgard, Clifton L.] Uniformed Serv Univ Hlth Sci, Collaborat Hlth Initiat Res Program, Dept Anat Physiol & Genet, Bethesda, MD 20814 USA.
   [Zhang, Shimin; Sesterhenn, Isabell A.] Joint Pathol Ctr, Genitourinary Pathol, Silver Spring, MD 20910 USA.
   [Kagan, Jacob; Srivastava, Sudhir] NCI, Canc Biomarkers Res Grp, Canc Prevent Div, Bethesda, MD 20892 USA.
   [Takeda, David; Loda, Massimo; Freedman, Matthew] Eli & Edythe L Broad Inst, Cambridge, MA USA.
   [Gaiser, Timo] Heidelberg Univ, Med Fak Mannheim, Univ Med Mannheim, Inst Pathol, D-68167 Mannheim, Germany.
   [McLeod, David G.] Walter Reed Natl Mil Med Ctr, Urol Serv, Bethesda, MD 20814 USA.
   [Szallasi, Zoltan] Harvard Univ, Sch Med, Harvard Mit Div Hlth Sci & Technol, Childrens Hosp Informat Program, Boston, MA 02115 USA.
   [Szallasi, Zoltan] Semmelweis Univ, Dept Pathol 2, Hungarian Acad Sci, Brain Metastasis Res Grp,MTA SE NAP, H-1091 Budapest, Hungary.
   [Werner, Thomas] Univ Michigan, Div Nephrol, Internal Med, Ann Arbor, MI 48109 USA.
   [Werner, Thomas] Univ Michigan, Ctr Computat Med & Bioinformat, Ann Arbor, MI 48109 USA.
RP Freedman, M (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02215 USA.
EM freedman@broadinstitute.org; adobi@cpdr.org; ssrivastava@cpdr.org
OI Tan, Shyh-Han/0000-0001-8250-7005; Csabai, Istvan/0000-0001-9232-9898
FU NCI NIH HHS [R01 CA162383, R01 CA162383-05]
NR 57
TC 7
Z9 7
U1 1
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 2352-3964
J9 EBIOMEDICINE
JI EBioMedicine
PD DEC
PY 2015
VL 2
IS 12
BP 1957
EP 1964
DI 10.1016/j.ebiom.2015.10.028
PG 8
WC Medicine, General & Internal
SC General & Internal Medicine
GA DA1EC
UT WOS:000367538100028
PM 26844274
ER

PT J
AU Mazet, JAK
   Wei, Q
   Zhao, GP
   Cummings, DAT
   Desmond, JS
   Rosenthal, J
   King, CH
   Cao, WC
   Chmura, AA
   Hagan, EA
   Zhang, SY
   Xiao, XM
   Xu, JG
   Shi, ZL
   Feng, F
   Liu, XP
   Pan, WQ
   Zhu, GJ
   Zuo, LY
   Daszak, P
AF Mazet, Jonna A. K.
   Wei, Qin
   Zhao, Guoping
   Cummings, Derek A. T.
   Desmond, James Stephen
   Rosenthal, Joshua
   King, Charles H.
   Cao, Wuchun
   Chmura, Aleksei A.
   Hagan, Emily A.
   Zhang, Shuyi
   Xiao, Xiangming
   Xu, Jianguo
   Shi, Zhengli
   Feng, Feng
   Liu, Xiuping
   Pan, Weiqing
   Zhu, Guangjian
   Zuo, Liyao
   Daszak, Peter
TI Joint China-US Call for Employing a Transdisciplinary Approach to
   Emerging Infectious Diseases
SO ECOHEALTH
LA English
DT Editorial Material
ID LAND-USE CHANGE; CLIMATE-CHANGE; EMERGENCE; HEALTH; LANDSCAPES; ECOLOGY
C1 [Mazet, Jonna A. K.] Univ Calif Davis, Sch Vet Med, Hlth Inst 1, Davis, CA 95616 USA.
   [Wei, Qin; Feng, Feng; Liu, Xiuping; Zuo, Liyao] Natl Nat Sci Fdn China, Beijing, Peoples R China.
   [Zhao, Guoping] Shanghai Inst Biol Sci, Shanghai, Peoples R China.
   [Cummings, Derek A. T.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
   [Desmond, James Stephen; Chmura, Aleksei A.; Hagan, Emily A.; Zhu, Guangjian; Daszak, Peter] EcoHlth Alliance, New York, NY USA.
   [Rosenthal, Joshua] NIH, Div Epidemiol & Populat Studies, Fogarty Int Ctr, New York, NY USA.
   [King, Charles H.] Case Western Reserve Univ, Cleveland, OH 44106 USA.
   [Cao, Wuchun] Acad Mil Med Sci, Beijing, Peoples R China.
   [Zhang, Shuyi] E China Normal Univ, Shanghai 200062, Peoples R China.
   [Xiao, Xiangming] Univ Oklahoma, Norman, OK 73019 USA.
   [Xu, Jianguo] Natl Inst Communicable Dis Control & Prevent, Beijing, Peoples R China.
   [Shi, Zhengli] Chinese Acad Sci, Wuhan Inst Virol, Wuhan, Peoples R China.
   [Pan, Weiqing] Second Mil Med Univ, Shanghai, Peoples R China.
RP Mazet, JAK (reprint author), Univ Calif Davis, Sch Vet Med, Hlth Inst 1, Davis, CA 95616 USA.
EM jkmazet@ucdavis.edu
NR 21
TC 1
Z9 1
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1612-9202
EI 1612-9210
J9 ECOHEALTH
JI EcoHealth
PD DEC
PY 2015
VL 12
IS 4
BP 555
EP 559
DI 10.1007/s10393-015-1060-1
PG 5
WC Biodiversity Conservation; Ecology; Environmental Sciences
SC Biodiversity & Conservation; Environmental Sciences & Ecology
GA DA2LW
UT WOS:000367627300003
PM 26646835
ER

PT J
AU Schwarzman, MR
   Ackerman, JM
   Dairkee, SH
   Fenton, SE
   Johnson, D
   Navarro, KM
   Osborne, G
   Rudel, RA
   Solomon, GM
   Zeise, L
   Janssen, S
AF Schwarzman, Megan R.
   Ackerman, Janet M.
   Dairkee, Shanaz H.
   Fenton, Suzanne E.
   Johnson, Dale
   Navarro, Kathleen M.
   Osborne, Gwendolyn
   Rudel, Ruthann A.
   Solomon, Gina M.
   Zeise, Lauren
   Janssen, Sarah
TI Screening for Chemical Contributions to Breast Cancer Risk: A Case Study
   for Chemical Safety Evaluation
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Review
ID MAMMARY-GLAND DEVELOPMENT; ESTROGEN-RECEPTOR-ALPHA; IN-UTERO;
   PROGESTERONE-RECEPTOR; ENDOCRINE DISRUPTORS; BISPHENOL-A;
   2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN TCDD; LACTATIONAL EXPOSURE; TOXCAST
   CHEMICALS; GENE-EXPRESSION
AB BACKGROUND: Current approaches to chemical screening, prioritization, and assessment are being reenvisioned, driven by innovations in chemical safety testing, new chemical regulations, and demand for information on human and environmental impacts of chemicals. To conceptualize these changes through the lens of a prevalent disease, the Breast Cancer and Chemicals Policy project convened an interdisciplinary expert panel to investigate methods for identifying chemicals that may increase breast cancer risk.
   METHODS: Based on a review of current evidence, the panel identified key biological processes whose perturbation may alter breast cancer risk. We identified corresponding assays to develop the Hazard Identification Approach for Breast Carcinogens (HIA-BC), a method for detecting chemicals that may raise breast cancer risk. Finally, we conducted a literature-based pilot test of the HIA-BC.
   RESULTS: The HIA-BC identifies assays capable of detecting alterations to biological processes relevant to breast cancer, including cellular and molecular events, tissue changes, and factors that alter susceptibility. In the pilot test of the HIA-BC, chemicals associated with breast cancer all demonstrated genotoxic or endocrine activity, but not necessarily both. Significant data gaps persist.
   CONCLUSIONS: This approach could inform the development of toxicity testing that targets mechanisms relevant to breast cancer, providing a basis for identifying safer chemicals. The study identified important end points not currently evaluated by federal testing programs, including altered mammary gland development, Her2 activation, progesterone receptor activity, prolactin effects, and aspects of estrogen receptor beta activity. This approach could be extended to identify the biological processes and screening methods relevant for other common diseases.
C1 [Schwarzman, Megan R.; Osborne, Gwendolyn] Univ Calif Berkeley, Sch Publ Hlth, Ctr Occupat & Environm Hlth, Berkeley, CA 94720 USA.
   [Ackerman, Janet M.; Rudel, Ruthann A.] Silent Spring Inst, Newton, MA USA.
   [Dairkee, Shanaz H.] Calif Pacific Med Ctr, Res Inst, San Francisco, CA USA.
   [Fenton, Suzanne E.] NIEHS, Div Natl Toxicol Program, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
   [Johnson, Dale] Univ Calif Berkeley, Dept Nutr Sci & Toxicol, Berkeley, CA 94720 USA.
   [Navarro, Kathleen M.] Univ Calif Berkeley, Dept Environm Hlth, Berkeley, CA 94720 USA.
   [Solomon, Gina M.] Calif Environm Protect Agcy, Sacramento, CA USA.
   [Zeise, Lauren] Calif Environm Protect Agcy, Off Environm Hlth Hazard Assessment, Sacramento, CA USA.
   [Janssen, Sarah] Univ Calif San Francisco, Div Occupat & Environm Med, San Francisco, CA 94143 USA.
   [Janssen, Sarah] NRDC, San Francisco, CA USA.
RP Schwarzman, MR (reprint author), 50 Univ Hall,7360, Berkeley, CA 94720 USA.
EM mschwarzman@berkeley.edu
FU California Breast Cancer Research Program; University of California
   Office of the President [15QB-8001]; Avon Foundation for Women
FX This work was funded by the California Breast Cancer Research Program,
   University of California Office of the President (grant # 15QB-8001),
   with partial support for J.M.A. and R.A.R. from a grant from Avon
   Foundation for Women.
NR 101
TC 4
Z9 4
U1 6
U2 18
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
   RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
EI 1552-9924
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD DEC
PY 2015
VL 123
IS 12
BP 1255
EP 1264
DI 10.1289/ehp.1408337
PG 10
WC Environmental Sciences; Public, Environmental & Occupational Health;
   Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
   Health; Toxicology
GA DA1WS
UT WOS:000367587000012
PM 26032647
ER

PT J
AU Verner, MA
   Loccisano, AE
   Morken, NH
   Yoon, M
   Wu, HL
   McDougall, R
   Maisonet, M
   Marcus, M
   Kishi, R
   Miyashita, C
   Chen, MH
   Hsieh, WS
   Andersen, ME
   Clewell, HJ
   Longnecker, MP
AF Verner, Marc-Andre
   Loccisano, Anne E.
   Morken, Nils-Halvdan
   Yoon, Miyoung
   Wu, Huali
   McDougall, Robin
   Maisonet, Mildred
   Marcus, Michele
   Kishi, Reiko
   Miyashita, Chihiro
   Chen, Mei-Huei
   Hsieh, Wu-Shiun
   Andersen, Melvin E.
   Clewell, Harvey J., III
   Longnecker, Matthew P.
TI Associations of Perfluoroalkyl Substances (PFAS) with Lower Birth
   Weight: An Evaluation of Potential Confounding by Glomerular Filtration
   Rate Using a Physiologically Based Pharmacokinetic Model (PBPK)
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
ID PERFLUOROOCTANOIC ACID EXPOSURE; EVIDENCE-BASED MEDICINE; FETAL-GROWTH;
   PERFLUORINATED COMPOUNDS; RENAL HEMODYNAMICS; HUMAN-PREGNANCY; SERUM;
   PFOA; CHEMICALS; HEALTH
AB BACKGROUND: Prenatal exposure to perfluoroalkyl substances (PFAS) has been associated with lower birth weight in epidemiologic studies. This association could be attributable to glomerular filtration rate (GFR), which is related to PFAS concentration and birth weight.
   OBJECTIVES: We used a physiologically based pharmacokinetic (PBPK) model of pregnancy to assess how much of the PFAS-birth weight association observed in epidemiologic studies might be attributable to GFR.
   METHODS: We modified a PBPK model to reflect the association of GFR with birth weight (estimated from three studies of GFR and birth weight) and used it to simulate PFAS concentrations in maternal and cord plasma. The model was run 250,000 times, with variation in parameters, to simulate a population. Simulated data were analyzed to evaluate the association between PFAS levels and birth weight due to GFR. We compared simulated estimates with those from a meta-analysis of epidemiologic data.
   RESULTS: The reduction in birth weight for each 1-ng/mL increase in simulated cord plasma for perfluorooctane sulfonate (PFOS) was 2.72g (95% CI: -3.40, -2.04), and for perfluorooctanoic acid (PFOA) was 7.13 g (95% CI: -8.46, -5.80); results based on maternal plasma at term were similar. Results were sensitive to variations in PFAS level distributions and the strength of the GFR-birth weight association. In comparison, our meta-analysis of epidemiologic studies suggested that each 1-ng/mL increase in prenatal PFOS and PFOA levels was associated with 5.00 g (95% CI: -21.66, -7.78) and 14.72 g (95% CI: -8.92, -1.09) reductions in birth weight, respectively.
   CONCLUSION: Results of our simulations suggest that a substantial proportion of the association between prenatal PFAS and birth weight may be attributable to confounding by GFR and that confounding by GFR may be more important in studies with sample collection later in pregnancy.
C1 [Verner, Marc-Andre] Harvard Univ, TH Chan Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
   [Verner, Marc-Andre] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden.
   [Loccisano, Anne E.; Yoon, Miyoung; Wu, Huali; Andersen, Melvin E.; Clewell, Harvey J., III] Hamner Inst Hlth Sci, Ctr Human Hlth Assessment, Res Triangle Pk, NC USA.
   [Morken, Nils-Halvdan] Univ Bergen, Dept Global Publ Hlth & Primary Care, Bergen, Norway.
   [Morken, Nils-Halvdan] Haukeland Hosp, Dept Obstet & Gynecol, N-5021 Bergen, Norway.
   [McDougall, Robin] Aegis Technol, Huntsville, AL USA.
   [Maisonet, Mildred] E Tennessee State Univ, Coll Publ Hlth, Biostat & Epidemiol Dept, Johnson City, TN 37614 USA.
   [Marcus, Michele] Emory Univ, Rollins Sch Publ Hlth, Dept Epidemiol, Atlanta, GA 30322 USA.
   [Kishi, Reiko; Miyashita, Chihiro] Hokkaido Univ, Ctr Environm & Hlth Sci, Sapporo, Hokkaido, Japan.
   [Chen, Mei-Huei; Hsieh, Wu-Shiun] Natl Taiwan Univ, Coll Med, Natl Taiwan Univ Hosp, Dept Pediat, Taipei 10764, Taiwan.
   [Longnecker, Matthew P.] NIEHS, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
RP Verner, MA (reprint author), Univ Montreal, Sch Publ Hlth, Dept Occupat & Environm Hlth, 2375 Chemin Cote St Catherine,Suite 4105, Montreal, PQ H3T 1A8, Canada.
EM verner.marcandre@gmail.com
OI Maisonet, Mildred/0000-0003-3561-2632; Yoon,
   Miyoung/0000-0002-3653-3488; Longnecker, Matthew/0000-0001-6073-5322
FU DuPont; 3M; Intramural Research Program of the National Institutes of
   Environmental Health Sciences (NIEHS), the National Institutes of Health
   (NIH)
FX This study was supported by grants from DuPont and 3M, and by the
   Intramural Research Program of the National Institutes of Environmental
   Health Sciences (NIEHS), the National Institutes of Health (NIH).
NR 47
TC 10
Z9 10
U1 8
U2 24
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
   RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
EI 1552-9924
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD DEC
PY 2015
VL 123
IS 12
BP 1317
EP 1324
DI 10.1289/ehp.1408837
PG 8
WC Environmental Sciences; Public, Environmental & Occupational Health;
   Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
   Health; Toxicology
GA DA1WS
UT WOS:000367587000020
PM 26008903
ER

PT J
AU Neychev, V
   Straughan, D
   Pacak, K
   Kebebew, E
AF Neychev, Vladimir
   Straughan, David
   Pacak, Karel
   Kebebew, Electron
TI Multidisciplinary management of locally advanced and widely metastatic
   paraganglioma in a patient with life-threatening compressive symptoms
SO HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND
   NECK
LA English
DT Article
DE paraganglioma; succinate dehydrogenase gene (SDHB); metastatic disease;
   compressive symptoms; management approach
ID NECK PARAGANGLIOMAS; PHEOCHROMOCYTOMA; HEAD; MUTATIONS; FEATURES; SDHB
AB Background. Patients presenting with locally advanced, metastatic paraganglioma with life-threatening compressive symptoms of critical anatomic structure pose a significant management challenge.
   Methods. We present a case of a 15-year-old patient with enlarging right neck mass causing dysphagia and respiratory compromise from near complete obstruction of the oropharynx.
   Results. Evaluation of the patient's family history led to the identification of a mutation in the succinate dehydrogenase subunit B (SDSD) gene (G725A). Laboratory and imaging workup revealed an 8.8 x 6.6 x 4.1 cm metabolically and biochemically active right neck mass, a tumor in the left para-aortic region, and multiple bony lesions consistent with widely metastatic disease. Multidisciplinary management included pre-operative clinical optimization, coil embolization, and palliative resection of the neck mass.
   Conclusion. Although the currently available treatment options for patients with advanced metastatic paraganglioma render no survival benefit, a multidisciplinary management approach aimed at relief of tumor-related symptoms and catecholamine excess should be undertaken. (C) 2015 Wiley Periodicals, Inc.
C1 [Neychev, Vladimir; Kebebew, Electron] NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
   [Straughan, David] NCI, Thorac & Gastrointestinal Oncol Branch, NIH, Bethesda, MD 20892 USA.
   [Pacak, Karel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Endocrinol & Genet, NIH, Bethesda, MD USA.
RP Kebebew, E (reprint author), Endocrine Oncol Branch EOB, Bldg 10-CRC,Room 4-5952,10 Ctr Dr, Bethesda, MD 20892 USA.
EM kebebewe@mail.nih.gov
FU Intramural Research Program of Center for Cancer Research, National
   Cancer Institute
FX Contract grant sponsor: This work was supported in part by the
   Intramural Research Program of the Center for Cancer Research, National
   Cancer Institute.
NR 12
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1043-3074
EI 1097-0347
J9 HEAD NECK-J SCI SPEC
JI Head Neck-J. Sci. Spec. Head Neck
PD DEC
PY 2015
VL 37
IS 12
BP E205
EP E208
DI 10.1002/hed.24069
PG 4
WC Otorhinolaryngology; Surgery
SC Otorhinolaryngology; Surgery
GA DA3CW
UT WOS:000367674600008
PM 25899001
ER

PT J
AU Lee, YS
   Filie, A
   Arthur, D
   Fojo, AT
   Jaffe, ES
AF Lee, Yi-Shan
   Filie, Armando
   Arthur, Diane
   Fojo, Antonio T.
   Jaffe, Elaine S.
TI Breast implant-associated anaplastic large cell lymphoma in a patient
   with Li-Fraumeni syndrome
SO HISTOPATHOLOGY
LA English
DT Letter
C1 [Lee, Yi-Shan; Filie, Armando; Arthur, Diane; Jaffe, Elaine S.] NCI, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Fojo, Antonio T.] NCI, Genitourinary Malignancies Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Lee, YS (reprint author), NCI, Pathol Lab, Ctr Canc Res, Bldg 10, Bethesda, MD 20892 USA.
FU Intramural NIH HHS [ZIA SC000550-34]
NR 10
TC 2
Z9 2
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0309-0167
EI 1365-2559
J9 HISTOPATHOLOGY
JI Histopathology
PD DEC
PY 2015
VL 67
IS 6
BP 925
EP 927
DI 10.1111/his.12737
PG 4
WC Cell Biology; Pathology
SC Cell Biology; Pathology
GA DA5CT
UT WOS:000367820500021
PM 25974645
ER

PT J
AU Elshal, MF
   Aldahlawi, AM
   Saadah, OI
   McCoy, JP
AF Elshal, Mohamed F.
   Aldahlawi, Alia M.
   Saadah, Omar I.
   McCoy, J. Philip
TI Reduced Dendritic Cells Expressing CD200R1 in Children with Inflammatory
   Bowel Disease: Correlation with Th17 and Regulatory T Cells
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE inflammatory bowel disease; ulcerative colitis; Crohn's disease;
   plasmacytoid dendritic cells; myeloid dendritic cells; CD200R1; CD200;
   TH17 and regulatory T cells
ID ULCERATIVE-COLITIS; CROHNS-DISEASE; ORAL TOLERANCE; PATHOGENESIS;
   ACTIVATION; AUTOIMMUNE; RECEPTOR; DIFFERENTIATION; MECHANISMS;
   INHIBITION
AB Loss of tolerance of the adaptive immune system towards indigenous flora contributes to the development of inflammatory bowel diseases (IBD). Defects in dendritic cell (DC)-mediated innate and adoptive immune responses are conceivable. The aim of this study was to investigate the expression of the inhibitory molecules CD200R1 and their ligand CD200 on DCs, to clarify the role of the DCs in the pathogenesis of IBD. Thirty-seven pediatric IBD patients (23 with Crohn's disease (CD) and 14 with ulcerative colitis (UC)) with mean age 13.25 +/- 2.9 years were included. Fourteen age-matched healthy pediatric volunteers (five males and nine females) served as a control group (HC). The percentage of CD11c(+) myeloid dendritic cells (mDCs) and CD123(+) plasmacytoid DCs (pDCs) expressing CD200R1 and CD200 were evaluated in peripheral blood using flow cytometry and were correlated with routine biochemical, serological markers, serum levels of cytokines and with the percentages of circulating regulatory T cells (Treg) and CD4(+) producing IL-17 (Th17). IBD patients showed a significant decrease in the percentage of pDCs and mDCs expressing CD200R1 compared to that of HC. Patients with UC showed increased expressions of the CD200 molecule on pDCs as compared to HC. DCs expressing CD200R1 were found to be correlated positively with Treg and negatively with TH17 and erythrocyte sedimentation rate (ESR). Our findings suggest that IBD is associated with dysregulation in the CD200R1/CD200 axis and that the decrease in DCs expressing CD200R1 may contribute to the imbalance of Th17 and Treg cells and in the pathogenesis of IBD.
C1 [Elshal, Mohamed F.] King Abdulaziz Univ, Fac Sci, Dept Biochem, Jeddah 21589, Saudi Arabia.
   [Elshal, Mohamed F.; Aldahlawi, Alia M.; Saadah, Omar I.; McCoy, J. Philip] King Abdulaziz Univ, Inflammatory Bowel Dis Res Grp, Jeddah 21589, Saudi Arabia.
   [Elshal, Mohamed F.] Sadat City Univ, Dept Mol Biol, Genet Engn & Biotechnol Res Inst, Sadat City 32897, Egypt.
   [Aldahlawi, Alia M.] King Abdulaziz Univ, Dept Biol Sci, Fac Sci, Jeddah 21589, Saudi Arabia.
   [Aldahlawi, Alia M.] King Abdulaziz Univ, Immunol Unit, King Fahd Med Res Ctr, Jeddah 21589, Saudi Arabia.
   [Saadah, Omar I.] King Abdulaziz Univ, Dept Pediat, Fac Med, Jeddah 21589, Saudi Arabia.
   [McCoy, J. Philip] NHLBI, Flow Cytometry Core Facil, NIH, Bethesda, MD 20892 USA.
RP Elshal, MF (reprint author), King Abdulaziz Univ, Fac Sci, Dept Biochem, Jeddah 21589, Saudi Arabia.
EM melshal@kau.edu.sa; alia008@hotmail.com; osaadah@kau.edu.sa;
   mccoyj@nhlbi.nih.gov
RI Genetic Engineering & Biotechnology, Research Institute /E-7221-2017;
   Faculty of, Sciences, KAU/E-7305-2017; Fac Sci,  KAU,  Biol Sci
   Dept/L-4228-2013
FU Deanship of Scientific Research at King Abdulaziz University, Jeddah,
   Saudi Arabia [RG/32/02]
FX The authors would like to express their sincere appreciation to the
   Deanship of Scientific Research at the King Abdulaziz University,
   Jeddah, Saudi Arabia, for funding this Research Group Project No.
   RG/32/02.
NR 51
TC 1
Z9 1
U1 0
U2 2
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD DEC
PY 2015
VL 16
IS 12
BP 28998
EP 29010
DI 10.3390/ijms161226143
PG 13
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
SC Biochemistry & Molecular Biology; Chemistry
GA DA1DD
UT WOS:000367535600064
PM 26690123
ER

PT J
AU O'Donohoe, PK
   Taylor, JG
AF O'Donohoe, P. K.
   Taylor, J. G.
TI MICRO RNA EXPRESSION AND VASO-OCCLUSIVE PAIN CRISES IN SICKLE CELL
   ANAEMIA
SO IRISH JOURNAL OF MEDICAL SCIENCE
LA English
DT Meeting Abstract
C1 [O'Donohoe, P. K.] Natl Univ Ireland Univ Coll Dublin, UCD Sch Med, Dublin 4, Ireland.
   [Taylor, J. G.] NHLBI, Bethesda, MD 20892 USA.
NR 2
TC 0
Z9 0
U1 1
U2 1
PU SPRINGER LONDON LTD
PI LONDON
PA 236 GRAYS INN RD, 6TH FLOOR, LONDON WC1X 8HL, ENGLAND
SN 0021-1265
EI 1863-4362
J9 IRISH J MED SCI
JI Irish J. Med. Sci.
PD DEC
PY 2015
VL 184
SU 12
MA 10
BP 554
EP 555
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA DA5LA
UT WOS:000367843400011
ER

PT J
AU Hasin, DS
   Saha, TD
   Kerridge, BT
   Goldstein, RB
   Chou, SP
   Zhang, HT
   Jung, J
   Pickering, RP
   Ruan, WJ
   Smith, SM
   Huang, BJ
   Grant, BF
AF Hasin, Deborah S.
   Saha, Tulshi D.
   Kerridge, Bradley T.
   Goldstein, Rise B.
   Chou, S. Patricia
   Zhang, Haitao
   Jung, Jeesun
   Pickering, Roger P.
   Ruan, W. June
   Smith, Sharon M.
   Huang, Boji
   Grant, Bridget F.
TI Prevalence of Marijuana Use Disorders in the United States Between
   2001-2002 and 2012-2013
SO JAMA PSYCHIATRY
LA English
DT Article
ID ALCOHOL-USE DISORDER; NATIONAL EPIDEMIOLOGIC SURVEY; INTERVIEW SCHEDULE
   AUDADIS; GENERAL-POPULATION SAMPLE; SUBSTANCE USE DISORDERS; CANNABIS
   CONTROL POLICY; SOCIAL STRESS MODEL; DRUG-USE DISORDERS;
   QUALITY-OF-LIFE; DSM-IV ALCOHOL
AB IMPORTANCE Laws and attitudes toward marijuana in the United States are becoming more permissive but little is known about whether the prevalence rates of marijuana use and marijuana use disorders have changed in the 21st century.
   OBJECTIVE To present nationally representative information on the past-year prevalence rates of marijuana use, marijuana use disorder, and marijuana use disorder among marijuana users in the US adult general population and whether this has changed between 2001-2002 and 2012-2013.
   DESIGN, SETTING, AND PARTICIPANTS Face-to-face interviews conducted in surveys of 2 nationally representative samples of US adults: the National Epidemiologic Survey on Alcohol and Related Conditions (data collected April 2001-April 2002; N = 43 093) and the National Epidemiologic Survey on Alcohol and Related Conditions-III (data collected April 2012-June 2013; N = 36 309). Data were analyzed March through May 2015.
   MAIN OUTCOMES AND MEASURES Past-year marijuana use and DSM-IV marijuana use disorder (abuse or dependence).
   RESULTS The past-year prevalence of marijuana use was 4.1% (SE, 0.15) in 2001-2002 and 9.5% (SE, 0.27) in 2012-2013, a significant increase (P < .05). Significant increases were also found across demographic subgroups (sex, age, race/ethnicity, education, marital status, income, urban/rural, and region). The past-year prevalence of DSM-IV marijuana use disorder was 1.5% (0.08) in 2001-2002 and 2.9% (SE, 0.13) in 2012-2013 (P < .05). With few exceptions, increases in the prevalence of marijuana use disorder between 2001-2002 and 2012-2013 were also statistically significant (P < .05) across demographic subgroups. However, the prevalence of marijuana use disorder among marijuana users decreased significantly from 2001-2002 (35.6%; SE, 1.37) to 2012-2013 (30.6%; SE, 1.04).
   CONCLUSIONS AND RELEVANCE The prevalence of marijuana use more than doubled between 2001-2002 and 2012-2013, and there was a large increase in marijuana use disorders during that time. While not all marijuana users experience problems, nearly 3 of 10 marijuana users manifested a marijuana use disorder in 2012-2013. Because the risk for marijuana use disorder did not increase among users, the increase in prevalence of marijuana use disorder is owing to an increase in prevalence of users in the US adult population. Given changing laws and attitudes toward marijuana, a balanced presentation of the likelihood of adverse consequences of marijuana use to policy makers, professionals, and the public is needed.
C1 [Hasin, Deborah S.] Columbia Univ, Coll Phys & Surg, Dept Psychiat, New York, NY USA.
   [Hasin, Deborah S.] Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA.
   [Hasin, Deborah S.] New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
   [Saha, Tulshi D.; Goldstein, Rise B.; Chou, S. Patricia; Zhang, Haitao; Jung, Jeesun; Pickering, Roger P.; Ruan, W. June; Smith, Sharon M.; Huang, Boji; Grant, Bridget F.] NIAAA, Lab Epidemiol & Biometry, Div Intramural Clin & Biol Res, NIH, Rockville, MD 20852 USA.
   [Kerridge, Bradley T.] Columbia Univ, Dept Epidemiol, Mailman Sch Publ Hlth, New York, NY USA.
RP Grant, BF (reprint author), NIAAA, Lab Epidemiol & Biometry, Div Intramural Clin & Biol Res, NIH, 5635 Fishers Ln,Room 3077, Rockville, MD 20852 USA.
EM bgrant@mail.nih.gov
OI Goldstein, Rise/0000-0002-9603-9473
FU National Institute on Alcohol Abuse and Alcoholism; National Institute
   on Drug Abuse [R01DA034244-01, F32DA0364431]; New York State Psychiatric
   Institute; intramural program, National Institute on Alcohol Abuse and
   Alcoholism, National Institutes of Health
FX The National Epidemiologic Survey on Alcohol and Related Conditions-III
   was sponsored by the National Institute on Alcohol Abuse and Alcoholism,
   with supplemental support from the National Institute on Drug Abuse.
   Support for this study was received from National Institute on Drug
   Abuse grant R01DA034244-01 and New York State Psychiatric Institute (Dr
   Hasin); National Institute on Drug Abuse grant F32DA0364431 (Dr
   Kerridge); and the intramural program, National Institute on Alcohol
   Abuse and Alcoholism, National Institutes of Health.
NR 88
TC 49
Z9 49
U1 8
U2 24
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-622X
EI 2168-6238
J9 JAMA PSYCHIAT
JI JAMA Psychiatry
PD DEC
PY 2015
VL 72
IS 12
BP 1235
EP 1242
DI 10.1001/jamapsychiatry.2015.1858
PG 8
WC Psychiatry
SC Psychiatry
GA DA1UY
UT WOS:000367582200016
PM 26502112
ER

PT J
AU Jha, S
   Wang, Z
   Laucis, N
   Bhattacharyya, T
AF Jha, Smita
   Wang, Zhong
   Laucis, Nicholas
   Bhattacharyya, Timothy
TI Trends in Media Reports, Oral Bisphosphonate Prescriptions, and Hip
   Fractures 1996-2012: An Ecological Analysis
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Article
DE OSTEOPOROSIS; FRACTURE PREVENTION; ANTIRESORPTIVES; GENERAL POPULATION
   STUDIES; EPIDEMIOLOGY; BISPHOSPHONATE
ID FEMORAL-SHAFT FRACTURES; MINERAL-RESEARCH; UNITED-STATES; OSTEOPOROSIS;
   RISK; BENEFITS; COVERAGE; CANADA; CANCER; RATES
AB Bisphosphonates are effective for the treatment of osteoporosis despite recent reports of safety concerns such as atypical femur fracture. We conducted an ecological analysis of relevant media reports, oral bisphosphonate use, and fracture outcomes in the United States. Trends in media reports and public interest of bisphosphonates were quantified using data from Google Trends. Data from the Medical Expenditure Panel Survey (MEPS) and the National Inpatient Sample (NIS) were used to estimate the trends in oral bisphosphonate use among patients aged 55 years and older and hospitalizations for intertrochanteric and subtrochanteric fractures, respectively. These trends in the prevalence of oral bisphosphonate use and the age-adjusted incidence rate of intertrochanteric and subtrochanteric fractures were examined from 1996 to 2012. A series of spikes in Internet search activity for alendronate (Fosamax) occurred between 2006 and 2010 immediately following media reports of safety concerns. Oral bisphosphonate use declined by greater than 50% between 2008 and 2012 (p < 0.001) after increasing use for more than a decade. The decline was more common in patients with lower education levels. Intertrochanteric hip fractures declined from 1996 through 2006 (p < 0.001) and continued to decline from 2008 to 2012 (p < 0.05). Subtrochanteric and diaphyseal fractures showed a steady and significant increase from 2002 to 2011 (p < 0.05). However, the incidence decreased from a peak of 30.5 per 100,000 in 2011 to 26.7 per 100,000 in 2012. The plateauing and subsequent decline in oral bisphosphonate use since 2006 coincided with reports of safety concerns of bisphosphonates, despite the fact that U.S. Food and Drug Administration (FDA) and American Society of Bone and Mineral Research (ASBMR) reports did not recommend any safety restrictions on their use. This decline in oral bisphosphonate use was followed by the decline in the incidence of subtrochanteric and diaphyseal fractures. (C) 2015 American Society for Bone and Mineral Research.
C1 [Jha, Smita] Natl Inst Child Hlth & Human Dev NICHD, NIH, Bethesda, MD USA.
   [Wang, Zhong; Laucis, Nicholas] Natl Inst Arthrit & Musculoskeletal & Skin Dis NI, Clin & Investigat Orthoped Surg, Intramural Res Program, NIH, Bethesda, MD USA.
   [Bhattacharyya, Timothy] Natl Inst Arthrit & Musculoskeletal & Skin Dis NI, NIH, Bethesda, MD USA.
RP Bhattacharyya, T (reprint author), NIAMS, NIH, 1 AMS Circle, Bethesda, MD 20892 USA.
EM timothy.bhattacharyya@nih.gov
FU National Institute of Arthritis and Musculoskeletal and Skin Diseases
   (NIAMS) of the National Institutes of Health (NIH)
FX This research was supported by the Intramural Research Program of the
   National Institute of Arthritis and Musculoskeletal and Skin Diseases
   (NIAMS) of the National Institutes of Health (NIH).
NR 31
TC 15
Z9 15
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0884-0431
EI 1523-4681
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD DEC
PY 2015
VL 30
IS 12
BP 2179
EP 2187
DI 10.1002/jbmr.2565
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA DA3JD
UT WOS:000367692100006
PM 26018247
ER

PT J
AU Forcina, GC
   Castro, A
   Bokesch, HR
   Spakowicz, DJ
   Legaspi, ME
   Kucera, K
   Villota, S
   Narvaez-Trujillo, A
   McMahon, JB
   Gustafson, KR
   Strobelt, SA
AF Forcina, Giovanni C.
   Castro, Amaya
   Bokesch, Heidi R.
   Spakowicz, Daniel J.
   Legaspi, Michelle E.
   Kucera, Kaury
   Villota, Stephany
   Narvaez-Trujillo, Alexandra
   McMahon, James B.
   Gustafson, Kirk R.
   Strobelt, Scott A.
TI Stelliosphaerols A and B, Sesquiterpene-Polyol Conjugates from an
   Ecuadorian Fungal Endophyte
SO JOURNAL OF NATURAL PRODUCTS
LA English
DT Article
ID NATURAL-PRODUCTS; DRUG DISCOVERY; LARGE PHYLOGENIES; MODELS; TOOL
AB Endophytic fungi are plant tissue-associated fungi that represent a rich resource of unexplored biological and chemical diversity. As part of an ongoing effort to characterize Amazon rainforest-derived endophytes, numerous fungi were isolated and cultured from plants collected in the Yasuni National Park in Ecuador. Of these samples, phylogenetic and morphological data revealed a previously undescribed fungus in the order Pleosporales that was cultured from the tropical tree Duroia hirsuta. Extracts from this fungal isolate displayed activity against Staphylococcus aureus and were thus subjected to detailed chemical studies. Two compounds with modest antibacterial activity were isolated, and their structures were elucidated using a combination of NMR spectroscopic analysis, LC-MS studies, and chemical degradation. These efforts led to the identification of stelliosphaerols A (1) and B (2), new sesquiterpene-polyol conjugates that are responsible, at least in part, for the S. aureus inhibitory activity of the fungal extract.
C1 [Forcina, Giovanni C.; Spakowicz, Daniel J.; Legaspi, Michelle E.; Kucera, Kaury; Strobelt, Scott A.] Yale Univ, Dept Mol Biophys & Biochem, New Haven, CT 06520 USA.
   [Castro, Amaya; Bokesch, Heidi R.; McMahon, James B.; Gustafson, Kirk R.] Natl Canc Inst, Ctr Canc Res, Mol Targets Lab, Frederick, MD 21702 USA.
   [Bokesch, Heidi R.] Leidos Biomed Res Inc, Frederick Natl Lab, Basic Sci Program, Frederick, MD 21702 USA.
   [Villota, Stephany; Narvaez-Trujillo, Alexandra] Pontificia Univ Catolica Ecuador, Lab Biotecnol Vegetal, Quito 17012184, Ecuador.
RP Gustafson, KR (reprint author), Natl Canc Inst, Ctr Canc Res, Mol Targets Lab, Frederick, MD 21702 USA.
EM gustafki@mail.nih.gov; strobel@yale.edu
FU HHMI Professorship; NSF [OISE 853408]; 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 thank the Ministerio del Ambiente of Ecuador for a collecting and
   research permit provided to S.A.S. We thank P. Vargus Nunez for help
   with host plant identification, D. Spakowicz for guidance with
   phylogenetic analysis, the Endophyte Collection Quito Catolica (CEQCA)
   for cataloging the microbial isolates, and S. Tarasov and M. Dyba
   (Biophysics Resource Core, Structural Biophysics Laboratory, CCR) for
   assistance with high-resolution mass spectrometry. This research was
   funded in part by an HHMI Professorship and NSF grant OISE 853408
   awarded to S.A.S. It was also supported by the Intramural Research
   Program of the NIH, National Cancer Institute, Center for Cancer
   Research, and 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 20
TC 0
Z9 0
U1 6
U2 11
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0163-3864
EI 1520-6025
J9 J NAT PROD
JI J. Nat. Prod.
PD DEC
PY 2015
VL 78
IS 12
BP 3005
EP 3010
DI 10.1021/acs.jnatprod.5b00749
PG 6
WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy
SC Plant Sciences; Pharmacology & Pharmacy
GA DA1NN
UT WOS:000367562600017
PM 26651879
ER

PT J
AU Talegawkar, SA
   Tanaka, T
   Maras, JE
   Ferrucci, L
   Tucker, KL
AF Talegawkar, S. A.
   Tanaka, T.
   Maras, J. E.
   Ferrucci, L.
   Tucker, K. L.
TI Validation of nutrient intake estimates derived using a
   semi-quantitative FFQ against 3 day diet records in the Baltimore
   Longitudinal Study of Aging
SO JOURNAL OF NUTRITION HEALTH & AGING
LA English
DT Article
DE Food frequency questionnaire; diet records; validation; Baltimore
   Longitudinal Study of Aging
ID FOOD FREQUENCY QUESTIONNAIRE; BODY-MASS INDEX; HISPANIC ADULTS;
   OLDER-ADULTS; VALIDITY; WOMEN; REPRODUCIBILITY; PATTERNS; FAT; MEN
AB Objective: To examine the relative validity of a multicultural FFQ used to derive nutrient intake estimates in a community dwelling cohort of younger and older men and women compared with those derived from 3 day (3d) diet records during the same time-frame. Design: Cross-sectional analyses. Setting: The Baltimore Longitudinal Study of Aging (BLSA) conducted in the Baltimore, MD and District of Columbia areas. Participants: A subset (n=468, aged 26 to 95 years (y), 47% female, 65% non-Hispanic white) from the BLSA, with complete data for nutrient estimates from a FFQ and 3d diet records. Measurements: Pearson's correlation coefficients (energy adjusted and de-attenuated) for intakes of energy and 26 nutrients estimated from the FFQ and the mean of 3d diet records were calculated in a cross-sectional analysis. Rankings of individuals based on FFQ for various nutrient intakes were compared to corresponding rankings based on the average of the 3d diet records. Bland Altman plots were examined for a visual representation of agreement between both assessment methods. All analyses were stratified by sex and age (above and below 65 y). Results: Median nutrient intake estimates tended to be higher from the FFQ compared to average 3d diet records. Energy adjusted and de-attenuated correlations between FFQ intake estimates and records ranged from 0.23 (sodium intake in men) to 0.81 (alcohol intake in women). The FFQ classified more than 70 percent of participants in either the same or adjacent quartile categories for all nutrients examined. Bland Altman plots demonstrated good agreement between the assessment methods for most nutrients. Conclusions: This FFQ provides reasonably valid estimates of dietary intakes of younger and older participants of the BLSA.
C1 [Talegawkar, S. A.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD 21205 USA.
   [Tanaka, T.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
   [Maras, J. E.] Northeastern Univ, Dept Hlth Sci, Boston, MA 02115 USA.
   [Tucker, K. L.] Univ Massachusetts, Coll Hlth Sci, Dept Clin Lab & Nutr Sci, Lowell, MA USA.
RP Talegawkar, SA (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD 21205 USA.
EM sameera.talegawkar@alumni.tufts.edu
NR 42
TC 1
Z9 1
U1 3
U2 6
PU SPRINGER FRANCE
PI PARIS
PA 22 RUE DE PALESTRO, PARIS, 75002, FRANCE
SN 1279-7707
EI 1760-4788
J9 J NUTR HEALTH AGING
JI J. Nutr. Health Aging
PD DEC
PY 2015
VL 19
IS 10
BP 994
EP 1002
DI 10.1007/s12603-015-0659-9
PG 9
WC Geriatrics & Gerontology; Nutrition & Dietetics
SC Geriatrics & Gerontology; Nutrition & Dietetics
GA DA3KU
UT WOS:000367696400005
PM 26624210
ER

PT J
AU Desai, CS
   Ning, HY
   Liu, K
   Reis, JP
   Gidding, SS
   Armstrong, A
   Lima, JAC
   Lloyd-Jones, DM
AF Desai, Chintan S.
   Ning, Hongyan
   Liu, Kiang
   Reis, Jared P.
   Gidding, Samuel S.
   Armstrong, Anderson
   Lima, Joao A. C.
   Lloyd-Jones, Donald M.
TI Cardiovascular Health in Young Adulthood and Association with Left
   Ventricular Structure and Function Later in Life: The Coronary Artery
   Risk Development in Young Adults Study
SO JOURNAL OF THE AMERICAN SOCIETY OF ECHOCARDIOGRAPHY
LA English
DT Article
DE Echocardiography; Cardiovascular health; Left ventricular mass
ID DIASTOLIC DYSFUNCTION; CARDIA; MASS; ECHOCARDIOGRAPHY; RECOMMENDATIONS;
   HYPERTENSION; PREVALENCE; COMMUNITY; GEOMETRY; BEHAVIOR
AB Background: The aim of this study was to determine the association between cardiovascular health (CVH) in young adulthood and left ventricular (LV) structure and function later in life.
   Methods: Participants from the Coronary Artery Risk Development in Young Adults study, which recruited black and white participants aged 18 to 30 years at baseline, were included; echocardiography was performed at year 25. CVH at year 0 was defined on the basis of blood pressure, total cholesterol, fasting glucose, body mass index, smoking status, diet, and physical activity. Two, 1, or 0 points were assigned to each component for ideal, intermediate, and poor levels of each component. Participants were stratified into CVH groups on the basis of point score: <= 8 (poor), 9 to 11 (intermediate), and 12 to 14 (ideal).
   Results: The distribution of CVH at year 0 was as follows: poor, n = 264 (9%); intermediate, n = 1,315 (47%); and ideal, n = 1,224 (44%). Individuals with ideal and intermediate CVH at year 0 had significantly lower LV end-diastolic volume and lower LV mass index at year 25. In participants with ideal and intermediate CVH, the multivariate-adjusted odds ratios for diastolic dysfunction at year 25 was 0.52 (95% CI, 0.37-0.73) and 0.63 (95% CI, 0.46-0.83), respectively, compared with participants with poor CVH. Participants with ideal and intermediate CVH had significantly lower odds for LV hypertrophy; the LV mass index was 5.3 to 8.7 g/m(2.7) lower (P <.001 for both) than in participants with poor CVH.
   Conclusion: Greater levels of CVH in young adulthood are associated with lower LV mass and lower risk for diastolic dysfunction 25 years later. (J Am Soc Echocardiogr 2015; 28: 1452-61.)
C1 [Desai, Chintan S.; Armstrong, Anderson; Lima, Joao A. C.] Johns Hopkins Univ Hosp, Div Cardiol, Baltimore, MD 21287 USA.
   [Ning, Hongyan; Liu, Kiang; Lloyd-Jones, Donald M.] Northwestern Univ, Dept Prevent Med, Feinberg Sch Med, Chicago, IL 60611 USA.
   [Reis, Jared P.] NHLBI, Bethesda, MD 20892 USA.
   [Gidding, Samuel S.] Thomas Jefferson Med Ctr, Philadelphia, PA USA.
RP Lloyd-Jones, DM (reprint author), Northwestern Univ, Clin & Translat Sci Inst, Feinberg Sch Med, 680 N Lake Shore Dr,Suite 1400, Chicago, IL 60611 USA.
EM dlj@northwestern.edu
FU National Heart, Lung, and Blood Institute [N01-HC95095, N01-HC48047];
   University of Minnesota [N01-HC48048]; Northwestern University
   [N01-HC48049]; Kaiser Foundation Research Institute [N01-HC48050];
   National Institutes of Health [T32 HL 69771-8]
FX The Coronary Artery Risk Development in Young Adults study was conducted
   and supported by the National Heart, Lung, and Blood Institute in
   collaboration with the University of Alabama at Birmingham (grants
   N01-HC95095 and N01-HC48047), the University of Minnesota (grant
   N01-HC48048), Northwestern University (grant N01-HC48049), and the
   Kaiser Foundation Research Institute (grant N01-HC48050). Dr Desai was
   supported by National Institutes of Health grant T32 HL 69771-8.
NR 27
TC 3
Z9 3
U1 1
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0894-7317
J9 J AM SOC ECHOCARDIOG
JI J. Am. Soc. Echocardiogr.
PD DEC
PY 2015
VL 28
IS 12
BP 1452
EP 1461
DI 10.1016/j.echo.2015.07.026
PG 10
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA DA3DV
UT WOS:000367677700012
PM 26341123
ER

PT J
AU Okada, T
   Linguraru, MG
   Hori, M
   Summers, RM
   Tomiyama, N
   Sato, Y
AF Okada, Toshiyuki
   Linguraru, Marius George
   Hori, Masatoshi
   Summers, Ronald M.
   Tomiyama, Noriyuki
   Sato, Yoshinobu
TI Abdominal multi-organ segmentation from CT images using conditional
   shape-location and unsupervised intensity priors
SO MEDICAL IMAGE ANALYSIS
LA English
DT Article
DE Subject-specific priors; Partial least squares regression; Computational
   anatomy; Statistical shape model; Probabilistic atlas
ID AUTOMATIC LIVER SEGMENTATION; PROBABILISTIC ATLAS; COMPUTED-TOMOGRAPHY;
   MODEL; REGRESSION; AORTA; CUT
AB This paper addresses the automated segmentation of multiple organs in upper abdominal computed tomography (CT) data. The aim of our study is to develop methods to effectively construct the conditional priors and use their prediction power for more accurate segmentation as well as easy adaptation to various imaging conditions in CT images, as observed in clinical practice. We propose a general framework of multi-organ segmentation which effectively incorporates interrelations among multiple organs and easily adapts to various imaging conditions without the need for supervised intensity information. The features of the framework are as follows: (1) A method for modeling conditional shape and location (shape-location) priors, which we call prediction-based priors, is developed to derive accurate priors specific to each subject, which enables the estimation of intensity priors without the need for supervised intensity information. (2) Organ correlation graph is introduced, which defines how the conditional priors are constructed and segmentation processes of multiple organs are executed. In our framework, predictor organs, whose segmentation is sufficiently accurate by using conventional single-organ segmentation methods, are pre-segmented, and the remaining organs are hierarchically segmented using conditional shape-location priors. The proposed framework was evaluated through the segmentation of eight abdominal organs (liver, spleen, left and right kidneys, pancreas, gallbladder, aorta, and inferior vena cava) from 134 CT data from 86 patients obtained under six imaging conditions at two hospitals. The experimental results show the effectiveness of the proposed prediction-based priors and the applicability to various imaging conditions without the need for supervised intensity information. Average Dice coefficients for the liver, spleen, and kidneys were more than 92%, and were around 73% and 67% for the pancreas and gallbladder, respectively. (C) 2015 Elsevier B.V. All rights reserved.
C1 [Okada, Toshiyuki] Univ Tsukuba, Fac Med, Dept Surg, Tsukuba, Ibaraki 3058575, Japan.
   [Linguraru, Marius George] Childrens Natl Med Ctr, Sheikh Zayed Inst Pediat Surg Innovat, Washington, DC 20010 USA.
   [Linguraru, Marius George] George Washington Univ, Sch Med & Hlth Sci, Dept Radiol, Washington, DC 20037 USA.
   [Linguraru, Marius George] George Washington Univ, Sch Med & Hlth Sci, Dept Pediat, Washington, DC 20037 USA.
   [Hori, Masatoshi; Tomiyama, Noriyuki] Osaka Univ, Grad Sch Med, Dept Radiol, Suita, Osaka 5650871, Japan.
   [Summers, Ronald M.] NIH, Ctr Clin, Radiol & Imaging Sci, Bethesda, MD 20892 USA.
   [Sato, Yoshinobu] Nara Inst Sci & Technol, Grad Sch Informat Sci, Ikoma, Nara 6300192, Japan.
RP Sato, Y (reprint author), Nara Inst Sci & Technol, Grad Sch Informat Sci, 8916-5 Takayama Cho, Ikoma, Nara 6300192, Japan.
EM yoshi@is.naist.jp
OI Hori, Masatoshi/0000-0002-2523-3789
FU MEXT/JSPS [21103003, 26108004]; Intramural Research Program of the
   National Institutes of Health, Clinical Center
FX This work was partly supported by MEXT/JSPS Grand-in-Aid for Scientific
   Research on Innovative Areas No. 21103003 and No. 26108004, and the
   Intramural Research Program of the National Institutes of Health,
   Clinical Center, and a philanthropic gift from the Government of Abu
   Dhabi to Children's National Medical Center.
NR 59
TC 13
Z9 14
U1 4
U2 8
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1361-8415
EI 1361-8423
J9 MED IMAGE ANAL
JI Med. Image Anal.
PD DEC
PY 2015
VL 26
IS 1
BP 1
EP 18
DI 10.1016/j.media.2015.06.009
PG 18
WC Computer Science, Artificial Intelligence; Computer Science,
   Interdisciplinary Applications; Engineering, Biomedical; Radiology,
   Nuclear Medicine & Medical Imaging
SC Computer Science; Engineering; Radiology, Nuclear Medicine & Medical
   Imaging
GA DA0MI
UT WOS:000367490800001
PM 26277022
ER

PT J
AU Albright, RA
   Stabach, P
   Cao, WX
   Kavanagh, D
   Mullen, I
   Braddock, AA
   Covo, MS
   Tehan, M
   Yang, GX
   Cheng, ZL
   Bouchard, K
   Yu, ZX
   Thorn, S
   Wang, XN
   Folta-Stogniew, EJ
   Negrete, A
   Sinusas, AJ
   Shiloach, J
   Zubal, G
   Madri, JA
   De La Cruz, EM
   Braddock, DT
AF Albright, Ronald A.
   Stabach, Paul
   Cao, Wenxiang
   Kavanagh, Dillon
   Mullen, Isabelle
   Braddock, Alexander A.
   Covo, Mariel S.
   Tehan, Martin
   Yang, Guangxiao
   Cheng, Zhiliang
   Bouchard, Keith
   Yu, Zhao-Xue
   Thorn, Stephanie
   Wang, Xiangning
   Folta-Stogniew, Ewa J.
   Negrete, Alejandro
   Sinusas, Albert J.
   Shiloach, Joseph
   Zubal, George
   Madri, Joseph A.
   De La Cruz, Enrique M.
   Braddock, Demetrios T.
TI ENPP1-Fc prevents mortality and vascular calcifications in rodent model
   of generalized arterial calcification of infancy
SO NATURE COMMUNICATIONS
LA English
DT Article
ID PSEUDOXANTHOMA ELASTICUM; ECTOPIC MINERALIZATION; LIGHT-SCATTERING;
   PYROPHOSPHATE; MUTATIONS; ABCC6; MICE; PRESENTATIONS; DEFICIENCY;
   FAILURE
AB Diseases of ectopic calcification of the vascular wall range from lethal orphan diseases such as generalized arterial calcification of infancy (GACI), to common diseases such as hardening of the arteries associated with aging and calciphylaxis of chronic kidney disease (CKD). GACI is a lethal orphan disease in which infants calcify the internal elastic lamina of their medium and large arteries and expire of cardiac failure as neonates, while calciphylaxis of CKD is a ubiquitous vascular calcification in patients with renal failure. Both disorders are characterized by vascular Monckeburg's sclerosis accompanied by decreased concentrations of plasma inorganic pyrophosphate (PPi). Here we demonstrate that subcutaneous administration of an ENPP1-Fc fusion protein prevents the mortality, vascular calcifications and sequela of disease in animal models of GACI, and is accompanied by a complete clinical and biomarker response. Our findings have implications for the treatment of rare and common diseases of ectopic vascular calcification.
C1 [Albright, Ronald A.; Stabach, Paul; Kavanagh, Dillon; Mullen, Isabelle; Braddock, Alexander A.; Covo, Mariel S.; Tehan, Martin; Yang, Guangxiao; Madri, Joseph A.; Braddock, Demetrios T.] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06510 USA.
   [Cao, Wenxiang; De La Cruz, Enrique M.] Yale Univ, Dept Mol Biophys & Biochem, New Haven, CT 06520 USA.
   [Cheng, Zhiliang; Bouchard, Keith; Yu, Zhao-Xue] Alexion, Cheshire, CT 06410 USA.
   [Thorn, Stephanie; Wang, Xiangning; Sinusas, Albert J.] Yale Univ, Dept Med & Diagnost Radiol, Sch Med, New Haven, CT 06510 USA.
   [Folta-Stogniew, Ewa J.] Yale Univ, WM Keck Biotechnol Res Lab, Sch Med, New Haven, CT 06511 USA.
   [Negrete, Alejandro; Shiloach, Joseph] NIDDK, Biotechnol Core Lab, NIH, Rockville, MD 20852 USA.
   [Zubal, George] Z Concepts LLC, East Haven, CT 06512 USA.
RP Braddock, DT (reprint author), Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06510 USA.
EM demetrios.braddock@yale.edu
FU Alexion Pharmaceuticals Inc.; Connecticut Bioscience Innovation Fund;
   Yale University Department of Pathology; State of Connecticut under the
   Connecticut Bioscience Innovations Fund
FX These studies were financially supported by research grants from Alexion
   Pharmaceuticals Inc., The Connecticut Bioscience Innovation Fund, and
   Yale University Department of Pathology. DTB acknowledges helpful
   conversations with Michael Hodsdon (Eli Lily), Elias Lolis (Yale), and
   John Louis (NIH/NIDDK/Laboratory of Chemical Physics), and Dr Jon Morrow
   (Yale) for his enthusiastic support and encouragement throughout the
   course of this study. This material is based on work supported in part
   by the State of Connecticut under the Connecticut Bioscience Innovations
   Fund. Its contents are solely the responsibility of the authors and do
   not necessarily represent the official views of the State of Connecticut
   or Connecticut Innovations, Incorporated.
NR 39
TC 7
Z9 8
U1 2
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC
PY 2015
VL 6
AR 10006
DI 10.1038/ncomms10006
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA DA1PG
UT WOS:000367567100001
PM 26624227
ER

PT J
AU Alioto, TS
   Buchhalter, I
   Derdak, S
   Hutter, B
   Eldridge, MD
   Hovig, E
   Heisler, LE
   Beck, TA
   Simpson, JT
   Tonon, L
   Sertier, AS
   Patch, AM
   Jager, N
   Ginsbach, P
   Drews, R
   Paramasivam, N
   Kabbe, R
   Chotewutmontri, S
   Diessl, N
   Previti, C
   Schmidt, S
   Brors, B
   Feuerbach, L
   Heinold, M
   Grobner, S
   Korshunov, A
   Tarpey, PS
   Butler, AP
   Hinton, J
   Jones, D
   Menzies, A
   Raine, K
   Shepherd, R
   Stebbings, L
   Teague, JW
   Ribeca, P
   Giner, FC
   Beltran, S
   Raineri, E
   Dabad, M
   Heath, SC
   Gut, M
   Denroche, RE
   Harding, NJ
   Yamaguchi, TN
   Fujimoto, A
   Nakagawa, H
   Quesada, C
   Valdes-Mas, R
   Nakken, S
   Vodak, D
   Bower, L
   Lynch, AG
   Anderson, CL
   Waddell, N
   Pearson, JV
   Grimmond, SM
   Peto, M
   Spellman, P
   He, MH
   Kandoth, C
   Lee, S
   Zhang, J
   Letourneau, L
   Ma, S
   Seth, S
   Torrents, D
   Xi, L
   Wheeler, DA
   Lopez-Otin, C
   Campo, E
   Campbell, PJ
   Boutros, PC
   Puente, XS
   Gerhard, DS
   Pfister, SM
   McPherson, JD
   Hudson, TJ
   Schlesner, M
   Lichter, P
   Eils, R
   Jones, DTW
   Gut, IG
AF Alioto, Tyler S.
   Buchhalter, Ivo
   Derdak, Sophia
   Hutter, Barbara
   Eldridge, Matthew D.
   Hovig, Eivind
   Heisler, Lawrence E.
   Beck, Timothy A.
   Simpson, Jared T.
   Tonon, Laurie
   Sertier, Anne-Sophie
   Patch, Ann-Marie
   Jaeger, Natalie
   Ginsbach, Philip
   Drews, Ruben
   Paramasivam, Nagarajan
   Kabbe, Rolf
   Chotewutmontri, Sasithorn
   Diessl, Nicolle
   Previti, Christopher
   Schmidt, Sabine
   Brors, Benedikt
   Feuerbach, Lars
   Heinold, Michael
   Groebner, Susanne
   Korshunov, Andrey
   Tarpey, Patrick S.
   Butler, Adam P.
   Hinton, Jonathan
   Jones, David
   Menzies, Andrew
   Raine, Keiran
   Shepherd, Rebecca
   Stebbings, Lucy
   Teague, Jon W.
   Ribeca, Paolo
   Giner, Francesc Castro
   Beltran, Sergi
   Raineri, Emanuele
   Dabad, Marc
   Heath, Simon C.
   Gut, Marta
   Denroche, Robert E.
   Harding, Nicholas J.
   Yamaguchi, Takafumi N.
   Fujimoto, Akihiro
   Nakagawa, Hidewaki
   Quesada, Ctor
   Valdes-Mas, Rafael
   Nakken, Sigve
   Vodak, Daniel
   Bower, Lawrence
   Lynch, Andrew G.
   Anderson, Charlotte L.
   Waddell, Nicola
   Pearson, John V.
   Grimmond, Sean M.
   Peto, Myron
   Spellman, Paul
   He, Minghui
   Kandoth, Cyriac
   Lee, Semin
   Zhang, John
   Letourneau, Louis
   Ma, Singer
   Seth, Sahil
   Torrents, David
   Xi, Liu
   Wheeler, David A.
   Lopez-Otin, Carlos
   Campo, Elias
   Campbell, Peter J.
   Boutros, Paul C.
   Puente, Xose S.
   Gerhard, Daniela S.
   Pfister, Stefan M.
   McPherson, John D.
   Hudson, Thomas J.
   Schlesner, Matthias
   Lichter, Peter
   Eils, Roland
   Jones, David T. W.
   Gut, Ivo G.
TI A comprehensive assessment of somatic mutation detection in cancer using
   whole-genome sequencing
SO NATURE COMMUNICATIONS
LA English
DT Article
ID ACUTE MYELOID-LEUKEMIA; VARIANT ANALYSIS; POINT MUTATIONS; EXOME;
   ACCURATE; MEDULLOBLASTOMA; SIGNATURES; FRAMEWORK; CONSENSUS; ALIGNMENT
AB As whole-genome sequencing for cancer genome analysis becomes a clinical tool, a full understanding of the variables affecting sequencing analysis output is required. Here using tumour-normal sample pairs from two different types of cancer, chronic lymphocytic leukaemia and medulloblastoma, we conduct a benchmarking exercise within the context of the International Cancer Genome Consortium. We compare sequencing methods, analysis pipelines and validation methods. We show that using PCR-free methods and increasing sequencing depth to similar to 100 x shows benefits, as long as the tumour: control coverage ratio remains balanced. We observe widely varying mutation call rates and low concordance among analysis pipelines, reflecting the artefact-prone nature of the raw data and lack of standards for dealing with the artefacts. However, we show that, using the benchmark mutation set we have created, many issues are in fact easy to remedy and have an immediate positive impact on mutation detection accuracy.
C1 [Alioto, Tyler S.; Derdak, Sophia; Ribeca, Paolo; Giner, Francesc Castro; Beltran, Sergi; Raineri, Emanuele; Dabad, Marc; Heath, Simon C.; Gut, Marta; Gut, Ivo G.] BIST, Ctr Genom Regulat, CNAG CRG, Barcelona 08028, Spain.
   [Alioto, Tyler S.; Derdak, Sophia; Ribeca, Paolo; Giner, Francesc Castro; Beltran, Sergi; Raineri, Emanuele; Dabad, Marc; Heath, Simon C.; Gut, Marta; Gut, Ivo G.] Univ Pompeu Fabra, Barcelona 08002, Spain.
   [Buchhalter, Ivo; Jaeger, Natalie; Ginsbach, Philip; Drews, Ruben; Paramasivam, Nagarajan; Kabbe, Rolf; Schlesner, Matthias; Eils, Roland] German Canc Res Ctr, Div Theoret Bioinformat, D-69120 Heidelberg, Germany.
   [Buchhalter, Ivo; Hutter, Barbara; Schmidt, Sabine; Brors, Benedikt; Feuerbach, Lars] German Canc Res Ctr, Div Appl Bioinformat, D-69120 Heidelberg, Germany.
   [Eldridge, Matthew D.; Bower, Lawrence; Lynch, Andrew G.; Anderson, Charlotte L.] Univ Cambridge, Li Ka Shing Ctr, Canc Res, UK Cambridge Inst, Cambridge CB2 0RE, England.
   [Hovig, Eivind; Nakken, Sigve; Vodak, Daniel] Oslo Univ Hosp, Inst Canc Res, Dept Tumor Biol, N-0424 Oslo, Norway.
   [Hovig, Eivind] Univ Oslo, Dept Informat, N-0373 Oslo, Norway.
   [Heisler, Lawrence E.; Beck, Timothy A.; Simpson, Jared T.; Denroche, Robert E.; Harding, Nicholas J.; Yamaguchi, Takafumi N.; McPherson, John D.; Hudson, Thomas J.] Ontario Inst Canc Res, Toronto, ON M5G 0A3, Canada.
   [Tonon, Laurie; Sertier, Anne-Sophie; Boutros, Paul C.] Ctr Leon Berard, Synergie Lyon Canc Fdn, F-69373 Lyon, France.
   [Patch, Ann-Marie; Waddell, Nicola; Pearson, John V.; Grimmond, Sean M.] Univ Queensland, Inst Mol Biosci, Queensland Ctr Med Gen, Brisbane, Qld 4072, Australia.
   [Patch, Ann-Marie; Waddell, Nicola; Pearson, John V.] QIMR Berghofer Med Res Inst, Brisbane, Qld 4006, Australia.
   [Jaeger, Natalie] Stanford Univ, Dept Genet, Stanford, CA 94305 USA.
   [Chotewutmontri, Sasithorn; Diessl, Nicolle; Previti, Christopher] German Canc Res Ctr, Genome & Proteome Core Facil, D-69120 Heidelberg, Germany.
   [Heinold, Michael; Pfister, Stefan M.] Univ Heidelberg Hosp, Dept Pediat Hematol & Oncol, D-69120 Heidelberg, Germany.
   [Groebner, Susanne] Univ Heidelberg Hosp, Dept Neuropathol, D-69120 Heidelberg, Germany.
   [Korshunov, Andrey; Tarpey, Patrick S.; Butler, Adam P.; Hinton, Jonathan; Jones, David; Menzies, Andrew; Raine, Keiran; Shepherd, Rebecca; Stebbings, Lucy; Teague, Jon W.; Campbell, Peter J.] Wellcome Trust Sanger Inst, Cambridge CB10 1SA, England.
   [Fujimoto, Akihiro; Nakagawa, Hidewaki] RIKEN, Ctr Integrat Med Sci, Minato Ku, Tokyo 1088639, Japan.
   [Quesada, Ctor; Valdes-Mas, Rafael; Lopez-Otin, Carlos; Puente, Xose S.] Univ Oviedo IUOPA, Oviedo 33006, Spain.
   [Vodak, Daniel] Oslo Univ Hosp, Inst Canc Genet & Informat, Bioinformat Core Facil, N-0310 Oslo, Norway.
   [Anderson, Charlotte L.] Univ Melbourne, Victorian Life Sci Computat Initiat, Melbourne, Vic 3053, Australia.
   [Grimmond, Sean M.] Univ Glasgow, Inst Canc Sci, WolfsonWohl Canc Res Ctr, Glasgow G61 1QH, Lanark, Scotland.
   [Peto, Myron; Spellman, Paul] Oregon Hlth & Sci Univ, Knight Canc Inst, Portland, OR 97239 USA.
   [He, Minghui] BGI Shenzhen, Shenzhen 518083, Peoples R China.
   [Kandoth, Cyriac] Washington Univ, Genome Inst, St Louis, MO 63108 USA.
   [Lee, Semin; Zhang, John] Harvard Univ, Sch Med, Boston, MA 02115 USA.
   [Zhang, John; Seth, Sahil] MD Anderson Canc Ctr, Houston, TX 77030 USA.
   [Letourneau, Louis] McGill Univ, Montreal, PQ H3A 0G4, Canada.
   [Ma, Singer] Univ Calif Santa Cruz, Ctr Biomol Sci & Engn, Santa Cruz, CA 95064 USA.
   [Torrents, David] Barcelona Supercomputing Ctr, IRB BSC Joint Res Program Computat Biol, Barcelona 08034, Spain.
   [Xi, Liu; Wheeler, David A.] Baylor Coll Med, Human Genome Sequencing Ctr, Houston, TX 77030 USA.
   [Campo, Elias] Univ Barcelona, Hosp Clin, Dept Pathol, Inst Invest Biomed August Pi & Sunyer,Hematopatho, Barcelona 08036, Spain.
   [Boutros, Paul C.; McPherson, John D.; Hudson, Thomas J.] Univ Toronto, Dept Med Biophys, Toronto, ON M5G 1L7, Canada.
   [Gerhard, Daniela S.] NCI, Off Canc Gen, Bethesda, MD 20892 USA.
   [Pfister, Stefan M.] German Canc Res Ctr, Div Pediat Neurooncol, D-69120 Heidelberg, Germany.
   [Hudson, Thomas J.] Univ Toronto, Dept Mol Genet, Toronto, ON M5S 1A8, Canada.
   [Lichter, Peter] German Canc Res Ctr, Div Mol Genet, D-69120 Heidelberg, Germany.
   [Lichter, Peter; Eils, Roland] German Canc Res Ctr, Heidelberg Ctr Personalised Oncol DKFZ HIPO, Heidelberg, Germany.
   [Eils, Roland] Heidelberg Univ, Inst Pharm & Mol Biotechnol, D-69120 Heidelberg, Germany.
   [Eils, Roland] Heidelberg Univ, Bioquant Ctr, D-69120 Heidelberg, Germany.
   [Jones, David T. W.] German Canc Res Ctr, Div Pediat Neurooncol, D-69120 Heidelberg, Germany.
RP Gut, IG (reprint author), DNAnexus, 1975W El Camino Real,Suite 101, Mountain View, CA 94040 USA.
EM ivo.gut@cnag.crg.eu
RI Eils, Roland/B-6121-2009; Alioto, Tyler/K-7267-2015; Torrents,
   David/G-5785-2015; Dabad, Marc/M-9522-2015; Lee, Semin/S-2629-2016;
   McPherson, John/D-2633-2017; Quesada, Victor/B-6557-2014; Hovig,
   Eivind/H-2474-2011; Pfister, Stefan/F-6860-2013; Beltran,
   Sergi/I-3408-2015; Waddell, Nic/H-4929-2015; Grimmond, Sean/J-5304-2016;
   Lopez-Otin, Carlos/C-6657-2013; Brors, Benedikt/E-5620-2013; Pearson,
   John/F-2249-2011; Campo, elias/O-7192-2016; 
OI Eils, Roland/0000-0002-0034-4036; Alioto, Tyler/0000-0002-2960-5420;
   Castro-Giner, Francesc/0000-0001-6111-0754; Torrents,
   David/0000-0002-6086-9037; Vodak, Daniel/0000-0003-0015-6577;
   Suarez-Puente, Xose/0000-0001-9525-1483; Hutter,
   Barbara/0000-0002-9034-0329; Buchhalter, Ivo/0000-0003-0764-5832;
   Yamaguchi, Takafumi/0000-0003-1082-3871; Dabad,
   Marc/0000-0002-6094-747X; Lee, Semin/0000-0002-9015-6046; McPherson,
   John/0000-0001-8049-9347; Quesada, Victor/0000-0002-8398-3457; Hovig,
   Eivind/0000-0002-9103-1077; Pfister, Stefan/0000-0002-5447-5322;
   Beltran, Sergi/0000-0002-2810-3445; Grimmond, Sean/0000-0002-8102-7998;
   Lopez-Otin, Carlos/0000-0001-6964-1904; Brors,
   Benedikt/0000-0001-5940-3101; Pearson, John/0000-0003-0904-4598; Campo,
   elias/0000-0001-9850-9793; Drews, Ruben/0000-0001-7360-4970; Nakken,
   Sigve/0000-0001-8468-2050
FU European Commission Framework Programme 7 [FP7 Health-F42008-201418,
   262055, 261123]; ICGC-CLL through the Spanish Ministry of Science and
   Innovation (MICINN); Instituto de Salud Carlos III (ISCIII); Generalitat
   de Catalunya; PedBrain Tumor Project - German Cancer Aid [109252];
   German Federal Ministry of Education and Research (BMBF) [01KU1201A,
   0315416C, 01GS0883]; BMBF [01KU1001A, 01KU1002B, 031A537A, 031A537C];
   Ontario Institute for Cancer Research; Government of Ontario, Ministry
   of Research and Innovation; Canada Foundation for Innovation; Movember
   Foundation; Terry Fox Research Institute New Investigator Award; CIHR
   New Investigator Award; Genome Canada Large-Scale Applied Project
   Contract; French National Institute of Cancer (INCa); ABS4NGS ANR
   [ANR-11-BINF-0001-06]; RIKEN President's Fund; Cancer Research UK, the
   University of Cambridge; Torres Quevedo subprogramme (MICINN)
   [PTQ-12-05391]; Research Council of Norway [221580, 218241]; Norwegian
   Cancer Society [71220-PR-20060433]; Genome Canada; Prostate Cancer
   Canada; Hutchison-Whampoa Limited
FX We thank the DKFZ Genomics and Proteomics Core Facility and the OICR
   Genome Technologies Platform for provision of sequencing services.
   Financial support was provided by the consortium projects READNA under
   grant agreement FP7 Health-F42008-201418, ESGI under grant agreement
   262055, GEUVADIS under grant agreement 261123 of the European Commission
   Framework Programme 7, ICGC-CLL through the Spanish Ministry of Science
   and Innovation (MICINN), the Instituto de Salud Carlos III (ISCIII) and
   the Generalitat de Catalunya. Additional financial support was provided
   by the PedBrain Tumor Project contributing to the ICGC, funded by German
   Cancer Aid (109252) and by the German Federal Ministry of Education and
   Research (BMBF, grants #01KU1201A, MedSys #0315416C and NGFNplus
   #01GS0883), the BMBF-funded ICGC projects on early-onset prostate cancer
   and malignant lymphoma (#01KU1001A, #01KU1002B) and via the BMBF-funded
   de. NBI HD-HuB network (#031A537A, #031A537C); the Ontario Institute for
   Cancer Research to PCB and JDM through funding provided by the
   Government of Ontario, Ministry of Research and Innovation; Genome
   Canada; the Canada Foundation for Innovation and Prostate Cancer Canada
   with funding from the Movember Foundation (PCB). P.C.B. was also
   supported by a Terry Fox Research Institute New Investigator Award, a
   CIHR New Investigator Award and a Genome Canada Large-Scale Applied
   Project Contract. The Synergie Lyon Cancer platform has received support
   from the French National Institute of Cancer (INCa) and from the ABS4NGS
   ANR project (ANR-11-BINF-0001-06). The ICGC RIKEN study was supported
   partially by RIKEN President's Fund 2011, and the supercomputing
   resource for the RIKEN study was provided by the Human Genome Center,
   University of Tokyo. M.D.E., L.B., A.G.L. and C.L.A. were supported by
   Cancer Research UK, the University of Cambridge and Hutchison-Whampoa
   Limited. S.D. is supported by the Torres Quevedo subprogramme (MICINN)
   under grant agreement PTQ-12-05391. E.H. is supported by the Research
   Council of Norway under grant agreements 221580 and 218241 and by the
   Norwegian Cancer Society under grant agreement 71220-PR-20060433. We
   specially thank Jennifer Jennings for administrating the activity of the
   ICGC Verification Working Group and Anna Borrell for administrative
   support.
NR 40
TC 19
Z9 19
U1 2
U2 25
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC
PY 2015
VL 6
AR 10001
DI 10.1038/ncomms10001
PG 13
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA DA1TU
UT WOS:000367579200001
PM 26647970
ER

PT J
AU Dal Monte, O
   Costa, VD
   Noble, PL
   Murray, EA
   Averbeck, BB
AF Dal Monte, Olga
   Costa, Vincent D.
   Noble, Pamela L.
   Murray, Elisabeth A.
   Averbeck, Bruno B.
TI Amygdala lesions in rhesus macaques decrease attention to threat
SO NATURE COMMUNICATIONS
LA English
DT Article
ID FACIAL EXPRESSIONS; MONKEY AMYGDALA; NEURAL RESPONSES; CINGULATE CORTEX;
   EYE CONTACT; EMOTION; DAMAGE; FACES; FEAR; RECOGNITION
AB Evidence from animal and human studies has suggested that the amygdala plays a role in detecting threat and in directing attention to the eyes. Nevertheless, there has been no systematic investigation of whether the amygdala specifically facilitates attention to the eyes or whether other features can also drive attention via amygdala processing. The goal of the present study was to examine the effects of amygdala lesions in rhesus monkeys on attentional capture by specific facial features, as well as gaze patterns and changes in pupil dilation during free viewing. Here we show reduced attentional capture by threat stimuli, specifically the mouth, and reduced exploration of the eyes in free viewing in monkeys with amygdala lesions. Our findings support a role for the amygdala in detecting threat signals and in directing attention to the eye region of faces when freely viewing different expressions.
C1 [Dal Monte, Olga; Costa, Vincent D.; Noble, Pamela L.; Murray, Elisabeth A.; Averbeck, Bruno B.] NIMH, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA.
RP Averbeck, BB (reprint author), NIMH, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA.
EM averbeckbb@mail.nih.gov
OI Murray, Elisabeth/0000-0003-1450-1642; Costa,
   Vincent/0000-0002-5412-8945
FU National Institute of Mental Health Intramural Research Programme
FX We are grateful to the staff of the Veterinary Medicine and Resources
   Branch at National Institute of Mental Health, NIH, for offering their
   facilities and support during data collection. We thank Andrew Mitz,
   David Ide, and George Dold for their technical support, and Daniel Reed
   Lucas III for his help with animal training. This study was supported by
   the National Institute of Mental Health Intramural Research Programme
   (O.D.M., V.D.C., P.L.N., E.A.M. and B.B.A).
NR 49
TC 3
Z9 3
U1 3
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC
PY 2015
VL 6
AR 10161
DI 10.1038/ncomms10161
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA DA1RQ
UT WOS:000367573600001
PM 26658670
ER

PT J
AU Perlman, EJ
   Gadd, S
   Arold, ST
   Radhakrishnan, A
   Gerhard, DS
   Jennings, L
   Huff, V
   Auvil, JMG
   Davidsen, TM
   Dome, JS
   Meerzaman, D
   Hsu, CH
   Nguyen, C
   Anderson, J
   Ma, Y
   Mungall, AJ
   Moore, RA
   Marra, MA
   Mullighan, CG
   Ma, J
   Wheeler, DA
   Hampton, OA
   Gastier-Foster, JM
   Ross, N
   Smith, MA
AF Perlman, Elizabeth J.
   Gadd, Samantha
   Arold, Stefan T.
   Radhakrishnan, Anand
   Gerhard, Daniela S.
   Jennings, Lawrence
   Huff, Vicki
   Auvil, Jaime M. Guidry
   Davidsen, Tanja M.
   Dome, Jeffrey S.
   Meerzaman, Daoud
   Hsu, Chih Hao
   Cu Nguyen
   Anderson, James
   Ma, Yussanne
   Mungall, Andrew J.
   Moore, Richard A.
   Marra, Marco A.
   Mullighan, Charles G.
   Ma, Jing
   Wheeler, David A.
   Hampton, Oliver A.
   Gastier-Foster, Julie M.
   Ross, Nicole
   Smith, Malcolm A.
TI MLLT1 YEATS domain mutations in clinically distinctive Favourable
   Histology Wilms tumours
SO NATURE COMMUNICATIONS
LA English
DT Article
ID RNA-POLYMERASE-II; ELONGATION COMPLEX SEC; CHILDRENS ONCOLOGY GROUP;
   MIXED-LINEAGE LEUKEMIA; TRANSCRIPTIONAL ELONGATION; CHROMATIN
   MODIFICATION; H3K79 METHYLATION; GENETIC-VARIATION; CANCER; PROTEIN
AB Wilms tumour is an embryonal tumour of childhood that closely resembles the developing kidney. Genomic changes responsible for the development of the majority of Wilms tumours remain largely unknown. Here we identify recurrent mutations within Wilms tumours that involve the highly conserved YEATS domain of MLLT1 (ENL), a gene known to be involved in transcriptional elongation during early development. The mutant MLLT1 protein shows altered binding to acetylated histone tails. Moreover, MLLT1-mutant tumours show an increase in MYC gene expression and HOX dysregulation. Patients with MLLT1-mutant tumours present at a younger age and have a high prevalence of precursor intralobar nephrogenic rests. These data support a model whereby activating MLLT1 mutations early in renal development result in the development of Wilms tumour.
C1 [Perlman, Elizabeth J.; Gadd, Samantha; Jennings, Lawrence] Northwestern Univ, Ann & Robert H Lurie Childrens Hosp Chicago, Feinberg Sch Med, Dept Pathol, Chicago, IL 60611 USA.
   [Arold, Stefan T.; Radhakrishnan, Anand] King Abdullah Univ Sci & Technol, Dept Biochem & Mol Biol, Div Biol & Environm Sci & Engn, Computat Biosci Res Ctr, Thuwal 23955, Saudi Arabia.
   [Gerhard, Daniela S.; Auvil, Jaime M. Guidry; Davidsen, Tanja M.] NCI, Off Canc Gen, Bethesda, MD 20892 USA.
   [Huff, Vicki] Univ Texas MD Anderson Canc Ctr, Dept Genet, Houston, TX 77030 USA.
   [Dome, Jeffrey S.] Childrens Natl Med Ctr, Div Pediat Hematol Oncol, Dept Pediat, Washington, DC 20010 USA.
   [Meerzaman, Daoud; Hsu, Chih Hao; Cu Nguyen] NCI, NIH, Ctr Biomed Informat & Informat Technol, Bethesda, MD 20892 USA.
   [Anderson, James] Frontier Sci & Technol Res Fdn Inc, Madison, WI 53719 USA.
   [Ma, Yussanne; Mungall, Andrew J.; Moore, Richard A.; Marra, Marco A.] British Columbia Canc Agcy, Canadas Michael Smith Genome Sci Ctr, Vancouver, BC V5Z 4S6, Canada.
   [Mullighan, Charles G.; Ma, Jing] St Jude Childrens Res Hosp, Dept Pathol, Memphis, TN 38105 USA.
   [Wheeler, David A.; Hampton, Oliver A.] Ohio State Univ, Nationwide Childrens Hosp, Dept Pathol & Lab Med, Columbus, OH 43205 USA.
   [Gastier-Foster, Julie M.; Ross, Nicole] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
   [Gastier-Foster, Julie M.] Ohio State Univ, Coll Med, Dept Pathol, Columbus, OH 43205 USA.
   [Gastier-Foster, Julie M.] Ohio State Univ, Coll Med, Dept Pediat, Columbus, OH 43205 USA.
   [Smith, Malcolm A.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Perlman, EJ (reprint author), Northwestern Univ, Ann & Robert H Lurie Childrens Hosp Chicago, Feinberg Sch Med, Dept Pathol, 225 E Chicago Ave, Chicago, IL 60611 USA.
EM Eperlman@luriechildrens.org
RI Marra, Marco/B-5987-2008
FU NCI [U10 CA98543]; National Cancer Institute, US National Institutes of
   Health [HHSN261200800001E]; Data Coordinating Center; NIH [U10CA42326,
   U10CA98543, U24 CA114766, UO1CA88131]; IDP Foundation; American and
   Lebanese Syrian Associated Charities of St Jude; King Abdullah
   University of Science and Technology
FX The TARGET initiative is supported by NCI Grant U10 CA98543. Work
   performed under contracts from the National Cancer Institute, US
   National Institutes of Health within HHSN261200800001E include specimen
   processing (the Children's Oncology Group Biopathology Center (BPC),
   whole genomic sequencing (Complete Genomics, Inc), whole exomic
   sequencing (Baylor College of Medicine) and specific capture followed by
   sequencing (British Columbia Cancer Agency Genome Sciences Centre). The
   content of this publication does not necessarily reflect the views of
   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. The authors thank Patee Gesuwan and
   Leandro Hermida and the Data Coordinating Center for their support. We
   thank Karen Carty and Franceline Huser and for help and assistance with
   the recombinant protein production and DSF analysis. We thank the KAUST
   bioscience core lab for access to the MicroCal ITC200 microcalorimeter.
   We also thank the Clinical Applications of Core Technology Laboratory of
   the Hartwell Center for Bioinformatics and Biotechnology of St Jude
   Children's Research Hospital for performing the copy number analysis.
   The authors are grateful for the project management expertize of Karen
   Novik and Laura Monovich, and for the technical expertize of Patricia
   Beezhold, Donna Kersey, Debbie-Payne Turner, Mary McNulty and Yvonne
   Moyer. This work would not be possible without the dedication of all the
   experts within the many disciplines both at the local institutions and
   centrally within the Children's Oncology Group. They enable the
   coordination and accurate annotation required for the therapeutic and
   biology protocols that form the basis for the TARGET studies. Financial
   Support: NCI U10 CA98543 (E.J.P., J.M.G.-F. and M.A.M.); NIH U10CA42326
   (E.J.P.); U10CA98543 (J.S.D. and E.J.P.); U24 CA114766; UO1CA88131
   (E.J.P.), the IDP Foundation (E.J.P.), the American and Lebanese Syrian
   Associated Charities of St Jude (J.M. and C.M.) and the King Abdullah
   University of Science and Technology (S.T.A. and A.R.).
NR 64
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PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC
PY 2015
VL 6
AR 10013
DI 10.1038/ncomms10013
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA DA1PJ
UT WOS:000367567400001
PM 26635203
ER

PT J
AU Poldrack, RA
   Laumann, TO
   Koyejo, O
   Gregory, B
   Hover, A
   Chen, MY
   Gorgolewski, KJ
   Luci, J
   Joo, SJ
   Boyd, RL
   Hunicke-Smith, S
   Simpson, ZB
   Caven, T
   Sochat, V
   Shine, JM
   Gordon, E
   Snyder, AZ
   Adeyemo, B
   Petersen, SE
   Glahn, DC
   Mckay, DR
   Curran, JE
   Goring, HHH
   Carless, MA
   Blangero, J
   Dougherty, R
   Leemans, A
   Handwerker, DA
   Frick, L
   Marcotte, EM
   Mumford, JA
AF Poldrack, Russell A.
   Laumann, Timothy O.
   Koyejo, Oluwasanmi
   Gregory, Brenda
   Hover, Ashleigh
   Chen, Mei-Yen
   Gorgolewski, Krzysztof J.
   Luci, Jeffrey
   Joo, Sung Jun
   Boyd, Ryan L.
   Hunicke-Smith, Scott
   Simpson, Zack Booth
   Caven, Thomas
   Sochat, Vanessa
   Shine, James M.
   Gordon, Evan
   Snyder, Abraham Z.
   Adeyemo, Babatunde
   Petersen, Steven E.
   Glahn, David C.
   Mckay, D. Reese
   Curran, Joanne E.
   Goering, Harald H. H.
   Carless, Melanie A.
   Blangero, John
   Dougherty, Robert
   Leemans, Alexander
   Handwerker, Daniel A.
   Frick, Laurie
   Marcotte, Edward M.
   Mumford, Jeanette A.
TI Long-term neural and physiological phenotyping of a single human
SO NATURE COMMUNICATIONS
LA English
DT Article
ID HUMAN CONNECTOME PROJECT; SURFACE-BASED ANALYSIS; HUMAN BRAIN; NETWORK
   ANALYSIS; CEREBRAL-CORTEX; MOOD DISORDERS; TIME-SERIES; FMRI; SYSTEM;
   MRI
AB Psychiatric disorders are characterized by major fluctuations in psychological function over the course of weeks and months, but the dynamic characteristics of brain function over this timescale in healthy individuals are unknown. Here, as a proof of concept to address this question, we present the MyConnectome project. An intensive phenome-wide assessment of a single human was performed over a period of 18 months, including functional and structural brain connectivity using magnetic resonance imaging, psychological function and physical health, gene expression and metabolomics. A reproducible analysis workflow is provided, along with open access to the data and an online browser for results. We demonstrate dynamic changes in brain connectivity over the timescales of days to months, and relations between brain connectivity, gene expression and metabolites. This resource can serve as a testbed to study the joint dynamics of human brain and metabolic function over time, an approach that is critical for the development of precision medicine strategies for brain disorders.
C1 [Poldrack, Russell A.; Chen, Mei-Yen; Joo, Sung Jun; Boyd, Ryan L.; Mumford, Jeanette A.] Univ Texas Austin, Dept Psychol, Austin, TX 78712 USA.
   [Poldrack, Russell A.; Luci, Jeffrey] Univ Texas Austin, Dept Neurosci, Austin, TX 78712 USA.
   [Poldrack, Russell A.; Gregory, Brenda; Hover, Ashleigh; Luci, Jeffrey; Frick, Laurie] Univ Texas Austin, Imaging Res Ctr, Austin, TX 78712 USA.
   [Poldrack, Russell A.; Koyejo, Oluwasanmi; Gorgolewski, Krzysztof J.; Shine, James M.] Stanford Univ, Dept Psychol, Stanford, CA 94305 USA.
   [Laumann, Timothy O.; Gordon, Evan; Snyder, Abraham Z.; Adeyemo, Babatunde; Petersen, Steven E.] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA.
   [Hunicke-Smith, Scott] Univ Texas Austin, Genome Sequencing & Anal Facil, Austin, TX 78712 USA.
   [Simpson, Zack Booth; Marcotte, Edward M.] Univ Texas Austin, Ctr Syst & Synthet Biol, Austin, TX 78712 USA.
   [Caven, Thomas] Univ Med Ctr Brackenridge, Austin, TX 78701 USA.
   [Sochat, Vanessa] Stanford Univ, Biomed Informat Program, Stanford, CA 94305 USA.
   [Glahn, David C.; Mckay, D. Reese] Inst Living, Olin Neuropsychiat Res Ctr, Hartford, CT 06114 USA.
   [Glahn, David C.; Mckay, D. Reese] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT 06511 USA.
   [Curran, Joanne E.; Blangero, John] Univ Texas Rio Grande Valley, South Texas Diabet & Obes Inst, Sch Med, Brownsville, TX 78520 USA.
   [Goering, Harald H. H.; Carless, Melanie A.] Texas Biomed Res Inst, San Antonio, TX 78227 USA.
   [Dougherty, Robert] Stanford Univ, Ctr Neurobiol Imaging, Stanford, CA 94305 USA.
   [Leemans, Alexander] Univ Med Ctr Utrecht, Image Sci Inst, NL-3584 CX Utrecht, Netherlands.
   [Handwerker, Daniel A.] NIMH, Bethesda, MD 20892 USA.
   [Marcotte, Edward M.] Univ Texas Austin, Dept Mol Biosci, Austin, TX 78712 USA.
RP Poldrack, RA (reprint author), Univ Texas Austin, Dept Psychol, Austin, TX 78712 USA.
EM poldrack@stanford.edu
RI Leemans, Alexander/A-1784-2011; 
OI Gorgolewski, Krzysztof/0000-0003-3321-7583; Leemans,
   Alexander/0000-0002-9306-6126; Gordon, Evan/0000-0002-2276-5237;
   Poldrack, Russell/0000-0001-6755-0259
FU Texas Emerging Technology Fund; James S. McDonnell Foundation
   Collaborative Activity award; National Institutes of Health [MH100872,
   NS0046424, GM076536, OD009572, MH078143, MH078111, MH083824]; National
   Science Foundation [1131441, 1237975]; Netherlands Organisation for
   Scientific Research (VIDI Grant) [639.072.411]; Welch Foundation
   [F1515]; Australian National Health and Medical Research Council
   [GNT1072403]; William R. Hewlett Stanford Graduate Fellowship; Cancer
   Prevention Research Institute of Texas; Population Research Center at UT
   Austin [5R24HD042849]
FX This research was supported by the Texas Emerging Technology Fund (to
   Daniel Johnston, PI), James S. McDonnell Foundation Collaborative
   Activity award (to S.E.P.), National Institutes of Health (MH100872 to
   T.L., NS0046424 to S.E.P., GM076536 and OD009572 to E.M.M., MH078143 to
   D.G., MH078111 to J.B., MH083824 to D.G. and J.B.), National Science
   Foundation (1131441 to R.A.P., 1237975 to E.M.M.), Netherlands
   Organisation for Scientific Research (VIDI Grant 639.072.411 to A.L.),
   Welch Foundation (F1515 to E.M.M.), Australian National Health and
   Medical Research Council (GNT1072403 to J.M.S.), William R. Hewlett
   Stanford Graduate Fellowship (to V.S.) and the Cancer Prevention
   Research Institute of Texas (to E.M.M.). REDCap at UT is supported by
   5R24HD042849 awarded to the Population Research Center at UT Austin. The
   content is solely the responsibility of the authors and does not
   necessarily represent the official views of the National Institutes of
   Health. Thanks to Neeta Bakhta for assistance with blood draws and
   laboratory analyses, Terry Heckman and Margaret Lutz for processing of
   blood samples, Dhivya Arasappan for assistance with bioinformatics, Joan
   Balash for assistance with audiometry, and Jacy Anthis, Ashley Armenita,
   Adiel Carlo, Andrew Coulter, Jave Del Rosario, Dustin Fry, Kristie
   Garza, Kelly Jameson, Seorin Kim, Christina Leuker, Lakshya Nagar, Jacob
   Perez, Grace Shearrer and Sheila Zare for assistance with MRI scanning.
   Thanks to Kalanit Grill-Spector, Anthony Stigliani and Evelina Federenko
   for providing localizer task software. We also thank the following
   individuals for helpful discussion and assistance at various points in
   the project: Tim Behrens, Robert Bilder, Randy Buckner, Rui Chen, Eliza
   Congdon, Maude David, George Georgiou, Matt Glasser, Steve Hanson, Alex
   Huk, Saad Jbabdi, Michael Milham, Nolan Nichols, Tom Nichols, James
   Pennebaker, Katie Pollard, Rajeev Raizada, Tom Schonberg, Michael
   Snyder, Stamatios Sotiropoulos, Emily Tsang, David Van Essen, Gael
   Varoquaux and Michael Waskom.
NR 74
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U2 19
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC
PY 2015
VL 6
AR 8885
DI 10.1038/ncomms9885
PG 15
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA DA1TC
UT WOS:000367577400002
PM 26648521
ER

PT J
AU Tran, DT
   Masedunskas, A
   Weigert, R
   Ten Hagen, KG
AF Tran, Duy T.
   Masedunskas, Andrius
   Weigert, Roberto
   Ten Hagen, Kelly G.
TI Arp2/3-mediated F-actin formation controls regulated exocytosis in vivo
SO NATURE COMMUNICATIONS
LA English
DT Article
ID FUSED SECRETORY VESICLES; ARP2/3 COMPLEX; COMPENSATORY ENDOCYTOSIS;
   CHROMAFFIN CELLS; MUC2 MUCIN; MYOSIN-II; INTRAVITAL MICROSCOPY;
   SALIVARY-GLAND; DROSOPHILA; PROTEIN
AB The actin cytoskeleton plays crucial roles in many cellular processes, including regulated secretion. However, the mechanisms controlling F-actin dynamics in this process are largely unknown. Through 3D time-lapse imaging in a secreting organ, we show that F-actin is actively disassembled along the apical plasma membrane at the site of secretory vesicle fusion and re-assembled directionally on vesicle membranes. Moreover, we show that fusion pore formation and PIP2 redistribution precedes actin and myosin recruitment to secretory vesicle membranes. Finally, we show essential roles for the branched actin nucleators Arp2/3- and WASp in the process of secretory cargo expulsion and integration of vesicular membranes with the apical plasma membrane. Our results highlight previously unknown roles for branched actin in exocytosis and provide a genetically tractable system to image the temporal and spatial dynamics of polarized secretion in vivo.
C1 [Tran, Duy T.; Ten Hagen, Kelly G.] NIDCR, Dev Glycobiol Sect, NIH, Bethesda, MD 20892 USA.
   [Masedunskas, Andrius; Weigert, Roberto] NIDCR, Intracellular Membrane Trafficking Sect, NIH, Bethesda, MD 20892 USA.
   [Masedunskas, Andrius] Univ New S Wales, Sch Med Sci, Oncol Res Unit, Sydney, NSW 2052, Australia.
RP Ten Hagen, KG (reprint author), NIDCR, Dev Glycobiol Sect, NIH, Bldg 30,Room 426,30 Convent Dr,MSC 4370, Bethesda, MD 20892 USA.
EM Kelly.Tenhagen@nih.gov
FU Intramural Research Program of the NIDCR, National Institutes of Health
   [Z01-DE-000713]
FX We thank our colleagues for many helpful discussions. We thank Jia Guo
   for technical assistance. We also thank the Vienna Drosophila RNAi
   Center, the Bloomington Stock Center and the Developmental Studies
   Hybridoma Bank for fly stocks and other reagents. This work was
   supported by the Intramural Research Program of the NIDCR, National
   Institutes of Health (Z01-DE-000713 to K.G.T.H.).
NR 51
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PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC
PY 2015
VL 6
AR 10098
DI 10.1038/ncomms10098
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA DA1QG
UT WOS:000367569800004
PM 26639106
ER

PT J
AU Semba, RD
   Lam, M
   Sun, K
   Zhang, PB
   Schaumberg, DA
   Ferrucci, L
   Ping, PP
   Van Eyk, JE
AF Semba, Richard D.
   Lam, Maggie
   Sun, Kai
   Zhang, Pingbo
   Schaumberg, Debra A.
   Ferrucci, Luigi
   Ping, Peipei
   Van Eyk, Jennifer E.
TI Priorities and trends in the study of proteins in eye research,
   1924-2014
SO PROTEOMICS CLINICAL APPLICATIONS
LA English
DT Article
DE Biological processes; Eye; Human proteome project; Mouse; MS; Proteomics
ID HOMEOBOX-CONTAINING GENE; RETINAL GANGLION-CELLS; COMPLEMENT FACTOR-H;
   MACULAR DEGENERATION; MASS-SPECTROMETRY; STRUCTURAL BASIS; VEGF-A;
   MUTATIONS; PEDF; MECHANISMS
AB Purpose: To identify the proteins that are relevant to eye research and develop assays for the study of a set of these proteins.
   Experimental design: We conducted a bibliometric analysis by merging gene lists for human and mouse from the National Center for Biotechnology Information FTP site and combining them with PubMed references that were retrieved with the search terms "eye" [MeSH Terms] OR "eye" [All Fields] OR "eyes" [All Fields].
   Results: For human and mouse eye studies, respectively, the total number of publications was 13 525 and 23 895 and the total number of proteins was 4050 and 4717. For proteins in human andmouse eye studies, respectively, 88.7 and 81.7% had five or fewer citations. The top 50 most intensively studied proteins for human and mouse eye studies were generally in the areas of photoreceptors and phototransduction, inflammation, and angiogenesis, neurodevelopment, lens transparency, and cell-cycle and cellular processes. We proposed selected reaction monitoring assays that were developed in silico for the top fifty most intensively studied proteins in human and mouse eye research.
   Conclusions and clinical relevance: We conclude that scientists engaged in eye research tend to focus on the same proteins. Newer resources and tools in proteomics can expand the investigations to lesser-known proteins of the eye.
C1 [Semba, Richard D.; Sun, Kai; Zhang, Pingbo] Johns Hopkins Univ, Sch Med, Wilmer Eye Inst, Baltimore, MD 21287 USA.
   [Lam, Maggie; Ping, Peipei] Univ Calif Los Angeles, David Geffen Sch Med, Dept Physiol, Cardiac Prote & Signaling Lab, Los Angeles, CA 90095 USA.
   [Schaumberg, Debra A.] Univ Utah, Sch Med, Moran Eye Ctr, Ctr Translat Med, Salt Lake City, UT USA.
   [Schaumberg, Debra A.] Harvard Univ, TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
   [Ferrucci, Luigi] NIA, NIH, Baltimore, MD 21224 USA.
   [Van Eyk, Jennifer E.] Cedars Sinai Med Ctr, Inst Heart, Adv Clin BioSyst Res Inst, Los Angeles, CA 90048 USA.
   [Van Eyk, Jennifer E.] Cedars Sinai Med Ctr, Dept Med, Los Angeles, CA 90048 USA.
RP Semba, RD (reprint author), Johns Hopkins Univ, Sch Med, Wilmer Eye Inst, Smith Bldg M015,400 N Broadway, Baltimore, MD 21287 USA.
EM rdsemba@jhmi.edu
FU National Institutes of Health [R01 EY024596, R01 AG027012]; Joint King
   Khaled Eye Specialist Hospital; Wilmer Eye Institute Research Grant
   Program; Edward N. & Della L. Thome Memorial Foundation; Research to
   Prevent Blindness
FX This work was supported by the National Institutes of Health grants R01
   EY024596, R01 AG027012, the Joint King Khaled Eye Specialist Hospital
   and Wilmer Eye Institute Research Grant Program, the Edward N. & Della
   L. Thome Memorial Foundation, and Research to Prevent Blindness.
NR 66
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U1 0
U2 4
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA POSTFACH 101161, 69451 WEINHEIM, GERMANY
SN 1862-8346
EI 1862-8354
J9 PROTEOM CLIN APPL
JI Proteom. Clin. Appl.
PD DEC
PY 2015
VL 9
IS 11-12
SI SI
BP 1105
EP 1122
DI 10.1002/prca.201500006
PG 18
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA DA3UD
UT WOS:000367723600014
PM 26123431
ER

PT J
AU Heindel, JJ
   Newbold, RR
   Bucher, JR
   Camacho, L
   Delclos, KB
   Lewis, SM
   Vanlandingham, M
   Churchwell, MI
   Twaddle, NC
   McLellen, M
   Chidambaram, M
   Bryant, M
   Woodling, K
   da Costa, GG
   Ferguson, SA
   Flaws, J
   Howard, PC
   Walker, NJ
   Zoeller, RT
   Fostel, J
   Favaro, C
   Schug, TT
AF Heindel, Jerrold J.
   Newbold, Retha R.
   Bucher, John R.
   Camacho, Luisa
   Delclos, K. Barry
   Lewis, Sherry M.
   Vanlandingham, Michelle
   Churchwell, Mona I.
   Twaddle, Nathan C.
   McLellen, Michelle
   Chidambaram, Mani
   Bryant, Matthew
   Woodling, Kellie
   da Costa, Goncalo Gamboa
   Ferguson, Sherry A.
   Flaws, Jodi
   Howard, Paul C.
   Walker, Nigel J.
   Zoeller, R. Thomas
   Fostel, Jennifer
   Favaro, Carolyn
   Schug, Thaddeus T.
TI NIEHS/FDA CLARITY-BPA research program update
SO REPRODUCTIVE TOXICOLOGY
LA English
DT Review
DE Bisphenol A; NIEHS; FDA; NTP; CLARITY-BPA; Consortium; Endocrine
   disruptors
ID SPRAGUE-DAWLEY RATS; ESTROGEN-RECEPTOR EXPRESSION; BISPHENOL-A; ETHINYL
   ESTRADIOL; THYROID-HORMONES; DNA METHYLATION; ORAL-EXPOSURE; CELL
   BIOLOGY; FEMALE; TOXICITY
AB Bisphenol A (BPA) is a chemical used in the production of numerous consumer products resulting in potential daily human exposure to this chemical. The FDA previously evaluated the body of BPA toxicology data and determined that BPA is safe at current exposure levels. Although consistent with the assessment of some other regulatory agencies around the world, this determination of BPA safety continues to be debated in scientific and popular publications, resulting in conflicting messages to the public. Thus, the National Toxicology Program (NTP), National Institute of Environmental Health Sciences (NIEHS), and U.S. Food and Drug Administration (FDA) developed a consortium-based research program to link more effectively a variety of hypothesis-based research investigations and guideline-compliant safety testing with BPA. This collaboration is known as the Consortium Linking Academic and Regulatory Insights on BPA Toxicity (CLARITY-BPA). This paper provides a detailed description of the conduct of the study and a midterm update on progress of the CLARITY-BPA research program. Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
C1 [Heindel, Jerrold J.; Schug, Thaddeus T.] NIEHS, NIH, Div Extramural Res & Training, Res Triangle Pk, NC 27709 USA.
   [Newbold, Retha R.; Bucher, John R.; Walker, Nigel J.; Fostel, Jennifer] NIEHS, NIH, Div Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
   [Camacho, Luisa; Delclos, K. Barry; Vanlandingham, Michelle; Churchwell, Mona I.; Twaddle, Nathan C.; McLellen, Michelle; Chidambaram, Mani; Bryant, Matthew; Woodling, Kellie; da Costa, Goncalo Gamboa] USDA, Div Biochem Toxicol, Natl Ctr Toxicol Res, Jefferson, AR 72079 USA.
   [Ferguson, Sherry A.] USDA, Div Neurotoxicol, Natl Ctr Toxicol Res, Jefferson, AR 72079 USA.
   [Flaws, Jodi] Univ Illinois, Dept Comparat Biosci, Urbana, IL 61802 USA.
   [Lewis, Sherry M.; Howard, Paul C.] USDA, Off Sci Coordinat, Natl Ctr Toxicol Res, Jefferson, AR 72079 USA.
   [Zoeller, R. Thomas] Univ Massachusetts, Dept Biol, Amherst, MA 01003 USA.
   [Favaro, Carolyn] NIEHS, Team Vistronix, NTP Comp & User Support, NIH,Div Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
RP Heindel, JJ (reprint author), NIEHS, NIH, Div Extramural Res & Training, POB 12233, Res Triangle Pk, NC 27709 USA.
EM heindelj@niehs.nih.gov
RI Walker, Nigel/D-6583-2012
OI Walker, Nigel/0000-0002-9111-6855
FU National Toxicology Program; Food and Drug Administration; National
   Institute of Environmental Health Sciences/National Institutes of Health
   [FDA IAG: 224-12-0003, NIEHS IAG: AES12013]
FX The NCTR portion of the study was conducted under the auspices of the
   National Toxicology Program and funded by an Interagency agreement (JAG)
   between the Food and Drug Administration and the National Institute of
   Environmental Health Sciences/National Institutes of Health (FDA IAG:
   224-12-0003; NIEHS IAG: AES12013). We are grateful for the extraordinary
   efforts of the NCTR Animal Care, Diet Preparation, Information
   Technology, Microbiology, Pathology, Quality Assurance, and Veterinary
   Services staffs, the NIP Statistical Support Team of the Division of
   Bioinformatics and Biostatistics, as well as Ms. Kathy Carroll of the
   Office of Scientific Coordination, in the planning and conduct of this
   study. This manuscript was reviewed in accordance with USFDA and NIEHS
   procedures prior to submission. The opinions expressed in this paper do
   not necessarily reflect those of the USFDA.
NR 34
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U2 23
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0890-6238
J9 REPROD TOXICOL
JI Reprod. Toxicol.
PD DEC
PY 2015
VL 58
BP 33
EP 44
DI 10.1016/j.reprotox.2015.07.075
PG 12
WC Reproductive Biology; Toxicology
SC Reproductive Biology; Toxicology
GA DA1MJ
UT WOS:000367559600005
PM 26232693
ER

PT J
AU Song, K
   Huang, P
   Yi, CL
   Ning, B
   Hu, S
   Nie, LM
   Chen, XY
   Nie, ZH
AF Song, Kai
   Huang, Peng
   Yi, Chenglin
   Ning, Bo
   Hu, Song
   Nie, Liming
   Chen, Xiaoyuan
   Nie, Zhihong
TI Photoacoustic and Colorimetric Visualization of Latent Fingerprints
SO ACS NANO
LA English
DT Article
DE latent fingerprints; colorimetric imaging; photoacoustic imaging; block
   copolymer; gold nanoparticles
ID GOLD NANOPARTICLES; ELECTROCHEMILUMINESCENCE; IDENTIFICATION;
   FINGERMARKS; METABOLITES; THERAPY
AB There is a high demand on a simple, rapid, accurate, user-friendly, cost-effective, and nondestructive universal method for latent fingerprint (LFP) detection. Herein, we describe a combination imaging strategy for LFP visualization with high resolution using poly(styrene-alt-maleic anhydride)-b-polystyrene (PSMA-b-PS) functionalized gold nanoparticles (GNPs). This general approach integrates the merits of both colorimetric imaging and photoacoustic imaging. In comparison with the previous methods, our strategy is single-step and does not require the signal amplification by silver staining. The PSMA-b-PS functionalized GNPs have good stability, tunable color, and high affinity for universal secretions (proteins/polypeptides/amino acids), which makes our approach general and flexible for visualizing LFPs on different substrates (presumably with different colors) and from different people. Moreover, the unique optical property of GNPs enables the photoacoustic imaging of GNPs-deposited LFPs with high resolution. This allows observation of level 3 hyperfine features of LFPs such as the pores and ridge contours by photoacoustic imaging. This technique can potentially be used to identify chemicals within LFP residues. We believe that this dual-modality-imaging of LFPs will find widespread use in forensic investigations and medical diagnostics.
C1 [Song, Kai] Changchun Normal Univ, Sch Life Sci, Changchun 130032, Peoples R China.
   [Huang, Peng] Shenzhen Univ, Guangdong Key Lab Biomed Measurements & Ultrasoun, Dept Biomed Engn, Sch Med, Shenzhen 518060, Peoples R China.
   [Song, Kai; Yi, Chenglin; Nie, Zhihong] Univ Maryland, Dept Chem & Biochem, College Pk, MD 20742 USA.
   [Ning, Bo; Hu, Song] Univ Virginia, Dept Biomed Engn, Charlottesville, VA 22903 USA.
   [Huang, Peng; Nie, Liming; Chen, Xiaoyuan] Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed, NIH, Bethesda, MD 20892 USA.
RP Huang, P (reprint author), Shenzhen Univ, Guangdong Key Lab Biomed Measurements & Ultrasoun, Dept Biomed Engn, Sch Med, Shenzhen 518060, Peoples R China.
EM peng.huang@nih.gov; shawn.chen@nih.gov; znie@umd.edu
RI Nie, Zhihong/D-7495-2011; Huang, Peng/R-2480-2016; 
OI Nie, Zhihong/0000-0001-9639-905X; Huang, Peng/0000-0003-3651-7813; Ning,
   Bo/0000-0002-6006-5696
FU Shenzhen University; University of Maryland; National Natural Science
   Foundation of China [81401465, 51573096, 11204021, 81272987]; National
   Science Foundation [CHE-1505839]; Intramural Research Program (IRP) of
   the NIBIB/NIH
FX This work was supported by the startup funds from the Shenzhen
   University and University of Maryland, the National Natural Science
   Foundation of China (81401465, 51573096, 11204021, 81272987), the
   National Science Foundation (CHE-1505839) and the Intramural Research
   Program (IRP) of the NIBIB/NIH.
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U2 78
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1936-0851
EI 1936-086X
J9 ACS NANO
JI ACS Nano
PD DEC
PY 2015
VL 9
IS 12
BP 12344
EP 12348
DI 10.1021/acsnano.5b05629
PG 5
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
   Nanotechnology; Materials Science, Multidisciplinary
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA CZ7LE
UT WOS:000367280100085
PM 26528550
ER

PT J
AU Tian, Q
   Resnick, SM
   Ferrucci, L
   Studenski, SA
AF Tian, Qu
   Resnick, Susan M.
   Ferrucci, Luigi
   Studenski, Stephanie A.
TI Intra-individual lap time variation of the 400-m walk, an early mobility
   indicator of executive function decline in high-functioning older
   adults?
SO AGE
LA English
DT Article
DE Lap time variation; Executive function; Longitudinal study; Aging
ID MILD COGNITIVE IMPAIRMENT; GAIT SPEED; BODY-COMPOSITION; SLOWER GAIT;
   HEALTH ABC; VARIABILITY; ASSOCIATION; PERFORMANCE; DISEASE; POPULATION
AB Higher intra-individual lap time variation (LTV) of the 400-m walk is cross-sectionally associated with poorer attention in older adults. Whether higher LTV predicts decline in executive function and whether the relationship is accounted for by slower walking remain unanswered. The main objective of this study was to examine the relationship between baseline LTV and longitudinal change in executive function. We used data from 347 participants aged 60 years and older (50.7 % female) from the Baltimore Longitudinal Study of Aging. Longitudinal assessments of executive function were conducted between 2007 and 2013, including attention (Trails A, Digit Span Forward Test), cognitive flexibility and set shifting (Trails B, Delta TMT: Trials B minus Trials A), visuoperceptual speed (Digit Symbol Substitution Test), and working memory (Digit Span Backward Test). LTV and mean lap time (MLT) were obtained from the 400-m walk test concurrent with the baseline executive function assessment. LTV was computed as variability of lap time across ten 40-m laps based on individual trajectories. A linear mixed-effects model was used to examine LTV in relation to changes in executive function, adjusted for age, sex, education, and MLT. Higher LTV was associated with greater decline in performance on Trails B (beta=4.322, p<0.001) and delta TMT (beta=4.230, p<0.001), independent of covariates. Findings remained largely unchanged after further adjustment for MLT. LTV was not associated with changes in other executive function measures (all p>0.05). In high-functioning older adults, higher LTV in the 400-m walk predicts executive function decline involving cognitive flexibility and set shifting over a long period of time. High LTV may be an early indicator of executive function decline independent of MLT.
C1 [Tian, Qu; Ferrucci, Luigi; Studenski, Stephanie A.] Natl Inst Aging, Translat Gerontol Branch, Longitudinal Studies Sect, Baltimore, MD 21224 USA.
   [Resnick, Susan M.] Natl Inst Aging, Lab Behav Neurosci, Baltimore, MD 21224 USA.
RP Tian, Q (reprint author), 251 Bayview Blvd,Suite 100,Rm 04B316, Baltimore, MD 21224 USA.
EM qu.tian@nih.gov
RI Tian, Qu/E-5266-2015
OI Tian, Qu/0000-0003-2706-1439
FU Intramural Research Program of the National Institute on Aging
FX This research was supported by the Intramural Research Program of the
   National Institute on Aging.
NR 47
TC 0
Z9 0
U1 3
U2 6
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0161-9152
EI 1574-4647
J9 AGE
JI Age
PD DEC
PY 2015
VL 37
IS 6
AR 115
DI 10.1007/s11357-015-9855-0
PG 9
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA CZ9ET
UT WOS:000367401300011
PM 26561401
ER

PT J
AU Talani, G
   Lovinger, DM
AF Talani, Giuseppe
   Lovinger, David M.
TI Interactions between ethanol and the endocannabinoid system at GABAergic
   synapses on basolateral amygdala principal neurons
SO ALCOHOL
LA English
DT Article
DE Alcohol; CB1 receptor; Synapse; Inhibition; Arachidonoyl ethanolamide;
   Cyclic AMP
ID CONDITIONED PLACE PREFERENCE; CANNABINOID CB1 RECEPTORS; NEURON/SYNAPTIC
   BOUTON PREPARATION; ACID AMIDE HYDROLASE; ENDOGENOUS CANNABINOIDS;
   SEEKING BEHAVIOR; SYNAPTIC-TRANSMISSION; GABA(B) RECEPTORS;
   ADENYLATE-CYCLASE; MODULATE ANXIETY
AB The basolateral amygdala (BLA) plays crucial roles in stimulus value coding, as well as drug and alcohol dependence. Ethanol alters synaptic transmission in the BLA, while endocannabinoids (eCBs) produce presynaptic depression at BLA synapses. Recent studies suggest interactions between ethanol and eCBs that have important consequences for alcohol drinking behavior. To determine how ethanol and eCBs interact in the BLA, we examined the physiology and pharmacology of GABAergic synapses onto BLA pyramidal neurons in neurons from young rats. Application of ethanol at concentrations relevant to intoxication increased, in both young and adult animals, the frequency of spontaneous and miniature GABAergic inhibitory postsynaptic currents, indicating a presynaptic site of ethanol action. Ethanol did not potentiate sIPSCs during inhibition of adenylyl cyclase while still exerting its effect during inhibition of protein kinase A. Activation of type 1 cannabinoid receptors (CBI) in the BLA inhibited GABAergic transmission via an apparent presynaptic mechanism, and prevented ethanol potentiation. Surprisingly, ethanol potentiation was also prevented by CBI antagonists/inverse agonists. Brief depolarization of BLA pyramidal neurons suppressed GABAergic transmission (depolarization-induced suppression of inhibition [DSI]), an effect previously shown to be mediated by postsynaptic eCB release and presynaptic CBI activation. A CBI-mediated suppression of GABAergic transmission was also produced by combined afferent stimulation at 0.1 Hz (LFS), and postsynaptic loading with the eCB arachidonoyl ethanolamide (AEA). Both DSI and LFS-induced synaptic depression were prevented by ethanol. Our findings indicate antagonistic interactions between ethanol and eCB/CB1 modulation at GABAergic BLA synapses that may contribute to eCB roles in ethanol seeking and drinking. Published by Elsevier Inc.
C1 [Talani, Giuseppe; Lovinger, David M.] NIAAA, Sect Synapt Pharmacol, Lab Integrat Neurosci, NIH, Bethesda, MD 20892 USA.
   [Talani, Giuseppe] CNR, Inst Neurosci, Cagliari, Italy.
RP Lovinger, DM (reprint author), NIAAA, Lab Integrat Neurosci, 5625 Fishers Lane,Room TS-11, Bethesda, MD 20892 USA.
EM lovindav@mail.nih.gov
FU Division of Intramural Clinical and Biological Research of the National
   Institute on Alcohol Abuse and Alcoholism [ZIAAA000407]
FX We acknowledge members of the Section on Synaptic Pharmacology,
   Laboratory for Integrative Neuroscience for helping us with the research
   and preparation of this manuscript, with a special thanks to Dr. Anton
   Sheinin for training in the vibrodissociation technique. This work was
   supported by the Division of Intramural Clinical and Biological Research
   of the National Institute on Alcohol Abuse and Alcoholism ZIAAA000407.
NR 94
TC 1
Z9 1
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-8329
EI 1873-6823
J9 ALCOHOL
JI Alcohol
PD DEC
PY 2015
VL 49
IS 8
BP 781
EP 794
DI 10.1016/j.alcohol.2015.08.006
PG 14
WC Substance Abuse; Pharmacology & Pharmacy; Toxicology
SC Substance Abuse; Pharmacology & Pharmacy; Toxicology
GA CZ9MJ
UT WOS:000367421400004
PM 26603632
ER

PT J
AU Edwards, S
   Little, HJ
   Richardson, HN
   Vendruscolo, LF
AF Edwards, Scott
   Little, Hilary J.
   Richardson, Heather N.
   Vendruscolo, Leandro F.
TI Divergent regulation of distinct glucocorticoid systems in alcohol
   dependence
SO ALCOHOL
LA English
DT Article
DE Alcohol-use disorder; Amygdala; Cognition; Corticotropin-releasing
   factor; Glucocorticoids; Prefrontal cortex
ID CORTICOTROPIN-RELEASING-FACTOR; PITUITARY-ADRENAL AXIS; STEROID-RECEPTOR
   COACTIVATOR-1; POSTTRAUMATIC-STRESS-DISORDER; ANXIETY-LIKE BEHAVIOR;
   ETHANOL WITHDRAWAL; ARGININE-VASOPRESSIN; PREFRONTAL CORTEX; CENTRAL
   NUCLEUS; V1B RECEPTOR
AB Chronic alcohol consumption disrupts glucocorticoid signaling at multiple physiological levels to interact with several disease-related processes associated with neuroendocrine and psychiatric disorders. Excessive alcohol use produces stress-related neuroadaptations at the level of the hypothalamic-pituitary-adrenal (HPA) axis as well as within central (extra-hypothalamic) neural circuitry, including the central amygdala (CeA) and prefrontal cortex (PFC). Altered glucocorticoid receptor (GR) signaling in these areas following excessive alcohol exposure is postulated to mediate the transition from recreational drinking to dependence, as well as the manifestation of a host of cognitive and neurological deficits. Specifically, a bidirectional regulation of stress systems by glucocorticoids leads to the development of an HPA axis tolerance and a concomitant sensitization of cortical and subcortical circuitries. A greater understanding of how hypothalamic and extra-hypothalamic glucocorticoid systems interact to mediate excessive drinking and related pathologies will lead to more effective therapeutic strategies for alcohol use disorder (AUD) and closely related comorbidities. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Edwards, Scott] Louisiana State Univ, Hlth Sci Ctr, Alcohol & Drug Abuse Ctr Excellence, Dept Physiol, New Orleans, LA 70112 USA.
   [Little, Hilary J.] Kings Coll London, Inst Psychiat Psychol & Neurosci, London WC2R 2LS, England.
   [Richardson, Heather N.] Univ Massachusetts, Dept Psychol & Brain Sci, Amherst, MA 01003 USA.
   [Vendruscolo, Leandro F.] NIDA, NIH, Baltimore, MD USA.
RP Edwards, S (reprint author), Louisiana State Univ, Hlth Sci Ctr, Alcohol & Drug Abuse Ctr Excellence, Dept Physiol, 1901 Perdido St, New Orleans, LA 70112 USA.
EM sedwa5@lsuhsc.edu
FU National Institute on Alcohol Abuse and Alcoholism [AA020839]; National
   Institute on Drug Abuse, Intramural Research Program;  [AA017581]
FX Preparation of this review was supported by the National Institute on
   Alcohol Abuse and Alcoholism (AA020839, SE) and the National Institute
   on Drug Abuse, Intramural Research Program (LFV). We thank Dr. Marisa
   Roberto and all of the individuals who allowed us to share our work at
   the 2014 Alcoholism and Stress Conference in Volterra, Italy (supported
   by AA017581).
NR 97
TC 6
Z9 6
U1 2
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-8329
EI 1873-6823
J9 ALCOHOL
JI Alcohol
PD DEC
PY 2015
VL 49
IS 8
BP 811
EP 816
DI 10.1016/j.alcohol.2015.04.004
PG 6
WC Substance Abuse; Pharmacology & Pharmacy; Toxicology
SC Substance Abuse; Pharmacology & Pharmacy; Toxicology
GA CZ9MJ
UT WOS:000367421400007
PM 26003866
ER

PT J
AU Hiroshima, Y
   Maawy, A
   Zhang, Y
   Guzman, MG
   Heim, R
   Makings, L
   Luiken, GA
   Kobayashi, H
   Tanaka, K
   Endo, I
   Hoffman, RM
   Bouvet, M
AF Hiroshima, Yukihiko
   Maawy, Ali
   Zhang, Yong
   Guzman, Miguel Garcia
   Heim, Roger
   Makings, Lew
   Luiken, George A.
   Kobayashi, Hisataka
   Tanaka, Kuniya
   Endo, Itaru
   Hoffman, Robert M.
   Bouvet, Michael
TI Photoimmunotherapy Inhibits Tumor Recurrence After Surgical Resection on
   a Pancreatic Cancer Patient-Derived Orthotopic Xenograft (PDOX) Nude
   Mouse Model
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article
ID MICE; CARCINOMA; SPECIMENS; TRANSPLANTATION; TISSUE; CEA
AB Background. Photoimmunotherapy (PIT) uses a target-specific photosensitizer based on a near-infrared (NIR) phthalocyanine dye, IR700, to induce tumor necrosis after irradiation with NIR light to kill cancer cells, such as those that remain after surgery. The purpose of the present study was to sterilize the surgical bed after pancreatic cancer resection with PIT in carcinoembryonic antigen (CEA)expressing, patient-derived, orthotopic xenograft (PDOX) nude mouse models.
   Methods. After confirmation of tumor engraftment, mice were randomized to two groups: bright light surgery (BLS)-only and BLS + PIT. Each treatment arm consisted of seven tumor-bearing mice. BLS was performed under standard bright-field with an MVX10 long-working distance, high-magnification microscope on all mice. For BLS + PIT, anti-CEA antibody conjugated with IR700 (anti-CEA-IR700) (50 mu g) was injected intravenously in all mice 24 h before surgery. After the surgery, the resection bed was then irradiated with a red-light-emitting diode at 690 +/- 5 nm with a power density of 150 mW/cm(2).
   Results. Anti-CEA-IR700 labelled and illuminated the pancreatic cancer PDOX. Minimal residual cancer of the PDOX was detected by fluorescence after BLS. The local recurrence rate was 85.7 % for BLS-only and 28.6 % for BLS + PIT-treated mice (p = 0.05). The average recurrent tumor weight was 1149.0 +/- 794.6 mg for BLS-only and 210.8 +/- 336.9 mg for BLS + PIT-treated mice (p = 0.015).
   Conclusion. Anti-CEA-IR700 was able to label and illuminate a pancreatic cancer PDOX nude mouse model sufficiently for PIT. PIT reduced recurrence by eliminating remaining residual cancer cells after BLS.
C1 [Hiroshima, Yukihiko; Maawy, Ali; Hoffman, Robert M.; Bouvet, Michael] Univ Calif San Diego, Moores Canc Ctr, Dept Surg, San Diego, CA 92103 USA.
   [Hiroshima, Yukihiko; Zhang, Yong; Hoffman, Robert M.] AntiCanc Inc, San Diego, CA USA.
   [Hiroshima, Yukihiko; Tanaka, Kuniya; Endo, Itaru] Yokohama City Univ, Grad Sch Med, Yokohama, Kanagawa 232, Japan.
   [Guzman, Miguel Garcia; Heim, Roger; Makings, Lew] Aspyrian Therapeut Inc, San Diego, CA USA.
   [Luiken, George A.] OncoFluor Inc, San Diego, CA USA.
   [Kobayashi, Hisataka] NIH, Bethesda, MD 20892 USA.
   [Bouvet, Michael] VA San Diego Healthcare Syst, San Diego, CA USA.
RP Hiroshima, Y (reprint author), Univ Calif San Diego, Moores Canc Ctr, Dept Surg, San Diego, CA 92103 USA.
EM mbouvet@ucsd.edu
FU National Cancer Institute [CA132971, 142669]; JSPS KAKENHI [26830081,
   26462070, 24592009]
FX This study was supported in part by National Cancer Institute grants
   CA132971 and 142669 (to Michael Bouvet and AntiCancer, Inc.) and JSPS
   KAKENHI Grant Numbers 26830081 to Yukihiko Hiroshima, 26462070 to Itaru
   Endo and 24592009 to Kuniya Tanaka.
NR 17
TC 1
Z9 1
U1 3
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
EI 1534-4681
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD DEC
PY 2015
VL 22
SU 3
BP S1469
EP S1474
DI 10.1245/s10434-015-4553-9
PG 6
WC Oncology; Surgery
SC Oncology; Surgery
GA CZ7OG
UT WOS:000367288100150
PM 25893411
ER

PT J
AU Neychev, V
   Steinberg, SM
   Yang, LL
   Mehta, A
   Nilubol, N
   Keil, MF
   Nieman, L
   Stratakis, CA
   Kebebew, E
AF Neychev, Vladimir
   Steinberg, Seth M.
   Yang, Lily
   Mehta, Amit
   Nilubol, Naris
   Keil, Margaret F.
   Nieman, Lynnette
   Stratakis, Constantine A.
   Kebebew, Electron
TI Long-Term Outcome of Bilateral Laparoscopic Adrenalectomy Measured by
   Disease-Specific Questionnaire in a Unique Group of Patients with
   Cushing's Syndrome
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article
ID QUALITY-OF-LIFE; 100 CONSECUTIVE PROCEDURES; UNILATERAL ADRENALECTOMY;
   FOLLOW-UP; CONSENSUS STATEMENT; 10-YEAR EXPERIENCE; HYPERPLASIA;
   MANAGEMENT; DIAGNOSIS; TRANSPERITONEAL
AB Background. Laparoscopic bilateral adrenalectomy (LBA) is recommended for patients with bilateral adrenal disease and occult or unresectable ectopic Cushing's syndrome (CS). There are limited data on long-term outcomes after LBA, partly due to the lack of disease-specific tools for the measurement of impact on patients' health and quality of life.
   Methods. We used a disease-specific questionnaire covering all major clinicopathologic characteristics of CS. We compared the outcome from LBA to a control group of 60 patients who had thyroidectomy (matched for age, gender, and time of surgery, 2: 1 control-to-CS).
   Results. Twenty-eight patients (20 women and 8 men) underwent LBA for CS. Of them, 24 patients (86 %) provided responses to our questionnaire. Ninety-two percent of patients' responses indicated a significant improvement of general Cushing's physical features with complete resolution reported in 59 % of responses. Significant improvement of associated biochemical abnormalities and comorbidities was reported in 83 % of patients' responses including complete reversal in 58 %. Significant improvement in emotional-behavioral symptoms was reported in 84 % of patients' responses with complete recovery in 53 %. All patients expressed satisfaction with LBA and significant improvement in their general health and selfreported quality of life. All of the improvements after LBA were statistically significant compared with the control group.
   Conclusions. Our disease-specific questionnaire enables a clearer understanding of the association between the clinical, metabolic, and emotional-behavioral features of CS, its treatment with LBA, and long-term impact on patient-reported quality of life. This disease-specific questionnaire may be useful for future studies in patients with CS.
C1 [Neychev, Vladimir; Yang, Lily; Mehta, Amit; Nilubol, Naris; Kebebew, Electron] NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
   [Steinberg, Seth M.] NCI, Biostat & Data Management Sect, NIH, Bethesda, MD 20892 USA.
   [Keil, Margaret F.; Stratakis, Constantine A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Endocrinol & Genet, NIH, Bethesda, MD USA.
   [Nieman, Lynnette] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Reprod Endocrinol, NIH, Bethesda, MD USA.
RP Neychev, V (reprint author), NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
EM vladimir.neychev@nih.gov
FU NIH [NCT00005927, NCT01005654, NCT02001051]
FX The study was supported by the NIH clinical protocols NCT00005927,
   NCT01005654, and NCT02001051.
NR 59
TC 2
Z9 2
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
EI 1534-4681
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD DEC
PY 2015
VL 22
SU 3
BP S699
EP S706
DI 10.1245/s10434-015-4605-1
PG 8
WC Oncology; Surgery
SC Oncology; Surgery
GA CZ7OG
UT WOS:000367288100057
PM 25968622
ER

PT J
AU Sadowski, SM
   Millo, C
   Neychev, V
   Aufforth, R
   Keutgen, X
   Glanville, J
   Alimchandani, M
   Nilubol, N
   Herscovitch, P
   Quezado, M
   Kebebew, E
AF Sadowski, Samira M.
   Millo, Corina
   Neychev, Vladimir
   Aufforth, Rachel
   Keutgen, Xavier
   Glanville, Joanne
   Alimchandani, Meghna
   Nilubol, Naris
   Herscovitch, Peter
   Quezado, Martha
   Kebebew, Electron
TI Feasibility of Radio-Guided Surgery with (68)Gallium-DOTATATE in
   Patients with Gastro-Entero-Pancreatic Neuroendocrine Tumors
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article
ID SOMATOSTATIN RECEPTOR SCINTIGRAPHY; RADIOGUIDED SURGERY; UNITED-STATES;
   MANAGEMENT; GUIDELINES; SYSTEM; EPIDEMIOLOGY; DIAGNOSIS; ENETS; PET
AB Background. Surgery is the only definitive therapy for gastro-entero-pancreatic neuroendocrine tumors (GEP-NETs), and achieving complete tumor resection is an important prognostic factor. Radiopharmaceuticals such as 68 Ga-DOTA peptides have been developed that offer superior accuracy for localization of GEPNETs. The study aim was to determine the feasibility of radio-guided surgery (RGS) using Ga-68-DOTATATE in patients with primary and recurrent GEPNETs
   . Methods. Fourteen patients with GEPNETs were enrolled onto a prospective study to determine the feasibility of RGS with Ga-68-DOTATATE. Findings from preoperative imaging, intraoperative exploration, RGS, and pathology were analyzed.
   Results. The median decay corrected target count rate was 172.6 (range 28.15-2341) for tumors, with a tumor-to-background ratio (TBR) of 4.46 (range 1.6-43.56). The median lesion size was 1.55 (range 0.5-15) cm. There was no significant correlation between preoperative imaging maximum standardized uptake value (SUVmax) of the lesions and TBR (Spearman r = -0.01, p = 0.9), TBR and tumor size (Spearman r = 0.29, p = 0.14), and SUVmax and tumor size (Spearman r = 0.22, p = 0.28). The probe showed correct identification for gastric and small intestine neuroendocrine tumor (NET), including lymph node metastasis in 17 (81.0 %) of 21 cases, with a median TBR of 3.5 (1.6-40.2). For pancreatic NETs and lymph node metastasis, 16 (66.7 %) of 24 were correctly identified by RGS.
   Conclusions. Our study shows that RGS with Ga-68-DOTATATE is feasible and correctly confirms bowel NETs and metastatic mesenteric lymph nodes. Further studies are needed to determine the benefit of RGS with Ga-68-DOTATATE.
C1 [Sadowski, Samira M.; Neychev, Vladimir; Aufforth, Rachel; Keutgen, Xavier; Glanville, Joanne; Nilubol, Naris; Kebebew, Electron] NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
   [Millo, Corina; Herscovitch, Peter] NIH, Positron Emiss Tomog Dept, Warren Grant Magnusson Clin Ctr, Bethesda, MD 20892 USA.
   [Alimchandani, Meghna; Quezado, Martha] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
RP Sadowski, SM (reprint author), NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
EM kebebewe@mail.nih.gov
FU Center for Cancer Research, National Cancer Institute
FX We would like to thank Candice Cottle-Delisle, RN, and Roxanne Merkel,
   RN, for their help coordinating the clinical protocol and study
   subjects; Lily A. Yang for data management; Maureen George for technical
   surgical support for the gamma probe; and the staff at the U.S. National
   Institutes of Health PET department. This research was supported by the
   intramural research programs of the Center for Cancer Research, National
   Cancer Institute.
NR 29
TC 1
Z9 1
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
EI 1534-4681
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD DEC
PY 2015
VL 22
SU 3
BP S676
EP S682
DI 10.1245/s10434-015-4857-9
PG 7
WC Oncology; Surgery
SC Oncology; Surgery
GA CZ7OG
UT WOS:000367288100054
PM 26350374
ER

PT J
AU Satoh, K
   Patel, D
   Dieckmann, W
   Nilubol, N
   Kebebew, E
AF Satoh, Kei
   Patel, Dhaval
   Dieckmann, William
   Nilubol, Naris
   Kebebew, Electron
TI Whole Body Metabolic Tumor Volume and Total Lesion Glycolysis Predict
   Survival in Patients with Adrenocortical Carcinoma
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article
ID POSITRON-EMISSION-TOMOGRAPHY; ADRENAL INCIDENTALOMAS; PROGNOSTIC VALUE;
   MANAGEMENT; PET/CT; DIAGNOSIS; RECURRENT; CANCER; PREVALENCE; MALIGNANCY
AB Background. Adrenocortical carcinoma (ACC) is a rare but lethal malignancy with few reliable prognostic markers. FDG-PET metabolic parameters have been shown to predict survival in several cancers. The objective was to determine if metabolic tumor volume (MTV), total lesion glycolysis (TLG), and maximum standardized uptake value (SUVmax) could serve as prognostic markers in patients with ACC.
   Methods. A total of 30 patients with ACC prospectively underwent 18F-FDG PET/CT prior to treatment. Whole body MTV, TLG, and SUVmax were measured by a semiautomatic method. A median cutoff was used to determine an association with overall survival (OS) from the time of 18F-FDG PET/CT by the Kaplan-Meier method.
   Results. Patients with high whole body MTV (>87.0 mL), TLG (>229.4 SUVlbm*mL), or SUVmax (>8.9 SUV) had a worse OS compared with those with low whole body MTV (median OS, 24 vs 45.1 months, p < .01), TLG (median OS, 24 vs 40.3 months, p < .005), or SUVmax (median OS, 23.7 vs 35.5 months, p < .02). In patients who had operable disease (n = 23), high whole body MTV (>87.0 mL) and TLG (>229.4 SUVlbm*mL) had a worse OS compared with those with low whole body MTV (median OS, 25.1 vs 45.1 months, p < .05) and TLG (median OS, 25.1 vs 40.3 months, p < .05), but a high SUVmax (>8.9 SUV) was not associated with worse OS (p = .11).
   Conclusions. Patients with ACC and a high whole body MTV, TLG, and SUVmax have a worse prognosis and OS. Measurement of whole body MTV and TLG may be helpful for guiding therapy for patients with ACC.
C1 [Satoh, Kei; Patel, Dhaval; Nilubol, Naris; Kebebew, Electron] NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
   [Satoh, Kei] Icahn Sch Med Mt Sinai, New York, NY 10029 USA.
   [Dieckmann, William] NIH, Ctr Clin, PET Dept, Bethesda, MD 20892 USA.
RP Satoh, K (reprint author), NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
EM divot999@gmail.com
OI Patel, Dhaval/0000-0002-5744-568X
FU Center for Cancer Research, National Cancer Institute, National
   Institutes of Health; National Institutes of Health (NIH); NIH; Pfizer
   Inc.; Doris Duke Charitable Foundation; Newport Foundation; American
   Association for Dental Research; Howard Hughes Medical Institute;
   Colgate-Palmolive Company
FX This research was supported by the intramural research program of the
   Center for Cancer Research, National Cancer Institute, National
   Institutes of Health and the National Institutes of Health (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 Newport
   Foundation, The American Association for Dental Research, The Howard
   Hughes Medical Institute, and the Colgate-Palmolive Company, as well as
   other private donors. For a complete list, please visit the Foundation
   website at:
   http://fnih.org/work/education-training-0/medical-research-scholars-prog
   ram.
NR 34
TC 1
Z9 1
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
EI 1534-4681
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD DEC
PY 2015
VL 22
SU 3
BP S714
EP S720
DI 10.1245/s10434-015-4813-8
PG 7
WC Oncology; Surgery
SC Oncology; Surgery
GA CZ7OG
UT WOS:000367288100059
PM 26282908
ER

PT J
AU Dunleavy, K
AF Dunleavy, Kieron
TI Aggressive B cell Lymphoma: Optimal Therapy for MYC-positive,
   Double-Hit, and Triple-Hit DLBCL
SO CURRENT TREATMENT OPTIONS IN ONCOLOGY
LA English
DT Review
DE Double-hit; MYC; BCL2; BCL6; Double-expresser; DA-EPOCH-R
ID RITUXIMAB PLUS CYCLOPHOSPHAMIDE; BURKITT-LYMPHOMA; GERMINAL CENTER;
   GENE-EXPRESSION; PROGNOSTIC-SIGNIFICANCE; MOLECULAR SUBTYPES;
   ANTITUMOR-ACTIVITY; PREDICTS SURVIVAL; POOR-PROGNOSIS; PHASE-II
AB Approximately 10 % of cases of diffuse large B cell lymphoma (DLBCL) harbor a MYC rearrangement and this has been associated with an inferior outcome following standard therapy across many different studies. Double-hit and triple-hit lymphomas harbor concurrent rearrangements of MYC and BCL2 and/or BCL6 and are also associated with a very aggressive course and poor clinical outcome. It is unclear and there is lack of consensus on how these diseases should be approached therapeutically. They are characterized typically by high tumor proliferation and likely require Burkitt lymphoma-type strategies and several retrospective studies suggest that more intensive approaches than rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) may be beneficial. One challenge in this respect is that most patients with these diseases are older than 60 years and generally have poor tolerability of regimens typically used in Burkitt lymphoma. Dose-adjusted EPOCH-R is an alternative effective immunochemotherapy platform for DLBCL and is effective in Burkitt lymphoma, and retrospective studies suggest that it is effective and feasible in patients with DLBCL that harbors a MYC rearrangement with or without a BCL-2 translocation (double-hit). A multicenter study of this approach in MYC-rearranged DLBCL is ongoing and preliminary results are very encouraging. There is a lack of consensus on the role of consolidation stem cell transplantation in patients who achieve a good response to initial therapy but at this point in time, no (retrospective) studies have demonstrated any benefit. These diseases are also associated with a high rate of CNS involvement and progression and checking for cerebrospinal fluid by cytology and flow cytometry at initial diagnosis should be considered. In summary, based on retrospective data and preliminary prospective data (as more mature data is awaited), while Burkitt-type regimens may be feasible in young patients, DA-EPOCH-R is a reasonable approach for patients with these diseases, particularly for those over the age of 60 years. CNS prophylaxis is a reasonable consideration (depending on clinical characteristics) given that the rate of CNS progression is high. Many exciting new small molecule inhibitors such as BCL-2 and MYC inhibitors are in development and are exciting for these diseases and attempts are underway to combine them with effective immunochemotherapy platforms.
C1 [Dunleavy, Kieron] NCI, Lymphoid Malignancies Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Dunleavy, K (reprint author), NCI, Lymphoid Malignancies Branch, Ctr Canc Res, Bldg 10,Room 4N-115,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM dunleavk@mail.nih.gov
FU National Cancer Institute
FX This work was supported by the intramural program of the National Cancer
   Institute.
NR 56
TC 9
Z9 9
U1 3
U2 12
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1527-2729
EI 1534-6277
J9 CURR TREAT OPTION ON
JI Curr. Treat. Options Oncol.
PD DEC
PY 2015
VL 16
IS 12
AR 58
DI 10.1007/s11864-015-0374-0
PG 11
WC Oncology
SC Oncology
GA DA0VS
UT WOS:000367516300004
PM 26634708
ER

PT J
AU Caglayan, M
   Wilson, SH
AF Caglayan, Melike
   Wilson, Samuel H.
TI Reprint of "Oxidant and environmental toxicant-induced effects
   compromise DNA ligation during base excision DNA repair"
SO DNA REPAIR
LA English
DT Article
DE Base excision repair (BER); DNA polymerase beta (pol beta); DNA ligase;
   8-oxo-7,8-dihydro-2 '-deoxyguanosine (8-oxoG); Ligation failure;
   Abortive ligation products
ID STRAND BREAK REPAIR; TEMPLATING 8-OXOGUANINE LESION; POLYMERASE
   ACTIVE-SITE; ABASIC SITES; APURINIC/APYRIMIDINIC ENDONUCLEASE-1;
   NEURODEGENERATIVE DISEASE; APRATAXIN DEFICIENCY; CATALYTIC MECHANISM; AP
   ENDONUCLEASE-1; OXIDATIVE DAMAGE
AB DNA lesions arise from many endogenous and environmental agents, and such lesions can promote deleterious events leading to genomic instability and cell death. Base excision repair (BER) is the main DNA repair pathway responsible for repairing single strand breaks, base lesions and abasic sites in mammalian cells. During BER, DNA substrates and repair intermediates are channeled from one step to the next in a sequential fashion so that release of toxic repair intermediates is minimized. This includes handoff of the product of gap-filling DNA synthesis to the DNA ligation step. The conformational differences in DNA polymerase beta (pol beta) associated with incorrect or oxidized nucleotide (8-oxodGMP) insertion could impact channeling of the repair intermediate to the final step of BER, i.e., DNA ligation by DNA ligase I or the DNA Ligase III/XRCC1 complex. Thus, modified DNA ligase substrates produced by faulty pol beta gap-filling could impair coordination between pol beta and DNA ligase. Ligation failure is associated with 5'-AMP addition to the repair intermediate and accumulation of strand breaks that could be more toxic than the initial DNA lesions. Here, we provide an overview of the consequences of ligation failure in the last step of BER. We also discuss DNA-end processing mechanisms that could play roles in reversal of impaired BER. Published by Elsevier B.V.
C1 [Caglayan, Melike; Wilson, Samuel H.] NIEHS, Genome Integr & Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Wilson, SH (reprint author), NIEHS, Genome Integr & Struct Biol Lab, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM wilson5@niehs.nih.gov
FU Intramural Research Program of the NIH, National Institute of
   Environmental Health Sciences [Z01-ES050158, Z01-ES050159]
FX This research was supported by grants Z01-ES050158 and Z01-ES050159 from
   the Intramural Research Program of the NIH, National Institute of
   Environmental Health Sciences.
NR 73
TC 2
Z9 3
U1 0
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-7864
EI 1568-7856
J9 DNA REPAIR
JI DNA Repair
PD DEC
PY 2015
VL 36
SI SI
BP 86
EP 90
DI 10.1016/j.dnarep.2015.11.002
PG 5
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA DA0MT
UT WOS:000367491900014
PM 26596511
ER

PT J
AU Sun, X
   Yang, HW
   Sturgill, D
   Oliver, B
   Rabinow, L
   Samson, ML
AF Sun, Xia
   Yang, Haiwang
   Sturgill, David
   Oliver, Brian
   Rabinow, Leonard
   Samson, Marie-Laure
TI Sxl-Dependent, tra/tra2-Independent Alternative Splicing of the
   Drosophila melanogaster X-Linked Gene found in neurons
SO G3-GENES GENOMES GENETICS
LA English
DT Article
DE Sex lethal; found in neurons; alternative splicing; sex-specific
   regulation
ID RNA-SEQ DATA; DOSAGE COMPENSATION; SEXUAL-DIFFERENTIATION;
   MESSENGER-RNA; BINDING PROTEIN; SOMATIC TISSUES; LETHAL; EXPRESSION;
   SWITCH; TRANSCRIPTS
AB Somatic sexual determination and behavior in Drosophila melanogaster are under the control of a genetic cascade initiated by Sex lethal (Sxl). In the female soma, SXL RNA-binding protein regulates the splicing of transformer (tra) transcripts into a female-specific form. The RNA-binding protein TRA and its cofactor TRA2 function in concert in females, whereas SXL, TRA, and TRA2 are thought to not function in males. To better understand sex-specific regulation of gene expression, we analyzed male and female head transcriptome datasets for expression levels and splicing, quantifying sex-biased gene expression via RNA-Seq and qPCR. Our data uncouple the effects of Sxl and tra/tra2 in females in the-sex-biased alternative splicing of head transcripts from the X-linked locus found in neurons (fne), encoding a pan-neuronal RNA-binding protein of the ELAV family. We show that FNE protein levels are downregulated by Sxl in female heads, also independently of tra/tra2. We argue that this regulation may have important sexually dimorphic consequences for the regulation of nervous system development or function.
C1 [Sun, Xia; Rabinow, Leonard; Samson, Marie-Laure] Univ Paris 11, Ctr Neurosci Paris Sud, UMR 8195, F-91405 Orsay, France.
   [Sun, Xia; Rabinow, Leonard; Samson, Marie-Laure] Univ Paris 11, CNRS UMR 8195, F-91405 Orsay, France.
   [Yang, Haiwang; Sturgill, David; Oliver, Brian] NIDDK, NIH, Bethesda, MD 20892 USA.
   [Sturgill, David] Univ Maryland, Program Computat Biol Bioinformat & Gen, College Pk, MD 20742 USA.
RP Samson, ML (reprint author), Univ Paris 11, Ctr Neurosci Paris Sud, CNRS, UMR 8195, Batiment 442 Bis, F-91405 Orsay, France.
EM Marie-Laure.Samson@u-psud.fr
FU Indo-French Center for the Promotion of Advanced Research (IFCPAR)
   [4903A]; Universite Paris Sud; Centre National de la Recherche
   Scientifique (CNRS); Intramural Research Program of the National
   Institute of Diabetes and Digestive and Kidney Diseases at NIH (NIDDK);
   China Scholarship Council
FX We thank Tom Cline for constructive criticisms of a prior version of the
   manuscript and for kindly providing the Sxl mutant stocks. More stocks
   were graciously provided by William Mattox, Bruce Baker, Trudy Mackay,
   the Indiana University Drosophila stock center, and the Drosophila
   Genetic Resource Center, Kyoto, Japan. We thank Karine Tuphile for
   cloning and sequencing of fne cDNAs and Bernadette Wiszniowski for
   assistance with stocks. We particularly thank S. Bate for providing the
   InVivoStat software. Financial support was provided to M.-L. S. and L.R.
   by the Indo-French Center for the Promotion of Advanced Research
   (IFCPAR, award #4903A), the Universite Paris Sud, and the Centre
   National de la Recherche Scientifique (CNRS). This work was supported in
   part by the Intramural Research Program of the National Institute of
   Diabetes and Digestive and Kidney Diseases at NIH (NIDDK, to B.O.). X.S.
   was supported by a graduate fellowship from the China Scholarship
   Council. This work was submitted as a partial requirement for completion
   of a doctoral thesis (by X.S.).
NR 57
TC 1
Z9 1
U1 4
U2 6
PU GENETICS SOCIETY AMERICA
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 2160-1836
J9 G3-GENES GENOM GENET
JI G3-Genes Genomes Genet.
PD DEC
PY 2015
VL 5
IS 12
BP 2865
EP 2874
DI 10.1534/g3.115.023721
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA CZ7CM
UT WOS:000367257500034
PM 26511498
ER

PT J
AU Lingala, S
   Ghany, MG
AF Lingala, Shilpa
   Ghany, Marc G.
TI Natural History of Hepatitis C
SO GASTROENTEROLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Natural history; Hepatitis C virus; Chronic hepatitis C; Fibrosis;
   Cirrhosis; Decompensated liver disease
ID HUMAN-IMMUNODEFICIENCY-VIRUS; LONG-TERM TREATMENT; NUTRITION EXAMINATION
   SURVEY; TYPE-2 DIABETES-MELLITUS; GENOME-WIDE ASSOCIATION; LIVER-RELATED
   MORTALITY; UNITED-STATES COHORT; BODY-MASS INDEX;
   HEPATOCELLULAR-CARCINOMA; FIBROSIS PROGRESSION
AB Hepatitis C infection is a common cause of cirrhosis and indication for liver transplantation in the United States. The incidence of chronic hepatitis C has been declining, but rates of cirrhosis and hepatocellular carcinoma are projected to increase. The outcome of chronic hepatitis C is variable. It is estimated that 20% to 25% will develop cirrhosis over a 25-year to 30-year period. The rate of disease progression is influenced by many host, viral, and environmental factors. Few can be modified.
C1 [Lingala, Shilpa; Ghany, Marc G.] NIDDKD, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Ghany, MG (reprint author), NIDDKD, Liver Dis Branch, NIH, Bldg 10,Room 9B-16,10 Ctr Dr,MSC 1800, Bethesda, MD 20892 USA.
EM marcg@intra.niddk.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases,
   National Institutes of Health [ZIA DK075009 09]
FX This work was supported by the Intramural Program of the National
   Institute of Diabetes and Digestive and Kidney Diseases, National
   Institutes of Health (ZIA DK075009 09).
NR 128
TC 9
Z9 9
U1 2
U2 5
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8553
EI 1558-1942
J9 GASTROENTEROL CLIN N
JI Gastroenterol. Clin. North Am.
PD DEC
PY 2015
VL 44
IS 4
BP 717
EP +
DI 10.1016/j.gtc.2015.07.003
PG 19
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CZ8PG
UT WOS:000367361000004
PM 26600216
ER

PT J
AU Maholmes, V
AF Maholmes, Valerie
TI Championing research on traumatised and injured children
SO INJURY PREVENTION
LA English
DT Editorial Material
C1 [Maholmes, Valerie] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20852 USA.
RP Maholmes, V (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20852 USA.
EM maholmev@mail.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1353-8047
EI 1475-5785
J9 INJURY PREV
JI Inj. Prev.
PD DEC
PY 2015
VL 21
IS 6
BP 441
EP 441
DI 10.1136/injuryprev-2015-041881
PG 1
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA DA0GF
UT WOS:000367474900014
PM 26609060
ER

PT J
AU Lau, AF
   Fahle, GA
   Kemp, MA
   Jassem, AN
   Dekker, JP
   Frank, KM
AF Lau, Anna F.
   Fahle, Gary A.
   Kemp, Margaret A.
   Jassem, Agatha N.
   Dekker, John P.
   Frank, Karen M.
TI Clinical Performance of Check-Direct CPE, a Multiplex PCR for Direct
   Detection of bla(KPC), bla(NDM) and/or bla(VIM), and bla(OXA-48) from
   Perirectal Swabs
SO JOURNAL OF CLINICAL MICROBIOLOGY
LA English
DT Article
ID CARBAPENEMASE-PRODUCING ENTEROBACTERIACEAE; REAL-TIME PCR; GRAM-NEGATIVE
   BACILLI; RESISTANT ENTEROBACTERIACEAE; RAPID DETECTION; RECTAL SWABS;
   CHROMAGAR KPC; MEDIA; ASSAY; SURVEILLANCE
AB We evaluated the clinical performance of Check-Direct CPE for carbapenemase detection directly from 301 perirectal swabs (258 patients) in a nonoutbreak setting. Culture of a PCR-confirmed, carbapenemase-containing organism, or history of colonization with such organism within the previous 2 weeks, was used as the reference standard. Check-Direct CPE demonstrated a sensitivity value, specificity value, positive predictive value (PPV), and negative predictive value (NPV) of 100% (all bla(KPC)), 88%, 21%, and 100%, respectively. False positives accounted for 79% (n = 34) of samples for which a cycle threshold (C-T) value was reached. Simulated studies to evaluate specimen pooling as an approach to minimize costs showed no difference in C-T values for pooled groups of three or five that each contained a single specimen spiked with similar to 1,500 CFU bla(KPC) Klebsiella pneumoniae; however, the detection rate dropped to 60% at a seeded concentration of similar to 150 CFU. When data were pooled, C-T values for bla(KPC) were higher for heavy-feces-containing than for light-feces-containing liquid-suspended specimens. Furthermore, C-T values for liquid-suspended specimens were 4 to 5 C-T values lower (i.e., represented greater sensitivity) than those seen in direct swab analysis. Culture was equivalent to or better than Check-Direct CPE for 13/15 (87%) isolates tested in a limit-of-detection analysis. Detection of a carbapenemase gene at a C-T cutoff value of <= 35 was culture confirmed in 23/24 (96%) of cases; however, C-T values of >35 overlapped broadly between culture-positive (n = 21) and culture-negative (n = 36) specimens. Check-Direct CPE will likely prove most useful in high-prevalence areas or in outbreak settings where rapid carbapenemase detection is critical for infection control management.
C1 [Lau, Anna F.; Fahle, Gary A.; Kemp, Margaret A.; Jassem, Agatha N.; Dekker, John P.; Frank, Karen M.] NIH, Microbiol Serv, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Lau, AF (reprint author), NIH, Microbiol Serv, Dept Lab Med, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA.
EM Anna.Lau@nih.gov
FU Intramural Research Program of the National Institutes of Health
FX This work was supported by the Intramural Research Program of the
   National Institutes of Health. The content is solely our responsibility
   and does not represent the official views of the National Institutes of
   Health.
NR 33
TC 6
Z9 6
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0095-1137
EI 1098-660X
J9 J CLIN MICROBIOL
JI J. Clin. Microbiol.
PD DEC
PY 2015
VL 53
IS 12
BP 3729
EP 3737
DI 10.1128/JCM.01921-15
PG 9
WC Microbiology
SC Microbiology
GA DA1CB
UT WOS:000367532800006
PM 26338860
ER

PT J
AU Hussam, A
   Hong, J
AF Hussam, Abul
   Hong, Jinsoo
TI A novel field deployable filter paper based amperometric gas sensor for
   the measurement of arsenic in water
SO JOURNAL OF ELECTROANALYTICAL CHEMISTRY
LA English
DT Article
DE Arsenic; Arsine; Groundwater; Amperometry; Electrochemical sensor
ID PHASE CHEMI-LUMINESCENCE; DRINKING-WATER; CHEMILUMINESCENCE;
   SPECTROMETRY; GROUNDWATER; ANALYZER; SAMPLES; ARSINE; OZONE; GOLD
AB The presence of toxic levels of inorganic arsenic in drinking water is a worldwide problem. Measurement of millions of samples in the field for arsenic is an analytical challenge and the first step to solve the problem. Here, we developed a novel electrochemical arsine sensor and system based on the cell: C(s)/I3-I2, AsH3(g/aq)//I-3(-), I-2 AgI(s)/Ag(s), where I-3(-)/I-2 mediated AsH3(g/l) oxidation which occurred on the C(s) electrode. The sensor system requires 50 mu L of 10 mM iodine solution and a small piece of filter paper placed inside a novel electrochemical cell. The cell exhibited highly efficient arsine mass transport with a limit of detection of 15 mu g/L As(III) in water. A mathematical model of mass transfer of AsH3(g/aq) and following electrochemical reaction was developed and applied to explain the experimental data. Groundwater samples containing arsenic were measured to prove its utility in a field deployable instrument Published by Elsevier B.V.
C1 [Hussam, Abul; Hong, Jinsoo] George Mason Univ, Dept Chem & Biochem, Ctr Clean Water & Sustainable Technol, Fairfax, VA 22030 USA.
RP Hong, J (reprint author), NIMH, PET Radiochem, NIH, Bldg 10,Room B3C355, Bethesda, MD 20892 USA.
EM jinsoohong@mail.nih.gov
NR 20
TC 1
Z9 1
U1 5
U2 18
PU ELSEVIER SCIENCE SA
PI LAUSANNE
PA PO BOX 564, 1001 LAUSANNE, SWITZERLAND
SN 1572-6657
EI 1873-2569
J9 J ELECTROANAL CHEM
JI J. Electroanal. Chem.
PD DEC 1
PY 2015
VL 758
BP 156
EP 162
DI 10.1016/j.jelechem.2015.10.007
PG 7
WC Chemistry, Analytical; Electrochemistry
SC Chemistry; Electrochemistry
GA CZ7KN
UT WOS:000367278400021
ER

PT J
AU Miyake, S
   Wakita, H
   Bernstock, JD
   Castri, P
   Ruetzler, C
   Miyake, J
   Lee, YJ
   Hallenbeck, JM
AF Miyake, Shin-ichi
   Wakita, Hideaki
   Bernstock, Joshua D.
   Castri, Paola
   Ruetzler, Christl
   Miyake, Junko
   Lee, Yang-ja
   Hallenbeck, John M.
TI Hypophosphorylation of ribosomal protein S6 is a molecular mechanism
   underlying ischemic tolerance induced by either hibernation or
   preconditioning.
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Article
DE hibernation; ischemic tolerance; protein translation; ribosomal protein
   S6; rpS6 kinase
ID MAMMALIAN TARGET; CEREBRAL-ISCHEMIA; GROUND-SQUIRRELS; INFARCT VOLUME;
   RAPAMYCIN MTOR; P70S6 KINASE; PHOSPHORYLATION; TRANSLATION; BRAIN;
   IDENTIFICATION
AB Thirteen-lined ground squirrels (Ictidomys tridecemlineatus) have an extraordinary capacity to withstand prolonged and profound reductions in blood flow and oxygen delivery to the brain without incurring any cellular damage. As such, the hibernation torpor of I. tridecemlineatus provides a valuable model of tolerance to ischemic stress. Herein, we report that during hibernation torpor, a marked reduction in the phosphorylation of the ribosomal protein S6 (rpS6) occurs within the brains of I. tridecemlineatus. Of note, rpS6 phosphorylation was shown to increase in the brains of rats that underwent an occlusion of the middle cerebral artery. However, such an increase was attenuated after the implementation of an ischemic preconditioning paradigm. In addition, cultured cortical neurons treated with the rpS6 kinase (S6K) inhibitors, nglucosamine or PF4708671, displayed a decrease in rpS6 phosphorylation and a subsequent increase in tolerance to oxygen/glucose deprivation, an in vitro model of ischemic stroke. Collectively, such evidence suggests that the downregulation of rpS6 signal transduction may account for a substantial part of the observed increase in cellular tolerance to brain ischemia that occurs during hibernation torpor and after ischemic preconditioning. Further identification and characterization of the mechanisms used by hibernating species to increase ischemic tolerance may eventually clarify how the loss of homeostatic control that occurs during and after cerebral ischemia in the clinic can ultimately be minimized and/or prevented.
C1 [Miyake, Shin-ichi; Wakita, Hideaki; Bernstock, Joshua D.; Castri, Paola; Ruetzler, Christl; Miyake, Junko; Lee, Yang-ja; Hallenbeck, John M.] NINDS, Stroke Branch, NIH, Bethesda, MD 20892 USA.
RP Hallenbeck, JM (reprint author), NINDS, Stroke Branch, NIH, Bldg10 Rm5B02,MSC 1401,10 Ctr Dr, Bethesda, MD 20892 USA.
EM hallenbj@ninds.nih.gov
FU Intramural Research Program of the NINDS/NIH
FX This work was supported by the Intramural Research Program of the
   NINDS/NIH. The authors declare no competing financial interests.
NR 46
TC 2
Z9 2
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3042
EI 1471-4159
J9 J NEUROCHEM
JI J. Neurochem.
PD DEC
PY 2015
VL 135
IS 5
BP 943
EP 957
DI 10.1111/jnc.13368
PG 15
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA CZ6DN
UT WOS:000367191500010
PM 26375300
ER

PT J
AU Zand, R
   Male, S
   Lynch, JK
AF Zand, Ramin
   Male, Shailesh
   Lynch, John K.
TI Diffuse Fluid-Attenuated Inversion Recovery Hyperintensity in
   Subarachnoid Space Following Cerebral Angiography and Intravenous
   Thrombolysis
SO JOURNAL OF STROKE & CEREBROVASCULAR DISEASES
LA English
DT Article
DE Cortical; blindness; angiography; magnetic resonance imaging
ID TRANSIENT CORTICAL BLINDNESS; BLOOD-BRAIN-BARRIER; CORONARY-ANGIOGRAPHY;
   CONTRAST; MRI
AB Objective: Transient cortical blindness (TCB) is a relatively rare but well-recognized complication following cardiovascular and cerebral angiography. Methods: A 68-year-old male developed TCB following cerebral angiography along with punctate diffusion lesion evident on emergent magnetic resonance imaging (MRI). The patient received intravenous tissue plasminogen activator (IV-tPA) for suspected stroke. Results: Follow-up MRI revealed diffuse hyperintensities in subarachnoid space in fluid-attenuated inversion recovery (FLAIR) sequence mostly in bilateral occipital lobes. Conclusion: The finding on the FLAIR as described in this case is an indication of diffuse disruption of the blood-brain barrier perhaps secondary to cerebral angiography, high blood pressure, and IV-tPA. To the best of our knowledge, this is the first reported case of TCB with diffuse postcontrast FLAIR changes.
C1 [Zand, Ramin; Lynch, John K.] NINDS, Sect Stroke Diagnost & Therapeut, Bethesda, MD 20892 USA.
   [Male, Shailesh] Univ Tennessee, Ctr Hlth Sci, Dept Neurol, Memphis, TN 38163 USA.
RP Zand, R (reprint author), NINDS, Stroke Branch, NIH, Stroke Program, 10 Ctr Dr,Room B1D-733, Bethesda, MD 20892 USA.
EM ramin.zand@gmail.com
OI Zand, Ramin/0000-0002-9477-0094
NR 10
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1052-3057
EI 1532-8511
J9 J STROKE CEREBROVASC
JI J. Stroke Cerebrovasc. Dis.
PD DEC
PY 2015
VL 24
IS 12
BP E1
EP E3
DI 10.1016/j.jstrokecerebrovasdis.2015.08.021
PG 3
WC Neurosciences; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA CZ8ZY
UT WOS:000367388800001
PM 26476586
ER

PT J
AU Shetty, V
   Harrell, L
   Murphy, DA
   Vitero, S
   Gutierrez, A
   Belin, TR
   Dye, BA
   Spolsky, VW
AF Shetty, Vivek
   Harrell, Lauren
   Murphy, Debra A.
   Vitero, Steven
   Gutierrez, Alexis
   Belin, Thomas R.
   Dye, Bruce A.
   Spolsky, Vladimir W.
TI Dental disease patterns in methamphetamine users Findings in a large
   urban sample
SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION
LA English
DT Article
DE Dental disease; methamphetamine use; patterns; severity
ID EXAMINATION SURVEY NHANES; ORAL-HEALTH COMPONENT; QUALITY-ASSURANCE;
   NATIONAL-HEALTH; METH-MOUTH; UNITED-STATES; ROOT CARIES; PREVALENCE;
   PERIODONTITIS; POPULATION
AB Background. The authors used a large community sample of methamphetamine (MA) users to verify the patterns and severity of dental disease and establish a hierarchy of caries susceptibility by tooth type and tooth surface.
   Methods. Using a stratified sampling approach, 571 MA users received comprehensive oral examinations and psychosocial assessments. Three calibrated dentists characterized dental and periodontal disease by using National Health and Nutrition Examination Survey protocols. The authors also collected data on substance use history and other attributes linked to dental disease.
   Results. On all dental outcome measures, MA users evidenced high dental and periodontal disease, with older (>= 30 years) and moderate or heavy MA users disproportionately affected. Women had higher rates of tooth loss and caries, as well as a greater prevalence of anterior caries. Current cigarette smokers were more likely to manifest 5 or more anterior surfaces with untreated caries and 3 or more teeth with root caries. Nearly 3% were edentulous, and a significant percentage (40%) indicated embarrassment with their dental appearance.
   Conclusions. MA users have high rates of dental and periodontal disease and manifest a dose-response relationship, with greater levels of MA use associated with higher rates of dental disease. Women and current cigarette smokers are affected disproportionately. The intraoral patterns and hierarchy of caries susceptibility in MA users are distinctive.
   Practical Implications. The prevalence and patterns of dental and periodontal disease could be used to alert dentists to possible covert MA use and to plan treatment. Concerns about dental appearance have potential as triggers for behavioral interventions.
C1 [Shetty, Vivek] Univ Calif Los Angeles, Sch Dent, UCLA Ctr Hlth Sci 230009, Los Angeles, CA 90095 USA.
   [Harrell, Lauren; Gutierrez, Alexis; Spolsky, Vladimir W.] Univ Calif Los Angeles, Sch Dent, Los Angeles, CA 90095 USA.
   [Harrell, Lauren; Belin, Thomas R.] Univ Calif Los Angeles, Dept Biostat, Fielding Sch Publ Hlth, Los Angeles, CA 90095 USA.
   [Murphy, Debra A.] Univ Calif Los Angeles, Integrated Subst Abuse Programs, Los Angeles, CA 90095 USA.
   [Vitero, Steven] AIDS Project Los Angeles, Dent Serv, Los Angeles, CA USA.
   [Dye, Bruce A.] Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD USA.
RP Shetty, V (reprint author), Univ Calif Los Angeles, Sch Dent, UCLA Ctr Hlth Sci 230009, 10833 Le Conte Ave, Los Angeles, CA 90095 USA.
EM vshetty@ucla.edu
FU National Institutes of Health, National Institute on Drug Abuse [R01
   DA026014]; National Institutes of Health, University of California, Los
   Angeles Clinical and Translational Science Institute grant [UL1TR000124]
FX This study was funded by the National Institutes of Health, National
   Institute on Drug Abuse (R01 DA026014) (V.S.), which had no role in the
   design of the study; in the collection, analysis, and interpretation of
   data; or in the writing of the report. Additional support for Dr. Belin
   was provided by a National Institutes of Health, University of
   California, Los Angeles Clinical and Translational Science Institute
   grant (UL1TR000124). The findings and conclusions in this report are
   those of the authors and do not necessarily represent the views of the
   National Institute on Drug Abuse or the National Institutes of Health.
NR 48
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PU AMER DENTAL ASSOC
PI CHICAGO
PA 211 E CHICAGO AVE, CHICAGO, IL 60611 USA
SN 0002-8177
EI 1943-4723
J9 J AM DENT ASSOC
JI J. Am. Dent. Assoc.
PD DEC
PY 2015
VL 146
IS 12
BP 875
EP 885
DI 10.1016/j.adaj.2015.09.012
PG 11
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA CZ8KB
UT WOS:000367347500021
PM 26610832
ER

PT J
AU Hall, KD
AF Hall, Kevin D.
TI Prescribing low-fat diets: useless for long-term weight loss?
SO LANCET DIABETES & ENDOCRINOLOGY
LA English
DT Editorial Material
ID ENERGY-INTAKE; ACCURATE
C1 [Hall, Kevin D.] NIDDK, Bethesda, MD 20892 USA.
RP Hall, KD (reprint author), NIDDK, Bethesda, MD 20892 USA.
EM kevinh@niddk.nih.gov
FU Intramural NIH HHS
NR 10
TC 0
Z9 0
U1 4
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 2213-8587
J9 LANCET DIABETES ENDO
JI Lancet Diabetes Endocrinol.
PD DEC
PY 2015
VL 3
IS 12
BP 920
EP 921
DI 10.1016/S2213-8587(15)00413-1
PG 3
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CZ8ZM
UT WOS:000367387600007
PM 26527510
ER

PT J
AU Baird, NJ
   Inglese, J
   Ferre-D'Amare, AR
AF Baird, Nathan J.
   Inglese, James
   Ferre-D'Amare, Adrian R.
TI Rapid RNA-ligand interaction analysis through high-information content
   conformational and stability landscapes
SO NATURE COMMUNICATIONS
LA English
DT Article
ID DI-GMP RIBOSWITCH; ANTIBACTERIAL DRUG TARGETS; 16S RIBOSOMAL-RNA;
   PROTEIN INTERACTIONS; RESPONSE REGULATOR; SMALL MOLECULES; BINDING;
   RIBOZYME; ANTIBIOTICS; RECOGNITION
AB The structure and biological properties of RNAs are a function of changing cellular conditions, but comprehensive, simultaneous investigation of the effect of multiple interacting environmental variables is not easily achieved. We have developed an efficient, high-throughput method to characterize RNA structure and thermodynamic stability as a function of multiplexed solution conditions using Forster resonance energy transfer (FRET). In a single FRET experiment using conventional quantitative PCR instrumentation, 19,400 conditions of MgCl2, ligand and temperature are analysed to generate detailed empirical conformational and stability landscapes of the cyclic diguanylate (c-di-GMP) riboswitch. The method allows rapid comparison of RNA structure modulation by cognate and non-cognate ligands. Landscape analysis reveals that kanamycin B stabilizes a non-native, idiosyncratic conformation of the riboswitch that inhibits c-di-GMP binding. This demonstrates that allosteric control of folding, rather than direct competition with cognate effectors, is a viable approach for pharmacologically targeting riboswitches and other structured RNA molecules.
C1 [Baird, Nathan J.; Ferre-D'Amare, Adrian R.] NHLBI, NIH, Bethesda, MD 20892 USA.
   [Inglese, James] NIH, Natl Ctr Adv Translat Sci, Rockville, MD 20850 USA.
RP Baird, NJ (reprint author), Univ Sci, Dept Chem & Biochem, 600 South 43rd St, Philadelphia, PA 19104 USA.
EM n.baird@usciences.edu
FU National Heart, Lung and Blood Institute, NIH; National Center for
   Advancing Translational Sciences, NIH; Director's Challenge Innovation
   Award, NIH; K22 NHLBI Career Transition Award [K22-HL121113A]
FX We thank J. Hogg for use of the microplate fluorometer; T. Christopher
   and R. Bonasio for use of qPCR instrumentation for single-fluorophore
   control experiments; P. Berget for use of the microplate fluorometer for
   single-fluorophore control experiments, G. Piszczek for support with ITC
   and initial fluorescence experiments; R. Macarthur for discussions
   aiding data analysis; Y.-X. Wang and X. Zuo for experimental SAXS beam
   time and support, respectively; and J. Zhang, M. Lau, C. Jones and S.
   Bachas for insightful comments. This work was supported by the
   intramural programmes of the National Heart, Lung and Blood Institute,
   NIH and the National Center for Advancing Translational Sciences, NIH
   and a 2013 Director's Challenge Innovation Award, NIH. N.J.B. is a
   recipient of a K22 NHLBI Career Transition Award (K22-HL121113A).
NR 55
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U2 17
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC
PY 2015
VL 6
AR 8898
DI 10.1038/ncomms9898
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA DA1WO
UT WOS:000367586600001
PM 26638992
ER

PT J
AU Jiang, CT
   Xie, C
   Lv, Y
   Li, J
   Krausz, KW
   Shi, JM
   Brocker, CN
   Desai, D
   Amin, SG
   Bisson, WH
   Liu, YL
   Gavrilova, O
   Patterson, AD
   Gonzalez, FJ
AF Jiang, Changtao
   Xie, Cen
   Lv, Ying
   Li, Jing
   Krausz, Kristopher W.
   Shi, Jingmin
   Brocker, Chad N.
   Desai, Dhimant
   Amin, Shantu G.
   Bisson, William H.
   Liu, Yulan
   Gavrilova, Oksana
   Patterson, Andrew D.
   Gonzalez, Frank J.
TI Intestine-selective farnesoid X receptor inhibition improves
   obesity-related metabolic dysfunction
SO NATURE COMMUNICATIONS
LA English
DT Article
ID BILE-ACID; BEIGE FAT; INSULIN-RESISTANCE; GLUCOSE-HOMEOSTASIS;
   ENERGY-EXPENDITURE; ADIPOSE-TISSUE; BROWN ADIPOCYTES; MURICHOLIC ACID;
   LIVER; MICE
AB The farnesoid X receptor (FXR) regulates bile acid, lipid and glucose metabolism. Here we show that treatment of mice with glycine-beta-muricholic acid (Gly-MCA) inhibits FXR signalling exclusively in intestine, and improves metabolic parameters in mouse models of obesity. Gly-MCA is a selective high-affinity FXR inhibitor that can be administered orally and prevents, or reverses, high-fat diet-induced and genetic obesity, insulin resistance and hepatic steatosis in mice. The high-affinity FXR agonist GW4064 blocks Gly-MCA action in the gut, and intestine-specific Fxr-null mice are unresponsive to the beneficial effects of Gly-MCA. Mechanistically, the metabolic improvements with Gly-MCA depend on reduced biosynthesis of intestinal-derived ceramides, which directly compromise beige fat thermogenic function. Consequently, ceramide treatment reverses the action of Gly-MCA in high-fat diet-induced obese mice. We further show that FXR signalling in ileum biopsies of humans positively correlates with body mass index. These data suggest that Gly-MCA may be a candidate for the treatment of metabolic disorders.
C1 [Jiang, Changtao; Xie, Cen; Krausz, Kristopher W.; Shi, Jingmin; Brocker, Chad N.; Gonzalez, Frank J.] NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Jiang, Changtao; Lv, Ying] Peking Univ, Sch Basic Med Sci, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China.
   [Jiang, Changtao; Lv, Ying] Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100191, Peoples R China.
   [Li, Jing; Liu, Yulan] Peking Univ, Peoples Hosp, Dept Gastroenterol, Beijing 100044, Peoples R China.
   [Desai, Dhimant; Amin, Shantu G.] Penn State Univ, Coll Med, Dept Pharmacol, Hershey, PA 17033 USA.
   [Bisson, William H.] Oregon State Univ, Dept Environm & Mol Toxicol, Corvallis, OR 97331 USA.
   [Gavrilova, Oksana] NIAID, Mouse Metab Core Lab, NIH, Bethesda, MD 20892 USA.
   [Patterson, Andrew D.] Penn State Univ, Dept Vet & Biomed Sci, University Pk, PA 16802 USA.
   [Patterson, Andrew D.] Penn State Univ, Ctr Mol Toxicol & Carcinogenesis, University Pk, PA 16802 USA.
RP Patterson, AD (reprint author), Penn State Univ, Dept Vet & Biomed Sci, University Pk, PA 16802 USA.
EM adp117@psu.edu; gonzalef@mail.nih.gov
RI Patterson, Andrew/G-3852-2012
OI Patterson, Andrew/0000-0003-2073-0070
FU Intramural Research Program, Center for Cancer Research, National Cancer
   Institute, National Institutes of Health; National Institutes of
   Environmental Health Sciences [ES022186]; National Natural Science
   Foundation of China [31401011, 81200626]; Pennsylvania Department of
   Health using Tobacco CURE Funds
FX We thank Linda G. Byrd and John Buckley for technical assistance with
   the mouse studies. We thank Paul A. Dawson, Makoto Miyazaki and Kristina
   Schoonjans for recombinant plasmids and Jerry T. Thompson for assistance
   with the FXR reporter assays. This work was supported by the Intramural
   Research Program, Center for Cancer Research, National Cancer Institute,
   National Institutes of Health, and by the National Institutes of
   Environmental Health Sciences (ES022186 (A.D.P.)). This project was
   funded in part by grants from the National Natural Science Foundation of
   China (31401011 to C.J. and 81200626 to J.L.) and in part by a grant
   with the Pennsylvania Department of Health using Tobacco CURE Funds (to
   A.D.P.). The Pennsylvania Department of Health specifically disclaims
   responsibility for any analyses, interpretations or conclusions of this
   work.
NR 57
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U1 14
U2 23
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC
PY 2015
VL 6
AR 10166
DI 10.1038/ncomms10166
PG 18
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA DA1RT
UT WOS:000367573900001
PM 26670557
ER

PT J
AU Macpherson, LJ
   Zaharieva, EE
   Kearney, PJ
   Alpert, MH
   Lin, TY
   Turan, Z
   Lee, CH
   Gallio, M
AF Macpherson, Lindsey J.
   Zaharieva, Emanuela E.
   Kearney, Patrick J.
   Alpert, Michael H.
   Lin, Tzu-Yang
   Turan, Zeynep
   Lee, Chi-Hon
   Gallio, Marco
TI Dynamic labelling of neural connections in multiple colours by
   trans-synaptic fluorescence complementation
SO NATURE COMMUNICATIONS
LA English
DT Article
ID IN-VIVO; DROSOPHILA BRAIN; PROTEIN; CIRCUITS; SYSTEMS; PHOTORECEPTORS;
   CONNECTOMICS; LOCALIZATION; TEMPERATURE; SYNAPSES
AB Determining the pattern of activity of individual connections within a neural circuit could provide insights into the computational processes that underlie brain function. Here, we develop new strategies to label active synapses by trans-synaptic fluorescence complementation in Drosophila. First, we demonstrate that a synaptobrevin-GRASP chimera functions as a powerful activity-dependent marker for synapses in vivo. Next, we create cyan and yellow variants, achieving activity-dependent, multi-colour fluorescence reconstitution across synapses (X-RASP). Our system allows for the first time retrospective labelling of synapses (rather than whole neurons) based on their activity, in multiple colours, in the same animal. As individual synapses often act as computational units in the brain, our method will promote the design of experiments that are not possible using existing techniques. Moreover, our strategies are easily adaptable to circuit mapping in any genetic system.
C1 [Macpherson, Lindsey J.; Turan, Zeynep] Columbia Univ, Howard Hughes Med Inst, New York, NY 10032 USA.
   [Macpherson, Lindsey J.; Turan, Zeynep] Columbia Univ, Dept Biochem & Mol Biophys, New York, NY 10032 USA.
   [Zaharieva, Emanuela E.; Kearney, Patrick J.; Alpert, Michael H.; Gallio, Marco] Northwestern Univ, Dept Neurobiol, Evanston, IL 60208 USA.
   [Lin, Tzu-Yang; Lee, Chi-Hon] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Neuronal Connect, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA.
RP Gallio, M (reprint author), Northwestern Univ, Dept Neurobiol, Evanston, IL 60208 USA.
EM marco.gallio@northwestern.edu
OI Kearney, Patrick/0000-0002-7145-5964; Gallio, Marco/0000-0003-2132-0639
FU NIH [RC1NS069014, R01NS076774, R01NS086859]; Eunice Kennedy Shriver
   National Institute of Child Health and Human Development [Z01-HD008776];
   Intramural Research Programs of the NIH;  [T32HL007909]
FX This work was initially conceived and carried out in the laboratory of
   Charles Zuker, supported by NIH grants RC1NS069014 and R01NS076774. Work
   in the Gallio Lab was supported by NIH grant R01NS086859 to M.G.
   Additional support: the Intramural Research Programs of the NIH and the
   Eunice Kennedy Shriver National Institute of Child Health and Human
   Development (grant Z01-HD008776 to C.-H.L.). L.J.M. was a fellow of the
   Jane Coffin Childs Foundation. M.H.A. is supported by training grant
   T32HL007909. We thank Charles Zuker for experimental suggestions,
   discussions and support. We thank A. Kuang, M. Schmidt and B. Dick, HHMI
   EXROP students C. Washington and C. Gonzalez, summer intern M.
   Morgenstern for technical help, I. de la Rosa for fly maintenance and R.
   Barretto for insightful comments.
NR 38
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U1 5
U2 18
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC
PY 2015
VL 6
AR 10024
DI 10.1038/ncomms10024
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA DA1UQ
UT WOS:000367581400001
PM 26635273
ER

PT J
AU Sun, B
   Pandey, M
   Inman, JT
   Yang, Y
   Kashlev, M
   Patel, SS
   Wang, MD
AF Sun, Bo
   Pandey, Manjula
   Inman, James T.
   Yang, Yi
   Kashlev, Mikhail
   Patel, Smita S.
   Wang, Michelle D.
TI T7 replisome directly overcomes DNA damage
SO NATURE COMMUNICATIONS
LA English
DT Article
ID SINGLE-STRANDED-DNA; REPLICATION FORK; ESCHERICHIA-COLI; BACTERIOPHAGE
   T7; HELICASE PROTEINS; RNA-POLYMERASE; CIS-SYN; MOLECULES;
   PHOTOPRODUCTS; PROCESSIVITY
AB Cells and viruses possess several known 'restart' pathways to overcome lesions during DNA replication. However, these 'bypass' pathways leave a gap in replicated DNA or require recruitment of accessory proteins, resulting in significant delays to fork movement or even cell division arrest. Using single-molecule and ensemble methods, we demonstrate that the bacteriophage T7 replisome is able to directly replicate through a leading-strand cyclobutane pyrimidine dimer (CPD) lesion. We show that when a replisome encounters the lesion, a substantial fraction of DNA polymerase (DNAP) and helicase stay together at the lesion, the replisome does not dissociate and the helicase does not move forward on its own. The DNAP is able to directly replicate through the lesion by working in conjunction with helicase through specific helicase-DNAP interactions. These observations suggest that the T7 replisome is fundamentally permissive of DNA lesions via pathways that do not require fork adjustment or replisome reassembly.
C1 [Sun, Bo; Inman, James T.; Yang, Yi; Wang, Michelle D.] Cornell Univ, Dept Phys, Lab Atom & Solid State Phys, Ithaca, NY 14853 USA.
   [Sun, Bo; Inman, James T.; Yang, Yi; Wang, Michelle D.] Cornell Univ, Howard Hughes Med Inst, Ithaca, NY 14853 USA.
   [Sun, Bo] ShanghaiTech Univ, Sch Life Sci & Technol, Shanghai 201210, Peoples R China.
   [Pandey, Manjula; Patel, Smita S.] Rutgers Robert Wood Johnson Med Sch, Dept Biochem & Mol Biol, Piscataway, NJ 08854 USA.
   [Kashlev, Mikhail] NCI Ctr Canc Res, Frederick, MD 21702 USA.
RP Wang, MD (reprint author), Cornell Univ, Dept Phys, Lab Atom & Solid State Phys, Ithaca, NY 14853 USA.
EM mwang@physics.cornell.edu
FU National Institutes of Health [GM059849, GM55310]; National Science
   Foundation [MCB-0820293]
FX We thank members of the Wang laboratory for critical reading of the
   manuscript. We wish to acknowledge support from the National Institutes
   of Health grants (GM059849 to M.D.W. and GM55310 to S.S.P.) and the
   National Science Foundation grant (MCB-0820293 to M.D.W.).
NR 50
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U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC
PY 2015
VL 6
AR 10260
DI 10.1038/ncomms10260
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA DA1VN
UT WOS:000367583700001
PM 26675048
ER

PT J
AU Li, NZ
   An, L
   Shen, J
AF Li, Ningzhi
   An, Li
   Shen, Jun
TI Spectral fitting using basis set modified by measured B-0 field
   distribution
SO NMR IN BIOMEDICINE
LA English
DT Article
DE metabolite quantification; non-linear fitting; field map; prefrontal
   lobe; deep brain gray matter
ID MAGNETIC-RESONANCE-SPECTROSCOPY; ACETYL-ASPARTYL-GLUTAMATE; ECHO TIME
   OPTIMIZATION; DISORDER PATIENTS; METABOLITE CONCENTRATIONS; PREFRONTAL
   CORTEX; BIPOLAR DISORDER; HUMAN BRAIN; IN-VIVO; H-1 MRS
AB This study sought to demonstrate and evaluate a novel spectral fitting method to improve quantification accuracy in the presence of large magnetic field distortion, especially with high fields. MRS experiments were performed using a point-resolved spectroscopy (PRESS)-type sequence at 7 T. A double-echo gradient echo (GRE) sequence was used to acquire B-0 maps following MRS experiments. The basis set was modified based on the measured B-0 distribution within the MRS voxel. Quantification results were obtained after fitting the measured MRS data using the modified basis set. The proposed method was validated using numerical Monte Carlo simulations, phantom measurements, and comparison of occipital lobe MRS measurements under homogeneous and inhomogeneous magnetic field conditions. In vivo results acquired from voxels placed in thalamus and prefrontal cortex regions close to the frontal sinus agreed well with published values. Instead of noise-amplifying complex division, the proposed method treats field variations as part of the signal model, thereby avoiding inherent statistical bias associated with regularization. Simulations and experiments showed that the proposed approach reliably quantified results in the presence of relatively large magnetic field distortion. Published 2015. This article is a U.S. Government work and is in the public domain in the USA.
C1 [Li, Ningzhi; An, Li; Shen, Jun] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
RP Li, NZ (reprint author), NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
EM ymlnz2008@gmail.com
FU Intramural NIH HHS [Z99 MH999999, ZIA MH002803-12]
NR 26
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U1 0
U2 4
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 DEC
PY 2015
VL 28
IS 12
BP 1707
EP 1715
DI 10.1002/nbm.3430
PG 9
WC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy
SC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy
GA CZ7XX
UT WOS:000367315100011
PM 26503305
ER

PT J
AU Bai, RL
   Klausc, A
   Bellay, T
   Stewart, C
   Pajevic, S
   Nevo, U
   Merkle, H
   Plenz, D
   Basser, PJ
AF Bai, Ruiliang
   Klausc, Andreas
   Bellay, Tim
   Stewart, Craig
   Pajevic, Sinisa
   Nevo, Uri
   Merkle, Hellmut
   Plenz, Dietmar
   Basser, Peter J.
TI Simultaneous calcium fluorescence imaging and MR of ex vivo organotypic
   cortical cultures: a new test bed for functional MRI
SO NMR IN BIOMEDICINE
LA English
DT Article
DE MRI; functional MRI; calcium; fluorescence; BOLD; organotypic culture;
   brain; neuronal activity
ID MAGNETIC-RESONANCE MICROSCOPY; NEAR-INFRARED SPECTROSCOPY; HIPPOCAMPAL
   SLICE MODEL; NEURONAL-ACTIVITY; HUMAN BRAIN; WATER DIFFUSION; IN-VITRO;
   SENSORY STIMULATION; OXYGENATION CHANGES; RAT NEOCORTEX
AB Recently, several new functional (f)MRI contrast mechanisms including diffusion, phase imaging, proton density, etc. have been proposed to measure neuronal activity more directly and accurately than blood-oxygen-level dependent (BOLD) fMRI. However, these approaches have proved difficult to reproduce, mainly because of the dearth of reliable and robust test systems to vet and validate them. Here we describe the development and testing of such a test bed for non-BOLD fMRI. Organotypic cortical cultures were used as a stable and reproducible biological model of neuronal activity that shows spontaneous activity similar to that of in vivo brain cortex without any hemodynamic confounds. An open-access, single-sided magnetic resonance (MR) "profiler" consisting of four permanent magnets with magnetic field of 0.32 T was used in this study to perform MR acquisition. A fluorescence microscope with long working distance objective was mounted on the top of a custom-designed chamber that keeps the organotypic culture vital, and the MR system was mounted on the bottom of the chamber to achieve real-time simultaneous calcium fluorescence optical imaging and MR acquisition on the same specimen. In this study, the reliability and performance of the proposed test bed were demonstrated by a conventional CPMG MR sequence acquired simultaneously with calcium imaging, which is a well-characterized measurement of neuronal activity. This experimental design will make it possible to correlate directly the other candidate functional MR signals to the optical indicia of neuronal activity in the future. Copyright (C) 2015 John Wiley & Sons, Ltd.
C1 [Bai, Ruiliang; Basser, Peter J.] NICHD, Sect Tissue Biophys & Biomimet, PPITS, NIH, Bethesda, MD 20892 USA.
   [Bai, Ruiliang] Univ Maryland, Inst Phys Sci & Technol, Biophys Program, College Pk, MD 20742 USA.
   [Klausc, Andreas; Bellay, Tim; Stewart, Craig; Plenz, Dietmar] NIMH, Sect Crit Brain Dynam, LSN, NIH, Bethesda, MD 20892 USA.
   [Pajevic, Sinisa] NIH, Math & Stat Comp Lab, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
   [Nevo, Uri] Tel Aviv Univ, Dept Biomed Engn, IL-69978 Tel Aviv, Israel.
   [Merkle, Hellmut] NINDS, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20892 USA.
RP Basser, PJ (reprint author), 13 South Dr,Bldg 13,Room 3W16, Bethesda, MD 20892 USA.
EM pjbasser@helix.nih.gov
OI Klaus, Andreas/0000-0002-4133-351X
FU Intramural Research Program (IRP) of the Eunice Kennedy Shriver National
   Institute of Child Health and Human Development (NICHD), NIH; IRP of
   NINDS
FX This work was supported by the Intramural Research Program (IRP) of the
   Eunice Kennedy Shriver National Institute of Child Health and Human
   Development (NICHD), NIH. Special thanks to Ms. Lynne A. Holtzclaw and
   Dr. James T. Russell from the Microscopy and Imaging Core (MIC) Facility
   at NICHD, NIH for assistance in immunohistochemistry and confocal
   imaging and Ms. L. Salak for editing the manuscript. We are also
   grateful to Dr. Alan P. Koretsky from the Laboratory of Functional and
   Molecular Imaging at the National Institute of Neurological Disorders
   and Stroke (NINDS) for useful discussion and the support from the IRP of
   NINDS.
NR 80
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U1 0
U2 7
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 DEC
PY 2015
VL 28
IS 12
BP 1726
EP 1738
DI 10.1002/nbm.3424
PG 13
WC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy
SC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy
GA CZ7XX
UT WOS:000367315100013
PM 26510537
ER

PT J
AU Kazak, AE
   Abrams, AN
   Banks, J
   Christofferson, J
   DiDonato, S
   Grootenhuis, MA
   Kabour, M
   Madan-Swain, A
   Patel, SK
   Zadeh, S
   Kupst, MJ
AF Kazak, Anne E.
   Abrams, Annah N.
   Banks, Jaime
   Christofferson, Jennifer
   DiDonato, Stephen
   Grootenhuis, Martha A.
   Kabour, Marianne
   Madan-Swain, Avi
   Patel, Sunita K.
   Zadeh, Sima
   Kupst, Mary Jo
TI Psychosocial Assessment as a Standard of Care in Pediatric Cancer
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE pediatric oncology; psychosocial assessment; screening; standards of
   care
ID QUALITY-OF-LIFE; POSTTRAUMATIC STRESS SYMPTOMS;
   BONE-MARROW-TRANSPLANTATION; ACUTE LYMPHOBLASTIC-LEUKEMIA; STEM-CELL
   TRANSPLANTATION; CHRONIC HEALTH CONDITIONS; CHRONICALLY ILL CHILDREN;
   ASSESSMENT-TOOL PAT2.0; YOUNG-ADULT SURVIVORS; LONG-TERM SURVIVORS
AB This paper presents the evidence for a standard of care for psychosocial assessment in pediatric cancer. An interdisciplinary group of investigators utilized EBSCO, PubMed, PsycINFO, Ovid, and Google Scholar search databases, focusing on five areas: youth/family psychosocial adjustment, family resources, family/social support, previous history/premorbid functioning, and family structure/function. Descriptive quantitative studies, systematic reviews, and meta-analyses (n = 149) were reviewed and evaluated using grading of recommendations, assessment development, and evaluation (GRADE) criteria. There is high quality evidence to support a strong recommendation for multifaceted, systematic assessments of psychosocial health care needs of youth with cancer and their families as a standard of care in pediatric oncology. (C) 2015 Wiley Periodicals, Inc.
C1 [Kazak, Anne E.; Christofferson, Jennifer; DiDonato, Stephen] Nemours Childrens Hlth Syst, Ctr Healthcare Delivery Sci, Wilmington, DE USA.
   [Kazak, Anne E.; Christofferson, Jennifer; DiDonato, Stephen] Nemours Childrens Hlth Syst, Ctr Pediat Traumat Stress, Wilmington, DE USA.
   [Kazak, Anne E.] Thomas Jefferson Univ, Sidney Kimmel Med Coll, Philadelphia, PA 19107 USA.
   [Abrams, Annah N.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
   [Abrams, Annah N.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
   [Banks, Jaime] Parent Advocate, Bethesda, MD USA.
   [Grootenhuis, Martha A.] Univ Amsterdam, Acad Med Ctr, Emma Childrens Hosp, NL-1105 AZ Amsterdam, Netherlands.
   [Kabour, Marianne] Transit Profess Ctr, Portland, OR USA.
   [Madan-Swain, Avi] Univ Alabama Birmingham, Childrens Alabama, Birmingham, AL USA.
   [Patel, Sunita K.] City Hope Med Ctr, Duarte, CA USA.
   [Patel, Sunita K.] City Hope Natl Med Ctr, Beckman Res Inst, Duarte, CA 91010 USA.
   [Zadeh, Sima] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
   [Kupst, Mary Jo] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
RP Kazak, AE (reprint author), AI Du Pont Hosp Children, Nemours Ctr Healthcare Delivery Sci, 1701 Rockland Rd,Suite 160, Wilmington, DE 19803 USA.
EM anne.kazak@nemours.org
FU Mattie Miracle Foundation; National Institutes of Health; Center for
   Pediatric Traumatic Stress [U79SM061255]
FX Grant sponsor: Mattie Miracle Foundation; Grant sponsor: National
   Institutes of Health and the Center for Pediatric Traumatic Stress;
   Grant number: U79SM061255
NR 166
TC 2
Z9 2
U1 5
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1545-5009
EI 1545-5017
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD DEC
PY 2015
VL 62
SU 5
BP S426
EP +
DI 10.1002/pbc.25730
PG 34
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA CZ7OZ
UT WOS:000367290000003
PM 26700916
ER

PT J
AU Lichtenthal, WG
   Sweeney, CR
   Roberts, KE
   Corner, GW
   Donovan, LA
   Prigerson, HG
   Wiener, L
AF Lichtenthal, Wendy G.
   Sweeney, Corinne R.
   Roberts, Kailey E.
   Corner, Geoffrey W.
   Donovan, Leigh A.
   Prigerson, Holly G.
   Wiener, Lori
TI Bereavement Follow-Up After the Death of a Child as a Standard of Care
   in Pediatric Oncology
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE bereaved parents; bereavement; cancer; death of a child; palliative
   care; pediatric oncology
ID RANDOMIZED CONTROLLED-TRIAL; PROLONGED GRIEF DISORDER;
   MENTAL-HEALTH-SERVICES; OF-LIFE CARE; PALLIATIVE CARE; PARENTAL GRIEF;
   SOCIAL SUPPORT; FAMILY PERSPECTIVES; MOTHERS EXPERIENCE; COMPLICATED
   GRIEF
AB After a child's death to cancer, families commonly want continued connection with the healthcare team that cared for their child, yet bereavement follow-up is often sporadic. A comprehensive literature search found that many bereaved parents experience poor psychological outcomes during bereavement and that parents want follow-up and benefit from continued connection with their child's healthcare providers. Evidence suggests that the standard of care should consist of at least one meaningful contact between the healthcare team and bereaved parents to identify those at risk for negative psychosocial sequelae and to provide resources for bereavement support. (C) 2015 Wiley Periodicals, Inc.
C1 [Lichtenthal, Wendy G.; Sweeney, Corinne R.; Roberts, Kailey E.; Corner, Geoffrey W.] Mem Sloan Kettering Canc Ctr, Dept Psychiat & Behav Sci, New York, NY 10022 USA.
   [Sweeney, Corinne R.] Fairleigh Dickinson Univ, Dept Psychol, Teaneck, NJ USA.
   [Corner, Geoffrey W.] Univ So Calif, Dept Psychol, Los Angeles, CA 90089 USA.
   [Donovan, Leigh A.] Univ New S Wales, Sch Womens & Childrens Hlth, Sydney, NSW, Australia.
   [Prigerson, Holly G.] Weill Cornell Med Coll, Dept Med, New York, NY USA.
   [Wiener, Lori] NCI, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Lichtenthal, WG (reprint author), Mem Sloan Kettering Canc Ctr, Dept Psychiat & Behav Sci, 641 Lexington Ave,7th Floor, New York, NY 10022 USA.
EM lichtenw@mskcc.org
OI Lichtenthal, Wendy/0000-0003-3597-7826
FU National Cancer Institute (NCI) [K07 CA172216, T32 CA009461]
FX Grant sponsor: National Cancer Institute (NCI); Grant number: K07
   CA172216 and T32 CA009461
NR 140
TC 6
Z9 6
U1 5
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1545-5009
EI 1545-5017
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD DEC
PY 2015
VL 62
SU 5
BP S834
EP +
DI 10.1002/pbc.25700
PG 36
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA CZ7OZ
UT WOS:000367290000016
PM 26700929
ER

PT J
AU Thompson, AL
   Christiansen, HL
   Elam, M
   Hoag, J
   Irwin, MK
   Pao, M
   Voll, M
   Noll, RB
   Kelly, KP
AF Thompson, Amanda L.
   Christiansen, Heather L.
   Elam, Megan
   Hoag, Jennifer
   Irwin, Mary Kay
   Pao, Maryland
   Voll, Megan
   Noll, Robert B.
   Kelly, Katherine Patterson
TI Academic Continuity and School Reentry Support as a Standard of Care in
   Pediatric Oncology
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE childhood cancer; psychosocial; school reentry
ID CHRONIC HEALTH CONDITIONS; CHILDHOOD-CANCER; REINTEGRATION PROGRAM;
   CHRONIC ILLNESS; BRAIN-TUMORS; CHILDREN; SURVIVORS; EDUCATION;
   PERCEPTIONS; TEACHERS
AB Clinicians agree that return to school after diagnosis promotes the positive adjustment of children and adolescents with cancer; however, the school reentry process can present challenges. The aim of this review was to critically evaluate the literature on school reentry support for youth with cancer. Seventeen publications were identified. School reentry services were well-received by families and educators; increased teacher and peer knowledge about childhood cancer; influenced peer and educator attitudes toward the patient; and improved communication and collaboration between patients/families, school, and the healthcare team. Evidence supports a strong recommendation for school reentry support for youth with cancer. (C) 2015 Wiley Periodicals, Inc.
C1 [Thompson, Amanda L.] Childrens Natl Hlth Syst, Ctr Canc & Blood Disorders, Washington, DC 20010 USA.
   [Christiansen, Heather L.] Blank Childrens Hosp, Canc & Blood Disorders Ctr, Des Moines, IA USA.
   [Elam, Megan] Cincinnati Childrens Hosp Med Ctr, Canc & Blood Dis Inst, Cincinnati, OH 45229 USA.
   [Hoag, Jennifer] Med Coll Wisconsin, Dept Pediat Hematol Oncol BMT, Milwaukee, WI 53226 USA.
   [Irwin, Mary Kay] Nationwide Childrens Hosp, Sch Hlth Serv, Columbus, OH USA.
   [Pao, Maryland] NIMH, Bethesda, MD 20892 USA.
   [Voll, Megan; Noll, Robert B.] Univ Pittsburgh, Dept Pediat, Pittsburgh, PA 15260 USA.
   [Kelly, Katherine Patterson] Childrens Natl Hlth Syst, Dept Nursing Res & Qual Outcomes, Washington, DC USA.
RP Kelly, KP (reprint author), Childrens Natl Hlth Syst, Washington, DC 20010 USA.
EM Kakelly@childrensnational.org
FU Intramural NIH HHS [ZIA MH002922-01]
NR 35
TC 2
Z9 2
U1 2
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1545-5009
EI 1545-5017
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD DEC
PY 2015
VL 62
SU 5
BP S805
EP +
DI 10.1002/pbc.25760
PG 13
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA CZ7OZ
UT WOS:000367290000014
PM 26700927
ER

PT J
AU Weaver, MS
   Heinze, KE
   Kelly, KP
   Wiener, L
   Casey, RL
   Bell, CJ
   Wolfe, J
   Garee, AM
   Watson, A
   Hinds, PS
AF Weaver, Meaghann S.
   Heinze, Katherine E.
   Kelly, Katherine P.
   Wiener, Lori
   Casey, Robert L.
   Bell, Cynthia J.
   Wolfe, Joanne
   Garee, Amy M.
   Watson, Anne
   Hinds, Pamela S.
TI Palliative Care as a Standard of Care in Pediatric Oncology
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE communication; family-centered care; palliative care; psychosocial
   support; quality of life
ID QUALITY-OF-LIFE; PATIENT-REPORTED OUTCOMES; YOUNG-ADULT ONCOLOGY;
   ADVANCED CANCER; BRAIN-TUMORS; CHILDREN; END; DEATH; PARENTS;
   PERSPECTIVES
AB The study team conducted a systematic review of pediatric and adolescent palliative cancer care literature from 1995 to 2015 using four databases to inform development of a palliative care psychosocial standard. A total of 209 papers were reviewed with inclusion of 73 papers for final synthesis. Revealed topics of urgent consideration include the following: symptom assessment and intervention, direct patient report, effective communication, and shared decision-making. Standardization of palliative care assessments and interventions in pediatric oncology has the potential to foster improved quality of care across the cancer trajectory for children and adolescents with cancer and their family members. (C) 2015 Wiley Periodicals, Inc.
C1 [Weaver, Meaghann S.] Childrens Natl Hlth Syst, Dept Oncol, Washington, DC USA.
   [Weaver, Meaghann S.] St Jude Childrens Res Hosp, Dept Oncol, Memphis, TN 38105 USA.
   [Heinze, Katherine E.] Johns Hopkins Univ, Sch Nursing, Baltimore, MD USA.
   [Kelly, Katherine P.; Hinds, Pamela S.] Childrens Natl Hlth Syst, Dept Nursing Res & Qual Outcomes, Washington, DC USA.
   [Wiener, Lori] NCI, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA.
   [Casey, Robert L.] Univ Colorado, Childrens Hosp Colorado, Ctr Canc & Blood Disorders, Denver, CO 80202 USA.
   [Bell, Cynthia J.] Wayne State Univ, Coll Nursing, Detroit, MI 48202 USA.
   [Bell, Cynthia J.] Hosp Michigan Inst, Detroit, MI USA.
   [Wolfe, Joanne] Dana Farber Canc Inst, Dept Psychosocial Oncol & Palliat Care, Boston, MA 02115 USA.
   [Garee, Amy M.] Nationwide Childrens Hosp, Dept Oncol, Columbus, OH USA.
   [Watson, Anne] Childrens Natl Hlth Syst, Dept Crit Care Med, Washington, DC USA.
   [Hinds, Pamela S.] George Washington Univ, Dept Pediat, Washington, DC 20052 USA.
RP Weaver, MS (reprint author), St Jude Childrens Res Hosp, 262 Danny Thomas Pl,MS 260, Memphis, TN 38105 USA.
EM Meaghann.Weaver@StJude.org
OI Bell, Cynthia/0000-0002-9026-0986
FU Intramural NIH HHS [Z99 CA999999]
NR 61
TC 4
Z9 4
U1 5
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1545-5009
EI 1545-5017
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD DEC
PY 2015
VL 62
SU 5
BP S829
EP S833
DI 10.1002/pbc.25695
PG 5
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA CZ7OZ
UT WOS:000367290000015
PM 26700928
ER

PT J
AU Wiener, L
   Kazak, AE
   Noll, RB
   Patenaude, AF
   Kupst, MJ
AF Wiener, Lori
   Kazak, Anne E.
   Noll, Robert B.
   Patenaude, Andrea Farkas
   Kupst, Mary Jo
TI Interdisciplinary Collaboration in Standards of Psychosocial Care
SO PEDIATRIC BLOOD & CANCER
LA English
DT Editorial Material
C1 [Wiener, Lori] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Kazak, Anne E.] Nemours Childrens Hlth Syst, Wilmington, DE USA.
   [Kazak, Anne E.] Thomas Jefferson Univ, Sidney Kimmel Med Sch, Philadelphia, PA 19107 USA.
   [Noll, Robert B.] Univ Pittsburgh, Dept Pediat, Pittsburgh, PA 15260 USA.
   [Patenaude, Andrea Farkas] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
   [Kupst, Mary Jo] Med Coll Wisconsin, Dept Pediat, Milwaukee, WI 53226 USA.
RP Wiener, L (reprint author), NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM wienerl@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 1
TC 1
Z9 1
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 DEC
PY 2015
VL 62
SU 5
BP S425
EP S425
DI 10.1002/pbc.25718
PG 1
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA CZ7OZ
UT WOS:000367290000002
PM 26700915
ER

PT J
AU Wiener, L
   Kazak, AE
   Noll, RB
   Patenaude, AF
   Kupst, MJ
AF Wiener, Lori
   Kazak, Anne E.
   Noll, Robert B.
   Patenaude, Andrea Farkas
   Kupst, Mary Jo
TI Standards for the Psychosocial Care of Children With Cancer and Their
   Families: An Introduction to the Special Issue
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE cancer; child; family; pediatric; psychosocial; standards
ID RECOMMENDATIONS; GUIDELINES; CONSENSUS; ONCOLOGY; GRADE
AB Pediatric oncology psychosocial professionals collaborated with an interdisciplinary group of experts and stakeholders and developed evidence-based standards for pediatric psychosocial care. Given the breadth of research evidence and traditions of clinical care, 15 standards were derived. Each standard is based on a systematic review of relevant literature and used the AGREE II process to evaluate the quality of the evidence. This article describes the methods used to develop the standards and introduces the 15 articles included in this special issue. Established standards help ensure that all children with cancer and their families receive essential psychosocial care. (C) 2015 Wiley Periodicals, Inc.
C1 [Wiener, Lori] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Kazak, Anne E.] Thomas Jefferson Univ, Sidney Kimmel Med Sch, Nemours Childrens Hlth Syst, Philadelphia, PA 19107 USA.
   [Noll, Robert B.] Univ Pittsburgh, Pittsburgh, PA USA.
   [Patenaude, Andrea Farkas] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
   [Kupst, Mary Jo] Med Coll Wisconsin, Dept Pediat, Milwaukee, WI 53226 USA.
RP Wiener, L (reprint author), NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM wienerl@mail.nih.gov
FU Mattie Miracle Cancer Foundation; National Cancer Institute; Center for
   Pediatric Traumatic Stress [5U79SM061255-03]
FX Grant sponsor: Mattie Miracle Cancer Foundation; Grant sponsor: National
   Cancer Institute; Grant sponsor: Center for Pediatric Traumatic Stress;
   Grant number: 5U79SM061255-03
NR 25
TC 7
Z9 7
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 DEC
PY 2015
VL 62
SU 5
BP S419
EP S424
DI 10.1002/pbc.25675
PG 6
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA CZ7OZ
UT WOS:000367290000001
PM 26397836
ER

PT J
AU Goldstein, RB
   Smith, SM
   Dawson, DA
   Grant, BF
AF Goldstein, Rise B.
   Smith, Sharon M.
   Dawson, Deborah A.
   Grant, Bridget F.
TI Sociodemographic and Psychiatric Diagnostic Predictors of 3-Year
   Incidence of DSM-IV Substance Use Disorders Among Men and Women in the
   National Epidemiologic Survey on Alcohol and Related Conditions
SO PSYCHOLOGY OF ADDICTIVE BEHAVIORS
LA English
DT Article
DE substance use disorders; incidence; predictors; epidemiology; gender
   differences
ID GENERAL-POPULATION SAMPLE; AGE-OF-ONSET; UNITED-STATES; CANNABIS USE;
   PERSONALITY-DISORDERS; HEALTH SURVEY; RISK-FACTORS; DRUG-USE;
   AUDADIS-IV; DEPENDENCE
AB Incidence rates of alcohol and drug use disorders (AUDs and DUDs) are consistently higher in men than women, but information on whether sociodemographic and psychiatric diagnostic predictors of AUD and DUD incidence differ by sex is limited. Using data from Waves 1 and 2 of the National Epidemiologic Survey on Alcohol and Related Conditions, sex-specific 3-year incidence rates of AUDs and DUDs among United States adults were compared by sociodemographic variables and baseline psychiatric disorders. Sex-specific logistic regression models estimated odds ratios for prediction of incident AUDs and DUDs, adjusting for potentially confounding baseline sociodemographic and diagnostic variables. Few statistically significant sex differences in predictive relationships were identified and those observed were generally modest. Prospective research is needed to identify predictors of incident DSM-5 AUDs and DUDs and their underlying mechanisms, including whether there is sex specificity by developmental phase, in the role of additional comorbidity in etiology and course, and in outcomes of prevention and treatment.
C1 [Goldstein, Rise B.; Smith, Sharon M.; Dawson, Deborah A.; Grant, Bridget F.] NIAAA, Lab Epidemiol & Biometry, Div Intramural Clin & Biol Res, NIH, Bethesda, MD 20892 USA.
   [Dawson, Deborah A.] Kelly Govt Serv, Rockville, MD USA.
RP Goldstein, RB (reprint author), NIAAA, Lab Epidemiol & Biometry, Div Intramural Clin & Biol Res, NIH, Room 3071,MS 9304,5635 Fishers Lane, Bethesda, MD 20892 USA.
EM goldster@mail.nih.gov
OI Goldstein, Rise/0000-0002-9603-9473
FU National Institute on Alcohol Abuse and Alcoholism (NIAAA); Intramural
   Program of National Institutes of Health, NIAAA
FX The National Epidemiologic Survey on Alcohol and Related Conditions
   (NESARC) is funded by the National Institute on Alcohol Abuse and
   Alcoholism (NIAAA) with supplemental support from the National Institute
   on Drug Abuse. This research was supported in part by the Intramural
   Program of the National Institutes of Health, NIAAA. A preliminary
   version of parts of this article was presented at the 167th Annual
   Meeting of the American Psychiatric Association, May, 2014, New York,
   NY. The authors extend their thanks to S. Patricia Chou, PhD, and Tulshi
   D. Saha, PhD, for invaluable assistance with the revision of this
   article. The views and opinions expressed in this report are those of
   the authors and should not be construed to represent the views of
   sponsoring organizations, agencies, or the U.S. government.
NR 55
TC 1
Z9 1
U1 3
U2 13
PU EDUCATIONAL PUBLISHING FOUNDATION-AMERICAN PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST, NE, WASHINGTON, DC 20002-4242 USA
SN 0893-164X
EI 1939-1501
J9 PSYCHOL ADDICT BEHAV
JI Psychol. Addict. Behav.
PD DEC
PY 2015
VL 29
IS 4
BP 924
EP 932
DI 10.1037/adb0000080
PG 9
WC Substance Abuse; Psychology, Multidisciplinary
SC Substance Abuse; Psychology
GA DA0BE
UT WOS:000367460900011
PM 26727008
ER

PT J
AU Jang, S
   Yu, LR
   Abdelmegeed, MA
   Gao, Y
   Banerjee, A
   Song, BJ
AF Jang, Sehwan
   Yu, Li-Rong
   Abdelmegeed, Mohamed A.
   Gao, Yuan
   Banerjee, Atrayee
   Song, Byoung-Joon
TI Critical role of c-jun N-terminal protein kinase in promoting
   mitochondrial dysfunction and acute liver injury
SO REDOX BIOLOGY
LA English
DT Article
DE Acute liver injury; Carbon tetrachloride; JNK; Protein phosphorylation;
   Mitochondria; Differential proteomics
ID CARBON-TETRACHLORIDE; RAT-LIVER; JNK INHIBITOR; ACETAMINOPHEN
   HEPATOTOXICITY; APOPTOSIS; TOXICITY; TRANSLOCATION; ACTIVATION; ALCOHOL;
   DAMAGE
AB The mechanism by which c-Jun N-terminal protein kinase (JNK) promotes tissue injury is poorly understood. Thus we aimed at studying the roles of JNK and its phospho-target proteins in mouse models of acute liver injury. Young male mice were exposed to a single dose of CCl4 (50 mg/kg, IP) and euthanized at different time points. Liver histology, blood alanine aminotransferase, and other enzyme activities were measured in CCl4-exposed mice without or with the highly-specific JNK inhibitors. Phosphoproteins were purified from control or CCl4-exposed mice and analyzed by differential mass-spectrometry followed by further characterizations of immunoprecipitation and activity measurements. JNK was activated within 1 h while liver damage was maximal at 24 h post-CCl4 injection. Markedly increased phosphorylation of many mitochondrial proteins was observed between 1 and 8 h following CCl4 exposure. Pretreatment with the selective JNK inhibitor SU3327 or the mitochondria-targeted antioxidant mito-TEMPO markedly reduced the levels of p-JNK, mitochondrial phosphoproteins and liver damage in CCl4-exposed mice. Differential proteomic analysis identified many phosphorylated mitochondrial proteins involved in anti-oxidant defense, electron transfer, energy supply, fatty acid oxidation, etc. Aldehyde dehydrogenase, NADH-ubiquinone oxidoreductase, and alpha-ketoglutarate dehydrogenase were phosphorylated in CCl4-exposed mice but dephosphorylated after SU3327 pretreatment. Consistently, the suppressed activities of these enzymes were restored by SU3327 pretreatment in CCl4-exposed mice. These data provide a novel mechanism by which JNK, rapidly activated by CCl4, promotes mitochondrial dysfunction and acute hepatotoxicity through robust phosphorylation of numerous mitochondrial proteins. Published by Elsevier B.V.
C1 [Jang, Sehwan; Abdelmegeed, Mohamed A.; Banerjee, Atrayee; Song, Byoung-Joon] NIAAA, Lab Membrane Biochem & Biophys, Bethesda, MD 20892 USA.
   [Yu, Li-Rong; Gao, Yuan] US FDA, Biomarkers & Alternat Models Branch, Div Syst Biol, Natl Ctr Toxicol Res, Jefferson, AR 72079 USA.
RP Song, BJ (reprint author), NIAAA, Lab Membrane Biochem & Biophys, Bethesda, MD 20892 USA.
EM sehwan.jang@upr.edu; abdelmegeedm@mail.nih.gov; yuangao2000@gmail.com;
   atrayee.liver@gmail.com; bj.song@nih.gov
FU Intramural Research Program of National Institute of Alcohol Abuse and
   Alcoholism (NIAAA); Intramural Fund of National Center for Toxicological
   Research, U.S. Food and Drug Administration (NCTR/FDA)
FX This study was supported by the Intramural Research Program of National
   Institute of Alcohol Abuse and Alcoholism (NIAAA) and in part with funds
   from the Intramural Fund of National Center for Toxicological Research,
   U.S. Food and Drug Administration (NCTR/FDA). The views presented in
   this article do not necessarily reflect those of the U.S. Food and Drug
   Administration. The authors are also grateful to Drs. Youngshim Choi and
   Klaus Gawrisch for the excellent technical help and support for this
   study, respectively.
NR 59
TC 8
Z9 8
U1 0
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 2213-2317
J9 REDOX BIOL
JI Redox Biol.
PD DEC
PY 2015
VL 6
BP 552
EP 564
DI 10.1016/j.redox.2015.09.040
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CZ8GR
UT WOS:000367338700054
PM 26491845
ER

PT J
AU Bergman, A
   Becher, G
   Blumberg, B
   Bjerregaard, P
   Bornman, R
   Brandt, I
   Casey, SC
   Frouin, H
   Giudice, LC
   Heindel, JJ
   Iguchi, T
   Jobling, S
   Kidd, KA
   Kortenkamp, A
   Lind, PM
   Muir, D
   Ochieng, R
   Ropstad, E
   Ross, PS
   Skakkebaek, NE
   Toppari, J
   Vandenberg, LN
   Woodruff, TJ
   Zoeller, RT
AF Bergman, Ake
   Becher, Georg
   Blumberg, Bruce
   Bjerregaard, Poul
   Bornman, Riana
   Brandt, Ingvar
   Casey, Stephanie C.
   Frouin, Heloise
   Giudice, Linda C.
   Heindel, Jerrold J.
   Iguchi, Taisen
   Jobling, Susan
   Kidd, Karen A.
   Kortenkamp, Andreas
   Lind, P. Monica
   Muir, Derek
   Ochieng, Roseline
   Ropstad, Erik
   Ross, Peter S.
   Skakkebaek, Niels Erik
   Toppari, Jorma
   Vandenberg, Laura N.
   Woodruff, Tracey J.
   Zoeller, R. Thomas
TI Manufacturing doubt about endocrine disrupter science - A rebuttal of
   industry-sponsored critical comments on the UNEP/WHO report "State of
   the Science of Endocrine Disrupting Chemicals 2012"
SO REGULATORY TOXICOLOGY AND PHARMACOLOGY
LA English
DT Editorial Material
DE Endocrine disruption; EDCs; Endocrine disruptors
ID EPIDEMIOLOGY; FRAMEWORK; CAUSATION; MODE
AB We present a detailed response to the critique of "State of the Science of Endocrine Disrupting Chemicals 2012" (UNEP/WHO, 2013) by financial stakeholders, authored by Lamb et al. (2014). Lamb et al.'s claim that UNEP/WHO (2013) does not provide a balanced perspective on endocrine disruption is based on incomplete and misleading quoting of the report through omission of qualifying statements and inaccurate description of study objectives, results and conclusions. Lamb et al. define extremely narrow standards for synthesizing evidence which are then used to dismiss the UNEP/WHO 2013 report as flawed. We show that Lamb et al. misuse conceptual frameworks for assessing causality, especially the Bradford Hill criteria, by ignoring the fundamental problems that exist with inferring causality from empirical observations. We conclude that Lamb et al.'s attempt of deconstructing the UNEP/WHO (2013) report is not particularly erudite and that their critique is not intended to be convincing to the scientific community, but to confuse the scientific data. Consequently, it promotes misinterpretation of the UNEP/WHO (2013) report by non-specialists, bureaucrats, politicians and other decision makers not intimately familiar with the topic of endocrine disruption and therefore susceptible to false generalizations of bias and subjectivity. (C) 2015 The Authors. Published by Elsevier Inc.
C1 [Bergman, Ake] Swedish Toxicol Sci Res Ctr Swetox, Sodertalje, Sweden.
   [Becher, Georg] Norwegian Inst Publ Hlth, Oslo, Norway.
   [Blumberg, Bruce; Casey, Stephanie C.] Univ Calif Irvine, Irvine, CA USA.
   [Bjerregaard, Poul] Univ Southern Denmark, Odense, Denmark.
   [Bornman, Riana] Univ Pretoria, Sch Hlth Syst & Publ Hlth, ZA-0002 Pretoria, South Africa.
   [Brandt, Ingvar; Lind, P. Monica] Uppsala Univ, Uppsala, Sweden.
   [Frouin, Heloise; Ross, Peter S.] Vancouver Aquarium Marine Sci Ctr, Vancouver, BC, Canada.
   [Giudice, Linda C.; Woodruff, Tracey J.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
   [Heindel, Jerrold J.] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
   [Iguchi, Taisen] Natl Inst Basic Biol, Okazaki, Aichi 444, Japan.
   [Jobling, Susan; Kortenkamp, Andreas] Brunel Univ London, Uxbridge, Middx, England.
   [Kidd, Karen A.] Univ New Brunswick, New Brunswick, NJ USA.
   [Muir, Derek] Environm Canada, Burlington, ON L7R 4A6, Canada.
   [Ochieng, Roseline] Aga Khan Univ Hosp, Nairobi, Kenya.
   [Ropstad, Erik] Norwegian Univ Life Sci, Oslo, Norway.
   [Skakkebaek, Niels Erik] Univ Copenhagen, Copenhagen Univ Hosp, Copenhagen, Denmark.
   [Toppari, Jorma] Univ Turku, Turku, Finland.
   [Vandenberg, Laura N.; Zoeller, R. Thomas] Univ Massachusetts, Amherst, MA 01003 USA.
RP Bergman, A (reprint author), Swedish Toxicol Sci Res Ctr Swetox, Sodertalje, Sweden.
EM ake.bergman@swetox.se
RI jobling, susan/N-9316-2016; 
OI Brandt, Ingvar/0000-0002-5386-2400; Bergman, Ake/0000-0003-3403-093X;
   Kidd, Karen/0000-0002-5619-1358; Bjerregaard, Poul/0000-0002-2065-7232
NR 22
TC 8
Z9 8
U1 6
U2 18
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0273-2300
EI 1096-0295
J9 REGUL TOXICOL PHARM
JI Regul. Toxicol. Pharmacol.
PD DEC
PY 2015
VL 73
IS 3
BP 1007
EP 1017
DI 10.1016/j.yrtph.2015.07.026
PG 11
WC Medicine, Legal; Pharmacology & Pharmacy; Toxicology
SC Legal Medicine; Pharmacology & Pharmacy; Toxicology
GA CZ7KX
UT WOS:000367279400042
PM 26239693
ER

PT J
AU Gao, J
   Adams, RP
   Swain, SM
AF Gao, J.
   Adams, R. P.
   Swain, S. M.
TI Does CDKN2A loss predict palbociclib benefit?
SO CURRENT ONCOLOGY
LA English
DT Article
DE Medical oncology; breast cancer
ID ADVANCED BREAST-CANCER; KINASE 4/6 INHIBITOR; CDK4; P16
AB Palbociclib, an oral small-molecule inhibitor of cyclin-dependent kinases 4 and 6, was recently approved by the U.S. Food and Drug Administration in combination with letrozole for postmenopausal women with advanced hormone receptor-positive, HER2-negative breast cancer. Patients with loss of CDKN2A (p16), an inherent negative regulator of cyclin-dependent kinases 4 and 6, were not separately studied because of the significant response of the patients selected based only on receptor status. Here, we report a patient with metastatic estrogen receptor-positive, HER2-negative breast cancer with CDKN2A loss who experienced a clinical response to palbociclib.
C1 [Gao, J.] NCI, NIH, Bethesda, MD 20892 USA.
   [Adams, R. P.; Swain, S. M.] MedStar Washington Hosp Ctr, Washington Canc Inst, Washington, DC 20010 USA.
RP Swain, SM (reprint author), MedStar Washington Hosp Ctr, Washington Canc Inst, 110 Irving St NW, Washington, DC 20010 USA.
EM sandra.m.swain@medstar.net
OI Swain, Sandra/0000-0002-1320-3830
FU Pfizer; Incyte
FX We have read and understood Current Oncology's policy on disclosing
   conflicts of interest, and we declare the following interests: SMS's
   institution has received research funding from Pfizer and Incyte. SMS is
   also a paid advisory board consultant for Pfizer. The other authors
   declare that they have no conflicts of interest. All authors contributed
   to the writing and revision of the report and approved the final
   version.
NR 13
TC 2
Z9 2
U1 0
U2 2
PU MULTIMED INC
PI TORONTO
PA 66 MARTIN ST, TORONTO, ON L9T 2R2, CANADA
SN 1198-0052
J9 CURR ONCOL
JI Curr. Oncol.
PD DEC
PY 2015
VL 22
IS 6
BP E498
EP E501
DI 10.3747/co.22.2700
PG 4
WC Oncology
SC Oncology
GA CZ3DB
UT WOS:000366983500012
PM 26715889
ER

PT J
AU Natrajan, MS
   Komori, M
   Kosa, P
   Johnson, KR
   Wu, TX
   Franklin, RJM
   Bielekova, B
AF Natrajan, Muktha S.
   Komori, Mika
   Kosa, Peter
   Johnson, Kory R.
   Wu, Tianxia
   Franklin, Robin J. M.
   Bielekova, Bibiana
TI Pioglitazone regulates myelin phagocytosis and multiple sclerosis
   monocytes
SO ANNALS OF CLINICAL AND TRANSLATIONAL NEUROLOGY
LA English
DT Article
ID CENTRAL-NERVOUS-SYSTEM; CEREBROSPINAL-FLUID; CNS REMYELINATION;
   MACROPHAGE POLARIZATION; INFLAMMATORY RESPONSES; INDUCED DEMYELINATION;
   SOLUBLE CD14; MRI ACTIVITY; CELLS; ACTIVATION
AB Objective: Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). Myeloid phagocytes, including blood monocytes recruited to demyelinating lesions, may play a dual role in MS: on one hand, they might enhance CNS damage after differentiating toward a proinflammatory phenotype; on the other, they promote remyelination and repair through effective phagocytosis of myelin debris. We have previously determined that the retinoid X receptor (RXR) plays an important role in monocyte phagocytosis of myelin. Peroxisome proliferator-activated receptor gamma is an RXR binding partner that plays a key role in myeloid cell biology and is targeted by the thiazolidinedione group of antidiabetics such as pioglitazone. Consequently, the purpose of this study was to determine if monocyte functions and differentiation profiles differ in MS patients compared to healthy volunteers (HV) and whether pioglitazone can reverse these differences to promote CNS recovery. Methods: Monocytes were isolated from MS patients and HV (n >= 36/group), and their ability to phagocytose myelin and modulate inflammation in the presence/absence of 1 mu mol/L pioglitazone (the in vivo achievable concentration) was quantified by flow cytometry, transcriptional profiling, and proteomic assays. Results: MS monocytes display impaired phagocytosis of myelin debris and enhanced proinflammatory differentiation. Pioglitazone treatment causes partial normalization of identified monocyte abnormalities in MS and fully reverses the deficit in myelin phagocytosis. Interpretation: These findings suggest that by inhibiting proinflammatory differentiation of monocytes and enhancing their phagocytosis of myelin, pioglitazone may be a useful adjunct therapy to immunomodulatory agents that target dysregulated adaptive immunity in MS.
C1 [Natrajan, Muktha S.; Komori, Mika; Kosa, Peter; Bielekova, Bibiana] NINDS, Neuroimmunol Dis Unit, NIH, Bethesda, MD 20892 USA.
   [Natrajan, Muktha S.; Franklin, Robin J. M.] Univ Cambridge, Wellcome Trust MRC Cambridge Stem Cell Inst, Cambridge CB2 0AH, England.
   [Natrajan, Muktha S.; Franklin, Robin J. M.] Univ Cambridge, Dept Clin Neurosci, Cambridge CB2 0AH, England.
   [Johnson, Kory R.; Wu, Tianxia] NINDS, NIH, Bethesda, MD 20892 USA.
RP Bielekova, B (reprint author), NINDS, Neuroimmunol Dis Unit, NIH, Bethesda, MD 20892 USA.
EM bibi.bielekova@nih.gov
NR 61
TC 1
Z9 1
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2328-9503
J9 ANN CLIN TRANSL NEUR
JI Ann. Clin. Transl. Neurol.
PD DEC
PY 2015
VL 2
IS 12
BP 1071
EP 1084
DI 10.1002/acn3.260
PG 14
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA CZ6WA
UT WOS:000367240500003
PM 26734659
ER

PT J
AU Peng, SY
   Xu, JH
   Pelkey, KA
   Chandra, G
   Zhang, ZJ
   Bagh, MB
   Yuan, XQ
   Wu, LG
   McBain, CJ
   Mukherjee, AB
AF Peng, Shiyong
   Xu, Jianhua
   Pelkey, Kenneth A.
   Chandra, Goutam
   Zhang, Zhongjian
   Bagh, Maria B.
   Yuan, Xiaoqing
   Wu, Ling-Gang
   McBain, Chris J.
   Mukherjee, Anil B.
TI Suppression of agrin-22 production and synaptic dysfunction in Cln1(-/-)
   mice
SO ANNALS OF CLINICAL AND TRANSLATIONAL NEUROLOGY
LA English
DT Article
ID NEURONAL CEROID-LIPOFUSCINOSIS; PALMITOYL-PROTEIN THIOESTERASE;
   LYSOSOMAL STORAGE DISORDERS; MENTAL-RETARDATION; OXIDATIVE STRESS; MOUSE
   MODEL; NERVOUS-SYSTEM; KNOCKOUT MICE; NEUROTRYPSIN; NEUROPATHOLOGY
AB Objective: Oxidative stress in the brain is highly prevalent in many neurodegenerative disorders including lysosomal storage disorders, in which neurodegeneration is a devastating manifestation. Despite intense studies, a precise mechanism linking oxidative stress to neuropathology in specific neurodegenerative diseases remains largely unclear. Methods: Infantile neuronal ceroid lipofuscinosis (INCL) is a devastating neurodegenerative lysosomal storage disease caused by mutations in the ceroid lipofuscinosis neuronal-1 (CLN1) gene encoding palmitoyl-protein thioesterase-1. Previously, we reported that in the brain of Cln1(-/-) mice, which mimic INCL, and in postmortem brain tissues from INCL patients, increased oxidative stress is readily detectable. We used molecular, biochemical, immunohistological, and electrophysiological analyses of brain tissues of Cln1(-/-) mice to study the role(s) of oxidative stress in mediating neuropathology. Results: Our results show that in Cln1(-/-) mice oxidative stress in the brain via upregulation of the transcription factor, CCAAT/enhancer-binding protein-delta, stimulated expression of serpina1, which is an inhibitor of a serine protease, neurotrypsin. Moreover, in the Cln1(-/-) mice, suppression of neurotrypsin activity by serpina1 inhibited the cleavage of agrin (a large proteoglycan), which substantially reduced the production of agrin-22, essential for synaptic homeostasis. Direct whole-cell recordings at the nerve terminals of Cln1(-/-) mice showed inhibition of Ca2+ currents attesting to synaptic dysfunction. Treatment of these mice with a thioesterase-mimetic small molecule, N-tert (Butyl) hydroxylamine (NtBuHA), increased agrin-22 levels. Interpretation: Our findings provide insight into a novel pathway linking oxidative stress with synaptic pathology in Cln1(-/-) mice and suggest that NtBuHA, which increased agrin-22 levels, may ameliorate synaptic dysfunction in this devastating neurodegenerative disease.
C1 [Peng, Shiyong; Chandra, Goutam; Zhang, Zhongjian; Bagh, Maria B.; Mukherjee, Anil B.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Dev Genet, Program Dev Endocrinol & Genet, NIH, Bethesda, MD 20892 USA.
   [Xu, Jianhua; Wu, Ling-Gang] NINDS, Synapt Transmiss Sect HNQ23 R, NIH, Bethesda, MD 20892 USA.
   [Pelkey, Kenneth A.; Yuan, Xiaoqing; McBain, Chris J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Dev Neurosci, NIH, Bethesda, MD 20892 USA.
RP Mukherjee, AB (reprint author), NIH, Bldg 10,Room 9D42, Bethesda, MD 20892 USA.
EM mukherja@exchange.nih.gov
NR 52
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2328-9503
J9 ANN CLIN TRANSL NEUR
JI Ann. Clin. Transl. Neurol.
PD DEC
PY 2015
VL 2
IS 12
BP 1085
EP 1104
DI 10.1002/acn3.261
PG 20
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA CZ6WA
UT WOS:000367240500004
PM 26734660
ER

PT J
AU Wang, X
   Wang, H
   Bi, C
   Zhang, X
   Huang, X
   Zhang, X
   Iqbal, J
   Wright, GW
   Staudt, LM
   Chan, WC
   McKeithan, TW
   Wang, P
   Zhang, H
   Fu, K
AF Wang, X.
   Wang, H.
   Bi, C.
   Zhang, X.
   Huang, X.
   Zhang, X.
   Iqbal, J.
   Wright, G. W.
   Staudt, L. M.
   Chan, W. C.
   McKeithan, T. W.
   Wang, P.
   Zhang, H.
   Fu, K.
TI miR-17 similar to 92 activates the canonical NF-kappa B signaling by
   targeting TNFAIP3, CYLD and Rnf11 in ABC-DLBCL lymphoma
SO ANNALS OF ONCOLOGY
LA English
DT Meeting Abstract
CT Asia Congress of the European-Society-for-Medical-Oncology (ESMO)
CY DEC 18-21, 2015
CL Singapore, SINGAPORE
SP European Soc Med Oncol
C1 [Wang, X.; Wang, H.; Wang, P.; Zhang, H.] Tianjin Med Univ, Dept Lymphoma, Canc Inst & Hosp, Tianjin, Peoples R China.
   [Bi, C.; Huang, X.; Zhang, X.; Iqbal, J.; Fu, K.] Univ Nebraska Med Ctr, Dept Pathol & Microbiol & Internal Med, Omaha, NE USA.
   [Zhang, X.] Chinese Acad Med Sci, Inst Hematol, Dept Pediat, Tianjin, Peoples R China.
   [Zhang, X.] Chinese Acad Med Sci, Blood Dis Hosp, Tianjin, Peoples R China.
   [Zhang, X.] Peking Union Med Coll, Tianjin, Peoples R China.
   [Wright, G. W.] NCI, Biometr Res Branch, Div Canc Treatment & Diag, NIH, Bethlehem, MD USA.
   [Staudt, L. M.; Chan, W. C.] NCI, Lymphoid Malignancies Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
   [McKeithan, T. W.] City Hope Natl Med Ctr, Dept Pathol, Duarte, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
EI 1569-8041
J9 ANN ONCOL
JI Ann. Oncol.
PD DEC
PY 2015
VL 26
SU 9
MA 296P
BP 88
EP 88
PG 1
WC Oncology
SC Oncology
GA CZ5RC
UT WOS:000367158700295
ER

PT J
AU Viollet, C
   Ragoussis, J
   Yarchoan, R
   Pezzella, F
AF Viollet, C.
   Ragoussis, J.
   Yarchoan, R.
   Pezzella, F.
TI A whole genome approach to better understand the link between Kaposi's
   sarcoma-associated herpesvirus and human cancers
SO ANNALS OF ONCOLOGY
LA English
DT Meeting Abstract
CT Asia Congress of the European-Society-for-Medical-Oncology (ESMO)
CY DEC 18-21, 2015
CL Singapore, SINGAPORE
SP European Soc Med Oncol
C1 [Viollet, C.; Yarchoan, R.] Natl Canc Inst, Ctr Canc Res, Bethesda, MD USA.
   [Ragoussis, J.] McGill Univ, Genome Sci, Montreal, PQ, Canada.
   [Pezzella, F.] Univ Oxford, John Radcliffe Hosp, RDM Clin Lab Sci, Oxford OX3 9DU, England.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
EI 1569-8041
J9 ANN ONCOL
JI Ann. Oncol.
PD DEC
PY 2015
VL 26
SU 9
MA 359O
BP 108
EP 108
PG 1
WC Oncology
SC Oncology
GA CZ5RC
UT WOS:000367158700358
ER

PT J
AU Chen, JF
   Xiao, YY
   Gai, ZX
   Li, R
   Zhu, ZX
   Bai, CL
   Tanguay, RL
   Xu, XJ
   Huang, CJ
   Dong, QX
AF Chen, Jiangfei
   Xiao, Yanyan
   Gai, Zengxin
   Li, Rong
   Zhu, Zixu
   Bai, Chenglian
   Tanguay, Robert L.
   Xu, Xiaojiang
   Huang, Changjiang
   Dong, Qiaoxiang
TI Reproductive toxicity of low level bisphenol A exposures in a
   two-generation zebrafish assay: Evidence of male-specific effects
SO AQUATIC TOXICOLOGY
LA English
DT Article
DE Zebrafish; Chronic exposure; BPA; Sperm; Mitochondrial biogenesis; Wnt
   signaling
ID MEDAKA ORYZIAS-LATIPES; PIMEPHALES-PROMELAS; PERINATAL EXPOSURE; SEX
   DETERMINATION; FATHEAD MINNOW; TERM EXPOSURE; MALE GOLDFISH; SPERM;
   QUALITY; DIFFERENTIATION
AB Bisphenol A (BPA), a high-volume chemical used to make polycarbonate plastic and epoxy resins, is a ubiquitous contaminant in environment and human body. To investigate the reproductive effects of longterm exposure to low concentrations of BPA, a two-generation study was conducted using the aquatic model species of zebrafish. Our findings revealed that exposure to 1 nM (0.228 mu g/L) BPA for continuous two generations resulted in female-biased sex ratio in both F1 and F2 adult population, decreased sperm density, and decreased sperm quality as measured by motility, velocity, ATP content and lipid peroxidation in F1 and F2 males. Females were less sensitive to BPA exposures than males as no adverse effects were found in female gonads or gametes. Delayed hatching at 48 hpf and increased malformation and mortality were found in the offspring from BPA exposed F2, but not F1 parents. Most importantly, the adverse effect on larval development and survival from BPA exposed F2 parents was paternal-specific, resulting mainly from BPA exposed males. Subsequent transcription analysis of F2 male gonads revealed dysregulated mitochondrial biogenesis and significant activation of non-canonical Wnt/planar cell polarity and Wnt/Calcium signaling pathways. Gene expression analysis of larvae from BPA exposed F2 parents showed significant reduced expression of DNA methyltransferases such as dnmt1, dnmt3, and dnmt5. In conclusion, low level BPA exposures for continuous two generations not only affects sex ratio and sperm quantity/quality in F1 and F2 adults, reproductive success in offspring from F2 parents, but also perturbs various molecular pathways potentially contributing to these BPA induced male-specific reproductive defects. (C) 2015 Elsevier B.V. All rights reserved.
C1 [Chen, Jiangfei; Xiao, Yanyan; Gai, Zengxin; Li, Rong; Zhu, Zixu; Bai, Chenglian; Huang, Changjiang; Dong, Qiaoxiang] Wenzhou Med Univ, Sch Lab Med & Life Sci, Zhejiang Prov Key Lab Technol & Applicat Model Or, Wenzhou 325035, Peoples R China.
   [Chen, Jiangfei; Xiao, Yanyan; Gai, Zengxin; Li, Rong; Zhu, Zixu; Bai, Chenglian; Huang, Changjiang; Dong, Qiaoxiang] Wenzhou Med Univ, Inst Environm Safety & Human Hlth, Wenzhou 325035, Peoples R China.
   [Tanguay, Robert L.] Oregon State Univ, Sinnhuber Aquat Res Lab, Environm & Mol Toxicol, Corvallis, OR 97333 USA.
   [Tanguay, Robert L.] Oregon State Univ, Environm Hlth Sci Ctr, Corvallis, OR 97333 USA.
   [Xu, Xiaojiang] NIEHS, Integrated Bioinformat, Res Triangle Pk, NC 27709 USA.
RP Huang, CJ (reprint author), Wenzhou Med Univ, Sch Lab Med & Life Sci, Zhejiang Prov Key Lab Technol & Applicat Model Or, Wenzhou 325035, Peoples R China.
EM cjhuang5711@163.com; dqxdong@163.com
RI Huang, Changjiang/F-2644-2010; Dong, Qiaoxiang/F-1918-2010
FU National Natural Science Foundation of China [41271491]; National
   Environmental Protection Public Welfare Science and Technology Research
   Program of China [201309047]
FX This work was supported in part by funding from the National Natural
   Science Foundation of China (No. 41271491) and the National
   Environmental Protection Public Welfare Science and Technology Research
   Program of China (No. 201309047).
NR 51
TC 6
Z9 7
U1 11
U2 49
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-445X
EI 1879-1514
J9 AQUAT TOXICOL
JI Aquat. Toxicol.
PD DEC
PY 2015
VL 169
BP 204
EP 214
DI 10.1016/j.aquatox.2015.10.020
PG 11
WC Marine & Freshwater Biology; Toxicology
SC Marine & Freshwater Biology; Toxicology
GA CZ3TV
UT WOS:000367027800021
PM 26562050
ER

PT J
AU Henderson, M
   Simeon-Dubach, D
   Albert, M
AF Henderson, Marianne
   Simeon-Dubach, Daniel
   Albert, Monique
TI Finding the Path to Biobank Sustainability Through Sound Business
   Planning
SO BIOPRESERVATION AND BIOBANKING
LA English
DT Editorial Material
C1 [Henderson, Marianne] NCI, NIH, Bethesda, MD 20892 USA.
   [Simeon-Dubach, Daniel] Medservice, Walchwil, Switzerland.
   [Albert, Monique] Ontario Inst Canc Res, Toronto, ON, Canada.
RP Henderson, M (reprint author), NCI, NIH, Bethesda, MD 20892 USA.
EM hendersm@mail.nih.gov
NR 4
TC 6
Z9 6
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1947-5535
EI 1947-5543
J9 BIOPRESERV BIOBANK
JI Biopreserv. Biobank.
PD DEC 1
PY 2015
VL 13
IS 6
SI SI
BP 385
EP 386
DI 10.1089/bio.2015.29039.mh
PG 2
WC Cell Biology; Chemistry, Applied; Medical Laboratory Technology
SC Cell Biology; Chemistry; Medical Laboratory Technology
GA CZ3MU
UT WOS:000367009000001
PM 26697906
ER

PT J
AU Odeh, H
   Miranda, L
   Rao, A
   Vaught, J
   Greenman, H
   McLean, J
   Reed, D
   Memon, S
   Fombonne, B
   Guan, P
   Moore, HM
AF Odeh, Hana
   Miranda, Lisa
   Rao, Abhi
   Vaught, Jim
   Greenman, Howard
   McLean, Jeffrey
   Reed, Daniel
   Memon, Sarfraz
   Fombonne, Benjamin
   Guan, Ping
   Moore, Helen M.
TI The Biobank Economic Modeling Tool (BEMT): Online Financial Planning to
   Facilitate Biobank Sustainability
SO BIOPRESERVATION AND BIOBANKING
LA English
DT Article
ID BUSINESS MODEL; USER FEES; BIOREPOSITORIES; CHALLENGES; GAP
AB Background: Biospecimens are essential resources for advancing basic and translational research. However, there are little data available regarding the costs associated with operating a biobank, and few resources to enable their long-term sustainability. To support the research community in this effort, the National Institutes of Health, National Cancer Institute's Biorepositories and Biospecimen Research Branch has developed the Biobank Economic Modeling Tool (BEMT). The tool is accessible at http://biospecimens.cancer.gov/resources/bemt.asp. Methods: To obtain market-based cost information and to inform the development of the tool, a survey was designed and sent to 423 biobank managers and directors across the world. The survey contained questions regarding infrastructure investments, salary costs, funding options, types of biospecimen resources and services offered, as well as biospecimen pricing and service-related costs. Results: A total of 106 responses were received. The data were anonymized, aggregated, and used to create a comprehensive database of cost and pricing information that was integrated into the web-based tool, the BEMT. The BEMT was built to allow the user to input cost and pricing data through a seven-step process to build a cost profile for their biobank, define direct and indirect costs, determine cost recovery fees, perform financial forecasting, and query the anonymized survey data from comparable biobanks. Conclusion: A survey was conducted to obtain a greater understanding of the costs involved in operating a biobank. The anonymized survey data was then used to develop the BEMT, a cost modeling tool for biobanks. Users of the tool will be able to create a cost profile for their biobanks' specimens, products and services, establish pricing, and allocate costs for biospecimens based on percent cost recovered, and perform project-specific cost analyses and financial forecasting.
C1 [Odeh, Hana; Rao, Abhi; Vaught, Jim; Memon, Sarfraz; Fombonne, Benjamin; Guan, Ping; Moore, Helen M.] NCI, Biorepositories & Biospecimen Res Branch, Bethesda, MD 20892 USA.
   [Odeh, Hana; Fombonne, Benjamin] Kelly Govt Solut, Rockville, MD USA.
   [Miranda, Lisa] Biobusiness Consulting Inc, Newburyport, MA USA.
   [Vaught, Jim] Gray Sourcing, San Diego, CA USA.
   [Greenman, Howard] Provia Labs LLC, Littleton, MA USA.
   [McLean, Jeffrey] Leidos Biomed Res Inc, Rockville, MD USA.
   [Reed, Daniel] Wrycan Inc, Cambridge, MA USA.
RP Moore, HM (reprint author), NCI, 9609 Med Ctr Dr,3W 428, Rockville, MD 20850 USA.
EM moorehe@mail.nih.gov
FU Biorepositories and Biospecimen Research Branch at the National Cancer
   Institute, National Institutes of Health
FX Funding: This project has been funded in whole or in part with federal
   funds from the American Recovery and Re-investment Act (ARRA) from the
   Biorepositories and Biospecimen Research Branch at the National Cancer
   Institute, National Institutes of Health.
NR 19
TC 4
Z9 4
U1 1
U2 4
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1947-5535
EI 1947-5543
J9 BIOPRESERV BIOBANK
JI Biopreserv. Biobank.
PD DEC 1
PY 2015
VL 13
IS 6
SI SI
BP 421
EP 429
DI 10.1089/bio.2015.0089
PG 9
WC Cell Biology; Chemistry, Applied; Medical Laboratory Technology
SC Cell Biology; Chemistry; Medical Laboratory Technology
GA CZ3MU
UT WOS:000367009000006
PM 26697911
ER

PT J
AU Lheureux, S
   Oza, AM
   Laurie, SA
   Halford, R
   Jonker, D
   Chen, E
   Keller, D
   Bourade, V
   Wang, L
   Doyle, L
   Siu, LL
   Goel, R
AF Lheureux, S.
   Oza, A. M.
   Laurie, S. A.
   Halford, R.
   Jonker, D.
   Chen, E.
   Keller, D.
   Bourade, V.
   Wang, L.
   Doyle, L.
   Siu, L. L.
   Goel, R.
TI A phase I combination dose-escalation study of eribulin mesylate and
   gemcitabine in patients with advanced solid tumours: a study of the
   Princess Margaret Consortium
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE eribulin; gemcitabine; advanced cancer; phase I; solid tumours; safety;
   gynaecological cancer
ID METASTATIC BREAST-CANCER; VIVO ANTICANCER ACTIVITIES; CELL LUNG-CANCER;
   HALICHONDRIN-B; ANALOG; E7389; CISPLATIN; MONOTHERAPY; MECHANISMS; VITRO
AB Background: Eribulin mesylate is a synthetic microtubule inhibitor that showed cytotoxic synergy in combination with gemcitabine preclinically. This combination was assessed in a Phase I dose-finding trial in patients diagnosed with advanced solid tumours who had received up to two prior chemotherapy regimens for metastatic disease (CP cohort).
   Methods: Dose escalation was performed in a 3+3 design to identify the recommended phase II dose (RP2D). Two additional expansion cohorts in women with gynaecologic cancers at the RP2D (G), and further dose escalation of metastatic chemotherapy-naive patients (CN), were evaluated.
   Results: 45 patients were treated: 21 (CP), 10 (G) and 14 (CN). The initial combination of eribulin and gemcitabine was administered on days 1, 8, and 15 of a 28-day cycle; however, due to 2 out of 6 dose-limiting haematological toxicities at the first dose level, a reduced dose-intense schedule was assessed. The RP2D was defined at 1.0mgm(-2) eribulin and 1000mgm(-2) gemcitabine day 1 and 8 q3 weeks. No other significant toxicities were observed in the G expansion cohort. Neutropenia prevented further dose escalation in the CN cohort. Objective responses were seen in all three cohorts -2/21 (CP), 1/10 (G) and 2/14 (CN).
   Conclusions: The combination of eribulin and gemcitabine was well tolerated at the RP2D.
C1 [Lheureux, S.; Oza, A. M.; Halford, R.; Chen, E.; Wang, L.; Siu, L. L.] Princess Margaret Canc Ctr, Dept Med Oncol, Toronto, ON M5G 2M9, Canada.
   [Laurie, S. A.; Jonker, D.; Keller, D.; Bourade, V.; Goel, R.] Ottawa Hosp Canc Ctr, Dept Med Oncol, Ottawa, ON K1H 8M5, Canada.
   [Doyle, L.] NCI, CTEP, Bethesda, MD 20892 USA.
RP Goel, R (reprint author), Ottawa Hosp Canc Ctr, Dept Med Oncol, Ottawa, ON K1H 8M5, Canada.
EM rgoel@toh.on.ca
FU NCI US grant [HHSN261201100032C]
FX We acknowledge the NCI US grant; Contract # HHSN261201100032C.
NR 28
TC 1
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U1 1
U2 2
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 DEC 1
PY 2015
VL 113
IS 11
BP 1534
EP 1540
DI 10.1038/bjc.2015.343
PG 7
WC Oncology
SC Oncology
GA CZ5UL
UT WOS:000367167400002
PM 26554651
ER

PT J
AU Bogdanova, TI
   Zurnadzhy, LY
   Nikiforov, YE
   Leeman-Neill, RJ
   Tronko, MD
   Chanock, S
   Mabuchi, K
   Likhtarov, IA
   Kovgan, LM
   Drozdovitch, V
   Little, MP
   Hatch, M
   Zablotska, LB
   Shpak, VM
   McConnell, RJ
   Brenner, AV
AF Bogdanova, Tetiana I.
   Zurnadzhy, Liudmyla Yu
   Nikiforov, Yuri E.
   Leeman-Neill, Rebecca J.
   Tronko, Mykola D.
   Chanock, Stephen
   Mabuchi, Kiyohiko
   Likhtarov, Ilya A.
   Kovgan, Leonila M.
   Drozdovitch, Vladimir
   Little, Mark P.
   Hatch, Maureen
   Zablotska, Lydia B.
   Shpak, Viktor M.
   McConnell, Robert J.
   Brenner, Alina V.
TI Histopathological features of papillary thyroid carcinomas detected
   during four screening examinations of a Ukrainian-American cohort
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE thyroid cancer; papillary thyroid carcinoma; radiation; iodine-131;
   pathology; Chernobyl; Chornobyl
ID ATOMIC-BOMB SURVIVORS; CHERNOBYL ACCIDENT; CANCER; RADIATION; CHILDREN;
   DISEASES; I-131; REARRANGEMENTS; MUTATION; RET/PTC
AB Background: There are limited data on the histopathology of papillary thyroid carcinomas (PTCs) diagnosed in irradiated populations. We evaluated the associations between iodine-131 dose and the histopathological characteristics of post-Chernobyl PTCs, the changes in these characteristics over time, and their associations with selected somatic mutations.
   Methods: This study included 115 PTCs diagnosed in a Ukrainian-American cohort (n = 13 243) during prescreening and four successive thyroid screenings. Of these PTCs, 65 were subjected to somatic mutation profiling. All individuals were <18 years at the time of the Chernobyl accident and had direct thyroid radioactivity measurements. Statistical analyses included multivariate linear and logistic regression.
   Results: We identified a borderline significant linear-quadratic association (P = 0.063) between iodine-131 dose and overall tumour invasiveness (presence of extrathyroidal extension, lymphatic/vascular invasion, and regional or distant metastases). Irrespective of dose, tumours with chromosomal rearrangements were more likely to have lymphatic/vascular invasion than tumours without chromosomal rearrangements (P = 0.020) or tumours with BRAF or RAS point mutations (P = 0.008). Controlling for age, there were significant time trends in decreasing tumour size (Po0.001), the extent of lymphatic/vascular invasion (P = 0.005), and overall invasiveness (P = 0.026).
   Conclusions: We determined that the invasive properties of PTCs that develop in iodine-131-exposed children may be associated with radiation dose. In addition, based on a subset of cases, tumours with chromosomal rearrangements appear to have a more invasive phenotype. The increase in small, less invasive PTCs over time is a consequence of repeated screening examinations.
C1 [Bogdanova, Tetiana I.; Zurnadzhy, Liudmyla Yu] Ukraine Acad Med Sci, Lab Morphol Endocrine Syst, State Inst VP Komisarenko Inst Endocrinol & Metab, UA-254114 Kiev, Ukraine.
   [Nikiforov, Yuri E.; Leeman-Neill, Rebecca J.] Univ Pittsburgh, Sch Med, Dept Pathol, Pittsburgh, PA 15213 USA.
   [Tronko, Mykola D.] Ukraine Acad Med Sci, State Inst VP Komisarenko Inst Endocrinol & Metab, Dept Fundamental & Appl Problems Endocrinol, UA-254114 Kiev, Ukraine.
   [Chanock, Stephen; Mabuchi, Kiyohiko; Drozdovitch, Vladimir; Little, Mark P.; Hatch, Maureen; Brenner, Alina V.] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Likhtarov, Ilya A.] Ukraine Acad Med Sci, State Inst Natl Res Ctr Radiat Med, Dept Dosimetry & Radiat Protect, UA-04050 Kiev, Ukraine.
   [Kovgan, Leonila M.] Ukraine Acad Med Sci, State Inst Natl Res Ctr Radiat Med, Lab Radiat Protect, UA-04050 Kiev, Ukraine.
   [Zablotska, Lydia B.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94118 USA.
   [Shpak, Viktor M.] Ukraine Acad Med Sci, State Inst VP Komisarenko Inst Endocrinol & Metab, Dept Med Consequences Chernobyl Accid & Int Coope, UA-254114 Kiev, Ukraine.
   [McConnell, Robert J.] Columbia Univ, Thyroid Ctr, New York, NY 10032 USA.
   [McConnell, Robert J.] Columbia Univ, Coll Phys & Surg, Dept Med, New York, NY USA.
RP Brenner, AV (reprint author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, 9609 Med Ctr Dr,MSC 9778, Bethesda, MD 20892 USA.
EM brennera@mail.nih.gov
OI Little, Mark/0000-0003-0980-7567
FU NIH [R01 CA88041, NO1-CP-21178, CA132918]; Intramural Research Program
   of the National Institutes of Health, National Cancer Institute;
   Department of Energy; US Nuclear Regulatory Commission
FX We acknowledge the commitment of our Colleagues at the Institute of
   Endocrinology and Metabolism (IEM) in Ukraine who performed all four
   screening examinations, particularly the staff of the Laboratory of
   Endocrine System Morphology who collected histopathological samples from
   the Ukrainian-American cohort and staff of the Surgery Department who
   operated on these patients. We also acknowledge our American colleagues,
   Drs. J Robbins, E Greenebaum, and P O'Kane, who collaborated with us
   over many years and participated in discussions of clinical and
   histopathological data. We gratefully acknowledge the confirmation of
   diagnoses provided by the International Pathology Panel of the Chernobyl
   Tissue Bank: Professors A Abrosimov, T Bogdanova, G Fadda, J Hunt, M
   Ito, V Livolsi, J Rosai, and ED Williams. This research was supported by
   the Intramural Research Program of the National Institutes of Health,
   National Cancer Institute, and the Department of Energy. The US Nuclear
   Regulatory Commission provided the initial funds for equipment purchase.
   The work of Drs. Nikiforov and Leeman-Neill was in part supported by NIH
   grant R01 CA88041 to YEN; Drs. Zablotska and McConnell by contract
   NO1-CP-21178 to LBZ and RJM and grant CA132918 to LBZ
NR 41
TC 2
Z9 5
U1 2
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD DEC 1
PY 2015
VL 113
IS 11
BP 1556
EP 1564
DI 10.1038/bjc.2015.372
PG 9
WC Oncology
SC Oncology
GA CZ5UL
UT WOS:000367167400005
PM 26625214
ER

PT J
AU Alexander, SPH
   Kelly, E
   Marrion, N
   Peters, JA
   Benson, HE
   Faccenda, E
   Pawson, AJ
   Sharman, JL
   Southan, C
   Buneman, OP
   Catterall, WA
   Cidlowski, JA
   Davenport, AP
   Fabbro, D
   Fan, G
   McGrath, JC
   Spedding, M
   Davies, JA
   Aldrich, R
   Attali, B
   Back, M
   Barnes, NM
   Bathgate, R
   Beart, PM
   Becirovic, E
   Biel, M
   Birdsall, NJ
   Boison, D
   Brauner-Osborne, H
   Broer, S
   Bryant, C
   Burnstock, G
   Burris, T
   Cain, D
   Calo, G
   Chan, SL
   Chandy, KG
   Chiang, N
   Christakos, S
   Christopoulos, A
   Chun, JJ
   Chung, JJ
   Clapham, DE
   Connor, MA
   Coons, L
   Cox, HM
   Dautzenberg, FM
   Dent, G
   Douglas, SD
   Dubocovich, ML
   Edwards, DP
   Farndale, R
   Fong, TM
   Forrest, D
   Fowler, CJ
   Fuller, P
   Gainetdinov, RR
   Gershengorn, MA
   Goldin, A
   Goldstein, SAN
   Grimm, SL
   Grissmer, S
   Gundlach, AL
   Hagenbuch, B
   Hammond, JR
   Hancox, JC
   Hartig, S
   Hauger, RL
   Hay, DL
   Hebert, T
   Hollenberg, AN
   Holliday, ND
   Hoyer, D
   Ijzerman, AP
   Inui, KI
   Ishii, S
   Jacobson, KA
   Jan, LY
   Jarvis, GE
   Jensen, R
   Jetten, A
   Jockers, R
   Kaczmarek, LK
   Kanai, Y
   Kang, HS
   Karnik, S
   Kerr, ID
   Korach, KS
   Lange, CA
   Larhammar, D
   Leeb-Lundberg, F
   Leurs, R
   Lolait, SJ
   Macewan, D
   Maguire, JJ
   May, JM
   Mazella, J
   McArdle, CA
   McDonnell, DP
   Michel, MC
   Miller, LJ
   Mitolo, V
   Monie, T
   Monk, PN
   Mouillac, B
   Murphy, PM
   Nahon, JL
   Nerbonne, J
   Nichols, CG
   Norel, X
   Oakley, R
   Offermanns, S
   Palmer, LG
   Panaro, MA
   Perez-Reyes, E
   Pertwee, RG
   Pike, JW
   Pin, JP
   Pintor, S
   Plant, LD
   Poyner, DR
   Prossnitz, ER
   Pyne, S
   Ren, D
   Richer, JK
   Rondard, P
   Ross, RA
   Sackin, H
   Safi, R
   Sanguinetti, MC
   Sartorius, CA
   Segaloff, DL
   Sladek, FM
   Stewart, G
   Stoddart, LA
   Striessnig, J
   Summers, RJ
   Takeda, Y
   Tetel, M
   Toll, L
   Trimmer, JS
   Tsai, MJ
   Tsai, SY
   Tucker, S
   Usdin, TB
   Vilargada, JP
   Vore, M
   Ward, DT
   Waxman, SG
   Webb, P
   Wei, AD
   Weigel, N
   Willars, GB
   Winrow, C
   Wong, SS
   Wulff, H
   Ye, RD
   Young, M
   Zajac, JM
AF Alexander, Stephen P. H.
   Kelly, Eamonn
   Marrion, Neil
   Peters, John A.
   Benson, Helen E.
   Faccenda, Elena
   Pawson, Adam J.
   Sharman, Joanna L.
   Southan, Christopher
   Buneman, O. Peter
   Catterall, William A.
   Cidlowski, John A.
   Davenport, Anthony P.
   Fabbro, Doriano
   Fan, Grace
   McGrath, John C.
   Spedding, Michael
   Davies, Jamie A.
   Aldrich, R.
   Attali, B.
   Back, M.
   Barnes, N. M.
   Bathgate, R.
   Beart, P. M.
   Becirovic, E.
   Biel, M.
   Birdsall, N. J.
   Boison, D.
   Brauner-Osborne, H.
   Broeer, S.
   Bryant, C.
   Burnstock, G.
   Burris, T.
   Cain, D.
   Calo, G.
   Chan, S. L.
   Chandy, K. G.
   Chiang, N.
   Christakos, S.
   Christopoulos, A.
   Chun, J. J.
   Chung, J. -J.
   Clapham, D. E.
   Connor, M. A.
   Coons, L.
   Cox, H. M.
   Dautzenberg, F. M.
   Dent, G.
   Douglas, S. D.
   Dubocovich, M. L.
   Edwards, D. P.
   Farndale, R.
   Fong, T. M.
   Forrest, D.
   Fowler, C. J.
   Fuller, P.
   Gainetdinov, R. R.
   Gershengorn, M. A.
   Goldin, A.
   Goldstein, S. A. N.
   Grimm, S. L.
   Grissmer, S.
   Gundlach, A. L.
   Hagenbuch, B.
   Hammond, J. R.
   Hancox, J. C.
   Hartig, S.
   Hauger, R. L.
   Hay, D. L.
   Hebert, T.
   Hollenberg, A. N.
   Holliday, N. D.
   Hoyer, D.
   Ijzerman, A. P.
   Inui, K. I.
   Ishii, S.
   Jacobson, K. A.
   Jan, L. Y.
   Jarvis, G. E.
   Jensen, R.
   Jetten, A.
   Jockers, R.
   Kaczmarek, L. K.
   Kanai, Y.
   Kang, H. S.
   Karnik, S.
   Kerr, I. D.
   Korach, K. S.
   Lange, C. A.
   Larhammar, D.
   Leeb-Lundberg, F.
   Leurs, R.
   Lolait, S. J.
   Macewan, D.
   Maguire, J. J.
   May, J. M.
   Mazella, J.
   McArdle, C. A.
   McDonnell, D. P.
   Michel, M. C.
   Miller, L. J.
   Mitolo, V.
   Monie, T.
   Monk, P. N.
   Mouillac, B.
   Murphy, P. M.
   Nahon, J. -L.
   Nerbonne, J.
   Nichols, C. G.
   Norel, X.
   Oakley, R.
   Offermanns, S.
   Palmer, L. G.
   Panaro, M. A.
   Perez-Reyes, E.
   Pertwee, R. G.
   Pike, J. W.
   Pin, J. P.
   Pintor, S.
   Plant, L. D.
   Poyner, D. R.
   Prossnitz, E. R.
   Pyne, S.
   Ren, D.
   Richer, J. K.
   Rondard, P.
   Ross, R. A.
   Sackin, H.
   Safi, R.
   Sanguinetti, M. C.
   Sartorius, C. A.
   Segaloff, D. L.
   Sladek, F. M.
   Stewart, G.
   Stoddart, L. A.
   Striessnig, J.
   Summers, R. J.
   Takeda, Y.
   Tetel, M.
   Toll, L.
   Trimmer, J. S.
   Tsai, M. -J.
   Tsai, S. Y.
   Tucker, S.
   Usdin, T. B.
   Vilargada, J. -P.
   Vore, M.
   Ward, D. T.
   Waxman, S. G.
   Webb, P.
   Wei, A. D.
   Weigel, N.
   Willars, G. B.
   Winrow, C.
   Wong, S. S.
   Wulff, H.
   Ye, R. D.
   Young, M.
   Zajac, J. -M.
CA CGTP Collaborators
TI THE CONCISE GUIDE TO PHARMACOLOGY 2015/16: Overview
SO BRITISH JOURNAL OF PHARMACOLOGY
LA English
DT Article
AB The Concise Guide to PHARMACOLOGY 2015/16 provides concise overviews of the key properties of over 1750 human drug targets with their pharmacology, plus links to an open access knowledgebase of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. The full contents can be found at http://onlinelibrary.wiley.com/doi/10.1111/bph.13347/full. This compilation of the major pharmacological targets is divided into eight areas of focus: G protein-coupled receptors, ligand-gated ion channels, voltage-gated ion channels, other ion channels, nuclear hormone receptors, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The Concise Guide is published in landscape format in order to facilitate comparison of related targets. It is a condensed version of material contemporary to late 2015, which is presented in greater detail and constantly updated on the website www.guidetopharmacology.org, superseding data presented in the previous Guides to Receptors & Channels and the Concise Guide to PHARMACOLOGY 2013/14. It is produced in conjunction with NC-IUPHAR and provides the official IUPHAR classification and nomenclature for human drug targets, where appropriate. It consolidates information previously curated and displayed separately in IUPHAR-DB and GRAC and provides a permanent, citable, point-in-time record that will survive database updates.
C1 [Alexander, Stephen P. H.] Univ Nottingham, Sch Med, Sch Biomed Sci, Nottingham NG7 2UH, England.
   [Kelly, Eamonn; Marrion, Neil] Univ Bristol, Sch Physiol & Pharmacol, Bristol BS8 1TD, Avon, England.
   [Peters, John A.] Univ Dundee, Med Educ Inst, Ninewells Hosp & Med Sch, Neurosci Div, Dundee DD1 9SY, Scotland.
   [Benson, Helen E.; Faccenda, Elena; Pawson, Adam J.; Sharman, Joanna L.; Southan, Christopher; Davies, Jamie A.] Univ Edinburgh, Ctr Integrat Physiol, Edinburgh EH8 9XD, Midlothian, Scotland.
   [Buneman, O. Peter] Univ Edinburgh, Sch Informat, Lab Foundat Comp Sci, Edinburgh EH8 9LE, Midlothian, Scotland.
   [Catterall, William A.] Univ Washington, Dept Pharmacol, Seattle, WA 98195 USA.
   [Cidlowski, John A.] NIEHS, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
   [Davenport, Anthony P.] Univ Cambridge, Clin Pharmacol Unit, Cambridge CB2 0QQ, England.
   [Fabbro, Doriano] PIQUR Therapeut, CH-4057 Basel, Switzerland.
   [Fan, Grace] Agnes Irwin Sch, Rosemont, PA USA.
   [McGrath, John C.] Univ Glasgow, Sch Life Sci, Glasgow G12 8QQ, Lanark, Scotland.
   [Spedding, Michael] Spedding Res Solut SARL, F-78110 Le Vesinet, France.
RP Alexander, SPH (reprint author), Univ Nottingham, Sch Med, Sch Biomed Sci, Nottingham NG7 2UH, England.
RI Alexander, Steve/B-8105-2009; Brauner-Osborne, Hans/D-7260-2011; Zajac,
   jean-marie/E-5129-2010; Winrow, Christopher/K-1864-2014; Connor,
   Mark/A-4197-2008; Monk, Peter/C-6155-2008; Ye, Richard/O-5223-2016;
   Mazella, Jean/A-6767-2012; NAHON, Jean-Louis/O-7977-2016; Gainetdinov,
   Raul/G-5875-2011; Jacobson, Kenneth/A-1530-2009; Pawson,
   Adam/Q-5678-2016
OI Sharman, Joanna/0000-0002-5275-6446; Norel, Xavier/0000-0003-0734-3359;
   McArdle, Craig/0000-0003-4836-5351; Gainetdinov,
   Raul/0000-0003-2951-6038; Alexander, Steve/0000-0003-4417-497X;
   Brauner-Osborne, Hans/0000-0001-9495-7388; Connor,
   Mark/0000-0003-2538-2001; Monk, Peter/0000-0003-4637-3059; Ye,
   Richard/0000-0002-2164-5620; Mazella, Jean/0000-0002-5627-0742; NAHON,
   Jean-Louis/0000-0001-9572-7779; Jacobson, Kenneth/0000-0001-8104-1493;
   Pawson, Adam/0000-0003-2280-845X
FU British Pharmacological Society; International Union of Basic and
   Clinical Pharmacology; Wellcome Trust [099156/Z/12/Z]; University of
   Edinburgh
FX We are extremely grateful for the financial contributions from the
   British Pharmacological Society, the International Union of Basic and
   Clinical Pharmacology, the Wellcome Trust (099156/Z/12/Z]), which
   support the website and the University of Edinburgh, who host the
   guidetopharmacology.org website. We are also tremendously grateful to
   the long list of collaborators from NC-IUPHAR subcommittees and beyond,
   who have assisted in the construction of the Concise Guide to
   PHARMACOLOGY 2015/16 and the online database
   www.GuideToPHARMACOLOGY.org.
NR 10
TC 49
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U1 3
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 DEC
PY 2015
VL 172
IS 24
SI SI
BP 5729
EP 5743
DI 10.1111/bph.13347
PG 15
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA CY6HT
UT WOS:000366510500001
PM 26650438
ER

PT J
AU Alexander, SPH
   Cidlowski, JA
   Kelly, E
   Marrion, N
   Peters, JA
   Benson, HE
   Faccenda, E
   Pawson, AJ
   Sharman, JL
   Southan, C
   Davies, JA
   Aldrich, R
   Attali, B
   Back, M
   Barnes, NM
   Bathgate, R
   Beart, PM
   Becirovic, E
   Biel, M
   Birdsall, NJ
   Boison, D
   Brauner-Osborne, H
   Broer, S
   Bryant, C
   Burnstock, G
   Burris, T
   Cain, D
   Calo, G
   Chan, SL
   Chandy, KG
   Chiang, N
   Christakos, S
   Christopoulos, A
   Chun, JJ
   Chung, JJ
   Clapham, DE
   Connor, MA
   Coons, L
   Cox, HM
   Dautzenberg, FM
   Dent, G
   Douglas, SD
   Dubocovich, ML
   Edwards, DP
   Farndale, R
   Fong, TM
   Forrest, D
   Fowler, CJ
   Fuller, P
   Gainetdinov, RR
   Gershengorn, MA
   Goldin, A
   Goldstein, SAN
   Grimm, SL
   Grissmer, S
   Gundlach, AL
   Hagenbuch, B
   Hammond, JR
   Hancox, JC
   Hartig, S
   Hauger, RL
   Hay, DL
   Hebert, T
   Hollenberg, AN
   Holliday, ND
   Hoyer, D
   Ijzerman, AP
   Inui, KI
   Ishii, S
   Jacobson, KA
   Jan, LY
   Jarvis, GE
   Jensen, R
   Jetten, A
   Jockers, R
   Kaczmarek, LK
   Kanai, Y
   Kang, HS
   Karnik, S
   Kerr, ID
   Korach, KS
   Lange, CA
   Larhammar, D
   Leeb-Lundberg, F
   Leurs, R
   Lolait, SJ
   Macewan, D
   Maguire, JJ
   May, JM
   Mazella, J
   McArdle, CA
   McDonnell, DP
   Michel, MC
   Miller, LJ
   Mitolo, V
   Monie, T
   Monk, PN
   Mouillac, B
   Murphy, PM
   Nahon, JL
   Nerbonne, J
   Nichols, CG
   Norel, X
   Oakley, R
   Offermanns, S
   Palmer, LG
   Panaro, MA
   Perez-Reyes, E
   Pertwee, RG
   Pike, JW
   Pin, JP
   Pintor, S
   Plant, LD
   Poyner, DR
   Prossnitz, ER
   Pyne, S
   Ren, D
   Richer, JK
   Rondard, P
   Ross, RA
   Sackin, H
   Safi, R
   Sanguinetti, MC
   Sartorius, CA
   Segaloff, DL
   Sladek, FM
   Stewart, G
   Stoddart, LA
   Striessnig, J
   Summers, RJ
   Takeda, Y
   Tetel, M
   Toll, L
   Trimmer, JS
   Tsai, MJ
   Tsai, SY
   Tucker, S
   Usdin, TB
   J-P, V
   Vore, M
   Ward, DT
   Waxman, SG
   Webb, P
   Wei, AD
   Weigel, N
   Willars, GB
   Winrow, C
   Wong, SS
   Wulff, H
   Ye, RD
   Young, M
   Zajac, JM
AF Alexander, Stephen P. H.
   Cidlowski, John A.
   Kelly, Eamonn
   Marrion, Neil
   Peters, John A.
   Benson, Helen E.
   Faccenda, Elena
   Pawson, Adam J.
   Sharman, Joanna L.
   Southan, Christopher
   Davies, Jamie A.
   Aldrich, R.
   Attali, B.
   Back, M.
   Barnes, N. M.
   Bathgate, R.
   Beart, P. M.
   Becirovic, E.
   Biel, M.
   Birdsall, N. J.
   Boison, D.
   Brauner-Osborne, H.
   Broeer, S.
   Bryant, C.
   Burnstock, G.
   Burris, T.
   Cain, D.
   Calo, G.
   Chan, S. L.
   Chandy, K. G.
   Chiang, N.
   Christakos, S.
   Christopoulos, A.
   Chun, J. J.
   Chung, J. -J.
   Clapham, D. E.
   Connor, M. A.
   Coons, L.
   Cox, H. M.
   Dautzenberg, F. M.
   Dent, G.
   Douglas, S. D.
   Dubocovich, M. L.
   Edwards, D. P.
   Farndale, R.
   Fong, T. M.
   Forrest, D.
   Fowler, C. J.
   Fuller, P.
   Gainetdinov, R. R.
   Gershengorn, M. A.
   Goldin, A.
   Goldstein, S. A. N.
   Grimm, S. L.
   Grissmer, S.
   Gundlach, A. L.
   Hagenbuch, B.
   Hammond, J. R.
   Hancox, J. C.
   Hartig, S.
   Hauger, R. L.
   Hay, D. L.
   Hebert, T.
   Hollenberg, A. N.
   Holliday, N. D.
   Hoyer, D.
   Ijzerman, A. P.
   Inui, K. I.
   Ishii, S.
   Jacobson, K. A.
   Jan, L. Y.
   Jarvis, G. E.
   Jensen, R.
   Jetten, A.
   Jockers, R.
   Kaczmarek, L. K.
   Kanai, Y.
   Kang, H. S.
   Karnik, S.
   Kerr, I. D.
   Korach, K. S.
   Lange, C. A.
   Larhammar, D.
   Leeb-Lundberg, F.
   Leurs, R.
   Lolait, S. J.
   Macewan, D.
   Maguire, J. J.
   May, J. M.
   Mazella, J.
   McArdle, C. A.
   McDonnell, D. P.
   Michel, M. C.
   Miller, L. J.
   Mitolo, V.
   Monie, T.
   Monk, P. N.
   Mouillac, B.
   Murphy, P. M.
   Nahon, J. -L.
   Nerbonne, J.
   Nichols, C. G.
   Norel, X.
   Oakley, R.
   Offermanns, S.
   Palmer, L. G.
   Panaro, M. A.
   Perez-Reyes, E.
   Pertwee, R. G.
   Pike, J. W.
   Pin, J. P.
   Pintor, S.
   Plant, L. D.
   Poyner, D. R.
   Prossnitz, E. R.
   Pyne, S.
   Ren, D.
   Richer, J. K.
   Rondard, P.
   Ross, R. A.
   Sackin, H.
   Safi, R.
   Sanguinetti, M. C.
   Sartorius, C. A.
   Segaloff, D. L.
   Sladek, F. M.
   Stewart, G.
   Stoddart, L. A.
   Striessnig, J.
   Summers, R. J.
   Takeda, Y.
   Tetel, M.
   Toll, L.
   Trimmer, J. S.
   Tsai, M. -J.
   Tsai, S. Y.
   Tucker, S.
   Usdin, T. B.
   Vilargada, J. -P.
   Vore, M.
   Ward, D. T.
   Waxman, S. G.
   Webb, P.
   Wei, A. D.
   Weigel, N.
   Willars, G. B.
   Winrow, C.
   Wong, S. S.
   Wulff, H.
   Ye, R. D.
   Young, M.
   Zajac, J. -M.
CA CGTP Collaborators
TI THE CONCISE GUIDE TO PHARMACOLOGY 2015/16: Nuclear hormone receptors
SO BRITISH JOURNAL OF PHARMACOLOGY
LA English
DT Article
AB The Concise Guide to PHARMACOLOGY 2015/16 provides concise overviews of the key properties of over 1750 human drug targets with their pharmacology, plus links to an open access knowledgebase of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. The full contents can be found at http://onlinelibrary.wiley.com/doi/10.1111/bph.13352/full. Nuclear hormone receptors are one of the eight major pharmacological targets into which the Guide is divided, with the others being: G protein-coupled receptors, ligand-gated ion channels, voltage-gated ion channels, other ion channels, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The Concise Guide is published in landscape format in order to facilitate comparison of related targets. It is a condensed version of material contemporary to late 2015, which is presented in greater detail and constantly updated on the website www.guidetopharmacology.org, superseding data presented in the previous Guides to Receptors & Channels and the Concise Guide to PHARMACOLOGY 2013/14. It is produced in conjunction with NC-IUPHAR and provides the official IUPHAR classification and nomenclature for human drug targets, where appropriate. It consolidates information previously curated and displayed separately in IUPHAR-DB and GRAC and provides a permanent, citable, point-in-time record that will survive database updates.
C1 [Alexander, Stephen P. H.] Univ Nottingham, Sch Med, Sch Biomed Sci, Nottingham NG7 2UH, England.
   [Cidlowski, John A.] NIEHS, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
   [Kelly, Eamonn; Marrion, Neil] Univ Bristol, Sch Physiol & Pharmacol, Bristol BS8 1TD, Avon, England.
   [Peters, John A.] Univ Dundee, Med Educ Inst, Ninewells Hosp & Med Sch, Neurosci Div, Dundee DD1 9SY, Scotland.
   [Benson, Helen E.; Faccenda, Elena; Pawson, Adam J.; Sharman, Joanna L.; Southan, Christopher; Davies, Jamie A.] Univ Edinburgh, Ctr Integrat Physiol, Edinburgh EH8 9XD, Midlothian, Scotland.
RP Alexander, SPH (reprint author), Univ Nottingham, Sch Med, Sch Biomed Sci, Nottingham NG7 2UH, England.
RI Alexander, Steve/B-8105-2009; Connor, Mark/A-4197-2008; Ye,
   Richard/O-5223-2016; Mazella, Jean/A-6767-2012; Gainetdinov,
   Raul/G-5875-2011; Jacobson, Kenneth/A-1530-2009; Pawson,
   Adam/Q-5678-2016; Safi, Rachid/A-5909-2010; 
OI Alexander, Steve/0000-0003-4417-497X; Connor, Mark/0000-0003-2538-2001;
   Ye, Richard/0000-0002-2164-5620; Mazella, Jean/0000-0002-5627-0742;
   Jacobson, Kenneth/0000-0001-8104-1493; Pawson, Adam/0000-0003-2280-845X;
   Sharman, Joanna/0000-0002-5275-6446; Southan,
   Christopher/0000-0001-9580-0446
NR 0
TC 26
Z9 26
U1 0
U2 4
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 DEC
PY 2015
VL 172
IS 24
SI SI
BP 5956
EP 5978
DI 10.1111/bph.13352
PG 23
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA CY6HT
UT WOS:000366510500006
PM 26650443
ER

PT J
AU Klar, AJS
AF Klar, Amar J. S.
TI Selective chromatid segregation mechanism proposed for the human split
   hand/foot malformation development by chromosome 2 translocations: A
   perspective
SO DEVELOPMENTAL BIOLOGY
LA English
DT Article
DE Limb development; Split hand/split foot malformation; Monochromatid gene
   expression; Selective strand/chromatid segregation mechanism; Asymmetric
   cell division mechanism; Epigenetic developmental mechanism
ID LEFT-RIGHT ASYMMETRY; FISSION YEAST; DNA STRANDS; FOOT MALFORMATION;
   EPIGENETIC STATES; CELL-DIVISION; INHERITANCE; LOCUS; MODEL;
   SCHIZOPHRENIA
AB Three unrelated chromosome 2q14.1-14.2 region translocations caused the split hand/foot limb malformation development in humans by an unknown mechanism. Their etiology was described by the autosomal dominant inheritance with incomplete penetrance genetic model although authors stated, "the understanding of the genotype-to-phenotype relationship has been most challenging". The conundrums are that no mutation was found in known genes located at or near the translocation breakpoints, some limbs were malformed while others were not in the same patient and surprisingly breakpoints lie at relatively large distance of more than 2.5 million bases to have caused disorder-causing gene mutations in a single gene. To help understand translocations etiology for limb development, we invoke the selective DNA strand/chromatid-specific epigenetic imprinting and segregation mechanism employed by the two highly diverged fission yeasts to produce daughter cells of different cell types by mitosis. By this mechanism, an anterior- and posterior-limb-tissues-generating pair of daughter cells is produced by a single deterministic cell dividing in the anlagen of the limb bud. Accordingly, malformation develops simply because translocations hinder the proper distribution of chromatid-specific epialleles of a limb developmental gene during the deterministic cell's mitosis. It is tempting to speculate that such a mechanism might involve the HOXD-cluster genes situated centromere-distal to the translocation breakpoints many million bases away at the 2q31.1 region. Further genetic tests of the hypothesis are proposed for the human and mouse limb development. In sum, genetic analysis of translocations suggests that the sequence asymmetry of strands in the double-helical DNA structure of a developmental gene forms the physical basis of daughter cells' developmental asymmetry, thus opposing the morphogen-gradient research paradigm of limb development. Published by Elsevier Inc.
C1 [Klar, Amar J. S.] NCI, Gene Regulat & Chromosome Biol Lab, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
RP Klar, AJS (reprint author), NCI, Gene Regulat & Chromosome Biol Lab, Ctr Canc Res, NIH, Bldg 539,Room 154, Frederick, MD 21702 USA.
EM klara@mail.nih.gov
FU Intramural Research Program of the National Cancer Institute, National
   Institutes of Health
FX The Intramural Research Program of the National Cancer Institute,
   National Institutes of Health, supports this research.
NR 46
TC 3
Z9 3
U1 0
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0012-1606
EI 1095-564X
J9 DEV BIOL
JI Dev. Biol.
PD DEC 1
PY 2015
VL 408
IS 1
BP 7
EP 13
DI 10.1016/j.ydbio.2015.10.013
PG 7
WC Developmental Biology
SC Developmental Biology
GA CZ2TE
UT WOS:000366956700004
PM 26477560
ER

PT J
AU Ajima, R
   Bisson, JA
   Helt, JC
   Nakaya, MA
   Habas, R
   Tessarollo, L
   He, X
   Morrisey, EE
   Yamaguchi, TP
   Cohen, ED
AF Ajima, Rieko
   Bisson, Joseph A.
   Helt, Jay-Christian
   Nakaya, Masa-Aki
   Habas, Raymond
   Tessarollo, Lino
   He, Xi
   Morrisey, Edward E.
   Yamaguchi, Terry P.
   Cohen, Ethan David
TI DAAM1 and DAAM2 are co-required for myocardial maturation and sarcomere
   assembly
SO DEVELOPMENTAL BIOLOGY
LA English
DT Article
ID PLANAR CELL POLARITY; 2ND HEART FIELD; LEFT-VENTRICULAR NONCOMPACTION;
   NON-COMPACTION CARDIOMYOPATHY; CARDIAC PROGENITOR CELLS; TYROSINE KINASE
   ROR2; RICTOR-MTOR COMPLEX; SIGNALING PATHWAY; OUTFLOW TRACT; MAMMALIAN
   CARDIOMYOCYTES
AB Wnt ligands regulate heart morphogenesis but the underlying mechanisms remain unclear. Two Formin-related proteins, DAAM1 and 2, were previously found to bind the Wnt effector Disheveled. Here, since DAAM1 and 2 nucleate actin and mediate Wnt-induced cytoskeletal changes, a foxed-allele of Daam1 was used to disrupt its function specifically in the myocardium and investigate Wnt-associated pathways. Homozygous Daam1 conditional knockout (CKO) mice were viable but had misshapen hearts and poor cardiac function. The defects in Daam1 CKO mice were observed by mid-gestation and were associated with a loss of protrusions from cardiomyocytes invading the outflow tract. Further, these mice exhibited noncompaction cardiomyopathy (NCM) and deranged cardiomyocyte polarity. Interestingly, Daam1 CKO mice that were also homozygous for an insertion disrupting Daam2 (DKO) had stronger NCM, severely reduced cardiac function, disrupted sarcomere structure, and increased myocardial proliferation, suggesting that DAAM1 and DAAM2 have redundant functions. While RhoA was unaffected in the hearts of Daam1/2 DM mice, AKT activity was lower than in controls, raising the issue of whether DAAM1/2 are only mediating Wnt signaling. Daam/-floxed mice were thus bred to Wnt5a null mice to identify genetic interactions. The hearts of Daam1 CKO mice that were also heterozygous for the null allele of Wnt5a had stronger NCM and more severe loss of cardiac function than Daam1 CKO mice, consistent with DAAM1 and Wnt5a acting in a common pathway. However, deleting Daam1 further disrupted Wnt5a homozygous-null hearts, suggesting that DAAM1 also has Wnt5a-independent roles in cardiac development. Published by Elsevier Inc.
C1 [Ajima, Rieko] Natl Inst Genet, Mammalian Dev Lab, Mishima, Shizuoka 4118540, Japan.
   [Bisson, Joseph A.; Helt, Jay-Christian; Cohen, Ethan David] Univ Rochester, Sch Med & Dent, Dept Med, Rochester, NY 14642 USA.
   [Nakaya, Masa-Aki; Yamaguchi, Terry P.] NCI, Canc & Dev Biol Lab, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
   [Habas, Raymond] Temple Univ, Coll Sci & Technol, Dept Biol, Philadelphia, PA 19122 USA.
   [Tessarollo, Lino] NCI, Neural Dev Sect, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21702 USA.
   [He, Xi] Harvard Univ, Boston Childrens Hosp, Sch Med, FM Kirby Neurobiol Ctr,Dept Neurol, Boston, MA 02115 USA.
   [Morrisey, Edward E.] Univ Penn, Dept Med & Cell & Dev Biol, Philadelphia, PA 19104 USA.
RP Yamaguchi, TP (reprint author), NCI, Canc & Dev Biol Lab, NIH, POB B 1050,Boyles St Bldg 539,Rm 218, Frederick, MD 21702 USA.
EM yamagute@mail.nih.gov; ethan_cohen@urmc.rochester.edu
FU Intramural Research Program of the NIH, National Cancer Institute,
   Center for Cancer Research; Progenitor Cell Biology Consortium Grant
   [HL100405]; American Heart Association [10SDG2610019, 15GRNT23020024]
FX This research was supported by the Intramural Research Program of the
   NIH, National Cancer Institute, Center for Cancer Research, as well as
   the Progenitor Cell Biology Consortium Grant (HL100405) and American
   Heart Association (10SDG2610019 and 15GRNT23020024).
NR 85
TC 0
Z9 0
U1 1
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0012-1606
EI 1095-564X
J9 DEV BIOL
JI Dev. Biol.
PD DEC 1
PY 2015
VL 408
IS 1
BP 126
EP 139
DI 10.1016/j.ydbio.2015.10.003
PG 14
WC Developmental Biology
SC Developmental Biology
GA CZ2TE
UT WOS:000366956700014
PM 26526197
ER

PT J
AU Soeiro-de-Souza, MG
   Henning, A
   Machado-Vieira, R
   Moreno, RA
   Pastorello, BF
   Leite, CD
   Vallada, H
   Otaduy, MCG
AF Soeiro-de-Souza, Marcio Gerhardt
   Henning, Anke
   Machado-Vieira, Rodrigo
   Moreno, Ricardo A.
   Pastorello, Bruno F.
   Leite, Claudia da Costa
   Vallada, Homero
   Garcia Otaduy, Maria Concepcion
TI Anterior cingulate Glutamate-Glutamine cycle metabolites are altered in
   euthymic bipolar I disorder
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE GABA; Glutamine; Glutamate; Bipolar; Spectroscopy
ID MAGNETIC-RESONANCE-SPECTROSCOPY; AMINOBUTYRIC-ACID CONCENTRATIONS; MOOD
   DISORDERS; BRAIN-METABOLITES; PRIOR-KNOWLEDGE; RATING-SCALE; PROTON MRS;
   GABA; SCHIZOPHRENIA; NMR
AB Bipolar disorder (BD) has been consistently associated with abnormalities in the Glutamate/GABA-Glutamine cycle. Magnetic resonance spectroscopy (MRS) studies have reported increased brain Glutamate (Glu) and Glx (Glu+Glutamine) in subjects with BD. However, data on separate measures of GABA and Glutamine (Gln) in BD are sparse due to overlapping resonant signals. The development of new sequence methods in the quantification of these metabolites has allowed a better understanding of the Glu/GABA-Gln cycle but data on this field of research remains sparse in BD. Eighty-eight subjects (50 euthymic BD and 38 HC) underwent 3T proton magnetic resonance spectroscopy (1H MRS) in the anterior cingulate cortex (ACC; 2 x 2 x4.5 cm(3)) using a two-dimensional JPRESS sequence. GABA, Glutamine (Gln) and Glutamate (Glu) were quantified with the Pro Fit program. Using image segmentation and known creatine (Cre) concentrations for white and grey matter, metabolite concentrations were calculated for the excited MRS voxel. GABA levels did not differ between groups. Gin level was higher in euthymic BD patients than in healthy controls. The Glu level and Glu/Gln ratio were lower in BD patients than in controls. The use of anticonvulsants was associated with Gln increase but did not affect Glu or Glu/Gln. Neither lithium nor antipsychotic use influenced metabolite levels. The ACC MRS findings indicate that the glutamatergic function in euthymic medicated BD patients is altered relative to controls. Whether this feature is a metabolic signature of euthymic BD subjects should be the focus of future studies. (C) 2015 Elsevier B.V. and ECNR All rights reserved.
C1 [Soeiro-de-Souza, Marcio Gerhardt; Moreno, Ricardo A.] Univ Sao Paulo IPq FMUSP, Sch Med, Inst Psychiat, Mood Disorders Unit GRUDA, Sao Paulo, Brazil.
   [Machado-Vieira, Rodrigo] NIMH, NIH, Bethesda, MD 20892 USA.
   [Pastorello, Bruno F.; Leite, Claudia da Costa; Garcia Otaduy, Maria Concepcion] Univ Sao Paulo InRad FMUSP, Dept & Inst Radiol, Lab Magnet Resonance LIM44, Sao Paulo, Brazil.
   [Soeiro-de-Souza, Marcio Gerhardt; Vallada, Homero] Univ Sao Paulo InRad FMUSP, Sch Med, Inst Psychiat, Genet & Pharmacogenet Unit PROGENE, Sao Paulo, Brazil.
   [Henning, Anke] Inst Biomed Engn Univ, Zurich, Switzerland.
   [Henning, Anke] Swiss Fed Inst Technol, Zurich, Switzerland.
   [Henning, Anke] Max Planck Inst Biol Cybernet, D-72076 Tubingen, Germany.
RP Soeiro-de-Souza, MG (reprint author), Hosp Clin Sao Paulo, Inst Psiquiatria, Dr Ovidio Pires Campos S-N,Third Floor, BR-05403010 Sao Paulo, Brazil.
EM marciogss@gmail.com
RI Soeiro-de-Souza, Marcio/J-9430-2012; Vallada, Homero/D-1333-2014;
   MACHADO-VIEIRA, RODRIGO/D-8293-2012; 
OI Soeiro-de-Souza, Marcio/0000-0002-9293-3128; Vallada,
   Homero/0000-0001-5123-8295; MACHADO-VIEIRA, RODRIGO/0000-0002-4830-1190;
   Henning, Anke/0000-0002-2267-4861
NR 64
TC 6
Z9 6
U1 2
U2 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
EI 1873-7862
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD DEC
PY 2015
VL 25
IS 12
BP 2221
EP 2229
DI 10.1016/j.euroneuro.2015.09.020
PG 9
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CZ2PO
UT WOS:000366947300004
PM 26476706
ER

PT J
AU Machado-Vieira, R
   Gattaz, WF
   Zanetti, MV
   De Sousa, RT
   Carvalho, AF
   Soeiro-de-Souza, MG
   Leite, CC
   Otaduy, MC
AF Machado-Vieira, Rodrigo
   Gattaz, Wagner F.
   Zanetti, Marcus V.
   De Sousa, Rafael T.
   Carvalho, Andre F.
   Soeiro-de-Souza, Marcio G.
   Leite, Claudia C.
   Otaduy, Maria C.
TI A Longitudinal (6-week) 3T H-1-MRS Study on the Effects of Lithium
   Treatment on Anterior Cingulate Cortex Metabolites in Bipolar Depression
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE Bipolar disorder; Depression; Magnetic resonance spectroscopy; Lithium;
   Glutamate; Imaging
ID MAGNETIC-RESONANCE-SPECTROSCOPY; N-ACETYL-ASPARTATE; GRAY-MATTER VOLUME;
   MOOD DISORDERS; UNIFYING HYPOTHESIS; CORTICAL GLUTAMATE; OXIDATIVE
   STRESS; RATING-SCALE; NITRIC-OXIDE; HUMAN BRAIN
AB The anterior cingulate cortex (ACC) is a key area in mood regulation. To date, no Longitudinal study has specifically evaluated lithium's effects on ACC metabolites using H-1-MRS, as well as its association with clinical improvement in bipolar depression. This H-1-MRS (TE=35 ms) study evaluated 24 drug-free BD patients during depressive episodes and after lithium treatment at therapeutic levels. Brain metabolite levels (N-acetyl aspartate (NM), creatine (tCr), choline, myo-inositol, and glutamate levels) were measured in the ACC at baseline (week 0) and after lithium monotherapy (week 6). The present investigation showed that ACC glutamate (Glu/tCr) and glutamate +glutamine (Glx/tCr) significantly increased after six weeks of lithium therapy. Regarding the association with clinical improvement, remitters showed an increase in myoinositol levels (ml/tCr) after lithium treatment compared to non-remitters. The present findings reinforce a role for ACC glutamate-glutamine cycling and myoinositol pathway as key targets for lithium's therapeutic effects in BD. Published by Elsevier B.V.
C1 [Machado-Vieira, Rodrigo; Gattaz, Wagner F.; Zanetti, Marcus V.; De Sousa, Rafael T.] Univ Sao Paulo, Dept & Inst Psychiat, Lab Neurosci, LIM 27, BR-05508 Sao Paulo, Brazil.
   [Machado-Vieira, Rodrigo; Gattaz, Wagner F.; Zanetti, Marcus V.; De Sousa, Rafael T.] Univ Sao Paulo, Ctr Interdisciplinary Res Appl Neurosci NAPNA, BR-05508 Sao Paulo, Brazil.
   [Machado-Vieira, Rodrigo; De Sousa, Rafael T.] NIMH, Expt Therapeut & Pathophysiol Branch, NIH, Bethesda, MD 20892 USA.
   [Carvalho, Andre F.] Univ Fed Ceara, Fac Med, Dept Clin Med, Fortaleza, Ceara, Brazil.
   [Carvalho, Andre F.] Univ Fed Ceara, Fac Med, Translat Psychiat Res Grp, Fortaleza, Ceara, Brazil.
   [Soeiro-de-Souza, Marcio G.] Univ Sao Paulo, Dept Psychiat, GRUDA, Mood Disorders Program, BR-05508 Sao Paulo, Brazil.
   [Leite, Claudia C.; Otaduy, Maria C.] Univ Sao Paulo, Dept & Inst Psychiat, Lab Magnet Resonance Neuroradiol, LIM 44, BR-05508 Sao Paulo, Brazil.
RP Machado-Vieira, R (reprint author), Univ Sao Paulo, Dept & Inst Psychiat, Lab Neurosci LIM27, BR-05508 Sao Paulo, Brazil.
EM machadovieirar@mail.nih.gov
RI Soeiro-de-Souza, Marcio/J-9430-2012; Leite, Claudia/B-6036-2013;
   MACHADO-VIEIRA, RODRIGO/D-8293-2012
OI Soeiro-de-Souza, Marcio/0000-0002-9293-3128; MACHADO-VIEIRA,
   RODRIGO/0000-0002-4830-1190
NR 49
TC 4
Z9 4
U1 2
U2 13
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
EI 1873-7862
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD DEC
PY 2015
VL 25
IS 12
BP 2311
EP 2317
DI 10.1016/j.euroneuro.2015.08.023
PG 7
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CZ2PO
UT WOS:000366947300013
PM 26428274
ER

PT J
AU Begley, DA
   Sundberg, JP
   Krupke, DM
   Neuhauser, SB
   Bult, CJ
   Eppig, JT
   Morse, HC
   Ward, JM
AF Begley, Dale A.
   Sundberg, John P.
   Krupke, Debra M.
   Neuhauser, Steven B.
   Bult, Carol J.
   Eppig, Janan T.
   Morse, Herbert C., III
   Ward, Jerrold M.
TI Finding mouse models of human lymphomas and leukemia's using the Jackson
   laboratory mouse tumor biology database
SO EXPERIMENTAL AND MOLECULAR PATHOLOGY
LA English
DT Article
DE Lymphoma; Leukemia; Mice; Mouse tumor biology database; Digital slides;
   Virtual slides
ID BETHESDA PROPOSALS; ANIMAL-MODELS; CANCER; MICE; NEOPLASMS; DISEASE;
   CLASSIFICATION; PATHBASE; UTILITY; LESIONS
AB Many mouse models have been created to study hematopoietic cancer types. There are over thirty hematopoietic tumor types and subtypes, both human and mouse, with various origins, characteristics and clinical prognoses. Determining the specific type of hematopoietic lesion produced in a mouse model and identifying mouse models that correspond to the human subtypes of these lesions has been a continuing challenge for the scientific community. The Mouse Tumor Biology Database (MTB; http://tumor.informatics.jax.org) is designed to facilitate use of mouse models of human cancer by providing detailed histopathologic and molecular information on lymphoma subtypes, including expertly annotated, on line, whole slide scans, and providing a repository for storing information on and querying these data for specific lymphoma models. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Begley, Dale A.; Sundberg, John P.; Krupke, Debra M.; Neuhauser, Steven B.; Bult, Carol J.; Eppig, Janan T.] Jackson Lab, Bar Harbor, ME 04609 USA.
   [Morse, Herbert C., III] NIAID, Virol & Cellular Immunol Sect, Immunogenet Lab, NIH, Bethesda, MD 20892 USA.
   [Ward, Jerrold M.] Global VetPathol, Montgomery Village, MD USA.
RP Begley, DA (reprint author), Jackson Lab, 600 Main St, Bar Harbor, ME 04609 USA.
EM dale.begley@jax.org
OI Krupke, Debra/0000-0002-3165-2891
FU National Institutes of Health [CA089713]; Intramural Research Program of
   the NIH, NIAID; Basic Cancer Center Core Grant from the National Cancer
   Institute [CA034196]
FX This work was supported by grants from the National Institutes of Health
   (CA089713, for the Mouse Tumor Biology Database) and the Intramural
   Research Program of the NIH, NIAID. The Jackson Laboratory Shared
   Scientific Services were supported in part by a Basic Cancer Center Core
   Grant from the National Cancer Institute (CA034196, to The Jackson
   Laboratory).
NR 34
TC 1
Z9 1
U1 1
U2 5
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4800
EI 1096-0945
J9 EXP MOL PATHOL
JI Exp. Mol. Pathol.
PD DEC
PY 2015
VL 99
IS 3
BP 533
EP 536
DI 10.1016/j.yexmp.2015.07.004
PG 4
WC Pathology
SC Pathology
GA CZ2SI
UT WOS:000366954500020
PM 26302176
ER

PT J
AU Neuman, MG
   Malnick, S
   Maor, Y
   Nanau, RM
   Melzer, E
   Ferenci, P
   Seitz, HK
   Mueller, S
   Mell, H
   Samuel, D
   Cohen, LB
   Kharbanda, KK
   Osna, NA
   Ganesan, M
   Thompson, KJ
   McKillop, LH
   Bautista, A
   Bataller, R
   French, SW
AF Neuman, Manuela G.
   Malnick, Stephen
   Maor, Yaakov
   Nanau, Radu M.
   Melzer, Ehud
   Ferenci, Peter
   Seitz, Helmut K.
   Mueller, Sebastian
   Mell, Haim
   Samuel, Didier
   Cohen, Lawrence B.
   Kharbanda, Kusum K.
   Osna, Natalia A.
   Ganesan, Murali
   Thompson, Kyle J.
   McKillop, Lain H.
   Bautista, Abraham
   Bataller, Ramon
   French, Samuel W.
TI Alcoholic liver disease: Clinical and translational research
SO EXPERIMENTAL AND MOLECULAR PATHOLOGY
LA English
DT Review
DE Alcoholic liver disease; Alcohol dehydrogenase; Betaine; CYP2E1;
   Hepatocarcinogenesis; Liver fibrosis; Hepatitis B and C viral infection;
   Human immunodeficiency virus; Liver transplant
ID HEPATITIS-C VIRUS; GENOTYPE 1 INFECTION; TREATMENT-NAIVE PATIENTS;
   PEGYLATED INTERFERON-ALPHA; CACO-2 CELL MONOLAYER; CHRONIC HCV
   INFECTION; ELEVATED S-ADENOSYLHOMOCYSTEINE; SUSTAINED VIROLOGICAL
   RESPONSE; ACETALDEHYDE-INDUCED INCREASE; DACLATASVIR PLUS ASUNAPREVIR
AB The present review spans a broad spectrum of topics dealing with alcoholic liver disease (ALD), including clinical research, translational research, pathogenesis and therapies. A special accent is placed on alcohol misuse, as alcohol is a legally commercialized and taxable product. Drinking alcohol, particularly from a young age, is a major health problem. Alcoholism is known to contribute to morbidity and mortality. A systematic literature search was performed in order to obtain updated data (2008-2015). The review is focused on genetic polymorphisms of alcohol metabolizing enzymes and the role of cytochrome p450 2E1 and iron in ALD. Alcohol-mediated hepatocarcinogenesis is also discussed in the presence or absence of co-morbidities such as viral hepatitis C as well as therapeutic the role of innate immunity in ALD-HCV. Moreover, emphasis was placed on alcohol and drug interactions, as well as liver transplantation for end-stage ALD. Finally, the time came to eradicate alcohol-induced liver and intestinal damage by using betaine. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Neuman, Manuela G.; Nanau, Radu M.] Vitro Drug Safety & Biotechnol, Toronto, ON, Canada.
   [Neuman, Manuela G.] Univ Toronto, Fac Med, Dept Pharmacol & Toxicol, Toronto, ON, Canada.
   [Malnick, Stephen; Maor, Yaakov; Melzer, Ehud] Hebrew Univ Jerusalem, Fac Med, Kaplan Hlth Sci Ctr, Dept Med,Div Gastroenterol, IL-76100 Rehovot, Israel.
   [Ferenci, Peter] Med Univ Vienna, Vienna, Austria.
   [Seitz, Helmut K.; Mueller, Sebastian] Heidelberg Univ, Heidelberg, Germany.
   [Seitz, Helmut K.; Mueller, Sebastian] Salem Med Ctr, Alcohol Res Ctr, Dept Med Gastroenterol & Hepatol, Heidelberg, Germany.
   [Mell, Haim] Israel Antidrug & Alcohol Author, Jerusalem, Israel.
   [Samuel, Didier] Hop Paul Brousse, Ctr Hepatobiliaire, Res Inserm Paris Unit 785 11, Liver Transplant Unit, Paris, France.
   [Cohen, Lawrence B.] Univ Toronto, Sunnybrook Hlth Sci Ctr, Div Gastroenterol, Toronto, ON, Canada.
   [Cohen, Lawrence B.] Univ Toronto, Dept Internal Med, Toronto, ON, Canada.
   [Kharbanda, Kusum K.; Osna, Natalia A.; Ganesan, Murali] Univ Nebraska Med Ctr, Vet Affairs Nebraska Western Iowa Hlth Care Syst, Res Serv, Omaha, NE USA.
   [Thompson, Kyle J.; McKillop, Lain H.] Carolinas Med Ctr, Dept Surg, Charlotte, NC 28203 USA.
   [Bautista, Abraham] NIAAA, Off Extramural Act, NIH, Rockville, MD 20852 USA.
   [Bataller, Ramon] Univ N Carolina, Dept Med, Div Gastroenterol & Hepatol, Chapel Hill, NC USA.
   [Bataller, Ramon] Univ N Carolina, Dept Nutr, Chapel Hill, NC USA.
   [French, Samuel W.] Harbor UCLA Med Ctr, Torrance, CA 90509 USA.
RP Neuman, MG (reprint author), Banting & Best Inst, Dept Pharmacol & Toxicol Vitro Drug Safety & Biot, 100 Coll St,Lab 217, Toronto, ON M5G 0A3, Canada.
EM manuela.neuman@utoronto.ca
FU European Association for the Biological Research on Alcoholism (ESBRA);
   In Vitro Drug Safety and Biotechnology; Mahaffy Innovative Grant,
   Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada; 
   [5U01AA-021818-03]
FX The article is based upon the some of the presentations given at the
   "7TH Charles Lieber Annual symposium: Alcohol and Chronic Diseases"
   organized by M.G. Neuman, as a satellite symposium to the 38th Meeting
   of the Research Society for Alcoholism, June 2015, San Antonio, Texas,
   USA as well as International Symposium "Alcohol a New Challenge"
   organized by M. G. Neuman, Y. Maor, E. Melzer and S. Malnick, January
   2015, Kaplan Medical Center, Rehovot, Israel. We are grateful to the
   European Association for the Biological Research on Alcoholism (ESBRA)
   that sponsored two of our speakers for the Israeli Symposium and to
   Debra Sharp, Director RSA for her ongoing support with Lieber's
   satellite symposium. Dr. French thanks Adriana Flores for typing his
   manuscript. Dr. French research on betaine was supported by
   5U01AA-021818-03. The funding for the manuscript was provided by the In
   Vitro Drug Safety and Biotechnology and Mahaffy Innovative Grant,
   Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada.
NR 202
TC 6
Z9 6
U1 4
U2 17
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4800
EI 1096-0945
J9 EXP MOL PATHOL
JI Exp. Mol. Pathol.
PD DEC
PY 2015
VL 99
IS 3
BP 596
EP 610
DI 10.1016/j.yexmp.2015.09.001
PG 15
WC Pathology
SC Pathology
GA CZ2SI
UT WOS:000366954500030
PM 26342547
ER

PT J
AU Schwimmer, JB
   Lavine, JE
   Neuschwander-Tetri, BA
   Wilson, L
   Xanthakos, SA
   Barlow, SE
   Vos, MB
   Molleston, JP
   Whitington, PF
   Rosenthal, P
   Jain, AK
   Murray, KF
   Brunt, EM
   Kleiner, DE
   Van Natta, ML
   Clark, JM
   Tonascia, J
   Doo, E
AF Schwimmer, Jeffrey B.
   Lavine, Joel E.
   Neuschwander-Tetri, Brent A.
   Wilson, Laura
   Xanthakos, Stavra A.
   Barlow, Sarah E.
   Vos, Miriam B.
   Molleston, Jean P.
   Whitington, Peter F.
   Rosenthal, Philip
   Jain, Ajay K.
   Murray, Karen F.
   Brunt, Elizabeth M.
   Kleiner, David E.
   Van Natta, Mark L.
   Clark, Jeanne M.
   Tonascia, James
   Doo, Edward
TI Cysteamine Bitartrate Delayed-Release (DR) for the Treatment of
   Nonalcoholic Fatty Liver Disease (NAFLD) in Children (CyNCh) Trial
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 [Schwimmer, Jeffrey B.] Univ Calif San Diego, Pediat, San Diego, CA USA.
   [Schwimmer, Jeffrey B.] Rady Childrens Hosp, Gastroenterol, San Diego, CA USA.
   [Lavine, Joel E.] Columbia Univ, Pediat, New York, NY USA.
   [Neuschwander-Tetri, Brent A.] St Louis Univ, Med, St Louis, MO 63103 USA.
   [Wilson, Laura; Van Natta, Mark L.; Tonascia, James] Johns Hopkins, Sch Publ Hlth, Baltimore, MD USA.
   [Xanthakos, Stavra A.] Cincinnati Childrens Hosp, Pediat, Cincinnati, OH USA.
   [Barlow, Sarah E.] Texas Childrens Hosp, Pediat, Houston, TX 77030 USA.
   [Molleston, Jean P.] James Whitcomb Riley Hosp Children, Pediat, Indianapolis, IN 46202 USA.
   [Whitington, Peter F.] Ann & Robert H Lurie Childrens Hosp Chicago, Pediat, Chicago, IL 60611 USA.
   [Rosenthal, Philip] UCSF, Pediat, San Francisco, CA USA.
   [Jain, Ajay K.] St Louis Univ, Pediat, St Louis, MO 63103 USA.
   [Murray, Karen F.] Seattle Childrens Hosp, Pediat, Seattle, WA USA.
   [Brunt, Elizabeth M.] Washington Univ, Pathol, St Louis, MO USA.
   [Kleiner, David E.] NCI, Pathol, Bethesda, MD 20892 USA.
   [Clark, Jeanne M.] Johns Hopkins Univ, Med, Baltimore, MD USA.
   [Doo, Edward] NIDDK, Liver Dis, Bethesda, MD 20892 USA.
   [Vos, Miriam B.] Emory Univ, Pediat, Atlanta, GA 30322 USA.
NR 0
TC 1
Z9 1
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD DEC
PY 2015
VL 62
IS 6
MA LB-31
BP 1398A
EP 1399A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CZ3OF
UT WOS:000367013200032
ER

PT J
AU Sehgal, R
   Patra, S
   David, P
   Vyas, A
   Khanam, A
   Hissar, S
   Gupta, E
   Kumar, G
   Kottilil, S
   Maiwall, R
   Sarin, SK
   Trehanpati, N
AF Sehgal, Rashi
   Patra, Sharda
   David, Paul
   Vyas, Ashish
   Khanam, Arshi
   Hissar, Syed
   Gupta, Ekta
   Kumar, Guresh
   Kottilil, Shyam
   Maiwall, Rakhi
   Sarin, Shiv Kumar
   Trehanpati, Nirupama
TI Impaired Monocyte-Macrophage Functions and Defective Toll-Like Receptor
   Signaling in Hepatitis E Virus-Infected Pregnant Women With Acute Liver
   Failure
SO HEPATOLOGY
LA English
DT Article
ID VIRAL-HEPATITIS; IFN-GAMMA; C VIRUS; INJURY; PATHOGENESIS; ACTIVATION;
   MORTALITY; DISEASE; CELLS; INDIA
AB Acute viral hepatitis resulting due to hepatitis E viral infection (AVH-E) is often serious in pregnancy and could result in acute liver failure (ALF). The role of monocytes and macrophages (mono-macs) in the pathogenesis of AVH-E and development of ALF-E in pregnancy is unclear. We investigated the functions of mono-macs in pregnant (P), AVH-E (n = 44), ALF-E (n = 12), healthy controls (HC; n = 20) and compared with nonpregnant (NP) AVHE (n = 10), ALF-E (n = 5), and HC (n = 10). We also recruited non-hepatitis E virus-related pregnant (P), ALF-NE (n = 5) and non-pregnant (NP), ALF-NE (n = 12) patients with ALF. Mono-macs, dendritic cell (DC) phenotypes, and Toll-like receptor (TLR) expressions were studied by flow cytometry and reverse-transcriptase polymerase chain reaction. Mono-macs functionality was determined by analyzing their phagocytic activity and reactive oxygen species (ROS) generation by using flow cytometry. Frequency of mono-macs and DCs was increased during HEV infection compared to HC (P < 0.001). Macrophages were increased (P < 0.002) in ALF-E(P) compared to ALF-NE(P). The macrophage phagocytic activity and Escherichia coli-induced ROS production was significantly impaired in ALF-E(P) compared to AVH-E(P) (P < 0.001), ALF-E(NP), and ALF-NE(P) patients (P < 0.02). TLR3 and TLR9 expression and downstream MYD88 signalling molecules IRF3 and IRF7 were significantly down-regulated in ALF-E(P) (P < 0.00) compared to AVH-E(P) and ALF-NE(P). Conclusion: Functionality of mono-macs is impaired in pregnant ALF-E patients compared to AVH-E(P). Reduced TLR3 and TLR7 expression and TLR downstream-signaling molecules in pregnant ALF-E patients suggests inadequate triggers for the innate immune responses contributing to development and severity of ALF-E. Studies using TLR agonists to activate mono-macs may be of use and in vitro studies should be undertaken using patient samples.
C1 [Sehgal, Rashi; David, Paul; Vyas, Ashish; Khanam, Arshi; Hissar, Syed; Kumar, Guresh; Sarin, Shiv Kumar; Trehanpati, Nirupama] Inst Liver & Biliary Sci, Dept Res, New Delhi 110070, India.
   [Gupta, Ekta] Inst Liver & Biliary Sci, Dept Virol, New Delhi 110070, India.
   [Maiwall, Rakhi; Sarin, Shiv Kumar] Inst Liver & Biliary Sci, Dept Hepatol, New Delhi 110070, India.
   [Patra, Sharda] Lady Harding Med Coll, Gynecol & Obstet, New Delhi, India.
   [Kottilil, Shyam] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
RP Trehanpati, N (reprint author), Inst Liver & Biliary Sci, D-1, New Delhi 110070, India.
EM shivsarin@gmail.com; trehanpati@gmail.com
FU Indian Council of Medical Research, Government of India, New Delhi
   [VIR/17/2009/ECD-1]; National Institute of Allergy and Infectious
   Diseases, National Institutes of Health, Bethesda, MD
FX This study was funded by HEV grant no. VIR/17/2009/ECD-1 received from
   the Indian Council of Medical Research, Government of India, New Delhi
   and partially by the intramural program of the National Institute of
   Allergy and Infectious Diseases, National Institutes of Health,
   Bethesda, MD.
NR 40
TC 7
Z9 7
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD DEC
PY 2015
VL 62
IS 6
BP 1683
EP 1696
DI 10.1002/hep.28143
PG 14
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CZ3OF
UT WOS:000367013200041
PM 26331854
ER

PT J
AU Kwan, R
   Chen, L
   Looi, K
   Tao, GZ
   Weerasinghe, SV
   Snider, NT
   Conti, MA
   Adelstein, RS
   Xie, Q
   Omary, MB
AF Kwan, Raymond
   Chen, Lu
   Looi, Koksun
   Tao, Guo-Zhong
   Weerasinghe, Sujith V.
   Snider, Natasha T.
   Conti, Mary Anne
   Adelstein, Robert S.
   Xie, Qing
   Omary, M. Bishr
TI PKC412 Normalizes Mutation-Related Keratin Filament Disruption and
   Hepatic Injury in Mice by Promoting Keratin-Myosin Binding
SO HEPATOLOGY
LA English
DT Article
ID EPIDERMOLYSIS-BULLOSA SIMPLEX; SIMPLE EPITHELIAL KERATINS; ACUTE
   MYELOID-LEUKEMIA; LAMIN A/C GENE; TRANSGENIC MICE;
   INTERMEDIATE-FILAMENTS; DISEASE; INHIBITION; FRAGILITY; ACTIVATION
AB Keratins, among other cytoskeletal intermediate filament proteins, are mutated at a highly conserved arginine with consequent severe disease phenotypes due to disruption of keratin filament organization. We screened a kinase inhibitor library, using A549 cells that are transduced with a lentivirus keratin 18 (K18) construct, to identify compounds that normalize filament disruption due to K18 Arg90Cys mutation at the conserved arginine. High-throughput screening showed that PKC412, a multikinase inhibitor, ameliorated K18 Arg90Cys-mediated keratin filament disruption in cells and in the livers of previously described transgenic mice that overexpress K18 Arg90Cys. Furthermore, PKC412 protected cultured A549 cells that express mutant or wild-type K18 and mouse livers of the K18 Arg90Cys-overexpressing transgenic mice from Fas-induced apoptosis. Proteomic analysis of proteins that associated with keratins after exposure of K18-expressing A549 cells to PKC412 showed that nonmuscle myosin heavy chain-IIA (NMHC-IIA) partitions with the keratin fraction. The nonmuscle myosin-IIA (NM-IIA) association with keratins was confirmed by immune staining and by coimmunoprecipitation. The keratin-myosin association is myosin dephosphorylation-dependent; occurs with K8, the obligate K18 partner; is enhanced by PKC412 in cells and mouse liver; and is blocked by hyperphosphorylation conditions in cultured cells and mouse liver. Furthermore, NMHC-IIA knockdown inhibits PKC412-mediated normalization of K18 R90C filaments. Conclusion: The inhibitor PKC412 normalizes K18 Arg90Cys mutation-induced filament disruption and disorganization by enhancing keratin association with NM-IIA in a myosin dephosphorylation-regulated manner. Targeting of intermediate filament disorganization by compounds that alter keratin interaction with their associated proteins offers a potential novel therapeutic approach for keratin and possibly other intermediate filament protein-associated diseases.
C1 [Kwan, Raymond; Chen, Lu; Looi, Koksun; Weerasinghe, Sujith V.; Snider, Natasha T.; Omary, M. Bishr] Univ Michigan, Dept Mol & Integrat Physiol, Ann Arbor, MI 48109 USA.
   [Kwan, Raymond; Chen, Lu; Looi, Koksun; Weerasinghe, Sujith V.; Snider, Natasha T.; Omary, M. Bishr] Univ Michigan, Dept Med, Ann Arbor, MI 48109 USA.
   [Kwan, Raymond; Omary, M. Bishr] VA Ann Arbor Healthcare Syst, Ann Arbor, MI USA.
   [Chen, Lu; Xie, Qing] Shanghai Jiao Tong Univ, Dept Infect Dis, Ruijin Hosp, Sch Med, Shanghai 200030, Peoples R China.
   [Tao, Guo-Zhong] Stanford Univ, Dept Surg, Palo Alto, CA 94304 USA.
   [Conti, Mary Anne; Adelstein, Robert S.] NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA.
RP Omary, MB (reprint author), 1137 E Catherine St,7744 MSII, Ann Arbor, MI 48109 USA.
EM xieqingrjh@163.com; mbishr@med.umich.edu
OI Adelstein, Robert/0000-0002-8683-2144
FU National Institutes of Health [R01 DK47918, K01 DK093776]; Department of
   Veterans Affairs; China Scholarship Council; institutional National
   Institutes of Health grant [DK34933]
FX Supported by National Institutes of Health grants R01 DK47918 (to
   M.B.O.) and K01 DK093776 (to N.T.S.), the Department of Veterans Affairs
   (to M.B.O.), the China Scholarship Council (to L.C.), and institutional
   National Institutes of Health grant DK34933 to the University of
   Michigan.
NR 33
TC 2
Z9 2
U1 1
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD DEC
PY 2015
VL 62
IS 6
BP 1858
EP 1869
DI 10.1002/hep.27965
PG 12
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CZ3OF
UT WOS:000367013200056
PM 26126491
ER

PT J
AU Liang, TJ
   Block, TM
   McMahon, BJ
   Ghany, MG
   Urban, S
   Guo, JT
   Locarnini, S
   Zoulim, F
   Chang, KM
   Lok, AS
AF Liang, T. Jake
   Block, Timothy M.
   McMahon, Brian J.
   Ghany, Marc G.
   Urban, Stephan
   Guo, Ju-Tao
   Locarnini, Stephen
   Zoulim, Fabien
   Chang, Kyong-Mi
   Lok, Anna S.
TI Present and Future Therapies of Hepatitis B: From Discovery to Cure
SO HEPATOLOGY
LA English
DT Review
ID CLOSED CIRCULAR DNA; TENOFOVIR DISOPROXIL FUMARATE; TAUROCHOLATE
   COTRANSPORTING POLYPEPTIDE; COMPLEX THERAPEUTIC VACCINE; CHIMERIC
   ANTIGEN RECEPTOR; ANTIVIRAL IMMUNE-RESPONSE; LARGE SURFACE PROTEIN; D
   VIRUS ENTRY; T-CELLS; IN-VIVO
AB Hepatitis B virus (HBV) is a significant global pathogen, infecting more than 240 million people worldwide. While treatment for HBV has improved, HBV patients often require lifelong therapies and cure is still a challenging goal. Recent advances in technologies and pharmaceutical sciences have heralded a new horizon of innovative therapeutic approaches that are bringing us closer to the possibility of a functional cure of chronic HBV infection. In this article, we review the current state of science in HBV therapy and highlight new and exciting therapeutic strategies spurred by recent scientific advances. Some of these therapies have already entered into clinical phase, and we will likely see more of them moving along the development pipeline. Conclusion: With growing interest in developing and efforts to develop more effective therapies for HBV, the challenging goal of a cure may be well within reach in the near future.
C1 [Liang, T. Jake; Ghany, Marc G.] NIDDK, LDB, NIH, Bethesda, MD 20892 USA.
   [Block, Timothy M.] Baruch S Blumberg Inst, Doylestown, PA USA.
   [McMahon, Brian J.] Ctr Dis Control & Prevent, Natl Ctr Emerging & Zoonot Infect Dis, Anchorage, AK USA.
   [Urban, Stephan] Univ Heidelberg Hosp, Mol Virol, Dept Infect Dis, Heidelberg, Germany.
   [Urban, Stephan] Univ Heidelberg Hosp, German Ctr Infect Dis, Heidelberg, Germany.
   [Locarnini, Stephen] Lyon Univ, Hepatol Dept, Lyon, France.
   [Locarnini, Stephen] Canc Res Ctr Lyon, INSERM, U1052, Lyon, France.
   [Zoulim, Fabien] Doherty Inst, Victorian Infect Dis Reference Lab, Melbourne, Vic, Australia.
   [Chang, Kyong-Mi] Philadelphia Vet Affairs Med Ctr, Dept Med, Philadelphia, PA USA.
   [Chang, Kyong-Mi] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Lok, Anna S.] Univ Michigan, Div Gastroenterol & Hepatol, Ann Arbor, MI 48109 USA.
RP Liang, TJ (reprint author), NIDDK, LDB, NIH, Bldg 10-9B16,10 Ctr Dr, Bethesda, MD 20892 USA.
EM jliang@nih.gov
FU Janssen; Oncore-Tekmira; Gilead; Bristol-Myers Squibb; Roche; Novira;
   Arrowhead
FX Dr. Guo received grants from Janssen. Dr. Block is on the Board of and
   owns stock in Contravir. He received grants and holds intellectual
   property rights with Oncore-Tekmira. Dr. Lok consults and received
   grants from Gilead. She consults from GlaxoSmithKline, Merck, MYR, and
   Tekmira. She received grants from Bristol-Myers Squibb. Dr. Chang
   advises Genentech, Arbutus, and Alnylam. Dr. Zoulim consults and
   received grants from Roche, Gilead, and Novira. He consults for Janssen.
   Dr. Locarnini received royalties and holds intellectual property rights
   with Melbourne Health. He consults and received fees from Arrowhead. He
   consults for Gilead.
NR 154
TC 32
Z9 33
U1 6
U2 25
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD DEC
PY 2015
VL 62
IS 6
BP 1893
EP 1908
DI 10.1002/hep.28025
PG 16
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CZ3OF
UT WOS:000367013200059
PM 26239691
ER

PT J
AU Mezey, E
   Nemeth, K
AF Mezey, Eva
   Nemeth, Krisztian
TI Mesenchymal stem cells and infectious diseases: Smarter than drugs
SO IMMUNOLOGY LETTERS
LA English
DT Article
DE MSC; BMSC; Immune-regulatory effects of MSC; MSC and pathogen
   interactions
ID TOLL-LIKE RECEPTORS; INDUCED ACUTE LUNG; STAPHYLOCOCCUS-AUREUS
   INFECTION; STROMAL CELLS; IN-VITRO; EX-VIVO; EXPERIMENTAL COLITIS;
   BACTERIAL CLEARANCE; IMMUNE-RESPONSES; HBV INFECTION
AB After bone marrow stromal cells (BMSCs also known as mesenchymal stem cells of bone marrow origin) were used successfully to treat graft versus host disease in a single human subject [1], many investigators studied the immune-suppressive properties of BMSCs and later adipose tissue derived MSCs (AMSC). The field has expanded significantly and there are many ongoing clinical trials that are trying to exploit the amazing abilities of MSCs from many tissues to regulate the immune system. In addition to "supervising" cells of the innate immune system, MSCs have also been shown to have anti-microbial properties. They appear to make molecules with direct effects on bacteria. Many questions about MSCs remain, however. We still need to determine how to isolate subpopulations of cells with specific immunomodulatory or antibacterial actions from the heterogeneous pool of cultured BMSCs. We need to find ways to prime cells to improve their immune regulatory activities, and while we have some ideas about mechanisms that underlie MSC/immune cell interactions, there is still much to discover before we can take full advantage of the regulatory abilities of MSCs to treat human diseases. (C) 2015 Published by Elsevier B.V.
C1 [Mezey, Eva; Nemeth, Krisztian] Natl Inst Dent & Craniofacial Res, Adult Stem Cell Sect, Craniofacial & Skeletal Dis Branch, NIH,Hlth & Human Serv, Bethesda, MD 20892 USA.
   [Nemeth, Krisztian] Semmelweis Univ, Dept Dermatol, H-1085 Budapest, Hungary.
RP Mezey, E (reprint author), Natl Inst Dent & Craniofacial Res, Adult Stem Cell Sect, Craniofacial & Skeletal Dis Branch, NIH,Hlth & Human Serv, Bethesda, MD 20892 USA.
EM mezeye@mail.nih.gov; nemethk@mail.nih.gov
FU Division of Intramural Research program of NIDCR, Intramural Research
   Program, NIH, DHHS [ZIA DE000714, ZIA DE000676]
FX Work in the authors' laboratory is supported by the Division of
   Intramural Research program of NIDCR (ZIA DE000714 and ZIA DE000676), in
   the Intramural Research Program, NIH, DHHS.
NR 89
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U1 3
U2 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-2478
EI 1879-0542
J9 IMMUNOL LETT
JI Immunol. Lett.
PD DEC
PY 2015
VL 168
IS 2
SI SI
BP 208
EP 214
DI 10.1016/j.imlet.2015.05.020
PG 7
WC Immunology
SC Immunology
GA CZ5BE
UT WOS:000367116300013
PM 26051681
ER

PT J
AU Jiang, MS
   Yang, XY
   Esposito, D
   Nelson, E
   Yuan, JH
   Hopkins, RF
   Broadt, T
   Xiao, Z
   Colantonio, S
   Prieto, DA
   Welch, AR
   Creekmore, SP
   Mitra, G
   Zhu, JW
AF Jiang, Man-Shiow
   Yang, Xiaoyi
   Esposito, Dominic
   Nelson, Earl
   Yuan, Jinhui
   Hopkins, Ralph F.
   Broadt, Trevor
   Xiao, Zhen
   Colantonio, Simona
   Prieto, DaRue A.
   Welch, Anthony R.
   Creekmore, Stephen P.
   Mitra, George
   Zhu, Jianwei
TI Mammalian cell transient expression, non-affinity purification, and
   characterization of human recombinant IGFBP7, an IGF-1 targeting
   therapeutic protein
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Article
DE IGFBP7; Protein expression; Protein purification; Transient gene
   expression
ID GENE-EXPRESSION; HEPATOCELLULAR-CARCINOMA; SECRETED PROTEIN; GROWTH;
   TRANSFECTION; SENESCENCE; LEVEL
AB Targeted inhibiting insulin-like growth factor 1 is an effective approach for cancer therapy. Insulin-like growth factor binding protein 7 (IGFBP7) is considered as a potential therapeutic protein. However, producing high quality of such non-IgG proteins in mammalian cells is still a challenge in biopharmaceutical development Here, we report a rapid production process by using transient gene transfection in HEK 293E cells. A set of constructs combining several expression promoters, leader sequences, and 5' un-translated regions were generated and optimized, from which the best vector with expression level at similar to 50 mg/L was selected for production at 2 L cell culture scale. Comparison study in downstream purification methods led to development of a scalable, non-affinity chromatography strategy through Super Q Fast Flow Q and Heparin columns. The product was characterized in purity (99%), isoelectric point, molecule weight, glycosylation, and stability by using SEC-HPLC, SDS-PAGE, isoelectric focusing and mass spectrometry. The highly purified product shows IGF-1 binding activity and inhibits IGF-1-induced cell proliferation. This process not only provides a remarkable high expression at similar to 50 mg/L and pure glycosylated mammalian rhIGFBP7, also highlights that transient gene expression technology is practical to be used for production and early development of recombinant non-IgG therapeutic proteins. (C) 2015 Elsevier B.V. All rights reserved.
C1 [Jiang, Man-Shiow; Yang, Xiaoyi; Nelson, Earl; Yuan, Jinhui; Broadt, Trevor; Mitra, George; Zhu, Jianwei] Frederick Natl Lab Canc Res, Leidos Biomed Res Inc, Biopharmaceut Dev Program, Frederick, MD 21702 USA.
   [Esposito, Dominic; Hopkins, Ralph F.] Frederick Natl Lab Canc Res, Leidos Biomed Res Inc, Prot Express Lab, Canc Res Technol Program, Frederick, MD 21702 USA.
   [Xiao, Zhen; Colantonio, Simona; Prieto, DaRue A.] Frederick Natl Lab Canc Res, Leidos Biomed Res Inc, Prot Characterizat Lab, Canc Res Technol Program, Frederick, MD 21702 USA.
   [Welch, Anthony R.; Creekmore, Stephen P.] Natl Canc Inst, Biol Resources Branch, Frederick, MD 21702 USA.
RP Zhu, JW (reprint author), Frederick Natl Lab Canc Res, Leidos Biomed Res Inc, Biopharmaceut Dev Program, Frederick, MD 21702 USA.
EM jianweiz@sjtu.edu.cn
FU National Cancer Institute, National Institutes of Health
   [HHSN261200800001E]; Developmental Therapeutics Program in the Division
   of Cancer Treatment and Diagnosis of the National Cancer Institute
   [HHSN261200800001E]
FX The authors would like to express acknowledgment to Dr. M. Green for his
   expression plasmid from where we amplified the IGFBP7 cDNA. This project
   has been funded in whole or in part with federal funds from the National
   Cancer Institute, National Institutes of Health, under Contract No.
   HHSN261200800001E. The content of this publication does not necessarily
   reflect the views or policies of the Department of Health and Human
   Services, nor does mention of trade names, commercial products, or
   organizations imply endorsement by the U.S. Government This research was
   supported [in part] by the Developmental Therapeutics Program in the
   Division of Cancer Treatment and Diagnosis of the National Cancer
   Institute (Contract No. HHSN261200800001E).
NR 38
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U1 0
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PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD DEC
PY 2015
VL 29
IS 2
BP 476
EP 487
DI 10.1016/j.intimp.2015.10.008
PG 12
WC Immunology; Pharmacology & Pharmacy
SC Immunology; Pharmacology & Pharmacy
GA CY9ZL
UT WOS:000366764800031
PM 26474694
ER

PT J
AU Arai, AE
AF Arai, Andrew E.
TI Fuzzy or Sharp Borders of Acute Myocardial Ischemia and Infarction?
SO JACC-CARDIOVASCULAR IMAGING
LA English
DT Editorial Material
DE acute myocardial infarction; gadolinium; MRI; myocardial ischemia
ID BLOOD-FLOW; RISK; AREA; OCCLUSION; SIZE; DOGS
C1 [Arai, Andrew E.] NHLBI, Adv Cardiovasc Imaging, NIH, Bethesda, MD 20892 USA.
RP Arai, AE (reprint author), NHLBI, Adv Cardiovasc Imaging, NIH, Bldg 10,Room B1D416,MSC 1061,10 Ctr Dr, Bethesda, MD 20892 USA.
EM araia@nih.gov
FU Intramural NIH HHS; NHLBI NIH HHS [HL006136]
NR 9
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 1936-878X
EI 1876-7591
J9 JACC-CARDIOVASC IMAG
JI JACC-Cardiovasc. Imag.
PD DEC
PY 2015
VL 8
IS 12
BP 1390
EP 1392
DI 10.1016/j.jcmg.2015.10.003
PG 3
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
   Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
   Medical Imaging
GA CZ6IS
UT WOS:000367205100006
PM 26699108
ER

PT J
AU Dunn, BK
   Steele, VE
   Fagerstrom, RM
   Topp, CF
   Ransohoff, D
   Cunningham, C
   Lubet, R
   Ford, LG
   Kramer, BS
AF Dunn, Barbara K.
   Steele, Vernon E.
   Fagerstrom, Richard M.
   Topp, Carol F.
   Ransohoff, David
   Cunningham, Christopher
   Lubet, Ron
   Ford, Leslie G.
   Kramer, Barnett S.
TI Predictive Value Tools as an Aid in Chemopreventive Agent Development
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID DRUG DEVELOPMENT; RATES
AB Background: Over 25 years, the National Cancer Institute's Division of Cancer Prevention has entered some 800 agents into a chemopreventive agent testing program. Two critical steps involve: 1) in vitro/in vivo morphologic assays and 2) animal tumor assays (incidence/multiplicity reduction). We sought to determine how accurately the earlier-stage (morphologic) assays predict efficacy in the later-stage (animal tumor) assays.
   Methods: Focusing on 210 agents tested in both morphologic and animal tumor assays, we carried out statistical modeling of how well the six most commonly used morphologic assays predicted drug efficacy in animal tumor assays. Using multimodel inference, three statistical models were generated to evaluate the ability of these six morphologic assays to predict tumor outcomes in three different sets of animal tumor assays: 1) all tumor types, 2) mammary cancer only, and 3) colon cancer only. Using this statistical modeling approach, each morphologic assay was assigned a value reflecting how strongly it predicted outcomes in each of the three different sets of animal tumor assays.
   Results: We demonstrated differences in the predictive value of specific morphologic assays for positive animal tumor assay results. Some of the morphologic assays were strongly predictive of meaningful positive efficacy outcomes in animal tumor assays representing specific cancer types, particularly the aberrant crypt focus (ACF) assay for colon cancer. Moreover, less strongly predictive assays can be combined and sequenced, resulting in enhanced composite predictive ability.
   Conclusions: Predictive models such as these could be used to guide selection of preventive agents as well as morphologic and animal tumor assays, thereby improving the efficiency of our approach to chemopreventive agent development.
C1 [Dunn, Barbara K.; Steele, Vernon E.; Fagerstrom, Richard M.; Lubet, Ron; Ford, Leslie G.; Kramer, Barnett S.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
   [Topp, Carol F.] CCS Associates Inc, Mclean, VA USA.
   [Ransohoff, David] Univ N Carolina, Dept Med, Chapel Hill, NC USA.
   [Cunningham, Christopher] Informat Management Serv Inc, Rockville, MD USA.
RP Dunn, BK (reprint author), NCI, Canc Prevent Div, 9609 Med Ctr Dr,Room 5E534, Bethesda, MD 20892 USA.
EM dunnb@mail.nih.gov
NR 8
TC 2
Z9 2
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-J. Natl. Cancer Inst.
PD DEC
PY 2015
VL 107
IS 12
AR djv259
DI 10.1093/jnci/djv259
PG 8
WC Oncology
SC Oncology
GA CZ2YN
UT WOS:000366970900004
PM 26420882
ER

PT J
AU Sampson, JN
   Wheeler, WA
   Yeager, M
   Panagiotou, O
   Wang, Z
   Berndt, SI
   Lan, Q
   Abnet, CC
   Amundadottir, LT
   Figueroa, JD
   Landi, MT
   Mirabello, L
   Savage, SA
   Taylor, PR
   De Vivo, I
   McGlynn, KA
   Purdue, MP
   Rajaraman, P
   Adami, HO
   Ahlbom, A
   Albanes, D
   Amary, MF
   An, SJ
   Andersson, U
   Andriole, G
   Andrulis, IL
   Angelucci, E
   Ansell, SM
   Arici, C
   Armstrong, BK
   Arslan, AA
   Austin, MA
   Baris, D
   Barkauskas, DA
   Bassig, BA
   Becker, N
   Benavente, Y
   Benhamou, S
   Berg, C
   Van Den Berg, D
   Bernstein, L
   Bertrand, KA
   Birmann, BM
   Black, A
   Boeing, H
   Boffetta, P
   Boutron-Ruault, MC
   Bracci, PM
   Brinton, L
   Brooks-Wilson, AR
   Bueno-De-Mesquita, HB
   Burdett, L
   Buring, J
   Butler, MA
   Cai, QY
   Cancel-Tassin, G
   Canzian, F
   Carrato, A
   Carreon, T
   Carta, A
   Chan, JKC
   Chang, ET
   Chang, GC
   Chang, IS
   Chang, J
   Chang-Claude, J
   Chen, CJ
   Chen, CY
   Chen, C
   Chen, CH
   Chen, C
   Chen, HY
   Chen, KX
   Chen, KY
   Chen, KC
   Chen, Y
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   Chen, YS
   Chen, YM
   Chien, LH
   Chirlaque, MD
   Choi, JE
   Choi, YY
   Chow, WH
   Chung, CC
   Clavel, J
   Clavel-Chapelon, F
   Cocco, P
   Colt, JS
   Comperat, E
   Conde, L
   Connors, JM
   Conti, D
   Cortessis, VK
   Cotterchio, M
   Cozen, W
   Crouch, S
   Crous-Bou, M
   Cussenot, O
   Davis, FG
   Ding, T
   Diver, WR
   Dorronsoro, M
   Dossus, L
   Duell, EJ
   Ennas, MG
   Erickson, RL
   Feychting, M
   Flanagan, AM
   Foretova, L
   Fraumeni, JF
   Freedman, ND
   Freeman, LEB
   Fuchs, C
   Gago-Dominguez, M
   Gallinger, S
   Gao, YT
   Gapstur, SM
   Garcia-Closas, M
   Garcia-Closas, R
   Gascoyne, RD
   Gastier-Foster, J
   Gaudet, MM
   Gaziano, JM
   Giffen, C
   Giles, GG
   Giovannucci, E
   Glimelius, B
   Goggins, M
   Gokgoz, N
   Goldstein, AM
   Gorlick, R
   Gross, M
   Grubb, R
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   Guan, P
   Gunter, M
   Guo, H
   Habermann, TM
   Haiman, CA
   Halai, D
   Hallmans, G
   Hassan, M
   Hattinger, C
   He, QC
   He, XZ
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   Henderson, B
   Henriksson, R
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   Hoffman-Bolton, J
   Hohensee, C
   Holford, TR
   Holly, EA
   Hong, YC
   Hoover, RN
   Horn-Ross, PL
   Hosain, GMM
   Hosgood, HD
   Hsiao, CF
   Hu, N
   Hu, W
   Hu, ZB
   Huang, MS
   Huerta, JM
   Hung, JY
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   Inskip, PD
   Jackson, RD
   Jacobs, EJ
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   Jeon, HS
   Ji, BT
   Jin, GF
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   Johansen, C
   Johnson, A
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   Chatterjee, N
AF Sampson, Joshua N.
   Wheeler, William A.
   Yeager, Meredith
   Panagiotou, Orestis
   Wang, Zhaoming
   Berndt, Sonja I.
   Lan, Qing
   Abnet, Christian C.
   Amundadottir, Laufey T.
   Figueroa, Jonine D.
   Landi, Maria Teresa
   Mirabello, Lisa
   Savage, Sharon A.
   Taylor, Philip R.
   De Vivo, Immaculata
   McGlynn, Katherine A.
   Purdue, Mark P.
   Rajaraman, Preetha
   Adami, Hans-Olov
   Ahlbom, Anders
   Albanes, Demetrius
   Amary, Maria Fernanda
   An, She-Juan
   Andersson, Ulrika
   Andriole, Gerald, Jr.
   Andrulis, Irene L.
   Angelucci, Emanuele
   Ansell, Stephen M.
   Arici, Cecilia
   Armstrong, Bruce K.
   Arslan, Alan A.
   Austin, Melissa A.
   Baris, Dalsu
   Barkauskas, Donald A.
   Bassig, Bryan A.
   Becker, Nikolaus
   Benavente, Yolanda
   Benhamou, Simone
   Berg, Christine
   Van Den Berg, David
   Bernstein, Leslie
   Bertrand, Kimberly A.
   Birmann, Brenda M.
   Black, Amanda
   Boeing, Heiner
   Boffetta, Paolo
   Boutron-Ruault, Marie-Christine
   Bracci, Paige M.
   Brinton, Louise
   Brooks-Wilson, Angela R.
   Bueno-de-Mesquita, H. Bas
   Burdett, Laurie
   Buring, Julie
   Butler, Mary Ann
   Cai, Qiuyin
   Cancel-Tassin, Geraldine
   Canzian, Federico
   Carrato, Alfredo
   Carreon, Tania
   Carta, Angela
   Chan, John K. C.
   Chang, Ellen T.
   Chang, Gee-Chen
   Chang, I-Shou
   Chang, Jiang
   Chang-Claude, Jenny
   Chen, Chien-Jen
   Chen, Chih-Yi
   Chen, Chu
   Chen, Chung-Hsing
   Chen, Constance
   Chen, Hongyan
   Chen, Kexin
   Chen, Kuan-Yu
   Chen, Kun-Chieh
   Chen, Ying
   Chen, Ying-Hsiang
   Chen, Yi-Song
   Chen, Yuh-Min
   Chien, Li-Hsin
   Chirlaque, Maria-Dolores
   Choi, Jin Eun
   Choi, Yi Young
   Chow, Wong-Ho
   Chung, Charles C.
   Clavel, Jacqueline
   Clavel-Chapelon, Franoise
   Cocco, Pierluigi
   Colt, Joanne S.
   Comperat, Eva
   Conde, Lucia
   Connors, Joseph M.
   Conti, David
   Cortessis, Victoria K.
   Cotterchio, Michelle
   Cozen, Wendy
   Crouch, Simon
   Crous-Bou, Marta
   Cussenot, Olivier
   Davis, Faith G.
   Ding, Ti
   Diver, W. Ryan
   Dorronsoro, Miren
   Dossus, Laure
   Duell, Eric J.
   Ennas, Maria Grazia
   Erickson, Ralph L.
   Feychting, Maria
   Flanagan, Adrienne M.
   Foretova, Lenka
   Fraumeni, Joseph F., Jr.
   Freedman, Neal D.
   Freeman, Laura E. Beane
   Fuchs, Charles
   Gago-Dominguez, Manuela
   Gallinger, Steven
   Gao, Yu-Tang
   Gapstur, Susan M.
   Garcia-Closas, Montserrat
   Garcia-Closas, Reina
   Gascoyne, Randy D.
   Gastier-Foster, Julie
   Gaudet, Mia M.
   Gaziano, J. Michael
   Giffen, Carol
   Giles, Graham G.
   Giovannucci, Edward
   Glimelius, Bengt
   Goggins, Michael
   Gokgoz, Nalan
   Goldstein, Alisa M.
   Gorlick, Richard
   Gross, Myron
   Grubb, Robert, III
   Gu, Jian
   Guan, Peng
   Gunter, Marc
   Guo, Huan
   Habermann, Thomas M.
   Haiman, Christopher A.
   Halai, Dina
   Hallmans, Goran
   Hassan, Manal
   Hattinger, Claudia
   He, Qincheng
   He, Xingzhou
   Helzlsouer, Kathy
   Henderson, Brian
   Henriksson, Roger
   Hjalgrim, Henrik
   Hoffman-Bolton, Judith
   Hohensee, Chancellor
   Holford, Theodore R.
   Holly, Elizabeth A.
   Hong, Yun-Chul
   Hoover, Robert N.
   Horn-Ross, Pamela L.
   Hosain, G. M. Monawar
   Hosgood, H. Dean, III
   Hsiao, Chin-Fu
   Hu, Nan
   Hu, Wei
   Hu, Zhibin
   Huang, Ming-Shyan
   Huerta, Jose-Maria
   Hung, Jen-Yu
   Hutchinson, Amy
   Inskip, Peter D.
   Jackson, Rebecca D.
   Jacobs, Eric J.
   Jenab, Mazda
   Jeon, Hyo-Sung
   Ji, Bu-Tian
   Jin, Guangfu
   Jin, Li
   Johansen, Christoffer
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TI Analysis of Heritability and Shared Heritability Based on Genome-Wide
   Association Studies for 13 Cancer Types
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID MULTIPLE SUSCEPTIBILITY LOCI; LUNG-CANCER; FAMILIAL RISK;
   PANCREATIC-CANCER; SWEDEN; INDIVIDUALS; MUTATIONS; RELATIVES; LYMPHOMA;
   DATABASE
AB Background: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites.
   Methods: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers.
   Results: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, h(l)(2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (rho = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (rho = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (rho = 0.51, SE = 0.18), and bladder and lung (rho = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures.
   Conclusion: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.
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   [Picci, Piero; Schwartz, Kendra; Serra, Massimo] Orthopaed Rizzoli Inst, Expt Oncol Lab, Bologna, Italy.
   [He, Xingzhou] Chinese Ctr Dis Control & Prevent, Beijing, Peoples R China.
   [Helzlsouer, Kathy; Hoffman-Bolton, Judith; Klein, Alison P.; Visvanathan, Kala] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
   [Hjalgrim, Henrik; Melbye, Mads] Statens Serum Inst, Dept Epidemiol Res, Div Hlth Surveillance & Res, DK-2300 Copenhagen, Denmark.
   [Holford, Theodore R.] Yale Univ, Sch Publ Hlth, Dept Biostat, New Haven, CT USA.
   [Hong, Yun-Chul] Seoul Natl Univ, Coll Med, Dept Prevent Med, Seoul, South Korea.
   [Horn-Ross, Pamela L.] Canc Prevent Inst Calif, Fremont, CA USA.
   [Hosain, G. M. Monawar] New Hampshire State Canc Registry, Concord, NH USA.
   [Hosgood, H. Dean, III] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA.
   [Hsiao, Chin-Fu] Natl Hlth Res Inst, Taiwan Lung Canc Tissue Specimen Informat Resourc, Zhunan, Taiwan.
   [Hu, Zhibin; Jin, Guangfu; Shen, Hongbing; Shen, Wei] Nanjing Med Univ, Jiangsu Collaborat Innovat Ctr Canc Personalized, Nanjing, Jiangsu, Peoples R China.
   [Hu, Zhibin; Jin, Guangfu; Shen, Hongbing; Shen, Wei] Nanjing Med Univ, Sch Publ Hlth, Ctr Canc, Jiangsu Key Lab Canc Biomarkers Prevent & Treatme, Nanjing, Jiangsu, Peoples R China.
   [Huang, Ming-Shyan; Hung, Jen-Yu] Kaohsiung Med Univ, Sch Med, Kaohsiung Med Univ Hosp, Dept Internal Med, Kaohsiung, Taiwan.
   [Jackson, Rebecca D.] Ohio State Univ, Div Endocrinol Diabet & Metab, Columbus, OH 43210 USA.
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   [Jeon, Hyo-Sung] Kyungpook Natl Univ, Mol Diagnost & Imaging Ctr, Daegu, South Korea.
   [Johansen, Christoffer] Danish Canc Soc Res Ctr, Unit Survivorship, Copenhagen, Denmark.
   [Johnson, Alison] Vermont Canc Registry, Burlington, VT USA.
   [Jung, Yoo Jin; Kang, Chang Hyun; Kim, Young Tae; Park, In Kyu] Seoul Natl Univ, Coll Med, Canc Res Inst, Dept Thorac & Cardiovasc Surg, Seoul, South Korea.
   [Kamineni, Aruna] Grp Hlth Res Inst, Seattle, WA USA.
   [Karagas, Margaret R.; Schned, Alan] Dartmouth Coll, Geisel Sch Med, Hanover, NH 03755 USA.
   [Kelly, Rachel S.; Vineis, Paolo] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, MRC PHE Ctr Environm & Hlth, London, England.
   [Khaw, Kay-Tee] Univ Cambridge, Cambridge CB2 1TN, England.
   [Kim, Hee Nam] Chonnam Natl Univ, Ctr Creat Biomed Scientists, Gwangju, South Korea.
   [Kim, Jin Hee] Seoul Natl Univ, Grad Sch Publ Hlth, Dept Environm Hlth, Seoul, South Korea.
   [Kim, Jun Suk] Korea Univ, Guro Hosp, Coll Med, Dept Internal Med,Div Med Oncol, Seoul, South Korea.
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   [Kogevinas, Manolis] Hosp del Mar, Municipal Inst Med Res IMIM, Barcelona, Spain.
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   [Liu, Li] Huazhong Univ Sci & Technol, Ctr Canc, Union Hosp, Wuhan 430074, Peoples R China.
   Umea Univ, Dept Surg & Perioperat Sci Urol & Androl, Umea, Sweden.
   Univ Florence, Dept Surg & Translat Med, Sect Anatomopathol, Florence, Italy.
   [Lund, Eiluv; Weiderpass, Elisabete] Univ Tromso, Arctic Univ Norway, Fac Hlth Sci, Dept Community Med, Tromso, Norway.
   Spanish Natl Canc Res Ctr CNIO, Genet & Mol Epidemiol Grp, Madrid, Spain.
   [Mannisto, Satu; Virtamo, Jarmo] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
   [Le Marchand, Loic; Yu, Herbert] Univ Hawaii, Ctr Canc, Canc Epidemiol Program, Honolulu, HI 96822 USA.
   Stanford Univ, Lucile Packard Childrens Hosp, Palo Alto, CA 94304 USA.
   [Masala, Giovanna; Palli, Domenico] Canc Res & Prevent Inst ISPO, Mol & Nutr Epidemiol Unit, Florence, Italy.
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   [Matsuo, Keitaro] Aichi Canc Res Inst, Div Mol Med, Nagoya, Aichi, Japan.
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   [Maynadie, Marc] Dijon Univ Hosp, Dijon, France.
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   Brown Univ, Dept Epidemiol, Div Biol & Med, Providence, RI 02912 USA.
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   [Mitsudomi, Tetsuya] Kinki Univ, Sch Med, Div Thorac Surg, Sayama, Osaka 589, Japan.
   [Monnereau, Alain] Inst Bergonie, Registre Hemopathies Malignes Gironde, Bordeaux, France.
   Aarhus Univ, Epidemiol Sect, DK-8000 Aarhus C, Denmark.
   Aalborg Univ Hosp, Dept Cardiol, Aalborg, Denmark.
   [Nieters, Alexandra] Univ Med Ctr Freiburg, Ctr Chron Immunodeficiency, Freiburg, Baden Wurttembe, Germany.
   [North, Kari E.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
   [North, Kari E.] Univ N Carolina, Carolina Ctr Genome Sci, Chapel Hill, NC USA.
   [Oberg, Ann L.] Mayo Clin, Dept Hlth Sci Res, Div Biomed Stat & Informat, Rochester, MN USA.
   [Olson, Sara H.; Pike, Malcolm C.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
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   [Park, Jae Yong] Kyungpook Natl Univ, Med Ctr, Lung Canc Ctr, Daegu, South Korea.
   [Peeters, Petra H. M.; Vermeulen, Roel C. H.] Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care 194, Utrecht, Netherlands.
   [Peeters, Petra H. M.] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, Dept Primary Care & Publ Hlth, London, England.
   [Petersen, Gloria M.] Mayo Clin, Div Epidemiol, Dept Hlth Sci Res, Rochester, MN USA.
   [Qian, Biyun] Acad Sinica, Genom Res Ctr, Taipei 115, Taiwan.
   [Qiao, You-Lin] Chinese Acad Med Sci, Canc Inst & Hosp, Dept Epidemiol, Beijing 100730, Peoples R China.
   [Risch, Harvey A.] Yale Univ, Sch Publ Hlth, Dept Chron Dis Epidemiol, New Haven, CT USA.
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   Karmanos Canc Inst, Detroit, MI USA.
   [Schwenn, Molly] Maine Canc Registry, Augusta, ME USA.
   [Serra, Consol] Univ Pompeu Fabra, Dept Ciencies Experimentals & Salut, Barcelona, Spain.
   [Severi, Gianluca; Vineis, Paolo] Human Genet Fdn, Turin, Italy.
   [Sihoe, Alan Dart Loon] Queen Mary Hosp, Div Cardiothorac Surg, Dept Surg, Hong Kong, Hong Kong, Peoples R China.
   Univ Melbourne, Dept Pathol, Parkville, Vic 3052, Australia.
   [Spinelli, John J.] BC Canc Agcy, Canc Control Res, Vancouver, BC, Canada.
   [Spinelli, John J.] Univ British Columbia, Sch Populat & Publ Hlth, Vancouver, BC V5Z 1M9, Canada.
   [Staines, Anthony] Dublin City Univ, Sch Nursing & Human Sci, Dublin 9, Ireland.
   [Su, Wu-Chou] Natl Cheng Kung Univ, Med Coll & Hosp, Tainan 701, Taiwan.
   [Sund, Malin] Umea Univ, Dept Surg & Perioperat Sci, Surg, Umea, Sweden.
   [Sung, Jae Sook] Korea Univ, Canc Res Inst, Seoul, South Korea.
   [Sung, Sook Whan] Seoul St Marys Hosp, Dept Thorac & Cardiovasc Surg, Seoul, South Korea.
   [Tardon, Adonina] Univ Oviedo, Inst Univ Oncol, Oviedo, Spain.
   [Thomas, David] St Vincents Hosp, Garvan Inst Med Res, Kinghorn Canc Ctr, Darlinghurst, NSW 2010, Australia.
   [Tjonneland, Anne] Danish Canc Soc, Res Ctr, Copenhagen, Denmark.
   [Travis, Ruth C.] Univ Oxford, Canc Epidemiol Unit, Oxford, England.
   [Trichopoulos, Dimitrios] Acad Athens, Bur Epidemiol Res, Athens, Greece.
   [Trichopoulos, Dimitrios] Hellen Hlth Fdn, Athens, Greece.
   [Tsai, Ying-Huang] Chang Gung Mem Hosp, Dept Resp Thearpy, Chiayi, Taiwan.
   [Turner, Jenny] Macquarie Univ, Australian Sch Adv Med, Sydney, NSW 2109, Australia.
   [Turner, Jenny] Douglass Hanly Moir Pathol, Dept Histopathol, Macquarie Pk, NSW, Australia.
   [Vajdic, Claire M.] Univ New S Wales, Prince Wales Clin Sch, Sydney, NSW, Australia.
   [Vermeulen, Roel C. H.] Univ Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands.
   [Wactawski-Wende, Jean] SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA.
   [Wang, Chih-Liang] Chang Gung Mem Hosp, Dept Pulm & Crit Care, Taoyuan, Taiwan.
   [Wang, Jiu-Cun] Fudan Univ, Sch Life Sci, State Key Lab Genet Engn, Shanghai, Peoples R China.
   [Wang, Junwen] Univ Hong Kong, Li Ka Shing Fac Med, Ctr Genom Sci, Hong Kong, Peoples R China.
   [Wang, Junwen] Univ Hong Kong, Li Ka Shing Fac Med, Dept Biochem, Hong Kong, Hong Kong, Peoples R China.
   [Wei, Fusheng; Wu, Guoping] China Natl Environm Monitoring Ctr, Beijing, Peoples R China.
   [Weiderpass, Elisabete] Canc Registry Norway, Oslo, Norway.
   [Weiderpass, Elisabete] Folkhalsan Res Ctr, Dept Genet Epidemiol, Helsinki, Finland.
   [Wolpin, Brian M.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
   [Wolpin, Brian M.] Harvard Univ, Sch Med, Boston, MA USA.
   [Wong, Maria Pik] Univ Hong Kong, Li Ka Shing Fac Med, Dept Pathol, Hong Kong, Hong Kong, Peoples R China.
   [Wu, Chen] Chinese Acad Med Sci, Canc Inst & Hosp, State Key Lab Mol Oncol, Beijing 100730, Peoples R China.
   [Wu, Chen] Peking Union Med Coll, Beijing 100021, Peoples R China.
   [Xiang, Yong-Bing] Shanghai Jiao Tong Univ, Sch Med, Renji Hosp, Shanghai Canc Inst, Shanghai 200030, Peoples R China.
   [Xu, Jun] Univ Hong Kong, Sch Publ Hlth, Hong Kong, Hong Kong, Peoples R China.
   [Xu, Ping] Wuhan Iron & Steel Corp Staff Worker Hosp, Dept Oncol, Wuhan, Peoples R China.
   [Yang, Pan-Chyr] Natl Taiwan Univ, Coll Med, Dept Internal Med, Taipei, Taiwan.
   [Yokota, Jun] Inst Predict & Personalized Med Canc IMPPC, Barcelona, Spain.
   [Yoon, Ho-Il] Seoul Natl Univ, Bundang Hosp, Dept Internal Med, Songnam, South Korea.
   [Yuan, Jian-Min] Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
   Georgetown Univ, Med Ctr, Innovat Ctr Biomed Informat, Washington, DC USA.
   Georgetown Univ, Med Ctr, Dept Oncol, Washington, DC 20007 USA.
   [Cerhan, James R.; Slager, Susan L.] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
   [Ferri, Giovanni M.] Univ Bari, Interdisciplinary Dept Med, Bari, Italy.
   [Magnani, Corrado] Univ Piemonte Orientale, Dept Translat Med, CPO Piemonte & Unit Med Stat & Epidemiol, Novara, Italy.
   [Mirabello, Lisa] Canc Prevent & Res Inst ISPO, Environm & Occupat Epidemiol Unit, Florence, Italy.
   [Smedby, Karin E.] Karolinska Univ Hosp, Karolinska Inst, Dept Med, Stockholm, Sweden.
   [Hunter, David J.] Broad Inst Harvard, Cambridge, MA USA.
   [Hunter, David J.] MIT, Cambridge, MA 02139 USA.
   [Kraft, Peter] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
RP Sampson, JN (reprint author), NCI, Biostat Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,7E594, Rockville, MD 20815 USA.
EM joshua.sampson@nih.gov; nilanjan.chatterjee@nih.gov
RI Wang, Junwen/D-3700-2011; Qiao, You-Lin/B-4139-2012; Clavel,
   Jacqueline/Q-2750-2016; Hattinger, Claudia/Q-1212-2016; Beane Freeman,
   Laura/C-4468-2015; Kitahara, Cari/R-8267-2016; Jung, Yoojin/G-2519-2015;
   Kogevinas, Manolis/C-3918-2017; Brooks-Wilson, Angela/E-9399-2012;
   Weiderpass, Elisabete/M-4029-2016; Abnet, Christian/C-4111-2015; Purdue,
   Mark/C-9228-2016; Jin, Li/C-1468-2009; Savage, Sharon/B-9747-2015; de
   Sanjose Llongueras, Silvia/H-6339-2014; Andrulis, Irene/E-7267-2013;
   Gallinger, Steven/E-4575-2013; Benhamou, Simone/K-6554-2015; Krogh,
   Vittorio/K-2628-2016
OI Wang, Junwen/0000-0002-4432-4707; Qiao, You-Lin/0000-0001-6380-0871;
   Clavel, Jacqueline/0000-0002-3616-7676; Hattinger,
   Claudia/0000-0002-9316-5095; Beane Freeman, Laura/0000-0003-1294-4124;
   Joseph, Vijai/0000-0002-7933-151X; Brooks-Wilson,
   Angela/0000-0003-1009-6408; Weiderpass, Elisabete/0000-0003-2237-0128;
   Abnet, Christian/0000-0002-3008-7843; Purdue, Mark/0000-0003-1177-3108;
   Jin, Li/0000-0002-4546-2415; Savage, Sharon/0000-0001-6006-0740; Krogh,
   Vittorio/0000-0003-0122-8624
FU Intramural Research Program of the National Institutes of Health
FX This study was supported by the Intramural Research Program of the
   National Institutes of Health.
NR 35
TC 14
Z9 14
U1 7
U2 63
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-J. Natl. Cancer Inst.
PD DEC
PY 2015
VL 107
IS 12
AR djv279
DI 10.1093/jnci/djv279
PG 11
WC Oncology
SC Oncology
GA CZ2YN
UT WOS:000366970900015
PM 26464424
ER

PT J
AU Wentzensen, N
   Fetterman, B
   Castle, PE
   Schiffman, M
   Wood, SN
   Stiemerling, E
   Tokugawa, D
   Bodelon, C
   Poitras, N
   Lorey, T
   Kinney, W
AF Wentzensen, Nicolas
   Fetterman, Barbara
   Castle, Philip E.
   Schiffman, Mark
   Wood, Shannon N.
   Stiemerling, Eric
   Tokugawa, Diane
   Bodelon, Clara
   Poitras, Nancy
   Lorey, Thomas
   Kinney, Walter
TI p16/Ki-67 Dual Stain Cytology for Detection of Cervical Precancer in
   HPV-Positive Women
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID HUMAN-PAPILLOMAVIRUS DNA; RANDOMIZED CONTROLLED-TRIAL; CANCER
   PRECURSORS; INTRAEPITHELIAL NEOPLASIA; PREDICTIVE VALUES;
   SCREENING-TESTS; FOLLOW-UP; PERFORMANCE; COLPOSCOPY; PREVENTION
AB Background: Human papillomavirus (HPV)-based cervical cancer screening requires triage markers to decide who should be referred to colposcopy. p16/Ki-67 dual stain cytology has been proposed as a biomarker for cervical precancers. We evaluated the dual stain in a large population of HPV-positive women.
   Methods: One thousand five hundred and nine HPV-positive women screened with HPV/cytology cotesting at Kaiser Permanente California were enrolled into a prospective observational study in 2012. Dual stain cytology was performed on residual Surepath material, and slides were evaluated for dual stain-positive cells. Disease endpoints were ascertained from the clinical database at KPNC. We evaluated the clinical performance of the assay among all HPV-positive women and among HPV-positive, cytology-negative women. We used internal benchmarks for clinical management to evaluate the clinical relevance of the dual stain assay. We evaluated sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of the dual stain compared with Pap cytology. All statistical tests were two-sided.
   Results: The dual stain had lower positivity (45.9%) compared with cytology at an ASC-US threshold (53.4%). For detection of CIN2+, the dual stain had similar sensitivity (83.4% vs 76.6%, P = .1), and statistically higher specificity (58.9% vs 49.6%, P < .001), PPV (21.0% vs 16.6%, P < .001), and NPV (96.4% vs 94.2%, P = .01) compared with cytology. Similar patterns were observed for CIN3+. Women with a positive test had high enough risk for referral to colposcopy, while the risk for women with negative tests was below a one-year return threshold based on current US management guidelines.
   Conclusion: Dual stain cytology showed good risk stratification for all HPV-positive women and for HPV-positive women with normal cytology. Additional follow-up is needed to determine how long dual stain negative women remain at low risk of precancer.
C1 [Wentzensen, Nicolas; Schiffman, Mark; Wood, Shannon N.; Bodelon, Clara] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Fetterman, Barbara; Stiemerling, Eric; Tokugawa, Diane; Poitras, Nancy; Lorey, Thomas] Kaiser Permanente, TPMG Reg Lab, Berkeley, CA USA.
   [Castle, Philip E.] Global Coalit Cerv Canc, Arlington, VA USA.
   [Castle, Philip E.] Albert Einstein Coll Med, Bronx, NY 10467 USA.
   [Kinney, Walter] Kaiser Permanente Med Care Program, Div Gynecol Oncol, Oakland, CA USA.
RP Wentzensen, N (reprint author), NCI, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Room 7-E114, Bethesda, MD 20892 USA.
EM wentzenn@mail.nih.gov
NR 26
TC 6
Z9 8
U1 1
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-J. Natl. Cancer Inst.
PD DEC
PY 2015
VL 107
IS 12
AR djv257
DI 10.1093/jnci/djv257
PG 8
WC Oncology
SC Oncology
GA CZ2YN
UT WOS:000366970900002
PM 26376685
ER

PT J
AU Yamazaki, Y
   Kodama, S
   Kakizaki, S
   Yamada, M
   Negishi, M
AF Yamazaki, Y.
   Kodama, S.
   Kakizaki, S.
   Yamada, M.
   Negishi, M.
TI IGFBP1 mediates pregnane X receptor-induced morphological changes and
   migration of hepatocellular carcinoma cells
SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Meeting Abstract
C1 [Yamazaki, Y.; Kodama, S.; Negishi, M.] NIEHS, Pharmacogenet Sect, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC 27709 USA.
   [Yamazaki, Y.; Kakizaki, S.; Yamada, M.] Gunma Univ, Grad Sch Med, Dept Med & Mol Sci, Maebashi, Gunma 371, Japan.
   [Kodama, S.] Tohoku Univ, Grad Sch Pharmaceut Sci, Lab Pharmacotherapy Life Style Related Dis, Sendai, Miyagi 980, Japan.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0815-9319
EI 1440-1746
J9 J GASTROEN HEPATOL
JI J. Gastroenterol. Hepatol.
PD DEC
PY 2015
VL 30
SU 4
SI SI
MA 1010
BP 329
EP 329
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CX4NI
UT WOS:000365677202018
ER

PT J
AU Kirklin, JK
   Naftel, DC
   Pagani, FD
   Kormos, RL
   Stevenson, LW
   Blume, ED
   Myers, SL
   Miller, MA
   Baldwin, JT
   Young, JB
AF Kirklin, James K.
   Naftel, David C.
   Pagani, Francis D.
   Kormos, Robert L.
   Stevenson, Lynne W.
   Blume, Elizabeth D.
   Myers, Susan L.
   Miller, Marissa A.
   Baldwin, J. Timothy
   Young, James B.
TI Seventh INTERMACS annual report: 15,000 patients and counting
SO JOURNAL OF HEART AND LUNG TRANSPLANTATION
LA English
DT Article
DE advanced heart failure; destination therapy; INTERMACS; mechanical
   support; ventricular assist device
ID VENTRICULAR ASSIST DEVICE; THROMBOSIS
AB The seventh annual report of the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) summarizes the first 9 years of patient enrollment. The Registry includes >15,000 patients from 158 participating hospitals. Trends in device strategy, patient profile at implant and survival are presented. Risk factors for mortality with continuous-flow pumps are updated, and the major causes/modes of death are presented. The adverse event burden is compared between eras, and health-related quality of life is reviewed. A detailed analysis of outcomes after mechanical circulatory support for ambulatory heart failure is presented. Recent summary data from PediMACS and MedaMACS is included. With the current continuous-flow devices, survival at 1 and 2 years is 80% and 70%, respectively. (C) 2015 International Society for Heart and Lung Transplantation. All rights reserved.
C1 [Kirklin, James K.; Naftel, David C.; Myers, Susan L.] Univ Alabama Birmingham, Dept Surg, Birmingham, AL 35294 USA.
   [Pagani, Francis D.] Univ Michigan, Dept Surg, Ann Arbor, MI 48109 USA.
   [Kormos, Robert L.] Univ Pittsburgh, Presbyterian Univ Hosp, Med Ctr, Dept Surg, Pittsburgh, PA USA.
   [Stevenson, Lynne W.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
   [Blume, Elizabeth D.] Boston Childrens Hosp, Dept Pediat, Boston, MA USA.
   [Miller, Marissa A.; Baldwin, J. Timothy] NHLBI, Div Cardiovasc Dis, Adv Technol & Surg Branch, Bethesda, MD 20892 USA.
   [Young, James B.] Cleveland Clin Fdn, Lerner Coll Med, Dept Med, Cleveland, OH 44195 USA.
RP Kirklin, JK (reprint author), Univ Alabama Birmingham, Dept Surg, 1900 Univ Blvd, Birmingham, AL 35294 USA.
EM jkirklin@uab.edu
FU National Heart, Lung and Blood Institute [HHSN2682011000250]
FX D.C.N. is a consultant for HeartWare and F.D.P. participates in contract
   research managed by the University of Michigan for HeartWare and
   Thoratec. The remaining authors have no conflicts of interest to
   disclose. This analysis and the INTERMACS device database are funded by
   a contract grant (HHSN2682011000250) from the National Heart, Lung and
   Blood Institute.
NR 4
TC 142
Z9 143
U1 10
U2 18
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1053-2498
EI 1557-3117
J9 J HEART LUNG TRANSPL
JI J. Heart Lung Transplant.
PD DEC
PY 2015
VL 34
IS 12
SI SI
BP 1495
EP 1504
DI 10.1016/j.healun.2015.10.003
PG 10
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery;
   Transplantation
SC Cardiovascular System & Cardiology; Respiratory System; Surgery;
   Transplantation
GA CZ2SU
UT WOS:000366955700001
PM 26520247
ER

PT J
AU Jeffries, N
   Miller, MA
   Taddei-Peters, WC
   Burke, C
   Baldwin, JT
   Young, JB
AF Jeffries, Neal
   Miller, Marissa A.
   Taddei-Peters, Wendy C.
   Burke, Catherine
   Baldwin, J. Timothy
   Young, James B.
TI What is the truth behind pump thrombosis in the HeartMate II device? A
   National Heart, Lung, and Blood Institute perspective based on data from
   the Interagency Registry for Mechanically Assisted Circulatory Support
SO JOURNAL OF HEART AND LUNG TRANSPLANTATION
LA English
DT Editorial Material
C1 [Jeffries, Neal; Miller, Marissa A.; Taddei-Peters, Wendy C.; Burke, Catherine; Baldwin, J. Timothy] NHLBI, Bethesda, MD 20892 USA.
   [Young, James B.] Cleveland Clin, Cleveland, OH 44106 USA.
RP Jeffries, N (reprint author), NHLBI, NIH, Room 9194,MSC 7913,6701 Rockledge Dr, Bethesda, MD 20892 USA.
EM nealjeff@nhIbi.nih.gov
FU PHS HHS [HHSN268201100025C]
NR 15
TC 5
Z9 5
U1 1
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1053-2498
EI 1557-3117
J9 J HEART LUNG TRANSPL
JI J. Heart Lung Transplant.
PD DEC
PY 2015
VL 34
IS 12
SI SI
BP 1505
EP 1510
DI 10.1016/j.healun.2015.10.036
PG 6
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery;
   Transplantation
SC Cardiovascular System & Cardiology; Respiratory System; Surgery;
   Transplantation
GA CZ2SU
UT WOS:000366955700002
PM 26681119
ER

PT J
AU Malicdan, MCV
   Vilboux, T
   Stephen, J
   Maglic, D
   Mian, L
   Konzman, D
   Guo, J
   Yildirimli, D
   Bryant, J
   Fischer, R
   Zein, WM
   Snow, J
   Vemulapalli, M
   Mullikin, JC
   Toro, C
   Solomon, BD
   Niederhuber, JE
   Gahl, WA
   Gunay-Aygun, M
AF Malicdan, May Christine V.
   Vilboux, Thierry
   Stephen, Joshi
   Maglic, Dino
   Mian, Luhe
   Konzman, Daniel
   Guo, Jennifer
   Yildirimli, Deniz
   Bryant, Joy
   Fischer, Roxanne
   Zein, Wadih M.
   Snow, Joseph
   Vemulapalli, Meghana
   Mullikin, James C.
   Toro, Camilo
   Solomon, Benjamin D.
   Niederhuber, John E.
   Gahl, William A.
   Gunay-Aygun, Meral
CA NISC Comparative Sequencing Progra
TI Mutations in human homologue of chicken talpid3 gene (KIAA0586) cause a
   hybrid ciliopathy with overlapping features of Jeune and Joubert
   syndromes
SO JOURNAL OF MEDICAL GENETICS
LA English
DT Article
ID ASPHYXIATING THORACIC DYSTROPHY; CILIA; PROTEINS; ABNORMALITIES;
   EXPRESSION; REVEALS; ENCODES; DISEASE; MUTANT; CEP120
AB Background In chicken, loss of TALPID3 results in non-functional cilia and short-rib polydactyly syndrome. This phenotype is caused by a frameshift mutation in the chicken ortholog of the human KIAA0586 gene, which encodes a novel coiled-coil domain protein essential for primary ciliogenesis, suggesting that KIAA0586 can be associated with ciliopathy in human beings.
   Methods In our patients with ciliopathy (http://www.clinicaltrials.gov: NCT00068224), we have collected extensive clinical and neuroimaging data from affected individuals, and performed whole exome sequencing on DNA from affected individuals and their parents. We analysed gene expression on fibroblast cell line, and determined the effect of gene mutation on ciliogenesis in cells derived from patients.
   Results We identified biallelic mutations in the human TALPID3 ortholog, KIAA0586, in six children with findings of overlapping Jeune and Joubert syndromes. Fibroblasts cultured from one of the patients with Jeune-Joubert syndrome exhibited more severe cilia defects than fibroblasts from patients with only Joubert syndrome; this difference was reflected in KIAA0586 RNA expression levels. Rescue of the cilia defect with full-length wild type KIAA0586 indicated a causal link between cilia formation and KIAA0586 function.
   Conclusions Our results show that biallelic deleterious mutations in KIAA0586 lead to Joubert syndrome with or without Jeune asphyxiating thoracic dystrophy. Furthermore, our results confirm that KIAA0586/TALPID3 is essential in cilia formation in human beings, expand the KIAA0586 phenotype to include features of Jeune syndrome and provide a pathogenetic connection between Joubert and Jeune syndromes, based on aberrant ciliogenesis.
C1 [Malicdan, May Christine V.; Toro, Camilo; Gahl, William A.] NIH, Undiagnosed Dis Program, Common Fund, Off Director, Bethesda, MD 20892 USA.
   [Malicdan, May Christine V.; Vilboux, Thierry; Stephen, Joshi; Maglic, Dino; Mian, Luhe; Konzman, Daniel; Guo, Jennifer; Yildirimli, Deniz; Bryant, Joy; Fischer, Roxanne; Gahl, William A.; Gunay-Aygun, Meral] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
   [Vilboux, Thierry; Solomon, Benjamin D.] Inova Translat Med Inst, Div Med Genom, Falls Church, VA USA.
   [Zein, Wadih M.] NEI, Ophthalm Genet & Visual Funct Branch, NIH, Bethesda, MD 20892 USA.
   [Snow, Joseph] NIMH, Off Clin Director, NIH, Bethesda, MD 20892 USA.
   [Vemulapalli, Meghana; Mullikin, James C.; NISC Comparative Sequencing Progra] NHGRI, NISC, NIH, Bethesda, MD 20892 USA.
   [Gahl, William A.; Gunay-Aygun, Meral] NHGRI, Off Clin Director, NIH, Bethesda, MD 20892 USA.
   [Niederhuber, John E.] Inova Translat Med Inst, Inova Hlth Syst, Falls Church, VA USA.
RP Gunay-Aygun, M (reprint author), NHGRI, NIH, 10 Ctr Dr,Bldg 10,Rm 10C103C, Bethesda, MD 20892 USA.
EM mgaygun@mail.nih.gov
FU Intramural Research Programs of National Human Genome Research
   Institute; National Eye Institute; National Institute of Mental Health
   of National Institutes of Health, Bethesda, Maryland, USA
FX This research was supported by the Intramural Research Programs of the
   National Human Genome Research Institute, National Eye Institute and the
   National Institute of Mental Health of the National Institutes of
   Health, Bethesda, Maryland, USA. We also thank the patients and their
   families for participating in this study.
NR 30
TC 6
Z9 6
U1 3
U2 6
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 DEC
PY 2015
VL 52
IS 12
BP 830
EP 839
DI 10.1136/jmedgenet-2015-103316
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA CZ2YF
UT WOS:000366970000006
PM 26386044
ER

PT J
AU Hoque, MT
   Shah, A
   More, V
   Miller, DS
   Bendayan, R
AF Hoque, Md. Tozammel
   Shah, Arpit
   More, Vijay
   Miller, David S.
   Bendayan, Reina
TI In vivo and ex vivo regulation of breast cancer resistant protein (Bcrp)
   by peroxisome proliferator-activated receptor alpha (Ppar alpha) at the
   blood-brain barrier
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Article
DE Blood-brain barrier; brain capillaries; breast cancer resistant protein;
   nuclear receptors; peroxisome proliferator-activated receptor alpha;
   regulation of drug transport
ID XENOBIOTIC EFFLUX TRANSPORTERS; MICROVESSEL ENDOTHELIAL-CELLS;
   ARYL-HYDROCARBON RECEPTOR; MEDIATED UP-REGULATION; P-GLYCOPROTEIN;
   NUCLEAR RECEPTORS; ABC TRANSPORTERS; RODENT BRAIN; EXPRESSION;
   LOCALIZATION
AB Breast cancer resistance protein (Bcrp/Abcg2) localized at the blood-brain barrier (BBB) limits permeability into the brain of many xenobiotics, including pharmacological agents. Peroxisome proliferator-activated receptor alpha (Ppar alpha), a ligand-activated transcription factor, primarily involved in lipid metabolism, has been shown to regulate the functional expression of Bcrp in human cerebral microvascular endothelial cells (hCMEC/D3). The aim of this study was to investigate ex vivo and in vivo, the regulation of Bcrp by Ppar alpha in an intact BBB. Ex vivo quantitative real-time PCR and immunoblot analyses showed significant up-regulation of Abcg2/Bcrp mRNA and protein levels in CD-1 mouse brain capillaries incubated with clofibrate, alpha Ppar alpha ligand. Fluorescence-based transport assays in CD-1 and C57BL/6 brain capillaries showed that exposure to clofibrate significantly increased Bcrp transport activity. This increase was not observed in capillaries isolated from Ppar alpha knockout mice. In vivo, we found: i) significant Bcrp protein up-regulation in clofibrate-dosed CD-1 and C57BL/6 capillary lysates, but no effect in Ppar alpha knockout capillary lysates, and ii) significantly increased Bcrp transport activity in capillaries isolated from clofibrate-treated mice. These results demonstrate an increase in Bcrp functional expression by Ppar alpha in brain capillaries, and suggest that Ppar alpha is another nuclear receptor that can contribute to the regulation of membrane efflux transporters and drug permeability at the BBB.
C1 [Hoque, Md. Tozammel; Shah, Arpit; Bendayan, Reina] Univ Toronto, Dept Pharmaceut Sci, Leslie Dan Fac Pharm, Toronto, ON, Canada.
   [More, Vijay; Miller, David S.] NIEHS, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA.
RP Bendayan, R (reprint author), Univ Toronto, Dept Pharmaceut Sci, Leslie Dan Fac Pharm, Toronto, ON, Canada.
EM r.bendayan@utoronto.ca
FU Canadian Institutes of Health Research (CIHR) [MOP56976]; Ontario HIV
   Treatment Network (OHTN) Career Scientist award; CIHR Strategic Training
   Program in Biological Therapeutics; Intramural Research Program of the
   National Institute of Environmental Health Sciences, National Institutes
   of Health
FX This research is supported by a grant from the Canadian Institutes of
   Health Research (CIHR, Grant No. MOP56976) awarded to Dr Reina Bendayan.
   Dr Bendayan is the recipient of the Ontario HIV Treatment Network (OHTN)
   Career Scientist award. Arpit Shah is the recipient of a graduate
   scholarship from the CIHR Strategic Training Program in Biological
   Therapeutics. Supported by the Intramural Research Program of the
   National Institute of Environmental Health Sciences, National Institutes
   of Health.
NR 47
TC 2
Z9 2
U1 3
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3042
EI 1471-4159
J9 J NEUROCHEM
JI J. Neurochem.
PD DEC
PY 2015
VL 135
IS 6
BP 1113
EP 1122
DI 10.1111/jnc.13389
PG 10
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA CZ6DT
UT WOS:000367192100006
PM 26465636
ER

PT J
AU Li, YZ
   Bader, M
   Tamargo, I
   Rubovitch, V
   Tweedie, D
   Pick, CG
   Greig, NH
AF Li, Yazhou
   Bader, Miaad
   Tamargo, Ian
   Rubovitch, Vardit
   Tweedie, David
   Pick, Chaim G.
   Greig, Nigel H.
TI Liraglutide is neurotrophic and neuroprotective in neuronal cultures and
   mitigates mild traumatic brain injury in mice
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Article
DE apoptosis; cAMP-response element binding protein; glucagon-like
   peptide-1; liraglutide; neuroprotection; traumatic brain injury
ID GLUCAGON-LIKE PEPTIDE-1; REVERSES BEHAVIORAL IMPAIRMENTS;
   ALZHEIMERS-DISEASE; NEURODEGENERATIVE DISORDERS; PARKINSONS-DISEASE;
   COGNITIVE DEFICITS; GENE-EXPRESSION; ANIMAL-MODEL; HEAD-INJURY;
   BETA-CELLS
AB Traumatic brain injury (TBI), a brain dysfunction for which there is no present effective treatment, is often caused by a concussive impact to the head and affects an estimated 1.7 million Americans annually. Our laboratory previously demonstrated that exendin-4, a long-lasting glucagon-like peptide 1 receptor (GLP-1R) agonist, has neuroprotective effects in cellular and animal models of TBI. Here, we demonstrate neurotrophic and neuroprotective effects of a different GLP-1R agonist, liraglutide, in neuronal cultures and a mouse model of mild TBI (mTBI). Liraglutide promoted dose-dependent proliferation in SH-SY5Y cells and in a GLP-1R over-expressing cell line at reduced concentrations. Pre-treatment with liraglutide rescued neuronal cells from oxidative stress-and glutamate excitotoxicity-induced cell death. Liraglutide produced neurotrophic and neuroprotective effects similar to those of exendin-4 in vitro. The cAMP/PKA/pCREB pathway appears to play an important role in this neuroprotective activity of liraglutide. Furthermore, our findings in cell culture were well-translated in a weight drop mTBI mouse model. Post-treatment with a clinically relevant dose of liraglutide for 7 days in mice ameliorated memory impairments caused by mTBI when evaluated 7 and 30 days post trauma. These data cross-validate former studies of exendin-4 and suggest that liraglutide holds therapeutic potential for the treatment of mTBI.
C1 [Li, Yazhou; Tamargo, Ian; Tweedie, David; Greig, Nigel H.] NIA, Translat Gerontol Branch, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
   [Bader, Miaad; Rubovitch, Vardit; Pick, Chaim G.] Tel Aviv Univ, Sackler Fac Med, Dept Anat & Anthropol, IL-69978 Tel Aviv, Israel.
   [Pick, Chaim G.] Tel Aviv Univ, Sagol Sch Neurosci, IL-69978 Tel Aviv, Israel.
RP Li, YZ (reprint author), Biomed Res Ctr, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM liyaz@mail.nih.gov; greign@mail.nih.gov
FU Intramural Research Program of the National Institute on Aging, National
   Institutes of Health; Ari and Regine Aprijaskis Fund at Tel-Aviv
   University; Israel Science Foundation [108/09]
FX This research was supported in part by (i) the Intramural Research
   Program of the National Institute on Aging, National Institutes of
   Health, (ii) the Ari and Regine Aprijaskis Fund at Tel-Aviv University,
   and (iii) a grant from the Israel Science Foundation, grant number
   108/09. No competing financial interests exist.
NR 82
TC 13
Z9 13
U1 4
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3042
EI 1471-4159
J9 J NEUROCHEM
JI J. Neurochem.
PD DEC
PY 2015
VL 135
IS 6
BP 1203
EP 1217
DI 10.1111/jnc.13169
PG 15
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA CZ6DT
UT WOS:000367192100014
PM 25982185
ER

PT J
AU Civiero, L
   Cirnaru, MD
   Beilina, A
   Rodella, U
   Russo, I
   Belluzzi, E
   Lobbestael, E
   Reyniers, L
   Hondhamuni, G
   Lewis, PA
   Van den Haute, C
   Baekelandt, V
   Bandopadhyay, R
   Bubacco, L
   Piccoli, G
   Cookson, MR
   Taymans, JM
   Greggio, E
AF Civiero, Laura
   Cirnaru, Maria Daniela
   Beilina, Alexandra
   Rodella, Umberto
   Russo, Isabella
   Belluzzi, Elisa
   Lobbestael, Evy
   Reyniers, Lauran
   Hondhamuni, Geshanthi
   Lewis, Patrick A.
   Van den Haute, Chris
   Baekelandt, Veerle
   Bandopadhyay, Rina
   Bubacco, Luigi
   Piccoli, Giovanni
   Cookson, Mark R.
   Taymans, Jean-Marc
   Greggio, Elisa
TI Leucine-rich repeat kinase 2 interacts with p21-activated kinase 6 to
   control neurite complexity in mammalian brain
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Article
DE LRRK2; neurodegeneration; neuronal cytoskeleton; p21-activated kinases;
   Parkinson's disease
ID PARKINSONS-DISEASE; CYTOPLASMIC LOCALIZATION; DOPAMINERGIC-NEURONS;
   ACTIN CYTOSKELETON; 14-3-3 BINDING; LRRK2 CONTROLS; GTP-BINDING;
   MOUSE-BRAIN; PHOSPHORYLATION; INHIBITION
AB Leucine-rich repeat kinase 2 (LRRK2) is a causative gene for Parkinson's disease, but the physiological function and the mechanism(s) by which the cellular activity of LRRK2 is regulated are poorly understood. Here, we identified p21-activated kinase 6 (PAK6) as a novel interactor of the GTPase/ROC domain of LRRK2. p21-activated kinases are serine-threonine kinases that serve as targets for the small GTP binding proteins Cdc42 and Rac1 and have been implicated in different morphogenetic processes through remodeling of the actin cytoskeleton such as synapse formation and neuritogenesis. Using an in vivo neuromorphology assay, we show that PAK6 is a positive regulator of neurite outgrowth and that LRRK2 is required for this function. Analyses of post-mortem brain tissue from idiopathic and LRRK2 G2019S carriers reveal an increase in PAK6 activation state, whereas knock-out LRRK2mice display reduced PAK6 activation and phosphorylation of PAK6 substrates. Taken together, these results support a critical role of LRRK2 GTPase domain in cytoskeletal dynamics in vivo through the novel interactor PAK6, and provide a valuable platform to unravel the mechanism underlying LRRK2-mediated pathophysiology.
C1 [Civiero, Laura; Rodella, Umberto; Russo, Isabella; Belluzzi, Elisa; Bubacco, Luigi; Greggio, Elisa] Univ Padua, Dept Biol, I-35131 Padua, Italy.
   [Cirnaru, Maria Daniela; Piccoli, Giovanni] Univ Vita Salute San Raffaele, Milan, Italy.
   [Beilina, Alexandra; Cookson, Mark R.] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
   [Rodella, Umberto; Lobbestael, Evy; Reyniers, Lauran; Van den Haute, Chris; Baekelandt, Veerle; Taymans, Jean-Marc] Katholieke Univ Leuven, Lab Neurobiol & Gene Therapy, Leuven, Belgium.
   [Hondhamuni, Geshanthi; Bandopadhyay, Rina] UCL, Dept Mol Neurosci, Reta Lila Weston Inst Neurol Studies, Inst Neurol, London, England.
   [Lewis, Patrick A.] Univ Reading, Sch Pharm, Reading, Berks, England.
   [Lewis, Patrick A.] UCL, Inst Neurol, Dept Mol Neurosci, London, England.
   [Van den Haute, Chris] Katholieke Univ Leuven, Leuven Viral Vector Core, Leuven, Belgium.
RP Greggio, E (reprint author), Univ Padua, Dept Biol, I-35131 Padua, Italy.
EM cookson@mail.nih.gov; jean-marc.taymans@inserm.fr;
   elisa.greggio@unipd.it
RI Bandopadhyay, Rina /C-7926-2009; 
OI Russo, Isabella/0000-0002-6151-2451; Lewis, Patrick/0000-0003-4537-0489;
   Belluzzi, Elisa/0000-0003-1129-2574; Bubacco, Luigi/0000-0001-7927-9208
FU Michael J Fox Foundation; Telethon - Italy [GGP12237]; CARIPLO
   Foundation [2011-0540]; EMBO fellowship [MBO ASTF 526-2012];
   FWO-Vlaanderen [G.0666.09, KAN2012 1.5.216.12]; IWT [SBO/80020,
   SBO/100042]; Fund Druwe-Eerdekens; Intramural Research Program of the
   NIH, National Institute on Aging; MRC [MR/L010933/1]; Parkinson's UK
   [F1002]; Wellcome Trust/MRC Joint Call in Neurodegeneration award
   [WT089698]; University of Sheffield; MRC Protein Phosphorylation Unit at
   the University of Dundee
FX We are grateful to the Michael J Fox Foundation for supporting this
   study. We also thank the financial support of Telethon - Italy (Grant
   no. GGP12237) and the CARIPLO Foundation (grant 2011-0540). LC was
   supported by a short-term EMBO fellowship (MBO ASTF 526-2012/Award). We
   thank the FWO-Vlaanderen (FWO projects G.0666.09, KAN2012 1.5.216.12 and
   fellowship to JMT), the IWT SBO/80020 and SBO/100042 projects and the
   Fund Druwe-Eerdekens managed by the King Baudouin Foundation for their
   support. This research was supported in part by the Intramural Research
   Program of the NIH, National Institute on Aging. This project is
   supported by an MRC grant to PAL (MR/L010933/1). PAL is a Parkinson's UK
   research fellow (grant F1002). This work was supported in part by the
   Wellcome Trust/MRC Joint Call in Neurodegeneration award (WT089698) to
   the UK Parkinson's Disease Consortium (UKPDC) whose members are from the
   UCL Institute of Neurology, the University of Sheffield and the MRC
   Protein Phosphorylation Unit at the University of Dundee. We thank
   Professor Johan Hofkens and Charlotte David (Molecular Imaging and
   Photonics, KU Leuven) for the use of the confocal laser scanning
   microscope. We also acknowledge the technical assistance of Fangye Gao
   and Caroline Van Heijningen and the Leuven Viral Vector Core
   (http://www.kuleuven.be/molmed/lvvc/vectorproduction.html) for the
   production of LV and AAV vectors. We gratefully thank Dr. Heather
   Melrose for providing LRRK2 knock-out mice. The authors have no conflict
   of interest to declare.
NR 75
TC 5
Z9 5
U1 2
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3042
EI 1471-4159
J9 J NEUROCHEM
JI J. Neurochem.
PD DEC
PY 2015
VL 135
IS 6
BP 1242
EP 1256
DI 10.1111/jnc.13369
PG 15
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA CZ6DT
UT WOS:000367192100017
PM 26375402
ER

PT J
AU Tempero, M
AF Tempero, Margaret
TI Paying Less for High-Value Care-Are You Kidding Me?
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Editorial Material
C1 [Tempero, Margaret] UCSF, Med, San Francisco, CA 94143 USA.
   [Tempero, Margaret] UCSF, Pancreas Ctr, San Francisco, CA USA.
   [Tempero, Margaret] NCI, Clin Oncol Study Sect, Bethesda, MD 20892 USA.
   [Tempero, Margaret] Mayo Clin, Pancreas SPOREs, Rochester, MN USA.
   [Tempero, Margaret] UAB Minnesota, Minneapolis, MN USA.
   [Tempero, Margaret] Univ Arizona, GI SPORE, Tucson, AZ 85721 USA.
   [Tempero, Margaret] Lustgarten Fdn, Bethpage, NY USA.
   [Tempero, Margaret] V Fdn, Cary, NY USA.
   [Tempero, Margaret] Alberta Canada Canc Board, Edmonton, AB, Canada.
   [Tempero, Margaret] UNMC, Eppley Canc Ctr, Omaha, NE USA.
   [Tempero, Margaret] UCSF, Div Med Oncol, San Francisco, CA USA.
   [Tempero, Margaret] UCSF, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA USA.
RP Tempero, M (reprint author), UCSF, Med, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU HARBORSIDE PRESS
PI COLD SPRING HARBOR
PA 37 MAIN ST, COLD SPRING HARBOR, NY 11724 USA
SN 1540-1405
EI 1540-1413
J9 J NATL COMPR CANC NE
JI J. Natl. Compr. Cancer Netw.
PD DEC
PY 2015
VL 13
IS 12
BP 1453
EP 1453
PG 1
WC Oncology
SC Oncology
GA CZ3RG
UT WOS:000367021100001
PM 26656513
ER

PT J
AU Hoa, M
   Friedman, RA
   Fisher, LM
   Derebery, MJ
AF Hoa, Michael
   Friedman, Rick A.
   Fisher, Laurel M.
   Derebery, M. Jennifer
TI Prognostic Implications of and Audiometric Evidence for Hearing
   Fluctuation in Meniere's Disease
SO LARYNGOSCOPE
LA English
DT Article
DE Meniere's disease; hearing loss; hearing fluctuation; efficacy;
   treatment; clinical trial
ID ENDOLYMPHATIC SAC DRAINAGE; TERM-FOLLOW-UP; HYDROPS; STEROIDS; ATTACKS;
   THRESHOLDS; MANAGEMENT
AB Objectives/Hypothesis: 1) To establish criteria for significant hearing fluctuation by assessing the range and occurrence of hearing fluctuations over the course of Meniere's disease; 2) to determine if audiometric evidence exists to support the notion that Meniere's disease is a pathophysiologic process involving the whole cochlea; and 3) to suggest prognostic implications for initial hearing fluctuation in patients with Meniere's disease.
   Study Design: Retrospective case series review.
   Methods: A total of 488 patients diagnosed by 1995 American Academy of Otolaryngology-Head and Neck Surgery Meniere's disease criteria for whom audiometric data were prospectively collected (2 cohorts: 341 and 146 patients initially seen between April 2002 to July 2003 and between January to December 2010, respectively). Based on several definitions for significant hearing fluctuation, change in hearing was categorized as "same," "worse," or "better" between any two consecutive evaluations. The relationship of initial hearing fluctuation to future hearing fluctuation and future hearing loss was evaluated.
   Results: Hearing fluctuation was evident in Meniere's disease patients with heterogeneous audiometric follow-up; and the characteristics of these hearing fluctuations, including the mean incidence, is described. Audiometric data suggests that there is a high congruence in Meniere's disease between changes in low-and high-frequency thresholds. Initial hearing fluctuation is associated with the occurrence of future and more frequent hearing fluctuations.
   Conclusion: Understanding the range of hearing fluctuations establishes a basis for determining audiometric thresholds used in evaluating future therapeutic trials aimed at the prevention of hearing loss in Meniere's disease. This knowledge will also inform the counseling directed toward patients diagnosed with Meniere's disease.
C1 [Hoa, Michael] Georgetown Univ, Dept Otolaryngol Head & Neck Surg, Med Ctr, Washington, DC 20007 USA.
   [Hoa, Michael] NIDCD, NIH, Otolaryngol Surgeon Sci Dev Program, Bethesda, MD USA.
   [Friedman, Rick A.; Fisher, Laurel M.] Univ So Calif, Dept Otolaryngol, Keck Sch Med, Los Angeles, CA USA.
   [Derebery, M. Jennifer] House Clin, Los Angeles, CA USA.
RP Hoa, M (reprint author), Georgetown Univ, Dept Otolaryngol Head & Neck Surg, Med Ctr, 3800 Reservoir Rd,NW,Gorman Bldg,1st Fl, Washington, DC 20007 USA.
EM michael.hoa@nih.gov
NR 24
TC 2
Z9 3
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0023-852X
EI 1531-4995
J9 LARYNGOSCOPE
JI Laryngoscope
PD DEC
PY 2015
VL 125
SU 12
BP S1
EP S12
DI 10.1002/lary.25579
PG 12
WC Medicine, Research & Experimental; Otorhinolaryngology
SC Research & Experimental Medicine; Otorhinolaryngology
GA CZ6CK
UT WOS:000367188500001
PM 26343803
ER

PT J
AU Panda, D
   Cherry, S
AF Panda, Debasis
   Cherry, Sara
TI A genome-wide RNAi screening method to discover novel genes involved in
   virus infection
SO METHODS
LA English
DT Article
DE siRNA screening protocol; Image-based screening; Virus-host
   interactions; Arrayed screen; High-content screening
ID WEST-NILE-VIRUS; HOST FACTORS; FALSE DISCOVERY; HIT SELECTION; DENGUE
   VIRUS; REPLICATION; REVEALS; ENTRY
AB Systematic and comprehensive analysis of host cell proteins involved in virus infection has been difficult in large part due to the lack of robust unbiased methods for their identification. Recent technological breakthroughs allowing development of cell-based genetic screens have greatly facilitated our understanding of virus-host interactions. These include instrumentation for processing in microtiter plates (e.g., 384 well), coupled with sensitive readers and off-the-shelf analysis and informatics pipelines. Because viruses are a significant threat to human health, a better understanding of the cellular factors that impact infection would pave the way for the development of new therapeutics. Here we describe the development and implementation of a genome-wide siRNA screen against a virus using human cells. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Panda, Debasis] NIAID, NIH, Viral Dis Lab, Bethesda, MD 20892 USA.
   [Cherry, Sara] Univ Penn, Dept Microbiol, Philadelphia, PA 19104 USA.
RP Panda, D (reprint author), Bldg 33,Room 1E13,33 North Dr, Bethesda, MD 20892 USA.
EM debasis.panda@nih.gov; cherrys@mail.med.upenn.edu
FU National Institute of Health [R01AI074951, U54AI057168, R21AI103441,
   R01AI095500]; Burroughs Wellcome Investigators in the Pathogenesis of
   Infectious Disease Award
FX This work was supported by National Institute of Health Grants
   R01AI074951, U54AI057168, R21AI103441 and R01AI095500 to SC. SC is a
   recipient of the Burroughs Wellcome Investigators in the Pathogenesis of
   Infectious Disease Award.
NR 21
TC 2
Z9 2
U1 1
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1046-2023
EI 1095-9130
J9 METHODS
JI Methods
PD DEC
PY 2015
VL 91
BP 75
EP 81
DI 10.1016/j.ymeth.2015.07.002
PG 7
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CZ0GM
UT WOS:000366783100010
PM 26164699
ER

PT J
AU Taruscio, D
   Groft, SC
   Cederroth, H
   Melegh, B
   Lasko, P
   Kosaki, K
   Baynam, G
   McCray, A
   Gahl, WA
AF Taruscio, Domenica
   Groft, Stephen C.
   Cederroth, Helene
   Melegh, Bela
   Lasko, Paul
   Kosaki, Kenjiro
   Baynam, Gareth
   McCray, Alexa
   Gahl, William A.
TI Undiagnosed Diseases Network International (UDNI): White paper for
   global actions to meet patient needs
SO MOLECULAR GENETICS AND METABOLISM
LA English
DT Editorial Material
DE Undiagnosed; Global health; Rare diseases; Omics; Ontology; Diagnosis
ID PROGRAM
AB In 2008, the National Institutes of Health's (NIH) Undiagnosed Disease Program (UDP) was initiated to provide diagnoses for individuals who had long sought one without success. As a result of two international conferences (Rome 2014 and Budapest 2015), the Undiagnosed Diseases Network International (UDNI) was established, modeled in part after the NIH UDP. Undiagnosed diseases are a global health issue, calling for an international scientific and healthcare effort. To meet this demand, the UDNI has built a consensus framework of principles, best practices and governance; the Board of Directors reflects its international character, as it includes experts from Australia, Canada, Hungary, Italy, Japan and the USA. The UDNI involves centers with internationally recognized expertise, and its scientific resources and know-how aim to fill the knowledge gaps that impede diagnosis. Consequently, the UDNI fosters the translation of research into medical practice. Active patient involvement is critical; the Patient Advisory Group is expected to play an increasing role in UDNI activities. All information for physicians and patients will be available at the UDNI website. (C) 2015 Published by Elsevier Inc.
C1 [Taruscio, Domenica] Ist Super Sanita, Natl Ctr Rare Dis, I-00161 Rome, Italy.
   [Groft, Stephen C.] NIH, Natl Ctr Adv Translat Sci, Bethesda, MD USA.
   [Cederroth, Helene] Wilhelm Fdn, Brottby, Sweden.
   [Melegh, Bela] Univ Pecs, Dept Med Genet, Pecs, Hungary.
   [Lasko, Paul] McGill Univ, Dept Biol, Montreal, PQ H3A 1B1, Canada.
   [Kosaki, Kenjiro] Keio Univ, Sch Med, Ctr Med Genet, Tokyo, Japan.
   [Baynam, Gareth] Princess Margaret Hosp, Perth, WA, Australia.
   [Baynam, Gareth] King Edward Mem Hosp, Perth, WA, Australia.
   [Baynam, Gareth] WA Dept Hlth, Publ Hlth Div, Off Populat Hlth, Melbourne, Vic, Australia.
   [Baynam, Gareth] Telethon Kids Inst, Perth, WA, Australia.
   [Baynam, Gareth] Western Australian Registry Dev Anomalies, Perth, WA, Australia.
   [Baynam, Gareth] Univ Western Australia, Sch Paediat & Child Hlth, Perth, WA 6009, Australia.
   [Baynam, Gareth] Murdoch Univ, Inst Immunol & Infect Dis, Perth, WA, Australia.
   [McCray, Alexa] Harvard Univ, Sch Med, Dept Med, Ctr Biomed Informat, Boston, MA USA.
   [Gahl, William A.] NHGRI, NIH Undiagnosed Dis Program, NIH, Bethesda, MD USA.
RP Taruscio, D (reprint author), Ist Super Sanita, Natl Ctr Rare Dis, Viale Regina Elena 299, I-00161 Rome, Italy.
EM domenica.taruscio@iss.it
NR 7
TC 10
Z9 10
U1 1
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1096-7192
EI 1096-7206
J9 MOL GENET METAB
JI Mol. Genet. Metab.
PD DEC
PY 2015
VL 116
IS 4
BP 223
EP 225
DI 10.1016/j.ymgme.2015.11.003
PG 3
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
   Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
   Medicine
GA CZ7KH
UT WOS:000367277800001
PM 26596705
ER

PT J
AU Tekola-Ayele, F
   Doumatey, AP
   Shriner, D
   Bentley, AR
   Chen, GJ
   Zhou, J
   Fasanmade, O
   Johnson, T
   Oli, J
   Okafor, G
   Eghan, BA
   Agyenim-Boateng, K
   Adebamowo, C
   Amoah, A
   Acheampong, J
   Adeyemo, A
   Rotimi, CN
AF Tekola-Ayele, Fasil
   Doumatey, Ayo P.
   Shriner, Daniel
   Bentley, Amy R.
   Chen, Guanjie
   Zhou, Jie
   Fasanmade, Olufemi
   Johnson, Thomas
   Oli, Johnnie
   Okafor, Godfrey
   Eghan, Benjami A., Jr.
   Agyenim-Boateng, Kofi
   Adebamowo, Clement
   Amoah, Albert
   Acheampong, Joseph
   Adeyemo, Adebowale
   Rotimi, Charles N.
TI Genome-wide association study identifies African-ancestry specific
   variants for metabolic syndrome
SO MOLECULAR GENETICS AND METABOLISM
LA English
DT Article
DE Metabolic syndrome; Pleiotropy; Genome-wide association study; African
   ancestry
ID CARBONIC-ANHYDRASE INHIBITORS; ENDOPLASMIC-RETICULUM STRESS; ACTIVATED
   RECEPTOR-GAMMA; ALPHA-T-CATENIN; TRANSCRIPTION FACTORS;
   INSULIN-RESISTANCE; DIABETES-MELLITUS; ADIPOCYTE DIFFERENTIATION;
   SUSCEPTIBILITY GENES; QUANTITATIVE TRAITS
AB The metabolic syndrome (MetS) is a constellation of metabolic disorders that increase the risk of developing several diseases including type 2 diabetes and cardiovascular diseases. Although genome-wide association studies (GWAS) have successfully identified variants associated with individual traits comprising MetS, the genetic basis and pathophysiological mechanisms underlying the clustering of these traits remain unclear. We conducted GWAS of MetS in 1427 Africans from Ghana and Nigeria followed by replication testing and meta-analysis in another continental African sample from Kenya. Further replication testing was performed in an African American sample from the Atherosclerosis Risk in Communities (ARIC) study. We found two African-ancestry specific variants that were significantly associated with MetS: SNP rs73989312[A] near CA10 that conferred increased risk (P = 3.86 x 10(-8), OR = 6.80) and SNP rs77244975[C] in CTNNA3 that conferred protection against MetS (P = 1.63 x 10(-8), OR = 0.15). Given the exclusive expression of CA10 in the brain, our CA10 finding strengthens previously reported link between brain function and MetS. We also identified two variants that are not African specific: rs76822696[A] near RALYL associated with increased MetS risk (P = 7.37 x 10(-9), OR = 1.59) and rs7964157[T] near KSR2 associated with reduced MetS risk (P = 4.52 x 10(-8), P-meta = 7.82 x 10(-9), OR = 0.53). The KSR2 locus displayed pleiotropic associations with triglyceride and measures of blood pressure. Rare KSR2 mutations have been reported to be associated with early onset obesity and insulin resistance. Finally, we replicated the LPL and CETP loci previously found to be associated with MetS in Europeans. These findings provide novel insights into the genetics of MetS in Africans and demonstrate the utility of conducting trans-ethnic disease gene mapping studies for testing the cosmopolitan significance of GWAS signals of cardio-metabolic traits. Published by Elsevier Inc.
C1 [Tekola-Ayele, Fasil; Doumatey, Ayo P.; Shriner, Daniel; Bentley, Amy R.; Chen, Guanjie; Zhou, Jie; Adeyemo, Adebowale; Rotimi, Charles N.] NHGRI, Ctr Res Genom & Global Hlth, NIH, Bethesda, MD 20892 USA.
   [Fasanmade, Olufemi; Johnson, Thomas] Univ Lagos, Lagos, Nigeria.
   [Oli, Johnnie; Okafor, Godfrey] Univ Nigeria, Teaching Hosp, Enugu, Nigeria.
   [Eghan, Benjami A., Jr.; Agyenim-Boateng, Kofi; Acheampong, Joseph] Univ Sci & Technol, Dept Med, Kumasi, Ghana.
   [Adebamowo, Clement] Univ Maryland, Sch Med, Dept Epidemiol & Publ Hlth, Baltimore, MD 21201 USA.
   [Amoah, Albert] Univ Ghana, Sch Med, Dept Med, Accra, Ghana.
RP Tekola-Ayele, F (reprint author), NHGRI, Ctr Res Genom & Global Hlth, NIH, Bldg 12A,Room 4047,12 South Dr, Bethesda, MD 20892 USA.
EM ayeleft@mail.nih.gov; rotimic@mail.nih.gov
OI Adeyemo, Adebowale/0000-0002-3105-3231; Tekola-Ayele,
   Fasil/0000-0003-4194-9370
FU Intramural Research Program of National Institutes of Health in Center
   for Research on Genomics and Global Health (CRGGH); National Human
   Genome Research Institute; National Institute of Diabetes and Digestive
   and Kidney Diseases; Center for Information Technology; Office of the
   Director at National Institutes of Health [1ZIAHG200362]; NIH from
   Office of Research on Minority Health [3T37TW00041-03S2]; National
   Center for Research Resources; National Heart, Lung, and Blood Institute
   [HHSN268201100005C, HHSN268201100006C, HHSN268201100007C,
   HHSN268201100008C, HHSN268201100009C, HHSN268201100010C,
   HHSN268201100011C, HHSN268201100012C]; Human Genome Research Institute
   grant [U01HG004402]
FX This work was supported in part by the Intramural Research Program of
   the National Institutes of Health in the Center for Research on Genomics
   and Global Health (CRGGH). The CRGGH is supported by the National Human
   Genome Research Institute, the National Institute of Diabetes and
   Digestive and Kidney Diseases, the Center for Information Technology,
   and the Office of the Director at the National Institutes of Health
   (1ZIAHG200362). Support for participant recruitment and initial genetic
   studies of the AADM study was provided by NIH grant No. 3T37TW00041-03S2
   from the Office of Research on Minority Health. The project was also
   supported in part by the National Center for Research Resources. The
   Atherosclerosis Risk in Communities (ARIC) Study is carried out as a
   collaborative study supported by National Heart, Lung, and Blood
   Institute contracts (HHSN268201100005C, HHSN268201100006C,
   HHSN268201100007C, HHSN268201100008C, HHSN268201100009C,
   HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C). The
   authors thank the staff and participants of the ARIC study for their
   important contributions. Funding for ARIC Gene Environment Association
   Studies (GENEVA) was provided by National Human Genome Research
   Institute grant U01HG004402 (E. Boerwinkle).
NR 87
TC 2
Z9 2
U1 0
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1096-7192
EI 1096-7206
J9 MOL GENET METAB
JI Mol. Genet. Metab.
PD DEC
PY 2015
VL 116
IS 4
BP 305
EP 313
DI 10.1016/j.ymgme.2015.10.008
PG 9
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
   Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
   Medicine
GA CZ7KH
UT WOS:000367277800012
PM 26507551
ER

PT J
AU Rizvi, SM
   Salam, N
   Geng, J
   Qi, Y
   Bream, JH
   Duggal, P
   Hussain, SK
   Martinson, J
   Wolinsky, S
   Carrington, M
   Raghavan, M
AF Rizvi, Syed Monem
   Salam, Nasir
   Geng, Jie
   Qi, Ying
   Bream, Jay H.
   Duggal, Priya
   Hussain, Shehnaz K.
   Martinson, Jeremy
   Wolinsky, Steven
   Carrington, Mary
   Raghavan, Malini
TI Distinct assembly profiles of HLA-B molecules
SO MOLECULAR IMMUNOLOGY
LA English
DT Meeting Abstract
CT 8th International Workshop on Antigen Processing and Presentation
CY JUN 10-13, 2014
CL Philadelphia, PA
C1 [Rizvi, Syed Monem; Salam, Nasir; Geng, Jie; Raghavan, Malini] Univ Michigan, Sch Med, Dept Microbiol & Immunol, Ann Arbor, MI 48109 USA.
   [Qi, Ying; Carrington, Mary] SAIC Frederick Inc, Canc & Inflammat Program, Expt Immunol Lab, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
   [Qi, Ying; Carrington, Mary] Ragon Inst MGH MIT & Harvard, Cambridge, MA 02139 USA.
   [Bream, Jay H.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Mol Microbiol & Immunol, Baltimore, MD 21205 USA.
   [Duggal, Priya] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA.
   [Hussain, Shehnaz K.] Univ Calif Los Angeles, Fielding Sch Publ Hlth, Dept Epidemiol, Los Angeles, CA 90095 USA.
   [Hussain, Shehnaz K.] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90095 USA.
   [Martinson, Jeremy] Univ Pittsburgh, Med Ctr, Sch Med, Dept Pathol, Pittsburgh, PA 15261 USA.
   [Wolinsky, Steven] Northwestern Univ, Feinberg Sch Med, Div Infect Dis, Chicago, IL 60611 USA.
EM malinir@umich.edu
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD DEC
PY 2015
VL 68
IS 2
BP 136
EP 136
PN A
PG 1
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA CZ0AO
UT WOS:000366767700028
ER

PT J
AU Wei, JJ
   Gibbs, J
   Bennink, JR
   Yewdell, JW
AF Wei, Jiajie
   Gibbs, James
   Bennink, Jack R.
   Yewdell, Jonathan W.
TI Illuminating DRiPs with GFP
SO MOLECULAR IMMUNOLOGY
LA English
DT Meeting Abstract
CT 8th International Workshop on Antigen Processing and Presentation
CY JUN 10-13, 2014
CL Philadelphia, PA
C1 [Wei, Jiajie; Gibbs, James; Bennink, Jack R.; Yewdell, Jonathan W.] Natl Inst Allergy & Infect, Bethesda, MD 20892 USA.
EM jyewdell@nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD DEC
PY 2015
VL 68
IS 2
BP 142
EP 143
PN A
PG 2
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA CZ0AO
UT WOS:000366767700048
ER

PT J
AU Cho, KJ
   Furuta, K
   Walseng, E
   Roche, PA
AF Cho, Kyung-Jin
   Furuta, Kazuyuki
   Walseng, Even
   Roche, Paul A.
TI Ubiquitination by march-I prevents pMHC-II recycling
SO MOLECULAR IMMUNOLOGY
LA English
DT Meeting Abstract
CT 8th International Workshop on Antigen Processing and Presentation
CY JUN 10-13, 2014
CL Philadelphia, PA
C1 [Cho, Kyung-Jin; Furuta, Kazuyuki; Walseng, Even; Roche, Paul A.] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
EM paul.roche@nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD DEC
PY 2015
VL 68
IS 2
BP 149
EP 150
PN A
PG 2
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA CZ0AO
UT WOS:000366767700069
ER

PT J
AU Morozov, GI
   Zhao, HY
   Mage, MG
   Boyd, LF
   Hildebrand, WH
   McMurtrey, C
   Schuck, P
   Natarajan, K
   Margulies, DH
AF Morozov, Giora I.
   Zhao, Huayung
   Mage, Michael G.
   Boyd, Lisa F.
   Hildebrand, William H.
   McMurtrey, Curtis
   Schuck, Peter
   Natarajan, Kannan
   Margulies, David H.
TI Tapasin-related protein TAPBP-R interacts directly with peptide-free
   MHC-I/beta 2-microglobulin complexes and is released by high affinity
   peptides
SO MOLECULAR IMMUNOLOGY
LA English
DT Meeting Abstract
CT 8th International Workshop on Antigen Processing and Presentation
CY JUN 10-13, 2014
CL Philadelphia, PA
C1 [Morozov, Giora I.; Mage, Michael G.; Boyd, Lisa F.; Natarajan, Kannan; Margulies, David H.] NIAID, Mol Biol Sect, Immunol Lab, NIH, Bethesda, MD 20892 USA.
   [Zhao, Huayung; Schuck, Peter] NIBIB, Dynam Macromol Assembly Sect, Lab Cellular Imaging & Macromol Biophys, NIH, Bethesda, MD 20892 USA.
   [Hildebrand, William H.; McMurtrey, Curtis] Univ Oklahoma, Hlth Sci Ctr, Dept Microbiol & Immunol, Oklahoma City, OK 73104 USA.
EM giora.morozov@nih.gov; zhaoh3@mail.nih.gov; mmage@niaid.nih.gov;
   lboyd@niaid.nih.gov; William-Hildebrand@ouhsc.edu;
   Curtis-McMurtrey@ouhsc.edu; schuckp@mail.nih.gov;
   knatarajan@niaid.nih.gov; dhm@nih.gov
NR 0
TC 0
Z9 0
U1 1
U2 5
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD DEC
PY 2015
VL 68
IS 2
BP 149
EP 149
PN A
PG 1
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA CZ0AO
UT WOS:000366767700068
ER

PT J
AU Jung, M
   Dunbar, CE
   Winkler, T
AF Jung, Moonjung
   Dunbar, Cynthia E.
   Winkler, Thomas
TI Modeling Human Bone Marrow Failure Syndromes Using Pluripotent Stem
   Cells and Genome Engineering
SO MOLECULAR THERAPY
LA English
DT Review
ID DIAMOND-BLACKFAN ANEMIA; PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA; FAMILIAL
   PLATELET DISORDER; ACUTE MYELOGENOUS LEUKEMIA; FANCONI-ANEMIA;
   DYSKERATOSIS-CONGENITA; HEMATOPOIETIC PROGENITORS; APLASTIC-ANEMIA;
   MYELODYSPLASTIC SYNDROMES; IPS CELLS
AB The combination of epigenetic reprogramming with advanced genome editing technologies opened a new avenue to study disease mechanisms, particularly of disorders with depleted target tissue. Bone marrow failure syndromes (BMFS) typically present with a marked reduction of peripheral blood cells due to a destroyed or dysfunctional bone marrow compartment. Somatic and germline mutations have been etiologically linked to many cases of BMFS. However, without the ability to study primary patient material, the exact pathogenesis for many entities remained fragmentary. Capturing the pathological genotype in induced pluripotent stem cells (iPSCs) allows studying potential developmental defects leading to a particular phenotype. The lack of hematopoietic stem and progenitor cells in these patients can also be overcome by differentiating patientderived iPSCs into hematopoietic lineages. With fast growing genome editing techniques, such as CRISPR/Cas9, correction of disease-causing mutations in iPSCs or introduction of mutations in cells from healthy individuals enable comparative studies that may identify other genetic or epigenetic events contributing to a specific disease phenotype. In this review, we present recent progresses in disease modeling of inherited and acquired BMFS using reprogramming and genome editing techniques. We also discuss the challenges and potential shortcomings of iPSC-based models for hematological diseases.
C1 [Jung, Moonjung; Dunbar, Cynthia E.; Winkler, Thomas] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Winkler, T (reprint author), NHLBI, Hematol Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM winklert@nhlbi.nih.gov
FU Division of Intramural Research at the National Heart, Lung, and Blood
   Institute
FX The authors were supported by the Division of Intramural Research at the
   National Heart, Lung, and Blood Institute. The authors declare no
   conflict of interest.
NR 118
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U1 4
U2 17
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 DEC
PY 2015
VL 23
IS 12
BP 1832
EP 1842
DI 10.1038/mt.2015.180
PG 11
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine
GA CZ3IH
UT WOS:000366997200007
PM 26435409
ER

PT J
AU Case, LK
   Pineda, J
   Ramachandran, VS
AF Case, Laura K.
   Pineda, Jaime
   Ramachandran, Vilayanur S.
TI Common coding and dynamic interactions between observed, imagined, and
   experienced motor and somatosensory activity
SO NEUROPSYCHOLOGIA
LA English
DT Article
DE Simulation; Mirror neuron system; Sensory referral; Motor referral;
   Somatosensation; Imagery
ID POSITRON-EMISSION-TOMOGRAPHY; MIRROR-TOUCH SYNAESTHESIA; PHANTOM LIMB
   PAIN; TRANSCRANIAL MAGNETIC STIMULATION; MENTAL ROTATION; CORTICOSPINAL
   EXCITABILITY; CORTICAL EXCITABILITY; SENSORIMOTOR CORTEX; EXECUTED
   MOVEMENTS; FUNCTIONAL-ANATOMY
AB Motor imagery and perception - considered generally as forms of motor simulation - share overlapping neural representations with motor production. While much research has focused on the extent of this "common coding," less attention has been paid to how these overlapping representations interact. How do imagined, observed, or produced actions influence one another, and how do we maintain control over our perception and behavior? In the first part of this review we describe interactions between motor production and motor simulation, and explore apparent regulatory mechanisms that balance these processes. Next, we consider the somatosensory system. Numerous studies now support a "sensory mirror system" comprised of neural representations activated by either afferent sensation or vicarious sensation. In the second part of this review we summarize evidence for shared representations of sensation and sensory simulation (including imagery and observed sensation), and suggest that similar interactions and regulation of simulation occur in the somatosensory domain as in the motor domain. We suggest that both motor and somatosensory simulations are flexibly regulated to support simulations congruent with our sensorimotor experience and goals and suppress or separate the influence of those that are not. These regulatory mechanisms are frequently revealed by cases of brain injury but can also be employed to facilitate sensorimotor rehabilitation. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
C1 [Case, Laura K.; Ramachandran, Vilayanur S.] Univ Calif San Diego, Ctr Brain & Cognit, San Diego, CA 92103 USA.
   [Case, Laura K.] NIH, Pain & Integrat Neurosci Branch, Natl Ctr Complementary & Integrat Hlth, Bethesda, MD 20892 USA.
   [Pineda, Jaime] Univ Calif San Diego, Dept Cognit Sci, San Diego, CA 92103 USA.
RP Case, LK (reprint author), NIH, Natl Ctr Complementary & Integrat Hlth, Bldg 10, Bethesda, MD 20892 USA.
EM laura.case@nih.gov
FU University of California, San Diego; National Center for Complementary
   and Integrative Health (NCCIH)
FX The authors thank Pat Church land, Piotr Winkielman, Claire Laubacher,
   and M Catherine Bushnell for assistance and helpful conversations. The
   first author thanks the University of California, San Diego and the
   National Center for Complementary and Integrative Health (NCCIH) for
   support during the preparation of the manuscript. The views presented in
   this paper are solely those of the authors and do not necessarily
   reflect views of NCCIH.
NR 201
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U2 15
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3932
EI 1873-3514
J9 NEUROPSYCHOLOGIA
JI Neuropsychologia
PD DEC
PY 2015
VL 79
SI SI
BP 233
EP 245
DI 10.1016/j.neuropsychologia.2015.04.005
PN B
PG 13
WC Behavioral Sciences; Neurosciences; Psychology, Experimental
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA CZ1QC
UT WOS:000366879400008
PM 25863237
ER

PT J
AU Kim, BC
   Kim, MK
   Han, K
   Lee, SY
   Lee, SH
   Ko, SH
   Kwon, HS
   Merchant, AT
   Yim, HW
   Lee, WC
   Park, YG
   Park, YM
AF Kim, Byung Chul
   Kim, Mee Kyoung
   Han, Kyungdo
   Lee, Sae-Young
   Lee, Seung-Hwan
   Ko, Seung-Hyun
   Kwon, Hyuk-Sang
   Merchant, Anwar T.
   Yim, Hyeon Woo
   Lee, Won-Chul
   Park, Yong Gyu
   Park, Yong-Moon
TI Low muscle mass is associated with metabolic syndrome only in nonobese
   young adults: the Korea National Health and Nutrition Examination Survey
   2008-2010
SO NUTRITION RESEARCH
LA English
DT Article
DE Low muscle mass; Sarcopenia; Metabolic syndrome; Obesity; Young adults;
   Insulin resistance
ID CARDIOVASCULAR-DISEASE RISK; SKELETAL-MUSCLE; SARCOPENIC OBESITY;
   INSULIN-RESISTANCE; POSTMENOPAUSAL WOMEN; BODY-COMPOSITION; MEN;
   STRENGTH; GLUCOSE; TESTOSTERONE
AB Little is known about the relationship between body composition and metabolic risk factors in young adults. We hypothesized that low muscle mass (LMM) is associated with metabolic syndrome (MetS) and its components in young adults and that the associations vary by obesity. A cross-sectional analysis was conducted using the Korea National Health and Nutrition Examination Survey data. In total, 5300 young adults aged 19 to 39 years were evaluated. Low muscle mass was defined as an appendicular skeletal muscle mass/weight less than 1 SD below the mean for each participant's corresponding sex and age group. Obesity was defined as a body mass index greater than or equal to 25 kg/m(2). The prevalence of LMM was higher in obese than nonobese participants (37.6% vs 9.6%). In the nonobese participants, the prevalence of MetS, high waist circumference, high triglycerides, and high blood pressure was significantly greater in the LMM group than in the high muscle mass group. In the nonobese group, compared with high muscle mass participants, those with LMM had odds ratios for MetS of 3.6 (95% confidence interval, 1.48-8.76; P < .001) and 3.6 (95% confidence interval, 1.48-8.71; P < .001) in men and women, respectively, after adjusting for confounding factors. However, no significant association of LMM with MetS or its components was found in obese participants. In conclusion, our results suggest that young adults with LMM may have a high risk of MetS, especially when they are nonobese. Interventions aimed at increasing muscle mass at younger ages may have the potential to reduce MetS. Published by Elsevier Inc.
C1 [Kim, Byung Chul] Catholic Univ Korea, Sch Med, Seoul, South Korea.
   [Kim, Byung Chul] Catholic Univ Korea, Dept Surg, Seoul, South Korea.
   [Kim, Mee Kyoung; Lee, Seung-Hwan; Ko, Seung-Hyun; Kwon, Hyuk-Sang] Catholic Univ Korea, Dept Internal Med, Div Endocrinol & Metab, Seoul, South Korea.
   [Han, Kyungdo; Park, Yong Gyu] Catholic Univ Korea, Dept Biostat, Seoul, South Korea.
   [Lee, Sae-Young] Korea Ctr Dis Control & Prevent, Korea Natl Inst Hlth, Ctr Immunol & Pathol, Div Aids, Osong, Chungbuk, South Korea.
   [Lee, Sae-Young; Yim, Hyeon Woo; Lee, Won-Chul; Park, Yong-Moon] Catholic Univ Korea, Dept Prevent Med, Seoul, South Korea.
   [Merchant, Anwar T.; Park, Yong-Moon] Univ S Carolina, Arnold Sch Publ Hlth, Dept Epidemiol & Biostat, Columbia, SC 29208 USA.
   [Park, Yong-Moon] NIEHS, NIH, Dept Hlth & Human Serv, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
RP Park, YM (reprint author), NIEHS, Epidemiol Branch, 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM mark.park@nih.gov
OI Lee, Seung-Hwan/0000-0002-3964-3877; PARK, YONG-MOON/0000-0002-5879-6879
NR 36
TC 1
Z9 1
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0271-5317
J9 NUTR RES
JI Nutr. Res.
PD DEC
PY 2015
VL 35
IS 12
BP 1070
EP 1078
DI 10.1016/j.nutres.2015.09.020
PG 9
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA CZ1RQ
UT WOS:000366883400005
PM 26602833
ER

PT J
AU Risso, DS
   Howard, L
   VanWaes, C
   Drayna, D
AF Risso, Davide S.
   Howard, Louisa
   VanWaes, Carter
   Drayna, Dennis
TI A potential trigger for pine mouth: a case of a homozygous
   phenylthiocarbamide taster
SO NUTRITION RESEARCH
LA English
DT Article
DE Dysgeusia; Pine nuts; PTC; TAS2R38; Taste disturbance
ID NUTS; SENSITIVITY; DYSGEUSIA; CONSUMERS; MARKERS
AB Pine mouth, also known as pine nut syndrome, is an uncommon dysgeusia that generally begins 12 to 48 hours after consuming pine nuts. It is characterized by a bitter metallic taste, usually amplified by the consumption of other foods, which lasts 2 to 4 weeks. Recent findings have correlated this disorder with the consumption of nuts of the species Pinus armandii, but no potential triggers or common underlying medical causes have been identified in individuals affected by this syndrome. We report a 23-year-old patient affected by pine mouth who also underwent a phenylthiocarbamide taste test and was found to be a taster for this compound. TAS2R38 genotyping demonstrated that this subject was a homozygous carrier of the proline-alanine-valine taster haplotype.
   We, therefore, hypothesize that homozygous phenylthiocarbamide taster status may be a potential contributor for pine mouth events. Although based on a single observation, this research suggests a connection between genetically determined bitter taste perception and the occurrence of pine nut dysgeusia events. Published by Elsevier Inc.
C1 [Risso, Davide S.; Drayna, Dennis] Natl Inst Deafness & Other Commun Disorders, NIH, Bethesda, MD 20892 USA.
   [Risso, Davide S.] Univ Bologna, Dept BiGeA, Lab Mol Anthropol, I-40126 Bologna, Italy.
   [Risso, Davide S.] Univ Bologna, Ctr Genome Biol, I-40126 Bologna, Italy.
   [Howard, Louisa] NIAID, NIH, Bethesda, MD 20892 USA.
   [VanWaes, Carter] Natl Inst Deafness & Other Commun Disorders, NIH, Clin Genom Unit, Bethesda, MD 20892 USA.
   [VanWaes, Carter] Natl Inst Deafness & Other Commun Disorders, NIH, Tumor Biol Sect, Head & Neck Surg Branch, Bethesda, MD 20892 USA.
RP Risso, DS (reprint author), Natl Inst Deafness & Other Commun Disorders, NIH, Bethesda, MD 20892 USA.
EM davide.risso@nih.gov
OI Risso, Davide/0000-0001-9848-8996
FU National Institute on Deafness and Other Communication Disorders
   intramural grant [Z1A-000046-15, ZIA-DC-000075]
FX DR, CVW, and DD were supported by the National Institute on Deafness and
   Other Communication Disorders intramural grant numbers Z1A-000046-15 and
   ZIA-DC-000075.
NR 20
TC 2
Z9 2
U1 3
U2 12
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0271-5317
J9 NUTR RES
JI Nutr. Res.
PD DEC
PY 2015
VL 35
IS 12
BP 1122
EP 1125
DI 10.1016/j.nutres.2015.09.011
PG 4
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA CZ1RQ
UT WOS:000366883400011
PM 26463018
ER

PT J
AU Kumar, S
   Tchounwou, PB
AF Kumar, Sanjay
   Tchounwou, Paul B.
TI Molecular mechanisms of cisplatin cytotoxicity in acute promyelocytic
   leukemia cells
SO ONCOTARGET
LA English
DT Article
DE cisplatin; APL cell line; cell cycle modulation; AP-1 and p53
ID ARSENIC TRIOXIDE; DNA-DAMAGE; MITOCHONDRIAL PATHWAY; INDUCED APOPTOSIS;
   OXIDATIVE STRESS; RESISTANCE; CHEMOTHERAPY; HYPERTHERMIA; EXPRESSION;
   THERAPY
AB Cis-diamminedichloroplatinum (II) (cisplatin) is a widely used anti-tumor drug for the treatment of a broad range of human malignancies with successful therapeutic outcomes for head and neck, ovarian, and testicular cancers. It has been found to inhibit cell cycle progression and to induce oxidative stress and apoptosis in acute promyelocytic leukemia (APL) cells. However, its molecular mechanisms of cytotoxic action are poorly understood. We hypothesized that cisplatin induces cytotoxicity through DNA adduct formation, oxidative stress, transcriptional factors (p53 and AP-1), cell cycle regulation, stress signaling and apoptosis in APL cells. We used the APL cell line as a model, and applied a variety of molecular tools to elucidate the cytotoxic mode of action of cisplatin. We found that cisplatin inhibited cell proliferation by a cytotoxicity, characterized by DNA damage and modulation of oxidative stress. Cisplatin also activated p53 and phosphorylated activator protein (AP-1) component, c-Jun at serine (63, 73) residue simultaneously leading to cell cycle arrest through stimulation of p21 and down regulation of cyclins and cyclin dependent kinases in APL cell lines. It strongly activated the intrinsic pathway of apoptosis through alteration of the mitochondrial membrane potential, release of cytochrome C, and up-regulation of caspase 3 activity. It also down regulated the p38MAPK pathway. Overall, this study highlights the molecular mechanisms that underline cisplatin toxicity to APL cells, and provides insights into selection of novel targets and/or design of therapeutic agents to treat APL.
C1 [Kumar, Sanjay; Tchounwou, Paul B.] Jackson State Univ, Coll Sci Engn & Technol, NIH NIMHD RCMI Ctr Environm Hlth, Cell & Toxicogen Res Lab, Jackson, MS 39217 USA.
RP Tchounwou, PB (reprint author), Jackson State Univ, Coll Sci Engn & Technol, NIH NIMHD RCMI Ctr Environm Hlth, Cell & Toxicogen Res Lab, Jackson, MS 39217 USA.
EM paul.b.tchounwou@jsums.edu
FU National Institutes of Health NIMHD through the RCMI-Center for
   Environmental Health at Jackson State University [G12MD007581]
FX This research was financially supported by National Institutes of Health
   NIMHD Grant No. G12MD007581, through the RCMI-Center for Environmental
   Health at Jackson State University.
NR 32
TC 3
Z9 3
U1 1
U2 6
PU IMPACT JOURNALS LLC
PI ALBANY
PA 6211 TIPTON HOUSE, STE 6, ALBANY, NY 12203 USA
SN 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD DEC 1
PY 2015
VL 6
IS 38
BP 40734
EP 40746
PG 13
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA CY0SF
UT WOS:000366115500027
PM 26486083
ER

PT J
AU Al-Holou, SN
   Tucker, WR
   Agron, E
   Clemons, TE
   Cukras, C
   Ferris, FL
   Chew, EY
AF Al-Holou, Shaza N.
   Tucker, William R.
   Agron, Elvira
   Clemons, Traci E.
   Cukras, Catherine
   Ferris, Frederick L., III
   Chew, Emily Y.
CA Age-Related Eye Dis Study 2 Res
TI The Association of Statin Use with Age-Related Macular Degeneration
   Progression The Age-Related Eye Disease Study 2 Report Number 9
SO OPHTHALMOLOGY
LA English
DT Article
ID COA REDUCTASE INHIBITORS; C-REACTIVE PROTEIN; CORONARY-HEART-DISEASE;
   BRUCHS MEMBRANE; LOWERING DRUGS; MEDICATION USE; UNITED-STATES; EYE
   DISEASE; RISK; MACULOPATHY
AB Purpose: To evaluate the association of statin use with progression of age-related macular degeneration (AMD).
   Design: Preplanned, prospective cohort study within a controlled clinical trial of oral supplementation for age-related eye diseases.
   Participants: Age-Related Eye Disease Study 2 (AREDS2) participants, aged 50 to 85 years.
   Methods: Factors, including age, gender, smoking status, aspirin use, and history of diabetes, hypertension, heart disease, angina, and stroke-all known to be associated with statin use-were included in a logistic regression model to estimate propensity scores for each participant. Age-adjusted proportional hazards regression models, with and without propensity score matching, were performed to evaluate the association of statin use with progression to late AMD. Analyses adjusting for the competing risk of death were also performed.
   Main Outcome Measures: Baseline and annual stereoscopic fundus photographs were assessed centrally by masked graders for the development of late AMD, either neovascular AMD or geographic atrophy (GA).
   Results: Of the 3791 participants (2462 with bilateral large drusen and 1329 with unilateral late AMD at baseline), 1659 (43.8%) were statin users. The overall analysis, with no matching of propensity scores and no adjustment for death as a competing risk, showed that statin use was not associated with progression to late AMD (hazard ratio [HR], 1.08; 95% confidence interval [CI], 0.83-1.41; P = 0.56). When matched for propensity scores and adjusted for death as a competing risk, the result was not statistically significant (HR, 0.81; 95% CI, 0.55-1.20; P = 0.29). Furthermore, subgroup analyses of persons with or without late AMD at baseline and the various components of late AMD (neovascular AMD, central GA, or any GA) also showed no statistically significant association of statin use with progression to AMD.
   Conclusions: Statin use was not statistically significantly associated with progression to late AMD in the AREDS2 participants, and these findings are consistent with findings in the majority of previous studies. Statins have been demonstrated to reduce the risk of cardiovascular disease, but our data do not provide evidence of a beneficial effect on slowing AMD progression. (C) 2015 Published by Elsevier on behalf of the American Academy of Ophthalmology.
C1 [Al-Holou, Shaza N.; Agron, Elvira; Cukras, Catherine; Ferris, Frederick L., III; Chew, Emily Y.] NEI, Clin Trials Branch, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA.
   [Tucker, William R.] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
   [Clemons, Traci E.] EMMES Corp, Rockville, MD 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
FU National Eye Institute/National Institutes of Health (NIH), Department
   of Health and Human Services, Bethesda Maryland [HHS-N-260-2005-0007-C,
   NO1-EY-5-0007]; NIH institute: Office of Dietary Supplements, National
   Center for Complementary and Alternative Medicine; NIH institute:
   National Institute on Aging; National Heart, Lung, and Blood Institute;
   NIH institute: National Institute of Neurological Disorders and Stroke;
   NIH; Pfizer Inc.; Doris Duke Charitable Foundation; Alexandria Real
   Estate Equities, Inc.; Mr. and Mrs. Joel S. Marcus; Howard Hughes
   Medical Institute
FX Supported by intramural program funds and contracts from the National
   Eye Institute/National Institutes of Health (NIH), Department of Health
   and Human Services, Bethesda Maryland (contract HHS-N-260-2005-0007-C;
   ADB Contract NO1-EY-5-0007). Funds were generously contributed to these
   contracts by the following NIH institutes: Office of Dietary
   Supplements, National Center for Complementary and Alternative Medicine;
   National Institute on Aging; National Heart, Lung, and Blood Institute;
   and National Institute of Neurological Disorders and Stroke. The sponsor
   and funding organization participated in the design and conduct of the
   study; data collection, management, analysis, and interpretation; and
   the preparation, review, and approval of the manuscript. 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 Doris
   Duke Charitable Foundation, The Alexandria Real Estate Equities, Inc.,
   Mr. and Mrs. Joel S. Marcus, and the Howard Hughes Medical Institute, as
   well as other private donors. For a complete list, please see the
   Foundation website at:
   http://fnih.org/work/education-training-0/medical-research-scholars-prog
   ram.
NR 46
TC 1
Z9 1
U1 3
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0161-6420
EI 1549-4713
J9 OPHTHALMOLOGY
JI Ophthalmology
PD DEC
PY 2015
VL 122
IS 12
BP 2490
EP 2496
DI 10.1016/j.ophtha.2015.08.028
PG 7
WC Ophthalmology
SC Ophthalmology
GA CZ4EZ
UT WOS:000367057500028
PM 26435335
ER

PT J
AU Ying, GS
   Maguire, MG
   Daniel, E
   Ferris, FL
   Jaffe, GJ
   Grunwald, JE
   Toth, CA
   Huang, JY
   Martin, DF
AF Ying, Gui-shuang
   Maguire, Maureen G.
   Daniel, Ebenezer
   Ferris, Frederick L.
   Jaffe, Glenn J.
   Grunwald, Juan E.
   Toth, Cynthia A.
   Huang, Jiayan
   Martin, Daniel F.
CA Comparison Age-Related Macular
TI Association of Baseline Characteristics and Early Vision Response with
   2-Year Vision Outcomes in the Comparison of AMD Treatments Trials (CATT)
SO OPHTHALMOLOGY
LA English
DT Article
ID DEGENERATION TREATMENTS TRIALS; VISUAL-ACUITY LOSS; MACULAR
   DEGENERATION; RANIBIZUMAB; BEVACIZUMAB; AFLIBERCEPT; THERAPY
AB Purpose: To evaluate the association of baseline characteristics and early visual acuity (VA) response with visual outcomes at years 1 or 2 in the Comparison of Age-Related Macular Degeneration (AMD) Treatments Trials (CATT).
   Design: Secondary analysis of CATT.
   Participants: The 1185 CATT participants with baseline VA of 20/25 to 20/320. Methods: Participants were assigned to ranibizumab or bevacizumab and to 1 of 3 dosing regimens. Associations of baseline characteristics and early VA response (week 4 or 12) with VA response at years 1 or 2 were assessed by R-2 from linear regression analyses. Patients who had a poor initial response (VA 20/ 40 or worse with persistent fluid and without >= 1-line VA gain) were defined as candidates for changing treatment.
   Main Outcome Measures: Visual acuity change from baseline.
   Results: Statistically significant (P < 0.05) baseline predictors for less VA gain at year 2 were older age, VA of 20/40 or better, larger choroidal neovascularization area, presence of geographic atrophy, total foveal thickness <= 325 mu m or >= 425 mu m, and elevation of retinal pigment epithelium. Among 176 eyes gaining >= 3 lines at week 12, 78% had a >= 3-line gain at year 2, whereas among 113 eyes losing >= 1-line at week 12, 27% improved to a >= 1-line gain at year 2. Visual acuity response at week 12 was more predictive of VA response at year 2 (R-2 = 0.30) than VA response at week 4 (R-2 = 0.17) and baseline predictors (R-2 = 0.13; P < 0.0001). Among 126 candidates for changing treatment drug at week 12, mean VA improved by 2.8 letters (P = 0.050), mean total retinal thickness decreased 53 mu m (P < 0.0001), and fluid resolved in 33% (P < 0.0001) between week 12 and year 1 with continued use of the same drug and regimen. Similar improvements were observed among 83 candidates for changing drugs at week 24.
   Conclusions: Visual acuity response at week 12 is more predictive of 2-year vision outcomes than either several baseline characteristics or week 4 response. Eyes with poor initial response may benefit from continued treatment without switching to another drug. Ophthalmology 2015; 122:2523-2531 (C) 2015 by the American Academy of Ophthalmology.
C1 [Ying, Gui-shuang; Maguire, Maureen G.; Daniel, Ebenezer; Grunwald, Juan E.; Huang, Jiayan] Univ Penn, Dept Ophthalmol, Philadelphia, PA 19104 USA.
   [Ferris, Frederick L.] NEI, NIH, Bethesda, MD 20892 USA.
   [Jaffe, Glenn J.; Toth, Cynthia A.] Duke Univ, Dept Ophthalmol, Durham, NC USA.
   [Martin, Daniel F.] Cleveland Clin, Cole Eye Inst, Cleveland, OH 44106 USA.
RP Ying, GS (reprint author), Univ Penn, Dept Ophthalmol, 3535 Market St,Suite 700, Philadelphia, PA 19104 USA.
EM gsying@mail.med.upenn.edu
OI Grunwald, Juan/0000-0002-5973-6616; Maguire, Maureen/0000-0002-4249-2467
FU Bioptigen (Morrisville, NC); Genentech (San Francisco, CA); Physical
   Sciences Inc (Andover, MA); Consultant - Alcon Laboratories (Fort Worth,
   TX); Thrombogenics (Iselin, NJ); Consultant - Genentech (San Francisco,
   CA); National Eye Institute, National Institutes of Health, Bethesda,
   Maryland [U10 EY017823, U10 EY017825, U10 EY017826, U10 EY017828,
   R21EY023689]
FX The author(s) have no proprietary or commercial interest in any
   materials discussed in this article. G.-S. Y.: Consultant -Janssen
   (Titusville, NJ) C.A.T.: Financial Support - Bioptigen (Morrisville,
   NC), Genentech (San Francisco, CA), Physical Sciences Inc (Andover,
   MA).; Consultant - Alcon Laboratories (Fort Worth, TX), Thrombogenics
   (Iselin, NJ) M.G.M.: Consultant - Genentech (San Francisco, CA);
   Supported by the National Eye Institute, National Institutes of Health,
   Bethesda, Maryland (cooperative agreement nos.: U10 EY017823, U10
   EY017825, U10 EY017826, U10 EY017828, and R21EY023689).
NR 25
TC 6
Z9 7
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 DEC
PY 2015
VL 122
IS 12
BP 2523
EP +
DI 10.1016/j.ophtha.2015.08.015
PG 10
WC Ophthalmology
SC Ophthalmology
GA CZ4EZ
UT WOS:000367057500032
PM 26383996
ER

PT J
AU Swineford, LB
   Guthrie, W
   Thurm, A
AF Swineford, Lauren B.
   Guthrie, Whitney
   Thurm, Audrey
TI Convergent and Divergent Validity of the Mullen Scales of Early Learning
   in Young Children With and Without Autism Spectrum Disorder
SO PSYCHOLOGICAL ASSESSMENT
LA English
DT Article
DE factor structure; Mullen Scales of Early Learning; validity; autism
   spectrum disorder
ID CONFIRMATORY FACTOR-ANALYSIS; OF-FIT INDEXES; MEASUREMENT INVARIANCE;
   WISC-IV; INTELLIGENCE; BEHAVIOR; MODELS; SCORES; SAMPLE
AB The purpose of this study was to report on the construct, convergent, and divergent validity of the Mullen Scales of Early Learning (MSEL), a widely used test of development for young children. The sample consisted of 399 children with a mean age of 3.38 years (SD = 1.14) divided into a group of children with autism spectrum disorder (ASD) and a group of children not on the autism spectrum, with and without developmental delays. The study used the MSEL and several other measures assessing constructs relevant to the age range including developmental skills, autism symptoms, and psychopathology symptoms across multiple methods of assessment. Multiple group confirmatory factor analyses revealed good overall fit and equal form of the MSEL 1-factor model across the ASD and nonspectnnu 2roups, supporting the construct validity of the MSEL. However, neither full nor partial invariance of factor loadings was established because of the lower loadings in the, ASD group compared with the, nonspectrum 2roup. Exploratory structural equation modeling revealed that other measures of developmental skills loaded together with the MSEL domain scores on a Developmental Functioning factor, supporting convergent validity of the MSEL. Divergent validity- was supported by- the lack of loading of MSEL domain scores on Autism Symptoms or Emotion/Behavior Problems factors. Although factor structure, and loadings V a ri d across groups, Convergent and divergent V alidity findings were, similar in the ASD and nonspectrum samples. Together, these results demonstrate evidence for the construct, convergent, and divergent validity of the MSEL using powerful data analytic techniques.
C1 [Swineford, Lauren B.; Thurm, Audrey] NIMH, Pediat & Dev Neurosci Branch, Bethesda, MD 20892 USA.
   [Guthrie, Whitney] Florida State Univ, Dept Psychol, Tallahassee, FL 32306 USA.
RP Swineford, LB (reprint author), NIMH, Pediat & Dev Neurosci Branch, 10 Ctr Dr MSC 1255,Bldg 10,Room 1C250, Bethesda, MD 20892 USA.
EM swinefordlb@mail.nih.gov
FU National Institute of Mental Health [NCT00271622, 06-M-0065]
FX This research was supported by the Intramural Program of the National
   Institute of Mental Health, NCT00271622, 06-M-0065. Selected results
   were presented at the Society for Research on Child Development in
   Seattle, Washington, March 2013.
NR 56
TC 1
Z9 1
U1 2
U2 10
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 1040-3590
EI 1939-134X
J9 PSYCHOL ASSESSMENT
JI Psychol. Assess.
PD DEC
PY 2015
VL 27
IS 4
BP 1364
EP 1378
DI 10.1037/pas0000116
PG 15
WC Psychology, Clinical
SC Psychology
GA CZ0UG
UT WOS:000366820900022
PM 25894712
ER

PT J
AU Melo, DR
   Brill, AB
   Zanzonico, P
   Vicini, P
   Moroz, B
   Kwon, D
   Lamart, S
   Brenner, A
   Bouville, A
   Simon, SL
AF Melo, Dunstana R.
   Brill, Aaron B.
   Zanzonico, Pat
   Vicini, Paolo
   Moroz, Brian
   Kwon, Deukwoo
   Lamart, Stephanie
   Brenner, Alina
   Bouville, Andre
   Simon, Steven L.
TI Organ Dose Estimates for Hyperthyroid Patients Treated with I-131: An
   Update of the Thyrotoxicosis Follow-Up Study
SO RADIATION RESEARCH
LA English
DT Article
ID THYROXINE DISTRIBUTION; RADIATION-DOSIMETRY; NUCLEAR-MEDICINE;
   THYROID-CANCER; THERAPY; IODINE; EMPHASIS; SYSTEMS; FETUS
AB The Thyrotoxicosis Therapy Follow-up Study (TTFUS) is comprised of 35,593 hyperthyroid patients treated from the mid-1940s through the mid-1960s. One objective of the TTFUS was to evaluate the long-term effects of high-dose iodine-131 (I-131) treatment (1-4). In the TTFUS cohort, 23,020 patients were treated with I-131, including 21,536 patients with Graves disease (GD), 1,203 patients with toxic nodular goiter (TNG) and 281 patients with unknown disease. The study population constituted the largest group of hyperthyroid patients ever examined in a single health risk study. The average number (+/- 1 standard deviation) of I-131 treatments per patient was 1.7 +/- 1.4 for the GD patients and 2.1 +/- 2.1 for the TNG patients. The average total I-131 administered activity was 380 +/- 360 MBq for GD patients and 640 +/- 550 MBq for TNG patients. In this work, a biokinetic model for iodine was developed to derive organ residence times and to reconstruct the radiation-absorbed doses to the thyroid gland and to other organs resulting from administration of I-131 to hyperthyroid patients. Based on I-131 data for a small, kinetically well-characterized sub-cohort of patients, multivariate regression equations were developed to relate the numbers of disintegrations of I-131 in more than 50 organs and tissues to anatomical (thyroid mass) and clinical (percentage thyroid uptake and pulse rate) parameters. These equations were then applied to estimate the numbers of I-131 disintegrations in the organs and tissues of all other hyperthyroid patients in the TTFUS who were treated with I-131. The reference voxel phantoms adopted by the International Commission on Radiological Protection (ICRP) were then used to calculate the absorbed doses in more than 20 organs and tissues of the body. As expected, the absorbed doses were found to be highest in the thyroid (arithmetic means of 120 and 140 Gy for GD and TNG patients, respectively). Absorbed doses in organs other than the thyroid were much smaller, with arithmetic means of 1.6 Gy, 1.5 Gy and 0.65 Gy for esophagus, thymus and salivary glands, respectively. The arithmetic mean doses to all other organs and tissues were more than 100 times less than those to the thyroid gland. To our knowledge, this work represents the most comprehensive study to date of the doses received by persons treated with I-131 for hyperthyroidism. (C) 2015 by Radiation Research Society
C1 [Melo, Dunstana R.; Moroz, Brian; Lamart, Stephanie; Bouville, Andre; Simon, Steven L.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Brill, Aaron B.] Vanderbilt Univ, Nashville, TN 37232 USA.
   [Zanzonico, Pat] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
   [Vicini, Paolo] Univ Washington, Dept Bioengn, Seattle, WA 98195 USA.
   [Kwon, Deukwoo; Brenner, Alina] Univ Miami, Sylvester Comprehens Canc Ctr, Miami, FL 33136 USA.
   [Bouville, Andre] NCI, Bethesda, MD 20892 USA.
RP Melo, DR (reprint author), Lovelace Resp Res Inst, Ctr Countermeasures Radiat, 2425 Ridgecrest Dr SE, Albuquerque, NM 87108 USA.
EM dmelo@lrri.org
FU National Institute of Allergy and Infectious Diseases; National Cancer
   Institute (NIAID) [Y2-A1-5077, Y3-CO-5117]; NCI Intramural Research
   Program
FX This work was supported by the Intra-agency agreement between the
   National Institute of Allergy and Infectious Diseases and the National
   Cancer Institute (NIAID agreement no. Y2-A1-5077 and NCI agreement no.
   Y3-CO-5117) and the NCI Intramural Research Program. The authors thank
   Dr. Michael Stabin of Vanderbilt University for review of early versions
   of the biokinetic model, Dr. Choonsik Lee of the National Cancer
   Institute for assisting with calculation of S values and Dr. Elaine Ron
   (deceased) for her vision and commitment to reanalyze the TTFUS
   dosimetry and health risks, which ultimately resulted in this analysis.
NR 45
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U1 0
U2 2
PU RADIATION RESEARCH SOC
PI LAWRENCE
PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA
SN 0033-7587
EI 1938-5404
J9 RADIAT RES
JI Radiat. Res.
PD DEC
PY 2015
VL 184
IS 6
BP 595
EP 610
DI 10.1667/RR14160.1
PG 16
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
   Nuclear Medicine & Medical Imaging
GA CZ5RW
UT WOS:000367160700006
PM 26579944
ER

PT J
AU Mansfield, AS
   Tafur, AJ
   Vulih, D
   Smith, GL
   Harris, PJ
   Ivy, SP
AF Mansfield, A. S.
   Tafur, A. J.
   Vulih, D.
   Smith, G. L.
   Harris, P. J.
   Ivy, S. P.
TI Severe hepatic dysfunction is associated with venous thromboembolic
   events in phase 1 clinical trials
SO THROMBOSIS RESEARCH
LA English
DT Article
DE Clinical trials, phase 1; Liver diseases; Neoplasms; Pulmonary embolism;
   Venous thrombosis
ID DEEP-VEIN THROMBOSIS; CANCER-PATIENTS; PULMONARY-EMBOLISM;
   LIVER-DISEASES; RISK-FACTORS; CHEMOTHERAPY; SCORE; EPIDEMIOLOGY;
   METAANALYSIS; MORTALITY
AB Introduction: Venous thromboembolic events (VTEs) are a significant cause of death in patients with cancer. The incidence of VTE is not well characterized in early phase clinical trials of novel antineoplastic agents, or in hepatic dysfunction studies designed for patients with varying degrees of liver test abnormalities. We compared the incidences of VTE in phase 1 clinical trials (P1CTs) and hepatic dysfunction trials (HDCTs) sponsored by the Cancer Therapy Evaluation Program of the National Cancer Institute (NCI) of the United States.
   Materials & methods: We reviewed individual patient records of 1841 subjects for symptomatic VTE diagnosed while on study: 1328 subjects on 42 P1CTs, and 513 subjects on 9 HDCTs. The NCI's Organ Dysfunction Working Group definitions were used to categorize patients. The incidences of VTEs between patients were compared by the Chi square test. Confounders were evaluated with the Cochran-Mantel-Haenszel method.
   Results & conclusions: There were 43 VTEs identified among all subjects (2.3%). There were significantly more VTE observed in the subjects on P1CTs (n = 38, 2.9%) than in the subjects on HDCTs (n = 5, 1.0%; RR 0.341, 95% 0.13-0.86, p = 0.015). For patients on HDCTs, those with severe dysfunction had a high incidence of VTE (RR 10.5 (1.12-93.6), p = 0.021) that remained significant in a multivariate model.
   VTEs were observed less frequently in patients who were enrolled in HDCT than those who were enrolled in P1CT; however, patients with severe hepatic dysfunction were more likely to experience VTE. Severe liver test abnormalities may not be protective against VTE in patients with malignancies receiving chemotherapy. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Mansfield, A. S.] Mayo Clin, Div Med Oncol, Rochester, MN 55905 USA.
   [Tafur, A. J.] Northshore Univ Hlth Syst, Vasc Med, Evanston, IL 60201 USA.
   [Vulih, D.] Theradex, Princeton, NJ 08540 USA.
   [Smith, G. L.] NCI, Clin Trials Monitoring Branch, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
   [Harris, P. J.; Ivy, S. P.] NCI, Invest Drug Branch, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Mansfield, AS (reprint author), Mayo Clin, Div Med Oncol, 200 First St SW, Rochester, MN 55905 USA.
EM mansfield.aaron@mayo.edu; atafur@northshore.org; DVulih@theradex.com;
   SmithG@ctep.nci.nih.gov; harrispj@mail.nih.gov; ivyp@ctep.nci.nih.gov
OI Mansfield, Aaron/0000-0002-9483-6903
FU National Cancer Institutes of Health [K12CA090628]
FX This work was support in part by the National Cancer Institutes of
   Health [K12CA090628 to A.S.M.].
NR 19
TC 0
Z9 0
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0049-3848
J9 THROMB RES
JI Thromb. Res.
PD DEC
PY 2015
VL 136
IS 6
BP 1169
EP 1173
DI 10.1016/j.thromres.2015.10.024
PG 5
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA CY9FM
UT WOS:000366712800024
PM 26493604
ER

PT J
AU Patel, D
   Kitahara, CM
   Park, Y
   Liao, LM
   Linet, M
   Kebebew, E
   Nilubol, N
AF Patel, Dhaval
   Kitahara, Cari M.
   Park, Yikyung
   Liao, Linda M.
   Linet, Martha
   Kebebew, Electron
   Nilubol, Naris
TI Thyroid Cancer and Nonsteroidal Anti-Inflammatory Drug Use: A Pooled
   Analysis of Patients Older Than 40 Years of Age
SO THYROID
LA English
DT Article
ID CYCLOOXYGENASE-2 EXPRESSION; RADIOLOGIC TECHNOLOGISTS; PAPILLARY
   CARCINOMA; UNITED-STATES; COX-2; METAANALYSIS; ASSOCIATION; HEALTH;
   ASPIRIN; IMPACT
AB Background: Cyclooxygenase (COX-2) has been associated with tumor growth and metastasis in several cancers, including thyroid cancer. For this reason, several investigators have studied COX-2 inhibitors in preclinical models of thyroid cancer and found antineoplastic effects. Thus, the primary aim of this study was to assess if the use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with a reduced incidence of thyroid cancer. A second aim of the study was to determine additional risk or protective factors for thyroid cancer. Methods: Three large prospective population-based studies (the NIH-AARP Diet and Health Study; the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial; and the U.S. Radiologic Technologists Study) were pooled to investigate the association between self-reported frequency of aspirin and nonaspirin NSAID use one year prior to baseline (no use, 2/week, >2-6/week, and 7/week) and subsequent risk of thyroid cancer. A Cox regression proportional hazard model was used to estimate aggregated hazard ratios (HR) adjusted for cohort, sex, race/ethnicity, weight, smoking status, and alcohol intake. Results: There were 388,577 participants in the pooled cohort, with 481 cases of thyroid cancer. No significant risk reduction was observed with regular use of nonaspirin NSAIDs (HR=1.14 [confidence interval (CI) 0.84-1.55]), and/or regular use of aspirin (HR=1.06 [CI 0.82-1.39]). The multivariate regression analysis confirmed as previously reported in the literature that female sex, obesity class I (body mass index [BMI]=30-34.99kg/m(2)), and obesity class II (BMI=35-35.99kg/m(2)) were independently associated with an increased thyroid cancer risk. Current smoking status and moderate and excessive alcohol use were also confirmed as independent risk factors associated with a reduced thyroid cancer risk. Conclusions: Neither nonaspirin NSAIDs nor aspirin use is associated with a reduced risk of thyroid cancer. Women and obesity are associated with an increased risk of thyroid cancer, whereas smoking and alcohol use are associated with decreased risk of thyroid cancer.
C1 [Patel, Dhaval; Kebebew, Electron; Nilubol, Naris] NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
   [Kitahara, Cari M.] NCI, Div Canc Epidemiol & Genet, Radiat Epidemiol Branch, NIH, Bethesda, MD 20892 USA.
   [Park, Yikyung; Liao, Linda M.; Linet, Martha] NCI, Div Canc Epidemiol & Genet, Nutr Epidemiol Branch, NIH, Bethesda, MD 20892 USA.
   [Park, Yikyung] Washington Univ, Sch Med, Div Publ Hlth Sci, St Louis, MO USA.
RP Nilubol, N (reprint author), NCI, Endocrine Oncol Branch, NIH, Clin Res Ctr, Bldg 10-CRC,Room 3-5840, Bethesda, MD 20892 USA.
EM naris.nilubol@nih.gov
RI Kitahara, Cari/R-8267-2016; 
OI Liao, Linda/0000-0002-1923-5294; Patel, Dhaval/0000-0002-5744-568X
FU Intramural Research Program of the NIH, National Cancer Institute
FX The authors would like to acknowledge the staff and data managers who
   have worked to establish the PLCO, NIH-AARP, and USRT databases. The
   authors would like to acknowledge David Venzon for his statistical
   assistance. We are indebted to the participants in the NIH-AARP Diet and
   Health Study for their outstanding cooperation. We also thank Sigurd
   Hermansen and Kerry Grace Morrissey from Westat for study outcomes
   ascertainment and management and Leslie Carroll at Information
   Management Services for data support and analysis. This research was
   supported in part by the Intramural Research Program of the NIH,
   National Cancer Institute.
NR 32
TC 1
Z9 1
U1 1
U2 3
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1050-7256
EI 1557-9077
J9 THYROID
JI Thyroid
PD DEC 1
PY 2015
VL 25
IS 12
BP 1355
EP 1362
DI 10.1089/thy.2015.0198
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CY9CI
UT WOS:000366704600012
PM 26426828
ER

PT J
AU Webster, AF
   Zumbo, P
   Fostel, J
   Gandara, J
   Hester, SD
   Recio, L
   Williams, A
   Wood, CE
   Yauk, CL
   Mason, CE
AF Webster, A. Francina
   Zumbo, Paul
   Fostel, Jennifer
   Gandara, Jorge
   Hester, Susan D.
   Recio, Leslie
   Williams, Andrew
   Wood, Charles E.
   Yauk, Carole L.
   Mason, Christopher E.
TI Mining the Archives: A Cross-Platform Analysis of Gene Expression
   Profiles in Archival Formalin-Fixed Paraffin-Embedded Tissues
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE RNA-seq; microarray; toxicogenomics; FFPE; archival RNA; biorepositories
ID FEMALE B6C3F1 MICE; RNA-SEQ; RISK-ASSESSMENT; DIFFERENTIAL EXPRESSION;
   SYSTEMATIC VARIATION; CELL-PROLIFERATION; CARCINOGEN FURAN; MICROARRAY
   DATA; QUALITY-CONTROL; LINEAR-MODEL
AB Formalin-fixed paraffin-embedded (FFPE) tissue samples represent a potentially invaluable resource for transcriptomic research. However, use of FFPE samples in genomic studies has been limited by technical challenges resulting from nucleic acid degradation. Here we evaluated gene expression profiles derived from fresh-frozen (FRO) and FFPE mouse liver tissues preserved in formalin for different amounts of time using 2 DNA microarray protocols and 2 whole-transcriptome sequencing (RNA-seq) library preparation methodologies. The ribo-depletion protocol outperformed the other methods by having the highest correlations of differentially expressed genes (DEGs), and best overlap of pathways, between FRO and FFPE groups. The effect of sample time in formalin (18 h or 3 weeks) on gene expression profiles indicated that test article treatment, not preservation method, was the main driver of gene expression profiles. Meta- and pathway analyses indicated that biological responses were generally consistent for 18 h and 3 week FFPE samples compared with FRO samples. However, clear erosion of signal intensity with time in formalin was evident, and DEG numbers differed by platform and preservation method. Lastly, we investigated the effect of time in paraffin on genomic profiles. Ribo-depletion RNA-seq analysis of 8-, 19-, and 26-year-old control blocks resulted in comparable quality metrics, including expected distributions of mapped reads to exonic, untranslated region, intronic, and ribosomal fractions of the transcriptome. Overall, our results indicate that FFPE samples are appropriate for use in genomic studies in which frozen samples are not available, and that ribo-depletion RNA-seq is the preferred method for this type of analysis in archival and long-aged FFPE samples.
C1 [Webster, A. Francina; Williams, Andrew; Yauk, Carole L.] Hlth Canada, Environm Hlth Sci & Res Bur, Ottawa, ON K1A 0K9, Canada.
   [Webster, A. Francina] Carleton Univ, Dept Biol, Ottawa, ON K1S 5B6, Canada.
   [Zumbo, Paul; Gandara, Jorge; Mason, Christopher E.] Weill Cornell Med Coll, Dept Physiol & Biophys, New York, NY 10065 USA.
   [Fostel, Jennifer] NIEHS, Res Triangle Pk, NC 27709 USA.
   [Hester, Susan D.; Wood, Charles E.] US EPA, Off Res & Dev, Res Triangle Pk, NC 27709 USA.
   [Recio, Leslie] ILS Inc, Res Triangle Pk, NC 27709 USA.
   [Mason, Christopher E.] Feil Family Brain & Mind Res Inst BMRI, New York, NY 10021 USA.
   [Mason, Christopher E.] HRH Prince Alwaleed Bin Talal Bin Abdulaziz Alsau, New York, NY 10065 USA.
RP Yauk, CL (reprint author), Hlth Canada, HECSB, ERHSD, Environm Hlth Sci & Res Bur, Bldg 8,P-L 0803A,50 Colombine Driveway, Ottawa, ON K1A 0K9, Canada.
EM Carole.Yauk@hc-sc.gc.ca; chm2042@med.cornell.edu
FU NTP [NO1-ES-55536]
FX We thank the ILS animal care group for performing the furan mouse
   exposures and fixing these tissues, and the NTP contract NO1-ES-55536
   for preparing the archival RNA. The authors greatly acknowledge Weill
   Cornell Epigenomics Core contribution and technical support from
   Jennifer A. Busuttil and Caroline Sheridan. We also thank the Bert L.
   and N. Kuggie Vallee Foundation Young Investigator Award and the
   WorldQuant Foundation. The authors also acknowledge Dr. Matt Meier and
   Dr Ivy Moffat for helpful comments on the article.
NR 48
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Z9 4
U1 2
U2 8
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
EI 1096-0929
J9 TOXICOL SCI
JI Toxicol. Sci.
PD DEC
PY 2015
VL 148
IS 2
BP 460
EP 472
DI 10.1093/toxsci/kfv195
PG 13
WC Toxicology
SC Toxicology
GA CZ6FB
UT WOS:000367195500011
PM 26361796
ER

PT J
AU Howdeshell, KL
   Rider, CV
   Wilson, VS
   Furr, JR
   Lambright, CR
   Gray, LE
AF Howdeshell, Kembra L.
   Rider, Cynthia V.
   Wilson, Vickie S.
   Furr, Johnathan R.
   Lambright, Christy R.
   Gray, L. Earl, Jr.
TI Dose Addition Models Based on Biologically Relevant Reductions in Fetal
   Testosterone Accurately Predict Postnatal Reproductive Tract Alterations
   by a Phthalate Mixture in Rats
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE dose addition; phthalates; postnatal developmental toxicity; male
   reproductive tract; endocrine disruptors; mixture models
ID N-BUTYL PHTHALATE; ALTERS SEXUAL-DIFFERENTIATION; CUMULATIVE
   RISK-ASSESSMENT; SPRAGUE-DAWLEY RATS; IN-UTERO EXPOSURE; DI(N-BUTYL)
   PHTHALATE; BENZYL PHTHALATE; GENE-EXPRESSION; DIETHYLHEXYL PHTHALATE;
   DEVELOPMENTAL TOXICITY
AB Challenges in cumulative risk assessment of anti-androgenic phthalate mixtures include a lack of data on all the individual phthalates and difficulty determining the biological relevance of reduction in fetal testosterone (T) on postnatal development. The objectives of the current study were 2-fold: (1) to test whether a mixture model of dose addition based on the fetal T production data of individual phthalates would predict the effects of a 5 phthalate mixture on androgen-sensitive postnatal male reproductive tract development, and (2) to determine the biological relevance of the reductions in fetal T to induce abnormal postnatal reproductive tract development using data from the mixture study. We administered a dose range of the mixture (60, 40, 20, 10, and 5% of the top dose used in the previous fetal T production study consisting of 300 mg/kg per chemical of benzyl butyl (BBP), di(n)butyl (DBP), diethyl hexyl phthalate (DEHP), di-isobutyl phthalate (DiBP), and 100 mg dipentyl (DPP) phthalate/kg; the individual phthalates were present in equipotent doses based on their ability to reduce fetal T production) via gavage to Sprague Dawley rat dams on GD8-postnatal day 3. We compared observed mixture responses to predictions of dose addition based on the previously published potencies of the individual phthalates to reduce fetal T production relative to a reference chemical and published postnatal data for the reference chemical (called DA(ref)). In addition, we predicted DA (called DA(all)) and response addition (RA) based on logistic regression analysis of all 5 individual phthalates when complete data were available. DA (ref) and DA (all) accurately predicted the observed mixture effect for 11 of 14 endpoints. Furthermore, reproductive tract malformations were seen in 17-100% of F1 males when fetal T production was reduced by about 25-72%, respectively.
C1 [Howdeshell, Kembra L.; Rider, Cynthia V.] NIEHS, Div Natl Toxicol Program NTP, Res Triangle Pk, NC 27709 USA.
   [Wilson, Vickie S.; Furr, Johnathan R.; Lambright, Christy R.; Gray, L. Earl, Jr.] US EPA, Off Res & Dev, Natl Hlth & Environm Effects Res Labs, Toxicol Assessment Div TAD,Reprod Toxicol Branch, Res Triangle Pk, NC 27711 USA.
RP Howdeshell, KL (reprint author), NIEHS, Div Natl Toxicol Program NTP, POB 12233, Res Triangle Pk, NC 27709 USA.
EM howdeshellkl@niehs.nih.gov
OI Wilson, Vickie/0000-0003-1661-8481
FU NIH, National Institute of Environmental Health Sciences
FX We wish to thank Dr Eve Mylchreest for providing us the original data
   from her 1998 DBP study (Mylchreest et al., 1998). We thank Mary Cardon
   and Dr Phillip Hartig for their help in fetal necropsies, Dr Dieldrich
   Bermudez for his assistance with adult necropsies, and Dr Donald A.
   Smith for his mathematical advice. This work was supported in part by
   the NIH, National Institute of Environmental Health Sciences. This
   research described in this article has been reviewed by the National
   Health and Environmental Effects Research Laboratory, U.S. EPA, and has
   been approved for publication. Approval does not necessarily reflect the
   views and policies of the U.S. EPA nor does mention of trade names or
   commercial products constitute endorsement or recommendation for use.
NR 50
TC 5
Z9 5
U1 7
U2 14
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
EI 1096-0929
J9 TOXICOL SCI
JI Toxicol. Sci.
PD DEC
PY 2015
VL 148
IS 2
BP 488
EP 502
DI 10.1093/toxsci/kfv196
PG 15
WC Toxicology
SC Toxicology
GA CZ6FB
UT WOS:000367195500013
PM 26350170
ER

PT J
AU Suffredini, DA
   Sampath-Kumar, H
   Li, Y
   Ohanjanian, L
   Remy, KE
   Cui, XZ
   Eichacker, PQ
AF Suffredini, Dante A.
   Sampath-Kumar, Hanish
   Li, Yan
   Ohanjanian, Lernik
   Remy, Kenneth E.
   Cui, Xizhong
   Eichacker, Peter Q.
TI Does Bacillus anthracis Lethal Toxin Directly Depress Myocardial
   Function? A Review of Clinical Cases and Preclinical Studies
SO TOXINS
LA English
DT Review
DE Bacillus anthracis; anthrax; lethal and edema toxins; cardiovascular
   dysfunction; shock; treatment
ID FATAL INHALATIONAL ANTHRAX; EDEMA TOXINS; SEPTIC SHOCK; UNITED-STATES;
   SEVERE SEPSIS; HEROIN USERS; DYSFUNCTION; BIOTERRORISM; PATHOLOGY; RATS
AB The US outbreak of B.anthracis infection in 2001 and subsequent cases in the US and Europe demonstrate that anthrax is a continuing risk for the developed world. While several bacterial components contribute to the pathogenesis of B. anthracis, production of lethal toxin (LT) is strongly associated with the development of hypotension and lethality. However, the mechanisms underlying the cardiovascular instability LT produces are unclear. Some evidence suggests that LT causes shock by impairing the peripheral vasculature, effects consistent with the substantial extravasation of fluid in patients dying with B. anthracis. Other data suggests that LT directly depresses myocardial function. However a clinical correlate for this latter possibility is less evident since functional studies and post-mortem examination in patients demonstrate absent or minimal cardiac changes. The purposes of this review were to first present clinical studies of cardiac functional and histologic pathology with B. anthracis infection and to then examine in vivo, in vitro, and ex vivo preclinical studies of LT's myocardial effects. Together, these data suggest that it is unclear whether that LT directly depresses cardiac function. This question is important for the clinical management and development of new therapies for anthrax and efforts should continue to be made to answer it.
C1 [Suffredini, Dante A.; Sampath-Kumar, Hanish; Li, Yan; Ohanjanian, Lernik; Cui, Xizhong; Eichacker, Peter Q.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Remy, Kenneth E.] Washington Univ, Sch Med, Dept Pediat, Div Crit Care Med, St Louis, MO 63110 USA.
RP Suffredini, DA (reprint author), NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
EM dante.suffredini@nih.gov; hanishsampathkumar@gmail.com; yli3@cc.nih.gov;
   lernik.ohanjanian@nih.gov; Remy_K@kids.wustl.edu; CXizhong@cc.nih.gov;
   PEichacker@cc.nih.gov
NR 61
TC 1
Z9 1
U1 1
U2 5
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 2072-6651
J9 TOXINS
JI Toxins
PD DEC
PY 2015
VL 7
IS 12
BP 5417
EP 5434
DI 10.3390/toxins7124891
PG 18
WC Toxicology
SC Toxicology
GA CZ3OI
UT WOS:000367013500040
PM 26703730
ER

PT J
AU Goldstein, I
   Hager, GL
AF Goldstein, Ida
   Hager, Gordon L.
TI Transcriptional and Chromatin Regulation during Fasting - The Genomic
   Era
SO TRENDS IN ENDOCRINOLOGY AND METABOLISM
LA English
DT Review
ID GROWTH-FACTOR 21; THYROID-HORMONE RECEPTOR; FATTY-ACID OXIDATION;
   HEPATIC GLUCONEOGENESIS; GLUCOCORTICOID-RECEPTOR; LIPID-METABOLISM;
   PPAR-ALPHA; GLUCOSE-PRODUCTION; DIABETES-MELLITUS; NUCLEAR RECEPTORS
AB An elaborate metabolic response to fasting is orchestrated by the liver and is heavily reliant on transcriptional regulation. In response to hormones (glucagon, glucocorticoids) many transcription factors (TFs) are activated and regulate various genes involved in metabolic pathways aimed at restoring homeostasis: gluconeogenesis, fatty acid oxidation, ketogenesis, and amino acid shuttling. We summarize recent discoveries regarding fasting-related TFs with an emphasis on genome-wide binding patterns. Collectively, the findings we discuss reveal a large degree of cooperation between TFs during fasting that occurs at motif-rich DNA sites bound by a combination of TFs. These new findings implicate transcriptional and chromatin regulation as major determinants of the response to fasting and unravels the complex, multi-TF nature of this response.
C1 [Goldstein, Ida; Hager, Gordon L.] NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA.
RP Goldstein, I (reprint author), NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA.
EM goldstein.ido@gmail.com; hagerg@dce41.nci.nih.gov
OI Goldstein, Ido/0000-0003-0139-1499
FU Intramural NIH HHS [Z01 BC005450-24]
NR 96
TC 5
Z9 6
U1 0
U2 13
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 1043-2760
J9 TRENDS ENDOCRIN MET
JI Trends Endocrinol. Metab.
PD DEC
PY 2015
VL 26
IS 12
BP 699
EP 710
DI 10.1016/j.tem.2015.09.005
PG 12
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CZ3TA
UT WOS:000367025700006
PM 26520657
ER

PT J
AU Germain, RN
   Fowlkes, BJ
   Samelson, LE
   Leonard, WJ
AF Germain, Ronald N.
   Fowlkes, B. J.
   Samelson, Lawrence E.
   Leonard, Warren J.
TI William E. Paul, MD (1936-2015) In Memoriam
SO TRENDS IN IMMUNOLOGY
LA English
DT Biographical-Item
C1 [Germain, Ronald N.] NIAID, Lab Syst Biol, NIH, Bethesda, MD 20892 USA.
   [Fowlkes, B. J.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
   [Samelson, Lawrence E.] NCI, Cellular & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
   [Leonard, Warren J.] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
   [Leonard, Warren J.] NHLBI, Ctr Immunol, NIH, Bethesda, MD 20892 USA.
RP Germain, RN (reprint author), NIAID, Lab Syst Biol, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM rgermain@nlh.gov
NR 1
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1471-4906
EI 1471-4981
J9 TRENDS IMMUNOL
JI Trends Immunol.
PD DEC
PY 2015
VL 36
IS 12
BP 751
EP 753
DI 10.1016/j.it.2015.10.001
PG 3
WC Immunology
SC Immunology
GA CZ4ZD
UT WOS:000367110800001
PM 27064162
ER

PT J
AU Luciano, M
   Marioni, RE
   Hernandez, MV
   Maniega, SM
   Hamilton, IF
   Royle, NA
   Scotland, G
   Chauhan, G
   Bis, JC
   Debette, S
   DeCarli, C
   Fornage, M
   Schmidt, R
   Ikram, MA
   Launer, LJ
   Seshadri, S
   Bastin, ME
   Porteous, DJ
   Wardlaw, J
   Deary, IJ
AF Luciano, Michelle
   Marioni, Riccardo E.
   Hernandez, Maria Valdes
   Maniega, Susana Munoz
   Hamilton, Iona F.
   Royle, Natalie A.
   Scotland, Generation
   Chauhan, Ganesh
   Bis, Joshua C.
   Debette, Stephanie
   DeCarli, Charles
   Fornage, Myriam
   Schmidt, Reinhold
   Ikram, M. Arfan
   Launer, Lenore J.
   Seshadri, Sudha
   Bastin, Mark E.
   Porteous, David J.
   Wardlaw, Joanna
   Deary, Ian J.
CA CHARGE Consortium
TI Structural Brain MRI Trait Polygenic Score Prediction of Cognitive
   Abilities
SO TWIN RESEARCH AND HUMAN GENETICS
LA English
DT Article
DE polygenic prediction; white matter hyperintensities; brain infarct;
   intracranial volume; hippocampal volume; total brain volume; general
   cognitive ability
ID GENOME-WIDE ASSOCIATION; INTRACRANIAL VOLUME; HIPPOCAMPAL VOLUME; HUMAN
   INTELLIGENCE; COMMON VARIANTS; OLD-AGE; METAANALYSIS; INFARCTS;
   INDIVIDUALS; DISEASE
AB Structural brain magnetic resonance imaging (MRI) traits share part of their genetic variance with cognitive traits. Here, we use genetic association results from large meta-analytic studies of genome-wide association (GWA) for brain infarcts (BI), white matter hyperintensities, intracranial, hippocampal, and total brain volumes to estimate polygenic scores for these traits in three Scottish samples: Generation Scotland: Scottish Family Health Study (GS:SFHS), and the Lothian Birth Cohorts of 1936 (LBC1936) and 1921 (LBC1921). These five brain MRI trait polygenic scores were then used to: (1) predict corresponding MRI traits in the LBC1936 (numbers ranged 573 to 630 across traits), and (2) predict cognitive traits in all three cohorts (in 8,115-8,250 persons). In the LBC1936, all MRI phenotypic traits were correlated with at least one cognitive measure, and polygenic prediction of MRI traits was observed for intracranial volume. Meta-analysis of the correlations between MRI polygenic scores and cognitive traits revealed a significant negative correlation (maximal r = 0.08) between the HV polygenic score and measures of global cognitive ability collected in childhood and in old age in the Lothian Birth Cohorts. The lack of association to a related general cognitive measure when including the GS:SFHS points to either type 1 error or the importance of using prediction samples that closely match the demographics of the GWA samples from which prediction is based. Ideally, these analyses should be repeated in larger samples with data on both MRI and cognition, and using MRI GWA results from even larger meta-analysis studies.
C1 [Luciano, Michelle; Marioni, Riccardo E.; Hernandez, Maria Valdes; Maniega, Susana Munoz; Hamilton, Iona F.; Royle, Natalie A.; Bastin, Mark E.; Porteous, David J.; Wardlaw, Joanna; Deary, Ian J.] Univ Edinburgh, Ctr Cognit Ageing & Cognit Epidemiol, Edinburgh EH8 9JZ, Midlothian, Scotland.
   [Luciano, Michelle; Deary, Ian J.] Univ Edinburgh, Dept Psychol, Edinburgh EH8 9JZ, Midlothian, Scotland.
   [Marioni, Riccardo E.; Scotland, Generation; Porteous, David J.] Univ Edinburgh, Inst Genet & Mol Med, Med Genet Sect, Ctr Genom & Expt Med, Edinburgh EH8 9JZ, Midlothian, Scotland.
   [Marioni, Riccardo E.] Univ Queensland, Queensland Brain Inst, Brisbane, Qld, Australia.
   [Hernandez, Maria Valdes; Maniega, Susana Munoz; Hamilton, Iona F.; Royle, Natalie A.; Bastin, Mark E.; Wardlaw, Joanna] Univ Edinburgh, Brain Res Imaging Ctr, Edinburgh EH8 9JZ, Midlothian, Scotland.
   [Hernandez, Maria Valdes; Hamilton, Iona F.; Royle, Natalie A.; Bastin, Mark E.; Wardlaw, Joanna] Univ Edinburgh, Ctr Clin Brain Sci, Edinburgh EH8 9JZ, Midlothian, Scotland.
   [Hernandez, Maria Valdes; Maniega, Susana Munoz; Hamilton, Iona F.; Royle, Natalie A.; Bastin, Mark E.; Wardlaw, Joanna] Univ Edinburgh, Dept Neuroimaging Sci, SINAPSE, Edinburgh EH8 9JZ, Midlothian, Scotland.
   [Chauhan, Ganesh; Debette, Stephanie] INSERM, Res Ctr Epidemiol & Biostat U897, Team Neuroepidemiol, Bordeaux, France.
   [Chauhan, Ganesh; Debette, Stephanie] Univ Bordeaux, Bordeaux, France.
   [Bis, Joshua C.] Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
   [Bis, Joshua C.] Univ Washington, Dept Med, Seattle, WA USA.
   [Debette, Stephanie; Seshadri, Sudha] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02215 USA.
   [Debette, Stephanie] Bordeaux Univ Hosp, Dept Neurol, Bordeaux, France.
   [DeCarli, Charles] Univ Calif Davis, Dept Neurol, Davis, CA 95616 USA.
   [DeCarli, Charles] Univ Calif Davis, Ctr Neurosci, Davis, CA 95616 USA.
   [Fornage, Myriam] Univ Texas Hlth Sci Ctr Houston, Sch Publ Hlth, Div Epidemiol, Brown Fdn Inst Mol Med, Houston, TX 77030 USA.
   [Fornage, Myriam] Univ Texas Hlth Sci Ctr Houston, Sch Publ Hlth, Div Epidemiol, Ctr Human Genet, Houston, TX 77030 USA.
   [Schmidt, Reinhold] Med Univ Graz, Dept Neurol, Graz, Austria.
   [Ikram, M. Arfan] Eramus MC Univ, Med Ctr, Dept Epidemiol, Rotterdam, Netherlands.
   [Ikram, M. Arfan] Eramus MC Univ, Med Ctr, Dept Radiol & Neurol, Rotterdam, Netherlands.
   [Launer, Lenore J.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
   [Seshadri, Sudha; CHARGE Consortium] Framingham Heart Dis Epidemiol Study, Framingham, MA USA.
RP Luciano, M (reprint author), Univ Edinburgh, Psychol, 7 George Sq, Edinburgh EH8 9JZ, Midlothian, Scotland.
EM michelle.luciano@ed.ac.uk
OI Seshadri, Sudha/0000-0001-6135-2622
FU Chief Scientist Office (CSO) of the Scottish Government Health
   Directorates [CZD/16/6]; Scottish Funding Council [HR03006]; BBSRC; Age
   UK's The Disconnected Mind project; UK's Biotechnology and Biological
   Sciences Research Council (BBSRC); Medical Research Council; Scottish
   Funding Council SINAPSE Collaboration; National Heart, Lung, and Blood
   Institute (NHLBI) [HL105756]; National Institute on Ageing (NIA) [AG
   033193]; ADCC [P30 010129]; NIA [N01-AG-12100, AG023629, R01AG15928,
   R01AG20098, AG008122, AG033193]; NHLBI [HL105756, HHSN268201100005C,
   HHSN268201100006C, HHSN268201100007C, HHSN268201100008C,
   HHSN268201100009C, HHSN268201100010C, HHSN268201100011C,
   HHSN268201100012C, R01HL087641, R01HL59367, R01HL086694, N01-HC-55015,
   N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021,
   N01-HC-55022, R01-HL087641, U01 HL096917, R01-HL093029,
   HHSN268201200036C, HHSN268200800007C, N01HC55222, N01HC85079,
   N01HC85080, N01HC85081, N01HC85082, N01HC85083, N01HC85086, HL080295,
   HL087652, HL103612, HL068986, HL120393, HL093029, HL096917, NS087541];
   National Human Genome Research Institute [U01HG004402]; NIH
   [HHSN268200625226C]; National Institutes of Health [UL1RR025005]; ASPS:
   The Austrian Science Fund (FWF) [P20545-P05, P13180]; National Center
   for Advancing Translational Sciences, CTSI [UL1TR000124]; National
   Institute of Diabetes and Digestive, and Kidney Disease Diabetes
   Research Center (DRC) [DK063491]; NHLBI's Framingham Heart Study
   [N01-HC-25195]; Affymetrix, Inc [N02-HL-6-4278]; NINDS [R01 NS17950];
   Fondation pour la Recherche Medicale; Caisse Nationale Maladie des
   Travailleurs Salaries; Direction Generale de la Sante; Mutuelle Generale
   de l'Education Nationale (MGEN); Institut de la Longevite; Conseils
   Regionaux of Aquitaine and Bourgogne; Fondation de France; Ministry of
   Research-INSERM Programme 'Cohortes et collections de donnees
   biologiques'; Eisai; National Foundation for Alzheimer's Disease and
   Related Disorders; Institut Pasteur de Lille; Centre National de
   Genotypage; Fondation Leducq; Erasmus Medical Center; Erasmus
   University, Rotterdam; Netherlands Organization for the Health Research
   and Development (ZonMw); Research Institute for Diseases in the Elderly
   (RIDE); Ministry of Education, Culture and Science; Ministry for Health,
   Welfare and Sports; European Commission; Municipality of Rotterdam; NIH
   Roadmap for Medical Research
FX GS:SFHS has received core funding from the Chief Scientist Office (CSO)
   of the Scottish Government Health Directorates CZD/16/6 and the Scottish
   Funding Council HR03006. Phenotype collection in the LBC1921 was
   supported by the BBSRC, The Royal Society, and the CSO of the Scottish
   Government. LBC1936 phenotype collection was supported by Research Into
   Ageing (now part of Age UK's The Disconnected Mind project). LBC
   genotyping was supported by the UK's Biotechnology and Biological
   Sciences Research Council (BBSRC). The work was undertaken by The
   University of Edinburgh Centre for Cognitive Ageing and Cognitive
   Epidemiology, part of the cross-council Life-long Health and Wellbeing
   Initiative (MR/K026992/1), with funding from the BBSRC and Medical
   Research Council. Imaging was performed in the Brain Research Imaging
   Centre, Edinburgh, supported by the Scottish Funding Council SINAPSE
   Collaboration.; Infrastructure for the CHARGE Consortium is supported in
   part by the National Heart, Lung, and Blood Institute (NHLBI) grant
   HL105756 and for the neurology working group of CHARGE (neuroCHARGE)
   through a grant from the National Institute on Ageing (NIA), AG 033193.
   CDC acknowledges support from ADCC grant P30 010129. AGES: Age, Gene,
   Environment Susceptibility Reykjavik Study: This study has been funded
   by NIA contract N01-AG-12100 with contributions from NEI, NIDCD, and
   NHLBI, the NIA Intramural Research Program, Hjartavernd (the Icelandic
   Heart Association), and the Althingi (the Icelandic Parliament). ARIC:
   The Atherosclerosis Risk in Communities Study is carried out as a
   collaborative study supported by NHLBI contracts (HHSN268201100005C,
   HHSN268201100006C, HHSN268201100007C, HHSN268201100008C,
   HHSN268201100009C, HHSN268201100010C, HHSN268201100011C, and
   HHSN268201100012C), R01HL087641, R01HL59367, and R01HL086694; National
   Human Genome Research Institute contract U01HG004402; NIH contract
   HHSN268200625226C, NHLBI contracts N01-HC-55015, N01-HC-55016,
   N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021, N01-HC-55022,
   and grants R01-HL087641, U01 HL096917, and R01-HL093029 (Fornage).
   Infrastructure was partly supported by Grant Number UL1RR025005, a
   component of the National Institutes of Health and NIH Roadmap for
   Medical Research. ASPS: The Austrian Science Fund (FWF) grant number
   P20545-P05 and P13180. The Medical University of Graz. CHS:
   Cardiovascular Health Study: This CHS research was supported by NHLBI
   contracts HHSN268201200036C, HHSN268200800007C, N01HC55222, N01HC85079,
   N01HC85080, N01HC85081, N01HC85082, N01HC85083, N01HC85086; and NHLBI
   grants HL080295, HL087652, HL105756, HL103612, HL068986, and HL120393
   with additional contribution from the National Institute of Neurological
   Disorders and Stroke (NINDS). Additional support was provided through
   AG023629, R01AG15928, and R01AG20098 from NIA. A full list of principal
   CHS investigators and institutions can be found at CHS-NHLBI.org/. The
   provision of genotyping data was supported in part by the National
   Center for Advancing Translational Sciences, CTSI grant UL1TR000124, and
   the National Institute of Diabetes and Digestive, and Kidney Disease
   Diabetes Research Center (DRC) grant DK063491 to the Southern California
   Diabetes Endocrinology Research Center. FHS: Framingham Heart Study:
   This work was supported by the NHLBI's Framingham Heart Study (Contract
   No. N01-HC-25195) and its contract with Affymetrix, Inc for genotyping
   services (Contract No. N02-HL-6-4278). This study as also supported by
   grants from the NIA: AG008122 and AG033193, the NINDS (R01 NS17950), and
   the NHLBI (HL093029, HL096917, NS087541). Three City Study (3C): The 3C
   Study is conducted under a partnership agreement between the Institut
   National de la Sante et de la Recherche Medicale (INSERM), the Victor
   Segalen-Bordeaux II University, and Sanofi-Aventis. The Fondation pour
   la Recherche Medicale funded the preparation and initiation of the
   study. The 3C Study is also supported by the Caisse Nationale Maladie
   des Travailleurs Salaries, Direction Generale de la Sante, Mutuelle
   Generale de l'Education Nationale (MGEN), Institut de la Longevite,
   Conseils Regionaux of Aquitaine and Bourgogne, Fondation de France, and
   Ministry of Research-INSERM Programme 'Cohortes et collections de
   donnees biologiques'. Lille Genopole received an unconditional grant
   from Eisai.; This work was supported by the National Foundation for
   Alzheimer's Disease and Related Disorders, the Institut Pasteur de Lille
   and the Centre National de Genotypage. Ganesh Chauhan is supported by a
   grant from the Fondation Leducq. RS: The Rotterdam Study is funded by
   Erasmus Medical Center and Erasmus University, Rotterdam, the
   Netherlands Organization for the Health Research and Development
   (ZonMw), the Research Institute for Diseases in the Elderly (RIDE), the
   Ministry of Education, Culture and Science, the Ministry for Health,
   Welfare and Sports, the European Commission (DG XII), and the
   Municipality of Rotterdam.
NR 35
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PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1832-4274
EI 1839-2628
J9 TWIN RES HUM GENET
JI Twin Res. Hum. Genet.
PD DEC
PY 2015
VL 18
IS 6
BP 738
EP 745
DI 10.1017/thg.2015.71
PG 8
WC Genetics & Heredity; Obstetrics & Gynecology
SC Genetics & Heredity; Obstetrics & Gynecology
GA CZ5RF
UT WOS:000367159000013
PM 26427786
ER

PT J
AU Imbrogno, S
   Mazza, R
   Pugliese, C
   Filice, M
   Angelone, T
   Loh, YP
   Tota, B
   Cerra, MC
AF Imbrogno, S.
   Mazza, R.
   Pugliese, C.
   Filice, M.
   Angelone, T.
   Loh, Y. P.
   Tota, B.
   Cerra, M. C.
TI Myocardial actions of the chromogranin A-derived pyroglutaminated
   serpinin in the goldfish (Carassius auratus) and in the frog (Rana
   esculenta)
SO VASCULAR PHARMACOLOGY
LA English
DT Meeting Abstract
C1 [Imbrogno, S.; Mazza, R.; Pugliese, C.; Filice, M.; Angelone, T.; Tota, B.; Cerra, M. C.] Univ Calabria, Dept Biol Ecol & Earth Sci, I-87036 Arcavacata Di Rende, CS, Italy.
   [Loh, Y. P.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1537-1891
EI 1879-3649
J9 VASC PHARMACOL
JI Vasc. Pharmacol.
PD DEC
PY 2015
VL 75
BP 58
EP 59
DI 10.1016/j.vph.2015.11.080
PG 2
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA CZ3UH
UT WOS:000367029000052
ER

PT J
AU Rodenbach, KE
   Schneider, MF
   Furth, SL
   Moxey-Mims, MM
   Mitsnefes, MM
   Weaver, DJ
   Warady, BA
   Schwartz, GJ
AF Rodenbach, Kyle E.
   Schneider, Michael F.
   Furth, Susan L.
   Moxey-Mims, Marva M.
   Mitsnefes, Mark M.
   Weaver, Donald J.
   Warady, Bradley A.
   Schwartz, George J.
TI Hyperuricemia and Progression of CKD in Children and Adolescents: The
   Chronic Kidney Disease in Children (CKiD) Cohort Study
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Article
DE Uric acid; urate; hyperuricemia; risk factor; chronic kidney disease
   (CKD); CKD progression; disease trajectory; pediatric kidney disease;
   children; adolescents; CKiD (Chronic Kidney Disease in Children);
   end-stage renal disease (ESRD); glomerular filtration rate (GFR); renal
   replacement therapy (RRT); renal function decline
ID SERUM URIC-ACID; PEDIATRIC REFERENCE INTERVALS; BLOOD-PRESSURE;
   ESSENTIAL-HYPERTENSION; BIOCHEMICAL ANALYTES; CARDIOVASCULAR RISK;
   RENAL-DISEASE; FOLLOW-UP; ALLOPURINOL; HEALTHY
AB Background: Hyperuricemia is associated with essential hypertension in children. No previous studies have evaluated the effect of hyperuricemia on progression of chronic kidney disease (CKD) in children.
   Study Design: Prospective observational cohort study.
   Setting & Participants: Children and adolescents (n = 678 cross-sectional; n = 627 longitudinal) with a median age of 12.3 (IQR, 8.6-15.6) years enrolled at 52 North American sites of the CKiD (CKD in Children) Study.
   Predictor: Serum uric acid level (<5.5, 5.5-7.5, and >7.5 mg/dL).
   Outcomes: Composite end point of either >30% decline in glomerular filtration rate (GFR) or initiation of renal replacement therapy.
   Measurements: Age, sex, race, blood pressure status, GFR, CKD cause, urine protein-creatinine ratio (<0.5, 0.5-<2.0, and >= 2.0 mg/mg), age- and sex-specific body mass index > 95th percentile, use of diuretics, and serum uric acid level.
   Results: Older age, male sex, lower GFR, and body mass index. 95th percentile were associated with higher uric acid levels. 162, 294, and 171 participants had initial uric acid levels <5.5, 5.5 to >7.5, or.7.5 mg/dL, respectively. We observed 225 instances of the composite end point over 5 years. In a multivariable parametric time-to-event analysis, compared with participants with initial uric acid levels <5.5 mg/dL, those with uric acid levels of 5.5 to 7.5 or >7.5 mg/dL had 17% shorter (relative time, 0.83; 95% CI, 0.62-1.11) or 38% shorter (relative time, 0.62; 95% CI, 0.45-0.85) times to event, respectively. Hypertension, lower GFR, glomerular CKD cause, and elevated urine protein-creatinine ratio were also associated with faster times to the composite end point.
   Limitations: The study lacked sufficient data to examine how use of specific medications might influence serum uric acid levels and CKD progression.
   Conclusions: Hyperuricemia is a previously undescribed independent risk factor for faster progression of CKD in children and adolescents. It is possible that treatment of children and adolescents with CKD with urate-lowering therapy could slow disease progression. (C) 2015 by the National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
C1 [Rodenbach, Kyle E.; Schwartz, George J.] Univ Rochester, Med Ctr, Rochester, NY 14642 USA.
   [Schneider, Michael F.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
   [Furth, Susan L.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
   [Mitsnefes, Mark M.] NIDDK, Bethesda, MD 20892 USA.
   [Mitsnefes, Mark M.] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
   [Weaver, Donald J.] Levine Childrens Hosp, Charlotte, NC USA.
   [Warady, Bradley A.] Childrens Mercy Hosp, Kansas City, MO 64108 USA.
RP Schwartz, GJ (reprint author), Univ Rochester, Box 777,Room 4-8105,601 Elmwood Ave, Rochester, NY 14642 USA.
EM george_schwartz@urmc.rochester.edu
FU NIDDK; National Institute of Neurological Disorders and Stroke; Eunice
   Kennedy Shriver National Institute of Child Health and Human
   Development; National Heart, Lung and Blood Institute [U01 DK82194,
   U01-DK-66143, U01-DK-66174, U01-DK-66116]; Strong Children's Research
   Center of the University of Rochester Department of Pediatrics
FX The CKiD Study is funded by the NIDDK, with additional funding from the
   National Institute of Neurological Disorders and Stroke, the Eunice
   Kennedy Shriver National Institute of Child Health and Human
   Development, and the National Heart, Lung and Blood Institute (U01
   DK82194, U01-DK-66143, U01-DK-66174, and U01-DK-66116). The NIDDK had a
   role in the study design. Mr Rodenbach was also supported by the Strong
   Children's Research Center of the University of Rochester Department of
   Pediatrics for a summer fellowship in 2013, during which time he began
   work on the uric acid project. GE Healthcare provided the Omnipaque
   300<SUP>T</SUP> for the iohexol GFR studies, and Paula Maier performed
   data entry.
NR 41
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PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0272-6386
EI 1523-6838
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD DEC
PY 2015
VL 66
IS 6
BP 984
EP 992
DI 10.1053/j.ajkd.2015.06.015
PG 9
WC Urology & Nephrology
SC Urology & Nephrology
GA CZ0ZP
UT WOS:000366835700014
PM 26209544
ER

PT J
AU Paz-Soldan, VA
   Morrison, AC
   Lopez, JJC
   Lenhart, A
   Scott, TW
   Elder, JP
   Sihuincha, M
   Kochel, TJ
   Halsey, ES
   Astete, H
   McCall, PJ
AF Paz-Soldan, Valerie A.
   Morrison, Amy C.
   Cordova Lopez, Jhonny J.
   Lenhart, Audrey
   Scott, Thomas W.
   Elder, John P.
   Sihuincha, Moises
   Kochel, Tadeusz J.
   Halsey, Eric S.
   Astete, Helvio
   McCall, Philip J.
TI Dengue Knowledge and Preventive Practices in Iquitos, Peru
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID AEDES-AEGYPTI DIPTERA; CULICIDAE PRODUCTION; VIRUS TRANSMISSION;
   CONTROLLED-TRIAL; CONTROL PROGRAM; VECTOR; URBAN; ACCEPTABILITY;
   INTEREPIDEMIC; EPIDEMIOLOGY
AB As part of a cluster-randomized trial to evaluate insecticide-treated curtains for dengue prevention in Iquitos, Peru, we surveyed 1,333 study participants to examine knowledge and reported practices associated with dengue and its prevention. Entomological data from 1,133 of these households were linked to the survey. Most participants knew that dengue was transmitted by mosquito bite (85.6%), but only few (18.6%) knew that dengue vectors bite during daytime. Most commonly recognized dengue symptoms were fever (86.6%), headache (76.4%), and muscle/joint pain (67.9%). Most commonly reported correct practices for mosquito control were cleaning homes (61.6%), using insecticide sprays (23%), and avoiding having standing water at home (12.3%). Higher education was associated with higher knowledge about dengue, including transmission and vector control. Higher socioeconomic status was associated with increased reported use of preventive practices requiring money expenditure. We were less likely to find Aedes aegypti eggs, larvae, or pupae in households that had < 5-year-old children at home. Although dengue has been transmitted in Iquitos since the 1990s and the Regional Health Authority routinely fumigates households, treats domestic water containers with larvicide, and issues health education messages through mass media, knowledge of dengue transmission and household practices for prevention could be improved.
C1 [Paz-Soldan, Valerie A.] Tulane Univ, Sch Publ Hlth & Trop Med, Global Community Hlth & Behav Sci Dept, New Orleans, LA 70112 USA.
   Univ Peruana Cayetano Heredia, Fac Salud Publ & Adm, Lima, Peru.
   [Astete, Helvio] United States Naval Med Res Unit 6, Iquitos, Peru.
   [Morrison, Amy C.; Scott, Thomas W.] Univ Calif Davis, Dept Entomol & Nematol, Davis, CA 95616 USA.
   Univ Liverpool Liverpool Sch Trop Med, Iquitos, Peru.
   [McCall, Philip J.] Univ Liverpool, Liverpool Sch Trop Med, Vector Biol Dept, Liverpool L3 5QA, Merseyside, England.
   [Scott, Thomas W.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
   San Diego State Univ, IBACH, San Diego, CA 92182 USA.
   [Sihuincha, Moises] Hosp Apoyo, Dept Internal Med, Iquitos, Peru.
   [Kochel, Tadeusz J.] Naval Med Res Ctr, Dept Virol, Silver Spring, MD USA.
   Ctr Dis Control & Prevent, Malaria Branch, Atlanta, GA USA.
   [Cordova Lopez, Jhonny J.] US Naval Med Res Ctr Detachment, Iquitos, Peru.
   [Lenhart, Audrey] US Ctr Dis Control & Prevent, Entomol Branch, Div Parasit Dis & Malaria, Ctr Global Hlth, Atlanta, GA USA.
   [Elder, John P.] San Diego State Univ, Sch Publ Hlth, San Diego, CA 92182 USA.
   [Halsey, Eric S.] Ctr Dis Control & Prevent, Atlanta, GA USA.
RP Paz-Soldan, VA (reprint author), Tulane Univ, Sch Publ Hlth & Trop Med, Global Community Hlth & Behav Sci Dept, 1440 Canal St,Suite 2200, New Orleans, LA 70112 USA.
EM vpazsold@tulane.edu; amy.aegypti@gmail.com; jjcordova_2000@hotmail.com;
   aj18@cdc.gov; twscott@ucdavis.edu; jelder@mail.sdsu.edu;
   sihuincha@hotmail.com; Tadeusz.Kochel@nbacc.dhs.gov; ycw8@cdc.gov;
   astetehelvio@gmail.com; philip.mccall@lstmed.ac.uk
FU Wellcome Trust [WT085714MA]; U.S. National Institutes of Health,
   National Institute of Allergy and Infectious Diseases (NIH/MAID) [R01
   AI069341-01]; NIH/NIAID [P01 AI098670]; Armed Forces Health Surveillance
   Center Global Emerging Infections Systems Research Program
   [847705.82000.25GB.B0016]; Military Infectious Disease Research Program
   [S0263_10_LI, S0216_09_LI]; Fogarty International Center [K01
   TW008414-01A1]; Research and Policy for Infectious Disease Dynamics
   (RAPIDD) program of the Science and Technology Directorate, U.S.
   Department of Homeland Security; Fogarty International Center, National
   Institutes of Health
FX This research was supported by funding from the Wellcome Trust
   (WT085714MA), the U.S. National Institutes of Health, National Institute
   of Allergy and Infectious Diseases (NIH/MAID) award number R01
   AI069341-01, the NIH/NIAID award number P01 AI098670, the Armed Forces
   Health Surveillance Center Global Emerging Infections Systems Research
   Program (847705.82000.25GB.B0016), and the Military Infectious Disease
   Research Program (S0263_10_LI and S0216_09_LI). Valerie A. Paz-Soldan
   received supported from the Fogarty International Center, award number
   K01 TW008414-01A1. Thomas W. Scott received support from the Research
   and Policy for Infectious Disease Dynamics (RAPIDD) program of the
   Science and Technology Directorate, U.S. Department of Homeland
   Security, and the Fogarty International Center, National Institutes of
   Health.
NR 34
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PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
EI 1476-1645
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD DEC
PY 2015
VL 93
IS 6
BP 1330
EP 1337
DI 10.4269/ajtmh.15-0096
PG 8
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA CY6TD
UT WOS:000366540800034
PM 26503276
ER

PT J
AU Goedeke, L
   Rotllan, N
   Ramirez, CM
   Aranda, JF
   Canfran-Duque, A
   Araldi, E
   Fernandez-Hernando, A
   Langhi, C
   de Cabo, R
   Baldan, A
   Suarez, Y
   Fernandez-Hernando, C
AF Goedeke, Leigh
   Rotllan, Noemi
   Ramirez, Cristina M.
   Aranda, Juan F.
   Canfran-Duque, Alberto
   Araldi, Elisa
   Fernandez-Hernando, Ana
   Langhi, Cedric
   de Cabo, Rafael
   Baldan, Angel
   Suarez, Yajaira
   Fernandez-Hernando, Carlos
TI miR-27b inhibits LDLR and ABCA1 expression but does not influence plasma
   and hepatic lipid levels in mice
SO ATHEROSCLEROSIS
LA English
DT Article
DE miRNAs; miR-27b; LDLR; ABCA1; Lipid homeostasis; Atherosclerosis
ID CHOLESTEROL HOMEOSTASIS; FAMILIAL HYPERCHOLESTEROLEMIA; CELLULAR
   CHOLESTEROL; MOUSE MODELS; METABOLISM; MICRORNAS; RECEPTOR;
   ATHEROSCLEROSIS; PATHWAY; BINDING
AB Rationale: Recently, there has been significant interest in the therapeutic administration of miRNA mimics and inhibitors to treat cardiovascular disease. In particular, miR-27b has emerged as a regulatory hub in cholesterol and lipid metabolism and potential therapeutic target for treating atherosclerosis. Despite this, the impact of miR-27b on lipid levels in vivo remains to be determined. As such, here we set out to further characterize the role of miR-27b in regulating cholesterol metabolism in vitro and to determine the effect of miR-27b overexpression and inhibition on circulating and hepatic lipids in mice.
   Methods and results: Our results identify miR-27b as an important regulator of LDLR activity in human and mouse hepatic cells through direct targeting of LDLR and LDLRAP1. In addition, we report that modulation of miR-27b expression affects ABCA1 protein levels and cellular cholesterol efflux to ApoA1 in human hepatic Huh7 cells. Overexpression of pre-miR-27b in the livers of wild-type mice using AAV8 vectors increased pre-miR-27b levels 50efold and reduced hepatic ABCA1 and LDLR expression by 50% and 20%, respectively, without changing circulating and hepatic cholesterol and triglycerides. To determine the effect of endogenous miR-27b on circulating lipids, wild-type mice were fed a Western diet for one month and injected with 5 mg/kg of LNA control or LNA anti-miR-27b oligonucleotides. Following two weeks of treatment, the expression of ABCA1 and LDLR were increased by 10-20% in the liver, demonstrating effective inhibition of miR-27b function. Intriguingly, no differences in circulating and hepatic lipids were observed between treatment groups.
   Conclusions: The results presented here provide evidence that short-term modulation of miR-27b expression in wild-type mice regulates hepatic LDLR and ABCA1 expression but does not influence plasma and hepatic lipid levels. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
C1 [Goedeke, Leigh; Rotllan, Noemi; Ramirez, Cristina M.; Aranda, Juan F.; Canfran-Duque, Alberto; Araldi, Elisa; Fernandez-Hernando, Ana; Suarez, Yajaira; Fernandez-Hernando, Carlos] Yale Univ, Sch Med, Comparat Med Sect, Dept Pathol,Program Integrat Cell Signaling & Neu, New Haven, CT 06520 USA.
   [Goedeke, Leigh; Rotllan, Noemi; Ramirez, Cristina M.; Aranda, Juan F.; Canfran-Duque, Alberto; Araldi, Elisa; Fernandez-Hernando, Ana; Suarez, Yajaira; Fernandez-Hernando, Carlos] Yale Univ, Sch Med, Vasc Biol & Therapeut Program, New Haven, CT 06520 USA.
   [de Cabo, Rafael] NIA, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
   [Langhi, Cedric; Baldan, Angel] St Louis Univ, Sch Med, Ctr Cardiovasc Res, Edward A Doisy Dept Biochem & Mol Biol, St Louis, MO USA.
RP Fernandez-Hernando, C (reprint author), 10 Amistad St,Room 320, New Haven, CT 06520 USA.
EM carlos.fernandez@yale.edu
RI de Cabo, Rafael/J-5230-2016; 
OI de Cabo, Rafael/0000-0002-3354-2442; Ramirez, Cristina
   M/0000-0003-2589-0786; , rafael/0000-0003-2830-5693
FU National Institutes of Health [R01HL107953, R01HL107953-04S1,
   R01HL106063, R01HL105945, 1F31AG043318, R01HL107794]; American Heart
   Association [15SDG23000025, GRNT20460189]; Howard Hughes Medical
   Institute International Student Research Fellowship; Foundation Leducq
   Transatlantic Network of Excellence in Cardiovascular Research
FX This work was supported by grants from the National Institutes of Health
   (R01HL107953, R01HL107953-04S1, and R01HL106063 to CF-H; R01HL105945 to
   YS; 1F31AG043318 to LG; and R01HL107794 to AB), the American Heart
   Association (15SDG23000025 to CMR and GRNT20460189 to AB), the Howard
   Hughes Medical Institute International Student Research Fellowship (to
   EA), and the Foundation Leducq Transatlantic Network of Excellence in
   Cardiovascular Research (to CFH).
NR 41
TC 9
Z9 9
U1 1
U2 3
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 DEC
PY 2015
VL 243
IS 2
BP 499
EP 509
DI 10.1016/j.atherosclerosis.2015.09.033
PG 11
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA CY6QO
UT WOS:000366534100022
PM 26520906
ER

PT J
AU Kreitman, RJ
   Pastan, I
AF Kreitman, Robert J.
   Pastan, Ira
TI Immunoconjugates in the management of hairy cell leukemia
SO BEST PRACTICE & RESEARCH CLINICAL HAEMATOLOGY
LA English
DT Article
DE Moxetumomab pasudotox; BL22; CD22; CD25; Recombinant immunotoxin;
   Pseudomonas exotoxin
ID TERM-FOLLOW-UP; IMMUNOTOXIN RFB4(DSFV)-PE38 BL22; CHRONIC
   LYMPHOCYTIC-LEUKEMIA; SINGLE-CHAIN IMMUNOTOXIN; PHASE-I TRIAL;
   PSEUDOMONAS-EXOTOXIN; RECOMBINANT IMMUNOTOXIN; DIPHTHERIA-TOXIN;
   CYTOTOXIC ACTIVITY; ANTI-TAC
AB Hairy cell leukemia (HCL) is an indolent B-cell malignancy effectively treated but not often cured by purine analog therapy; after multiple courses of purine analogs, patients can become purine analog resistant and in need of alternative therapies. Complete remission to single-agent purine analog is often accompanied by minimal residual disease (MRD), residual HCL cells detectable by immunologic methods, considered a risk factor for eventual relapse. Several different non-chemotherapy approaches are being used to target relapsed and refractory HCL, including inhibitors of BRAF, but so far only monoclonal antibody (MAb)-based approaches have been reported to eliminate MRD in a high percentage of patients. One of the MAb-based options for HCL currently under clinical investigation involves recombinant immunotoxins, containing a fragment of a MAb and a bacterial toxin. The bacterial toxin, a highly potent fragment from Pseudomonas exotoxin, catalytically ADP-ribosylates elongation factor 2 (EF2), resulting in protein synthesis inhibition and apoptotic cell death. Recombinant immunotoxins tested in HCL patients include LMB-2, targeting CD25, and BL22, targeting CD22. An affinity matured version of BL22, termed moxetumomab pasudotox (formerly HA22 or CAT-8015) achieved high CR rates in phase I, and is currently undergoing multicenter Phase 3 testing. Phase I testing was without dose-limiting toxicity, although 2 patients had grade 2 hemolytic uremic syndrome (HUS) with transient grade 1 abnormalities in platelets and creatinine. Preclinical work is underway to identify residues on moxetumomab pasudotox leading to immunogenicity. Moxetumomab pasudotox is undergoing pivotal testing for relapsed and refractory HCL. Published by Elsevier Ltd.
C1 [Kreitman, Robert J.; Pastan, Ira] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Kreitman, RJ (reprint author), NCI, Mol Biol Lab, NIH, 37-5124B,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM kreitmar@mail.nih.gov
FU NIH; Hairy Cell Leukemia Foundation
FX Research in this review was supported in part by the intramural program
   of the NIH and the Hairy Cell Leukemia Foundation.
NR 79
TC 6
Z9 6
U1 0
U2 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1521-6926
EI 1532-1924
J9 BEST PRACT RES CL HA
JI Best Pract. Res. Clin. Haematol.
PD DEC
PY 2015
VL 28
IS 4
BP 236
EP 245
DI 10.1016/j.beha.2015.09.003
PG 10
WC Hematology
SC Hematology
GA CZ0BU
UT WOS:000366770900010
PM 26614902
ER

PT J
AU Natrajan, MS
   de la Fuente, AG
   Crawford, AH
   Linehan, E
   Nunez, V
   Johnson, KR
   Wu, TX
   Fitzgerald, DC
   Ricote, M
   Bielekova, B
   Franklin, RJM
AF Natrajan, Muktha S.
   de la Fuente, Alerie G.
   Crawford, Abbe H.
   Linehan, Eimear
   Nunez, Vanessa
   Johnson, Kory R.
   Wu, Tianxia
   Fitzgerald, Denise C.
   Ricote, Mercedes
   Bielekova, Bibiana
   Franklin, Robin J. M.
TI Retinoid X receptor activation reverses age-related deficiencies in
   myelin debris phagocytosis and remyelination
SO BRAIN
LA English
DT Article
DE remyelination; ageing; retinoid X receptor; myelin debris;
   monocyte-derived macrophages
ID CENTRAL-NERVOUS-SYSTEM; OLIGODENDROCYTE PRECURSOR CELLS;
   MULTIPLE-SCLEROSIS LESIONS; CNS REMYELINATION; ADULT CNS; ALTERNATIVE
   ACTIVATION; LUPUS-ERYTHEMATOSUS; T-CELLS; MACROPHAGES; MICROGLIA
AB The efficiency of central nervous system remyelination declines with age. This is in part due to an age-associated decline in the phagocytic removal of myelin debris, which contains inhibitors of oligodendrocyte progenitor cell differentiation. In this study, we show that expression of genes involved in the retinoid X receptor pathway are decreased with ageing in both myelin-phagocytosing human monocytes and mouse macrophages using a combination of in vivo and in vitro approaches. Disruption of retinoid X receptor function in young macrophages, using the antagonist HX531, mimics ageing by reducing myelin debris uptake. Macrophage-specific RXR alpha (Rxra) knockout mice revealed that loss of function in young mice caused delayed myelin debris uptake and slowed remyelination after experimentally-induced demyelination. Alternatively, retinoid X receptor agonists partially restored myelin debris phagocytosis in aged macrophages. The agonist bexarotene, when used in concentrations achievable in human subjects, caused a reversion of the gene expression profile in multiple sclerosis patient monocytes to a more youthful profile and enhanced myelin debris phagocytosis by patient cells. These results reveal the retinoid X receptor pathway as a positive regulator of myelin debris clearance and a key player in the age-related decline in remyelination that may be targeted by available or newly-developed therapeutics.
C1 [Natrajan, Muktha S.; de la Fuente, Alerie G.; Crawford, Abbe H.; Franklin, Robin J. M.] Univ Cambridge, Wellcome Trust MRC Cambridge Stem Cell Inst, Cambridge CB2 0AH, England.
   [Natrajan, Muktha S.; de la Fuente, Alerie G.; Crawford, Abbe H.; Franklin, Robin J. M.] Univ Cambridge, Dept Clin Neurosci, Cambridge CB2 0AH, England.
   [Natrajan, Muktha S.; Johnson, Kory R.; Wu, Tianxia; Bielekova, Bibiana] NINDS, Neuroimmunol Dis Unit, NIH, Bethesda, MD 20892 USA.
   [Linehan, Eimear; Fitzgerald, Denise C.] Queens Univ Belfast, Ctr Infect & Immun, Belfast BT7 1NN, Antrim, North Ireland.
   [Nunez, Vanessa; Ricote, Mercedes] Ctr Nacl Invest Cardiovasc Carlos III CNIC, Dept Cardiovasc Dev & Repair, Madrid, Spain.
RP Franklin, RJM (reprint author), Univ Cambridge, Wellcome Trust MRC Cambridge Stem Cell Inst, Clifford Allbutt Bldg,Cambridge Biomed Campus, Cambridge CB2 0AH, England.
EM Bibi.Bielekova@nih.gov; rjf1000@cam.ac.uk
RI Ricote, Mercedes/L-4615-2014
OI Ricote, Mercedes/0000-0002-8090-8902
FU UK Multiple Sclerosis Society; Wellcome-Trust; NINDS/NIH Intramural
   Research Program; Health Research Board Scholars Program;
   Gates-Cambridge Scholarship; Spanish Ministry of Economy and
   Competitiveness [SAF2012-31483]
FX This work was supported by grants from the UK Multiple Sclerosis
   Society, Wellcome-Trust, NINDS/NIH Intramural Research Program, Health
   Research Board Scholars Program, Gates-Cambridge Scholarship, and
   Spanish Ministry of Economy and Competitiveness (SAF2012-31483).
NR 70
TC 8
Z9 8
U1 1
U2 10
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0006-8950
EI 1460-2156
J9 BRAIN
JI Brain
PD DEC 1
PY 2015
VL 138
BP 3581
EP 3597
DI 10.1093/brain/awv289
PN 12
PG 17
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA CY4NK
UT WOS:000366384600020
PM 26463675
ER

PT J
AU Wang, TW
   Vermeulen, RCH
   Hu, W
   Liu, G
   Xiao, XH
   Alekseyev, Y
   Xu, J
   Reiss, B
   Steiling, K
   Downward, GS
   Silverman, DT
   Wei, FS
   Wu, GP
   Li, JH
   Lenburg, ME
   Rothman, N
   Spira, A
   Lan, Q
AF Wang, Teresa W.
   Vermeulen, Roel C. H.
   Hu, Wei
   Liu, Gang
   Xiao, Xiaohui
   Alekseyev, Yuriy
   Xu, Jun
   Reiss, Boris
   Steiling, Katrina
   Downward, George S.
   Silverman, Debra T.
   Wei, Fusheng
   Wu, Guoping
   Li, Jihua
   Lenburg, Marc E.
   Rothman, Nathaniel
   Spira, Avrum
   Lan, Qing
TI Gene-expression profiling of buccal epithelium among non-smoking women
   exposed to household air pollution from smoky coal
SO CARCINOGENESIS
LA English
DT Article
ID LUNG-CANCER RISK; ENDOTHELIAL GROWTH-FACTOR; XUAN-WEI; CIGARETTE-SMOKE;
   DIAGNOSTIC EVALUATION; COMBUSTION EMISSIONS; ENRICHMENT ANALYSIS;
   BRONCHIAL AIRWAY; FUYUAN COUNTIES; HEALTH IMPACTS
AB In China's rural counties of Xuanwei and Fuyuan, lung cancer rates are among the highest in the world. While the elevated disease risk in this population has been linked to the usage of smoky (bituminous) coal as compared to smokeless (anthracite) coal, the underlying molecular changes associated with this exposure remains unclear. To understand the physiologic effects of smoky coal exposure, we analyzed the genome-wide gene-expression profiles in buccal epithelial cells collected from healthy, non-smoking female residents of Xuanwei and Fuyuan who burn smoky (n = 26) and smokeless (n = 9) coal. Gene-expression was profiled via microarrays, and changes associated with coal type were correlated to household levels of fine particulate matter (PM 2.5) and polycyclic aromatic hydrocarbons (PAHs). Expression levels of 282 genes were altered with smoky versus smokeless coal exposure (P < 0.005), including the 2-fold increase of proinflammatory IL8 and decrease of proapoptotic CASP3. This signature was more correlated with carcinogenic PAHs (e.g. Benzo[a] pyrene; r = 0.41) than with non-carcinogenic PAHs (e.g. Fluorene; r = 0.08) or PM 2.5 (r = 0.05). Genes altered with smoky coal exposure were concordantly enriched with tobacco exposure in previously profiled buccal biopsies of smokers and non-smokers (GSEA, q < 0.05). This is the first study to identify a signature of buccal epithelial gene-expression that is associated with smoky coal exposure, which in part is similar to the molecular response to tobacco smoke, thereby lending biologic plausibility to prior epidemiological studies that have linked this exposure to lung cancer risk.
C1 [Wang, Teresa W.; Liu, Gang; Xiao, Xiaohui; Steiling, Katrina; Lenburg, Marc E.; Spira, Avrum] Boston Univ, Sch Med, Div Computat Biomed, Boston, MA 02118 USA.
   [Wang, Teresa W.; Steiling, Katrina; Lenburg, Marc E.; Spira, Avrum] Boston Univ, Bioinformat Program, Boston, MA 02215 USA.
   [Vermeulen, Roel C. H.; Reiss, Boris; Downward, George S.] Univ Utrecht, Div Environm Epidemiol, Inst Risk Assessment Sci, Utrecht, Netherlands.
   [Hu, Wei; Silverman, Debra T.; Rothman, Nathaniel; Lan, Qing] NCI, Div Canc Epidemiol & Genet, Rockville, MD 20850 USA.
   [Alekseyev, Yuriy; Lenburg, Marc E.; Spira, Avrum] Boston Univ, Sch Med, Dept Pathol & Lab Med, Boston, MA 02118 USA.
   [Xu, Jun] Univ Hong Kong, Sch Publ Hlth, Hong Kong, Hong Kong, Peoples R China.
   [Reiss, Boris] Univ Washington, Sch Publ Hlth, Seattle, WA 98195 USA.
   [Wei, Fusheng; Wu, Guoping] China Natl Environm Monitoring Ctr, Beijing, Peoples R China.
   [Li, Jihua] Qujing Ctr Dis Control & Prevent, Qujing, Peoples R China.
RP Spira, A (reprint author), Boston Univ, Sch Med, Div Computat Biomed, Boston, MA 02118 USA.
EM aspira@bu.edu; qingl@mail.nih.gov
RI Lenburg, Marc/B-8027-2008; Vermeulen, Roel/F-8037-2011
OI Lenburg, Marc/0000-0002-5760-4708; Vermeulen, Roel/0000-0003-4082-8163
FU National Institutes of Health/National Institute of Environmental Health
   Sciences [3U01ES16035-03S1]; Intramural Research Program of the US
   National Cancer Institute
FX National Institutes of Health/National Institute of Environmental Health
   Sciences (3U01ES16035-03S1); Intramural Research Program of the US
   National Cancer Institute.
NR 50
TC 1
Z9 1
U1 6
U2 16
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
EI 1460-2180
J9 CARCINOGENESIS
JI Carcinogenesis
PD DEC
PY 2015
VL 36
IS 12
BP 1494
EP 1501
DI 10.1093/carcin/bgv150
PG 8
WC Oncology
SC Oncology
GA CY4ON
UT WOS:000366387600005
PM 26468118
ER

PT J
AU La Maestra, S
   D'Agostini, F
   Izzotti, A
   Micale, RT
   Mastracci, L
   Camoirano, A
   Balansky, R
   Trosko, JE
   Steele, VE
   De Flora, S
AF La Maestra, Sebastiano
   D'Agostini, Francesco
   Izzotti, Alberto
   Micale, Rosanna T.
   Mastracci, Luca
   Camoirano, Anna
   Balansky, Roumen
   Trosko, James E.
   Steele, Vernon E.
   De Flora, Silvio
TI Modulation by aspirin and naproxen of nucleotide alterations and tumors
   in the lung of mice exposed to environmental cigarette smoke since birth
SO CARCINOGENESIS
LA English
DT Article
ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; STEM-CELL THEORY; TOBACCO-SMOKE;
   CANCER-RISK; N-ACETYLCYSTEINE; URINARY-BLADDER; GENE-EXPRESSION; RODENT
   MODELS; CARCINOGENESIS; INFLAMMATION
AB Chemoprevention provides an important strategy for cancer control in passive smokers. Due to the crucial role played by smoke-related chronic inflammation in lung carcinogenesis, of special interest are extensively used pharmacological agents, such as nonsteroidal anti-inflammatory drugs (NSAIDs). We evaluated the ability of aspirin and naproxen, inhibitors of both cyclooxygenase-1 and cyclooxygenase -2, to modulate environmental cigarette smoke (ECS)-induced lung carcinogenesis in A/J mice of both genders. Based on a subchronic toxicity study in 180 postweaning mice, we used 1600 mg/kg diet aspirin and 320 mg/kg diet naproxen. In the tumor chemoprevention study, using 320 mice, exposure to ECS started soon after birth and administration of NSAIDs started after weaning. At 10 weeks of life, the NSAIDs did not affect the presence of occult blood in feces. As assessed in a subset of 40 mice, bulky DNA adducts and 8-hydroxy-2'-deoxyguanosine levels were considerably increased in ECS-exposed mice and, irrespective of gender, both NSAIDs remarkably inhibited these nucleotide alterations. After exposure for 4 months followed by 5 months in filtered air, ECS induced a significant increase in the yield of surface lung tumors, the 43.7% of which were adenomas and the 56.3% were adenocarcinomas. Oct-4 (octamer-binding transcription factor 4), a marker of cell stemness, was detected in some adenocarcinoma cells. The NAIDs attenuated the yield of lung tumors, but prevention of ECS-induced lung adenomas was statistically significant only in female mice treated with aspirin, which supports a role for estrogens in ECS-related lung carcinogenesis and highlights the antiestrogenic properties of NSAIDs.
C1 [La Maestra, Sebastiano; D'Agostini, Francesco; Izzotti, Alberto; Micale, Rosanna T.; Camoirano, Anna; De Flora, Silvio] Univ Genoa, Dept Hlth Sci, I-16132 Genoa, Italy.
   [Mastracci, Luca] Univ Genoa, Dept Surg & Diagnost Sci, I-16132 Genoa, Italy.
   [Balansky, Roumen] Natl Oncol Ctr, Sofia 1756, Bulgaria.
   [Trosko, James E.] Michigan State Univ, Dept Pediat & Human Dev, Natl Food Safety Toxicol Ctr, E Lansing, MI 48824 USA.
   [Steele, Vernon E.] NCI, Canc Prevent Div, Chemoprevent Agent Dev Res Grp, Bethesda, MD 20892 USA.
RP De Flora, S (reprint author), Univ Genoa, Dept Hlth Sci, I-16132 Genoa, Italy.
EM sdf@unige.it
OI izzotti, alberto/0000-0002-8588-0347
FU United States National Cancer Institute [HHSN-261201200015I]
FX United States National Cancer Institute (Contract #HHSN-261201200015I).
NR 51
TC 3
Z9 3
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
EI 1460-2180
J9 CARCINOGENESIS
JI Carcinogenesis
PD DEC
PY 2015
VL 36
IS 12
BP 1531
EP 1538
DI 10.1093/carcin/bgv149
PG 8
WC Oncology
SC Oncology
GA CY4ON
UT WOS:000366387600009
PM 26464196
ER

PT J
AU Nicolaou, KC
   Rhoades, D
   Wang, YP
   Totokotsopoulos, S
   Bai, RL
   Hamel, E
AF Nicolaou, K. C.
   Rhoades, Derek
   Wang, Yanping
   Totokotsopoulos, Sotirios
   Bai, Ruoli
   Hamel, Ernest
TI Synthesis and Biological Evaluation of Novel EpothiloneB Side Chain
   Analogues
SO CHEMMEDCHEM
LA English
DT Article
DE antibody-drug conjugates; anticancer agents; epothilones; organic
   synthesis; tubulin binding agents
ID HIGHLY POTENT EPOTHILONE; STEREOSELECTIVE-SYNTHESIS; CHEMICAL-SYNTHESIS;
   STANNOUS CHLORIDE; (-)-EPOTHILONE B; TUBULIN; CONFORMATION; REDUCTION;
   CATALYSIS; STRATEGY
AB The design, synthesis, and biological evaluation of a series of epothilone analogues with novel side chains equipped with an amino group are described. Their design facilitates potential conjugation to selective drug delivery systems such as antibodies. Their synthesis proceeded efficiently via Stille coupling of a readily available vinyl iodide and heterocyclic stannanes. Cytotoxicity studies and tubulin binding assays revealed two of these analogues to be more potent than epothilonesA-D and the anticancer agent ixabepilone, currently in clinical use.
C1 [Nicolaou, K. C.; Rhoades, Derek; Wang, Yanping; Totokotsopoulos, Sotirios] Rice Univ, Dept Chem, Houston, TX 77005 USA.
   [Rhoades, Derek] Univ Calif San Diego, Dept Chem & Biochem, La Jolla, CA 92093 USA.
   [Totokotsopoulos, Sotirios] Scripps Res Inst, Dept Chem, La Jolla, CA 92037 USA.
   [Bai, Ruoli; Hamel, Ernest] NCI, Screening Technol Branch, Dev Therapeut Program,NIH, Div Canc Treatment & Diag,Frederick Natl Lab Canc, Frederick, MD 21702 USA.
RP Nicolaou, KC (reprint author), Rice Univ, Dept Chem, 6100 Main St, Houston, TX 77005 USA.
EM kcn@rice.edu
FU Cancer Prevention & Research Institute of Texas (CPRIT); Welch
   Foundation [C-1819]; Bristol-Myers Squibb
FX This work was partially carried out at The Scripps Research Institute
   (TSRI). We thank Drs. D. H. Huang (TSRI), L. Pasternack (TSRI), L. B.
   Alemany (Rice Univ.), and Q. Kleerekoper (Rice Univ.) for NMR
   spectroscopic assistance, and Drs. G. Siuzdak (TSRI) and C. Pennington
   (Rice Univ.) for assistance with mass spectrometry. This work was
   supported by the Cancer Prevention & Research Institute of Texas
   (CPRIT), the Welch Foundation (grant C-1819), and Bristol-Myers Squibb.
   Disclaimer by the co-authors based at NCI (R.L. and E.H.): The content
   of this article is the sole responsibility of the authors and does not
   necessarily reflect the official views of the US National Institutes of
   Health.
NR 52
TC 0
Z9 0
U1 6
U2 23
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA POSTFACH 101161, 69451 WEINHEIM, GERMANY
SN 1860-7179
EI 1860-7187
J9 CHEMMEDCHEM
JI ChemMedChem
PD DEC
PY 2015
VL 10
IS 12
BP 1974
EP 1979
DI 10.1002/cmdc.201500401
PG 6
WC Chemistry, Medicinal; Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA CY6HY
UT WOS:000366511000004
PM 26447977
ER

PT J
AU Tang, KS
   Klempner, MS
   Wormser, GP
   Marques, AR
   Alaedini, A
AF Tang, Kevin S.
   Klempner, Mark S.
   Wormser, Gary P.
   Marques, Adriana R.
   Alaedini, Armin
TI Association of Immune Response to Endothelial Cell Growth Factor With
   Early Disseminated and Late Manifestations of Lyme Disease but Not
   Posttreatment Lyme Disease Syndrome
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Editorial Material
DE Lyme disease; posttreatment Lyme disease syndrome; endothelial cell
   growth factor; antibody; Borrelia burgdorferi
ID SYMPTOMS
AB Endothelial cell growth factor has been recently proposed as a potential autoantigen in manifestations of Lyme disease that are thought to involve immune-mediated mechanisms. Our findings indicate that a humoral immune response to this protein is not associated with posttreatment Lyme disease syndrome.
C1 [Tang, Kevin S.; Alaedini, Armin] Columbia Univ, Med Ctr, Dept Med, New York, NY 10032 USA.
   [Klempner, Mark S.] Univ Massachusetts, Sch Med, MassBiol, Boston, MA 02125 USA.
   [Wormser, Gary P.] New York Med Coll, Dept Med, Div Infect Dis, Valhalla, NY 10595 USA.
   [Marques, Adriana R.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
RP Alaedini, A (reprint author), Columbia Univ, Med Ctr, Dept Med, 1130 St Nicholas Ave,Rm 937, New York, NY 10032 USA.
EM aa819@columbia.edu
FU Intramural NIH HHS; NIAID NIH HHS [N01AI65308, R56AI093763, R56
   AI093763]
NR 12
TC 2
Z9 2
U1 1
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
EI 1537-6591
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD DEC 1
PY 2015
VL 61
IS 11
BP 1703
EP 1706
DI 10.1093/cid/civ638
PG 4
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA CY5RF
UT WOS:000366464200011
PM 26219695
ER

PT J
AU Koo, PJ
   Kwak, JJ
   Pokharel, S
   Choyke, PL
AF Koo, Phillip J.
   Kwak, Jennifer J.
   Pokharel, Sajal
   Choyke, Peter L.
TI Novel Imaging of Prostate Cancer with MRI, MRI/US, and PET
SO CURRENT ONCOLOGY REPORTS
LA English
DT Review
DE Prostate cancer; MRI; MRI/US; Fusion; DWI; DKI; Hyperpolarized; PET;
   PET/CT; PSMA; FACBC; Acetate; Bombesin; GRP; FDHT
ID GASTRIN-RELEASING-PEPTIDE; POSITRON-EMISSION-TOMOGRAPHY; ACID SYNTHASE
   EXPRESSION; MEMBRANE ANTIGEN; ANDROGEN-RECEPTOR; RADICAL PROSTATECTOMY;
   ANTI-1-AMINO-3-F-18-FLUOROCYCLOBUTANE-1-CARBOXYLIC ACID; TARGETED
   BIOPSY; FUSION; CASTRATION
AB Imaging of prostate cancer presents many challenges to the imaging community. There has been much progress in this space in large part due to MRI and PET radiopharmaceuticals. Though MRI has been focused on the evaluation of local disease and PETon the detection of metastatic disease, these two areas do converge and will be complementary especially with the growth of new PET/MRI technologies. In this review article, we review novel MRI, MRI/US, and PET radiopharmaceuticals which will offer insight into the future direction of imaging in prostate cancer.
C1 [Koo, Phillip J.; Kwak, Jennifer J.] Univ Colorado, Sch Med, Dept Radiol, Div Nucl Med & Mol Imaging, Aurora, CO 80045 USA.
   [Pokharel, Sajal] Univ Colorado, Sch Med, Dept Radiol, Div Abdominal Imaging, Aurora, CO 80045 USA.
   [Choyke, Peter L.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Koo, PJ (reprint author), Univ Colorado, Sch Med, Dept Radiol, Div Nucl Med & Mol Imaging, Mail Stop L954,12401 E 17th Ave,Room 1512, Aurora, CO 80045 USA.
EM phillip.koo@ucdenver.edu; jennifer.kwak@ucdenver.edu;
   sajal.pokharel@ucdenver.edu; pchoyke@nih.gov
NR 85
TC 3
Z9 3
U1 2
U2 13
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1523-3790
EI 1534-6269
J9 CURR ONCOL REP
JI Curr. Oncol. Rep.
PD DEC
PY 2015
VL 17
IS 12
AR 56
DI 10.1007/s11912-015-0480-y
PG 10
WC Oncology
SC Oncology
GA CZ0PG
UT WOS:000366807600004
PM 26462919
ER

PT J
AU Lucas, CL
   Lenardo, MJ
AF Lucas, Carrie L.
   Lenardo, Michael J.
TI Identifying genetic-determinants of autoimmunity and immune
   dysregulation
SO CURRENT OPINION IN IMMUNOLOGY
LA English
DT Review
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; GENOME-WIDE ASSOCIATION; X-LINKED
   SYNDROME; LYMPHOPROLIFERATIVE-SYNDROME; RHEUMATOID-ARTHRITIS; HUMAN
   IMMUNODEFICIENCY; DEFECTIVE LYMPHOCYTE; AIRE GENE; MUTATIONS; DISEASE
AB Common autoimmune diseases are relatively heterogeneous with both genetic and environmental factors influencing disease susceptibility and progression. As the populations in developed countries age, these chronic diseases will become an increasing burden in human suffering and health care costs. By contrast, rare immune diseases that are severe and develop early in childhood are frequently monogenic and fully penetrant, often with a Mendelian inheritance pattern. Although these may be incompatible with survival or cured by hematopoietic stem cell transplantation, we will argue that they constitute a rich source of genetic insights into immunological diseases. Here, we discuss five examples of well-studied Mendelian disease-causing genes and their known or predicted roles in conferring susceptibility to common, polygenic diseases of autoimmunity. Mendelian disease mutations, as experiments of nature, reveal human loci that are indispensable for immune regulation and, therefore, most promising as therapeutic targets.
C1 [Lucas, Carrie L.; Lenardo, Michael J.] NIAID, Mol Dev Immune Syst Sect, Immunol Lab, Clin Genom Program,NIH, Bethesda, MD 20892 USA.
RP Lenardo, MJ (reprint author), NIAID, Mol Dev Immune Syst Sect, Immunol Lab, Clin Genom Program,NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM lenardo@nih.gov
FU Intramural Research Program of NIH, NIAID; Postdoctoral Research
   Associate (PRAT) Fellowship, NIGMS, NIH
FX This work was supported by the Intramural Research Program of NIH,
   NIAID. C.L.L. was supported by the Postdoctoral Research Associate
   (PRAT) Fellowship, NIGMS, NIH. The authors thank Drs. Helen Su and Yu
   Zhang for critically reading the manuscript.
NR 52
TC 2
Z9 2
U1 2
U2 6
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0952-7915
EI 1879-0372
J9 CURR OPIN IMMUNOL
JI Curr. Opin. Immunol.
PD DEC
PY 2015
VL 37
BP 28
EP 33
DI 10.1016/j.coi.2015.09.001
PG 6
WC Immunology
SC Immunology
GA CZ0FK
UT WOS:000366780300006
PM 26433354
ER

PT J
AU Boyd, A
   Killoran, K
   Mitre, E
   Nutman, TB
AF Boyd, Alexis
   Killoran, Kristin
   Mitre, Edward
   Nutman, Thomas B.
TI Pleural cavity type 2 innate lymphoid cells precede Th2 expansion in
   murine Litomosoides sigmodontis infection
SO EXPERIMENTAL PARASITOLOGY
LA English
DT Article
DE Lymphocytes; Filaria; Pleural cavity; Innate lymphoid cells; ILC2s
ID IMMUNITY; MICE; FILARIASIS; BASOPHILS; RESPONSES
AB Recently, a family of innate cells has been identified that respond to IL-25 and IL-33 in murine intestinal helminths. Termed Type 2 innate lymphoid cells (ILC2s) they facilitate the development of Th2 responses responsible for helminth clearance. We evaluated these cells in a tissue-invasive helminth model. Using Litomosides sigmodontis (a strong Th2 polarizing filarial infection) we observed a robust Th2 response in the pleural cavity, where adult worms reside, marked by increased levels of IL-5 and IL-13 in infected mice. In parallel, ILC2s were expanded in the pleural cavity early in the infection, peaking during the prepatent period. L sigmodontis also elicits a strong systemic Th2 response, which includes significantly increased levels of IgG1, IgE and IL-5 in the plasma of infected mice. Although ILC2s were expanded locally, they were not expanded in the spleen, blood, or mediastinal lymph nodes in response to L sigmodontis infection, suggesting that ILC2s function primarily at the site of infection. The increase in ILC2s in the pleural cavity and the expansion in Th2 responses indicates a probable role for these cells in initiating and maintaining the Th2 response and highlights the importance of these cells in helminth infections and their role in Th2 immunity. Published by Elsevier Ltd.
C1 [Boyd, Alexis; Nutman, Thomas B.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
   [Killoran, Kristin; Mitre, Edward] Uniformed Serv Univ Hlth Sci, Dept Microbiol & Immunol, F Edward Hebert Sch Med, Bethesda, MD 20892 USA.
RP Nutman, TB (reprint author), NIAID, Parasit Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM tnutman@niaid.nih.gov
FU Division of Intramural Research (DIR), NIAID
FX Alexis Boyd was a predoctoral student in the Microbiology and Immunology
   program of the Institute for Biomedical Sciences at the George
   Washington University. This work is from a dissertation that was
   presented in partial fulfillment of the requirements for the Ph.D.
   degree. The work was supported, in part, by the Division of Intramural
   Research (DIR), NIAID.
NR 19
TC 0
Z9 0
U1 1
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4894
EI 1090-2449
J9 EXP PARASITOL
JI Exp. Parasitol.
PD DEC
PY 2015
VL 159
BP 118
EP 126
DI 10.1016/j.exppara.2015.09.006
PG 11
WC Parasitology
SC Parasitology
GA CY5JC
UT WOS:000366442900016
PM 26394284
ER

PT J
AU Ehrenshaft, M
   Deterding, LJ
   Mason, RP
AF Ehrenshaft, Marilyn
   Deterding, Leesa J.
   Mason, Ronald P.
TI Tripping up Trp: Modification of protein tryptophan residues by reactive
   oxygen species, modes of detection, and biological consequences
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Review
DE Tryptophan; Protein; Oxidation; Radical; Singlet oxygen; Ozone;
   Kynurenine; N-formylkynurenine; Fluorescence; Mass spectrometry;
   Anti-NFK; ESR; ESR spin trapping; Lysozyme; hSOD1; alpha-crystallin;
   Apolipoprotein; Photosynthesis; MopE
ID LOW-DENSITY-LIPOPROTEIN; TORPEDO-CALIFORNICA ACETYLCHOLINESTERASE;
   AMYOTROPHIC-LATERAL-SCLEROSIS; TANDEM MASS-SPECTROMETRY; PHOTOSENSITIZER
   METHYLENE-BLUE; ZN-SUPEROXIDE-DISMUTASE; LENS ALPHA-CRYSTALLIN;
   EGG-WHITE LYSOZYME; N-FORMYLKYNURENINE; SINGLET OXYGEN
AB Proteins comprise a majority of the dry weight of a cell, rendering them a major target for oxidative modification. Oxidation of proteins can result in significant alterations in protein molecular mass such as breakage of the polypeptide backbone and/or polymerization of monomers into dimers, multimers, and sometimes insoluble aggregates. Protein oxidation can also result in structural changes to amino acid residue side chains, conversions that have only a modest effect on protein size but can have widespread consequences for protein function. There are a wide range of rate constants for amino acid reactivity, with cysteine, methionine, tyrosine, phenylalanine, and tryptophan having the highest rate constants with commonly encountered biological oxidants. Free tryptophan and tryptophan protein residues react at a diffusion-limited rate with hydroxyl radical and also have high rate constants for reactions with singlet oxygen and ozone. Although oxidation of proteins in general and tryptophan residues specifically can have effects detrimental to the health of cells and organisms, some modifications are neutral, whereas others contribute to the function of the protein in question or may act as a signal that damaged proteins need to be replaced. This review provides a brief overview of the chemical mechanisms by which tryptophan residues become oxidized, presents both the strengths and the weaknesses of some of the techniques used to detect these oxidative interactions, and discusses selected examples of the biological consequences of tryptophan oxidation in proteins from animals, plants, and microbes. Published by Elsevier Inc.
C1 [Ehrenshaft, Marilyn; Mason, Ronald P.] Immun Inflammat & Dis Lab, Res Triangle Pk, NC 27709 USA.
   [Ehrenshaft, Marilyn; Mason, Ronald P.] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
   [Deterding, Leesa J.] NIEHS, Epigenet & Stem Cell Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Ehrenshaft, M (reprint author), Immun Inflammat & Dis Lab, Res Triangle Pk, NC 27709 USA.
EM ehrensh1@niehs.nih.gov
FU Intramural Research Program of the NIEHS, NIH
FX We thank B. Jean Corbett, Dr. Ann Motten, and Mary J. Mason for valuable
   help in the preparation of the manuscript. This work was supported by
   the Intramural Research Program of the NIEHS, NIH.
NR 95
TC 4
Z9 4
U1 10
U2 40
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD DEC
PY 2015
VL 89
BP 220
EP 228
DI 10.1016/j.freeradbiomed.2015.08.003
PG 9
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA CY4CI
UT WOS:000366355800021
PM 26393422
ER

PT J
AU Delmastro-Greenwood, M
   Hughan, KS
   Vitturi, DA
   Salvatore, SR
   Grimes, G
   Potti, G
   Shiva, S
   Schopfer, FJ
   Gladwin, MT
   Freeman, BA
   Wendell, SG
AF Delmastro-Greenwood, Meghan
   Hughan, Kara S.
   Vitturi, Dario A.
   Salvatore, Sonia R.
   Grimes, George
   Potti, Gopal
   Shiva, Sruti
   Schopfer, Francisco J.
   Gladwin, Mark T.
   Freeman, Bruce A.
   Wendell, Stacy Gelhaus
TI Nitrite and nitrate-dependent generation of anti-inflammatory fatty acid
   nitroalkenes
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE Nitrogen metabolism; Diet; Redox signaling; Nitro-fatty acid; Conjugated
   linoleic acid; Nitrate; Nitrite
ID CONJUGATED LINOLEIC-ACID; HEALTHY HUMANS; OLEIC ACID; INFLAMMATION;
   CIS-9,TRANS-11; THERAPEUTICS; HYPERTENSION; MECHANISMS; LIPIDS
AB A gap in our understanding of the beneficial systemic responses to dietary constituents nitrate (NO3-), nitrite (NO2-) and conjugated linoleic acid (cLA) is the identification of the downstream metabolites that mediate their actions. To examine these reactions in a clinical context, investigational drug preparations of N-15-labeled NO3- and NO2- were orally administered to healthy humans with and without cLA. Mass spectrometry analysis of plasma and urine indicated that the nitrating species nitrogen dioxide was formed and reacted with the olefinic carbons of unsaturated fatty acids to yield the electrophilic fatty acid, nitro-cLA (NO2-cLA). These species mediate the post-translational modification (PTM) of proteins via reversible Michael addition with nucleophilic amino acids. The PTM of critical target proteins by electrophilic lipids has been described as a sensing mechanism that regulates adaptive cellular responses, but little is known about the endogenous generation of fatty acid nitroalkenes and their metabolites. We report that healthy humans consuming N-15-labeled NO3- or NO2-, with and without cLA supplementation, produce (NO2)-N-15-cLA and corresponding metabolites that are detected in plasma and urine. These data support that the dietary constituents NO3-, NO2- and cLA promote the further generation of secondary electrophilic lipid products that are absorbed into the circulation at concentrations sufficient to exert systemic effects before being catabolized or excreted. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Delmastro-Greenwood, Meghan; Vitturi, Dario A.; Salvatore, Sonia R.; Shiva, Sruti; Schopfer, Francisco J.; Freeman, Bruce A.; Wendell, Stacy Gelhaus] Univ Pittsburgh, Dept Pharmacol & Chem Biol, Pittsburgh, PA 15261 USA.
   [Hughan, Kara S.; Shiva, Sruti; Schopfer, Francisco J.; Gladwin, Mark T.; Freeman, Bruce A.; Wendell, Stacy Gelhaus] Univ Pittsburgh, Pittsburgh Heart Lung Blood & Vasc Med Inst, Pittsburgh, PA 15261 USA.
   [Grimes, George; Potti, Gopal] NIH, Pharmaceut Dev Sect, Dept Pharm, Ctr Clin, Bethesda, MD 20892 USA.
RP Freeman, BA (reprint author), Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, 200 Lothrop St,Biomed Sci Tower E1340, Pittsburgh, PA 15261 USA.
EM freerad@pitt.edu; gstacy@pitt.edu
OI Vitturi, Dario/0000-0003-0354-4567
FU NIH [R01-HL058115, R01-HL64937, P01-HL103455, AT00682, K12-HD052892];
   Cochrane Weber Fund of Children's Hospital of Pittsburgh of UPMC;
   Vascular Medicine Institute/CTSI Pilot Project Program in Hemostasis &
   Vascular Biology
FX The authors thank Ram Agarwal, Deborah Sperling and Judith Starling for
   formulating <SUP>15</SUP>NOx, Nydia Chien and Suchitra Barge for their
   IRB and regulatory assistance and Nicole Helbling and Alex Despines for
   trial implementation. This work was supported by NIH grants
   R01-HL058115, R01-HL64937 (BF), P01-HL103455 (MG, BF), AT00682 (FJS),
   K12-HD052892 (KSH), the Cochrane Weber Fund of Children's Hospital of
   Pittsburgh of UPMC and the Vascular Medicine Institute/CTSI Pilot
   Project Program in Hemostasis & Vascular Biology. FJS and BAF
   acknowledge interest in Complexa, Inc. MTG is co-inventor on a US
   Government Patent for the use of nitrite salts for cardiovascular
   indications (IND # 70,411) and has received royalties from the US
   Government.
NR 42
TC 6
Z9 6
U1 1
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD DEC
PY 2015
VL 89
BP 333
EP 341
DI 10.1016/j.freeradbiomed.2015.07.149
PG 9
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA CY4CI
UT WOS:000366355800031
PM 26385079
ER

PT J
AU Jiao, S
   Peters, U
   Berndt, S
   Bezieau, S
   Brenner, H
   Campbell, PT
   Chan, AT
   Chang-Claude, J
   Lemire, M
   Newcomb, PA
   Potter, JD
   Slattery, ML
   Woods, MO
   Hsu, L
AF Jiao, Shuo
   Peters, Ulrike
   Berndt, Sonja
   Bezieau, Stephane
   Brenner, Hermann
   Campbell, Peter T.
   Chan, Andrew T.
   Chang-Claude, Jenny
   Lemire, Mathieu
   Newcomb, Polly A.
   Potter, John D.
   Slattery, Martha L.
   Woods, Michael O.
   Hsu, Li
TI Powerful Set-Based Gene-Environment Interaction Testing Framework for
   Complex Diseases
SO GENETIC EPIDEMIOLOGY
LA English
DT Article
DE G x E screening statistics; eSBERUA; rare variants; GWAS
ID GENOME-WIDE ASSOCIATION; RARE-VARIANT ASSOCIATION; COLORECTAL-CANCER;
   COMMON VARIANTS; BLADDER-CANCER; MARKER-SET; SUSCEPTIBILITY;
   INDEPENDENCE; TRAITS; MODELS
AB Identification of gene-environment interaction (G x E) is important in understanding the etiology of complex diseases. Based on our previously developed Set Based gene EnviRonment InterAction test (SBERIA), in this paper we propose a powerful framework for enhanced set-based G x E testing (eSBERIA). The major challenge of signal aggregation within a set is how to tell signals from noise. eSBERIA tackles this challenge by adaptively aggregating the interaction signals within a set weighted by the strength of the marginal and correlation screening signals. eSBERIA then combines the screening-informed aggregate test with a variance component test to account for the residual signals. Additionally, we develop a case-only extension for eSBERIA (coSBERIA) and an existing set-based method, which boosts the power not only by exploiting the G-E independence assumption but also by avoiding the need to specify main effects for a large number of variants in the set. Through extensive simulation, we show that coSBERIA and eSBERIA are considerably more powerful than existing methods within the case-only and the case-control method categories across a wide range of scenarios. We conduct a genome-wide G x E search by applying our methods to Illumina HumanExome Beadchip data of 10,446 colorectal cancer cases and 10,191 controls and identify two novel interactions between nonsteroidal anti-inflammatory drugs (NSAIDs) and MINK1 and PTCHD3. (C) 2015 Wiley Periodicals, Inc.
C1 [Jiao, Shuo; Peters, Ulrike; Newcomb, Polly A.; Potter, John D.; Hsu, Li] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA.
   [Berndt, Sonja] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Bezieau, Stephane] CHU Nantes, Serv Genet Med, F-44035 Nantes 01, France.
   [Brenner, Hermann] German Canc Res Ctr, Div Clin Epidemiol & Aging Res, Heidelberg, Germany.
   [Brenner, Hermann] German Canc Consortium DKTK, Heidelberg, Germany.
   [Campbell, Peter T.] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
   [Chan, Andrew T.] Brigham & Womens Hosp, Channing Div Network Med, Boston, MA 02115 USA.
   [Chan, Andrew T.] Harvard Univ, Sch Med, Boston, MA USA.
   [Chang-Claude, Jenny] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
   [Lemire, Mathieu] Ontario Inst Canc Res, Toronto, ON, Canada.
   [Newcomb, Polly A.] Univ Washington, Sch Publ Hlth, Seattle, WA 98195 USA.
   [Potter, John D.] Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand.
   [Slattery, Martha L.] Univ Utah, Hlth Sci Ctr, Dept Internal Med, Salt Lake City, UT USA.
   [Woods, Michael O.] Mem Univ Newfoundland, Discipline Genet, St John, NF, Canada.
RP Hsu, L (reprint author), Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, 1100 Fairview Ave N,Mailstop M2-B500, Seattle, WA 98109 USA.
EM lih@fredhutch.org
RI Brenner, Hermann/B-4627-2017; 
OI Brenner, Hermann/0000-0002-6129-1572; Bezieau,
   stephane/0000-0003-0095-1319; Potter, John/0000-0001-5439-1500
FU NCI NIH HHS [P01 CA053996, K05 CA152715, P30 CA015704, R01 CA059045, R21
   CA191312, U01 CA137088, U01 CA164930]; NIA NIH HHS [R01 AG014358]; NIH
   HHS [S10 OD020069]
NR 29
TC 1
Z9 1
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0741-0395
EI 1098-2272
J9 GENET EPIDEMIOL
JI Genet. Epidemiol.
PD DEC
PY 2015
VL 39
IS 8
BP 609
EP 618
DI 10.1002/gepi.21908
PG 10
WC Genetics & Heredity; Mathematical & Computational Biology
SC Genetics & Heredity; Mathematical & Computational Biology
GA CY7RA
UT WOS:000366605200002
PM 26095235
ER

PT J
AU Asimit, JL
   Panoutsopoulou, K
   Wheeler, E
   Berndt, SI
   Cordell, HJ
   Morris, AP
   Zeggini, E
   Barroso, I
AF Asimit, Jennifer L.
   Panoutsopoulou, Kalliope
   Wheeler, Eleanor
   Berndt, Sonja I.
   Cordell, Heather J.
   Morris, Andrew P.
   Zeggini, Eleftheria
   Barroso, Ines
CA GIANT Consortium
   ArcOGEN Consortium
TI A Bayesian Approach to the Overlap Analysis of Epidemiologically Linked
   Traits
SO GENETIC EPIDEMIOLOGY
LA English
DT Article
DE Bayes' factor; P-value; obesity; osteoarthritis; overlap analysis;
   threshold calibration
ID GENOME-WIDE ASSOCIATION; GENETIC ASSOCIATION; SUSCEPTIBILITY LOCI;
   IDENTIFICATION; OSTEOARTHRITIS; IMPUTATION; VARIANTS; CANCER; TOOL
AB Diseases often cooccur in individuals more often than expected by chance, and may be explained by shared underlying genetic etiology. A common approach to genetic overlap analyses is to use summary genome-wide association study data to identify single-nucleotide polymorphisms (SNPs) that are associated with multiple traits at a selected P-value threshold. However, P-values do not account for differences in power, whereas Bayes' factors (BFs) do, and may be approximated using summary statistics. We use simulation studies to compare the power of frequentist and Bayesian approaches with overlap analyses, and to decide on appropriate thresholds for comparison between the two methods. It is empirically illustrated that BFs have the advantage over P-values of a decreasing type I error rate as study size increases for single-disease associations. Consequently, the overlap analysis of traits from different-sized studies encounters issues in fair P-value threshold selection, whereas BFs are adjusted automatically. Extensive simulations show that Bayesian overlap analyses tend to have higher power than those that assess association strength with P-values, particularly in low-power scenarios. Calibration tables between BFs and P-values are provided for a range of sample sizes, as well as an approximation approach for sample sizes that are not in the calibration table. Although P-values are sometimes thought more intuitive, these tables assist in removing the opaqueness of Bayesian thresholds and may also be used in the selection of a BF threshold to meet a certain type I error rate. An application of our methods is used to identify variants associated with both obesity and osteoarthritis. Published 2015 Wiley Periodicals, Inc.
C1 [Asimit, Jennifer L.; Panoutsopoulou, Kalliope; Wheeler, Eleanor; Zeggini, Eleftheria; Barroso, Ines] Wellcome Trust Sanger Inst, Cambridge CB10 1HH, England.
   [Berndt, Sonja I.] NCI, Div Canc Epidemiol & Genet, US Natl Inst Hlth, Bethesda, MD 20892 USA.
   [Cordell, Heather J.] Newcastle Univ, Inst Med Genet, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
   [Morris, Andrew P.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
   [Morris, Andrew P.] Univ Liverpool, Dept Biostat, Liverpool L69 3BX, Merseyside, England.
RP Asimit, JL (reprint author), Wellcome Trust Sanger Inst, Morgan Bldg,Wellcome Trust Genome Campus, Cambridge CB10 1HH, England.
EM ja11@sanger.ac.uk
OI Zeggini, Eleftheria/0000-0003-4238-659X; Asimit,
   Jennifer/0000-0002-4857-2249; Wheeler, Eleanor/0000-0002-8616-6444
FU Arthritis Research UK; Medical Research Council [MR/K021486/1]; Wellcome
   Trust [087436, WT098051]
NR 27
TC 1
Z9 1
U1 1
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0741-0395
EI 1098-2272
J9 GENET EPIDEMIOL
JI Genet. Epidemiol.
PD DEC
PY 2015
VL 39
IS 8
BP 624
EP 634
DI 10.1002/gepi.21919
PG 11
WC Genetics & Heredity; Mathematical & Computational Biology
SC Genetics & Heredity; Mathematical & Computational Biology
GA CY7RA
UT WOS:000366605200004
PM 26411566
ER

PT J
AU Amankwah, EK
   Lin, HY
   Tyrer, JP
   Lawrenson, K
   Dennis, J
   Chornokur, G
   Aben, KKH
   Anton-Culver, H
   Antonenkova, N
   Bruinsma, F
   Bandera, EV
   Bean, YT
   Beckmann, MW
   Bisogna, M
   Bjorge, L
   Bogdanova, N
   Brinton, LA
   Brooks-Wilson, A
   Bunker, CH
   Butzow, R
   Campbell, IG
   Carty, K
   Chen, ZH
   Chen, YA
   Chang-Claude, J
   Cook, LS
   Cramer, DW
   Cunningham, JM
   Cybulski, C
   Dansonka-Mieszkowska, A
   Du Bois, A
   Despierre, E
   Dicks, E
   Doherty, JA
   Doerk, T
   Duerst, M
   Easton, DF
   Eccles, DM
   Edwards, RP
   Ekici, AB
   Fasching, PA
   Fridley, BL
   Gao, YT
   Gentry-Maharaj, A
   Giles, GG
   Glasspool, R
   Goodman, MT
   Gronwald, J
   Harrington, P
   Harter, P
   Hasmad, HN
   Hein, A
   Heitz, F
   Hildebrandt, MAT
   Hillemanns, P
   Hogdall, CK
   Hogdall, E
   Hosono, S
   Iversen, ES
   Jakubowska, A
   Jensen, A
   Ji, BT
   Karlan, BY
   Jim, H
   Kellar, M
   Kiemeney, LA
   Krakstad, C
   Kjaer, SK
   Kupryjanczyk, J
   Lambrechts, D
   Lambrechts, S
   Le, ND
   Lee, AW
   Lele, S
   Leminen, A
   Lester, J
   Levine, DA
   Liang, D
   Lim, BK
   Lissowska, J
   Lu, K
   Lubinski, J
   Lundvall, L
   Massuger, LFAG
   Matsuo, K
   McGuire, V
   McLaughlin, JR
   McNeish, I
   Menon, U
   Milne, RL
   Modugno, F
   Moysich, KB
   Ness, RB
   Nevanlinna, H
   Eilber, U
   Odunsi, K
   Olson, SH
   Orlow, I
   Orsulic, S
   Weber, RP
   Paul, J
   Pearce, CL
   Pejovic, T
   Pelttari, LM
   Permuth-Wey, J
   Pike, MC
   Poole, EM
   Risch, HA
   Rosen, B
   Rossing, MA
   Rothstein, JH
   Rudolph, A
   Runnebaum, IB
   Rzepecka, IK
   Salvesen, HB
   Schernhammer, E
   Schwaab, I
   Shu, XO
   Shvetsov, YB
   Siddiqui, N
   Sieh, W
   Song, HL
   Southey, MC
   Spiewankiewicz, B
   Sucheston-Campbell, L
   Teo, SH
   Terry, KL
   Thompson, PJ
   Thomsen, L
   Tangen, IL
   Tworoger, SS
   Van Altena, AM
   Vierkant, RA
   Vergote, I
   Walsh, CS
   Wang-Gohrke, S
   Wentzensen, N
   Whittemore, AS
   Wicklund, KG
   Wilkens, LR
   Wu, AH
   Wu, XF
   Woo, YL
   Yang, H
   Zheng, W
   Ziogas, A
   Kelemen, LE
   Berchuck, A
   Chenevix-Trench, G
   Grp, AM
   Schildkraut, JM
   Ramus, SJ
   Goode, EL
   Monteiro, ANA
   Gayther, SA
   Narod, SA
   Pharoah, PDP
   Sellers, TA
   Phelan, CM
AF Amankwah, Ernest K.
   Lin, Hui-Yi
   Tyrer, Jonathan P.
   Lawrenson, Kate
   Dennis, Joe
   Chornokur, Ganna
   Aben, Katja K. H.
   Anton-Culver, Hoda
   Antonenkova, Natalia
   Bruinsma, Fiona
   Bandera, Elisa V.
   Bean, Yukie T.
   Beckmann, Matthias W.
   Bisogna, Maria
   Bjorge, Line
   Bogdanova, Natalia
   Brinton, Louise A.
   Brooks-Wilson, Angela
   Bunker, Clareann H.
   Butzow, Ralf
   Campbell, Ian G.
   Carty, Karen
   Chen, Zhihua
   Chen, Y. Ann
   Chang-Claude, Jenny
   Cook, Linda S.
   Cramer, Daniel W.
   Cunningham, Julie M.
   Cybulski, Cezary
   Dansonka-Mieszkowska, Agnieszka
   Du Bois, Andreas
   Despierre, Evelyn
   Dicks, Ed
   Doherty, Jennifer A.
   Doerk, Thilo
   Duerst, Matthias
   Easton, Douglas F.
   Eccles, Diana M.
   Edwards, Robert P.
   Ekici, Arif B.
   Fasching, Peter A.
   Fridley, Brooke L.
   Gao, Yu-Tang
   Gentry-Maharaj, Aleksandra
   Giles, Graham G.
   Glasspool, Rosalind
   Goodman, Marc T.
   Gronwald, Jacek
   Harrington, Patricia
   Harter, Philipp
   Hasmad, Hanis N.
   Hein, Alexander
   Heitz, Florian
   Hildebrandt, Michelle A. T.
   Hillemanns, Peter
   Hogdall, Claus K.
   Hogdall, Estrid
   Hosono, Satoyo
   Iversen, Edwin S.
   Jakubowska, Anna
   Jensen, Allan
   Ji, Bu-Tian
   Karlan, Beth Y.
   Jim, Heather
   Kellar, Melissa
   Kiemeney, Lambertus A.
   Krakstad, Camilla
   Kjaer, Susanne K.
   Kupryjanczyk, Jolanta
   Lambrechts, Diether
   Lambrechts, Sandrina
   Le, Nhu D.
   Lee, Alice W.
   Lele, Shashi
   Leminen, Arto
   Lester, Jenny
   Levine, Douglas A.
   Liang, Dong
   Lim, Boon Kiong
   Lissowska, Jolanta
   Lu, Karen
   Lubinski, Jan
   Lundvall, Lene
   Massuger, Leon F. A. G.
   Matsuo, Keitaro
   McGuire, Valerie
   McLaughlin, John R.
   McNeish, Ian
   Menon, Usha
   Milne, Roger L.
   Modugno, Francesmary
   Moysich, Kirsten B.
   Ness, Roberta B.
   Nevanlinna, Heli
   Eilber, Ursula
   Odunsi, Kunle
   Olson, Sara H.
   Orlow, Irene
   Orsulic, Sandra
   Weber, Rachel Palmieri
   Paul, James
   Pearce, Celeste L.
   Pejovic, Tanja
   Pelttari, Liisa M.
   Permuth-Wey, Jennifer
   Pike, Malcolm C.
   Poole, Elizabeth M.
   Risch, Harvey A.
   Rosen, Barry
   Rossing, Mary Anne
   Rothstein, Joseph H.
   Rudolph, Anja
   Runnebaum, Ingo B.
   Rzepecka, Iwona K.
   Salvesen, Helga B.
   Schernhammer, Eva
   Schwaab, Ira
   Shu, Xiao-Ou
   Shvetsov, Yurii B.
   Siddiqui, Nadeem
   Sieh, Weiva
   Song, Honglin
   Southey, Melissa C.
   Spiewankiewicz, Beata
   Sucheston-Campbell, Lara
   Teo, Soo-Hwang
   Terry, Kathryn L.
   Thompson, Pamela J.
   Thomsen, Lotte
   Tangen, Ingvild L.
   Tworoger, Shelley S.
   Van Altena, Anne M.
   Vierkant, Robert A.
   Vergote, Ignace
   Walsh, Christine S.
   Wang-Gohrke, Shan
   Wentzensen, Nicolas
   Whittemore, Alice S.
   Wicklund, Kristine G.
   Wilkens, Lynne R.
   Wu, Anna H.
   Wu, Xifeng
   Woo, Yin-Ling
   Yang, Hannah
   Zheng, Wei
   Ziogas, Argyrios
   Kelemen, Linda E.
   Berchuck, Andrew
   Chenevix-Trench, Georgia
   Grp, Aocs Management
   Schildkraut, Joellen M.
   Ramus, Susan J.
   Goode, Ellen L.
   Monteiro, Alvaro N. A.
   Gayther, Simon A.
   Narod, Steven A.
   Pharoah, Paul D. P.
   Sellers, Thomas A.
   Phelan, Catherine M.
TI Epithelial-Mesenchymal Transition (EMT) Gene Variants and Epithelial
   Ovarian Cancer (EOC) Risk
SO GENETIC EPIDEMIOLOGY
LA English
DT Article
DE ovarian cancer; epithelial-mesenchymal transition; single-nucleotide
   polymorphisms
ID SINGLE-NUCLEOTIDE POLYMORPHISMS; LUNG-CANCER; NEVER SMOKERS;
   SUSCEPTIBILITY; NEUROPILIN-1; SURVIVAL; DISEASE; METAANALYSIS;
   GLYPICANS; ONCOGENES
AB Epithelial-mesenchymal transition (EMT) is a process whereby epithelial cells assume mesenchymal characteristics to facilitate cancer metastasis. However, EMT also contributes to the initiation and development of primary tumors. Prior studies that explored the hypothesis that EMT gene variants contribute to epithelial ovarian carcinoma (EOC) risk have been based on small sample sizes and none have sought replication in an independent population. We screened 15,816 single-nucleotide polymorphisms (SNPs) in 296 genes in a discovery phase using data from a genome-wide association study of EOC among women of European ancestry (1,947 cases and 2,009 controls) and identified 793 variants in 278 EMT-related genes that were nominally (P < 0.05) associated with invasive EOC. These SNPs were then genotyped in a larger study of 14,525 invasive-cancer patients and 23,447 controls. A P-value < 0.05 and a false discovery rate (FDR) < 0.2 were considered statistically significant. In the larger dataset, GPC6/GPC5 rs17702471 was associated with the endometrioid subtype among Caucasians (odds ratio (OR) = 1.16, 95% CI = 1.07-1.25, P = 0.0003, FDR = 0.19), whereas F8 rs7053448 (OR = 1.69, 95% CI = 1.27-2.24, P = 0.0003, FDR = 0.12), F8 rs7058826 (OR = 1.69, 95% CI = 1.27-2.24, P = 0.0003, FDR = 0.12), and CAPN13 rs1983383 (OR = 0.79, 95% CI = 0.69-0.90, P = 0.0005, FDR = 0.12) were associated with combined invasive EOC among Asians. In silico functional analyses revealed that GPC6/GPC5 rs17702471 coincided with DNA regulatory elements. These results suggest that EMT gene variants do not appear to play a significant role in the susceptibility to EOC. (C) 2015 Wiley Periodicals, Inc.
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   [Dansonka-Mieszkowska, Agnieszka; Kupryjanczyk, Jolanta; Rzepecka, Iwona K.] Inst Oncol, Warsaw, Poland.
   [Du Bois, Andreas; Harter, Philipp; Heitz, Florian] Knappschaft GmbH, Evang Huyssens Stiftung, Kliniken Essen Mitte, Dept Gynaecol & Gynaecol Oncol, Essen, Germany.
   [Du Bois, Andreas; Harter, Philipp; Heitz, Florian] Dr Horst Schmidt Kliniken Wiesbaden, Dept Gynaecol & Gynaecol Oncol, Wiesbaden, Germany.
   [Despierre, Evelyn; Lambrechts, Sandrina; Vergote, Ignace] Katholieke Univ Leuven, Univ Hosp Leuven, Leuven Canc Inst, Div Gynecol, Leuven, Belgium.
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   [Doherty, Jennifer A.] Dartmouth Coll, Hitchcock Med Ctr, Dartmouth Med Sch, Sect Biostat & Epidemiol,Dept Community & Family, Hanover, NH 03756 USA.
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   [Easton, Douglas F.] Univ Cambridge, Dept Oncol, Ctr Canc Genet Epidemiol, Cambridge, England.
   [Easton, Douglas F.] Univ Cambridge, Dept Publ Hlth & Primary Care, Ctr Canc Genet Epidemiol, Cambridge, England.
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   [Giles, Graham G.; Milne, Roger L.] Univ Melbourne, Sch Populat & Global Hlth, Ctr Epidemiol & Biostat, Melbourne, Australia.
   [Goodman, Marc T.; Thompson, Pamela J.] Cedars Sinai Med Ctr, Samuel Oschin Comprehens Canc Inst, Canc Prevent & Control, Los Angeles, CA 90048 USA.
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   [Hogdall, Claus K.; Kjaer, Susanne K.; Lundvall, Lene] Univ Copenhagen, Rigshosp, Dept Gynaecol, DK-2100 Copenhagen, Denmark.
   [Hogdall, Estrid; Jensen, Allan; Kjaer, Susanne K.] Danish Canc Soc Res Ctr, Dept Virus Lifestyle & Genes, Copenhagen, Denmark.
   [Hogdall, Estrid] Univ Copenhagen, Herlev Hosp, Dept Pathol, Mol Unit, Copenhagen, Denmark.
   [Hosono, Satoyo; Matsuo, Keitaro] Aichi Canc Ctr Res Inst, Div Epidemiol & Prevent, Nagoya, Aichi, Japan.
   [Iversen, Edwin S.] Duke Univ, Dept Stat, Durham, NC USA.
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   [Lambrechts, Diether] Univ Leuven, VIB, Vesalius Res Ctr, Leuven, Belgium.
   [Lambrechts, Diether] Univ Leuven, Dept Oncol, Lab Translat Genet, Leuven, Belgium.
   [Le, Nhu D.] BC Canc Agcy, Canc Control Res, Vancouver, BC, Canada.
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   [Lissowska, Jolanta] M Sklodowska Curie Mem Canc Ctr, Dept Canc Epidemiol & Prevent, Warsaw, Poland.
   [Lissowska, Jolanta] Inst Oncol, Warsaw, Poland.
   [Lu, Karen] Univ Texas MD Anderson Canc Ctr, Dept Gynecol Oncol, Houston, TX 77030 USA.
   [Massuger, Leon F. A. G.; Van Altena, Anne M.] Radboud Inst Mol Life Sci, Radboud Univ Med Ctr, Nijmegen, Netherlands.
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   [Spiewankiewicz, Beata] Inst Oncol, Dept Gynecol Oncol, Warsaw, Poland.
   [Teo, Soo-Hwang] Univ Malaya, Med Ctr, Kuala Lumpur, Malaysia.
   [Thomsen, Lotte] Univ Copenhagen, Rigshosp, Dept Pathol, DK-2100 Copenhagen, Denmark.
   [Vierkant, Robert A.] Mayo Clin, Div Biomed Stat & Informat, Dept Hlth Sci Res, Rochester, MN USA.
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   [Kelemen, Linda E.] Med Univ S Carolina, Dept Publ Hlth Sci, Charleston, SC 29425 USA.
   [Berchuck, Andrew] Duke Univ, Med Ctr, Dept Obstet & Gynecol, Durham, NC USA.
   [Chenevix-Trench, Georgia; Grp, Aocs Management] QIMR Berghofer Med Res Inst, Brisbane, Qld, Australia.
   [Chenevix-Trench, Georgia; Grp, Aocs Management] Peter MacCallum Canc Ctr, East Melbourne, Australia.
   [Schildkraut, Joellen M.] Duke Canc Inst, Canc Prevent Detect & Control Res Program, Durham, NC USA.
   [Goode, Ellen L.] Mayo Clin, Div Epidemiol, Dept Hlth Sci Res, Rochester, MN USA.
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RP Phelan, CM (reprint author), H Lee Moffitt Canc Ctr & Res Inst, Dept Canc Epidemiol, 12902 Magnolia Dr, Tampa, FL 33612 USA.
EM catherine.phelan@moffitt.org
RI van Altena, Anne/B-9824-2016; Brooks-Wilson, Angela/E-9399-2012; Teo, 
   Soo-hwang/H-2353-2014; Aben, Katja/G-9686-2016; Hein,
   Alexander/F-6999-2010; Dork, Thilo/J-8620-2012; Gronwald,
   Jacek/A-4576-2017; Bjorge, Line/C-1307-2017; salvesen,
   Helga/C-1187-2017; 
OI Matsuo, Keitaro/0000-0003-1761-6314; Giles, Graham/0000-0003-4946-9099;
   Brooks-Wilson, Angela/0000-0003-1009-6408; Aben,
   Katja/0000-0002-0214-2147; Hein, Alexander/0000-0003-2601-3398;
   Gronwald, Jacek/0000-0002-3643-2871; Bjorge, Line/0000-0002-0240-2770;
   salvesen, Helga/0000-0002-4438-8831; Glasspool,
   Rosalind/0000-0002-5000-1680; Ramus, Susan/0000-0003-0005-7798;
   Krakstad, Camilla/0000-0002-0174-8139
FU Canadian Institutes of Health Research [MOP-86727]; Cancer Research UK
   [10124, C490/A10119, C490/A10124, C490/A6187]; NCI NIH HHS [K22
   CA138563, 1K99CA184415-01, K07 CA092044, K07 CA095666, K07 CA143047, K99
   CA184415, N01 CN025403, N01 PC035137, N01 PC067010, P01 CA017054, P01
   CA087969, P30 CA008748, P30 CA014089, P30 CA015083, P30 CA016056, P30
   CA072720, P50 CA105009, P50 CA136393, R01 CA-1491429, R01 CA049449, R01
   CA050385, R01 CA054419, R01 CA058598, R01 CA058860, R01 CA063678, R01
   CA063682, R01 CA067262, R01 CA074850, R01 CA076016, R01 CA080742, R01
   CA083918, R01 CA087538, R01 CA087696, R01 CA112523, R01 CA114343, R01
   CA122443, R01 CA126841, R01 CA136924, R01 CA149429, R01-CA076016, R03
   CA113148, R03 CA115195, R25 CA147832, R25T CA147832, U01 CA049449, U01
   CA058860, U01 CA067262, U01 CA069417, U19 CA148112]; NIEHS NIH HHS [T32
   ES013678, T32ES013678]
NR 36
TC 2
Z9 2
U1 1
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 DEC
PY 2015
VL 39
IS 8
BP 689
EP 697
DI 10.1002/gepi.21921
PG 9
WC Genetics & Heredity; Mathematical & Computational Biology
SC Genetics & Heredity; Mathematical & Computational Biology
GA CY7RA
UT WOS:000366605200009
PM 26399219
ER

PT J
AU Mastwal, S
   Ye, YZ
   Ren, M
   Jimenez, D
   Martinowich, K
   Gerfen, CR
   Wang, KH
AF Mastwal, Surjeet
   Ye, Yizhou
   Ren, Ming
   Jimenez, Dennisse
   Martinowich, Keri
   Gerfen, Charles R.
   Wang, Kuan Hong
TI Phasic dopamine neuron activity elicits unique mesofrontal plasticity in
   adolescence
SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE
LA English
DT Meeting Abstract
CT Joint Meeting of the 20th Biennial Meeting of the
   International-Society-for-Developmental-Neuroscience / 5th Annual
   NeuroDevNet Brain Development Conference
CY JUL 19-24, 2014
CL Montreal, CANADA
SP Int Soc Dev Neuroscience
C1 [Mastwal, Surjeet; Ye, Yizhou; Ren, Ming; Wang, Kuan Hong] NIMH, Unit Neural Circuits & Adapt Behav, Genes Cognit & Psychosis Program, NIH, Bethesda, MD 20892 USA.
   [Jimenez, Dennisse; Martinowich, Keri] Johns Hopkins Univ, Sch Med, Lieber Inst Brain Dev, Baltimore, MD 21205 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.
   [Gerfen, Charles R.] NIMH, Lab Syst Neurosci, NIH, Bethesda, MD 20892 USA.
EM wkuan@mail.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0736-5748
EI 1873-474X
J9 INT J DEV NEUROSCI
JI Int. J. Dev. Neurosci.
PD DEC
PY 2015
VL 47
SI SI
BP 95
EP 95
DI 10.1016/j.ijdevneu.2015.04.259
PN A
PG 1
WC Developmental Biology; Neurosciences
SC Developmental Biology; Neurosciences & Neurology
GA CY6QT
UT WOS:000366534600249
PM 26531581
ER

PT J
AU Wu, DY
AF Wu, Da-Yu
TI New research priorities of the National Institute on Drug Abuse (NIDA):
   Cannabis effects on brain development
SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE
LA English
DT Meeting Abstract
CT Joint Meeting of the 20th Biennial Meeting of the
   International-Society-for-Developmental-Neuroscience / 5th Annual
   NeuroDevNet Brain Development Conference
CY JUL 19-24, 2014
CL Montreal, CANADA
SP Int Soc Dev Neuroscience
C1 [Wu, Da-Yu] NIDA, Div Basic Neurosci & Behav Res, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 7
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0736-5748
EI 1873-474X
J9 INT J DEV NEUROSCI
JI Int. J. Dev. Neurosci.
PD DEC
PY 2015
VL 47
SI SI
BP 96
EP 96
DI 10.1016/j.ijdevneu.2015.04.263
PN A
PG 1
WC Developmental Biology; Neurosciences
SC Developmental Biology; Neurosciences & Neurology
GA CY6QT
UT WOS:000366534600253
PM 26531585
ER

PT J
AU Kim, C
   Prasad, V
AF Kim, Chul
   Prasad, Vinay
TI Cancer Drugs Approved on the Basis of a Surrogate End Point and
   Subsequent Overall Survival: An Analysis of 5 Years of US Food and Drug
   Administration Approvals
SO JAMA INTERNAL MEDICINE
LA English
DT Letter
C1 [Kim, Chul] NCI, Med Oncol Serv, NIH, Bethesda, MD 20892 USA.
   [Prasad, Vinay] Oregon Hlth & Sci Univ, Knight Canc Ctr, Div Hematol & Med Oncol, Portland, OR 97239 USA.
RP Prasad, V (reprint author), Oregon Hlth & Sci Univ, Knight Canc Ctr, Div Hematol & Med Oncol, 3181 SW Sam Jackson Pk Rd, Portland, OR 97239 USA.
EM prasad@ohsu.edu
NR 4
TC 24
Z9 25
U1 1
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-6106
EI 2168-6114
J9 JAMA INTERN MED
JI JAMA Intern. Med.
PD DEC
PY 2015
VL 175
IS 12
BP 1992
EP 1994
DI 10.1001/jamainternmed.2015.5868
PG 4
WC Medicine, General & Internal
SC General & Internal Medicine
GA CY3TE
UT WOS:000366332000031
PM 26502403
ER

PT J
AU Teach, SJ
   Gill, MA
   Togias, A
   Sorkness, CA
   Arbes, SJ
   Calatroni, A
   Wildfire, JJ
   Gergen, PJ
   Cohen, RT
   Pongracic, JA
   Kercsmar, CM
   Hershey, GKK
   Gruchalla, RS
   Liu, AH
   Zoratti, EM
   Kattan, M
   Grindle, KA
   Gern, JE
   Busse, WW
   Szefler, SJ
AF Teach, Stephen J.
   Gill, Michelle A.
   Togias, Alkis
   Sorkness, Christine A.
   Arbes, Samuel J., Jr.
   Calatroni, Agustin
   Wildfire, Jeremy J.
   Gergen, Peter J.
   Cohen, Robyn T.
   Pongracic, Jacqueline A.
   Kercsmar, Carolyn M.
   Hershey, Gurjit K. Khurana
   Gruchalla, Rebecca S.
   Liu, Andrew H.
   Zoratti, Edward M.
   Kattan, Meyer
   Grindle, Kristine A.
   Gern, James E.
   Busse, William W.
   Szefler, Stanley J.
TI Preseasonal treatment with either omalizumab or an inhaled
   corticosteroid boost to prevent fall asthma exacerbations
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Asthma; fall season; omalizumab; inhaled corticosteroid; asthma
   exacerbations; rhinovirus; IFN-alpha
ID INNER-CITY CHILDREN; ALLERGIC-ASTHMA; EOSINOPHILIC ASTHMA;
   IMMUNE-RESPONSES; RANDOMIZED-TRIAL; RISK-FACTORS; RHINOVIRUS; IGE;
   MEPOLIZUMAB; ADOLESCENTS
AB Background: Short-term targeted treatment can potentially prevent fall asthma exacerbations while limiting therapy exposure. Objective: We sought to compare (1) omalizumab with placebo and (2) omalizumab with an inhaled corticosteroid (ICS) boost with regard to fall exacerbation rates when initiated 4 to 6 weeks before return to school.
   Methods: A 3-arm, randomized, double-blind, double placebo-controlled, multicenter clinical trial was conducted among inner-city asthmatic children aged 6 to 17 years with 1 or more recent exacerbations (clincaltrials.gov #NCT01430403). Guidelines-based therapy was continued over a 4- to 9-month run-in phase and a 4-month intervention phase. In a subset the effects of omalizumab on IFN-alpha responses to rhinovirus in PBMCs were examined.
   Results: Before the falls of 2012 and 2013, 727 children were enrolled, 513 were randomized, and 478 were analyzed. The fall exacerbation rate was significantly lower in the omalizumab versus placebo arms (11.3% vs 21.0%; odds ratio [OR], 0.48; 95% CI, 0.25-0.92), but there was no significant difference between omalizumab and ICS boost (8.4% vs 11.1%; OR, 0.73; 95% CI, 0.33-1.64). In a prespecified subgroup analysis, among participants with an exacerbation during the run-in phase, omalizumab was significantly more efficacious than both placebo (6.4% vs 36.3%; OR, 0.12; 95% CI, 0.02-0.64) and ICS boost (2.0% vs 27.8%; OR, 0.05; 95% CI, 0.002-0.98). Omalizumab improved IFN-a responses to rhinovirus, and within the omalizumab group, greater IFN-a increases were associated with fewer exacerbations (OR, 0.14; 95% CI, 0.01-0.88). Adverse events were rare and similar among arms.
   Conclusions: Adding omalizumab before return to school to ongoing guidelines-based care among inner-city youth reduces fall asthma exacerbations, particularly among those with a recent exacerbation.
C1 [Teach, Stephen J.] Childrens Natl Hlth Syst, Div Emergency Med, Washington, DC 20010 USA.
   [Teach, Stephen J.] Childrens Natl Hlth Syst, Dept Pediat, Washington, DC 20010 USA.
   [Gill, Michelle A.; Gruchalla, Rebecca S.] Univ Texas SW Med Ctr Dallas, Dept Pediat, Dallas, TX 75390 USA.
   [Gill, Michelle A.] Univ Texas SW Med Ctr Dallas, Dept Immunol, Dallas, TX 75390 USA.
   [Togias, Alkis; Gergen, Peter J.] NIAID, Bethesda, MD 20892 USA.
   [Sorkness, Christine A.; Grindle, Kristine A.; Gern, James E.; Busse, William W.] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI USA.
   [Arbes, Samuel J., Jr.; Calatroni, Agustin; Wildfire, Jeremy J.] Rho Inc, Fed Syst Div, Chapel Hill, NC USA.
   [Cohen, Robyn T.] Boston Univ, Sch Med, Boston, MA 02215 USA.
   [Pongracic, Jacqueline A.] Ann & Robert H Lurie Childrens Hosp Chicago, Chicago, IL 60611 USA.
   [Kercsmar, Carolyn M.; Hershey, Gurjit K. Khurana] Cincinnati Childrens Hosp, Denver, CO USA.
   [Liu, Andrew H.] Natl Jewish Hlth, Denver, CO USA.
   [Zoratti, Edward M.] Henry Ford Hosp, Dept Internal Med, Div Allergy & Immunol, Detroit, MI 48202 USA.
   [Kattan, Meyer] Columbia Univ, Coll Phys & Surg, New York, NY USA.
   [Liu, Andrew H.; Szefler, Stanley J.] Childrens Hosp Colorado, Aurora, CO USA.
   [Liu, Andrew H.; Szefler, Stanley J.] Univ Colorado, Sch Med, Aurora, CO USA.
RP Teach, SJ (reprint author), Childrens Natl Hlth Syst, 111 Michigan Ave NW, Washington, DC 20010 USA.
EM steach@childrensnational.org
OI Togias, Alkis/0000-0001-9009-5717; Khurana Hershey,
   Gurjit/0000-0001-6663-977X; Cohen, Robyn/0000-0002-6902-3118
FU National Institute of Allergy and Infectious Diseases, National
   Institutes of Health, Department of Health and Human Services
   [HHSN272200900052C, HHSN272201000052I]; National Center for Research
   Resources; National Center for Advancing Translational Sciences,
   National Institutes of Health [NCRR/NIH UL1TR000451, 1UL1RR025780,
   UL1TR000075, NCATS/NIH UL1 TR000154, UL1 TR000077-04, NCATS/NIH
   UL1TR000040, UL1TR000150, UL1TR001105, NIH NIAID 5R01AI098077,
   UM1AI109565]
FX This project has been funded in whole or in part with federal funds from
   the National Institute of Allergy and Infectious Diseases, National
   Institutes of Health, Department of Health and Human Services, under
   contracts HHSN272200900052C and HHSN272201000052I. Additional support
   was provided by the National Center for Research Resources and the
   National Center for Advancing Translational Sciences, National
   Institutes of Health, under grants NCRR/NIH UL1TR000451, 1UL1RR025780,
   UL1TR000075 and NCATS/NIH UL1 TR000154, UL1 TR000077-04, NCATS/NIH
   UL1TR000040, UL1TR000150, and UL1TR001105, NIH NIAID 5R01AI098077, and
   UM1AI109565. The following were donated: omalizumab and matching placebo
   by Novartis and fluticasone and matching placebo by GlaxoSmithKline
   under a clinical trial agreement with the University of
   Wisconsin-Madison; EpiPens by Mylan; and Ayr nasal rinse by B.F. Ascher
   & Company.
NR 31
TC 34
Z9 36
U1 1
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
EI 1097-6825
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD DEC
PY 2015
VL 136
IS 6
BP 1476
EP 1485
DI 10.1016/j.jaci.2015.09.008
PG 10
WC Allergy; Immunology
SC Allergy; Immunology
GA CX9RZ
UT WOS:000366044300006
PM 26518090
ER

PT J
AU Carter, MC
   Clayton, ST
   Komarow, HD
   Brittain, EH
   Scott, LM
   Cantave, D
   Gaskins, DM
   Maric, I
   Metcalfe, DD
AF Carter, Melody C.
   Clayton, Sarah T.
   Komarow, Hirsh D.
   Brittain, Erica H.
   Scott, Linda M.
   Cantave, Daly
   Gaskins, Donna M.
   Maric, Irina
   Metcalfe, Dean D.
TI Assessment of clinical findings, tryptase levels, and bone marrow
   histopathology in the management of pediatric mastocytosis
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Mast cells; tryptase; urticaria pigmentosa; cutaneous mastocytosis;
   diffuse cutaneous mastocytosis; mastocytosis; bone marrow examination
ID CUTANEOUS MASTOCYTOSIS; SYSTEMIC MASTOCYTOSIS; URTICARIA-PIGMENTOSA;
   FOLLOW-UP; CHILDREN; ADULTS; ONSET; RECOMMENDATIONS; INVOLVEMENT;
   DIAGNOSIS
AB Background: The management of children with pediatric mastocytosis poses a challenge. This is because there is limited information as to the application of clinical and laboratory findings and bone marrow histopathology as they relate to medical intervention and communication.
   Objective: We sought to examine clinical aspects of pediatric mastocytosis in relationship to serum tryptase levels and bone marrow pathology to provide practical guidance for management.
   Methods: Between 1986 and 2012, 105 children were evaluated at the National Institutes of Health. Organomegaly was confirmed by means of ultrasound. Baseline tryptase levels and at least 1 subsequent tryptase measurement was available in 84 and 37 of these children, respectively. Fifty-three children underwent a bone marrow examination. These data were used to examine relationships between clinical findings, tryptase levels, and marrow histopathology.
   Results: In patients with high tryptase levels and severe mediator symptoms, all with organomegaly had systemic disease, and none without organomegaly had systemic disease. Serum tryptase levels differed significantly between patients with urticaria pigmentosa and those with diffuse cutaneous (P < .0001) and systemic mastocytosis (P < .0001) and in all 3 categories versus control subjects (P < .0001). Tryptase levels and symptoms decreased over time in most patients, and tryptase levels correlated with bone marrow mast cell burden in patients with systemic mastocytosis (P < .0001). There was a significant relationship between clinical resolution and the percentage decrease in tryptase levels (P = .0014).
   Conclusions: The majority of children experienced major or complete disease resolution (57%), whereas the remainder exhibited partial improvement. Organomegaly was a strong indicator of systemic disease. Serum tryptase levels furthered classification and reflected clinicopathologic findings, while sequential tryptase measurements were useful in supplementing clinical judgment as to disease course.
C1 [Carter, Melody C.; Clayton, Sarah T.; Komarow, Hirsh D.; Scott, Linda M.; Gaskins, Donna M.; Metcalfe, Dean D.] NIAID, Lab Allerg Dis, Bethesda, MD 20892 USA.
   [Brittain, Erica H.] NIAID, Biostat Res Branch, Bethesda, MD 20892 USA.
   [Cantave, Daly] NIH, Dept Nursing, Clin Ctr, Bethesda, MD 20892 USA.
   [Maric, Irina] NIH, Hematol Sect, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Carter, MC (reprint author), Bldg 10-11C207,10 Ctr Dr,MSC 1881, Bethesda, MD 20892 USA.
EM mcarter@niaid.nih.gov
FU Division of Intramural Research, National Institute of Allergy and
   Infectious Diseases, National Institutes of Health
FX Supported by the Division of Intramural Research, National Institute of
   Allergy and Infectious Diseases, National Institutes of Health.
NR 25
TC 3
Z9 3
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
EI 1097-6825
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD DEC
PY 2015
VL 136
IS 6
BP 1673
EP U378
DI 10.1016/j.jaci.2015.04.024
PG 10
WC Allergy; Immunology
SC Allergy; Immunology
GA CX9RZ
UT WOS:000366044300030
PM 26044856
ER

PT J
AU Bernhardt, ML
   Zhang, YP
   Erxleben, CF
   Padilla-Banks, E
   McDonough, CE
   Miao, YL
   Armstrong, DL
   Williams, CJ
AF Bernhardt, Miranda L.
   Zhang, Yingpei
   Erxleben, Christian F.
   Padilla-Banks, Elizabeth
   McDonough, Caitlin E.
   Miao, Yi-Liang
   Armstrong, David L.
   Williams, Carmen J.
TI Ca(V)3.2 T-type channels mediate Ca2+ entry during oocyte maturation and
   following fertilization
SO JOURNAL OF CELL SCIENCE
LA English
DT Article
DE Oocyte; Ca2+; T-type channel; Meiosis; Fertilization; Egg activation
ID MOUSE EGG ACTIVATION; REPETITIVE CALCIUM TRANSIENTS; MEIOTIC MATURATION;
   EMBRYO DEVELOPMENT; HYPERPOLARIZING RESPONSES; INTRACELLULAR CALCIUM;
   ENDOPLASMIC-RETICULUM; SPERMATOGENIC CELLS; COMPARATIVE BIOLOGY;
   POLYSPERMY BLOCK
AB Initiation of mouse embryonic development depends upon a series of fertilization-induced rises in intracellular Ca2+. Complete egg activation requires influx of extracellular Ca2+; however, the channels that mediate this influx remain unknown. Here, we tested whether the alpha 1 subunit of the T-type channel Ca(V)3.2, encoded by Cacna1h, mediates Ca2+ entry into oocytes. We show that mouse eggs express a robust voltage-activated Ca2+ current that is completely absent in Cacna1h(-/-) eggs. Cacna1h(-/-) females have reduced litter sizes, and careful analysis of Ca2+ oscillation patterns in Cacna1h(-/-) eggs following in vitro fertilization (IVF) revealed reductions in first transient length and oscillation persistence. Total and endoplasmic reticulum (ER) Ca2+ stores were also reduced in Cacna1h(-/-) eggs. Pharmacological inhibition of Ca(V)3.2 in wild-type CF-1 strain eggs using mibefradil or pimozide reduced Ca2+ store accumulation during oocyte maturation and reduced Ca2+ oscillation persistence, frequency and number following IVF. Overall, these data show that Ca(V)3.2 T-type channels have prev8iously unrecognized roles in supporting the meiotic-maturation-associated increase in ER Ca2+ stores and mediating Ca2+ influx required for the activation of development.
C1 [Bernhardt, Miranda L.; Zhang, Yingpei; Padilla-Banks, Elizabeth; McDonough, Caitlin E.; Williams, Carmen J.] NIH, Reprod & Dev Biol Lab, Res Triangle Pk, NC 27709 USA.
   [Erxleben, Christian F.; Armstrong, David L.] NIH, Neurobiol Lab, Res Triangle Pk, NC 27709 USA.
   [Miao, Yi-Liang] Huazhong Agr Univ, Coll Anim Sci & Technol, Key Lab Anim Genet Breeding & Reprod, Minist Educ, Wuhan 430070, Peoples R China.
RP Williams, CJ (reprint author), NIH, Reprod & Dev Biol Lab, Res Triangle Pk, NC 27709 USA.
EM williamsc5@niehs.nih.gov
FU Intramural Research Program of the National Institutes of Health,
   National Institutes of Environmental Health Sciences [1ZIAES102985]
FX This work was supported by the Intramural Research Program of the
   National Institutes of Health, National Institutes of Environmental
   Health Sciences [grant number 1ZIAES102985]. Deposited in PMC for
   release after 12 months.
NR 67
TC 5
Z9 5
U1 3
U2 9
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
   CAMBS, ENGLAND
SN 0021-9533
EI 1477-9137
J9 J CELL SCI
JI J. Cell Sci.
PD DEC 1
PY 2015
VL 128
IS 23
BP 4442
EP 4452
DI 10.1242/jcs.180026
PG 11
WC Cell Biology
SC Cell Biology
GA CY3NL
UT WOS:000366316400020
PM 26483387
ER

PT J
AU Gold, AL
   Jarcho, JM
   Rosen, DK
   Pine, DS
   Ernst, M
AF Gold, Andrea L.
   Jarcho, Johanna M.
   Rosen, Dana K.
   Pine, Daniel S.
   Ernst, Monique
TI Emotional and Nonemotional Conflict Processing in Pediatric and Adult
   Anxiety Disorders
SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY
LA English
DT Article
ID ERROR-RELATED NEGATIVITY; OBSESSIVE-COMPULSIVE DISORDER; GENERALIZED
   ANXIETY; COGNITIVE CONTROL; BRAIN ACTIVITY; TRAIT ANXIETY;
   BEHAVIORAL-INHIBITION; DEPRESSIVE-DISORDERS; IMPLICIT REGULATION;
   ADAPTATION
AB Objective: Perturbations in emotional conflict adaptation, an implicit regulatory process, have been observed in adult anxiety disorders. However, findings remain inconsistent and restricted to adults. The current study compares conflict adaptation in youth and adults, with and without anxiety disorders. We predicted conflict adaptation would be present in the healthy but not the anxious groups. Methods: In a clinic setting, 111 participants (27 healthy youth, 22 anxious youth, 41 healthy adults, and 21 anxious adults) completed emotional and nonemotional conflict tasks. Groups did not differ (all p's >0.1) on intelligence quotient (IQ), gender, and socioeconomic status; age did not differ between healthy and anxious subjects in either age cohort. Separate four way mixed-design analyses of variance were conducted to test hypotheses regarding the influence of diagnosis, age group, and task type on accuracy (percent correct) and reaction time (RT) for conflict adaptation (incongruent trials preceded by incongruent vs. congruent trials) and conflict detection (incongruent vs. congruent trials). Results: Measures of conflict adaptation did not interact with diagnosis or age. There was a significant main effect of conflict adaptation across the overall sample in the expected direction for accuracy, but not RT. The well-replicated conflict detection effect also did emerge across tasks, with slower RT and lower accuracy for incongruent than for congruent trials. These effects were greater for the emotional than for nonemotional tasks. Finally, there were age differences in accuracy-based conflict detection specific to the emotional task, for which the size of the effect was larger for youth than for adults. Conclusions: The current study of youth and adults did not replicate prior behavioral findings of failure to engage conflict adaptation in anxiety disorders. Therefore, more work is needed before widely adopting conflict adaptation paradigms as a standard neurocognitive marker for anxiety disorders.
C1 [Gold, Andrea L.; Jarcho, Johanna M.; Rosen, Dana K.; Pine, Daniel S.; Ernst, Monique] NIMH, Sect Dev & Affect Neurosci, NIH, Bethesda, MD 20892 USA.
RP Gold, AL (reprint author), NIH, 9000 Rockville Pike MSC 2670,Bldg 15K, Bethesda, MD 20892 USA.
EM andrea.gold@nih.gov
OI Jarcho, Johanna/0000-0001-9075-6968; Gold, Andrea/0000-0003-4447-776X
FU Intramural NIH HHS
NR 50
TC 0
Z9 0
U1 3
U2 8
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1044-5463
EI 1557-8992
J9 J CHILD ADOL PSYCHOP
JI J. Child Adolesc. Psychopharmacol.
PD DEC 1
PY 2015
VL 25
IS 10
BP 754
EP 763
DI 10.1089/cap.2015.0066
PG 10
WC Pediatrics; Pharmacology & Pharmacy; Psychiatry
SC Pediatrics; Pharmacology & Pharmacy; Psychiatry
GA CY9JT
UT WOS:000366723900004
PM 26544668
ER

PT J
AU Matsudaira, T
   Gow, RV
   Kelly, J
   Murphy, C
   Potts, L
   Sumich, A
   Ghebremeskel, K
   Crawford, MA
   Taylor, E
AF Matsudaira, Toshiko
   Gow, Rachel V.
   Kelly, Joanna
   Murphy, Caroline
   Potts, Laura
   Sumich, Alexander
   Ghebremeskel, Kebreab
   Crawford, Michael A.
   Taylor, Eric
TI Biochemical and Psychological Effects of Omega-3/6 Supplements in Male
   Adolescents with Attention-Deficit/Hyperactivity Disorder: A Randomized,
   Placebo-Controlled, Clinical Trial
SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY
LA English
DT Article
ID DEFICIT HYPERACTIVITY DISORDER; POLYUNSATURATED FATTY-ACIDS; BRAIN
   DOCOSAHEXAENOIC ACID; YOUNG-ADULT PRISONERS; DOUBLE-BLIND; LINOLENIC
   ACID; CHILDREN; BEHAVIOR; ADHD; RATS
AB Background: An abnormality in long chain-polyunsaturated fatty acid (LC-PUFA) levels has been implicated in attention-deficit/hyperactivity disorder (ADHD). Studies evaluating LC-PUFA supplementation for therapeutic efficacy in ADHD have shown mixed and, therefore, inconclusive results. Methods: Seventy-six male adolescents (age 12-16 years, mean=13.7) with ADHD were assessed for the effects of 12 weeks omega-3 and omega-6 supplements on biochemical and psychological outcomes in a randomized, placebo-controlled, clinical trial. The primary outcome measure was change in the Conners' Teacher Rating Scales (CTRS) following 12 weeks of supplementation of LC-PUFA or placebo. At baseline, the placebo and treatment groups had comparable levels of LC-PUFA as measured by red blood cell phosphatidylcholine. In the treatment group, supplementation enhanced eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and total omega-3 fatty acid levels. Results: No superiority of LC-PUFAs to placebo was observed on the primary outcome. Further, there were no reliable treatment effects on aggression, impulsivity, depression, and anxiety. Conclusions: Future studies should use larger sample sizes and longer supplementation period to detect small-modest effects for clinical recommendations in ADHD.
C1 [Matsudaira, Toshiko; Taylor, Eric] Inst Psychiat Psychol & Neurosci, Dept Adolescent & Child Psychiat, London, England.
   [Gow, Rachel V.] NIH, Sect Nutr Neurosci, Bethesda, MD 20892 USA.
   [Kelly, Joanna; Murphy, Caroline; Potts, Laura] Inst Psychiat, Dept Biostat, Kings Clin Trials Unit, London, England.
   [Sumich, Alexander] Nottingham Trent Univ, Sch Social Sci, Div Psychol, Nottingham, England.
   [Ghebremeskel, Kebreab] London Metropolitan Univ, Lipid & Nutr Res Ctr, London, England.
   [Crawford, Michael A.] Univ London Imperial Coll Sci Technol & Med, Fac Med, Reprod Physiol, London, England.
RP Matsudaira, T (reprint author), 1-15-9 Sekiguchi,Bunkyo Ku, Tokyo 1120014, Japan.
EM toshimatsudaira@yahoo.co.jp
NR 58
TC 2
Z9 2
U1 6
U2 20
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1044-5463
EI 1557-8992
J9 J CHILD ADOL PSYCHOP
JI J. Child Adolesc. Psychopharmacol.
PD DEC 1
PY 2015
VL 25
IS 10
BP 775
EP 782
DI 10.1089/cap.2015.0052
PG 8
WC Pediatrics; Pharmacology & Pharmacy; Psychiatry
SC Pediatrics; Pharmacology & Pharmacy; Psychiatry
GA CY9JT
UT WOS:000366723900006
PM 26682998
ER

PT J
AU Calkins, ME
   Merikangas, KR
   Moore, TM
   Burstein, M
   Behr, MA
   Satterthwaite, TD
   Ruparel, K
   Wolf, DH
   Roalf, DR
   Mentch, FD
   Qiu, HJ
   Chiavacci, R
   Connolly, JJ
   Sleiman, PMA
   Gur, RC
   Hakonarson, H
   Gur, RE
AF Calkins, Monica E.
   Merikangas, Kathleen R.
   Moore, Tyler M.
   Burstein, Marcy
   Behr, Meckenzie A.
   Satterthwaite, Theodore D.
   Ruparel, Kosha
   Wolf, Daniel H.
   Roalf, David R.
   Mentch, Frank D.
   Qiu, Haijun
   Chiavacci, Rosetta
   Connolly, John J.
   Sleiman, Patrick M. A.
   Gur, Ruben C.
   Hakonarson, Hakon
   Gur, Raquel E.
TI The Philadelphia Neurodevelopmental Cohort: constructing a deep
   phenotyping collaborative
SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY
LA English
DT Article
DE Community cohort; children; adolescents; young adults; psychopathology;
   mood; anxiety; behavior; psychosis; comorbidity; structure; genomics;
   neuroimaging; neurocognition; public domain
ID SUPPLEMENT NCS-A; COMMON MENTAL-DISORDERS; COMMUNITY SAMPLE; PSYCHOSIS
   SPECTRUM; SEX-DIFFERENCES; SUBSTANCE USE; RISK-FACTORS; FIT INDEXES;
   REPLICATION; COMORBIDITY
AB Background: An integrative multidisciplinary approach is required to elucidate the multiple factors that shape neurodevelopmental trajectories of mental disorders. The Philadelphia Neurodevelopmental Cohort (PNC), funded by the National Institute of Mental Health Grand Opportunity (GO) mechanism of the American Recovery and Reinvestment Act, was designed to characterize clinical and neurobehavioral phenotypes of genotyped youths. Data generated, which are recently available through the NIMH Database of Genotypes and Phenotypes (dbGaP), have garnered considerable interest. We provide an overview of PNC recruitment and clinical assessment methods to allow informed use and interpretation of the PNC resource by the scientific community. We also evaluate the structure of the assessment tools and their criterion validity. Methods: Participants were recruited from a large pool of youths (n = 13,958) previously identified and genotyped at The Children's Hospital of Philadelphia. A comprehensive computerized tool for structured evaluation of psychopathology domains (GOASSESS) was constructed. We administered GOASSESS to all participants and used factor analysis to evaluate its structure. Results: A total of 9,498 youths (aged 8-21; mean age = 14.2; European American = 55.8%; African American = 32.9%; Other = 11.4%) were enrolled. Factor analysis revealed a strong general psychopathology factor, and specific 'anxious-misery', 'fear', and 'behavior' factors. The 'behavior' factor had a small negative correlation (-0.21) with overall accuracy of neurocognitive performance, particularly in tests of executive and complex reasoning. Being female had a high association with the 'anxious-misery' and low association with the 'behavior' factors. The psychosis spectrum was also best characterized by a general factor and three specific factors: ideas about 'special abilities/persecution,' 'unusual thoughts/perceptions', and 'negative/disorganized' symptoms. Conclusions: The PNC assessment mechanism yielded psychopathology data with strong factorial validity in a large diverse community cohort of genotyped youths. Factor scores should be useful for dimensional integration with other modalities (neuroimaging, genomics). Thus, PNC public domain resources can advance understanding of complex interrelationships among genes, cognition, brain, and behavior involved in neurodevelopment of common mental disorders.
C1 [Calkins, Monica E.; Moore, Tyler M.; Satterthwaite, Theodore D.; Ruparel, Kosha; Wolf, Daniel H.; Roalf, David R.; Gur, Ruben C.; Gur, Raquel E.] Univ Penn, Dept Psychiat, Neuropsychiat Sect, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Merikangas, Kathleen R.; Burstein, Marcy] NIMH, Genet Epidemiol Res Branch, Intramural Res Program, Bethesda, MD 20892 USA.
   [Behr, Meckenzie A.; Mentch, Frank D.; Qiu, Haijun; Chiavacci, Rosetta; Connolly, John J.; Hakonarson, Hakon] Childrens Hosp Philadelphia, Ctr Appl Genom, Philadelphia, PA 19104 USA.
   [Sleiman, Patrick M. A.] Univ Penn, Dept Pediat, Perelman Sch Med, Philadelphia, PA 19104 USA.
RP Calkins, ME (reprint author), Univ Penn, Dept Psychiat, Neuropsychiat Sect, Perelman Sch Med, 9 Maloney,3600 Spruce St, Philadelphia, PA 19104 USA.
EM mcalkins@upenn.edu
FU National Institute of Mental Health [MH089983, MH089924, K08MH079364,
   K23MH098130]; Dowshen Program for Neuroscience; Marc Rapport Family
   Investigator grant through Brain and Behavior Foundation
FX This work was supported by the National Institute of Mental Health
   (R.E.G. and H.H, RC2 grant numbers MH089983 and MH089924), (M.E.C.,
   grant number K08MH079364), and (T.D.S., grant number K23MH098130); the
   Dowshen Program for Neuroscience; and the Marc Rapport Family
   Investigator grant through the Brain and Behavior Foundation (T.D.S.).
   The authors thank the participants of this study, and all the members of
   the Recruitment, Assessment, and Data Teams whose individual
   contributions collectively made this work possible. Also William G.
   Iacono and Genevieve Ryczek (University of Minnesota Center for Twin and
   Family Research; MCTFR) for their consultation while developing our
   recruitment strategy, and Iacono for allowing use, modification, and
   computerization of the MCFTR substance use measure. The authors have
   declared that they have no competing or potential conflicts of interest.
NR 43
TC 10
Z9 10
U1 3
U2 8
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 DEC
PY 2015
VL 56
IS 12
BP 1356
EP 1369
DI 10.1111/jcpp.12416
PG 14
WC Psychology, Developmental; Psychiatry; Psychology
SC Psychology; Psychiatry
GA CY6IK
UT WOS:000366512300010
PM 25858255
ER

PT J
AU Lee, C
   Kim, KP
   Bolch, WE
   Moroz, BE
   Folio, L
AF Lee, Choonsik
   Kim, Kwang Pyo
   Bolch, Wesley E.
   Moroz, Brian E.
   Folio, Les
TI NCICT: a computational solution to estimate organ doses for pediatric
   and adult patients undergoing CT scans
SO JOURNAL OF RADIOLOGICAL PROTECTION
LA English
DT Article
DE computed tomography; organ dose; computational phantoms; Monte Carlo
   simulation
ID COMPUTED-TOMOGRAPHY; RADIATION-EXPOSURE; HYBRID PHANTOMS; HUMAN ANATOMY;
   BRAIN-TUMORS; DOSIMETRY; MODELS; PROTECTION; LEUKEMIA; PROGRAM
AB We developed computational methods and tools to assess organ doses for pediatric and adult patients undergoing computed tomography (CT) examinations. We used the International Commission on Radiological Protection (ICRP) reference pediatric and adult phantoms combined with the Monte Carlo simulation of a reference CT scanner to establish comprehensive organ dose coefficients (DC), organ absorbed dose per unit volumetric CT Dose Index (CTDIvol) (mGy/mGy). We also developed methods to estimate organ doses with tube current modulation techniques and size specific dose estimates. A graphical user interface was designed to obtain user input of patient- and scan-specific parameters, and to calculate and display organ doses. A batch calculation routine was also integrated into the program to automatically calculate organ doses for a large number of patients. We entitled the computer program, National Cancer Institute dosimetry system for CT(NCICT). We compared our dose coefficients with those from CT-Expo, and evaluated the performance of our program using CT patient data. Our pediatric DCs show good agreements of organ dose estimation with those from CT-Expo except for thyroid. Our results support that the adult phantom in CT-Expo seems to represent a pediatric individual between 10 and 15 years rather than an adult. The comparison of CTDIvol values between NCICT and dose pages from 10 selected CT scans shows good agreements less than 12% except for two cases (up to 20%). The organ dose comparison between mean and modulated mAs shows that mean mAs-based calculation significantly overestimates dose (up to 2.4-fold) to the organs in close proximity to lungs in chest and chest-abdomen-pelvis scans. Our program provides more realistic anatomy based on the ICRP reference phantoms, higher age resolution, the most up-to-date bone marrow dosimetry, and several convenient features compared to previous tools. The NCICT will be available for research purpose in the near future.
C1 [Lee, Choonsik; Moroz, Brian E.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Kim, Kwang Pyo] Kyung Hee Univ, Dept Nucl Engn, Gyeonggi Do, South Korea.
   [Bolch, Wesley E.] Univ Florida, Dept Biomed Engn, Gainesville, FL 32611 USA.
   [Folio, Les] NIH, Radiol & Imaging Sci Clin Ctr, Bethesda, MD 20892 USA.
RP Lee, C (reprint author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20850 USA.
EM leechoonsik@mail.nih.gov
FU intramural research program of the National Institutes of Health,
   National Cancer Institute, Division of Cancer Epidemiology and Genetics
FX This work was supported by the intramural research program of the
   National Institutes of Health, National Cancer Institute, Division of
   Cancer Epidemiology and Genetics. This study utilised the
   high-performance computational capabilities of the Biowulf computing
   system at the National Institutes of Health, Bethesda, MD.
   (http://biowulf.nih.gov).
NR 42
TC 3
Z9 3
U1 2
U2 8
PU IOP PUBLISHING LTD
PI BRISTOL
PA TEMPLE CIRCUS, TEMPLE WAY, BRISTOL BS1 6BE, ENGLAND
SN 0952-4746
EI 1361-6498
J9 J RADIOL PROT
JI J. Radiol. Prot.
PD DEC
PY 2015
VL 35
IS 4
BP 891
EP 909
DI 10.1088/0952-4746/35/4/891
PG 19
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 CY4OU
UT WOS:000366388500011
ER

PT J
AU Rahu, K
   Rahu, M
   Tekkel, M
   Veidebaum, T
   Hakulinen, T
   Auvinen, A
   Bigbee, WL
   Hartshorne, MF
   Inskip, PD
   Boice, JD
AF Rahu, Kaja
   Rahu, Mati
   Tekkel, Mare
   Veidebaum, Toomas
   Hakulinen, Timo
   Auvinen, Anssi
   Bigbee, William L.
   Hartshorne, Michael F.
   Inskip, Peter D.
   Boice, John D., Jr.
TI Chernobyl cleanup workers from Estonia: cohort description and related
   epidemiological research
SO JOURNAL OF RADIOLOGICAL PROTECTION
LA English
DT Review
DE Chernobyl cleanup workers; cancer incidence; cohort; mortality;
   radiation exposure; record linkage; suicide
ID MINISATELLITE MUTATION-RATE; CANCER INCIDENCE; THYROID-CANCER;
   FOLLOW-UP; RISK; LIQUIDATORS; ACCIDENT; BIODOSIMETRY; MORTALITY;
   CHILDREN
AB The Estonian study of Chernobyl cleanup workers was one of the first investigations to evaluate the possible health consequences of working in the Chernobyl area (the 30 km exclusion zone and/or adjacent territories) after the 1986 reactor accident. The cohort consists of 4831 men who were dispatched in 1986-1991 for tasks involving decontamination, construction of buildings, transport, radiation measurement, guard duty or other activities. By 31 December 2012, the follow-up of the cohort yielded 102 158 person-years of observation. Exposure and health data were collected by postal questionnaires, biodosimetry evaluations, thyroid screenings, and record-linkages with cancer, causes of death and health insurance reimbursement registers and databases. These data cover socio-demographic factors, employment history, aspects of health behaviour, medical history, work and living conditions in the Chernobyl area, biomarkers of exposure, cancer and non-cancer disease occurrence and causes of death. Cancer incidence data were obtained for 1986-2008, mortality data for 1986-2011 and non-cancer morbidity data for 2004-2012. Although the cohort is relatively small, it has been extensively examined and benefited from comprehensive nationwide population and health registers. The major finding was an increased risk of suicide. Thyroid examinations did not reveal an association with thyroid nodular disease and radiation dose, but did indicate the importance of accounting for screening when making comparisons with unscreened populations. No risk of leukaemia was observed and risks higher than 2.5-fold could be excluded with 95% confidence. Biodosimetry included GPA analyses and chromosomal translocation analyses and indicated that the Estonian cleanup workers experienced a relatively low mean exposure of the order of 0.1 Gy. One value of the Estonian study is in the methodologic processes brought to bear in addressing possible health effects from the Chernobyl accident. Twenty-five years of research are summarised and opportunities for the future listed.
C1 [Rahu, Kaja; Rahu, Mati; Tekkel, Mare] Natl Inst Hlth Dev, Dept Epidemiol & Biostat, Tallinn, Estonia.
   [Veidebaum, Toomas] Natl Inst Hlth Dev, Tallinn, Estonia.
   [Hakulinen, Timo] Finnish Canc Registry, FIN-00170 Helsinki, Finland.
   [Auvinen, Anssi] Univ Tampere, Sch Hlth Sci, FIN-33101 Tampere, Finland.
   [Auvinen, Anssi] STUK Radiat & Nucl Safety Author, Helsinki, Finland.
   [Bigbee, William L.] Univ Pittsburgh, Sch Med, Dept Pathol, Pittsburgh, PA USA.
   [Bigbee, William L.] Univ Pittsburgh, Hillman Canc Ctr, Inst Canc, Pittsburgh, PA USA.
   [Hartshorne, Michael F.] Univ New Mexico, Dept Radiol, Albuquerque, NM 87131 USA.
   [Inskip, Peter D.] NCI, Dept Hlth & Human Serv, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet,NIH, Bethesda, MD 20892 USA.
   [Boice, John D., Jr.] Natl Council Radiat Protect & Measurements, Bethesda, MD USA.
   [Boice, John D., Jr.] Vanderbilt Univ, Sch Med, Div Epidemiol, Nashville, TN 37212 USA.
RP Rahu, K (reprint author), Natl Inst Hlth Dev, Dept Epidemiol & Biostat, Tallinn, Estonia.
EM kaja.rahu@tai.ee
RI Rahu, Mati/A-9981-2008
FU Estonian Research Council [IUT5-1]; US National Cancer Institute
   [N01-CP-85638-03]
FX This stage of the study was supported by the Estonian Research Council
   (IUT5-1). The initial work was financed by US National Cancer Institute
   Contract N01-CP-85638-03.
NR 31
TC 1
Z9 1
U1 1
U2 6
PU IOP PUBLISHING LTD
PI BRISTOL
PA TEMPLE CIRCUS, TEMPLE WAY, BRISTOL BS1 6BE, ENGLAND
SN 0952-4746
EI 1361-6498
J9 J RADIOL PROT
JI J. Radiol. Prot.
PD DEC
PY 2015
VL 35
IS 4
BP R35
EP R45
DI 10.1088/0952-4746/35/4/R35
PG 11
WC Environmental Sciences; Public, Environmental & Occupational Health;
   Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical
   Imaging
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
   Health; Nuclear Science & Technology; Radiology, Nuclear Medicine &
   Medical Imaging
GA CY4OU
UT WOS:000366388500003
PM 26512763
ER

PT J
AU Taylor, JK
   Coleman, CM
   Postel, S
   Sisk, JM
   Bernbaum, JG
   Venkataraman, T
   Sundberg, EJ
   Frieman, MB
AF Taylor, Justin K.
   Coleman, Christopher M.
   Postel, Sandra
   Sisk, Jeanne M.
   Bernbaum, John G.
   Venkataraman, Thiagarajan
   Sundberg, Eric J.
   Frieman, Matthew B.
TI Severe Acute Respiratory Syndrome Coronavirus ORF7a Inhibits Bone Marrow
   Stromal Antigen 2 Virion Tethering through a Novel Mechanism of
   Glycosylation Interference
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID PAPAIN-LIKE PROTEASE; SARS-CORONAVIRUS; CELL-SURFACE; MURINE
   CORONAVIRUS; MOLECULAR-CLONING; AIRWAY EPITHELIA; HIV-1 RELEASE; VIRUS;
   BST-2/TETHERIN; VPU
AB Severe acute respiratory syndrome (SARS) emerged in November 2002 as a case of atypical pneumonia in China, and the causative agent of SARS was identified to be a novel coronavirus, severe acute respiratory syndrome coronavirus (SARS-CoV). Bone marrow stromal antigen 2 (BST-2; also known as CD317 or tetherin) was initially identified to be a pre-B-cell growth promoter, but it also inhibits the release of virions of the retrovirus human immunodeficiency virus type 1 (HIV-1) by tethering budding virions to the host cell membrane. Further work has shown that BST-2 restricts the release of many other viruses, including the human coronavirus 229E (hCoV-229E), and the genomes of many of these viruses encode BST-2 antagonists to overcome BST-2 restriction. Given the previous studies on BST-2, we aimed to determine if BST-2 has the ability to restrict SARS-CoV and if the SARS-CoV genome encodes any proteins that modulate BST-2's antiviral function. Through an in vitro screen, we identified four potential BST-2 modulators encoded by the SARS-CoV genome: the papain-like protease (PLPro), nonstructural protein 1 (nsp1), ORF6, and ORF7a. As the function of ORF7a in SARS-CoV replication was previously unknown, we focused our study on ORF7a. We found that BST-2 does restrict SARS-CoV, but the loss of ORF7a leads to a much greater restriction, confirming the role of ORF7a as an inhibitor of BST-2. We further characterized the mechanism of BST-2 inhibition by ORF7a and found that ORF7a localization changes when BST-2 is overexpressed and ORF7a binds directly to BST-2. Finally, we also show that SARS-CoV ORF7a blocks the restriction activity of BST-2 by blocking the glycosylation of BST-2.
   IMPORTANCE
   The severe acute respiratory syndrome coronavirus (SARS-CoV) emerged from zoonotic sources in 2002 and caused over 8,000 infections and 800 deaths in 37 countries around the world. Identifying host factors that regulate SARS-CoV pathogenesis is critical to understanding how this lethal virus causes disease. We have found that BST-2 is capable of restricting SARS-CoV release from cells; however, we also identified a SARS-CoV protein that inhibits BST-2 function. We show that the SARS-CoV protein ORF7a inhibits BST-2 glycosylation, leading to a loss of BST-2's antiviral function.
C1 [Taylor, Justin K.; Coleman, Christopher M.; Sisk, Jeanne M.; Venkataraman, Thiagarajan; Sundberg, Eric J.; Frieman, Matthew B.] Univ Maryland, Dept Microbiol & Immunol, Baltimore, MD 21201 USA.
   [Postel, Sandra; Sundberg, Eric J.] Univ Maryland, Sch Med, Inst Human Virol, Baltimore, MD 21201 USA.
   [Bernbaum, John G.] NIH, Integrated Res Facil, Frederick, MD USA.
   [Sundberg, Eric J.] Univ Maryland, Sch Med, Dept Med, Baltimore, MD 21201 USA.
RP Frieman, MB (reprint author), Univ Maryland, Dept Microbiol & Immunol, Baltimore, MD 21201 USA.
EM mfrieman@som.umaryland.edu
OI Venkataraman, Thiagarajan/0000-0003-0921-6345
FU Division of Intramural Research of the National Institute of Allergy and
   Infectious Diseases (NIAID) [RO1AI1095569]; NIAID [R01AI087452]
FX This work was supported by the Division of Intramural Research of the
   National Institute of Allergy and Infectious Diseases (NIAID) with grant
   RO1AI1095569 (to M.B.F.) and by NIAID grant R01AI087452 (to E.J.S.).
NR 54
TC 1
Z9 1
U1 1
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 DEC
PY 2015
VL 89
IS 23
BP 11820
EP 11833
DI 10.1128/JVI.02274-15
PG 14
WC Virology
SC Virology
GA CZ1WM
UT WOS:000366896600008
PM 26378163
ER

PT J
AU Tekeste, SS
   Wilkinson, TA
   Weiner, EM
   Xu, XW
   Miller, JT
   Le Grice, SFJ
   Clubb, RT
   Chow, SA
AF Tekeste, Shewit S.
   Wilkinson, Thomas A.
   Weiner, Ethan M.
   Xu, Xiaowen
   Miller, Jennifer T.
   Le Grice, Stuart F. J.
   Clubb, Robert T.
   Chow, Samson A.
TI Interaction between Reverse Transcriptase and Integrase Is Required for
   Reverse Transcription during HIV-1 Replication
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; DOUBLE-STRANDED DNA; TYPE-1 INTEGRASE;
   RETROVIRAL INTEGRASE; NUCLEAR IMPORT; IN-VITRO; ANGSTROM RESOLUTION;
   CONSERVED RESIDUES; VIRAL REPLICATION; GENETIC-ANALYSIS
AB Human immunodeficiency virus type 1 (HIV-1) replication requires reverse transcription of its RNA genome into a double-stranded cDNA copy, which is then integrated into the host cell chromosome. The essential steps of reverse transcription and integration are catalyzed by the viral enzymes reverse transcriptase (RT) and integrase (IN), respectively. In vitro, HIV-1 RT can bind with IN, and the C-terminal domain (CTD) of IN is necessary and sufficient for this binding. To better define the RT-IN interaction, we performed nuclear magnetic resonance (NMR) spectroscopy experiments to map a binding surface on the IN CTD in the presence of RT prebound to a duplex DNA construct that mimics the primer-binding site in the HIV-1 genome. To determine the biological significance of the RT-IN interaction during viral replication, we used the NMR chemical shift mapping information as a guide to introduce single amino acid substitutions of nine different residues on the putative RT-binding surface in the IN CTD. We found that six viral clones bearing such IN substitutions (R231E, W243E, G247E, A248E, V250E, and I251E) were noninfectious. Further analyses of the replication-defective IN mutants indicated that the block in replication took place specifically during early reverse transcription. The recombinant INs purified from these mutants, though retaining enzymatic activities, had diminished ability to bind RT in a cosedimentation assay. The results indicate that the RT-IN interaction is functionally relevant during the reverse transcription step of the HIV-1 life cycle.
   IMPORTANCE
   To establish a productive infection, human immunodeficiency virus type 1 (HIV-1) needs to reverse transcribe its RNA genome to create a double-stranded DNA copy and then integrate this viral DNA genome into the chromosome of the host cell. These two essential steps are catalyzed by the HIV-1 enzymes reverse transcriptase (RT) and integrase (IN), respectively. We have shown previously that IN physically interacts with RT, but the importance of this interaction during HIV-1 replication has not been fully characterized. In this study, we have established the biological significance of the HIV-1 RT-IN interaction during the viral life cycle by demonstrating that altering the RT-binding surface on IN disrupts both reverse transcription and viral replication. These findings contribute to our understanding of the RT-IN binding mechanism, as well as indicate that the RT-IN interaction can be exploited as a new antiviral drug target.
C1 [Tekeste, Shewit S.; Wilkinson, Thomas A.; Xu, Xiaowen; Chow, Samson A.] Univ Calif Los Angeles, Dept Mol & Med Pharmacol, Los Angeles, CA 90024 USA.
   [Weiner, Ethan M.; Clubb, Robert T.] Univ Calif Los Angeles, Dept Chem & Biochem, Los Angeles, CA 90024 USA.
   [Miller, Jennifer T.; Le Grice, Stuart F. J.] NCI, Basic Res Lab, Frederick, MD 21701 USA.
RP Chow, SA (reprint author), Univ Calif Los Angeles, Dept Mol & Med Pharmacol, Los Angeles, CA 90024 USA.
EM schow@mednet.ucla.edu
RI Xu, Xiaowen/C-2139-2016
FU UCLA CFAR [5P30 AI028697]; NIH [GM101416]; Science Technology Department
   of Zhejiang Province, China [2012C24015]; Research Training in
   Pharmacological Sciences [NIH T32GM008652]; UCLA AIDS Institute/CFAR
   Fellowship Award; Intramural Research Program of the National Cancer
   Institute, NIH, Department of Health and Human Services
FX The ELISA for p24 was carried out by the Center for AIDS Research (CFAR)
   Virology Core Facility of the University of California, Los Angeles
   (UCLA), which is supported by UCLA CFAR grant 5P30 AI028697 and the UCLA
   AIDS Institute and by the UCLA Council of Bioscience Resources. This
   work was partly supported by NIH grant GM101416 and an International
   Collaborative grant (number 2012C24015) from the Science Technology
   Department of Zhejiang Province, China, to S.A.C. S.S.T. was partly
   supported by Research Training in Pharmacological Sciences (NIH
   T32GM008652) and a UCLA AIDS Institute/CFAR Fellowship Award. J.T.M. and
   S.F.J.L.G. are supported by the Intramural Research Program of the
   National Cancer Institute, NIH, Department of Health and Human Services.
NR 79
TC 6
Z9 6
U1 3
U2 13
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD DEC
PY 2015
VL 89
IS 23
BP 12058
EP 12069
DI 10.1128/JVI.01471-15
PG 12
WC Virology
SC Virology
GA CZ1WM
UT WOS:000366896600028
PM 26401032
ER

PT J
AU Altan-Bonnet, N
   Chen, YH
AF Altan-Bonnet, Nihal
   Chen, Ying-Han
TI Intercellular Transmission of Viral Populations with Vesicles
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID CELLS; VIRUS; REPLICATION; RNA; ENTEROVIRUSES; PARTICLES; RELEASE;
   PATHWAY; SPREAD
AB A common paradigm holds that during cell-to-cell transmission, viruses behave as lone soldiers. Recently, we discovered not only that enteroviruses are transmitted via vesicles as populations of viral particles but also that this type of transmission enhances their infection efficiency (Y. H. Chen et al., Cell 160:619-630, 2015). This mechanism could be advantageous for the overall fitness of the viral population, promoting genetic interplay by enabling viral quasispecies to collectively infect a susceptible host cell. Here, we discuss these findings in the context of viral pathogenesis and also propose that this novel type of vesicular transmission is widespread among different virus families and includes populations of both viral particles and naked viral genomes.
C1 [Altan-Bonnet, Nihal; Chen, Ying-Han] NHLBI, Lab Host Pathogen Dynam, NIH, Bethesda, MD 20892 USA.
RP Altan-Bonnet, N (reprint author), NHLBI, Lab Host Pathogen Dynam, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM nihal.altan-bonnet@nih.gov
NR 21
TC 5
Z9 5
U1 0
U2 6
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD DEC
PY 2015
VL 89
IS 24
BP 12242
EP 12244
DI 10.1128/JVI.01452-15
PG 3
WC Virology
SC Virology
GA CZ1WS
UT WOS:000366897200003
PM 26423944
ER

PT J
AU Lee, FH
   Mason, R
   Welles, H
   Learn, GH
   Keele, BF
   Roederer, M
   Bar, KJ
AF Lee, Fang-Hua
   Mason, Rosemarie
   Welles, Hugh
   Learn, Gerald H.
   Keele, Brandon F.
   Roederer, Mario
   Bar, Katharine J.
TI Breakthrough Virus Neutralization Resistance as a Correlate of
   Protection in a Nonhuman Primate Heterologous Simian Immunodeficiency
   Virus Vaccine Challenge Study
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID RECOMBINANT GLYCOPROTEIN-120 VACCINE; RHESUS MONOCLONAL-ANTIBODIES;
   PREVENT HIV-1 INFECTION; EFFICACY TRIAL; SIEVE ANALYSIS; GP120 VACCINE;
   SIV STRAIN; PHYLOGENIES; SIVSME660; RESPONSES
AB Comprehensive assessments of immune correlates of protection in human immunodeficiency virus (HIV) vaccine trials are essential to vaccine design. Neutralization sieve analysis compares the neutralization sensitivity of the breakthrough transmitted/founder (TF) viruses from vaccinated and control animals to infer the molecular mechanisms of vaccine protection. Here, we report a robust neutralization sieve effect in a nonhuman primate simian immunodeficiency virus (SIV) vaccine trial (DNA prime/recombinant adenovirus type 5 [rAd5] boost) (VRC-10-332) that demonstrated substantial protective efficacy and revealed a genetic signature of neutralization resistance in the C1 region of env. We found significant enrichment for neutralization resistance in the vaccine compared to control breakthrough TF viruses when tested with plasma from vaccinated study animals, plasma from chronically SIV-infected animals, and a panel of SIV-specific monoclonal antibodies targeting six discrete Env epitopes (P < 0.008 for all comparisons). Neutralization resistance was significantly associated with the previously identified genetic signature of resistance (P < 0.0001), and together, the results identify virus neutralization as a correlate of protection. These findings further demonstrate the in vivo relevance of our previous in vitro analyses of the SIVsmE660 challenge stock, which revealed a broad range of neutralization sensitivities of its component viruses. In sum, this report demonstrates proof-of-concept that phenotypic sieve analyses can elucidate mechanistic correlates of immune protection following vaccination and raises a cautionary note for SIV and SHIV (simian-human immunodeficiency virus) vaccine studies that employ challenge strains with envelope glycoproteins that fail to exhibit neutralization resistance profiles typical of TF viruses.
   IMPORTANCE
   With more than 2 million new infections annually, the development of an effective vaccine against HIV-1 is a global health priority. Understanding immunologic correlates of protection generated in vaccine trials is critical to advance vaccine development. Here, we assessed the role of vaccine-elicited neutralizing antibodies in a recent nonhuman primate study of a vaccine that showed significant protection against simian immunodeficiency virus (SIV) challenge and suggested a genetic signature of neutralization sensitivity. We found that breakthrough viruses able to establish infection in vaccinated animals were substantially more resistant to antibody-mediated neutralization than were viruses from controls. These findings suggest that vaccine-elicited neutralizing antibodies selectively blocked the transmission of more sensitive challenge viruses. Sieve analysis also corroborated a genetic signature of neutralization sensitivity and highlighted the impact of challenge swarm diversity. Our findings suggest an important role for neutralization sieve analyses as an informative component of comprehensive immune-correlates analyses.
C1 [Lee, Fang-Hua; Learn, Gerald H.; Bar, Katharine J.] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Mason, Rosemarie; Welles, Hugh; Roederer, Mario] NIAID, Vaccine Res Ctr, Bethesda, MD 20892 USA.
   [Keele, Brandon F.] Leidos Biomed Res Inc, AIDS & Canc Virus Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
RP Bar, KJ (reprint author), Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
EM bark@upenn.edu
OI Welles, Hugh/0000-0002-3336-1203
FU Penn Center for AIDS Research (CFAR), an NIH [P30 AI 045008]; University
   of Pennsylvania; National Cancer Institute, National institutes of
   Health [HHSN261200800001E]
FX This publication was made possible through statistical and sequencing
   core services and support from the Penn Center for AIDS Research (CFAR),
   an NIH-funded program (P30 AI 045008). We acknowledge funding from the
   University of Pennsylvania and federal funds from the National Cancer
   Institute, National institutes of Health, under contract no.
   HHSN261200800001E.
NR 58
TC 6
Z9 6
U1 0
U2 5
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD DEC
PY 2015
VL 89
IS 24
BP 12388
EP 12400
DI 10.1128/JVI.01531-15
PG 13
WC Virology
SC Virology
GA CZ1WS
UT WOS:000366897200016
PM 26423953
ER

PT J
AU Asokan, M
   Rudicell, RS
   Louder, M
   McKee, K
   O'Dell, S
   Stewart-Jones, G
   Wang, K
   Xu, L
   Chen, X
   Choe, M
   Chuang, G
   Georgiev, IS
   Joyce, MG
   Kirys, T
   Ko, S
   Pegu, A
   Shi, W
   Todd, JP
   Yang, Z
   Bailer, RT
   Rao, S
   Kwong, PD
   Nabel, GJ
   Mascola, JR
AF Asokan, M.
   Rudicell, R. S.
   Louder, M.
   McKee, K.
   O'Dell, S.
   Stewart-Jones, G.
   Wang, K.
   Xu, L.
   Chen, X.
   Choe, M.
   Chuang, G.
   Georgiev, I. S.
   Joyce, M. G.
   Kirys, T.
   Ko, S.
   Pegu, A.
   Shi, W.
   Todd, J. P.
   Yang, Z.
   Bailer, R. T.
   Rao, S.
   Kwong, P. D.
   Nabel, G. J.
   Mascola, J. R.
TI Bispecific Antibodies Targeting Different Epitopes on the HIV-1 Envelope
   Exhibit Broad and Potent Neutralization
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID MONOCLONAL-ANTIBODIES; IGG ANTIBODIES; IMPROVES PROTECTION; RATIONAL
   DESIGN; SHIV INFECTION; VACCINE; IMMUNIZATION; RECOGNITION; GENERATION;
   MACAQUES
AB The potency and breadth of the recently isolated neutralizing human monoclonal antibodies to HIV-1 have stimulated interest in their use to prevent or to treat HIV-1 infection. Due to the antigenically diverse nature of the HIV-1 envelope (Env), no single antibody is highly active against all viral strains. While the physical combination of two broadly neutralizing antibodies (bNAbs) can improve coverage against the majority of viruses, the clinical-grade manufacturing and testing of two independent antibody products are time and resource intensive. In this study, we constructed bispecific immunoglobulins (IgGs) composed of independent antigen-binding fragments with a common Fc region. We developed four different bispecific IgG variants that included antibodies targeting four major sites of HIV-1 neutralization. We show that these bispecific IgGs display features of both antibody specificities and, in some cases, display improved coverage over the individual parental antibodies. All four bispecific IgGs neutralized 94% to 97% of antigenically diverse viruses in a panel of 206 HIV-1 strains. Among the bispecific IgGs tested, VRC07 X PG9-16 displayed the most favorable neutralization profile. It was superior in breadth to either of the individual antibodies, neutralizing 97% of viruses with a median 50% inhibitory concentration (IC50) of 0.055 mu g/ml. This bispecific IgG also demonstrated in vivo pharmacokinetic parameters comparable to those of the parental bNAbs when administered to rhesus macaques. These results suggest that IgG-based bispecific antibodies are promising candidates for the prevention and treatment of HIV-1 infection in humans.
   IMPORTANCE
   To prevent or treat HIV-1 infection, antibodies must potently neutralize nearly all strains of HIV-1. Thus, the physical combination of two or more antibodies may be needed to broaden neutralization coverage and diminish the possibility of viral resistance. A bispecific antibody that has two different antibody binding arms could potentially display neutralization characteristics better than those of any single parental antibody. Here we show that bispecific antibodies contain the binding specificities of the two parental antibodies and that a single bispecific antibody can neutralize 97% of viral strains with a high overall potency. These findings support the use of bispecific antibodies for the prevention or treatment of HIV-1 infection.
C1 [Asokan, M.; Rudicell, R. S.; Louder, M.; McKee, K.; O'Dell, S.; Stewart-Jones, G.; Wang, K.; Xu, L.; Chen, X.; Choe, M.; Chuang, G.; Georgiev, I. S.; Joyce, M. G.; Kirys, T.; Ko, S.; Pegu, A.; Shi, W.; Todd, J. P.; Yang, Z.; Bailer, R. T.; Rao, S.; Kwong, P. D.; Nabel, G. J.; Mascola, J. R.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Mascola, JR (reprint author), NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM jmascola@nih.gov
FU intramural research program of the Vaccine Research Center, NIAID, NIH
FX This work was funded by the intramural research program of the Vaccine
   Research Center, NIAID, NIH.
NR 41
TC 10
Z9 10
U1 0
U2 11
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD DEC
PY 2015
VL 89
IS 24
BP 12501
EP 12512
DI 10.1128/JVI.02097-15
PG 12
WC Virology
SC Virology
GA CZ1WS
UT WOS:000366897200025
PM 26446600
ER

PT J
AU Ahn, K
   Kao, C
   Mentch, F
   Hakonarson, H
   Rapoport, J
AF Ahn, Kwangmi
   Kao, Charlly
   Mentch, Frank
   Hakonarson, Hakon
   Rapoport, Judith
TI Neurodevelopmental Copy Number Variants and Clinical Risk: A Pediatric
   Record Population Study
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE CNV; pediatric; penetrance; 22q11
C1 [Ahn, Kwangmi; Kao, Charlly; Mentch, Frank; Hakonarson, Hakon; Rapoport, Judith] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W32
BP S463
EP S464
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700760
ER

PT J
AU Alvarez, V
AF Alvarez, Veronica
TI Strengthening Accumbal Indirect Pathway Promotes Resilience to
   Compulsive Cocaine Use
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
C1 [Alvarez, Veronica] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA 28.2
BP S48
EP S48
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700095
ER

PT J
AU Aponte, Y
AF Aponte, Yeka
TI A Novel Microendoscopy System for Functional Imaging of Circuits that
   Drive Feeding-Reward Behaviors
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
C1 [Aponte, Yeka] NIDA, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA 5.1
BP S9
EP S9
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700018
ER

PT J
AU Arcurio, L
   Schwandt, M
   Zhu, X
   Momenan, R
   Leggio, L
AF Arcurio, Lindsay
   Schwandt, Melanie
   Zhu, Xi
   Momenan, Reza
   Leggio, Lorenzo
TI Characterization and Associated Risk-Factors of a Human Model of
   Chronic-Heavy-Intermittent-Drinking
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE alcohol use disorder; drinking; at-risk; epidemiology
C1 [Arcurio, Lindsay; Schwandt, Melanie; Zhu, Xi; Momenan, Reza; Leggio, Lorenzo] NIAAA, Bethesda, MD USA.
RI Leggio, Lorenzo/M-2972-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W223
BP S586
EP S587
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700947
ER

PT J
AU Ballard, E
   Cui, LH
   Machado-Vieira, R
   Zarate, C
   Merikangas, K
AF Ballard, Elizabeth
   Cui, Lihong
   Machado-Vieira, Rodrigo
   Zarate, Carlos
   Merikangas, Kathleen
TI Anxiety Disorders Underlie the Familial Transmission of Suicide Attempts
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE suicide; epidemiology; familial risk
C1 [Ballard, Elizabeth; Cui, Lihong; Machado-Vieira, Rodrigo; Zarate, Carlos; Merikangas, Kathleen] NIMH, Bethesda, MD 20892 USA.
RI MACHADO-VIEIRA, RODRIGO/D-8293-2012
OI MACHADO-VIEIRA, RODRIGO/0000-0002-4830-1190
NR 0
TC 0
Z9 0
U1 1
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA T5
BP S274
EP S275
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700476
ER

PT J
AU Blanco, C
   Wall, M
   Olfson, M
AF Blanco, Carlos
   Wall, Melanie
   Olfson, Mark
TI The Relationship between Pain and Prescription Drug Use Disorders: A
   National Prospective Study
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE chronic pain; Prescription drug abuse; national representative sample;
   national study
C1 [Blanco, Carlos; Wall, Melanie; Olfson, Mark] NIDA, Washington, DC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W230
BP S591
EP S591
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700954
ER

PT J
AU Bonci, A
AF Bonci, Antonello
TI From Optogenetics to rTMS: A Clinical Trials on Cocaine Craving
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
C1 [Bonci, Antonello] NIDA, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA 28.1
BP S47
EP S48
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700094
ER

PT J
AU Brotman, M
   Tseng, WL
   Wiggins, J
   Kircanski, K
   White, L
   Frank, H
   Pine, D
   Leibenluft, E
AF Brotman, Melissa
   Tseng, Wan-Ling
   Wiggins, Jillian
   Kircanski, Katharina
   White, Lauren
   Frank, Heather
   Pine, Daniel
   Leibenluft, Ellen
TI Neural Correlates of Attention Bias in Irritability and Anxiety
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE attentional bias; irritability; Anxiety; fMRI
C1 [Brotman, Melissa; Tseng, Wan-Ling; Wiggins, Jillian; Kircanski, Katharina; White, Lauren; Frank, Heather; Pine, Daniel; Leibenluft, Ellen] NIMH, Bethesda, MD 20892 USA.
RI Brotman, Melissa/H-7409-2013
NR 0
TC 0
Z9 0
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA T59
BP S308
EP S309
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700528
ER

PT J
AU Callicott, J
   Dickinson, D
   Weinberger, D
   Berman, K
AF Callicott, Joseph
   Dickinson, Dwight
   Weinberger, Daniel
   Berman, Karen
TI General Intelligence and Associated fMRI Networks in Schizophrenia
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE fMRI; Connectivity; DLPFC; schizophrenia; Cognition
C1 [Callicott, Joseph; Dickinson, Dwight; Weinberger, Daniel; Berman, Karen] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 3
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W165
BP S548
EP S548
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700889
ER

PT J
AU Cameron, H
AF Cameron, Heather
TI Stress, Unpredictability, and the Role of Adult Neurogenesis in Response
   to Threat
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
C1 [Cameron, Heather] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA 10.2
BP S16
EP S16
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700033
ER

PT J
AU Chaarani, B
   Mackey, S
   Spechler, P
   Higgins, S
   Potter, A
   Althoff, R
   Stein, E
   Garavan, H
AF Chaarani, Bader
   Mackey, Scott
   Spechler, Phil
   Higgins, Stephen
   Potter, Alexandra
   Althoff, Robert
   Stein, Elliot
   Garavan, Hugh
CA IMAGEN Consortium
TI Gene X Smoking Interactions in the Ventromedial PFC: Alpha 5 Nicotinic
   Cholinergic Receptor Gene Variation and Smoking Effects on Adolescent
   Grey Matter
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE nicotine addiction; vmPFC; nicotinic acetylcholine receptors; alpha 5
C1 [Chaarani, Bader; Mackey, Scott; Spechler, Phil; Higgins, Stephen; Potter, Alexandra; Althoff, Robert; Stein, Elliot; Garavan, Hugh; IMAGEN Consortium] NIDA, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W238
BP S595
EP S596
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700962
ER

PT J
AU Cuthbert, B
AF Cuthbert, Bruce
TI Data Sharing at NIMH
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
C1 [Cuthbert, Bruce] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA 15.1
BP S25
EP S25
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700052
ER

PT J
AU Dickinson, D
   Pratt, D
   Orel, J
   Giangrande, E
   Weinberger, DR
   Berman, K
AF Dickinson, Dwight
   Pratt, Danielle
   Orel, Jennifer
   Giangrande, Evan
   Weinberger, Daniel R.
   Berman, Karen
TI Resolving "Deficit'' and "Distress'' Schizophrenia Subgroups from
   Positive and Negative Syndrome Scale Data
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE PANSS; Schizophrenia; Cognition; Cluster Analysis; Psychosis
C1 [Dickinson, Dwight; Pratt, Danielle; Orel, Jennifer; Giangrande, Evan; Weinberger, Daniel R.; Berman, Karen] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA T204
BP S405
EP S405
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700671
ER

PT J
AU Driscoll, C
   Lindell, S
   Yepes, M
   Miller-Cruse, I
   Stephens, C
   McDonnell, S
   Barr, C
AF Driscoll, Carlos
   Lindell, Stephen
   Yepes, Maelys
   Miller-Cruse, Isaac
   Stephens, Clay
   McDonnell, Sue
   Barr, Christina
TI Oxytocin Receptor Gene (OXTR) Variation, Fear and Reward Sensitivity in
   Rhesus Macaque and Non-Traditional Model Animals
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE domesticate; OXTR; Animal Models; oxytocin; fear
C1 [Driscoll, Carlos; Lindell, Stephen; Yepes, Maelys; Miller-Cruse, Isaac; Stephens, Clay; McDonnell, Sue; Barr, Christina] NIAAA, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W146
BP S534
EP S535
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700870
ER

PT J
AU Edwards, E
AF Edwards, Emmeline
TI Complementary and Integrative Health Approaches for Mental Health
   Conditions
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
C1 [Edwards, Emmeline] NIH, Natl Ctr Complementary & Integrat Hlth, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA 27.4
BP S47
EP S47
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700093
ER

PT J
AU Eisenberg, D
   Ianni, A
   Hegarty, C
   Kohn, P
   Gregory, M
   Czarapata, J
   Masdeu, J
   Berman, K
AF Eisenberg, Daniel
   Ianni, Angela
   Hegarty, Catherine
   Kohn, Philip
   Gregory, Michael
   Czarapata, Jasmin
   Masdeu, Joseph
   Berman, Karen
TI Multi-Tracer Pet Characterization of Pre- and Post -Synaptic
   Dopaminergic Systems
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE Dopamine; striatum; PET
ID BRAIN
C1 [Eisenberg, Daniel; Ianni, Angela; Hegarty, Catherine; Kohn, Philip; Gregory, Michael; Czarapata, Jasmin; Masdeu, Joseph; Berman, Karen] NIMH, Bethesda, MD 20892 USA.
RI Eisenberg, Daniel/S-4342-2016
NR 7
TC 0
Z9 0
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA T135
BP S358
EP S358
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700603
ER

PT J
AU Enoch, MA
   Hodgkinson, C
   Shen, PH
   Yuan, QP
   Goldman, D
AF Enoch, Mary-Anne
   Hodgkinson, Colin
   Shen, Pei-Hong
   Yuan, Qiaoping
   Goldman, David
TI Genetic Influences on Resting EEG Alpha Power in an American Indian
   Tribe
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE CRHBP; GPHN; SLC6A4; HTR3B; FAAH
C1 [Enoch, Mary-Anne; Hodgkinson, Colin; Shen, Pei-Hong; Yuan, Qiaoping; Goldman, David] NIAAA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W14
BP S451
EP S452
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700742
ER

PT J
AU Ernst, M
   Davis, A
   Grillon, C
AF Ernst, Monique
   Davis, Andrew
   Grillon, Christian
TI Methylphenidate Decreases Anxiety-Induced Impairment of Working Memory
   Performance in Healthy Subjects
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE Threat of Shock; Working Memory Capacity; stimulant; anxiety state;
   propanolol
C1 [Ernst, Monique; Davis, Andrew; Grillon, Christian] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA T9
BP S276
EP S277
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700480
ER

PT J
AU Farokhnia, M
   Schwandt, ML
   Hodgkinson, CA
   Leggio, L
AF Farokhnia, Mehdi
   Schwandt, Melanie L.
   Hodgkinson, Colin A.
   Leggio, Lorenzo
TI Genetic Variation of the GABA(B) Receptor in Individuals with Alcohol
   Use Disorder and Association with Smoking Measures
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE GABAB; Alcohol dependence; Smoking; genetics
C1 [Farokhnia, Mehdi; Schwandt, Melanie L.; Hodgkinson, Colin A.; Leggio, Lorenzo] NIAAA, NIDA, Bethesda, MD USA.
RI Leggio, Lorenzo/M-2972-2016
NR 0
TC 0
Z9 0
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA M259
BP S269
EP S270
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700467
ER

PT J
AU Ferre, S
AF Ferre, Sergi
TI Changing Classical Pharmacology by Exploring the Allosteric Mechanisms
   of Caffeine Within the Adenosine A2A-Dopamine D2 Receptor Heterotetramer
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
C1 [Ferre, Sergi] NIDA, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 5
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA 31.2
BP S54
EP S54
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700107
ER

PT J
AU Goldman, D
   Kwako, L
   de Wit, H
   Ramchandani, V
   Schwandt, M
   Mason, B
   Voon, V
AF Goldman, David
   Kwako, Laura
   de Wit, Harriet
   Ramchandani, Vijay
   Schwandt, Melanie
   Mason, Barbara
   Voon, Valerie
TI Addictions Neuroclinical Assessment: The Search Continues
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
C1 [Goldman, David; Kwako, Laura; de Wit, Harriet; Ramchandani, Vijay; Schwandt, Melanie; Mason, Barbara; Voon, Valerie] NIAAA, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA 51
BP S89
EP S89
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700178
ER

PT J
AU Goldman, D
   Spagnolo, P
   Bonci, A
   Aston-Jones, G
   Robbins, T
   Creed, M
   Denys, D
   Green, A
   Holtzheimer, P
   Abulseoud, O
   Rezai, A
   Mayberg, H
AF Goldman, David
   Spagnolo, Primavera
   Bonci, Antonelle
   Aston-Jones, Gary
   Robbins, Trevor
   Creed, Meaghan
   Denys, DAmiaan
   Green, Alan
   Holtzheimer, Paul
   Abulseoud, Osama
   Rezai, Ali
   Mayberg, Helen
TI Neurocircuit-based Interventions in Addictions: When and How?
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
C1 [Goldman, David; Spagnolo, Primavera; Bonci, Antonelle; Aston-Jones, Gary; Robbins, Trevor; Creed, Meaghan; Denys, DAmiaan; Green, Alan; Holtzheimer, Paul; Abulseoud, Osama; Rezai, Ali; Mayberg, Helen] NIAAA, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA 43
BP S75
EP S75
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700149
ER

PT J
AU Gowin, J
   Coe, M
   Schwandt, M
   Tapocik, J
   Sun, H
   Singley, E
   Eskay, R
   Umhau, J
   Heilig, M
   Ramchandani, V
AF Gowin, Joshua
   Coe, Marion
   Schwandt, Melanie
   Tapocik, Jenica
   Sun, Hui
   Singley, Erick
   Eskay, Robert
   Umhau, John
   Heilig, Markus
   Ramchandani, Vijay
TI The Role of mu-Opioid Receptor (OPRM1) Gene A118G Polymorphism on
   Cortisol and beta-Endorphin Response to Alcohol
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE OPRM1 A118G; HPA axis; Opioid system; Alcohol
C1 [Gowin, Joshua; Coe, Marion; Schwandt, Melanie; Tapocik, Jenica; Sun, Hui; Singley, Erick; Eskay, Robert; Umhau, John; Heilig, Markus; Ramchandani, Vijay] NIAAA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA T224
BP S417
EP S418
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700691
ER

PT J
AU Grant, S
   Pariyadath, V
   Chiu, P
   Childress, AR
   Breiter, H
   Evins, A
   George, M
   Mackey, S
   Zubieta, JK
AF Grant, Steven
   Pariyadath, Vani
   Chiu, Pearl
   Childress, Anna Rose
   Breiter, Hans
   Evins, Anne
   George, Mark
   Mackey, Sean
   Zubieta, Jon-Kar
TI rt-fMRI Neurofeedback: Are We There Yet?
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
C1 [Grant, Steven; Pariyadath, Vani; Chiu, Pearl; Childress, Anna Rose; Breiter, Hans; Evins, Anne; George, Mark; Mackey, Sean; Zubieta, Jon-Kar] NIDA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA 17
BP S28
EP S28
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700058
ER

PT J
AU Gregory, MD
   Kippenhan, JS
   Nash, T
   Prabhakaran, R
   Eisenberg, D
   Yankowitz, L
   Insel, C
   Roe, K
   Sottile, M
   Kohn, P
   Mervis, C
   Berman, K
AF Gregory, Michael D.
   Kippenhan, J. Shane
   Nash, Tiffany
   Prabhakaran, Ranjani
   Eisenberg, Daniel
   Yankowitz, Lisa
   Insel, Crystal
   Roe, Katherine
   Sottile, Melanie
   Kohn, Philip
   Mervis, Carolyn
   Berman, Karen
TI Copy Number Variation of the 7q11.23 Williams Syndrome Chromosomal
   Region Affects Brain Gyrification and Skull Shape
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE Dup7; gyrification; skull shape; williams syndrome; 7q11.23
C1 [Gregory, Michael D.; Kippenhan, J. Shane; Nash, Tiffany; Prabhakaran, Ranjani; Eisenberg, Daniel; Yankowitz, Lisa; Insel, Crystal; Roe, Katherine; Sottile, Melanie; Kohn, Philip; Mervis, Carolyn; Berman, Karen] NIMH, Bethesda, MD 20892 USA.
RI Eisenberg, Daniel/S-4342-2016
NR 10
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W28
BP S460
EP S461
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700756
ER

PT J
AU Heilig, M
AF Heilig, Markus
TI The Role of Epigenetic Mechanisms in the Medial Prefrontal Cortex in the
   Transition to Alcohol Dependence
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
C1 [Heilig, Markus] NIAAA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA 11.1
BP S17
EP S18
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700036
ER

PT J
AU Hickie, I
   Scott, E
   Merikangas, K
AF Hickie, Ian
   Scott, Elizabeth
   Merikangas, Kathleen
TI Use of Mobile Technologies to Monitor Activity, Sleep, and Mood States
   to Identify Targets of Prevention of Mood Disorders
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE Mobile technology; accelerometry; mood disorders; big data; Actigraphy;
   mood and anxiety disorders
C1 [Hickie, Ian; Scott, Elizabeth; Merikangas, Kathleen] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W105
BP S507
EP S508
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700829
ER

PT J
AU Hodgkinson, C
   Perez-Rodriguez, MM
   Yuan, QP
   Leung, M
   Prat, M
   Casas, M
   Ferrer, M
   Ribases, M
   Andion, O
   New, A
   Siever, L
   Goldman, D
AF Hodgkinson, Colin
   Perez-Rodriguez, M. Mercedes
   Yuan, Qiaoping
   Leung, Ming
   Prat, Monica
   Casas, Miguel
   Ferrer, Marc
   Ribases, Marta
   Andion, Oscar
   New, Antonia
   Siever, Larry
   Goldman, David
TI Exome Sequencing of Borderline Personality Disorder Patients to Identify
   Functional Rare Variants
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE exome; borderline personaility disorder; sequencing
C1 [Hodgkinson, Colin; Perez-Rodriguez, M. Mercedes; Yuan, Qiaoping; Leung, Ming; Prat, Monica; Casas, Miguel; Ferrer, Marc; Ribases, Marta; Andion, Oscar; New, Antonia; Siever, Larry; Goldman, David] NIAAA, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W148
BP S536
EP S536
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700872
ER

PT J
AU Hoffman, J
   Dubey, N
   Schuebel, K
   Marietta, C
   Yuan, QP
   Martinez, P
   Nieman, L
   Rubinow, D
   Schmidt, P
   Goldman, D
AF Hoffman, Jessica
   Dubey, Neelima
   Schuebel, Kornel
   Marietta, Cheryl
   Yuan, Qiaoping
   Martinez, Pedro
   Nieman, Lynnette
   Rubinow, David
   Schmidt, Peter
   Goldman, David
TI Lymphoblast Cell Lines from Women with Premenstrual Dysphoric Disorder
   (PMDD) Differ in mRNA and Protein Expression Profiles of the ESC/E(Z)
   Pathway Compared with Asymptomatic Controls
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE mood disorder; ovarian steroids; Whole exome sequencing; RNA Sequencing;
   premenstrual dysphoric disorder
C1 [Hoffman, Jessica; Dubey, Neelima; Schuebel, Kornel; Marietta, Cheryl; Yuan, Qiaoping; Martinez, Pedro; Nieman, Lynnette; Rubinow, David; Schmidt, Peter; Goldman, David] NIMH, Rockville, MD 20857 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA M116
BP S180
EP S181
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700324
ER

PT J
AU Iadarola, M
   Sapio, M
   Mannes, A
AF Iadarola, Michael
   Sapio, Matthew
   Mannes, Andrew
TI Nociceptive Neural Transcriptional Plasticity in Rat Dorsal Horn in a
   Persistent Pain Model
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE chronic pain; gene expression; Transcriptomics; transcription factors;
   Synaptic Plasticity
C1 [Iadarola, Michael; Sapio, Matthew; Mannes, Andrew] NIH, Bethesda, MD 20892 USA.
RI Sapio, Matthew/J-5096-2016
OI Sapio, Matthew/0000-0002-8855-5419
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W143
BP S532
EP S533
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700867
ER

PT J
AU Ianni, A
   Eisenberg, D
   Hegarty, C
   Masdeu, J
   Gregory, M
   Kohn, P
   Berman, K
AF Ianni, Angela
   Eisenberg, Daniel
   Hegarty, Catherine
   Masdeu, Joseph
   Gregory, Michael
   Kohn, Philip
   Berman, Karen
TI Dopamine Synthesis and Receptor Profile are Associated with Body Mass
   Index in Humans
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE Dopamine; Obesity; Neuroreceptor imaging
C1 [Ianni, Angela; Eisenberg, Daniel; Hegarty, Catherine; Masdeu, Joseph; Gregory, Michael; Kohn, Philip; Berman, Karen] NIH, Bethesda, MD 20892 USA.
RI Eisenberg, Daniel/S-4342-2016
NR 0
TC 0
Z9 0
U1 2
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W45
BP S472
EP S473
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700773
ER

PT J
AU Ihne, J
   Nugent, A
   Furey, M
   Szczepanik, J
   Zarate, C
AF Ihne, Jessica
   Nugent, Allison
   Furey, Maura
   Szczepanik, Joanna
   Zarate, Carlos
TI Brain Activation Correlates of Negative Attentional Bias in Depression
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE depression; fMRI; attentional bias; brain based markers for depression
C1 [Ihne, Jessica; Nugent, Allison; Furey, Maura; Szczepanik, Joanna; Zarate, Carlos] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 3
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA M98
BP S169
EP S169
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700306
ER

PT J
AU Innis, R
AF Innis, Robert
TI Positron Emission Tomographic Imaging of Translocator Protein (TSPO) as
   a Biomarker of Neuroinflammation in Alzheimer's Disease
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
C1 [Innis, Robert] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA 40.1
BP S69
EP S69
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700137
ER

PT J
AU Jabbi, M
   Cropp, B
   Kohn, P
   Nash, T
   Kippenhan, JS
   Mattay, R
   Gregory, MD
   Pessiglione, M
   Masdeu, J
   Eisenberg, DP
   Berman, KF
AF Jabbi, Mbemba
   Cropp, Brett
   Kohn, Philip
   Nash, Tiffany
   Kippenhan, J. Shane
   Mattay, Raghav
   Gregory, Michael D.
   Pessiglione, Mathias
   Masdeu, Joseph
   Eisenberg, Daniel P.
   Berman, Karen F.
TI Presynaptic Midbrain Dopamine Modulates Adaptive Prediction Error
   Signals in Humans
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE Brain; Dopmaine; Adaptive Behavior; Learning
C1 [Jabbi, Mbemba; Cropp, Brett; Kohn, Philip; Nash, Tiffany; Kippenhan, J. Shane; Mattay, Raghav; Gregory, Michael D.; Pessiglione, Mathias; Masdeu, Joseph; Eisenberg, Daniel P.; Berman, Karen F.] NIMH, Bethesda, MD 20892 USA.
RI Eisenberg, Daniel/S-4342-2016; Pessiglione, Mathias/E-2141-2017
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA T136
BP S359
EP S359
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700604
ER

PT J
AU Lee, MR
   Rohn, MCH
   Tanda, G
   Newman, AH
   Leggio, L
AF Lee, Mary R.
   Rohn, Matthew C. H.
   Tanda, Gianluigi
   Newman, Amy H.
   Leggio, Lorenzo
TI The Effect of Oxytocin on Methylphenidate-Induced Stimulation of
   Dopamine Levels: Importance of Route of Administration for Oxytocin
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE oxytocin; Psychostimulant; Dopamine; addiction; Microdialysis
C1 [Lee, Mary R.; Rohn, Matthew C. H.; Tanda, Gianluigi; Newman, Amy H.; Leggio, Lorenzo] NIAAA, Bethesda, MD USA.
RI Tanda, Gianluigi/B-3318-2009; Leggio, Lorenzo/M-2972-2016
OI Tanda, Gianluigi/0000-0001-9526-9878; 
NR 0
TC 0
Z9 0
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W261
BP S611
EP S611
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700984
ER

PT J
AU Leibenluft, E
AF Leibenluft, Ellen
TI Do the Neural Mechanisms Mediating Irritability Differ Across Diagnoses?
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
C1 [Leibenluft, Ellen] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA 30.3
BP S52
EP S53
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700104
ER

PT J
AU Lemos, J
   Montesino, M
   Bocarsly, M
   Clark, M
   Alvarez, V
AF Lemos, Julia
   Montesino, Michael
   Bocarsly, Miriam
   Clark, Michael
   Alvarez, Veronica
TI The Actions of Corticotropin Releasing Hormone in the Nucleus Accumbens
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE CRH; Dopamine; genetic
C1 [Lemos, Julia; Montesino, Michael; Bocarsly, Miriam; Clark, Michael; Alvarez, Veronica] NIAAA, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W115
BP S514
EP S514
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700839
ER

PT J
AU Lesage, E
   Aronson, S
   Sutherland, M
   Ross, T
   Salmeron, BJ
   Stein, E
AF Lesage, Elise
   Aronson, Sarah
   Sutherland, Matthew
   Ross, Thomas
   Salmeron, Betty Jo
   Stein, Elliot
TI Nicotinic Receptor Stimulation Affects Reversal Learning in Smokers
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE nicotine; Varenicline; fMRI; Reward-based decision-making; reversal
   learning
C1 [Lesage, Elise; Aronson, Sarah; Sutherland, Matthew; Ross, Thomas; Salmeron, Betty Jo; Stein, Elliot] NIDA, Baltimore, MD USA.
RI Salmeron, Betty Jo/M-1793-2016
OI Salmeron, Betty Jo/0000-0003-1699-9333
NR 3
TC 0
Z9 0
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA T257
BP S438
EP S439
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700723
ER

PT J
AU Litten, R
   Ryan, M
   Fertig, J
   Falk, D
AF Litten, Raye
   Ryan, Megan
   Fertig, Joanne
   Falk, Daniel
TI Moderators of Varenicline Treatment Effects in a Double-Blind,
   Placebo-Controlled Trial for Alcohol Dependence
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE varenicline; CNS Clinical Trials; Alcohol dependence; moderators
C1 [Litten, Raye; Ryan, Megan; Fertig, Joanne; Falk, Daniel] NIAAA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA M253
BP S265
EP S266
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700461
ER

PT J
AU Machado-Vieira, R
   Guo, W
   Murrough, J
   Mathew, S
   Grunebaum, M
   Charney, D
   Iosifescu, D
   Yao, Y
   McMahon, F
   Zarate, C
AF Machado-Vieira, Rodrigo
   Guo, Wei
   Murrough, James
   Mathew, Sanjay
   Grunebaum, Michael
   Charney, Dennis
   Iosifescu, Dan
   Yao, Yin
   McMahon, Francis
   Zarate, Carlos, Jr.
TI Exploratory Genome-Wide Association Study of Acute Antidepressant
   Effects of Ketamine
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE GWAS; ketamine; antidepressant; genetics; treatment
C1 [Machado-Vieira, Rodrigo; Guo, Wei; Murrough, James; Mathew, Sanjay; Grunebaum, Michael; Charney, Dennis; Iosifescu, Dan; Yao, Yin; McMahon, Francis; Zarate, Carlos, Jr.] NIMH, Bethesda, MD 20892 USA.
RI MACHADO-VIEIRA, RODRIGO/D-8293-2012; Murrough, James/J-7129-2013
OI MACHADO-VIEIRA, RODRIGO/0000-0002-4830-1190; Murrough,
   James/0000-0001-6286-1242
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W78
BP S492
EP S492
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700804
ER

PT J
AU Marenco, S
   Meyer, CT
   van der Veen, JW
   Kelly, R
   Shen, J
   Weinberger, DR
   Apud, JA
   Berman, KF
AF Marenco, Stefano
   Meyer, Christian T.
   van der Veen, Jan Willem
   Kelly, Ryan
   Shen, Jun
   Weinberger, Daniel R.
   Apud, Jose A.
   Berman, Karen F.
TI Choline Increases in the Dorsal Anterior Cingulate of Patients with
   Psychosis Measured with Magnetic Resonance Spectroscopy
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE schizophrenia; choline; magnetic resonance spectroscopy; genetics;
   Antipsychotics
C1 [Marenco, Stefano; Meyer, Christian T.; van der Veen, Jan Willem; Kelly, Ryan; Shen, Jun; Weinberger, Daniel R.; Apud, Jose A.; Berman, Karen F.] NIMH, Bethesda, MD 20892 USA.
RI Marenco, Stefano/A-2409-2008
OI Marenco, Stefano/0000-0002-2488-2365
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA T157
BP S372
EP S373
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700624
ER

PT J
AU McMahon, F
AF McMahon, Francis
TI Genome Sequencing of Anabaptist Patients with Bipolar Disorder Reveals
   Enrichment of Rare, Functional Variants Within Genes Involved in GTPase
   Signaling
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
C1 [McMahon, Francis] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA 25.3
BP S44
EP S45
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700088
ER

PT J
AU Niciu, M
   Iadarola, N
   Luckenbaugh, D
   Banerjee, D
   Richards, E
   Ballard, E
   Brutsche, N
   McMahon, F
   Machado-Vieira, R
   Nugent, A
   Zarate, C
AF Niciu, Mark
   Iadarola, Nicolas
   Luckenbaugh, David
   Banerjee, Dipavo
   Richards, Erica
   Ballard, Elizabeth
   Brutsche, Nancy
   McMahon, Francis
   Machado-Vieira, Rodrigo
   Nugent, Allison
   Zarate, Carlos
TI Ketamine's Antidepressant Efficacy is Not Correlated with Baseline
   Subcortical Volumes in a Major Depressive Disorder Replication Sample
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE Major Depressive Disorder; Ketamine; brain volume; Thalamus; BDNF
C1 [Niciu, Mark; Iadarola, Nicolas; Luckenbaugh, David; Banerjee, Dipavo; Richards, Erica; Ballard, Elizabeth; Brutsche, Nancy; McMahon, Francis; Machado-Vieira, Rodrigo; Nugent, Allison; Zarate, Carlos] NIMH, Bethesda, MD 20892 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 NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA T74
BP S318
EP S319
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700543
ER

PT J
AU Preston, K
   Kowalczyk, W
   Phillips, K
   Jobes, M
   Furnari, M
   Ghitza, U
   Epstein, D
AF Preston, Kenzie
   Kowalczyk, William
   Phillips, Karran
   Jobes, Michelle
   Furnari, Melody
   Ghitza, Udi
   Epstein, David
TI Clonidine Increases the Likelihood that Abstinence can Withstand Leisure
   Time in Buprenorphine-Maintained Outpatients
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE ecological momentary assessment; opioids; clonidine; buprenorphine
   maintenance
C1 [Preston, Kenzie; Kowalczyk, William; Phillips, Karran; Jobes, Michelle; Furnari, Melody; Ghitza, Udi; Epstein, David] NIDA, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA M258
BP S269
EP S269
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700466
ER

PT J
AU Raznahan, A
AF Raznahan, Armin
TI Studying the where and how of Sexually Dimorphic Brain Development
   Through Cross-Species Neuroimaging and Genomics
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
C1 [Raznahan, Armin] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA 34.3
BP S60
EP S61
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700119
ER

PT J
AU Richards, E
   Zanotti-Fregonara, P
   Fujita, M
   Machado-Vieira, R
   Niciu, M
   Park, M
   Salvadore, G
   Kolb, H
   Zarate, C
   Innis, R
AF Richards, Erica
   Zanotti-Fregonara, Paolo
   Fujita, Masahiro
   Machado-Vieira, Rodrigo
   Niciu, Mark
   Park, Minkyung
   Salvadore, Giacomo
   Kolb, Hartmuth
   Zarate, Carlos
   Innis, Robert
TI Using Pet Imaging of Translocator Protein (TSPO) to Investigate the Link
   between Inflammation and Depression
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE TSPO and [11C]PBR-28 PET; neuroinflammation; Major Depressive Disorder
C1 [Richards, Erica; Zanotti-Fregonara, Paolo; Fujita, Masahiro; Machado-Vieira, Rodrigo; Niciu, Mark; Park, Minkyung; Salvadore, Giacomo; Kolb, Hartmuth; Zarate, Carlos; Innis, Robert] NIMH, Bethesda, MD 20892 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 NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA M89
BP S163
EP S164
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700297
ER

PT J
AU Richards, E
AF Richards, Erica
TI Using PET Imaging of Translocator Protein (TSPO) to Investigate the Link
   Between Inflammation and Depression
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
C1 [Richards, Erica] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA 40.3
BP S70
EP S70
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700139
ER

PT J
AU Salinas, A
   Davis, M
   Lovinger, D
   Mateo, Y
AF Salinas, Armando
   Davis, Margaret
   Lovinger, David
   Mateo, Yolanda
TI Dopamine Release and Cocaine Sensitivity Differ Between Striosome and
   Matrix Compartments of the Striatum
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE voltammetry; Substance abuse; Basal Ganglia; dopamine transporter
C1 [Salinas, Armando; Davis, Margaret; Lovinger, David; Mateo, Yolanda] NIAAA, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA M232
BP S252
EP S252
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700440
ER

PT J
AU Salmeron, BJ
   Geng, XJ
   Hu, YZ
   Gu, H
   Adinoff, B
   Stein, E
   Yang, YH
AF Salmeron, Betty Jo
   Geng, Xiujuan
   Hu, Yuzheng
   Gu, Hong
   Adinoff, Bryon
   Stein, Elliot
   Yang, Yihong
TI Temporal-Medial Prefrontal Circuitry Identified in Non-Treatment Seeking
   Cocaine Users Predicts Relapse in an Independent Cohort of Treated
   Cocaine Dependent Individuals
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE cocaine addiction; treatment outcome prediction; morphological and
   resting state brain activity
C1 [Salmeron, Betty Jo; Geng, Xiujuan; Hu, Yuzheng; Gu, Hong; Adinoff, Bryon; Stein, Elliot; Yang, Yihong] NIDA, Baltimore, MD USA.
RI Salmeron, Betty Jo/M-1793-2016
OI Salmeron, Betty Jo/0000-0003-1699-9333
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA M237
BP S255
EP S256
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700445
ER

PT J
AU Sapio, M
   Mannes, A
   Iadarola, M
AF Sapio, Matthew
   Mannes, Andrew
   Iadarola, Michael
TI Brain Activity and Transcriptional Programs in Frontal Lobe and
   Hippocampus: Uncoupling and Recoupling Following Anesthesia
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE Anesthetic; Cognitive Resilience; Transcriptomics; RNA-seq; neural
   plasticity
C1 [Sapio, Matthew; Mannes, Andrew; Iadarola, Michael] NIH, Bethesda, MD 20892 USA.
RI Sapio, Matthew/J-5096-2016
OI Sapio, Matthew/0000-0002-8855-5419
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA T54
BP S305
EP S306
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700523
ER

PT J
AU Shrestha, S
   Cortes, M
   Singh, P
   Jenko, K
   Gladding, R
   Morse, C
   Zoghbi, S
   Fujita, M
   Pike, V
   Innis, R
AF Shrestha, Stal
   Cortes, Michelle
   Singh, Prachi
   Jenko, Kimberly
   Gladding, Robert
   Morse, Cheryl
   Zoghbi, Sami
   Fujita, Masahiro
   Pike, Victor
   Innis, Robert
TI In Vivo Evaluation in Monkey Brain of the COX-1 and COX-2 Selective
   Positron Emission Tomographic Radioligands [11C]PS13 and [11C]MC1
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE Positron emission tomography; Inflammatory Markers; COX-1
C1 [Shrestha, Stal; Cortes, Michelle; Singh, Prachi; Jenko, Kimberly; Gladding, Robert; Morse, Cheryl; Zoghbi, Sami; Fujita, Masahiro; Pike, Victor; Innis, Robert] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 1
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA M54
BP S139
EP S140
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700262
ER

PT J
AU Sibley, D
   Free, RB
   Shin, JH
   Miller, B
   Doyle, T
   Moritz, A
   Conroy, J
   Brust, T
   Southall, N
   Ferrer, M
   Donthamsetti, P
   Javitch, J
   Watts, V
   Katz, J
   Stanwood, G
   Bertz, J
   Woods, J
   Emmitte, K
   Lindsley, C
   Alvarez, V
AF Sibley, David
   Free, R. Benjamin
   Shin, J. Hoon
   Miller, Brittney
   Doyle, Trevor
   Moritz, Amy
   Conroy, Jennie
   Brust, Tarsis
   Southall, Noel
   Ferrer, Marc
   Donthamsetti, Prashant
   Javitch, Jonathan
   Watts, Val
   Katz, Jonathan
   Stanwood, Gregg
   Bertz, Jeremiah
   Woods, James
   Emmitte, Kyle
   Lindsley, Craig
   Alvarez, Veronica
TI Characterization of a Novel Dopaminergic Agonist that Displays Spatial
   Bias and Functional Selectively at the D2 Dopamine Receptor
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE Dopamine; Dopamine (D2, D3) receptors; Functional Selectivity
C1 [Sibley, David; Free, R. Benjamin; Shin, J. Hoon; Miller, Brittney; Doyle, Trevor; Moritz, Amy; Conroy, Jennie; Brust, Tarsis; Southall, Noel; Ferrer, Marc; Donthamsetti, Prashant; Javitch, Jonathan; Watts, Val; Katz, Jonathan; Stanwood, Gregg; Bertz, Jeremiah; Woods, James; Emmitte, Kyle; Lindsley, Craig; Alvarez, Veronica] NINDS, Bethesda, MD 20892 USA.
RI Brust, Tarsis/D-5247-2017
OI Brust, Tarsis/0000-0003-0912-8273
NR 0
TC 0
Z9 0
U1 2
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA M176
BP S216
EP S217
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700384
ER

PT J
AU Stangl, B
   Corey, K
   Momenan, R
   Ramchandani, V
AF Stangl, Bethany
   Corey, Kristin
   Momenan, Reza
   Ramchandani, Vijay
TI Alcohol Sensitivity and Sex Effects on Cardiac Reactivity During Acute
   Intravenous Alcohol Exposure in Non-Dependent Drinkers
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE Cardiac Reactivity; Heart Rate Variability; IV Alcohol; Alcohol
   Sensitivity
C1 [Stangl, Bethany; Corey, Kristin; Momenan, Reza; Ramchandani, Vijay] NIAAA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA T262
BP S442
EP S442
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700728
ER

PT J
AU Stoddard, J
   Sharif-Askary, B
   Harkins, E
   Frank, H
   Brotman, M
   Penton-Voak, I
   Maoz, K
   Bar-Haim, Y
   Munafo, M
   Pine, D
   Leibenluft, E
AF Stoddard, Joel
   Sharif-Askary, Banafsheh
   Harkins, Elizabeth
   Frank, Heather
   Brotman, Melissa
   Penton-Voak, Ian
   Maoz, Keren
   Bar-Haim, Yair
   Munafo, Marcus
   Pine, Daniel
   Leibenluft, Ellen
TI Preliminary Evidence for Computer-based Training Targeting Hostile
   Interpretation Bias as a Treatment for DMDD
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE disruptive mood dysregulation disorder; interpretation bias;
   irritability
C1 [Stoddard, Joel; Sharif-Askary, Banafsheh; Harkins, Elizabeth; Frank, Heather; Brotman, Melissa; Penton-Voak, Ian; Maoz, Keren; Bar-Haim, Yair; Munafo, Marcus; Pine, Daniel; Leibenluft, Ellen] NIMH, Bethesda, MD 20892 USA.
RI Brotman, Melissa/H-7409-2013
NR 0
TC 0
Z9 0
U1 0
U2 11
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA T29
BP S290
EP S291
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700500
ER

PT J
AU Tomasi, D
   Wang, GJ
   Volkow, N
AF Tomasi, Dardo
   Wang, Gene-Jack
   Volkow, Nora
TI Involvement of Striatal Dopamine D2/D3 Receptors in the Modulation of
   Visual Attention During Rested Wakefulness and Sleep Deprivation
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE Dopamine; Attention; sleep disturbance; fMRI; PET
C1 [Tomasi, Dardo; Wang, Gene-Jack; Volkow, Nora] NIAAA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA M226
BP S247
EP S248
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700434
ER

PT J
AU Wang, GJ
   Kojori, ES
   Tomasi, D
   Wong, C
   Volkow, N
AF Wang, Gene-Jack
   Kojori, Ehsan Shokri
   Tomasi, Dardo
   Wong, Christopher
   Volkow, Nora
TI Lower Brain Responses during Cognitive Inhibition of Food Craving
   Elicited by Food Stimulation in Obese Subjects
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE neuroimaging; obesity; cognitive control
C1 [Wang, Gene-Jack; Kojori, Ehsan Shokri; Tomasi, Dardo; Wong, Christopher; Volkow, Nora] NIAAA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 2
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W226
BP S589
EP S589
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700950
ER

PT J
AU Wiers, CE
   Shokri-Kojori, E
   Cabrera, E
   Cunningham, S
   Tomasi, D
   Wang, GJ
   Volkow, ND
AF Wiers, Corinde E.
   Shokri-Kojori, Ehsan
   Cabrera, Elizabeth
   Cunningham, Samantha
   Tomasi, Dardo
   Wang, Gene-Jack
   Volkow, Nora D.
TI Social Economic Status Predicts Dopamine D2/3 Receptor Availability in
   Healthy Volunteers but Not Cocaine Abusers
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE Dopamine (D2, D3) receptors; social; cocaine addiction
C1 [Wiers, Corinde E.; Shokri-Kojori, Ehsan; Cabrera, Elizabeth; Cunningham, Samantha; Tomasi, Dardo; Wang, Gene-Jack; Volkow, Nora D.] NIAAA, Bethesda, DC USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W247
BP S602
EP S602
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700971
ER

PT J
AU Yao, Y
   McMahon, F
AF Yao, Yin
   McMahon, Francis
TI The Challenge: Estimating the Onset of Drug Effect in the STAR*D Data
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE Antidepressants; genetics; statistical methods
C1 [Yao, Yin; McMahon, Francis] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA W111
BP S511
EP S511
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700835
ER

PT J
AU Zanotti-Fregonara, P
   Veronese, M
   Xu, R
   Zoghbi, S
   Liow, JS
   Fujita, M
   Pike, V
   Innis, R
AF Zanotti-Fregonara, Paolo
   Veronese, Mattia
   Xu, Rong
   Zoghbi, Sami
   Liow, Jeih-San
   Fujita, Masahiro
   Pike, Victor
   Innis, Robert
TI A Novel Genetic Method of Measuring the Receptor-Specific Component of
   PET Radioligand Binding in Human Brain Without Pharmacological Blockade
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 54th Annual Meeting of the American-College-of-Neuropsychopharmacology
   (ACNP)
CY DEC 06-10, 2015
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
DE PET; metabotropic glutamate receptor; Genomics
C1 [Zanotti-Fregonara, Paolo; Veronese, Mattia; Xu, Rong; Zoghbi, Sami; Liow, Jeih-San; Fujita, Masahiro; Pike, Victor; Innis, Robert] NIMH, Bethesda, MD 20892 USA.
RI Veronese, Mattia/A-6012-2013
OI Veronese, Mattia/0000-0003-3562-0683
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2015
VL 40
SU 1
MA M123
BP S185
EP S185
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CY7OI
UT WOS:000366597700331
ER

PT J
AU Delitala, AP
   Filigheddu, F
   Orru, M
   AlGhatrif, M
   Steri, M
   Pilia, MG
   Scuteri, A
   Lobina, M
   Piras, MG
   Delitala, G
   Lakatta, EG
   Schlessinger, D
   Cucca, F
AF Delitala, A. P.
   Filigheddu, F.
   Orru, M.
   AlGhatrif, M.
   Steri, M.
   Pilia, M. G.
   Scuteri, A.
   Lobina, M.
   Piras, M. G.
   Delitala, G.
   Lakatta, E. G.
   Schlessinger, D.
   Cucca, F.
TI No evidence of association between subclinical thyroid disorders and
   common carotid intima medial thickness or atherosclerotic plaque
SO NUTRITION METABOLISM AND CARDIOVASCULAR DISEASES
LA English
DT Article
DE Subclinical thyroid disorders; Carotid intima-media thickness; Carotid
   plaques; Atherosclerosis; Arterial remodelling
ID CARDIOVASCULAR RISK-FACTORS; ARTERY-INTIMA; HORMONE REPLACEMENT;
   HEART-DISEASE; DOUBLE-BLIND; HYPOTHYROIDISM; HYPERTHYROIDISM;
   DYSFUNCTION; POPULATION; MORTALITY
AB Background and aims: Increased carotid artery intima-media thickness (IMT) and the presence of plaques have been shown to be predictors of cardiovascular disease. The cardiovascular risk in patients with overt thyroid diseases is related to increased risk of atherosclerosis, but there has been no clear evidence about subclinical disorders. We have assessed whether subclinical thyroid dysfunction is associated with arterial thickening and plaque.
   Methods and results: The SardiNIA study is a population-based survey on the Italian island of Sardinia. We reviewed data from 5815 subjects (aged 14-102 years), none of whom had overt hyperthyroidism or hypothyroidism or was taking thyroid medication. Serum thyrotropin (TSH), free thyroxine, together with carotid ultrasound IMT and the presence of common carotid plaques were analysed in all subjects. Possible association of IMT and carotid plaques with thyroid parameters was evaluated by univariate and multivariate analyses. IMT was significantly associated with age, sex, smoking, low density lipoprotein cholesterol (LDL), high density lipoprotein cholesterol, pulse pressure (PP), history of arterial hypertension, diabetes, and previous cardiovascular events (p = 0.001 or lower, R-2 = 0.47). Carotid plaques were predicted by age, sex, LDL, PP, history of diabetes, previous cardiovascular events, and the use of statins (p = 0.029 or lower). Thyroid hormone was not predictive of carotid atherosclerosis when adjusted for confounders.
   Conclusion: Thyroid hormone is not associated with increased IMT or with the presence of carotid artery plaque. Our data do not support the idea that treating subclinical disorders might help to prevent arterial remodelling or carotid atherosclerosis. (C) 2015 The Italian Society of Diabetology, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition, and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.
C1 [Delitala, A. P.] Univ Sassari, Azienda Osped, I-07100 Sassari, Italy.
   [Filigheddu, F.; Delitala, G.] Univ Sassari, Azienda Osped, Dept Clin & Expt Med, I-07100 Sassari, Italy.
   [Orru, M.; Steri, M.; Pilia, M. G.; Scuteri, A.; Lobina, M.; Piras, M. G.; Cucca, F.] Cittadella Univ Monserrato, Consiglio Nazl Ric, Ist Ric Genet & Biomed IRGB, Cagliari, Italy.
   [AlGhatrif, M.; Lakatta, E. G.; Schlessinger, D.] NIA, NIH, DHHS, Baltimore, MD 21224 USA.
   [Cucca, F.] Univ Sassari, Azienda Osped, Dept Biomed Sci, I-07100 Sassari, Italy.
RP Delitala, AP (reprint author), Univ Sassari, Azienda Osped, Via Michele Coppino 26, I-07100 Sassari, Italy.
EM aledelitala@tiscali.it
RI Delitala, Alessandro/L-3194-2016; 
OI Delitala, Alessandro/0000-0003-1729-8969; piras, maria
   grazia/0000-0001-9004-0900; Lobina, Monia/0000-0003-3620-3160; Steri,
   Anna Maristella/0000-0001-5869-3872
FU NIH, National Institute on Aging [N01-AG-1-2109]
FX This research was supported in part by the Intramural Research Program
   of the NIH, National Institute on Aging (N01-AG-1-2109).
NR 30
TC 3
Z9 3
U1 1
U2 7
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0939-4753
EI 1590-3729
J9 NUTR METAB CARDIOVAS
JI Nutr. Metab. Carbiovasc. Dis.
PD DEC
PY 2015
VL 25
IS 12
BP 1104
EP 1110
DI 10.1016/j.numecd.2015.09.001
PG 7
WC Cardiac & Cardiovascular Systems; Endocrinology & Metabolism; Nutrition
   & Dietetics
SC Cardiovascular System & Cardiology; Endocrinology & Metabolism;
   Nutrition & Dietetics
GA CY5RW
UT WOS:000366466000005
PM 26615224
ER

PT J
AU Belfort, MA
   Saade, GR
   Thom, E
   Blackwell, SC
   Reddy, UM
   Thorp, JM
   Tita, ATN
   Miller, RS
   Peaceman, AM
   McKenna, DS
   Chien, EKS
   Rouse, DJ
   Gibbs, RS
   El-Sayed, YY
   Sorokin, Y
   Caritis, SN
   VanDorsten, JP
AF Belfort, Michael A.
   Saade, George R.
   Thom, Elizabeth
   Blackwell, Sean C.
   Reddy, Uma M.
   Thorp, John M.
   Tita, Alan T. N.
   Miller, Russell S.
   Peaceman, Alan M.
   McKenna, David S.
   Chien, Edward K. S.
   Rouse, Dwight J.
   Gibbs, Ronald S.
   El-Sayed, Yasser Y.
   Sorokin, Yoram
   Caritis, Steve N.
   VanDorsten, J. Peter
CA Eunice Kennedy Shriver Natl Inst
TI A Randomized Trial of Intrapartum Fetal ECG ST-Segment Analysis
   EDITORIAL COMMENT
SO OBSTETRICAL & GYNECOLOGICAL SURVEY
LA English
DT Editorial Material
C1 [Belfort, Michael A.] Univ Utah, Hlth Sci Ctr, Salt Lake City, UT 84112 USA.
   [Saade, George R.] Univ Texas Med Branch, Galveston, TX 77555 USA.
   [Thom, Elizabeth] George Washington Univ, Ctr Biostat, Washington, DC USA.
   [Blackwell, Sean C.] Univ Texas Hlth Sci Ctr Houston, Childrens Mem Hermann Hosp, Houston, TX 77030 USA.
   [Reddy, Uma M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
   [Thorp, John M.] Univ N Carolina, Chapel Hill, NC USA.
   [Tita, Alan T. N.] Univ Alabama Birmingham, Birmingham, AL USA.
   [Miller, Russell S.] Columbia Univ, New York, NY USA.
   [Peaceman, Alan M.] Northwestern Univ, Chicago, IL 60611 USA.
   [McKenna, David S.] Ohio State Univ, Columbus, OH 43210 USA.
   [Chien, Edward K. S.] Case Western Reserve Univ, MetroHlth Med Ctr, Cleveland, OH 44106 USA.
   [Rouse, Dwight J.] Brown Univ, Providence, RI 02912 USA.
   [Gibbs, Ronald S.] Univ Colorado, Sch Med, Aurora, CO USA.
   [El-Sayed, Yasser Y.] Stanford Univ, Stanford, CA 94305 USA.
   [Sorokin, Yoram] Wayne State Univ, Detroit, MI USA.
   [Caritis, Steve N.] Univ Pittsburgh, Pittsburgh, PA USA.
   [VanDorsten, J. Peter] Med Univ S Carolina, Charleston, SC 29425 USA.
RP Belfort, MA (reprint author), Univ Utah, Hlth Sci Ctr, Salt Lake City, UT 84112 USA.
NR 0
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 0029-7828
EI 1533-9866
J9 OBSTET GYNECOL SURV
JI Obstet. Gynecol. Surv.
PD DEC
PY 2015
VL 70
IS 12
BP 735
EP 737
DI 10.1097/OGX.0000000000000276
PG 3
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA CY3RQ
UT WOS:000366327900003
ER

PT J
AU Diamond, MP
   Legro, RS
   Coutifaris, C
   Alvero, R
   Robinson, RD
   Casson, P
   Christman, GM
   Ager, J
   Huang, H
   Hansen, KR
   Baker, V
   Usadi, R
   Seungdamrong, A
   Bates, GW
   Rosen, RM
   Haisenleder, D
   Krawetz, SA
   Barnhart, K
   Trussell, JC
   Ohl, D
   Jin, YF
   Santoro, N
   Eisenberg, E
   Zhang, HP
AF Diamond, Michael P.
   Legro, Richard S.
   Coutifaris, Christos
   Alvero, Ruben
   Robinson, Randal D.
   Casson, Peter
   Christman, Gregory M.
   Ager, Joel
   Huang, Hao
   Hansen, Karl R.
   Baker, Valerie
   Usadi, Rebecca
   Seungdamrong, Aimee
   Bates, G. Wright
   Rosen, R. Mitchell
   Haisenleder, Daniel
   Krawetz, Stephen A.
   Barnhart, Kurt
   Trussell, J. C.
   Ohl, Dana
   Jin, Yufeng
   Santoro, Nanette
   Eisenberg, Esther
   Zhang, Heping
CA NICHD Reprod Med Network
TI Letrozole, Gonadotropin, or Clomiphene for Unexplained Infertility
   EDITORIAL COMMENT
SO OBSTETRICAL & GYNECOLOGICAL SURVEY
LA English
DT Editorial Material
C1 [Diamond, Michael P.] Georgia Regents Univ, Dept Obstet & Gynecol, Augusta, GA 30912 USA.
   [Diamond, Michael P.; Ager, Joel; Krawetz, Stephen A.] Wayne State Univ, Dept Obstet & Gynecol, Detroit, MI USA.
   [Legro, Richard S.] Penn State Univ, Dept Obstet & Gynecol, Hershey, PA USA.
   [Coutifaris, Christos; Barnhart, Kurt] Univ Penn, Sch Med, Dept Obstet & Gynecol, Philadelphia, PA 19104 USA.
   [Alvero, Ruben; Santoro, Nanette] Univ Colorado, Dept Obstet & Gynecol, Denver, CO 80202 USA.
   [Robinson, Randal D.] Univ Texas Hlth Sci Ctr San Antonio, Dept Obstet & Gynecol, San Antonio, TX 78229 USA.
   [Casson, Peter] Univ Vermont, Dept Obstet & Gynecol, Burlington, VT USA.
   [Christman, Gregory M.; Ohl, Dana] Univ Michigan, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA.
   [Huang, Hao; Jin, Yufeng; Zhang, Heping] Yale Univ, Dept Biostat, Sch Publ Hlth, New Haven, CT USA.
   [Hansen, Karl R.] Univ Oklahoma, Coll Med, Dept Obstet & Gynecol, Oklahoma City, OK 73190 USA.
   [Baker, Valerie] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
   [Usadi, Rebecca] Carolinas Med Ctr, Charlotte, NC 28203 USA.
   [Seungdamrong, Aimee] Univ Med & Dent New Jersey, Newark, NJ 07103 USA.
   [Bates, G. Wright] Univ Alabama Birmingham, Birmingham, AL USA.
   [Rosen, R. Mitchell] Univ Calif San Francisco, Dept Reprod Endocrinol & Infertil, San Francisco, CA 94143 USA.
   [Haisenleder, Daniel] Univ Virginia, Ctr Res Reprod, Ligand Core Lab, Charlottesville, VA USA.
   [Trussell, J. C.] Upstate Univ Hosp, Syracuse, NY USA.
   [Eisenberg, Esther] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Fertil & Infertil Branch, Rockville, MD USA.
RP Diamond, MP (reprint author), Georgia Regents Univ, Dept Obstet & Gynecol, Augusta, GA 30912 USA.
OI Diamond, Michael/0000-0001-6353-4489
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0029-7828
EI 1533-9866
J9 OBSTET GYNECOL SURV
JI Obstet. Gynecol. Surv.
PD DEC
PY 2015
VL 70
IS 12
BP 757
EP 758
DI 10.1097/OGX.0000000000000275
PG 2
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA CY3RQ
UT WOS:000366327900015
ER

PT J
AU Day, FR
   Ruth, KS
   Thompson, DJ
   Lunetta, KL
   Pervjakova, N
   Chasman, DI
   Stolk, L
   Finucane, HK
   Sulem, P
   Bulik-Sullivan, B
   Esko, T
   Johnson, AD
   Elks, CE
   Franceschini, N
   He, C
   Altmaier, E
   Brody, JA
   Franke, LL
   Huffman, JE
   Keller, MF
   McArdle, PF
   Nutile, T
   Porcu, E
   Robino, A
   Rose, LM
   Schick, UM
   Smith, JA
   Teumer, A
   Traglia, M
   Vuckovic, D
   Yao, J
   Zhao, W
   Albrecht, E
   Amin, N
   Corre, T
   Hottenga, JJ
   Mangino, M
   Smith, AV
   Tanaka, T
   Abecasis, GR
   Andrulis, IL
   Anton-Culver, H
   Antoniou, AC
   Arndt, V
   Arnold, AM
   Barbieri, C
   Beckmann, MW
   Beeghly-Fadiel, A
   Benitez, J
   Bernstein, L
   Bielinski, SJ
   Blomqvist, C
   Boerwinkle, E
   Bogdanova, NV
   Bojesen, SE
   Bolla, MK
   Borresen-Dale, AL
   Boutin, TS
   Brauch, H
   Brenner, H
   Bruning, T
   Burwinkel, B
   Campbell, A
   Campbell, H
   Chanock, SJ
   Chapman, JR
   Chen, YDI
   Chenevix-Trench, G
   Couch, FJ
   Coviello, AD
   Cox, A
   Czene, K
   Darabi, H
   De Vivo, I
   Demerath, EW
   Dennis, J
   Devilee, P
   Dork, T
   dos-Santos-Silva, I
   Dunning, AM
   Eicher, JD
   Fasching, PA
   Faul, JD
   Figueroa, J
   Flesch-Janys, D
   Gandin, I
   Garcia, ME
   Garcia-Closas, M
   Giles, GG
   Girotto, GG
   Goldberg, MS
   Gonzalez-Neira, A
   Goodarzi, MO
   Grove, ML
   Gudbjartsson, DF
   Guenel, P
   Guo, XQ
   Haiman, CA
   Hall, P
   Hamann, U
   Henderson, BE
   Hocking, LJ
   Hofman, A
   Homuth, G
   Hooning, MJ
   Hopper, JL
   Hu, FB
   Huang, JY
   Humphreys, K
   Hunter, DJ
   Jakubowska, A
   Jones, SE
   Kabisch, M
   Karasik, D
   Knight, JA
   Kolcic, I
   Kooperberg, C
   Kosma, VM
   Kriebel, J
   Kristensen, V
   Lambrechts, D
   Langenberg, C
   Li, JM
   Li, X
   Lindstrom, S
   Liu, YM
   Luan, JA
   Lubinski, J
   Magi, R
   Mannermaa, A
   Manz, J
   Margolin, S
   Marten, J
   Martin, NG
   Masciullo, C
   Meindl, A
   Michailidou, K
   Mihailov, E
   Milani, L
   Milne, RL
   Muller-Nurasyid, M
   Nalls, M
   Neale, BM
   Nevanlinna, H
   Neven, P
   Newman, AB
   Nordestgaard, BG
   Olson, JE
   Padmanabhan, S
   Peterlongo, P
   Peters, U
   Petersmann, A
   Peto, J
   Pharoah, PDP
   Pirastu, NN
   Pirie, A
   Pistis, G
   Polasek, O
   Porteous, D
   Psaty, BM
   Pylkas, K
   Radice, P
   Raffel, LJ
   Rivadeneira, F
   Rudan, I
   Rudolph, A
   Ruggiero, D
   Sala, CF
   Sanna, S
   Sawyer, EJ
   Schlessinger, D
   Schmidt, MK
   Schmidt, F
   Schmutzler, RK
   Schoemaker, MJ
   Scott, RA
   Seynaeve, CM
   Simard, J
   Sorice, R
   Southey, MC
   Stockl, D
   Strauch, K
   Swerdlow, A
   Taylor, KD
   Thorsteinsdottir, U
   Toland, AE
   Tomlinson, I
   Truong, T
   Tryggvadottir, L
   Turner, ST
   Vozzi, D
   Wang, Q
   Wellons, M
   Willemsen, G
   Wilson, JF
   Winqvist, R
   Wolffenbuttel, BBHR
   Wright, AF
   Yannoukakos, D
   Zemunik, T
   Zheng, W
   Zygmunt, M
   Bergmann, S
   Boomsma, DI
   Buring, JE
   Ferrucci, L
   Montgomery, GW
   Gudnason, V
   Spector, TD
   van Duijn, CM
   Alizadeh, BZ
   Ciullo, M
   Crisponi, L
   Easton, DF
   Gasparini, PP
   Gieger, C
   Harris, TB
   Hayward, C
   Kardia, SLR
   Kraft, P
   McKnight, B
   Metspalu, A
   Morrison, AC
   Reiner, AP
   Ridker, PM
   Rotter, JI
   Toniolo, D
   Uitterlinden, AG
   Ulivi, S
   Volzke, H
   Wareham, NJ
   Weir, DR
   Yerges-Armstrong, LM
   Price, AL
   Stefansson, K
   Visser, JA
   Ong, KK
   Chang-Claude, J
   Murabito, JM
   Perry, JRB
   Murray, A
AF Day, Felix R.
   Ruth, Katherine S.
   Thompson, Deborah J.
   Lunetta, Kathryn L.
   Pervjakova, Natalia
   Chasman, Daniel I.
   Stolk, Lisette
   Finucane, Hilary K.
   Sulem, Patrick
   Bulik-Sullivan, Brendan
   Esko, Tonu
   Johnson, Andrew D.
   Elks, Cathy E.
   Franceschini, Nora
   He, Chunyan
   Altmaier, Elisabeth
   Brody, Jennifer A.
   Franke, Lude L.
   Huffman, Jennifer E.
   Keller, Margaux F.
   McArdle, Patrick F.
   Nutile, Teresa
   Porcu, Eleonora
   Robino, Antonietta
   Rose, Lynda M.
   Schick, Ursula M.
   Smith, Jennifer A.
   Teumer, Alexander
   Traglia, Michela
   Vuckovic, Dragana
   Yao, Jie
   Zhao, Wei
   Albrecht, Eva
   Amin, Najaf
   Corre, Tanguy
   Hottenga, Jouke-Jan
   Mangino, Massimo
   Smith, Albert V.
   Tanaka, Toshiko
   Abecasis, Goncalo R.
   Andrulis, Irene L.
   Anton-Culver, Hoda
   Antoniou, Antonis C.
   Arndt, Volker
   Arnold, Alice M.
   Barbieri, Caterina
   Beckmann, Matthias W.
   Beeghly-Fadiel, Alicia
   Benitez, Javier
   Bernstein, Leslie
   Bielinski, Suzette J.
   Blomqvist, Carl
   Boerwinkle, Eric
   Bogdanova, Natalia V.
   Bojesen, Stig E.
   Bolla, Manjeet K.
   Borresen-Dale, Anne-Lise
   Boutin, Thibaud S.
   Brauch, Hiltrud
   Brenner, Hermann
   Bruening, Thomas
   Burwinkel, Barbara
   Campbell, Archie
   Campbell, Harry
   Chanock, Stephen J.
   Chapman, J. Ross
   Chen, Yii-Der Ida
   Chenevix-Trench, Georgia
   Couch, Fergus J.
   Coviello, Andrea D.
   Cox, Angela
   Czene, Kamila
   Darabi, Hatef
   De Vivo, Immaculata
   Demerath, Ellen W.
   Dennis, Joe
   Devilee, Peter
   Doerk, Thilo
   dos-Santos-Silva, Isabel
   Dunning, Alison M.
   Eicher, John D.
   Fasching, Peter A.
   Faul, Jessica D.
   Figueroa, Jonine
   Flesch-Janys, Dieter
   Gandin, Ilaria
   Garcia, Melissa E.
   Garcia-Closas, Montserrat
   Giles, Graham G.
   Girotto, Giorgia G.
   Goldberg, Mark S.
   Gonzalez-Neira, Anna
   Goodarzi, Mark O.
   Grove, Megan L.
   Gudbjartsson, Daniel F.
   Guenel, Pascal
   Guo, Xiuqing
   Haiman, Christopher A.
   Hall, Per
   Hamann, Ute
   Henderson, Brian E.
   Hocking, Lynne J.
   Hofman, Albert
   Homuth, Georg
   Hooning, Maartje J.
   Hopper, John L.
   Hu, Frank B.
   Huang, Jinyan
   Humphreys, Keith
   Hunter, David J.
   Jakubowska, Anna
   Jones, Samuel E.
   Kabisch, Maria
   Karasik, David
   Knight, Julia A.
   Kolcic, Ivana
   Kooperberg, Charles
   Kosma, Veli-Matti
   Kriebel, Jennifer
   Kristensen, Vessela
   Lambrechts, Diether
   Langenberg, Claudia
   Li, Jingmei
   Li, Xin
   Lindstroem, Sara
   Liu, Yongmei
   Luan, Jian'an
   Lubinski, Jan
   Maegi, Reedik
   Mannermaa, Arto
   Manz, Judith
   Margolin, Sara
   Marten, Jonathan
   Martin, Nicholas G.
   Masciullo, Corrado
   Meindl, Alfons
   Michailidou, Kyriaki
   Mihailov, Evelin
   Milani, Lili
   Milne, Roger L.
   Mueller-Nurasyid, Martina
   Nalls, Michael
   Neale, Benjamin M.
   Nevanlinna, Heli
   Neven, Patrick
   Newman, Anne B.
   Nordestgaard, Borge G.
   Olson, Janet E.
   Padmanabhan, Sandosh
   Peterlongo, Paolo
   Peters, Ulrike
   Petersmann, Astrid
   Peto, Julian
   Pharoah, Paul D. P.
   Pirastu, Nicola N.
   Pirie, Ailith
   Pistis, Giorgio
   Polasek, Ozren
   Porteous, David
   Psaty, Bruce M.
   Pylkaes, Katri
   Radice, Paolo
   Raffel, Leslie J.
   Rivadeneira, Fernando
   Rudan, Igor
   Rudolph, Anja
   Ruggiero, Daniela
   Sala, Cinzia F.
   Sanna, Serena
   Sawyer, Elinor J.
   Schlessinger, David
   Schmidt, Marjanka K.
   Schmidt, Frank
   Schmutzler, Rita K.
   Schoemaker, Minouk J.
   Scott, Robert A.
   Seynaeve, Caroline M.
   Simard, Jacques
   Sorice, Rossella
   Southey, Melissa C.
   Stoeckl, Doris
   Strauch, Konstantin
   Swerdlow, Anthony
   Taylor, Kent D.
   Thorsteinsdottir, Unnur
   Toland, Amanda E.
   Tomlinson, Ian
   Truong, Therese
   Tryggvadottir, Laufey
   Turner, Stephen T.
   Vozzi, Diego
   Wang, Qin
   Wellons, Melissa
   Willemsen, Gonneke
   Wilson, James F.
   Winqvist, Robert
   Wolffenbuttel, Bruce B. H. R.
   Wright, Alan F.
   Yannoukakos, Drakoulis
   Zemunik, Tatijana
   Zheng, Wei
   Zygmunt, Marek
   Bergmann, Sven
   Boomsma, Dorret I.
   Buring, Julie E.
   Ferrucci, Luigi
   Montgomery, Grant W.
   Gudnason, Vilmundur
   Spector, Tim D.
   van Duijn, Cornelia M.
   Alizadeh, Behrooz Z.
   Ciullo, Marina
   Crisponi, Laura
   Easton, Douglas F.
   Gasparini, Paolo P.
   Gieger, Christian
   Harris, Tamara B.
   Hayward, Caroline
   Kardia, Sharon L. R.
   Kraft, Peter
   McKnight, Barbara
   Metspalu, Andres
   Morrison, Alanna C.
   Reiner, Alex P.
   Ridker, Paul M.
   Rotter, Jerome I.
   Toniolo, Daniela
   Uitterlinden, Andre G.
   Ulivi, Sheila
   Voelzke, Henry
   Wareham, Nicholas J.
   Weir, David R.
   Yerges-Armstrong, Laura M.
   Price, Alkes L.
   Stefansson, Kari
   Visser, Jenny A.
   Ong, Ken K.
   Chang-Claude, Jenny
   Murabito, Joanne M.
   Perry, John R. B.
   Murray, Anna
CA PRACTICAL Consortium
   kConFab Investigators
   AOCS Investigators
   Generation Scotland
   EPIC-Interact Consortium
   LifeLines Cohort Study
TI Large-Scale Genomic Analyses Link Reproductive Aging to Hypothalamic
   Signaling, Breast Cancer Susceptibility, and BRCA1-Mediated DNA Repair
   EDITORIAL COMMENT
SO OBSTETRICAL & GYNECOLOGICAL SURVEY
LA English
DT Editorial Material
C1 [Day, Felix R.; Elks, Cathy E.; Langenberg, Claudia; Luan, Jian'an; Scott, Robert A.; Wareham, Nicholas J.; Ong, Ken K.; Perry, John R. B.] Univ Cambridge, Sch Clin Med, Med Res Council Epidemiol Unit, Inst Metab Sci, Cambridge, England.
   [Ruth, Katherine S.; Jones, Samuel E.; Murray, Anna] Univ Exeter, Univ Exeter Med Sch, Genet Complex Traits, Exeter, Devon, England.
   [Thompson, Deborah J.; Antoniou, Antonis C.; Bolla, Manjeet K.; Dennis, Joe; Michailidou, Kyriaki; Pharoah, Paul D. P.; Pirie, Ailith; Wang, Qin; Easton, Douglas F.] Univ Cambridge, Dept Publ Hlth & Primary Care, Ctr Canc Genet Epidemiol, Cambridge, England.
   [Lunetta, Kathryn L.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
   [Lunetta, Kathryn L.; Johnson, Andrew D.; Huffman, Jennifer E.; Eicher, John D.; Murabito, Joanne M.] NHLBI, Framingham, MA USA.
   [Lunetta, Kathryn L.; Johnson, Andrew D.; Huffman, Jennifer E.; Eicher, John D.; Murabito, Joanne M.] Boston Univ, Framingham Heart Study, Framingham, MA USA.
   [Pervjakova, Natalia; Esko, Tonu; Maegi, Reedik; Mihailov, Evelin; Milani, Lili; Metspalu, Andres] Univ Tartu, Estonian Genome Ctr, EE-50090 Tartu, Estonia.
   [Pervjakova, Natalia] Univ Tartu, Inst Mol & Cell Biol, EE-50090 Tartu, Estonia.
   [Chasman, Daniel I.; Rose, Lynda M.; Buring, Julie E.; Ridker, Paul M.] Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA.
   [Chasman, Daniel I.; Karasik, David; Buring, Julie E.; Ridker, Paul M.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
   [Stolk, Lisette; Rivadeneira, Fernando; Uitterlinden, Andre G.] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
   [Stolk, Lisette; Rivadeneira, Fernando; Uitterlinden, Andre G.] Netherlands Consortium Hlth Aging & Natl Genom In, Leiden, Netherlands.
   [Finucane, Hilary K.; De Vivo, Immaculata; Hu, Frank B.; Hunter, David J.; Li, Xin; Lindstroem, Sara; Kraft, Peter; Price, Alkes L.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
   [Finucane, Hilary K.] MA Inst Technol, Dept Math, Cambridge, MA USA.
   [Sulem, Patrick; Gudbjartsson, Daniel F.; Thorsteinsdottir, Unnur; Stefansson, Kari] deCODE Genet Amgen Inc, Reykjavik, Iceland.
   [Bulik-Sullivan, Brendan; Neale, Benjamin M.] Broad Inst MIT & Harvard, Stanley Ctr Psychiat Res, Cambridge, MA USA.
   [Bulik-Sullivan, Brendan; Neale, Benjamin M.] Massachusetts Gen Hosp, Dept Med, Analyt & Translat Genet Unit, Boston, MA 02114 USA.
   [Bulik-Sullivan, Brendan; Neale, Benjamin M.] Broad Inst, Med & Populat Genet, Cambridge, MA USA.
   [Esko, Tonu] Boston Childrens Hosp, Div Endocrinol, Boston, MA USA.
   [Esko, Tonu] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
   [Esko, Tonu; Hunter, David J.] Broad Inst MIT & Harvard, Cambridge, MA USA.
   [Franceschini, Nora] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
   [He, Chunyan] Indiana Univ, Richard M Fairbanks Sch Publ Hlth, Dept Epidemiol, Indianapolis, IN 46204 USA.
   [He, Chunyan] Indiana Univ, Melvin & Bren Simon Canc Ctr, Indianapolis, IN 46204 USA.
   [Altmaier, Elisabeth; Kriebel, Jennifer; Manz, Judith; Gieger, Christian] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Neuherberg, Germany.
   [Altmaier, Elisabeth; Albrecht, Eva; Mueller-Nurasyid, Martina; Strauch, Konstantin; Gieger, Christian] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Genet Epidemiol, Neuherberg, Germany.
   [Altmaier, Elisabeth; Kriebel, Jennifer; Manz, Judith; Gieger, Christian] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 2, Neuherberg, Germany.
   [Brody, Jennifer A.; Psaty, Bruce M.] Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
   [Franke, Lude L.] Univ Groningen, Univ Med Ctr Groningen, Dept Genet, Groningen, Netherlands.
   [Huffman, Jennifer E.; Boutin, Thibaud S.; Marten, Jonathan; Wilson, James F.; Wright, Alan F.; Hayward, Caroline] Univ Edinburgh, Inst Genet & Mol Med, MRC Human Genet Unit, Edinburgh, Midlothian, Scotland.
   [Keller, Margaux F.] Merck Pharmaceut, Boston, MA USA.
   [McArdle, Patrick F.; Yerges-Armstrong, Laura M.] Univ Maryland, Sch Med, Div Endocrinol Diabet & Nutr, Program Personalized Med, Baltimore, MD 21201 USA.
   [Nutile, Teresa; Ruggiero, Daniela; Sorice, Rossella; Ciullo, Marina] Inst Genet & Biophys, Natl Res Council, Naples, Italy.
   [Porcu, Eleonora; Pistis, Giorgio; Sanna, Serena; Crisponi, Laura] Inst Genet & Biomed Res, Natl Res Council, Cagliari, Italy.
   [Porcu, Eleonora; Pistis, Giorgio] Univ Sassari, Dept Biomed Sci, I-07100 Sassari, Italy.
   [Porcu, Eleonora; Abecasis, Goncalo R.; Pistis, Giorgio] Univ Michigan, Ctr Stat Genet, Ann Arbor, MI 48109 USA.
   [Robino, Antonietta; Vuckovic, Dragana; Barbieri, Caterina; Gandin, Ilaria; Pirastu, Nicola N.; Vozzi, Diego; Gasparini, Paolo P.; Ulivi, Sheila] Hospitalisat & Hlth Care BurloGarofolo, Inst Maternal & Child Hlth, Sci Inst Res, Trieste, Italy.
   [Schick, Ursula M.; Kooperberg, Charles; Peters, Ulrike; Reiner, Alex P.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.
   [Smith, Jennifer A.; Zhao, Wei; Kardia, Sharon L. R.] Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA.
   [Teumer, Alexander; Voelzke, Henry] Univ Med Greifswald, Inst Community Med, Greifswald, Germany.
   [Traglia, Michela; Barbieri, Caterina; Masciullo, Corrado; Sala, Cinzia F.; Toniolo, Daniela] Ist Sci San Raffaele, Div Genet & Cell Biol, I-20132 Milan, Italy.
   [Vuckovic, Dragana; Gandin, Ilaria; Girotto, Giorgia G.; Pirastu, Nicola N.; Gasparini, Paolo P.] Univ Trieste, Dept Clin Med Sci Surg & Hlth, Trieste, Italy.
   [Yao, Jie; Chen, Yii-Der Ida; Guo, Xiuqing; Taylor, Kent D.; Rotter, Jerome I.] Harbor UCLA Med Ctr, LABioMed, Dept Pediat, Inst Translat Genom & Populat Sci, Torrance, CA 90509 USA.
   [Amin, Najaf; Hofman, Albert; Rivadeneira, Fernando; van Duijn, Cornelia M.; Uitterlinden, Andre G.] Erasmus MC, Dept Epidemiol, Genet Epidemiol Unit, Rotterdam, Netherlands.
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   [Guenel, Pascal; Truong, Therese] Univ Paris Sud, UMRS 1018, Villejuif, France.
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   [Hamann, Ute; Kabisch, Maria] German Canc Res Ctr, Mol Genet Breast Canc, Heidelberg, Germany.
   [Hocking, Lynne J.] Univ Aberdeen, Div Appl Med, Musculoskeletal Res Programme, Aberdeen, Scotland.
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   [Wolffenbuttel, Bruce B. H. R.] Univ Groningen, Univ Med Ctr Groningen, Dept Endocrinol, Groningen, Netherlands.
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   [Yannoukakos, Drakoulis] Natl Ctr Sci Res Demokritos, Inst Radioisotopes & Radiodiagnost Prod, Mol Diagnost Lab, Athens, Greece.
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RP Day, FR (reprint author), Univ Cambridge, Sch Clin Med, Med Res Council Epidemiol Unit, Inst Metab Sci, Cambridge Biomed Campus, Cambridge, England.
RI Knight, Julia/A-6843-2012; Li, Jingmei/I-2904-2012; Bielinski,
   Suzette/A-2238-2009; Bruning, Thomas/G-8120-2015; Franke,
   Lude/P-7036-2016; Brenner, Hermann/B-4627-2017; Polasek,
   Ozren/B-6002-2011; Kolcic, Ivana/E-2713-2017
OI Li, Jingmei/0000-0001-8587-7511; Bielinski, Suzette/0000-0002-2905-5430;
   Bruning, Thomas/0000-0001-9560-5464; Franke, Lude/0000-0002-5159-8802;
   Brenner, Hermann/0000-0002-6129-1572; Polasek,
   Ozren/0000-0002-5765-1862; Kolcic, Ivana/0000-0001-7918-6052
FU Cancer Research UK [16561]
NR 0
TC 0
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U1 4
U2 16
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0029-7828
EI 1533-9866
J9 OBSTET GYNECOL SURV
JI Obstet. Gynecol. Surv.
PD DEC
PY 2015
VL 70
IS 12
BP 758
EP 762
DI 10.1097/01.ogx.0000473766.71624.99
PG 5
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA CY3RQ
UT WOS:000366327900016
ER

PT J
AU Chan, L
   Heinemann, AW
AF Chan, Leighton
   Heinemann, Allen W.
TI Clinical Trial Registration: The Time Has Come...
SO PM&R
LA English
DT Editorial Material
C1 [Chan, Leighton] NIH, Dept Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Heinemann, Allen W.] Northwestern Univ, Feinberg Sch Med, Chicago, IL USA.
RP Chan, L (reprint author), NIH, Dept Med, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA.
EM lchan@acrm.org
OI Heinemann, Allen/0000-0003-2782-7326
NR 3
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 1934-1482
EI 1934-1563
J9 PM&R
JI PM&R
PD DEC
PY 2015
VL 7
IS 12
BP 1203
EP 1204
DI 10.1016/j.pmrj.2015.11.003
PG 2
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA CZ1FP
UT WOS:000366851600001
PM 26709245
ER

PT J
AU Perkins, DO
   Jeffries, CD
   Cornblatt, BA
   Woods, SW
   Addington, J
   Bearden, CE
   Cadenhead, KS
   Cannon, TD
   Heinssen, R
   Mathalon, DH
   Seidman, LJ
   Tsuang, MT
   Walker, EF
   McGlashan, TH
AF Perkins, Diana O.
   Jeffries, Clark D.
   Cornblatt, Barbara A.
   Woods, Scott W.
   Addington, Jean
   Bearden, Carrie E.
   Cadenhead, Kristin S.
   Cannon, Tyrone D.
   Heinssen, Robert
   Mathalon, Daniel H.
   Seidman, Larry J.
   Tsuang, Ming T.
   Walker, Elaine F.
   McGlashan, Thomas H.
TI Severity of thought disorder predicts psychosis in persons at clinical
   high-risk
SO SCHIZOPHRENIA RESEARCH
LA English
DT Article
DE Psychosis; High-risk; Risk prediction; Symptom severity; Schizophrenia;
   Survival
ID ULTRA-HIGH-RISK; INTERRATER RELIABILITY; PRODROMAL SYNDROMES; FOLLOW-UP;
   VALIDITY; POPULATION; SCHIZOPHRENIA; VALIDATION; DIAGNOSIS;
   PSYCHOPATHOLOGY
AB Background: Improving predictive accuracy is of paramount importance for early detection and prevention of psychosis. We sought a symptom severity classifier that would improve psychosis risk prediction.
   Methods: Subjects were from two cohorts of the North American Prodrome Longitudinal Study. All subjects met Criteria of Psychosis-Risk States. In Cohort-1 (n=296) we developed a classifier that included those items of the Scale of Psychosis-Risk Symptoms that best distinguished subjects who converted to psychosis from nonconverters, with performance initially validated by randomization tests in Cohort-1. Cohort-2 (n=592) served as an independent test set.
   Results: We derived 2-Item and 4-Item subscales. Both included unusual thought content and suspiciousness; the latter added reduced ideational richness and difficulties with focus/concentration. The Concordance Index (C-Index), a measure of discrimination, was similar for each subscale across cohorts (4-Item subscale Cohort-2: 0.71, 95% CI=[0.64, 0.77], Cohort-1: 0.74, 95% CI=[0.69, 0.80]; 2-Item subscale Cohort-2: 0.68, 95% CI=[0.3, 0.76], Cohort-1: 0.72, 95% CI=[0.66-0.79]). The 4-Item performed better than the 2-Item subscale in 742/1000 random selections of 80% subsets of Cohort-2 subjects (p-value=1.3E-55). Subscale calibration between cohorts was proportional (higher scores/lower survival), but absolute conversion risk predicted from Cohort-1 was higher than that observed in Cohort-2, reflecting the cohorts' differences in 2-year conversion rates (Cohort-2: 0.16, 95% CI=[0.13, 0.19]; Cohort-1: 0.30, 95% CI=[0.24, 0.36]).
   Conclusion: Severity of unusual thought content, suspiciousness, reduced ideational richness, and difficulty with focus/concentration informed psychosis risk prediction. Scales based on these symptoms may have utility in research and, assuming further validation, eventual clinical applications. (C) 2015 Elsevier B.V. All rights reserved.
C1 [Perkins, Diana O.] Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27514 USA.
   [Jeffries, Clark D.] Univ N Carolina, Renaissance Comp Inst, Chapel Hill, NC USA.
   [Cornblatt, Barbara A.] Zucker Hillside Hosp, Dept Psychiat, Long Isl City, NY USA.
   [Woods, Scott W.; Cannon, Tyrone D.; McGlashan, Thomas H.] Yale Univ, Dept Psychiat, New Haven, CT 06520 USA.
   [Addington, Jean] Univ Calgary, Dept Psychiat, Hotchkiss Brain Inst, Calgary, AB T2N 1N4, Canada.
   [Bearden, Carrie E.] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA.
   [Bearden, Carrie E.] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90024 USA.
   [Cadenhead, Kristin S.; Tsuang, Ming T.] UCSD, Dept Psychiat, San Diego, CA USA.
   [Cannon, Tyrone D.] Yale Univ, Dept Psychol, New Haven, CT 06520 USA.
   [Heinssen, Robert] NIMH, Rockville, MD USA.
   [Mathalon, Daniel H.] UCSF, Dept Psychiat, San Francisco, CA USA.
   [Seidman, Larry J.] Harvard Univ, Sch Med, Dept Psychiat, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA.
   [Seidman, Larry J.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
   [Walker, Elaine F.] Emory Univ, Dept Psychol, Atlanta, GA 30322 USA.
   [Walker, Elaine F.] Emory Univ, Dept Psychiat, Atlanta, GA 30322 USA.
RP Perkins, DO (reprint author), Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27514 USA.
EM Diana_Perkins@unc.edu
FU National Institutes of Health
FX This project was a cooperative agreement between the investigator sites
   and the National Institutes of Health.
NR 53
TC 2
Z9 2
U1 3
U2 9
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
EI 1573-2509
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD DEC
PY 2015
VL 169
IS 1-3
BP 169
EP 177
DI 10.1016/j.schres.2015.09.008
PG 9
WC Psychiatry
SC Psychiatry
GA CY5PC
UT WOS:000366458600026
PM 26441004
ER

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   Panis, C
   Pantano, F
   Parslow, VR
   Pawelec, G
   Pedersen, PL
   Poore, B
   Poudyal, D
   Prakash, S
   Prince, M
   Raffaghello, L
   Rathmell, JC
   Rathmell, WK
   Ray, SK
   Reichrath, J
   Rezazadeh, S
   Ribatti, D
   Ricciardiello, L
   Robey, RB
   Rodier, F
   Rupasinghe, HPV
   Russo, GL
   Ryan, EP
   Samadi, AK
   Sanchez-Garcia, I
   Sanders, AJ
   Santini, D
   Sarkar, M
   Sasada, T
   Saxena, NK
   Shackelford, RE
   Kumara, HMCS
   Sharma, D
   Shin, DM
   Sidransky, D
   Siegelin, MD
   Signori, E
   Singh, N
   Sivanand, S
   Sliva, D
   Smythe, C
   Spagnuolo, C
   Stafforini, DM
   Stagg, J
   Subbarayan, PR
   Sundin, T
   Talib, WH
   Thompson, SK
   Tran, PT
   Ungefroren, H
   Vander Heiden, MG
   Venkateswaran, V
   Vinay, DS
   Vlachostergios, PJ
   Wang, ZW
   Wellendx, KE
   Whelan, RL
   Yang, ES
   Yang, HJ
   Yang, XJ
   Yaswen, P
   Yedjou, C
   Yin, X
   Zhu, JY
   Zollo, M
AF Block, Keith I.
   Gyllenhaal, Charlotte
   Lowe, Leroy
   Amedei, Amedeo
   Amin, A. R. M. Ruhul
   Amin, Amr
   Aquilano, Katia
   Arbiser, Jack
   Arreola, Alexandra
   Arzumanyan, Alla
   Ashraf, S. Salman
   Azmi, Asfar S.
   Benencia, Fabian
   Bhakta, Dipita
   Bilsland, Alan
   Bishayeen, Anupam
   Blain, Stacy W.
   Block, Penny B.
   Boosani, Chandra S.
   Carey, Thomas E.
   Carnero, Amancio
   Carotenuto, Marianeve
   Casey, Stephanie C.
   Chakrabarti, Mrinmay
   Chaturvedi, Rupesh
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   Chenx, Helen
   Chen, Sophie
   Chen, Yi Charlie
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   Ciriolo, Maria Rosa
   Coley, Helen M.
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   Connell, Marisa
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   Curran, Colleen S.
   Dabrosin, Charlotta
   Damia, Giovanna
   Dasgupta, Santanu
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   Decker, William K.
   Dhawan, Punita
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   Dong, Jin-Tang
   Dou, Q. Ping
   Drew, Janice E.
   Elkord, Eyad
   El-Rayes, Bassel
   Feitelson, Mark A.
   Felsher, Dean W.
   Ferguson, Lynnette R.
   Fimognari, Carmela
   Firestone, Gary L.
   Frezza, Christian
   Fujii, Hiromasa
   Fuster, Mark M.
   Generali, Daniele
   Georgakilas, Alexandros G.
   Gieseler, Frank
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   Guha, Gunjan
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   Lokeshwar, Bal L.
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   Marino, Maria
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   Sanchez-Garcia, Isidro
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   Kumara, H. M. C. Shantha
   Sharma, Dipali
   Shin, Dong M.
   Sidransky, David
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   Signori, Emanuela
   Singh, Neetu
   Sivanand, Sharanya
   Sliva, Daniel
   Smythe, Carl
   Spagnuolo, Carmela
   Stafforini, Diana M.
   Stagg, John
   Subbarayan, Pochi R.
   Sundin, Tabetha
   Talib, Wamidh H.
   Thompson, Sarah K.
   Tran, Phuoc T.
   Ungefroren, Hendrik
   Vander Heiden, Matthew G.
   Venkateswaran, Vasundara
   Vinay, Dass S.
   Vlachostergios, Panagiotis J.
   Wang, Zongwei
   Wellendx, Kathryn E.
   Whelan, Richard L.
   Yang, Eddy S.
   Yang, Huanjie
   Yang, Xujuan
   Yaswen, Paul
   Yedjou, Clement
   Yin, Xin
   Zhu, Jiyue
   Zollo, Massimo
TI Designing a broad-spectrum integrative approach for cancer prevention
   and treatment
SO SEMINARS IN CANCER BIOLOGY
LA English
DT Review
DE Multi-targeted; Cancer hallmarks; Phytochemicals; Targeted therapy;
   Integrative medicine
ID RANDOMIZED CONTROLLED-TRIALS; TEA POLYPHENOL
   (-)-EPIGALLOCATECHIN-3-GALLATE; BOTANICAL DIETARY-SUPPLEMENTS;
   TRADITIONAL CHINESE MEDICINE; CONTROLLED CLINICAL-TRIAL; METASTATIC
   BREAST-CANCER; ENDOTHELIAL-CELL-GROWTH; III COLON-CANCER; PHASE-I TRIAL;
   LOW-FAT DIETS
AB Targeted therapies and the consequent adoption of "personalized" oncology have achieved notable successes in some cancers; however, significant problems remain with this approach. Many targeted therapies are highly toxic, costs are extremely high, and most patients experience relapse after a few disease-free months. Relapses arise from genetic heterogeneity in tumors, which harbor therapy-resistant immortalized cells that have adopted alternate and compensatory pathways (i.e., pathways that are not reliant upon the same mechanisms as those which have been targeted). To address these limitations, an international task force of 180 scientists was assembled to explore the concept of a low-toxicity "broadspectrum" therapeutic approach that could simultaneously target many key pathways and mechanisms. Using cancer hallmark phenotypes and the tumor microenvironment to account for the various aspects of relevant cancer biology, interdisciplinary teams reviewed each hallmark area and nominated a wide range of high-priority targets (74 in total) that could be modified to improve patient outcomes. For these targets, corresponding low-toxicity therapeutic approaches were then suggested, many of which were phytochemicals. Proposed actions on each target and all of the approaches were further reviewed for known effects on other hallmark areas and the tumor microenvironment Potential contrary or procarcinogenic effects were found for 3.9% of the relationships between targets and hallmarks, and mixed evidence of complementary and contrary relationships was found for 7.1%. Approximately 67% of the relationships revealed potentially complementary effects, and the remainder had no known relationship. Among the approaches, 1.1% had contrary, 2.8% had mixed and 62.1% had complementary relationships. These results suggest that a broad-spectrum approach should be feasible from a safety standpoint. This novel approach has potential to be relatively inexpensive, it should help us address stages and types of cancer that lack conventional treatment, and it may reduce relapse risks. A proposed agenda for future research is offered. (C) 2015 The Authors. Published by Elsevier Ltd.
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RP Block, KI (reprint author), Block Ctr Integrat Canc Treatment, Skokie, IL 60077 USA.
EM drblock@blockmedical.com; Leroy.lowe@gettingtoknowcancer.org
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   CANCER/P-3323-2015; Keith, Nicol/D-3325-2009; Zollo,
   Massimo/K-5857-2016; niccolai, elena/K-6091-2016; Ciriolo, Maria
   /K-6572-2016; AQUILANO, KATIA/K-8888-2016; Jiang, Wen/B-1293-2010
OI Pantano, Francesco/0000-0002-2894-9686; Raffaghello,
   Lizzia/0000-0003-2357-0607; Bhakta-Guha, Dipita/0000-0002-7144-3947;
   Gieseler, Frank/0000-0001-6409-3822; RICCIARDIELLO,
   LUIGI/0000-0003-2568-6208; SANCHEZ-GARCIA, ISIDRO/0000-0001-6989-9905;
   Elkord, Eyad/0000-0002-3868-0318; Locasale, Jason/0000-0002-7766-3502;
   Ganji, Purna chandra N/0000-0002-4989-5234; Robey, R.
   Brooks/0000-0001-5059-3965; signori, emanuela/0000-0003-0286-7401;
   Heneberg, Petr/0000-0002-0703-951X; Keith, Nicol/0000-0001-7862-3580;
   Zollo, Massimo/0000-0002-0970-7243; niccolai, elena/0000-0002-9205-8079;
   AQUILANO, KATIA/0000-0002-5905-9870; Jiang, Wen/0000-0002-3283-1111
FU Terry Fox Foundation Grant [TF-13-20]; UAEU Program for Advanced
   Research (UPAR) [31S118]; NIH [AR47901, R21CA188818, R15 CA137499-01,
   F32CA177139, P20RR016477, P20GM103434, R01CA170378, U54CA149145,
   U54CA143907, R01-HL107652, R01CA166348, R01GM071725, R01 CA109335-04A1,
   <LF>109511<LF>R01CA151304<LF>CA168997 <LF> A1110613<LF>1R03CA1711326<LF>
   1P01AT003961<LF>RO1 CA100816<LF>P01AG034906 <LF>
   R01AG020642<LF>P01AG034906-01A1<LF>R01HL108006]; NIH NRSA Grant
   [F31CA154080]; NIH (NIAID) R01: Combination therapies for chronic HBV,
   liver disease, and cancer [AI076535]; Sky Foundation Inc. Michigan;
   University of Glasgow; Beatson Oncology Centre Fund; Spanish Ministry of
   Economy and Competitivity, ISCIII [PI12/00137, RTICC: RD12/0036/0028];
   FEDER from Regional Development European Funds (European Union),
   Consejeria de Ciencia e Innovacion [CTS-6844, CTS-1848]; Consejeria de
   Salud of the Junta de Andalucia [PI-0135-2010, PI-0306-2012]; ISCIII
   [PIE13/0004]; FEDER funds; United Soybean Board; NIH NCCAM Grant
   [K01AT007324]; NIH NCI Grant [R33 CA161873-02]; Michael Cuccione
   Childhood Cancer Foundation Graduate Studentship; Ovarian and Prostate
   Cancer Research Trust, UK; West Virginia Higher Education Policy
   Commission/Division of Science Research; National Institutes of Health;
   Italian Association for Cancer Research (AIRC) [IG10636, 15403]; GRACE
   Charity, UK; Breast Cancer Campaign, UK; Michael Cuccione Childhood
   Cancer Foundation Postdoctoral Fellowship; Connecticut State University;
   Swedish Research Council; Swedish Research Society; University of Texas
   Health Science Centre at Tyler, Elsa U. Pardee Foundation; CPRIT; Cancer
   Prevention and Research Institute of Texas; NIH National Institute of
   Diabetes and Digestive and Kidney Diseases (NIDDK); NIH National
   Institute on Alcohol Abuse and Alcoholism (NIAAA); Gilead and Shire
   Pharmaceuticals; NIH/NCI [1R01CA20009, 5R01CAl27258-05, R21CA184788, NIH
   P30 CA22453, NCI RO1 28704]; Scottish Government's Rural and Environment
   Science and Analytical Services Division; National Research Foundation;
   United Arab Emirates University; Terry Fox Foundation; Novartis
   Pharmaceutical; Aveo Pharmaceutical; Roche; Bristol Myers Squibb; Bayer
   Pharmaceutical; Pfizer; Kyowa Kirin; NIH/NIAID Grant [A1076535];
   Auckland Cancer Society; Cancer Society of New Zealand; NIH Public
   Service Grant from the National Cancer Institute [CA164095]; Medical
   Research Council CCU-Program Grant on cancer metabolism; EU Marie Curie
   Reintegration Grant [MC-CIG-303514]; Greek National funds through the
   Operational Program 'Educational and Lifelong Learning of the National
   Strategic Reference Framework (NSRF)-Research Funding Program THALES
   [MIS 379346]; COST Action CM1201 `Biomimetic Radical Chemistry'; Duke
   University Molecular Cancer Biology T32 Training Grant; National
   Sciences Engineering and Research Council Undergraduate Student Research
   Award in Canada; Charles University in Prague projects [UNCE 204015,
   PRVOUK P31/2012]; Czech Science Foundation projects [15-03834Y,
   P301/12/1686]; Czech Health Research Council AZV project [15-32432A];
   Internal Grant Agency of the Ministry of Health of the Czech Republic
   project [NT13663-3/2012]; National Institute of Aging [P30AG028716-01];
   NIH/NCI training grants to Duke University [T32-CA059365-19,
   5T32-CA059365]; Ministry of Education, Culture, Sports, Science and
   Technology, Japan [24590493]; Ministry of Health and Welfare
   [CCMP101-RD-031, CCMP102-RD-112]; Tzu-Chi University of Taiwan
   [61040055-10]; Svenska Sallskapet for Medicinsk Forskning; Cancer
   Research Wales; Albert Hung Foundation; Fong Family Foundation; Welsh
   Government A4B scheme; NIH NCI; University of Glasgow, Beatson Oncology
   Centre Fund, CRUK [C301/A14762]; NIH Intramural Research Program;
   National Science Foundation; American Cancer Society; National Cancer
   Center [NCC-1310430-2]; National Research Foundation [NRF-2005-0093837];
   Sol Goldman Pancreatic Cancer Research Fund Grant [80028595]; Lustgarten
   Fund Grant [90049125, NIHR21CA169757]; Alma Toorock Memorial for Cancer
   Research; National Research Foundation of Korea (NRF); Ministry of
   Science, ICT & Future Planning (MSIP), Republic of Korea [2011-0017639,
   2011-0030001]; Ministry of Education of Taiwan [TMUTOP103005-4];
   International Life Sciences Institute; United States' Public Health
   Services Grants [NIH R01CA156776]; VA-BLR&D Merit Review Grant
   [5101-BX001517-02]; V Foundation; Pancreatic Cancer Action Network;
   Damon Runyon Cancer Research Foundation; Children's Cancer Institute
   Australia; University Roma Tre; Italian Association for Cancer Research
   (AIRC-Grant) [IG15221]; Carlos III Health Institute; Feder funds [AM:
   CP10/00539, PI13/02277]; Basque Foundation for Science (IKERBASQUE);
   Marie Curie CIG Grant [2012/712404]; Canadian Institutes of Health
   Research; Avon Foundation for Women [OBC-134038]; Canadian Institutes of
   Health [MSH-136647, MOP 64308]; Bayer Healthcare System G4T
   (Grants4Targets); NIH NIDDK; NIH NIAAA; Shire Pharmaceuticals;
   Harvard-MIT Health Sciences and Technology Research Assistantship Award;
   Italian Ministry of University; University of Italy; Auckland Cancer
   Society Research Centre (ACSRC); German Federal Ministry of Education
   and Research (Bundesministerium fur Bildung und Forschung, BMBF)
   [16SV5536K]; European Commission [FP7 259679 "IDEAL"]; Cinque per Mille
   dell'IRPEF-Finanziamento della Ricerca Sanitaria; European Union Seventh
   Framework Programme (FP7) [278570]; AIRC [10216, 13837]; European
   Community's Seventh Framework Program FP7 [311876]; Canadian Institute
   for Health Research [MOP114962, MOP125857]; Fonds de Recherche Quebec
   Sante [22624]; Terry Fox Research Institute [1030]; FEDER; MICINN
   [SAF2012-32810]; Junta de Castilla y Leon [BIO/SA06/13]; ARIMMORA
   project [FP7-ENV-2011]; European Union; NIH NIDDK [K01DK077137,
   R03DK089130]; NIH NCI grants [R01CA131294, R21 CA155686]; Avon
   Foundation; Breast Cancer Research Foundation Grant [90047965]; National
   Institute of Health, NINDS Grant [K08NS083732]; AACR-National Brain
   Tumor Society Career Development Award for Translational Brain Tumor
   Research [13-20-23-SIEG]; Department of Science and Technology, New
   Delhi, India [SR/FT/LS-063/2008]; Yorkshire Cancer Research; Wellcome
   Trust, UK; Italian Ministry of Economy and Finance Project CAMPUS-QUARC,
   within program FESR Campania Region; National Cancer Institute
   [5P01CA073992]; IDEA Award from the Department of Defense
   [W81XWH-12-1-0515]; Huntsman Cancer Foundation; University of Miami
   Clinical and Translational Science Institute (CTSI) Pilot Research Grant
   [CTSI-2013-P03]; SEEDS You Choose Awards; DoD [W81XVVH-11-1-0272,
   W81XWH-13-1-0182]; Kimmel Translational Science Award [SKF-13-021]; ACS
   Scholar award [122688-RSG-12-196-01-TBG]; National Cancer Institute,
   Pancreatic Cancer Action Network, Pew Charitable Trusts; American
   Diabetes Association; Elsa U. Pardee Foundation; Scientific Research
   Foundation for the Returned Oversea Scholars, State Education Ministry
   and Scientific and Technological Innovation Project, Harbin
   [2012RFLX5011]; United States National Institutes of Health [ES019458];
   California Breast Cancer Research Program [17UB-8708]; National
   Institutes of Health through the RCMI-Center for Environmental Health
   [G1200MD007581]; NIH/National Heart, Lung, and Blood Institute Training
   Grant [T32HL098062]; European FP7-TuMIC [HEALTH-F2-2008-201662]; Italian
   Association for Cancer research (AIRC) Grant IG [11963]; Regione
   Campania L.R:N.5; European National Funds [PON01-02388/1 2007-2013]
FX Amr Amin was funded by Terry Fox Foundation Grant # TF-13-20 and UAEU
   Program for Advanced Research (UPAR) #31S118; Jack Arbiser was funded by
   NIH AR47901; Alexandra Arreola was funded by NIH NRSA Grant F31CA154080;
   Alla Arzumanyan was funded by NIH (NIAID) R01: Combination therapies for
   chronic HBV, liver disease, and cancer (AI076535); Work in the lab of
   Asfar S. Azmi is supported by NIH R21CA188818 as well as from Sky
   Foundation Inc. Michigan; Fabian Benencia was supported by NIH Grant R15
   CA137499-01; Alan Bilsland was supported by the University of Glasgow,
   Beatson Oncology Centre Fund, CRUK (www. cancerresearchuk.org) Grant
   C301/A14762; Amancio Carnero was supported by grants from the Spanish
   Ministry of Economy and Competitivity, ISCIII (Fis: PI12/00137, RTICC:
   RD12/0036/0028) co-funded by FEDER from Regional Development European
   Funds (European Union), Consejeria de Ciencia e Innovacion (CTS-6844 and
   CTS-1848) and Consejeria de Salud of the Junta de Andalucia
   (PI-0135-2010 and PI-0306-2012). His work on this project has also been
   made possible thanks to the Grant PIE13/0004 co-funded by the ISCIII and
   FEDER funds; Stephanie C. Casey was supported by NIH Grant F32CA177139;
   Mrinmay Chakrabarti was supported by the United Soybean Board; Rupesh
   Chaturvedi was supported by an NIH NCCAM Grant (K01AT007324); Georgia
   Zhuo Chen was supported by an NIH NCI Grant (R33 CA161873-02); Helen
   Chen acknowledges financial support from the Michael Cuccione Childhood
   Cancer Foundation Graduate Studentship; Sophie Chen acknowledges
   financial support from the Ovarian and Prostate Cancer Research Trust,
   UK; Yi Charlie Chen acknowledges financial support from the West
   Virginia Higher Education Policy Commission/Division of Science
   Research, his research was also supported by NIH grants (P20RR016477 and
   P20GM103434) from the National Institutes of Health awarded to the West
   Virginia IDeA Network of Biomedical Research Excellence; Maria Rosa
   Ciriolo was partially supported by the Italian Association for Cancer
   Research (AIRC) Grants #IG10636 and #15403; Helen M. Coley acknowledges
   financial support from the GRACE Charity, UK and the Breast Cancer
   Campaign, UK; Marisa Connell was supported by a Michael Cuccione
   Childhood Cancer Foundation Postdoctoral Fellowship; Sarah Crawford was
   supported by a research grant from Connecticut State University;
   Charlotta Dabrosin acknowledges financial support from the Swedish
   Research Council and the Swedish Research Society; Giovanna Damia
   gratefully acknowledges the generous contributions of The Italian
   Association for Cancer Research (IG14536 to G.D.); Santanu Dasgupta
   gratefully acknowledges the support of the University of Texas Health
   Science Centre at Tyler, Elsa U. Pardee Foundation; William K. Decker
   was supported in part by CPRIT, the Cancer Prevention and Research
   Institute of Texas; Anna Mae E. Diehl was supported by NIH National
   Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), the NIH
   National Institute on Alcohol Abuse and Alcoholism (NIAAA), Gilead and
   Shire Pharmaceuticals; Q. Ping Dou was partially supported by NIH/NCI
   (1R01CA20009, 5R01CAl27258-05 and R21CA184788), and NIH P30 CA22453 (to
   Karmanos Cancer Institute); Janice E.; Drew was supported by the
   Scottish Government's Rural and Environment Science and Analytical
   Services Division; Eyad Elkord thanks the National Research Foundation,
   United Arab Emirates University and the Terry Fox Foundation for
   supporting research projects in his lab; Bassel El-Rayes was supported
   by Novartis Pharmaceutical, Aveo Pharmaceutical, Roche, Bristol Myers
   Squibb, Bayer Pharmaceutical, Pfizer, and Kyowa Kirin; Mark A. Feitelson
   was supported by NIH/NIAID Grant A1076535; Dean W. Felsher was supported
   by NIH grants (R01CA170378, U54CA149145, and U54CA143907); Lynnette R
   Ferguson was financially supported by the Auckland Cancer Society and
   the Cancer Society of New Zealand; Gary L. Firestone was supported by
   NIH Public Service Grant CA164095 awarded from the National Cancer
   Institute; Christian Frezza "would like to acknowledge funding from a
   Medical Research Council CCU-Program Grant on cancer metabolism, and a
   unique applicant AICR project grant"; Mark M. Fuster was supported by
   NIH Grant R01-HL107652; Alexandros G. Georgakilas was supported by an EU
   Marie Curie Reintegration Grant MC-CIG-303514, Greek National funds
   through the Operational Program 'Educational and Lifelong Learning of
   the National Strategic Reference Framework (NSRF)-Research Funding
   Program THALES (Grant number MIS 379346) and COST Action CM1201
   `Biomimetic Radical Chemistry'; Michelle F. Green was supported by a
   Duke University Molecular Cancer Biology T32 Training Grant; Brendan
   Grue was supported by a National Sciences Engineering and Research
   Council Undergraduate Student Research Award in Canada; Dorota Halicka
   was supported by by NIH NCI grant NCI RO1 28704; Petr Heneberg was
   supported by the Charles University in Prague projects UNCE 204015 and
   PRVOUK P31/2012, by the Czech Science Foundation projects 15-03834Y and
   P301/12/1686, by the Czech Health Research Council AZV project
   15-32432A, and by the Internal Grant Agency of the Ministry of Health of
   the Czech Republic project NT13663-3/2012; Matthew D. Hirschey wishes to
   acknowledge Duke University Institutional Support, the Duke Pepper Older
   Americans Independence Center (OAIC) Program in Aging Research supported
   by the National Institute of Aging (P30AG028716-01) and NIH/NCI training
   grants to Duke University (T32-CA059365-19 and 5T32-CA059365); Lorne J.
   Hofseth was supported by NIH grants (1R01CA151304,1R03CA1711326, and
   1P01AT003961); Kanya Honoki was supported in part by the grant from the
   Ministry of Education, Culture, Sports, Science and Technology, Japan
   (No. 24590493); Hsue-Yin Hsu was supported in part by grants from the
   Ministry of Health and Welfare (CCMP101-RD-031 and CCMP102-RD-112) and
   Tzu-Chi University (61040055-10) of Taiwan; Lasse D. Jensen was
   supported by Svenska Sallskapet for Medicinsk Forskning, Gosta Fraenkels
   Stiftelse, Ak.e Wibergs Stiftelse, kopings Universitet and the
   Karolinska Institute, Sweden; Wen G. Jiang wishes to ackOllie och Elof
   Ericssons Stiftelse, Linnowledge the support by Cancer Research Wales,
   the Albert Hung Foundation, the Fong Family Foundation, and Welsh
   Government A4B scheme; Lee W. Jones was supported in part by grants from
   the NIH NCI; W Nicol Keith was supported by the University of Glasgow,
   Beatson Oncology Centre Fund, CRUK (www. cancerresearchuk.org) Grant
   C301/A14762; Sid P. Kerkar was supported by the NIH Intramural Research
   Program; Rob J. Kulathinal was supported by the National Science
   Foundation, and the American Cancer Society; Byoung S.; Kwon was
   supported in part by National Cancer Center (NCC-1310430-2) and National
   Research Foundation (NRF-2005-0093837); Anne Le was supported by Sol
   Goldman Pancreatic Cancer Research Fund Grant 80028595, a Lustgarten
   Fund Grant 90049125 and Grant NIHR21CA169757 (to Anne Le); Michael A.
   Lea was funded by the The Alma Toorock Memorial for Cancer Research;
   Ho-Young Lee This work was supported by grants from the National
   Research Foundation of Korea (NRF), the Ministry of Science, ICT &
   Future Planning (MSIP), Republic of Korea (Nos. 2011-0017639 and
   2011-0030001) and by a NIH Grant RO1 CA100816; Liang-Tzung Lin was
   supported in part by a grant from the Ministry of Education of Taiwan
   (TMUTOP103005-4); Jason W. Locasale acknowledges support from NIH awards
   (CA168997 and A1110613) and the International Life Sciences Institute;
   Bal L. Lokeshwar was supported in part by United States' Public Health
   Services Grants: NIH R01CA156776 and VA-BLR&D Merit Review Grant No.
   5101-BX001517-02; Valter D. Longo acknowleages support from NIH awards
   (P01AG034906 and R01AG020642) and from the V Foundation; Costas A.
   Lyssiotis was funded in part by the Pancreatic Cancer Action Network as
   a Pathway to Leadership Fellow and through a Dale F. Frey Breakthrough
   award from the Damon Runyon Cancer Research Foundation; Karen L.
   MacKenzie wishes to acknowledge the support from the Children's Cancer
   Institute Australia (affiliated with the University of New South Wales,
   Australia and the Sydney Children's Hospital Network); Maria Marino was
   supported by grant from University Roma Tre to M.M. (CLA 2013) and by
   the Italian Association for Cancer Research (AIRC-Grant #IG15221); Ander
   Matheu is funded by Carlos III Health Institute and Feder funds (AM:
   CP10/00539, PI13/02277), Basque Foundation for Science (IKERBASQUE) and
   Marie Curie CIG Grant (AM: 2012/712404); Christopher Maxwell was
   supported by funding from the Canadian Institutes of Health Research, in
   partnership with the Avon Foundation for Women (OBC-134038) and the
   Canadian Institutes of Health Research New Investigator Salary Award
   (MSH-136647); Eoin McDonnell received Duke University Institutional
   Support; Kapil Mehta was supported by Bayer Healthcare System G4T
   (Grants4Targets); Gregory A. Michelotti received support from NIH NIDDK,
   NIH NIAAA, and Shire Pharmaceuticals; Vinayak Muralidhar was supported
   by the Harvard-MIT Health Sciences and Technology Research Assistantship
   Award; Elena Niccolai was supported by the Italian Ministry of
   University and the University of Italy; Virginia R. Parslow gratefully
   acknowledges the financial support of the Auckland Cancer Society
   Research Centre (ACSRC); Graham Pawelec was supported by the German
   Federal Ministry of Education and Research (Bundesministerium fur
   Bildung und Forschung, BMBF) Grant number 16SV5536K, and by the European
   Commission (FP7 259679 "IDEAL"); Peter L. Pedersen was supported by NIH
   Grant CA-10951; Brad Poore was supported by Sol Goldman Pancreatic
   Cancer Research Fund Grant 80028595, the Lustgarten Fund Grant 90049125,
   and Grant NIHR21CA169757 (to Anne Le); Satya Prakash was supported by a
   Canadian Institutes of Health Research Grant (MOP 64308); Lizzia
   Raffaghello was supported by an NIH Grant (P01AG034906-01A1) and Cinque
   per Mille dell'IRPEF-Finanziamento della Ricerca Sanitaria; Jeffrey C.
   Rathmell was supported by an NIH Grant (R01HL108006); Swapan K.; Ray was
   supported by the United Soybean Board; Domenico Ribatti received funding
   from the European Union Seventh Framework Programme (FP7/2007-2013)
   under Grant agreement no 278570; Luigi Ricciardiello was supported by
   the AIRC Investigator Grants 10216 and 13837, and the European
   Community's Seventh Framework Program FP7/2007-2013 under Grant
   agreement 311876; Francis Rodier acknowledges the support of the
   Canadian Institute for Health Research (FR: MOP114962, MOP125857), Fonds
   de Recherche Quebec Sante (FR: 22624), and the Terry Fox Research
   Institute (FR: 1030); Gian Luigi Russo contributed to this effort while
   participating in the Fulbright Research Scholar Program 2013-14; Isidro
   Sanchez-Garcia is partially supported by FEDER and by MICINN
   (SAF2012-32810), by NIH Grant (R01 CA109335-04A1), by Junta de Castilla
   y Leon (BIO/SA06/13) and by the ARIMMORA project (FP7-ENV-2011, European
   Union Seventh Framework Program). Isidro SanchezGarcia's lab is also a
   member of the EuroSyStem and the DECIDE Network funded by the European
   Union under the FP7 program; Andrew J. Sanders wishes to acknowledge the
   support by Cancer Research Wales, the Albert Hung Foundation, the Fong
   Family Foundation, and Welsh Government A4B scheme; Neeraj K. Saxena was
   supported by grant funding from NIH NIDDK (K01DK077137, R03DK089130);
   Dipali Sharma was partially funded by NIH NCI grants (R01CA131294, R21
   CA155686), the Avon Foundation and a Breast Cancer Research Foundation
   Grant (90047965); Markus David Siegelin received funding from National
   Institute of Health, NINDS Grant K08NS083732, and the 2013 AACR-National
   Brain Tumor Society Career Development Award for Translational Brain
   Tumor Research, Grant Number 13-20-23-SIEG; Neetu Singh was supported by
   funds from the Department of Science and Technology (SR/FT/LS-063/2008),
   New Delhi, India; Carl Smythe was supported by Yorkshire Cancer Research
   and The Wellcome Trust, UK; Carmela Spagnuolo was supported by funding
   from Project C.I.S.I.A., act n. 191/2009 from the Italian Ministry of
   Economy and Finance Project CAMPUS-QUARC, within program FESR Campania
   Region 2007/2013, objectives 2.1, 2.2; Diana M. Stafforini was supported
   by grants from the National Cancer Institute (5P01CA073992), IDEA Award
   W81XWH-12-1-0515 from the Department of Defense, and by the Huntsman
   Cancer Foundation; John Stagg was supported by the Canadian Institutes
   of Health Research; Pochi R. Subbarayan was supported by the University
   of Miami Clinical and Translational Science Institute (CTSI) Pilot
   Research Grant (CTSI-2013-P03) and SEEDS You Choose Awards; Phuoc T.
   Tran was funded by the DoD (W81XVVH-11-1-0272 and W81XWH-13-1-0182), a
   Kimmel Translational Science Award (SKF-13-021), an ACS Scholar award
   (122688-RSG-12-196-01-TBG) and the NIH (R01CA166348); Kathryn E. Wellen
   receives funding from the National Cancer Institute, Pancreatic Cancer
   Action Network, Pew Charitable Trusts, American Diabetes Association,
   and Elsa U.; Pardee Foundation; Huanjie Yang was partially supported by
   the Scientific Research Foundation for the Returned Oversea Scholars,
   State Education Ministry and Scientific and Technological Innovation
   Project, Harbin (2012RFLX5011); Paul Yaswen was supported by funding
   from the United States National Institutes of Health (ES019458) and the
   California Breast Cancer Research Program (17UB-8708); Clement Yedjou
   was supported by a grant from the National Institutes of Health (Grant #
   G1200MD007581), through the RCMI-Center for Environmental Health; Xin
   Yin was supported by NIH/National Heart, Lung, and Blood Institute
   Training Grant T32HL098062.; Jiyue Zhu was supported by NIH Grant
   R01GM071725; Massimo Zollo was supported by the European FP7-TuMIC
   HEALTH-F2-2008-201662, the Italian Association for Cancer research
   (AIRC) Grant IG # 11963 and the Regione Campania L.R:N.5, the European
   National Funds PON01-02388/1 2007-2013.
NR 261
TC 31
Z9 31
U1 9
U2 33
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1044-579X
J9 SEMIN CANCER BIOL
JI Semin. Cancer Biol.
PD DEC
PY 2015
VL 35
SU S
BP S276
EP S304
DI 10.1016/j.semcancer.2015.09.007
PG 29
WC Oncology
SC Oncology
GA CY7WG
UT WOS:000366619400013
PM 26590477
ER

PT J
AU Casey, SC
   Amedei, A
   Aquilano, K
   Azmi, AS
   Benencia, F
   Bhakta, D
   Bilsland, AE
   Boosani, CS
   Chen, S
   Ciriolo, MR
   Crawford, S
   Fujii, H
   Georgakilas, AG
   Guha, G
   Halicka, D
   Helferich, WG
   Heneberg, P
   Honoki, K
   Keith, WN
   Kerkar, SP
   Mohammed, SI
   Niccolai, E
   Nowsheen, S
   Rupasinghe, HPV
   Samadi, A
   Singh, N
   Talib, WH
   Venkateswaran, V
   Whelan, RL
   Yang, XJ
   Felsher, DW
AF Casey, Stephanie C.
   Amedei, Amedeo
   Aquilano, Katia
   Azmi, Asfar S.
   Benencia, Fabian
   Bhakta, Dipita
   Bilsland, Alan E.
   Boosani, Chandra S.
   Chen, Sophie
   Ciriolo, Maria Rosa
   Crawford, Sarah
   Fujii, Hiromasa
   Georgakilas, Alexandros G.
   Guha, Gunjan
   Halicka, Dorota
   Helferich, William G.
   Heneberg, Petr
   Honoki, Kanya
   Keith, W. Nicol
   Kerkar, Sid P.
   Mohammed, Sulma I.
   Niccolai, Elena
   Nowsheen, Somaira
   Rupasinghe, H. P. Vasantha
   Samadi, Abbas
   Singh, Neetu
   Talib, Wamidh H.
   Venkateswaran, Vasundara
   Whelan, Richard L.
   Yang, Xujuan
   Felsher, Dean W.
TI Cancer prevention and therapy through the modulation of the tumor
   microenvironment
SO SEMINARS IN CANCER BIOLOGY
LA English
DT Review
DE Tumor microenvironment; Cancer biology; Cancer therapy; Cancer
   prevention
ID ENDOTHELIAL GROWTH-FACTOR; CELL-CYCLE ARREST; NF-KAPPA-B; REGULATORY
   T-CELLS; HUMAN PROSTATE-CANCER; HUMAN COLON-CANCER; INDOLEAMINE
   2,3-DIOXYGENASE EXPRESSION; EPITHELIAL-MESENCHYMAL TRANSITION;
   CARCINOMA-ASSOCIATED FIBROBLASTS; BERBERINE INDUCES APOPTOSIS
AB Cancer arises in the context of an in vivo tumor microenvironment This microenvironment is both a cause and consequence of tumorigenesis. Tumor and host cells co-evolve dynamically through indirect and direct cellular interactions, eliciting multiscale effects on many biological programs, including cellular proliferation, growth, and metabolism, as well as angiogenesis and hypoxia and innate and adaptive immunity. Here we highlight specific biological processes that could be exploited as targets for the prevention and therapy of cancer. Specifically, we describe how inhibition of targets such as cholesterol synthesis and metabolites, reactive oxygen species and hypoxia, macrophage activation and conversion, indoleamine 2,3-dioxygenase regulation of dendritic cells, vascular endothelial growth factor regulation of angiogenesis, fibrosis inhibition, endoglin, and Janus kinase signaling emerge as examples of important potential nexuses in the regulation of tumorigenesis and the tumor microenvironment that can be targeted. We have also identified therapeutic agents as approaches, in particular natural products such as berberine, resveratrol, onionin A, epigallocatechin gallate, genistein, curcumin, naringenin, desoxyrhapontigenin, piperine, and zerumbone, that may warrant further investigation to target the tumor microenvironment for the treatment and/or prevention of cancer. (C) 2015 Elsevier Ltd.
C1 [Casey, Stephanie C.; Felsher, Dean W.] Stanford Univ, Div Oncol, Dept Med, Sch Med, Stanford, CA 94305 USA.
   [Casey, Stephanie C.; Felsher, Dean W.] Stanford Univ, Div Oncol, Sch Med, Dept Pathol, Stanford, CA 94305 USA.
   [Amedei, Amedeo] Univ Florence, Dept Expt & Clin Med, Florence, Italy.
   [Aquilano, Katia; Ciriolo, Maria Rosa] Univ Roma Tor Vergata, Dept Biol, I-00173 Rome, Italy.
   [Azmi, Asfar S.] Wayne State Univ, Sch Med, Dept Oncol, Detroit, MI USA.
   [Benencia, Fabian] Ohio Univ, Dept Biomed Sci, Athens, OH 45701 USA.
   [Bhakta, Dipita] SASTRA Univ, Sch Chem & Biotechnol, Thanjavur 613401, Tamil Nadu, India.
   [Bilsland, Alan E.] Univ Glasgow, Inst Canc Sci, Glasgow, Lanark, Scotland.
   [Boosani, Chandra S.] Creighton Univ, Sch Med, Dept Biomed Sci, Omaha, NE 68178 USA.
   [Chen, Sophie] Ovarian & Prostate Canc Res Lab, Guildford, Surrey, England.
   [Crawford, Sarah] So Connecticut State Univ, Dept Biol, New Haven, CT 06515 USA.
   [Fujii, Hiromasa] Nara Med Univ, Dept Orthoped Surg, Kashihara, Nara 634, Japan.
   [Georgakilas, Alexandros G.] Natl Tech Univ Athens, Dept Phys, Sch Appl Math & Phys Sci, GR-15773 Athens, Greece.
   [Halicka, Dorota] New York Med Coll, Valhalla, NY 10595 USA.
   [Helferich, William G.] Univ Illinois, Champaign, IL USA.
   [Helferich, William G.] Univ Illinois, Urbana, IL USA.
   [Heneberg, Petr] Charles Univ Prague, Fac Med 3, Prague, Czech Republic.
   [Kerkar, Sid P.] NCI, NIH, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Mohammed, Sulma I.] Purdue Univ, Ctr Canc Res, Dept Comparat Pathobiol, W Lafayette, IN 47907 USA.
   [Niccolai, Elena] Univ Florence, Florence, Italy.
   [Nowsheen, Somaira] Mayo Clin, Mayo Med Sch, Mayo Grad Sch, Med Sci Training Program, Rochester, MN USA.
   [Rupasinghe, H. P. Vasantha] Dalhousie Univ, Fac Agr, Dept Environm Sci, Halifax, NS B3H 3J5, Canada.
   [Samadi, Abbas] Sanus Biosci, San Diego, CA USA.
   [Singh, Neetu] King Georges Med Univ, Adv Mol Sci Res Ctr, Ctr Adv Res, Lucknow, Uttar Pradesh, India.
   [Talib, Wamidh H.] Appl Sci Univ, Dept Clin Pharm & Therapeut, Amman, Jordan.
   [Venkateswaran, Vasundara] Sunnybrook Hlth Sci Ctr, Div Urol, Toronto, ON M4N 3M5, Canada.
   [Whelan, Richard L.] Icahn Sch Med Mt Sinai, Mt Sinai Roosevelt Hosp, New York, NY 10029 USA.
RP Felsher, DW (reprint author), Stanford Univ, Div Oncol, Dept Med, Stanford, CA 94305 USA.
EM dfelsher@stanford.edu
RI Heneberg, Petr/C-1881-2012; Keith, Nicol/D-3325-2009; niccolai,
   elena/K-6091-2016; Ciriolo, Maria /K-6572-2016; AQUILANO,
   KATIA/K-8888-2016; Bhakta-Guha, Dipita/E-8076-2012; 
OI Heneberg, Petr/0000-0002-0703-951X; Keith, Nicol/0000-0001-7862-3580;
   niccolai, elena/0000-0002-9205-8079; AQUILANO,
   KATIA/0000-0002-5905-9870; Bhakta-Guha, Dipita/0000-0002-7144-3947;
   Benencia, Fabian/0000-0003-3049-6150
FU Ohio University; EU [MC-CIG-303514]; Greek National funds through the
   Operational Program 'Educational and Lifelong Learning of the National
   Strategic Reference Framework (NSRF)-Research Funding Program: THALES
   [MIS 379346]; Charles University in Prague [UNCE 204015, PRVOUK
   P31/2012]; Czech Science Foundation [P301/12/1686]; Internal Grant
   Agency of the Ministry of Health of the Czech Republic [NT13663-3/2012];
   CRU [C301/A14762]; Heritage College of Osteopathic Medicine at OU
   [RP1206]; Ministry of Education, Culture, Sports, Science and
   Technology, Japan [24590493]
FX R.L.W. is conducting a Phase I trial for EGCG. The authors thank the
   Italian Ministry of University and Research (2009FZZ4XM_002 to E.N.,
   A.A.), the Intramural Research Program of the NIH, National Cancer
   Institute, Center for Cancer Research (S.P.K.), the National Institutes
   of Health (R01CA128704 to D.H.), National Institutes of Health
   F32CA177139, R01CA170378, U54CA149145, P50CA114747, R01CA184384, and
   R21CA169964 (to S.C.C., D.W.F.), an NIH R15 CA137499-01 (F.B.), a
   startup fund from Ohio University, an RSAC grant (RP1206) from the
   Heritage College of Osteopathic Medicine at OU (to F.B.), Prostate and
   Ovarian Cancer Research Trust in Surrey, UK (S. Chen), a Connecticut
   State University Research grant (S. Crawford), an EU Marie Curie
   Reintegration Grant MC-CIG-303514, Greek National funds through the
   Operational Program 'Educational and Lifelong Learning of the National
   Strategic Reference Framework (NSRF)-Research Funding Program: THALES
   (Grant number MIS 379346) and COST Action CM1201 'Biomimetic Radical
   Chemistry' (to A.G.G.), the Charles University in Prague projects UNCE
   204015 and PRVOUK P31/2012, by the Czech Science Foundation project
   P301/12/1686, and by the Internal Grant Agency of the Ministry of Health
   of the Czech Republic project NT13663-3/2012 (to P.H.), the Ministry of
   Education, Culture, Sports, Science and Technology, Japan (No. 24590493)
   (to K.H.), and private donations (R.L.W.). W.N.K. and A.E.B. acknowledge
   the University of Glasgow, Beatson Oncology Centre Fund, CRU
   (www.cancerresearchuk.org/) grant C301/A14762. Study sponsors had no
   involvement in the study. The authors also acknowledge the efforts of
   Leroy Lowe and the Getting to Know Cancer team.
NR 664
TC 20
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U1 7
U2 72
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1044-579X
J9 SEMIN CANCER BIOL
JI Semin. Cancer Biol.
PD DEC
PY 2015
VL 35
SU S
BP S199
EP S223
DI 10.1016/j.semcancer.2015.02.007
PG 25
WC Oncology
SC Oncology
GA CY7WG
UT WOS:000366619400010
PM 25865775
ER

PT J
AU Hallett, M
AF Hallett, Mark
TI Explanation of timing of botulinum neurotoxin effects, onset and
   duration, and clinical ways of influencing them
SO TOXICON
LA English
DT Article; Proceedings Paper
CT TOXINS 2015 Basic Science and Clinical Aspects of Botulinum and Other
   Neurotoxins
CY JAN 14-17, 2015
CL Lisbon, PORTUGAL
SP Intl Neurotoxin Assoc (INA)
DE Endplate; Uptake; Duration of action; Cooling; Muscle activity; Zinc
ID TOXIN TYPE-A; MUSCLE-ACTIVITY; ZINC; SUPPLEMENTATION; SPASTICITY;
   INJECTION; PHYTASE; ZONE
AB While the steps in the action of botulinum neurotoxin (BoNT) are well known, the factors underlying the timing of these steps are not fully understood. After toxin is injected into a muscle, it resides in the extracellular space and must be taken up into the nerve terminals. More toxin will be taken up if near the endplate. Toxin is distributed mainly by convection and there is likely little diffusion. Toxin that is not taken up will go into the general circulation where it may have a slight systemic effect. The uptake is activity and temperature dependent. Encouraging the unwanted muscle contractions after injection should be helpful. Cooling will decrease the uptake. The times for washout from the extracellular space and uptake of the toxin are not well established, but are likely measured in minutes. Toxin in the general circulation has a long halftime. The time from injection to weakness is determined by how long it takes to get sufficient damage of the SNARE proteins to interfere with synaptic release. Toxins are zinc dependent proteases, and supplemental zinc may produce a greater effect. There will be weakness as long as there is residual toxin in the nerve ending. Published by Elsevier Ltd.
C1 [Hallett, Mark] NINDS, Human Motor Control Sect, NIH, Bethesda, MD 20892 USA.
RP Hallett, M (reprint author), NINDS, Human Motor Control Sect, NIH, Bldg 10,Room 7D37,10 Ctr Dr, Bethesda, MD 20892 USA.
EM hallettm@ninds.nih.gov
OI Hallett, Mark/0000-0002-3180-6811
FU NINDS Intramural Program
FX Dr. Hallett's work is supported by the NINDS Intramural Program.
NR 22
TC 0
Z9 0
U1 1
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0041-0101
J9 TOXICON
JI Toxicon
PD DEC 1
PY 2015
VL 107
SI SI
BP 64
EP 67
DI 10.1016/j.toxicon.2015.07.013
PN A
PG 4
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA CY6SP
UT WOS:000366539400010
PM 26220801
ER

PT J
AU Radin, RG
   Sallmen, M
   Kristensen, P
AF Radin, Rose G.
   Sallmen, Markku
   Kristensen, Petter
TI RE: PARENTAL AGE AT BIRTH AND RISK OF HEMATOLOGICAL MALIGNANCIES IN
   OLDER ADULTS
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Letter
ID SELECTION BIAS
C1 [Radin, Rose G.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Intramural Populat Hlth Res, Bethesda, MD 20892 USA.
   [Sallmen, Markku] Finnish Inst Occupat Hlth, Work Related Dis, Helsinki, Finland.
   [Kristensen, Petter] Natl Inst Occupat Hlth, Oslo, Norway.
RP Radin, RG (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Intramural Populat Hlth Res, Bethesda, MD 20892 USA.
EM rose.radin@nih.gov
NR 8
TC 1
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U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
EI 1476-6256
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD DEC 1
PY 2015
VL 182
IS 11
BP 973
EP 974
DI 10.1093/aje/kwv288
PG 2
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA CY4IL
UT WOS:000366371700013
PM 26582779
ER

PT J
AU Grantz, KL
   Hinkle, SN
   Mendola, P
   Sjaarda, LA
   Albert, PS
AF Grantz, Katherine L.
   Hinkle, Stefanie N.
   Mendola, Pauline
   Sjaarda, Lindsey A.
   Albert, Paul S.
TI RE: "DIFFERENCES IN RISK FACTORS FOR RECURRENT VERSUS INCIDENT PRETERM
   DELIVERY" REPLY
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Letter
C1 [Grantz, Katherine L.; Hinkle, Stefanie N.; Mendola, Pauline; Sjaarda, Lindsey A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Intramural Populat Hlth Res, NIH, Rockville, MD 20852 USA.
   [Albert, Paul S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Biostat & Bioinformat Branch, Div Intramural Populat Hlth Res, NIH, Rockville, MD USA.
RP Grantz, KL (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Intramural Populat Hlth Res, NIH, Rockville, MD 20852 USA.
EM katherine.grantz@nih.gov
OI Grantz, Katherine/0000-0003-0276-8534
FU NICHD NIH HHS [HHSN275200800002C, HHSN275200800002I]
NR 3
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U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
EI 1476-6256
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD DEC 1
PY 2015
VL 182
IS 11
BP 976
EP 976
DI 10.1093/aje/kwv277
PG 1
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA CY4IL
UT WOS:000366371700016
PM 26568570
ER

PT J
AU Thorne, PS
   Mendy, A
   Metwali, N
   Salo, P
   Co, C
   Jaramillo, R
   Rose, KM
   Zeldin, DC
AF Thorne, Peter S.
   Mendy, Angelico
   Metwali, Nervana
   Salo, Paeivi
   Co, Caroll
   Jaramillo, Renee
   Rose, Kathryn M.
   Zeldin, Darryl C.
TI Endotoxin Exposure: Predictors and Prevalence of Associated Asthma
   Outcomes in the United States
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Article
DE allergy; asthma; house dust; indoor air; wheeze
ID SCHOOL-AGE-CHILDREN; INNER-CITY HOMES; AIRBORNE ENDOTOXIN;
   NATIONAL-SURVEY; MATTRESS DUST; GERMAN HOMES; SENSITIZATION; ALLERGENS;
   DETERMINANTS; ENVIRONMENTS
AB Rationale: Inhaled endotoxin induces airway inflammation and is an established risk factor for asthma. The 2005-2006 National Health and Nutrition Examination Survey included measures of endotoxin and allergens in homes as well as specific IgE to inhalant allergens.
   Objectives: To understand the relationships between endotoxin exposure, asthma outcomes, and sensitization status for 15 aeroallergens in a nationally representative sample.
   Methods: Participants were administered questionnaires in their homes. Reservoir dust was vacuum sampled to generate composite bedding and bedroom floor samples. We analyzed 7,450 National Health and Nutrition Examination Survey dust and quality assurance samples for their endotoxin content using extreme quality assurance measures. Data for 6,963 subjects were available, making this the largest study of endotoxin exposure to date. Log-transformed endotoxin concentrations were analyzed using logistic models and forward stepwise linear regression. Analyses were weighted to provide national prevalence estimates and unbiased variances.
   Measurements and Main Results: Endotoxin exposure was significantly associated with wheeze in the past 12 months, wheeze during exercise, doctor and/or emergency room visits for wheeze, and use of prescription medications for wheeze. Models adjusted for age, sex, race and/or ethnicity, and poverty-to-income ratio and stratified by allergy status showed that these relationships were not dependent upon sensitization status but were worsened among those living in poverty. Significant predictors of higher endotoxin exposures were lower family income; Hispanic ethnicity; participant age; dog(s), cat(s), cockroaches, and/or smoker(s) in the home; and carpeted floors.
   Conclusions: In this U.S. nationwide representative sample, higher endotoxin exposure was significantly associated with measures of wheeze, with no observed protective effect regardless of sensitization status.
C1 [Thorne, Peter S.; Mendy, Angelico; Metwali, Nervana] Univ Iowa, Coll Publ Hlth, Dept Occupat & Environm Hlth, Iowa City, IA 52242 USA.
   [Salo, Paeivi; Zeldin, Darryl C.] NIEHS, Div Intramural Res, NIH, Res Triangle Pk, NC 27709 USA.
   [Co, Caroll; Jaramillo, Renee; Rose, Kathryn M.] Social & Sci Syst Inc, Durham, NC USA.
RP Thorne, PS (reprint author), Univ Iowa, Coll Publ Hlth, Dept Occupat & Environm Hlth, 145 North Riverside Dr,S341A CPHB, Iowa City, IA 52242 USA.
EM peter-thorne@uiowa.edu
OI Thorne, Peter/0000-0002-5045-0929
FU National Center for Health Statistics, Centers for Disease Control and
   Prevention [200-2010-34238 NCE1]; (National Institutes of Health [NIH])
   [P30 ES005605]; Intramural Research Program of the NIH (National
   Institute of Environmental Health Sciences) [Z01 ES025041]
FX Sample extraction and endotoxin analysis done at the University of Iowa
   were funded by the National Center for Health Statistics, Centers for
   Disease Control and Prevention (grant 200-2010-34238 NCE1). Data
   analysis was funded through a grant to the University of Iowa
   Environmental Health Sciences Research Center (National Institutes of
   Health [NIH] grant P30 ES005605 [P.S.T.]) and through a contract to
   Social and Scientific Systems, Inc. (HMSN291200555553). This work was
   also funded in part by the Intramural Research Program of the NIH
   (National Institute of Environmental Health Sciences grant Z01 ES025041
   [D.C.Z.]).
NR 43
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U1 5
U2 15
PU AMER THORACIC SOC
PI NEW YORK
PA 25 BROADWAY, 18 FL, NEW YORK, NY 10004 USA
SN 1073-449X
EI 1535-4970
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD DEC 1
PY 2015
VL 192
IS 11
BP 1287
EP 1297
DI 10.1164/rccm.201502-0251OC
PG 11
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA CX6RU
UT WOS:000365829900009
PM 26258643
ER

PT J
AU Levy, BD
   Noel, PJ
   Freemer, MM
   Cloutier, MM
   Georas, SN
   Jarjour, NN
   Ober, C
   Woodruff, P
   Barnes, KC
   Bender, BG
   Camargo, CA
   Chupp, GL
   Denlinger, LC
   Fahy, JV
   Fitzpatrick, AM
   Fuhlbrigge, A
   Gaston, BM
   Hartert, TV
   Kolls, JK
   Lynch, SV
   Moore, WC
   Morgan, WJ
   Nadeau, KC
   Ownby, DR
   Solway, J
   Szefler, SJ
   Wenzel, SE
   Wright, RJ
   Smith, RA
   Erzurum, SC
AF Levy, Bruce D.
   Noel, Patricia J.
   Freemer, Michelle M.
   Cloutier, Michelle M.
   Georas, Steve N.
   Jarjour, Nizar N.
   Ober, Carole
   Woodruff, PrescottG.
   Barnes, Kathleen C.
   Bender, Bruce G.
   Camargo, Carlos A., Jr.
   Chupp, Geoff L.
   Denlinger, Loren C.
   Fahy, John V.
   Fitzpatrick, Anne M.
   Fuhlbrigge, Anne
   Gaston, Ben M.
   Hartert, Tina V.
   Kolls, Jay K.
   Lynch, Susan V.
   Moore, Wendy C.
   Morgan, Wayne J.
   Nadeau, Kari C.
   Ownby, Dennis R.
   Solway, Julian
   Szefler, Stanley J.
   Wenzel, Sally E.
   Wright, Rosalind J.
   Smith, Robert A.
   Erzurum, Serpil C.
TI Future Research Directions in Asthma An NHLBI Working Group Report
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Article
DE asthma; prevention; phenotype; disease modification; implementation
ID INNATE LYMPHOID-CELLS; CLUSTER-ANALYSIS; RESEARCH-PROGRAM; SYSTEMS
   BIOLOGY; PHENOTYPES; LUNG; INFLAMMATION; DISEASES; ADHERENCE; WORKSHOP
AB Asthma is a common chronic disease without cure. Our understanding of asthma onset, pathobiology, classification, and management has evolved substantially over the past decade; however, significant asthma-related morbidity and excess healthcare use and costs persist. To address this important clinical condition, the NHLBI convened a group of extramural investigators for an Asthma Research Strategic Planning workshop on September 18-19, 2014, to accelerate discoveries and their translation to patients. The workshop focused on (1) in utero and early-life origins of asthma, (2) the use of phenotypes and endotypes to classify disease, (3) defining disease modification, (4) disease management, and (5) implementation research. This report summarizes the workshop and produces recommendations to guide future research in asthma.
C1 [Levy, Bruce D.; Fuhlbrigge, Anne] Brigham & Womens Hosp, Boston, MA 02115 USA.
   [Noel, Patricia J.; Freemer, Michelle M.; Smith, Robert A.] NHLBI, Bethesda, MD 20892 USA.
   [Cloutier, Michelle M.] Univ Connecticut, Ctr Hlth, Hartford, CT 06112 USA.
   [Georas, Steve N.] Univ Rochester, Rochester, NY USA.
   [Jarjour, Nizar N.; Denlinger, Loren C.] Univ Wisconsin Hosp & Clin, Madison, WI 53792 USA.
   [Ober, Carole; Solway, Julian] Univ Chicago, Chicago, IL 60637 USA.
   [Woodruff, PrescottG.; Lynch, Susan V.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
   [Barnes, Kathleen C.] Johns Hopkins Univ, Baltimore, MD USA.
   [Bender, Bruce G.] Natl Jewish Hlth, Denver, CO USA.
   [Camargo, Carlos A., Jr.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
   [Chupp, Geoff L.] Yale Univ, Sch Med, New Haven, CT USA.
   [Fitzpatrick, Anne M.] Emory Univ, Sch Med, Atlanta, GA USA.
   [Gaston, Ben M.] Case Western Reserve Univ, Cleveland, OH 44106 USA.
   [Hartert, Tina V.] Vanderbilt Univ, Sch Med, Nashville, TN 37212 USA.
   [Kolls, Jay K.] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
   [Moore, Wendy C.] Wake Forest Sch Med, Winston Salem, NC USA.
   [Morgan, Wayne J.] Univ Arizona, Tucson, AZ USA.
   [Nadeau, Kari C.] Stanford Sch Med, Stanford, CA USA.
   [Ownby, Dennis R.] Georgia Regents Univ, Augusta, GA USA.
   [Szefler, Stanley J.] Childrens Hosp Colorado, Denver, CO USA.
   [Szefler, Stanley J.] Univ Colorado, Sch Med, Denver, CO USA.
   [Wright, Rosalind J.] Icahn Sch Med Mt Sinai, New York, NY 10029 USA.
   [Erzurum, Serpil C.] Cleveland Clin, Lerner Coll Med, Cleveland, OH 44106 USA.
RP Noel, PJ (reprint author), NHLBI, Div Lung Dis, Bldg 10, Bethesda, MD 20892 USA.
EM noelp@nih.gov
RI Morgan, Grace/C-8098-2013
OI Morgan, Grace/0000-0002-5467-0507
FU NHLBI, National Institutes of Health
FX Supported by the NHLBI, National Institutes of Health.
NR 40
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U2 7
PU AMER THORACIC SOC
PI NEW YORK
PA 25 BROADWAY, 18 FL, NEW YORK, NY 10004 USA
SN 1073-449X
EI 1535-4970
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD DEC 1
PY 2015
VL 192
IS 11
BP 1366
EP 1372
DI 10.1164/rccm.201505-0963WS
PG 7
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA CX6RU
UT WOS:000365829900017
PM 26305520
ER

PT J
AU Sapra, KJ
   McLain, AC
   Maisog, JM
   Sundaram, R
   Louis, GMB
AF Sapra, Katherine J.
   McLain, Alexander C.
   Maisog, Jose M.
   Sundaram, Rajeshwari
   Louis, Germaine M. Buck
TI Clustering of retrospectively reported and prospectively observed
   time-to-pregnancy
SO ANNALS OF EPIDEMIOLOGY
LA English
DT Article
DE Time-to-pregnancy; Fecundity; Conception; Conception delay
ID SEMEN QUALITY; LIFE-STYLE; COHORT; WOMEN; VALIDITY; RISK; QUESTIONNAIRE;
   FECUNDABILITY; RECURRENCE
AB Purpose: Given reportedly high clustering but limited validity of retrospectively reported time-to-pregnancy (TTP), we assessed within-woman clustering for retrospectively reported TTPs alone and including gold-standard prospectively observed TTPs among women with 2 or more retrospectively reported and 1 or more prospectively observed TTPs. We further investigated whether past trying times inform future trying time among women with 1 or more retrospectively reported and I or more prospectively observed TTPs.
   Methods: Five hundred one couples attempting pregnancy were prospectively observed until human chorionic gonadotropin pregnancy or 12 months of trying. Women reported TIT, for past planned pregnancies. Clustering as measured by the frailty variance was estimated using discrete Cox frailty models, adjusted for age, body mass index, smoking at each attempt. Utility of past attempts to inform future attempts was assessed with discrete Cox models and relative risk regression, adjusted for enrollment age, body mass index, smoking.
   Results: Seventy-five women with 2 or more prior pregnancies contributed 180 retrospective and 91 prospective TTPs for frailty modeling. Retrospectively reported TIT clustering was high (frailty variance = 0.89) but substantially lower when including prospectively observed TTPs (frailty variance = 0.42). Among 202 women with 1 or more prior pregnancies, past trying times did not inform future trying time.
   Conclusions: TIP recall rather than UP may account for clustering. Past trying times may not inform future trying times. Published by Elsevier Inc.
C1 [Sapra, Katherine J.; Sundaram, Rajeshwari; Louis, Germaine M. Buck] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, Rockville, MD 20852 USA.
   [McLain, Alexander C.] Univ S Carolina, Arnold Sch Publ Hlth, Dept Epidemiol & Biostat, Columbia, SC 29208 USA.
   [Maisog, Jose M.] Glotech Inc, Rockville, MD USA.
RP Sapra, KJ (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, 6100 Execut Blvd,Room 7805, Rockville, MD 20852 USA.
EM katherine.sapra@nih.gov
OI Sapra, Katherine/0000-0001-5659-6489; Sundaram,
   Rajeshwari/0000-0002-6918-5002; Buck Louis, Germaine/0000-0002-1774-4490
FU Intramural Research Program of the Eunice Kennedy Shriver National
   Institute of Child Health and Human Development [N01-HD-3-3355,
   N01-HD-3-3356, NOH-HD-3-3358]
FX This research was supported by the Intramural Research Program of the
   Eunice Kennedy Shriver National Institute of Child Health and Human
   Development (contracts N01-HD-3-3355, N01-HD-3-3356, and NOH-HD-3-3358).
   The study funders had no role in the study design; collection, analysis,
   or interpretation of data; writing of the report; or the decision to
   submit the article for publication.
NR 25
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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 DEC
PY 2015
VL 25
IS 12
BP 959
EP 963
DI 10.1016/j.annepidem.2015.04.005
PG 5
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA CY5IK
UT WOS:000366441100014
PM 26033375
ER

PT J
AU Knight, JS
   Subramanian, V
   O'Dell, AA
   Yalavarthi, S
   Zhao, WP
   Smith, CK
   Hodgin, JB
   Thompson, PR
   Kaplan, MJ
AF Knight, Jason S.
   Subramanian, Venkataraman
   O'Dell, Alexander A.
   Yalavarthi, Srilakshmi
   Zhao, Wenpu
   Smith, Carolyne K.
   Hodgin, Jeffrey B.
   Thompson, Paul R.
   Kaplan, Mariana J.
TI Peptidylarginine deiminase inhibition disrupts NET formation and
   protects against kidney, skin and vascular disease in lupus-prone
   MRL/lpr mice
SO ANNALS OF THE RHEUMATIC DISEASES
LA English
DT Article
ID CHRONIC GRANULOMATOUS-DISEASE; NEUTROPHIL EXTRACELLULAR TRAPS; NADPH
   OXIDASE; MURINE LUPUS; ERYTHEMATOSUS; GENE; ACTIVATION; PAD4;
   MANIFESTATIONS; INFLAMMASOME
AB Objectives An imbalance between neutrophil extracellular trap (NET) formation and degradation has been described in systemic lupus erythematosus (SLE), potentially contributing to autoantigen externalisation, type I interferon synthesis and endothelial damage. We have demonstrated that peptidylarginine deiminase (PAD) inhibition reduces NET formation and protects against lupus-related vascular damage in the New Zealand Mixed model of lupus. However, another strategy for inhibiting NETs-knockout of NOX2-accelerates lupus in a different murine model, MRL/lpr. Here, we test the effects of PAD inhibition on MRL/lpr mice in order to clarify whether some NET inhibitory pathways may be consistently therapeutic across models of SLE.
   Methods NET formation and autoantibodies to NETs were characterised in lupus-prone MRL/lpr mice. MRL/lpr mice were also treated with two different PAD inhibitors, Cl-amidine and the newly described BB-Cl-amidine. NET formation, endothelial function, interferon signature, nephritis and skin disease were examined in treated mice.
   Results Neutrophils from MRL/lpr mice demonstrate accelerated NET formation compared with controls. MRL/lpr mice also form autoantibodies to NETs and have evidence of endothelial dysfunction. PAD inhibition markedly improves endothelial function, while downregulating the expression of type I interferon-regulated genes. PAD inhibition also reduces proteinuria and immune complex deposition in the kidneys, while protecting against skin disease.
   Conclusions PAD inhibition reduces NET formation, while protecting against lupus-related damage to the vasculature, kidneys and skin in various lupus models. The strategy by which NETs are inhibited will have to be carefully considered if human studies are to be undertaken.
C1 [Knight, Jason S.; O'Dell, Alexander A.; Yalavarthi, Srilakshmi] Univ Michigan, Dept Internal Med, Div Rheumatol, Ann Arbor, MI 48109 USA.
   [Subramanian, Venkataraman; Thompson, Paul R.] Scripps Res Inst, Dept Chem, Jupiter, FL USA.
   [Zhao, Wenpu; Smith, Carolyne K.; Kaplan, Mariana J.] NIAMSD, System Autoimmun Branch, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
   [Hodgin, Jeffrey B.] Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA.
RP Kaplan, MJ (reprint author), NIAMSD, System Autoimmun Branch, Intramural Res Program, NIH, 10 Ctr Dr,10-6D47C, Bethesda, MD 20892 USA.
EM mariana.kaplan@nih.gov
FU Rheumatology Research Foundation Rheumatology Scientist Development
   Award; National Institutes of Health (NIH) through PHS [HL088419];
   Intramural Research Program at NIAMS; NIH [GM079357, CA151304]
FX Microscopy was performed in the Center for Live Cell Imaging (CLCI) at
   the University of Michigan and at the IRP at NIAMS. JSK was supported by
   a Rheumatology Research Foundation Rheumatology Scientist Development
   Award. This work was supported by the National Institutes of Health
   (NIH) through PHS grant HL088419 (to MJK) and by the Intramural Research
   Program at NIAMS. PRT is supported by NIH grants GM079357 and CA151304.
NR 53
TC 35
Z9 35
U1 2
U2 10
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0003-4967
EI 1468-2060
J9 ANN RHEUM DIS
JI Ann. Rheum. Dis.
PD DEC
PY 2015
VL 74
IS 12
BP 2199
EP 2206
DI 10.1136/annrheumdis-2014-205365
PG 8
WC Rheumatology
SC Rheumatology
GA CX6YA
UT WOS:000365846400023
PM 25104775
ER

PT J
AU Sharov, A
   Maran, T
   Tonnessen, M
AF Sharov, Alexei
   Maran, Timo
   Tonnessen, Morten
TI Organisms Reshape Sign Relations
SO BIOSEMIOTICS
LA English
DT Editorial Material
ID SPECIATION
C1 [Sharov, Alexei] NIA, Genet Lab, Baltimore, MD 21224 USA.
   [Maran, Timo] Univ Tartu, Dept Semiot, EE-50090 Tartu, Estonia.
   [Tonnessen, Morten] Univ Stavanger, Dept Social Studies, Stavanger, Norway.
   [Tonnessen, Morten] Univ Stavanger, Dept Hlth Studies, Stavanger, Norway.
RP Sharov, A (reprint author), NIA, Genet Lab, Baltimore, MD 21224 USA.
EM sharoval@mail.nih.gov
RI Maran, Timo/G-5504-2016
NR 15
TC 1
Z9 1
U1 3
U2 3
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1875-1342
EI 1875-1350
J9 BIOSEMIOTICS-NETH
JI Biosemiotics
PD DEC
PY 2015
VL 8
IS 3
BP 361
EP 365
DI 10.1007/s12304-015-9251-2
PG 5
WC Humanities, Multidisciplinary; History & Philosophy Of Science
SC Arts & Humanities - Other Topics; History & Philosophy of Science
GA CX4RC
UT WOS:000365687000001
ER

PT J
AU Wu, XC
   Prasad, PK
   Landry, I
   Harlan, LC
   Parsons, HM
   Lynch, CF
   Smith, AW
   Hamilton, AS
   Keegan, THM
AF Wu, Xiao-Cheng
   Prasad, Pinki K.
   Landry, Ian
   Harlan, Linda C.
   Parsons, Helen M.
   Lynch, Charles F.
   Smith, Ashley W.
   Hamilton, Ann S.
   Keegan, Theresa H. M.
CA AYA HOPE Study Collaborative Grp
TI Impact of the AYA HOPE Comorbidity Index on Assessing Health Care
   Service Needs and Health Status among Adolescents and Young Adults with
   Cancer
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID SURVIVAL; OBESITY; METAANALYSIS; VALIDATION; OVERWEIGHT; DISORDERS;
   MORTALITY; DIAGNOSIS; ONCOLOGY; CHILDREN
AB Background: Existing comorbidity indices were not developed for adolescent and young adults (AYA) 15 to 39 years of age. The aim of this study was to assess impact of comorbidities on health care service needs and health status among AYA cancer survivors using the newly developed AYA HOPE comorbidity index in comparison with the existing indices.
   Methods: Data on comorbid conditions were obtained from medical records and service needs and health status were from a survey of AYA cancer survivors. Prevalence of comorbidities was based on the AYA HOPE index. Charlson and NCI indices were compared. Multivariable logistic regression was used.
   Results: Of the 485 patients, 14.6% had >= 2 comorbidities based on the AYA HOPE Index. Prevalence of mental illness and obesity/overweight, which were not included in existing indices, were 8.2% and 5.8%, respectively. Prevalence of cardiovascular, endocrine, gastrointestinal, and neurologic conditions were higher with the AYA HOPE Index than the other two indices. Forty percent of AYA patients reported service needs, particularly for mental health services (25.2%) and support groups (17.7%). Having >= 2 comorbidities on the AYA index was associated with higher mental health service needs [OR, 2.05; 95% confidence interval (CI), 1.10-3.82] adjusting for demographic and clinical factors. Comorbidities were associated with fair/poor self-reported health status.
   Conclusion: The AYA HOPE Index is a more comprehensive comorbidity index for AYA cancer patients than existing indices, and the number of comorbidities is associated with service needs and health status.
   Impact: The AYA HOPE index could identify patients' additional service needs early in therapy. (C)2015 AACR.
C1 [Wu, Xiao-Cheng; Landry, Ian] LSUHSC, Dept Epidemiol, New Orleans, LA USA.
   [Prasad, Pinki K.] LSUSHC, Childrens Hosp New Orleans, Dept Pediat Hematol Oncol, New Orleans, LA USA.
   [Harlan, Linda C.] NCI, Appl Res Program, Bethesda, MD 20892 USA.
   [Parsons, Helen M.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
   [Lynch, Charles F.] Univ Iowa, Dept Epidemiol, Iowa City, IA USA.
   [Smith, Ashley W.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
   [Hamilton, Ann S.] Univ So Calif, Norris Canc Ctr, Prevent Med, Los Angeles, CA USA.
   [Keegan, Theresa H. M.] Univ Calif Davis, Div Hematol & Oncol, Dept Internal Med, Davis, CA 95616 USA.
RP Wu, XC (reprint author), LSU Hlth Sci Ctr, Sch Publ Hlth, 2020 Gravier St,3rd Floor, New Orleans, LA 70112 USA.
EM xwu@lsuhsce.du
FU [HHSN261201300004I];  [HHSN261201300005I];  [HHSN261201300011I]; 
   [HHSN261201300012I];  [HHSN261201300014I];  [HHSN261201300016I]; 
   [HHSN261201300020I]
FX This work was supported by HHSN261201300004I (A.S. Hamilton),
   HHSN261201300005I, HHSN261201300011I, HHSN261201300012I,
   HHSN261201300014I (T.H.M. Keegan), HHSN261201300016I (X.-C. Wu), and
   HHSN261201300020I (C.F. Lynch)
NR 35
TC 0
Z9 0
U1 1
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 DEC
PY 2015
VL 24
IS 12
BP 1844
EP 1849
DI 10.1158/1055-9965.EPI-15-0401
PG 6
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA CY0XB
UT WOS:000366129100005
PM 26420768
ER

PT J
AU Zhu, GJ
   Liu, Z
   Epstein, JI
   Davis, C
   Christudass, CS
   Carter, HB
   Landis, P
   Zhang, H
   Chung, JY
   Hewitt, SM
   Miller, MC
   Veltri, RW
AF Zhu, Guangjing
   Liu, Zhi
   Epstein, Jonathan I.
   Davis, Christine
   Christudass, Christhunesa S.
   Carter, H. Ballentine
   Landis, Patricia
   Zhang, Hui
   Chung, Joon-Yong
   Hewitt, Stephen M.
   Miller, M. Craig
   Veltri, Robert W.
TI A Novel Quantitative Multiplex Tissue Immunoblotting for Biomarkers
   Predicts a Prostate Cancer Aggressive Phenotype
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID DECISION CURVE ANALYSIS; TERM-FOLLOW-UP; RADICAL PROSTATECTOMY;
   HER-2/NEU EXPRESSION; ACTIVE SURVEILLANCE; PROGNOSTIC VALUE;
   NATURAL-HISTORY; DEATH; RISK; GLYCOPROTEINS
AB Background: Early prediction of disease progression in men with very low-risk (VLR) prostate cancer who selected active surveillance (AS) rather than immediate treatment could reduce morbidity associated with overtreatment.
   Methods: We evaluated the association of six biomarkers [Periostin, (-5, -7) proPSA, CACNA1D, HER2/neu, EZH2, and Ki-67] with different Gleason scores and biochemical recurrence (BCR) on prostate cancer TMAs of 80 radical prostatectomy (RP) cases. Multiplex tissue immunoblotting (MTI) was used to assess these biomarkers in cancer and adjacent benign areas of 5 mm sections. Multivariate logistic regression (MLR) was applied to model our results.
   Results: In the RP cases, CACNA1D, HER2/neu, and Periostin expression were significantly correlated with aggressive phenotype in cancer areas. An MLR model in the cancer area yielded a ROC-AUC = 0.98, whereas in cancer-adjacent benign areas, yielded a ROC-AUC = 0.94. CACNA1D and HER2/neu expression combined with Gleason score in a MLR model yielded a ROC-AUC = 0.79 for BCR prediction. In the small biopsies from an AS cohort of 61 VLR cases, an MLR model for prediction of progressors at diagnosis retained (-5, -7) proPSA and CACNA1D, yielding a ROC-AUC of 0.78, which was improved to 0.82 after adding tPSA into the model.
   Conclusions: The molecular profile of biomarkers is capable of accurately predicting aggressive prostate cancer on retrospective RP cases and identifying potential aggressive prostate cancer requiring immediate treatment on the AS diagnostic biopsy but limited in BCR prediction.
   Impact: Comprehensive profiling of biomarkers using MTI predicts prostate cancer aggressive phenotype in RP and AS biopsies. (C) 2015 AACR.
C1 [Zhu, Guangjing; Liu, Zhi; Davis, Christine; Christudass, Christhunesa S.; Carter, H. Ballentine; Landis, Patricia; Veltri, Robert W.] Johns Hopkins Univ, Sch Med, James Buchanan Brady Urol Inst, Baltimore, MD 21287 USA.
   [Epstein, Jonathan I.; Zhang, Hui] Johns Hopkins Univ Hosp, Dept Pathol, Baltimore, MD 21287 USA.
   [Chung, Joon-Yong; Hewitt, Stephen M.] NCI, Expt Pathol Lab, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Veltri, RW (reprint author), Johns Hopkins Univ, Sch Med, James Buchanan Brady Urol Inst, 600 N Wolfe St, Baltimore, MD 21287 USA.
EM rveltri1@jhmi.edu
OI Hewitt, Stephen/0000-0001-8283-1788; Chung,
   Joon-Yong/0000-0001-5041-5982
FU Brady Urological Institute at the Johns Hopkins University;  [EDRN/NCI
   U01CA152813]
FX This work was supported by two grants: EDRN/NCI U01CA152813 grant (to H.
   Zhang P.I.) with an administrative supplement to Dr. Robert W. Veltri,
   Prostate Cancer Foundation and Patana Fund of The Brady Urological
   Institute at the Johns Hopkins University.
NR 44
TC 2
Z9 2
U1 2
U2 3
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 DEC
PY 2015
VL 24
IS 12
BP 1864
EP 1872
DI 10.1158/1055-9965.EPI-15-0496
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA CY0XB
UT WOS:000366129100008
PM 26404961
ER

PT J
AU Arem, H
   Brinton, LA
   Moore, SC
   Gapstur, SM
   Habel, LA
   Johnson, K
   Kolonel, LN
   McCormack, VA
   Michels, KB
   Sesso, HD
   Ursin, G
   Van den Eeden, SK
   Weiderpass, E
   Cook, MB
   Matthews, CE
AF Arem, Hannah
   Brinton, Louise A.
   Moore, Steven C.
   Gapstur, Susan M.
   Habel, Laurel A.
   Johnson, Kenneth
   Kolonel, Laurence N.
   McCormack, Valerie A.
   Michels, Karin B.
   Sesso, Howard D.
   Ursin, Giske
   Van den Eeden, Stephen K.
   Weiderpass, Elisabete
   Cook, Michael B.
   Matthews, Charles E.
TI Physical Activity and Risk of Male Breast Cancer
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID BASE-LINE CHARACTERISTICS; COHORT; HEALTH; DESIGN
AB The association between leisure-time physical activity (LTPA) and male breast cancer risk is unclear. In the Male Breast Cancer Pooling Project, with 449 cases and 13,855 matched controls, we used logistic regression with study stratification to generate adjusted ORs and 95% confidence intervals (CI) for LTPA tertiles and male breast cancer risk. Compared with low LTPA, medium and high LTPA were not associated with male breast cancer risk (OR, 1.01; 95% CI, 0.79-1.29; 0.90, 0.69-1.18, respectively). In joint-effects analyses, compared with the referent of high body mass index (BMI; >= 25 kg/m(2))/low LTPA, neither medium nor high PA was associated with risk among high BMI men, but normal BMI men (<25 kg/m(2)) with low or medium LTPA were at a nonsignificant similar to 16% reduced risk and those with high LTPA were at a 27% reduced risk (OR, 0.73; 95% CI, 0.50-1.07). Physical activity alone may not confer protection against male breast cancer risk. (C)2015 AACR.
C1 [Arem, Hannah; Brinton, Louise A.; Moore, Steven C.; Cook, Michael B.; Matthews, Charles E.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Gapstur, Susan M.] Amer Canc Soc, Atlanta, GA 30329 USA.
   [Habel, Laurel A.; Van den Eeden, Stephen K.] Kaiser Permanente No Calif, Div Res, Oakland, CA USA.
   [Johnson, Kenneth] Univ Ottawa, Dept Epidemiol & Community Med, Ottawa, ON, Canada.
   [Kolonel, Laurence N.] Canc Res Ctr Hawaii, Honolulu, HI USA.
   [McCormack, Valerie A.] Int Agcy Res Canc, F-69372 Lyon, France.
   [Michels, Karin B.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Obstet & Gynecol Epidemiol Ctr,Dept Obstet Gyneco, Boston, MA 02115 USA.
   [Michels, Karin B.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
   [Michels, Karin B.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Channing Lab,Dept Med, Boston, MA 02115 USA.
   [Sesso, Howard D.] Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA.
   [Sesso, Howard D.] Brigham & Womens Hosp, Div Aging, Boston, MA 02115 USA.
   [Ursin, Giske; Weiderpass, Elisabete] Canc Registry Norway, Oslo, Norway.
   [Weiderpass, Elisabete] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
   [Weiderpass, Elisabete] Univ Tromso, Dept Community Med, Fac Hlth Sci, Tromso, Norway.
   [Weiderpass, Elisabete] Folkhalsan Res Ctr, Genet Epidemiol Grp, Helsinki, Finland.
RP Arem, H (reprint author), NCI, 9609 Med Ctr Dr,Rm 6E314, Rockville, MD 20892 USA.
EM Aremhe2@mail.nih.gov
RI Cook, Michael/A-5641-2009; Moore, Steven/D-8760-2016; Weiderpass,
   Elisabete/M-4029-2016
OI Cook, Michael/0000-0002-0533-7302; Moore, Steven/0000-0002-8169-1661;
   Weiderpass, Elisabete/0000-0003-2237-0128
FU NIH [CA 097193, CA 34944, CA 40360, HL 26490, HL 34595]; NCI, NIH
   [CA167552]; NIH/NCI [R37CA54281]; Intramural Research Program at the
   NIH, Bethesda, Maryland
FX H. Arem, L.A. Brinton, S.C. Moore, M.B. Cook, and C.E. Matthews are
   supported by the Intramural Research Program at the NIH, Bethesda,
   Maryland. The Physicians' Health Study was supported by grants CA
   097193, CA 34944, CA 40360, HL 26490, and HL 34595 from the NIH (to H.D.
   Sesso). The Health Professionals' Follow-Up Study was supported by
   research grant CA167552 from the NCI, NIH (to K.B. Michels). Support for
   MEC was provided by NIH/NCI under grant number R37CA54281 (to L.N.
   Kolonel). The American Cancer Society funds the creation, maintenance,
   and updating of the Cancer Prevention Study II cohort (to S.M. Gapstur).
NR 18
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD DEC
PY 2015
VL 24
IS 12
BP 1898
EP 1901
DI 10.1158/1055-9965.EPI-15-0588
PG 4
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA CY0XB
UT WOS:000366129100012
PM 26404962
ER

PT J
AU Reding, KW
   Young, MT
   Szpiro, AA
   Han, CJ
   DeRoo, LA
   Weinberg, C
   Kaufman, JD
   Sandler, DP
AF Reding, Kerryn W.
   Young, Michael T.
   Szpiro, Adam A.
   Han, Claire J.
   DeRoo, Lisa A.
   Weinberg, Clarice
   Kaufman, Joel D.
   Sandler, Dale P.
TI Breast Cancer Risk in Relation to Ambient Air Pollution Exposure at
   Residences in the Sister Study Cohort
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
AB Background: Some but not all past studies reported associations between components of air pollution and breast cancer, namely fine particulate matter <= 2.5 mm (PM2.5) and nitrogen dioxide (NO2). It is yet unclear whether risks differ according to estrogen receptor (ER) and progesterone receptor (PR) status.
   Methods: This analysis includes 47,591 women from the Sister Study cohort enrolled from August 2003 to July 2009, in whom 1,749 invasive breast cancer cases arose from enrollment to January 2013. Using Cox proportional hazards and polytomous logistic regression, we estimated breast cancer risk associated with residential exposure to NO2, PM2.5, and PM10.
   Results: Although breast cancer risk overall was not associated with PM2.5 [HR = 1.03; 95% confidence intervals (CI), 0.96-1.11], PM10 (HR = 0.99; 95% CI, 0.98-1.00), or NO2 (HR = 1.02; 95% CI, 0.97-1.07), the association with NO2 differed according to ER/PR subtype (P = 0.04). For an interquartile range (IQR) difference of 5.8 parts per billion (ppb) in NO2, the relative risk (RR) of ER+/PR+ breast cancer was 1.10 (95% CI, 1.02-1.19), while there was no evidence of association with ER-/PR- (RR = 0.92; 95% CI, 0.77-1.09; P-interaction = 0.04).
   Conclusions: Within the Sister Study cohort, we found no significant associations between air pollution and breast cancer risk overall. But we observed an increased risk of ER+/PR+ breast cancer associated with NO2.
   Impact: Though these results suggest there is no substantial increased risk for breast cancer overall in relation to air pollution, NO2, a marker of traffic-related air pollution, may differentially affect ER+/PR+ breast cancer. (C)2015 AACR.
C1 [Reding, Kerryn W.; Han, Claire J.] Univ Washington, Sch Nursing, Seattle, WA 98195 USA.
   [Reding, Kerryn W.] Fred Hutchinson Canc Res Ctr Publ Hlth Sci, Seattle, WA USA.
   [Young, Michael T.; Szpiro, Adam A.; Kaufman, Joel D.] Univ Washington, Sch Publ Hlth, Seattle, WA 98195 USA.
   [DeRoo, Lisa A.] Univ Bergen, Dept Global Publ Hlth & Primary Care, Bergen, Norway.
   [Weinberg, Clarice; Sandler, Dale P.] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
RP Reding, KW (reprint author), Fred Hutchinson Canc Res Ctr, 1100 Fairview Ave N,Mail Stop M3-B232, Seattle, WA 98109 USA.
EM kreding@uw.edu
RI Kaufman, Joel/B-5761-2008; 
OI Kaufman, Joel/0000-0003-4174-9037; Sandler, Dale/0000-0002-6776-0018
FU Intramural Research Program of the NIH, National Institute of
   Environmental Health Sciences [Z01 ES 044005]; National Institute of
   Nursing Research career development award [R00NR012232]
FX This work was funded in part by the Intramural Research Program of the
   NIH, National Institute of Environmental Health Sciences (Z01 ES 044005;
   PI: D.P. Sandler). This publication was also in part developed under
   STAR research assistance agreements (RD831697; PI: J.D. Kaufman; and
   RD83479601; PI: S. Vedal; Project Director: J.D. Kaufman) awarded by the
   U.S. EPA. It has not been formally reviewed by the EPA. Dr. Reding was
   supported by National Institute of Nursing Research career development
   award (R00NR012232; PI: K.W. Reding).
NR 8
TC 5
Z9 5
U1 0
U2 6
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD DEC
PY 2015
VL 24
IS 12
BP 1907
EP 1909
DI 10.1158/1055-9965.EPI-15-0787
PG 3
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA CY0XB
UT WOS:000366129100014
PM 26464427
ER

PT J
AU Keller, K
   Maass, M
   Dizayee, S
   Leiss, V
   Annala, S
   Koth, J
   Seemann, WK
   Muller-Ehmsen, J
   Mohr, K
   Nurnberg, B
   Engelhardt, S
   Herzig, S
   Birnbaumer, L
   Matthes, J
AF Keller, Kirsten
   Maass, Martina
   Dizayee, Sara
   Leiss, Veronika
   Annala, Suvi
   Koeth, Jessica
   Seemann, Wiebke K.
   Mueller-Ehmsen, Jochen
   Mohr, Klaus
   Nurnberg, Bernd
   Engelhardt, Stefan
   Herzig, Stefan
   Birnbaumer, Lutz
   Matthes, Jan
TI Lack of G alpha(i2) leads to dilative cardiomyopathy and increased
   mortality in beta(1)-adrenoceptor overexpressing mice
SO CARDIOVASCULAR RESEARCH
LA English
DT Article
DE Adrenergic receptor; Inhibitory G protein; Cardiomyopathy; Heart
   failure; Cardioprotection
ID SYMPATHETIC-NERVOUS-SYSTEM; CONGESTIVE-HEART-FAILURE; RECEPTOR
   TRANSGENIC MICE; G-PROTEINS; BETA(2)-ADRENERGIC RECEPTOR; ISCHEMIC
   CARDIOMYOPATHY; GENE KNOCKOUT; MOUSE HEARTS; TROPONIN-I; HYPERTROPHY
AB Inhibitory G (G(i)) proteins have been proposed to be cardioprotective. We investigated effects of G alpha(i2) knockout on cardiac function and survival in a murine heart failure model of cardiac beta(1)-adrenoceptor overexpression.
   beta(1)-transgenic mice lacking G alpha(i2) (beta(1)-tg/G alpha(-/-)(i2)) were compared with wild-type mice and littermates either overexpressing cardiac beta(1)-adrenoceptors (beta(1)-tg) or lacking G alpha(i2) (G alpha(-/-)(i2)). At 300 days, mortality of mice only lacking G alpha(i2) was already higher compared with wild-type or beta(1)-tg, but similar to beta(1)-tg/G alpha(-/-)(i2), mice. Beyond 300 days, mortality of beta(1)-tg/G alpha(-/-)(i2) mice was enhanced compared with all other genotypes (mean survival time: 363 +/- 21 days). At 300 days of age, echocardiography revealed similar cardiac function of wild-type, beta(1)-tg, and G alpha(-/-)(i2) mice, but significant impairment for beta(1)-tg/G alpha(-/-)(i2) mice (e.g. ejection fraction 14 +/- 2 vs. 40 +/- 4% in wild-type mice). Significantly increased ventricle-to-body weight ratio (0.71 +/- 0.06 vs. 0.48 +/- 0.02% in wild-type mice), left ventricular size (length 0.82 +/- 0.04 vs. 0.66 +/- 0.03 cm in wild types), and atrial natriuretic peptide and brain natriuretic peptide expression (mRNA: 2819 and 495% of wild-type mice, respectively) indicated hypertrophy. G alpha(i3) was significantly up-regulated in G alpha(i2) knockout mice (protein compared with wild type: 340 +/- 90% in G alpha(-/-)(i2) and 394 +/- 80% in beta(1)-tg/G alpha(-/-)(i2), respectively).
   G alpha(i2) deficiency combined with cardiac beta(1)-adrenoceptor overexpression strongly impaired survival and cardiac function. At 300 days of age, beta(1)-adrenoceptor overexpression alone had not induced cardiac hypertrophy or dysfunction while there was overt cardiomyopathy in mice additionally lacking G alpha(i2). We propose an enhanced effect of increased beta(1)-adrenergic drive by the lack of protection via G alpha(i2). G alpha(i3) up-regulation was not sufficient to compensate for G alpha(i2) deficiency, suggesting an isoform-specific or a concentration-dependent mechanism.
C1 [Keller, Kirsten; Dizayee, Sara; Annala, Suvi; Koeth, Jessica; Seemann, Wiebke K.; Herzig, Stefan; Matthes, Jan] Univ Cologne, Dept Pharmacol, D-50931 Cologne, Germany.
   [Maass, Martina] Univ Hosp, Dept Internal Med 3, Cologne, Germany.
   [Leiss, Veronika; Nurnberg, Bernd] Eberhard Karls Univ Tubingen, Inst Expt & Clin Pharmacol & Toxicol, Dept Pharmacol & Expt Therapy, Hosp & Clin, Tubingen, Germany.
   [Leiss, Veronika; Nurnberg, Bernd] Ctr Pharmacogen & Drug Res, Interfac, Tubingen, Germany.
   [Mueller-Ehmsen, Jochen] Asklepios Klin Altona, Hamburg, Germany.
   [Mohr, Klaus] Univ Bonn, Pharmacol & Toxicol Sect, Inst Pharm, Bonn, Germany.
   [Engelhardt, Stefan] Tech Univ Munich, Inst Pharmacol & Toxicol, D-80290 Munich, Germany.
   [Birnbaumer, Lutz] NIEHS, Neurobiol Lab, NIH, Dept Hlth & Human Serv, Durham, NC USA.
RP Matthes, J (reprint author), Univ Cologne, Dept Pharmacol, Gleueler Str 24, D-50931 Cologne, Germany.
EM jan.matthes@uni-koeln.de
FU NIH [Z01-ES-101643]; Deutsche Forschungsgemeinschaft (DFG) [He
   1578/13-1, He 1578/13-2]
FX This study was supported in part by the Intramural Research Program of
   the NIH (Project Z01-ES-101643) to L.B. and by Deutsche
   Forschungsgemeinschaft (DFG; He 1578/13-1 and 2) to S.H.
NR 56
TC 2
Z9 2
U1 0
U2 9
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0008-6363
EI 1755-3245
J9 CARDIOVASC RES
JI Cardiovasc. Res.
PD DEC 1
PY 2015
VL 108
IS 3
BP 348
EP 356
DI 10.1093/cvr/cvv235
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA CY4OQ
UT WOS:000366388000006
PM 26464333
ER

PT J
AU Tomic, M
   Bargi-Souza, P
   Leiva-Salcedo, E
   Nunes, MT
   Stojilkovic, SS
AF Tomic, Melanija
   Bargi-Souza, Paula
   Leiva-Salcedo, Elias
   Nunes, Maria Tereza
   Stojilkovic, Stanko S.
TI Calcium signaling properties of a thyrotroph cell line, mouse T alpha T1
   cells
SO CELL CALCIUM
LA English
DT Article
DE ATP; Calcium influx; Calcium mobilization; P2Y receptors; Thyrotrophs;
   Thyrotropin-releasing hormone; Triiodothryonine
ID ANTERIOR-PITUITARY-CELLS; NUCLEOTIDE-GATED CHANNELS; THYROID-HORMONE
   RECEPTOR; BETA-SUBUNIT GENE; RAT LACTOTROPHS; PROLACTIN-RELEASE;
   ACTION-POTENTIALS; POTASSIUM CURRENT; STORE DEPLETION; CA2+ ENTRY
AB T alpha T1 cells are mouse thyrotroph cell line frequently used for studies on thyroid-stimulating hormone beta subunit gene expression and other cellular functions. Here we have characterized calcium-signaling pathways in T alpha T1 cells, an issue not previously addressed in these cells and incompletely described in native thyrotrophs. T alpha T1 cells are excitable and fire action potentials spontaneously and in response to application of thyrotropin-releasing hormone (TRH), the native hypothalamic agonist for thyrotrophs. Spontaneous electrical activity is coupled to small amplitude fluctuations in intracellular calcium, whereas TRH stimulates both calcium mobilization from intracellular pools and calcium influx. Nonreceptor-mediated depletion of intracellular pool also leads to a prominent facilitation of calcium influx. Both receptor and non-receptor stimulated calcium influx is substantially attenuated but not completely abolished by inhibition of voltage-gated calcium channels, suggesting that depletion of intracellular calcium pool in these cells provides a signal for both voltage-independent and -dependent calcium influx, the latter by facilitating the pacemaking activity. These cells also express purinergic P2Y1 receptors and their activation by extracellular ATP mimics TRH action on calcium mobilization and influx. The thyroid hormone triiodothyronine prolongs duration of TRH-induced calcium spikes during 30-min exposure. These data indicate that Tan cells are capable of responding to natively feed-forward TRH signaling and intrapituitary ATP signaling with acute calcium mobilization and sustained calcium influx. Amplification of TRH-induced calcium signaling by triiodothyronine further suggests the existence of a pathway for positive feedback effects of thyroid hormones probably in a non-genomic manner. Published by Elsevier Ltd.
C1 [Tomic, Melanija; Bargi-Souza, Paula; Leiva-Salcedo, Elias; Stojilkovic, Stanko S.] Eunice Kennedy Shiver Natl Inst Child Hlth & Huma, Sect Cellular Signaling, NIH, Bethesda, MD 20892 USA.
   [Bargi-Souza, Paula; Nunes, Maria Tereza] Univ Sao Paulo, Dept Physiol & Biophys, Inst Biomed Sci, Sao Paulo, SP, Brazil.
RP Stojilkovic, SS (reprint author), NICHD, Bldg 49,Room 6A-36,9 Convent Dr, Bethesda, MD 20892 USA.
EM stojilks@mail.nih.gov
RI Tomic, Melanija/C-3371-2016; Bargi-Souza, Paula/J-5262-2015
OI Bargi-Souza, Paula/0000-0001-7746-0636
FU Intramural Research Program of the National Institute of Child Health
   and Human Development [ZIA DH000195-22]; Fundacao de Amparo a Pesquisa
   do Estado de Sao Paulo (FAPESP) [2013/05629-4]; Conselho Nacional de
   Pesquisa e Desenvolvimento (CNPq); FAPESP [2012/06643-8]
FX This work was supported by the Intramural Research Program of the
   National Institute of Child Health and Human Development (ZIA
   DH000195-22) and by a grant from the Fundacao de Amparo a Pesquisa do
   Estado de Sao Paulo (FAPESP: Proc. 2013/05629-4) to MTN. MTN is
   recipient of Conselho Nacional de Pesquisa e Desenvolvimento (CNPq)
   fellowships and PBS is recipient of a FAPESP fellowship (2012/06643-8).
NR 55
TC 0
Z9 0
U1 1
U2 2
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
   LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0143-4160
EI 1532-1991
J9 CELL CALCIUM
JI Cell Calcium
PD DEC
PY 2015
VL 58
IS 6
BP 598
EP 605
DI 10.1016/j.ceca.2015.09.003
PG 8
WC Cell Biology
SC Cell Biology
GA CY0AR
UT WOS:000366068900008
PM 26453278
ER

PT J
AU Bjornson, E
   Mukhopadhyay, B
   Asplund, A
   Pristovsek, N
   Cinar, R
   Romeo, S
   Uhlen, M
   Kunos, G
   Nielsen, J
   Mardinoglu, A
AF Bjornson, Elias
   Mukhopadhyay, Bani
   Asplund, Anna
   Pristovsek, Nusa
   Cinar, Resat
   Romeo, Stefano
   Uhlen, Mathias
   Kunos, George
   Nielsen, Jens
   Mardinoglu, Adil
TI Stratification of Hepatocellular Carcinoma Patients Based on Acetate
   Utilization
SO CELL REPORTS
LA English
DT Article
ID FATTY-ACID OXIDATION; GENOME-SCALE MODELS; METABOLIC NETWORK;
   GLUTAMINE-METABOLISM; CANCER METABOLISM; LEPTIN RESISTANCE; TUMOR-CELLS;
   EXPRESSION; TRANSCRIPTOMICS; IDENTIFICATION
AB Hepatocellular carcinoma (HCC) is a deadly form of liver cancer that is increasingly prevalent. We analyzed global gene expression profiling of 361 HCC tumors and 49 adjacent noncancerous liver samples by means of combinatorial network-based analysis. We investigated the correlation between transcriptome and proteome of HCC and reconstructed a functional genome-scale metabolic model (GEM) for HCC. We identified fundamental metabolic processes required for cell proliferation using the network centric view provided by the GEM. Our analysis revealed tight regulation of fatty acid biosynthesis (FAB) and highly significant deregulation of fatty acid oxidation in HCC. We predicted mitochondrial acetate as an emerging substrate for FAB through upregulation of mitochondrial acetyl-CoA synthetase (ACSS1) in HCC. We analyzed heterogeneous expression of ACSS1 and ACSS2 between HCC patients stratified by high and low ACSS1 and ACSS2 expression and revealed that ACSS1 is associated with tumor growth and malignancy under hypoxic conditions in human HCC.
C1 [Bjornson, Elias; Nielsen, Jens; Mardinoglu, Adil] Chalmers, Dept Biol & Biol Engn, S-41296 Gothenburg, Sweden.
   [Mukhopadhyay, Bani; Cinar, Resat; Kunos, George] NIAAA, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA.
   [Asplund, Anna; Pristovsek, Nusa] Uppsala Univ, Dept Immunol Genet & Pathol, Sci Life Lab, S-75185 Uppsala, Sweden.
   [Romeo, Stefano] Univ Gothenburg, Wallenberg Lab, Sahlgrenska Ctr Cardiovasc & Metab Res, Dept Mol & Clin Med, S-41345 Gothenburg, Sweden.
   [Romeo, Stefano] Sahlgrens Univ Hosp, Dept Cardiol, S-41650 Gothenburg, Sweden.
   [Romeo, Stefano] Magna Graecia Univ Catanzaro, Dept Med & Surg Sci, Clin Nutr Unit, I-88100 Catanzaro, Italy.
   [Uhlen, Mathias] KTH Royal Inst Technol, Dept Prote, S-10691 Stockholm, Sweden.
   [Uhlen, Mathias; Nielsen, Jens; Mardinoglu, Adil] KTH Royal Inst Technol, Sci Life Lab, S-17121 Stockholm, Sweden.
RP Mardinoglu, A (reprint author), Chalmers, Dept Biol & Biol Engn, S-41296 Gothenburg, Sweden.
EM adilm@scilifelab.se
RI romeo, stefano/L-6861-2015; 
OI romeo, stefano/0000-0001-9168-4898; Nielsen, Jens/0000-0002-9955-6003;
   CINAR, RESAT/0000-0002-8597-7253; Pristovsek, Nusa/0000-0002-5492-7085
FU Knut and Alice Wallenberg Foundation; Bill and Melinda Gates Foundation;
   Novo Nordisk A/S; Swedish Research Council; NovoNordisk Foundation Grant
   for Excellence in Endocrinology
FX This work was supported by grants from the Knut and Alice Wallenberg
   Foundation, Bill and Melinda Gates Foundation, and Novo Nordisk A/S.
   S.R. was supported by the Swedish Research Council and the NovoNordisk
   Foundation Grant for Excellence in Endocrinology.
NR 51
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U1 2
U2 7
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD DEC 1
PY 2015
VL 13
IS 9
BP 2014
EP 2026
DI 10.1016/j.celrep.2015.10.045
PG 13
WC Cell Biology
SC Cell Biology
GA CX9SY
UT WOS:000366047000025
PM 26655911
ER

PT J
AU Gonzalez-Castillo, J
   Hoy, CW
   Handwerker, DA
   Roopchansingh, V
   Inati, SJ
   Saad, ZS
   Cox, RW
   Bandettini, PA
AF Gonzalez-Castillo, Javier
   Hoy, Colin W.
   Handwerker, Daniel A.
   Roopchansingh, Vinai
   Inati, Souheil J.
   Saad, Ziad S.
   Cox, Robert W.
   Bandettini, Peter A.
TI Task Dependence, Tissue Specificity, and Spatial Distribution of
   Widespread Activations in Large Single-Subject Functional MRI Datasets
   at 7T
SO CEREBRAL CORTEX
LA English
DT Article
DE activation extent; negative BOLD; single subject; transients
ID NEURONAL-ACTIVITY; CORPUS-CALLOSUM; BOLD RESPONSES; WHITE-MATTER; FMRI
   SIGNALS; HUMAN BRAIN; TRANSIENT; HUMANS; EXTENT; TESLA
AB It was recently shown that when large amounts of task-based blood oxygen level-dependent (BOLD) data are combined to increase contrast- and temporal signal-to-noise ratios, the majority of the brain shows significant hemodynamic responses time-locked with the experimental paradigm. Here, we investigate the biological significance of such widespread activations. First, the relationship between activation extent and task demands was investigated by varying cognitive load across participants. Second, the tissue specificity of responses was probed using the better BOLD signal localization capabilities of a 7T scanner. Finally, the spatial distribution of 3 primary response types-namely positively sustained (pSUS), negatively sustained (nSUS), and transient-was evaluated using a newly defined voxel-wise wave-shape index that permits separation of responses based on their temporal signature. About 86% of gray matter (GM) became significantly active when all data entered the analysis for the most complex task. Activation extent scaled with task load and largely followed the GM contour. The most common response type was nSUS BOLD, irrespective of the task. Our results suggest that widespread activations associated with extremely large single-subject functional magnetic resonance imaging datasets can provide valuable information about the functional organization of the brain that goes undetected in smaller sample sizes.
C1 [Gonzalez-Castillo, Javier; Hoy, Colin W.; Handwerker, Daniel A.; Bandettini, Peter A.] NIMH, Sect Funct Imaging Methods, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
   [Roopchansingh, Vinai; Inati, Souheil J.; Bandettini, Peter A.] NIMH, Funct MRI Facil, NIH, Bethesda, MD 20892 USA.
   [Saad, Ziad S.; Cox, Robert W.] NIMH, Sci & Stat Comp Core, NIH, Bethesda, MD 20892 USA.
RP Gonzalez-Castillo, J (reprint author), NIMH, Sect Funct Imaging Methods, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
EM javier.gonzalez-castillo@nih.gov
OI Gonzalez-Castillo, Javier/0000-0002-6520-5125
FU Intramural Research Program of National Institute of Mental Health
   (NIMH) at National Institutes of Health (NIH)
FX This research was supported by the Intramural Research Program of the
   National Institute of Mental Health (NIMH) at the National Institutes of
   Health (NIH).
NR 39
TC 0
Z9 0
U1 0
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1047-3211
EI 1460-2199
J9 CEREB CORTEX
JI Cereb. Cortex
PD DEC
PY 2015
VL 25
IS 12
BP 4667
EP 4677
DI 10.1093/cercor/bhu148
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA CY5RB
UT WOS:000366463800003
PM 25405938
ER

PT J
AU Remaley, AT
AF Remaley, Alan T.
TI Six-Month-Old Boy with "Milky" Serum Commentary
SO CLINICAL CHEMISTRY
LA English
DT Editorial Material
C1 [Remaley, Alan T.] NHLBI, Lipoprot Metab Lab, Cardiopulm Branch, NIH, Bethesda, MD 20892 USA.
RP Remaley, AT (reprint author), NIH, Bldg 10,Rm 2C-433,10 Ctr Dr,MSC 1508, Bethesda, MD 20892 USA.
EM aremaley1@cc.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
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 DEC
PY 2015
VL 61
IS 12
BP 1444
EP 1445
DI 10.1373/clinchem.2015.243972
PG 2
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA CY0BT
UT WOS:000366071900006
PM 26614229
ER

PT J
AU Osafo, C
   Raji, YR
   Burke, D
   Tayo, BO
   Tiffin, N
   Moxey-Mims, MM
   Rasooly, RS
   Kimmel, PL
   Ojo, A
   Adu, D
   Parekh, RS
AF Osafo, Charlotte
   Raji, Yemi Raheem
   Burke, David
   Tayo, Bamidele O.
   Tiffin, Nicki
   Moxey-Mims, Marva M.
   Rasooly, Rebekah S.
   Kimmel, Paul L.
   Ojo, Akinlolu
   Adu, Dwomoa
   Parekh, Rulan S.
CA H3Arica Kidney Dis Res Network Inv
TI Human Heredity and Health (H3) in Africa Kidney Disease Research
   Network: A Focus on Methods in Sub-Saharan Africa
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID GLOMERULAR-FILTRATION-RATE; BASE-LINE CHARACTERISTICS; APOL1 RISK
   VARIANTS; POPULATION-GENETICS; COHORT; AMERICANS; ASSOCIATIONS;
   PREDICTION; EQUATION; CONSENT
AB CKD affects an estimated 14% of adults in sub-Saharan Africa, but very little research has been done on the cause, progression, and prevention of CKD there. As part of the Human Heredity and Health in Africa (H3Africa) Consortium, the H3Africa Kidney Disease Research Network was established to study prevalent forms of kidney disease in sub-Saharan Africa and increase the capacity for genetics and genomics research. The study is performing comprehensive phenotypic characterization and analyzing environmental and genetic factors from nine clinical centers in four African countries (Ghana, Nigeria, Ethiopia, and Kenya) over a 5-year period. Approximately 4000 participants with specified kidney disease diagnoses and 4000 control participants will be enrolled in the four African countries. In addition, approximately 50 families with hereditary glomerular disease will be enrolled. The study includes both pediatric and adult participants age <1 to 74 years across a broad spectrum of kidney diseases secondary to hypertension-attributed nephropathy, diabetes, HIV infection, sickle cell disease, biopsy-proven glomerular disease, and CKD of unknown origin. Clinical and demographic data with biospecimens are collected to assess clinical, biochemical, and genetic markers of kidney disease. As of March 2015, a total of 3499 patients and controls have been recruited and 1897 had complete entry data for analysis. Slightly more than half (50.2%) of the cohort is female. Initial quality control of clinical data collection and of biosample and DNA analysis is satisfactory, demonstrating that a clinical research infrastructure can be successfully established in Africa. This study will provide clinical, biochemical, and genotypic data that will greatly increase the understanding of CKD in sub-Saharan Africa.
C1 [Osafo, Charlotte; Adu, Dwomoa] Univ Ghana, Dept Med & Therapeut, Accra, Ghana.
   [Raji, Yemi Raheem] Univ Ibadan, Dept Med, Ibadan, Nigeria.
   [Burke, David] Univ Michigan, Sch Med, Dept Human Genet, Ann Arbor, MI USA.
   [Ojo, Akinlolu] Univ Michigan, Sch Med, Dept Med, Ann Arbor, MI 48104 USA.
   [Tayo, Bamidele O.] Loyola Univ Chicago, Dept Publ Hlth Sci, Maywood, IL USA.
   [Tiffin, Nicki] Univ Western Cape, South African Natl Bioinformat Inst, Med Res Council South Africa, Bioinformat Unit, Cape Town, South Africa.
   [Moxey-Mims, Marva M.; Rasooly, Rebekah S.; Kimmel, Paul L.] NIDDK, NIH, Bethesda, MD USA.
   [Parekh, Rulan S.] Univ Toronto, Dept Pediat, Univ Hlth Network, Hosp Sick Children, Toronto, ON, Canada.
   [Parekh, Rulan S.] Univ Toronto, Dept Med, Univ Hlth Network, Hosp Sick Children, Toronto, ON, Canada.
RP Adu, D (reprint author), Univ Ghana, POB 4236, Accra, Ghana.
EM dwoms15@gmail.com
OI Rasooly, Rebekah/0000-0002-6357-5528
FU National Human Genome Research Institute [1U54-HG006939-01]
FX The H3Kidney Disease Research Network study and investigators are funded
   under a cooperative agreement from the National Human Genome Research
   Institute (1U54-HG006939-01).
NR 33
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U1 1
U2 3
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1555-9041
EI 1555-905X
J9 CLIN J AM SOC NEPHRO
JI Clin. J. Am. Soc. Nephrol.
PD DEC
PY 2015
VL 10
IS 12
BP 2279
EP 2287
DI 10.2215/CJN.11951214
PG 9
WC Urology & Nephrology
SC Urology & Nephrology
GA CX9EF
UT WOS:000366007100023
PM 26138261
ER

PT J
AU Zeitler, P
   Hirst, K
   Copeland, KC
   El Ghormli, L
   Katz, LL
   Levitsky, LL
   Linder, B
   McGuigan, P
   White, NH
   Wilfley, D
AF Zeitler, Phil
   Hirst, Kathryn
   Copeland, Kenneth C.
   El Ghormli, Laure
   Katz, Lorraine Levitt
   Levitsky, Lynne L.
   Linder, Barbara
   McGuigan, Paul
   White, Neil H.
   Wilfley, Denise
CA TODAY Study Grp
TI HbA(1c) After a Short Period of Monotherapy With Metformin Identifies
   Durable Glycemic Control Among Adolescents With Type 2 Diabetes
SO DIABETES CARE
LA English
DT Article
ID BETA-CELL FUNCTION; GLUCOSE CONTROL; YOUTH; COMPLICATIONS; OUTCOMES;
   INSULIN; CURVE
AB OBJECTIVETo determine whether clinically accessible parameters early in the course of youth-onset type 2 diabetes predict likelihood of durable control on oral therapy.RESEARCH DESIGN AND METHODSTODAY was a randomized clinical trial of adolescents with type 2 diabetes. Two groups, including participants from all three treatments, were defined for analysis: 1) those who remained in glycemic control for at least 48 months of follow-up and 2) those who lost glycemic control before 48 months. Outcome group was analyzed in univariate and multivariate models as a function of baseline characteristics (age, sex, race/ethnicity, socioeconomic status, BMI, waist circumference, Tanner stage, disease duration, depressive symptoms) and biochemical measures (HbA(1c), C-peptide, lean and fat body mass, insulin inverse, insulinogenic index). Receiver operating characteristic curves were used to analyze HbA(1c) cut points.RESULTSIn multivariate models including factors significant in univariate analysis, only HbA(1c) and insulinogenic index at randomization remained significant (P < 0.0001 and P = 0.0002, respectively). An HbA(1c) cutoff of 6.3% (45 mmol/mol) (positive likelihood ratio [PLR] 3.7) was identified that optimally distinguished the groups; sex-specific cutoffs were 6.3% (45 mmol/mol) for females (PLR 4.4) and 5.6% (38 mmol/mol) for males (PLR 2.1).CONCLUSIONSIdentifying youth with type 2 diabetes at risk for rapid loss of glycemic control would allow more targeted therapy. HbA(1c) is a clinically accessible measure to identify high risk for loss of glycemic control on oral therapy. Adolescents with type 2 diabetes unable to attain a non-diabetes range HbA(1c) on metformin are at increased risk for rapid loss of glycemic control.
C1 [Zeitler, Phil] Univ Colorado, Sch Med, Dept Pediat, Endocrinol Sect, Aurora, CO USA.
   [Hirst, Kathryn; El Ghormli, Laure] George Washington Univ, Ctr Biostat, Rockville, MD 20852 USA.
   [Copeland, Kenneth C.] Univ Oklahoma, Coll Med, Oklahoma City, OK 73190 USA.
   [Katz, Lorraine Levitt] Univ Penn, Perelman Sch Med, Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
   [Levitsky, Lynne L.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
   [Linder, Barbara] Natl Inst Diabet & Digest & Kidney Dis, Div Diabet Endocrinol & Metab Dis, NIH, Bethesda, MD USA.
   [McGuigan, Paul] Case Western Reserve Univ, Rainbow Babies & Childrens Hosp, Cleveland, OH 44106 USA.
   [White, Neil H.; Wilfley, Denise] Washington Univ, Sch Med, St Louis, MO USA.
RP Hirst, K (reprint author), George Washington Univ, Ctr Biostat, Rockville, MD 20852 USA.
EM khirst@bsc.gwu.edu
OI Zeitler, Philip/0000-0001-5756-7858
FU NIDDK; National Institutes of Health Office of the Director
   [U01-DK-61212, U01-DK-61230, U01-DK-61239, U01-DK-61242, U01-DK-61254];
   National Center for Research Resources (NCRR) General Clinical Research
   Centers Program [M01-RR00036, M01-RR00043-45, M01-RR00069, M01-RR00084,
   M01-RR01066, M01-RR00125, M01-RR14467]; NCRR Clinical and Translational
   Science Awards [UL1-RR024134, UL1-RR024139, UL1-RR024153, UL1-RR024989,
   UL1-RR024992, UL1-RR025758, UL1-RR025780]
FX This work was completed with funding from NIDDK and the National
   Institutes of Health Office of the Director through grants U01-DK-61212,
   U01-DK-61230, U01-DK-61239, U01-DK-61242, and U01-DK-61254; from the
   National Center for Research Resources (NCRR) General Clinical Research
   Centers Program through grants M01-RR00036 (Washington University School
   of Medicine), M01-RR00043-45 (Children's Hospital Los Angeles),
   M01-RR00069 (University of Colorado Denver), M01-RR00084 (Children's
   Hospital of Pittsburgh), M01-RR01066 (Massachusetts General Hospital),
   M01-RR00125 (Yale University), and M01-RR14467 (University of Oklahoma
   Health Sciences Center); and from the NCRR Clinical and Translational
   Science Awards through grants UL1-RR024134 (Children's Hospital of
   Philadelphia), UL1-RR024139 (Yale University), UL1-RR024153 (Children's
   Hospital of Pittsburgh), UL1-RR024989 (Case Western Reserve University),
   UL1-RR024992 (Washington University in St. Louis), UL1-RR025758
   (Massachusetts General Hospital), and UL1-RR025780 (University of
   Colorado Denver). The NIDDK project office was involved in all aspects
   of the study, including design and conduct; collection, management,
   analysis, and interpretation of data; review and approval of the
   manuscript; and decision to submit the manuscript for publication.
NR 25
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U1 0
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PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD DEC
PY 2015
VL 38
IS 12
BP 2285
EP 2292
DI 10.2337/dc15-0848
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CY0TK
UT WOS:000366118800028
PM 26537182
ER

PT J
AU Espeland, MA
   Brinton, RD
   Hugenschmidt, C
   Manson, JE
   Craft, S
   Yaffe, K
   Weitlauf, J
   Vaughan, L
   Johnson, KC
   Padula, CB
   Jackson, RD
   Resnick, SM
AF Espeland, Mark A.
   Brinton, Roberta Diaz
   Hugenschmidt, Christina
   Manson, JoAnn E.
   Craft, Suzanne
   Yaffe, Kristine
   Weitlauf, Julie
   Vaughan, Leslie
   Johnson, Karen C.
   Padula, Claudia B.
   Jackson, Rebecca D.
   Resnick, Susan M.
CA WHIMS Study Grp
TI Impact of Type 2 Diabetes and Postmenopausal Hormone Therapy on
   Incidence of Cognitive Impairment in Older Women
SO DIABETES CARE
LA English
DT Article
ID HEALTH INITIATIVE MEMORY; ESTROGEN PLUS PROGESTIN; CONJUGATED EQUINE
   ESTROGENS; RANDOMIZED CONTROLLED-TRIAL; ALZHEIMERS-DISEASE; BRAIN
   VOLUMES; DEMENTIA; METAANALYSIS; VALIDITY; RISK
AB OBJECTIVEIn older women, higher levels of estrogen may exacerbate the increased risk for cognitive impairment conveyed by diabetes. We examined whether the effect of postmenopausal hormone therapy (HT) on cognitive impairment incidence differs depending on type 2 diabetes.RESEARCH DESIGN AND METHODSThe Women's Health Initiative (WHI) randomized clinical trials assigned women to HT (0.625 mg/day conjugated equine estrogens with or without [i.e., unopposed] 2.5 mg/day medroxyprogesterone acetate) or matching placebo for an average of 4.7-5.9 years. A total of 7,233 women, aged 65-80 years, were classified according to type 2 diabetes status and followed for probable dementia and cognitive impairment (mild cognitive impairment or dementia).RESULTSThrough a maximum of 18 years of follow-up, women with diabetes had increased risk of probable dementia (hazard ratio [HR] 1.54 [95% CI 1.16-2.06]) and cognitive impairment (HR 1.83 [1.50-2.23]). The combination of diabetes and random assignment to HT increased their risk of dementia (HR 2.12 [1.47-3.06]) and cognitive impairment (HR 2.20 [1.70-2.87]) compared with women without these conditions, interaction P = 0.09 and P = 0.08. These interactions appeared to be limited to women assigned to unopposed conjugated equine estrogens.CONCLUSIONSThese analyses provide additional support to a prior report that higher levels of estrogen may exacerbate risks that type 2 diabetes poses for cognitive function in older women. The role estrogen plays in suppressing non-glucose-based energy sources in the brain may explain this interaction.
C1 [Espeland, Mark A.] Wake Forest Sch Med, Dept Biostat Sci, Winston Salem, NC 27157 USA.
   [Brinton, Roberta Diaz] Univ So Calif, Dept Pharmacol & Pharmaceut Sci, Los Angeles, CA USA.
   [Brinton, Roberta Diaz] Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA.
   [Brinton, Roberta Diaz] Univ So Calif, Dept Neurol, Los Angeles, CA USA.
   [Hugenschmidt, Christina; Craft, Suzanne] Wake Forest Sch Med, Dept Internal Med, Winston Salem, NC USA.
   [Manson, JoAnn E.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Prevent Med, Boston, MA 02115 USA.
   [Yaffe, Kristine] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 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.
   [Weitlauf, Julie; Padula, Claudia B.] Stanford Univ, Sch Med, Vet Affairs Palo Alto Hlth Care Syst, Stanford, CA 94305 USA.
   [Weitlauf, Julie; Padula, Claudia B.] Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA.
   [Vaughan, Leslie] Wake Forest Sch Med, Dept Social Sci & Hlth Policy, Winston Salem, NC USA.
   [Johnson, Karen C.] Univ Tennessee, Ctr Hlth Sci, Dept Prevent Med, Memphis, TN 38163 USA.
   [Jackson, Rebecca D.] Ohio State Univ, Dept Internal Med, Columbus, OH 43210 USA.
   [Resnick, Susan M.] NIA, Lab Behav Neurosci, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Espeland, MA (reprint author), Wake Forest Sch Med, Dept Biostat Sci, Winston Salem, NC 27157 USA.
EM mespelan@wakehealth.edu
FU National Institute on Aging (NIA) [HHSN-271-2011-00004C]; National
   Heart, Lung, and Blood Institute, U.S. Department of Health and Human
   Services; NIA, National Institutes of Health
FX WHIMS-ECHO is funded by the National Institute on Aging (NIA), contract
   no. HHSN-271-2011-00004C, and WHI is funded by the National Heart, Lung,
   and Blood Institute, U.S. Department of Health and Human Services.
   S.M.R. is supported by the Intramural Research Program, NIA, National
   Institutes of Health.
NR 38
TC 2
Z9 4
U1 0
U2 5
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD DEC
PY 2015
VL 38
IS 12
BP 2316
EP 2324
DI 10.2337/dc15-1385
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CY0TK
UT WOS:000366118800032
PM 26486190
ER

PT J
AU Rotman, Y
AF Rotman, Yaron
TI Comment on "Resveratrol improves insulin resistance, glucose and lipid
   metabolism in patients with non-alcoholic fatty liver disease: A
   randomized controlled trial" by Shihui Chen et al. [Dig. Liver Dis.
   2015;47:226-32]
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Letter
C1 [Rotman, Yaron] NIDDK, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Rotman, Y (reprint author), NIDDK, Liver Dis Branch, NIH, 10 Ctr Dr,Bldg 10,Rm 9C434,MSC 1800, Bethesda, MD 20892 USA.
EM rotmany@mail.nih.gov
NR 3
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 1590-8658
EI 1878-3562
J9 DIGEST LIVER DIS
JI Dig. Liver Dis.
PD DEC
PY 2015
VL 47
IS 12
BP 1090
EP 1090
DI 10.1016/j.dld.2015.08.011
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CX7XJ
UT WOS:000365916000018
PM 26382727
ER

PT J
AU Rivero-Buceta, E
   Carrero, P
   Casanova, E
   Doyaguez, EG
   Madrona, A
   Quesada, E
   Perez-Perez, MJ
   Mateos, R
   Bravo, L
   Mathys, L
   Noppen, S
   Kiselev, E
   Marchand, C
   Pommier, Y
   Liekens, S
   Balzarini, J
   Camarasa, MJ
   San-Felix, A
AF Rivero-Buceta, Eva
   Carrero, Paula
   Casanova, Elena
   Doyaguuez, Elisa G.
   Madrona, Andres
   Quesada, Ernesto
   Jesus Perez-Perez, Maria
   Mateos, Raquel
   Bravo, Laura
   Mathys, Leen
   Noppen, Sam
   Kiselev, Evgeny
   Marchand, Christophe
   Pommier, Yves
   Liekens, Sandra
   Balzarini, Jan
   Jose Camarasa, Maria
   San-Felix, Ana
TI Anti-HIV-1 activity of a tripodal receptor that recognizes mannose
   oligomers
SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
DE Antiviral agents; AIDS; HIV; Integrase; Polyphenols
ID ANTIOXIDANT ACTIVITY; DERIVATIVES; ACID; HYDROXYTYROSOL; ENTEROBACTIN;
   INFECTION; THERAPY
AB The glycoprotein gp120 of the HIV-1 viral envelope has a high content in mannose residues, particularly alpha-1,2-mannose oligomers. Compounds that interact with these high-mannose type glycans may disturb the interaction between gp120 and its (co)receptors and are considered potential anti-HIV agents. Previously, we demonstrated that a tripodal receptor (1), with a central scaffold of 1,3,5-triethylbenzene substituted with three 2,3,4-trihydroxybenzoyl groups, selectively recognizes alpha-1,2-mannose polysaccharides. Here we present additional studies to determine the anti-HIV-1 activity and the mechanism of antiviral activity of this compound. Our studies indicate that 1 shows anti-HIV-1 activity in the low micromolar range and has pronounced gp120 binding and HIV-1 integrase inhibitory capacity. However, gp120 binding rather than integrase inhibition seems to be the primary mechanism of antiviral activity of 1. (C) 2015 Elsevier Masson SAS. All rights reserved.
C1 [Rivero-Buceta, Eva; Carrero, Paula; Casanova, Elena; Doyaguuez, Elisa G.; Madrona, Andres; Quesada, Ernesto; Jesus Perez-Perez, Maria; Jose Camarasa, Maria; San-Felix, Ana] Inst Quim Med IQM CSIC, Madrid 28006, Spain.
   [Carrero, Paula] ABG Patentes, Madrid 28036, Spain.
   [Casanova, Elena] Euroquim SA, Illescas, Toledo, Spain.
   [Doyaguuez, Elisa G.] Ctr Quim Organ Lora Tamayo CSIC, Madrid 28006, Spain.
   [Mateos, Raquel; Bravo, Laura] Inst Ciencia & Tecnol Alimentos & Nutr ICTAN CSIC, Madrid 28040, Spain.
   [Mathys, Leen; Noppen, Sam; Liekens, Sandra; Balzarini, Jan] Katholieke Univ Leuven, Rega Inst Med Res, B-3000 Leuven, Belgium.
   [Kiselev, Evgeny; Marchand, Christophe; Pommier, Yves] NCI, Dev Therapeut Branch, NIH, Bethesda, MD 20892 USA.
   [Kiselev, Evgeny; Marchand, Christophe; Pommier, Yves] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP San-Felix, A (reprint author), Inst Quim Med IQM CSIC, Juan Cierva 3, Madrid 28006, Spain.
EM anarosa@iqm.csic.es
RI Quesada del Sol, Ernesto/B-7823-2008; MATEOS BRIZ, Raquel/H-9125-2012;
   Marchand, Christophe/D-8559-2016; Camarasa, Maria-Jose/B-6340-2015;
   Perez-Perez, Maria-Jesus/O-4580-2014
OI Quesada del Sol, Ernesto/0000-0001-6886-0523; MATEOS BRIZ,
   Raquel/0000-0002-9722-1939; Camarasa, Maria-Jose/0000-0002-4978-6468;
   Perez-Perez, Maria-Jesus/0000-0003-1336-7760
FU Spanish MICINN/MINECO [SAF 2012-39760-C02-01]; FEDER programme; Plan
   Nacional de Cooperacion Pablico-Privada. Subprograma INNPACTO
   [IPT-2012-0213-060000]; Comunidad de Madrid [BIPEDD2-CM-S2010/BMD-2457];
   KU Leuven [GOA 10/14, PF 10/18]; FWO [G-0528.12N]; Center for Cancer
   Research, the Intramural Program of the National Cancer Institute, NIH
   [Z01-BC 007333]
FX The Spanish MICINN/MINECO (Project: SAF 2012-39760-C02-01, co-financed
   by the FEDER programme); Plan Nacional de Cooperacion Pablico-Privada.
   Subprograma INNPACTO (IPT-2012-0213-060000, co-financed by the FEDER
   programme) and the Comunidad de Madrid (BIPEDD2-CM-S2010/BMD-2457) are
   acknowledged for financial support. The Spanish MICINN/MINECCO is also
   acknowledged for a grant to E. Rivero-Buceta. We thank Leentje Persoons,
   Frieda De Meyer, Leen Ingels, Stijn Delmotte, Katrien Geerts, and Inge
   Vliegen for excellent technical assistance. Financial support of KU
   Leuven (GOA 10/14; PF 10/18) and the FWO (G-0528.12N) was provided for
   the antiviral experiments. The integrase studies were supported by the
   Center for Cancer Research, the Intramural Program of the National
   Cancer Institute, NIH (Z01-BC 007333).
NR 35
TC 0
Z9 0
U1 1
U2 5
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI PARIS
PA 23 RUE LINOIS, 75724 PARIS, FRANCE
SN 0223-5234
EI 1768-3254
J9 EUR J MED CHEM
JI Eur. J. Med. Chem.
PD DEC 1
PY 2015
VL 106
BP 132
EP 143
DI 10.1016/j.ejmech.2015.10.027
PG 12
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA CY2IM
UT WOS:000366232100013
PM 26540494
ER

PT J
AU Shi, F
   Cheng, J
   Wang, L
   Yap, PT
   Shen, D
AF Shi, Feng
   Cheng, Jian
   Wang, Li
   Yap, Pew-Thian
   Shen, Dinggang
TI LRTV: MR Image Super-Resolution With Low-Rank and Total Variation
   Regularizations
SO IEEE TRANSACTIONS ON MEDICAL IMAGING
LA English
DT Article
DE Image enhancement; image sampling; matrix completion; sparse learning;
   spatial resolution
ID DIFFUSION-WEIGHTED IMAGES; SPARSE REPRESENTATION; RECONSTRUCTION;
   RESOLUTION; REGISTRATION; ALGORITHMS
AB Image super-resolution (SR) aims to recover high-resolution images from their low-resolution counterparts for improving image analysis and visualization. Interpolation methods, widely used for this purpose, often result in images with blurred edges and blocking effects. More advanced methods such as total variation (TV) retain edge sharpness during image recovery. However, these methods only utilize information from local neighborhoods, neglecting useful information from remote voxels. In this paper, we propose a novel image SR method that integrates both local and global information for effective image recovery. This is achieved by, in addition to TV, low-rank regularization that enables utilization of information throughout the image. The optimization problem can be solved effectively via alternating direction method of multipliers (ADMM). Experiments on MR images of both adult and pediatric subjects demonstrate that the proposed method enhances the details in the recovered high-resolution images, and outperforms methods such as the nearest-neighbor interpolation, cubic interpolation, iterative back projection (IBP), non-local means (NLM), and TV-based up-sampling.
C1 [Shi, Feng; Cheng, Jian; Wang, Li; Yap, Pew-Thian; Shen, Dinggang] Univ N Carolina, Dept Radiol, Chapel Hill, NC 27599 USA.
   [Shi, Feng; Cheng, Jian; Wang, Li; Yap, Pew-Thian; Shen, Dinggang] Univ N Carolina, Biomed Res Imaging Ctr, Chapel Hill, NC 27599 USA.
   [Cheng, Jian] NICHHD, Sect Tissue Biophys & Biomimet, Program Pediat Imaging & Tissue Sci, NIH, Bethesda, MD 20892 USA.
   [Shen, Dinggang] Korea Univ, Dept Brain & Cognit Engn, Seoul 136713, South Korea.
RP Shen, D (reprint author), Univ N Carolina, Dept Radiol, Chapel Hill, NC 27599 USA.
EM fengshi@med.unc.edu; jian.cheng.1983@gmail.com; li_wang@med.unc.edu;
   pewthian_yap@med.unc.edu; dinggang_shen@med.unc.edu
FU National Institutes of Health [MH100217, EB006733, EB008374, EB009634,
   AG041721, AG042599, MH088520]; National Research Foundation from Korean
   government [2012-005741]
FX This work was supported in part by National Institutes of Health Grants
   MH100217, EB006733, EB008374, EB009634, AG041721, AG042599, MH088520,
   and the National Research Foundation under Grant 2012-005741 from the
   Korean government. F. Shi and J. Cheng contributed equally to this work.
NR 29
TC 2
Z9 2
U1 9
U2 24
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 0278-0062
EI 1558-254X
J9 IEEE T MED IMAGING
JI IEEE Trans. Med. Imaging
PD DEC
PY 2015
VL 34
IS 12
BP 2459
EP 2466
DI 10.1109/TMI.2015.2437894
PG 8
WC Computer Science, Interdisciplinary Applications; Engineering,
   Biomedical; Engineering, Electrical & Electronic; Imaging Science &
   Photographic Technology; Radiology, Nuclear Medicine & Medical Imaging
SC Computer Science; Engineering; Imaging Science & Photographic
   Technology; Radiology, Nuclear Medicine & Medical Imaging
GA CY0OD
UT WOS:000366104500004
PM 26641727
ER

PT J
AU Cahoon, EK
   Kitahara, CM
   Ntowe, E
   Bowen, EM
   Doody, MM
   Alexander, BH
   Lee, T
   Little, MP
   Linet, MS
   Freedman, DM
AF Cahoon, Elizabeth K.
   Kitahara, Cari M.
   Ntowe, Estelle
   Bowen, Emily M.
   Doody, Michele M.
   Alexander, Bruce H.
   Lee, Terrence
   Little, Mark P.
   Linet, Martha S.
   Freedman, D. Michal
TI Female Estrogen-Related Factors and Incidence of Basal Cell Carcinoma in
   a Nationwide US Cohort
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID NONMELANOMA SKIN-CANCER; STATES RADIOLOGIC TECHNOLOGISTS; HORMONE
   REPLACEMENT THERAPY; HEALTH-CARE SERVICES; UNITED-STATES;
   ORAL-CONTRACEPTIVES; ULTRAVIOLET-RADIATION; RISK; PHOTOSENSITIVITY;
   PREVALENCE
AB Purpose
   UV radiation exposure is the primary risk factor for basal cell carcinoma (BCC), the most common human malignancy. Although the photosensitizing properties of estrogens have been recognized for decades, few studies have examined the relationship between reproductive factors or exogenous estrogen use and BCC.
   Methods
   Using data from the US Radiologic Technologists Study, a large, nationwide, prospective cohort, we assessed the relationship between reproductive factors, exogenous estrogen use, and first primary BCC while accounting for sun exposure, personal sun sensitivity, and lifestyle factors for geographically dispersed women exposed to a wide range of ambient UV radiation.
   Results
   Elevated risk of BCC was associated with late age at natural menopause (hazard ratio [HR] for >= 55 years v 50 to 54 years, 1.50; 95% CI, 1.04 to 2.17) and any use of menopausal hormone therapy (MHT; HR, 1.16; 95% CI, 1.03 to 1.30; P for trend for duration = .001). BCC risk was most increased among women reporting natural menopause who used MHT for 10 or more years versus women who never used MHT (HR, 1.97; 95% CI, 1.35 to 2.87). Risk of BCC was not associated with age at menarche, parity, age at first birth, infertility, use of diethylstilbestrol by participant's mother, age at hysterectomy, or use of oral contraceptives.
   Conclusion
   These analyses confirm a previous finding of increased risk of BCC associated with MHT. Novel findings of increased BCC risk associated with MHT in women experiencing natural menopause and for late age at natural menopause warrant further investigation. Users of MHT may constitute an additional high-risk group in need of more frequent skin cancer screening. (C) 2015 by American Society of Clinical Oncology.
C1 [Cahoon, Elizabeth K.; Kitahara, Cari M.; Ntowe, Estelle; Bowen, Emily M.; Doody, Michele M.; Lee, Terrence; Little, Mark P.; Linet, Martha S.; Freedman, D. Michal] NCI, NIH, US Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
   [Alexander, Bruce H.] Univ Minnesota, Sch Publ Hlth, Minneapolis, MN USA.
RP Cahoon, EK (reprint author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, 9609 Med Ctr Dr,Rm 7E524, Bethesda, MD 20892 USA.
EM cahoonek@mail.nih.gov
RI Kitahara, Cari/R-8267-2016; 
OI Little, Mark/0000-0003-0980-7567
FU Intramural Research Program, Division of Cancer Epidemiology and
   Genetics, National Cancer Institute, National Institutes of Health, US
   Department of Health and Human Services, Bethesda, MD
FX Supported by the Intramural Research Program, Division of Cancer
   Epidemiology and Genetics, National Cancer Institute, National
   Institutes of Health, US Department of Health and Human Services,
   Bethesda, MD.
NR 39
TC 1
Z9 1
U1 0
U2 3
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD DEC 1
PY 2015
VL 33
IS 34
BP 4058
EP +
DI 10.1200/JCO.2015.62.0625
PG 10
WC Oncology
SC Oncology
GA CX9JE
UT WOS:000366021000014
PM 26527779
ER

PT J
AU Cheli, M
   Canepa, M
   Brunelli, C
   Bezante, GP
   Favorini, S
   Rollando, D
   Sivori, G
   Viani, E
   Finocchi, C
   Balbi, M
AF Cheli, Martino
   Canepa, Marco
   Brunelli, Claudio
   Bezante, Gian Paolo
   Favorini, Serena
   Rollando, Daniela
   Sivori, Giorgia
   Viani, Erica
   Finocchi, Cinzia
   Balbi, Manrico
TI Recurrent and Residual Shunts After Patent Foramen Ovale Closure:
   Results From a Long-Term Transcranial Doppler Study
SO JOURNAL OF INTERVENTIONAL CARDIOLOGY
LA English
DT Article
ID TO-LEFT SHUNT; PRESUMED PARADOXICAL EMBOLISM; PERCUTANEOUS CLOSURE;
   TRANSESOPHAGEAL ECHOCARDIOGRAPHY; TRANSCATHETER CLOSURE; CRYPTOGENIC
   STROKE; EVENTS; OCCLUDER; DEVICES; PFO
AB ObjectivesAssess the evolution of right-to-left shunt (RLS) after transcatheter patent foramen ovale (PFO) closure.
   BackgroundDespite the high number of interventional procedures performed worldwide, limited systematic data on the long-term abolition of RLS after percutaneous closure are available.
   MethodsAll patients treated at our Institution between February 2001 and July 2009 were included in this single center, prospective study, and were asked to repeat late contrast transcranial Doppler (cTCD). Rate of complete closure, residual RLS (i.e., a shunt that persists after closure), and recurrent RLS (i.e., a shunt that reappears after a previous negative cTCD) was assessed.
   ResultsLong-term follow-up was completed in 120 patients (56% male). RLS was still detectable 4.92.3 years (range 1.3-10.3) after the procedure in 55 patients; 20 (17%) had residual RLS and 35 (29%) had recurrent RLS. Multivariate analysis revealed that significant predictors of residual RLS included post-procedural shunt at transesophageal echocardiography (OR 3.07, 95%CI 0.97-9.7), use of a bigger device (35 vs 25mm, OR 3.85, 95%CI 1.22-12.2) and length of follow-up (OR 0.75, 95%CI 0.57-0.98), while only length of follow-up (OR 0.77, 95%CI 0.62-0.95) was associated with recurrent RLS. Neurological recurrences (1 stroke, 6 transient ischemic attacks) were equally distributed between the groups.
   ConclusionA significant number of recurrent and residual shunts may be observed by cTCD up to 5 years after PFO closure. Management of late RLSs includes periodic re-evaluation, exclusion of device-induced complications or secondary sources of RLS, and optimization of antithrombotic treatment with or without a second intervention. (J Interven Cardiol 2015;28:600-608)
C1 [Cheli, Martino; Canepa, Marco; Brunelli, Claudio; Bezante, Gian Paolo; Favorini, Serena; Rollando, Daniela; Balbi, Manrico] Univ Genoa, Dept Internal Med, Cardiol Unit, I-16126 Genoa, Italy.
   [Canepa, Marco] NIA, Longitudinal Studies Sect, Translat Gerontol Branch, NIH, Baltimore, MD USA.
   [Sivori, Giorgia; Viani, Erica; Finocchi, Cinzia] Univ Genoa, Dept Neurosci Rehabil Ophthalmol Genet & Maternal, I-16126 Genoa, Italy.
RP Cheli, M (reprint author), Univ Genoa, Dept Internal Med, Cardiol Unit, I-16126 Genoa, Italy.
EM martinocheli@gmail.com
NR 38
TC 2
Z9 2
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0896-4327
EI 1540-8183
J9 J INTERV CARDIOL
JI J. Interv. Cardiol.
PD DEC
PY 2015
VL 28
IS 6
BP 600
EP 608
DI 10.1111/joic.12255
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA CY4SI
UT WOS:000366398100011
PM 26643006
ER

PT J
AU Thompson, FE
   Kirkpatrick, SI
   Subar, AF
   Reedy, J
   Schap, TE
   Wilson, MM
   Krebs-Smith, SM
AF Thompson, Frances E.
   Kirkpatrick, Sharon I.
   Subar, Amy F.
   Reedy, Jill
   Schap, TusaRebecca E.
   Wilson, Magdalena M.
   Krebs-Smith, Susan M.
TI The National Cancer Institute's Dietary Assessment Primer: A Resource
   for Diet Research
SO JOURNAL OF THE ACADEMY OF NUTRITION AND DIETETICS
LA English
DT Article
DE Dietary assessment; Diet instrument; 24-Hour dietary recall; Food
   record; Food frequency questionnaire
ID FOOD FREQUENCY QUESTIONNAIRE; DOUBLY LABELED WATER; RECOVERY BIOMARKERS;
   MEASUREMENT ERROR; ASSESSMENT INSTRUMENTS; ENERGY; RECORDS; VALIDATION;
   POTASSIUM; VALIDITY
AB This monograph describes the National Cancer Institute's Dietary Assessment Primer, a web resource developed to help researchers choose the best available dietary assessment approach to achieve their research objective. All self-report instruments have error, but understanding the nature of that error can lead to better assessment, analysis, and interpretation of results. The Primer includes profiles of the major self-report dietary assessment instruments, including guidance on the best uses of each instrument; discussion of validation and measurement error generally and with respect to each instrument; guidance for choosing a dietary assessment approach for different research questions; and additional resources, such as a glossary, references, and overviews of specific/important issues in the field. This monograph also describes some future research needs in the field of dietary assessment.
C1 [Thompson, Frances E.; Subar, Amy F.; Reedy, Jill; Schap, TusaRebecca E.; Wilson, Magdalena M.; Krebs-Smith, Susan M.] NCI, Risk Factor Assessment Branch, Epidemiol & Genom Res Program, Div Canc Control & Populat Sci,NIH, Bethesda, MD 20892 USA.
   [Kirkpatrick, Sharon I.] Univ Waterloo, Sch Publ Hlth & Hlth Syst, Waterloo, ON N2L 3G1, Canada.
   [Schap, TusaRebecca E.] USDA, Ctr Nutr Policy & Promot, Alexandria, VA USA.
RP Thompson, FE (reprint author), NCI, Risk Factor Assessment Branch, Epidemiol & Genom Res Program, Div Canc Control & Populat Sci,NIH, 9609 Med Ctr Dr,MSC 9762, Bethesda, MD 20892 USA.
EM thompsof@mail.nih.gov
OI Kirkpatrick, Sharon/0000-0001-9896-5975
FU Intramural NIH HHS [Z99 CA999999]
NR 42
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Z9 8
U1 2
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 2212-2672
EI 2212-2680
J9 J ACAD NUTR DIET
JI J. Acad. Nutr. Diet.
PD DEC
PY 2015
VL 115
IS 12
BP 1986
EP 1995
DI 10.1016/j.jand.2015.08.016
PG 10
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA CX9DF
UT WOS:000366004400010
PM 26422452
ER

PT J
AU Essajee, S
   Vojnov, L
   Penazzato, M
   Jani, I
   Siberry, GK
   Fiscus, SA
   Markbyl, J
AF Essajee, Shaffiq
   Vojnov, Lara
   Penazzato, Martina
   Jani, Ilesh
   Siberry, George K.
   Fiscus, Susan A.
   Markbyl, Jessica
TI Reducing mortality in HIV-infected infants and achieving the 90-90-90
   target through innovative diagnosis approaches
SO JOURNAL OF THE INTERNATIONAL AIDS SOCIETY
LA English
DT Editorial Material
DE infant; HIV; diagnosis; treatment; point of care; SMS
ID POOLED ANALYSIS; SOUTH-AFRICA; COUNTRIES
AB Introduction: Despite significant gains in access to early infant diagnosis (EID) over the past decade, most HIV-exposed infants still do not get tested for HIV in the first two months of life. For those who are tested, the long turnaround time between when the sample is drawn and when the results are returned leads to a high rate of loss to follow-up, which in turn means that few infected infants start antiretroviral treatment. Consequently, there continues to be high mortality from perinatally acquired HIV, and the ambitious goals of 90% of infected children identified, 90% of identified children treated and 90% of treated children with sustained virologic suppression by 2020 seem far beyond our reach. The objective of this commentary is to review recent advances in the field of HIV diagnosis in infants and describe how these advances may overcome long-standing barriers to access to testing and treatment.
   Discussion: Several innovative approaches to EID have recently been described. These include point-of-care testing, use of SMS printers to connect the central laboratory and the health facility through a mobile phone network, expanding paediatric testing to other entry points where children access the health system and testing HIV-exposed infants at birth as a rapid way to identify in utero infection. Each of these interventions is discussed here, together with the opportunities and challenges associated with scale-up. Point-of-care testing has the potential to provide immediate results but is less cost-effective in settings where test volumes are low. Virological testing at birth has been piloted in some countries to identify those infants who need urgent treatment, but a negative test at birth does not obviate the need for additional testing at six weeks. Routine testing of infants in child health settings is a useful strategy to identify exposed and infected children whose mothers were not enrolled in programmes for the prevention of mother-to-child transmission. Facility-based SMS printers speed up the return of laboratory results and may be of value for other testing services apart from HIV infant diagnosis.
   Conclusions: New tools and strategies for HIV infant diagnosis could have a significant positive impact on the identification and retention of HIV-infected infants. In order to be most effective, national programmes should carefully consider which ideas to implement and how best to integrate novel strategies into existing systems. There is no single solution that will work everywhere. Rather, a number of approaches need to be considered and should be linked in order to achieve the greatest impact on the continuum of care from testing to treatment.
C1 [Essajee, Shaffiq; Penazzato, Martina; Markbyl, Jessica] WHO, CH-1205 Geneva, Switzerland.
   [Vojnov, Lara] Clinton Hlth Access Initiat, Boston, MA USA.
   [Jani, Ilesh] Inst Nacl Saude, Maputo, Mozambique.
   [Siberry, George K.] NIH, Bethesda, MD 20892 USA.
   [Fiscus, Susan A.] Univ N Carolina, Sch Med, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA.
RP Essajee, S (reprint author), WHO, HTM HIV TAC, D Bldg,Ave Appia 20, CH-1205 Geneva, Switzerland.
EM essajees@who.int
NR 18
TC 6
Z9 6
U1 1
U2 3
PU INT AIDS SOCIETY
PI GENEVA
PA AVENUE DE FRANCE 23, GENEVA, 1202, SWITZERLAND
SN 1758-2652
J9 J INT AIDS SOC
JI J. Int. AIDS Soc.
PD DEC
PY 2015
VL 18
SU 6
BP 14
EP 18
DI 10.7448/IAS.18.7.20299
PG 5
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA CX8QZ
UT WOS:000365970000003
PM 26639120
ER

PT J
AU Lee, S
   Hazra, R
AF Lee, Sonia
   Hazra, Rohan
TI Achieving 90-90-90 in paediatric HIV: adolescence as the touchstone for
   transition success
SO JOURNAL OF THE INTERNATIONAL AIDS SOCIETY
LA English
DT Editorial Material
DE children; adolescents; HIV; transition; guidelines
ID ADULT HEALTH-CARE; HUMAN-IMMUNODEFICIENCY-VIRUS; PERINATALLY ACQUIRED
   HIV; YOUNG-PEOPLE; INFECTED ADOLESCENTS; ANTIRETROVIRAL TREATMENT;
   POSITION PAPER; FOLLOW-UP; SERVICES; YOUTH
AB Introduction: The number of children less than 15 years estimated to be living with HIV globally approximated 3.2 million in 2013. Young people aged 15 to 24 years living with HIV approximated 4 million. The survival of these children and adolescents into adulthood poses new and urgent challenges of transition from the paediatric to adolescent to adult healthcare settings due to emerging developmental, psychosocial and comorbid issues. In order to achieve treatment targets of 90 90 90 across the continuum of care for paediatric HIV by 2020, focused efforts on the implementation of appropriate healthcare transition plans across the lifespan, with a focus on adolescence, should be prioritized.
   Discussion: Published data or empirical evidence examining implementation of transition models and association with clinical outcomes are limited. While some guidelines do exist that offer recommendations about how to promote seamless transitions, very few data are available to assess the adequacy of these guidelines and whether they are effectively adhered to in clinical care settings globally. Furthermore, paediatric and adolescent HIV infection, either acquired perinatally or behaviourally, is set apart from other chronic illnesses as a highly stigmatizing disease that disproportionately affects poor, minority and often marginalized populations. Focused efforts on adolescence as the touchstone for transition practices and policies need to be implemented.
   Conclusions: Optimal healthcare for these vulnerable populations, particularly in resource-limited settings, will require HIV-specific transitional care services and programmes that are coordinated, collaborative, integrated and, importantly, evidence-based.
C1 [Lee, Sonia; Hazra, Rohan] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Maternal & Pediat Infect Dis Branch, Bethesda, MD 20852 USA.
RP Lee, S (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Maternal & Pediat Infect Dis Branch, 6100 Execut Blvd,Room 4B11K, Bethesda, MD 20852 USA.
EM leesonia@mail.nih.gov
NR 38
TC 0
Z9 0
U1 5
U2 8
PU INT AIDS SOCIETY
PI GENEVA
PA AVENUE DE FRANCE 23, GENEVA, 1202, SWITZERLAND
SN 1758-2652
J9 J INT AIDS SOC
JI J. Int. AIDS Soc.
PD DEC
PY 2015
VL 18
SU 6
BP 68
EP 72
DI 10.7448/IAS.18.7.20257
PG 5
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA CX8QZ
UT WOS:000365970000010
ER

PT J
AU Snider, TH
   Wilhelm, CM
   Babin, MC
   Platoff, GE
   Yeung, DT
AF Snider, Thomas H.
   Wilhelm, Christina M.
   Babin, Michael C.
   Platoff, Gennady E., Jr.
   Yeung, David T.
TI Assessing the therapeutic efficacy of oxime therapies against
   percutaneous organophosphorus pesticide and nerve agent challenges in
   the Hartley guinea pig
SO JOURNAL OF TOXICOLOGICAL SCIENCES
LA English
DT Article
DE Nerve agent; Pesticide; Oxime therapy
ID HUMAN BUTYRYLCHOLINESTERASE; HUMAN ACETYLCHOLINESTERASE; REACTIVATION;
   SOMAN; CHOLINESTERASE; MECHANISM; ATROPINE; PLASMA; TABUN
AB Given the rapid onset of symptoms from intoxication by organophosphate (OP) compounds, a quick-acting, efficacious therapeutic regimen is needed. A primary component of anti-OP therapy is an oxime reactivator to rescue OP-inhibited acetylcholinesterases. Male guinea pigs, clipped of hair, received neat applications of either VR, VX, parathion, or phorate oxon (PHO) at the 85th percentile lethal dose, and, beginning with presentation of toxicosis, received the human equivalent dose therapy by intramuscular injection with two additional follow-on treatments at 3-hr intervals. Each therapy consisted of atropine free base at 0.4 mg/kg followed by one of eight candidate oximes. Lethality rates were obtained at 24 hr after VR, VX and PHO challenges, and at 48 hr after challenge with parathion. Lethality rates among symptomatic, oxime-treated groups were compared with that of positive control (OP-challenged and atropine-only treated) guinea pigs composited across the test days. Significant (p <= 0.05) protective therapy was afforded by 1,1-methylene bis(4(hydroxyimino- methyl)pyridinium) dimethanesulfonate (MMB4 DMS) against challenges of VR (p <= 0.001) and VX (p <= 0.05). Lethal effects of VX were also significantly (p <= 0.05) mitigated by treatments with oxo-[[1-[[4-(oxoazaniumylmethylidene)pyridin-1-yl] methoxymethyl]pyridin-4-ylidene]methyliazanium dichloride (obidoxime Cl-2) and 1-(((4-(aminocarbonyl) pyridinio)methoxy)methyl)-2,4-bis((hydroxyimino)methyl)pyridinium dimethanesulfonate (HLo-7 DMS). Against parathion, significant protective therapy was afforded by obidoxime dichloride (p <= 0.001) and 1,1'-propane-1,3-diylbis{4-[(E)-(hydroxyimino)methyl]pyridinium} dibromide (TM13-4, p <= 0.01). None of the oximes evaluated was therapeutically effective against PHO. Across the spectrum of OP chemicals tested, the oximes that offered the highest level of therapy were MMB4 DMS and obidoxime dichloride.
C1 [Snider, Thomas H.; Wilhelm, Christina M.; Babin, Michael C.] Battelle Mem Inst, Columbus, OH 43201 USA.
   [Platoff, Gennady E., Jr.] NIAID, NIH, Bethesda, MD 20892 USA.
   [Yeung, David T.] NINDS, NIH, Bethesda, MD 20892 USA.
RP Snider, TH (reprint author), Battelle Mem Inst, 505 King Ave,JM-7, Columbus, OH 43201 USA.
EM snidert@battelle.org
FU National Institutes of Health (NIH) Office of the Director [Y1-
   OD-0387-01]; NIH; NIAID; NINDS; DoD Defense Technical Information Center
   (DTIC) under the Chemical, Biological, Radiological & Nuclear Defense
   Information Analysis Center (CBRNIAC) program [SP0700-00-D-3180, 0687,
   832/CB-IO-OOI2]
FX This work was supported by the National Institutes of Health (NIH)
   Office of the Director through an interagency agreement (OD#: Y1-
   OD-0387-01) between the National Institute of Allergy and Infectious
   Diseases (NIAID) and Department of Defense (DoD) and prepared under the
   auspices of the NIH, NIAID, NINDS, and the DoD Defense Technical
   Information Center (DTIC) under the Chemical, Biological, Radiological &
   Nuclear Defense Information Analysis Center (CBRNIAC) program, Contract
   No. SP0700-00-D-3180, Delivery Order Number 0687, CBRNIAC Task
   832/CB-IO-OOI2.
NR 37
TC 1
Z9 1
U1 4
U2 10
PU JAPANESE SOC TOXICOLOGICAL SCIENCES
PI TOKYO
PA INTERNATIONAL MEDICAL INFORMATION CENTER, SHINANOMACHI RENGAKAN, 35
   SHINANO-MACHI, SHINJUKU-KU, TOKYO, 160-0016, JAPAN
SN 0388-1350
EI 1880-3989
J9 J TOXICOL SCI
JI J. Toxicol. Sci.
PD DEC
PY 2015
VL 40
IS 6
BP 759
EP 775
PG 17
WC Toxicology
SC Toxicology
GA CY2LF
UT WOS:000366239500010
PM 26558457
ER

PT J
AU Turo, D
   Otto, P
   Hossain, M
   Gebreab, T
   Armstrong, K
   Rosenberger, WF
   Shao, H
   Shah, JP
   Gerber, LH
   Sikdar, S
AF Turo, Diego
   Otto, Paul
   Hossain, Murad
   Gebreab, Tadesse
   Armstrong, Katherine
   Rosenberger, William F.
   Shao, Hui
   Shah, Jay P.
   Gerber, Lynn H.
   Sikdar, Siddhartha
TI Novel Use of Ultrasound Elastography to Quantify Muscle Tissue Changes
   After Dry Needling of Myofascial Trigger Points in Patients With Chronic
   Myofascial Pain
SO JOURNAL OF ULTRASOUND IN MEDICINE
LA English
DT Article
DE dry needling; musculoskeletal ultrasound; myofascial pain syndrome;
   myofascial trigger points; ultrasound elastography
ID UPPER TRAPEZIUS MUSCLE; SKELETAL-MUSCLE; MUSCULOSKELETAL PAIN;
   MANAGEMENT; TRIAL
AB Objectives-To compare a mechanical heterogeneity index derived from ultrasound vibration elastography with physical findings before and after dry-needling treatment of spontaneously painful active myofascial trigger points in the upper trapezius muscle.
   Methods-Forty-eight patients with chronic myofascial pain enrolled in a prospectiie interventional trial of 3 weekly dry-needling treatments for active myofascial trigger points. Trigger points were evaluated at baseline and at treatment completion using palpation, the pressure-pain threshold, and the mechanical heterogeneity index. Thirtypatients were reevaluated at 8 weeks. Trigger points that "responded" changed to tissue that was no longer spontaneously painful, with or without the presence of a palpable nodule. Trigger points that "resolved" changed to tissue without a palpable nodule. The mechanical heterogeneity index was defined as the proportion of the upper trapezius muscle that appeared mechanically stiffer on elastography. Statistical significance for comparisons was determined at P < .05.
   Results-Following 3 dry needle treatments, the mechanical heterogeneity index decreased significantly for the 38 myofascial trigger points (79% of 48) that responded to treatment. Among these, the baseline mechanical heterogeneity index was significantly lower for the 13 trigger points (27% of 38) that resolved, but the decrease after 3 dry needle treatments did not reach significance. The pressure-pain threshold improved significantly for both groups. At 8 weeks, the mechanical heterogeneity index decreased significantly for the 22 trigger points (73% of 30) that responded and for the 10(45% of 22) that resolved. The pressure-pain threshold improvement was significant for trigger points that responded but did not reach significance for resolved trigger points.
   Conclusions-The mechanical heterogeneity index identifies changes in muscle tissue. properties that correlate with changes in the myofascial trigger point status after dry needling.
C1 [Turo, Diego; Gebreab, Tadesse; Sikdar, Siddhartha] George Mason Univ, Dept Bioengn, Fairfax, VA 22030 USA.
   [Otto, Paul; Hossain, Murad] George Mason Univ, Dept Elect & Comp Engn, Fairfax, VA 22030 USA.
   [Rosenberger, William F.; Shao, Hui] George Mason Univ, Dept Stat, Fairfax, VA 22030 USA.
   [Armstrong, Katherine; Gerber, Lynn H.] George Mason Univ, Ctr Study Chron Illness & Disabil, Fairfax, VA 22030 USA.
   [Shah, Jay P.] NIH, Dept Rehabil Med, Bethesda, MD 20892 USA.
RP Sikdar, S (reprint author), George Mason Univ, Dept Bioengn, 4400 Univ Dr,MS 1GS, Fairfax, VA 22030 USA.
EM ssikdar@gmu.edu
FU National Institutes of Arthritis and Musculoskeletal and Skin Diseases,
   National Institutes of Health [1R01-AR057348]
FX This work was supported by grant 1R01-AR057348 from the National
   Institutes of Arthritis and Musculoskeletal and Skin Diseases, National
   Institutes of Health, and was presented in part at the 2014 Ultrasonic
   Imaging and Tissue Characterization Symposium; June 9-11,2014;
   Arlington, Virginia.
NR 27
TC 3
Z9 3
U1 2
U2 9
PU AMER INST ULTRASOUND MEDICINE
PI LAUREL
PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906
   USA
SN 0278-4297
EI 1550-9613
J9 J ULTRAS MED
JI J. Ultrasound Med.
PD DEC
PY 2015
VL 34
IS 12
BP 2149
EP 2161
DI 10.7863/ultra.14.08033
PG 13
WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
GA CY0CB
UT WOS:000366072700004
PM 26491094
ER

PT J
AU Prasad, V
   Vandross, A
AF Prasad, Vinay
   Vandross, Andrae
TI Characteristics of Exceptional or Super Responders to Cancer Drugs
SO MAYO CLINIC PROCEEDINGS
LA English
DT Article
ID ANAPLASTIC THYROID-CARCINOMA; PHASE-I; SOLID TUMORS; EVEROLIMUS;
   INHIBITOR; THERAPY; TRIAL; PATIENT; ACTIVATION; REMISSION
AB Objective: To summarize case reports of exceptional and super responders already published in the biomedical literature.
   Patients and Methods: We searched for published case reports or abstracts of exceptional or super responders to a cancer drug using PubMed and Google Scholar search engines. Pooling such reports is widely considered a promising research strategy and the subject of several ongoing investigations, including the National Cancer Institute's Exceptional Responders Initiative. All articles were read in full, including relevant references. We extracted clinical characteristics of exceptional or super responders, including age, tumor type, drug, genetic mutations, depth of response, duration of response, number of previous lines of therapy, duration of response to a previous line of therapy, and the number of patients treated similarly to identify the exceptional case. This study was performed between March 1, 2015, and April 30, 2015.
   Results: Among 489 articles, 32 exceptional responders were identified. The most common malignancies described were renal cell cancer (5 of 32 [16%]) and urothelial carcinoma (4 of 32 [13%]). The use of targeted agents was common in these cases (26 of 32 [81%]), particularly inhibitors of the mTOR pathway (16 of 32 [50%]). The median duration of response among responders was 17.5 months, and 59% (19 of 32) of the patients were last known to be alive with continuing response or stable disease. Notably, 46% (12 of 26) of the patients had received 2 or more previous lines of therapy and 6 of the 32 cases (19%) did not report this information. Few authors report the number of patients treated similarly to observe the super response (12 of 32 [38%]).
   Conclusion: Exceptional or super responders to cancer drugs have been described in the literature; however, there is incompleteness in the reporting of relevant data that may help clarify whether such responses are secondary to treatment or reflect underlying biology. (C) 2015 Mayo Foundation for Medical Education and Research
C1 [Prasad, Vinay] Oregon Hlth & Sci Univ, Dept Publ Hlth & Prevent Med, Knight Canc Inst, Div Hematol Oncol, Portland, OR 97201 USA.
   [Vandross, Andrae] Univ Calif Los Angeles, Div Med Oncol, Los Angeles, CA USA.
RP Prasad, V (reprint author), NCI, Div Med Oncol, NIH, 10 Ctr Dr 10-12N226, Bethesda, MD 20892 USA.
EM vinayak.k.prasad@gmail.com
NR 51
TC 10
Z9 10
U1 0
U2 1
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 DEC
PY 2015
VL 90
IS 12
BP 1639
EP 1649
DI 10.1016/j.mayocp.2015.08.017
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA CX9TC
UT WOS:000366047500009
PM 26546106
ER

PT J
AU Zhang, T
   Xu, Y
   Liu, YF
   Ye, YH
AF Zhang, Ting
   Xu, Yue
   Liu, Yanfen
   Ye, Yihong
TI gp78 functions downstream of Hrd1 to promote degradation of misfolded
   proteins of the endoplasmic reticulum
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID UBIQUITIN LIGASE GP78; ER-ASSOCIATED DEGRADATION; HMG COA REDUCTASE;
   QUALITY-CONTROL; RETRO-TRANSLOCATION; CONJUGATING ENZYME; MEMBRANE;
   DISLOCATION; ATPASE; RETROTRANSLOCATION
AB Eukaryotic cells eliminate misfolded proteins from the endoplasmic reticulum (ER) via a conserved process termed ER-associated degradation (ERAD). Central regulators of the ERAD system are membrane-bound ubiquitin ligases, which are thought to channel misfolded proteins through the ER membrane during retrotranslocation. Hrd1 and gp78 are mammalian ubiquitin ligases homologous to Hrd1p, an ubiquitin ligase essential for ERAD in Saccharomyces cerevisiae. However, the functional relevance of these proteins to Hrd1p is unclear. In this paper, we characterize the gp78-containing ubiquitin ligase complex and define its functional interplay with Hrd1 using biochemical and recently developed CRISPR-based genetic tools. Our data show that transient inactivation of the gp78 complex by short hairpin RNA-mediated gene silencing causes significant stabilization of both luminal and membrane ERAD substrates, but unlike Hrd1, which plays an essential role in retrotranslocation and ubiquitination of these ERAD substrates, knockdown of gp78 does not affect either of these processes. Instead, gp78 appears to act downstream of Hrd1 to promote ERAD via cooperation with the BAG6 chaperone complex. We conclude that the Hrd1 complex forms an essential retrotranslocation module that is evolutionarily conserved, but the mammalian ERAD system uses additional ubiquitin ligases to assist Hrd1 during retrotranslocation.
C1 [Zhang, Ting; Xu, Yue; Liu, Yanfen; Ye, Yihong] NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Ye, YH (reprint author), NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM yihongy@mail.nih.gov
FU Intramural Research Program of the National Institute of Diabetes,
   Digestive and Kidney Diseases
FX We thank members of the Ye lab for discussions and suggestions and Nia
   Soetandyo for creating the pCMV-MHC1-147-FLAG-S11 construct. This
   research was supported by the Intramural Research Program of the
   National Institute of Diabetes, Digestive and Kidney Diseases.
NR 53
TC 8
Z9 8
U1 0
U2 6
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC 1
PY 2015
VL 26
IS 24
BP 4438
EP 4450
DI 10.1091/mbc.E15-06-0354
PG 13
WC Cell Biology
SC Cell Biology
GA CY3RE
UT WOS:000366326500014
PM 26424800
ER

PT J
AU Binukumar, BK
   Shukla, V
   Amin, ND
   Grant, P
   Bhaskar, M
   Skuntz, S
   Steiner, J
   Pant, HC
AF Binukumar, B. K.
   Shukla, Varsha
   Amin, Niranjana D.
   Grant, Philip
   Bhaskar, M.
   Skuntz, Susan
   Steiner, Joseph
   Pant, Harish C.
TI Peptide TFP5/TP5 derived from Cdk5 activator P35 provides
   neuroprotection in the MPTP model of Parkinson's disease
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID CYCLIN-DEPENDENT KINASE-5; NIGROSTRIATAL DOPAMINERGIC-NEURONS;
   ALZHEIMERS-DISEASE; MOUSE MODEL; MICROGLIAL ACTIVATION; TREATED MICE;
   CDK5-MEDIATED PHOSPHORYLATION; MITOCHONDRIAL DYSFUNCTION; TAU
   HYPERPHOSPHORYLATION; OXIDATIVE STRESS
AB Parkinson's disease (PD) is a chronic neurodegenerative disorder characterized by the loss of dopamine neurons in the substantia nigra, decreased striatal dopamine levels, and consequent extrapyramidal motor dysfunction. Recent evidence indicates that cyclin-dependent kinase 5 (Cdk5) is inappropriately activated in several neurodegenerative conditions, including PD. To date, strategies to specifically inhibit Cdk5 hyperactivity have not been successful without affecting normal Cdk5 activity. Previously we reported that TFP5 peptide has neuroprotective effects in animal models of Alzheimer's disease. Here we show that TFP5/TP5 selective inhibition of Cdk5/p25 hyperactivation in vivo and in vitro rescues nigrostriatal dopaminergic neurodegeneration induced by 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine (MPTP/MPP+) in a mouse model of PD. TP5 peptide treatment also blocked dopamine depletion in the striatum and improved gait dysfunction after MPTP administration. The neuroprotective effect of TFP5/TP5 peptide is also associated with marked reduction in neuroinflammation and apoptosis. Here we show selective inhibition of Cdk5/p25 hyperactivation by TFP5/TP5 peptide, which identifies the kinase as a potential therapeutic target to reduce neurodegeneration in Parkinson's disease.
C1 [Binukumar, B. K.; Shukla, Varsha; Amin, Niranjana D.; Grant, Philip; Bhaskar, M.; Skuntz, Susan; Steiner, Joseph; Pant, Harish C.] NINDS, NIH, Bethesda, MD 20892 USA.
RP Pant, HC (reprint author), NINDS, NIH, Bethesda, MD 20892 USA.
EM panth@ninds.nih.gov
FU Intramural Research Program of the National Institutes of Health;
   Intramural Research Program of the National Institute of Neurological
   Disorders and Stroke
FX This research was supported by the Intramural Research Programs of the
   National Institutes of Health, National Institute of Neurological
   Disorders and Stroke.
NR 67
TC 4
Z9 5
U1 1
U2 4
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC 1
PY 2015
VL 26
IS 24
BP 4478
EP 4491
DI 10.1091/mbc.E15-06-0415
PG 14
WC Cell Biology
SC Cell Biology
GA CY3RE
UT WOS:000366326500017
PM 26399293
ER

PT J
AU Mazor, R
   Zhang, JL
   Xiang, LM
   Addissie, S
   Awuah, P
   Beers, R
   Hassan, R
   Pastan, I
AF Mazor, Ronit
   Zhang, Jingli
   Xiang, Laiman
   Addissie, Selamawit
   Awuah, Prince
   Beers, Richard
   Hassan, Raffit
   Pastan, Ira
TI Recombinant Immunotoxin with T-cell Epitope Mutations That Greatly
   Reduce Immunogenicity for Treatment of Mesothelin-Expressing Tumors
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID PHASE-I TRIAL; ANTITUMOR-ACTIVITY; OVARIAN-CANCER; IDENTIFICATION;
   EFFICACY; SS1P; DETERMINANTS; ELIMINATION; INFUSION; RG7787
AB SS1P is a recombinant immunotoxin (RIT) that targets mesothelin. It consists of an antimesothelin Fv fused to a portion of Pseudomonas exotoxin A. In clinical studies, it has produced dramatic responses in patients with advanced mesothelioma, when combined with immunosuppressive therapy so that several treatment cycles could be given. Otherwise its activity is limited by its immunogenicity. In this work, we describe the development and characterization of LMB-T20, a highly potent RIT targeted at mesothelin-expressing cancers with low immunogenicity due to removal of its eight T-cell epitopes. LMB-T20 was more active than SS1P when tested on four different mesothelin-expressing cell lines as well as on cells obtained from patients with mesothelioma. It also has potent antitumor activity in mice, and has reduced immunogenicity as measured by cytokine secretion assays. In conclusion, LMB-T20 is a favorable candidate for evaluation in clinical trials due to its reduced immunogenicity and excellent activity. (C)2015 AACR.
C1 [Mazor, Ronit; Zhang, Jingli; Xiang, Laiman; Addissie, Selamawit; Awuah, Prince; Beers, Richard; Hassan, Raffit; Pastan, Ira] NCI, Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Pastan, I (reprint author), NCI, NIH, 37 Convent Dr,Room 5106, Bethesda, MD 20892 USA.
EM pastani@mail.nih.gov
FU Intramural Research Program of the NIH, National Cancer Institute,
   Center for Cancer Research [2791]; Roche Pharmaceuticals
FX This research was supported by the Intramural Research Program of the
   NIH, National Cancer Institute, Center for Cancer Research and with a
   Cooperative Research and Development Agreement (#2791) with Roche
   Pharmaceuticals.
NR 30
TC 4
Z9 4
U1 0
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
EI 1538-8514
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD DEC
PY 2015
VL 14
IS 12
BP 2789
EP 2796
DI 10.1158/1535-7163.MCT-15-0532
PG 8
WC Oncology
SC Oncology
GA CX9VZ
UT WOS:000366055100012
PM 26443804
ER

PT J
AU McMillin, M
   Frampton, G
   Quinn, M
   Divan, A
   Grant, S
   Patel, N
   Newell-Rogers, K
   DeMorrow, S
AF McMillin, Matthew
   Frampton, Gabriel
   Quinn, Matthew
   Divan, Ali
   Grant, Stephanie
   Patel, Nisha
   Newell-Rogers, Karen
   DeMorrow, Sharon
TI Suppression of the HPA Axis During Cholestasis Can Be Attributed to
   Hypothalamic Bile Acid Signaling
SO MOLECULAR ENDOCRINOLOGY
LA English
DT Article
ID PITUITARY-ADRENAL AXIS; BILIARY OBSTRUCTION; CHOLANGIOCARCINOMA GROWTH;
   HEPATIC-ENCEPHALOPATHY; DUCT LIGATION; SEPTIC SHOCK; RATS; LIVER;
   INSUFFICIENCY; ACTIVATION
AB Suppression of the hypothalamic-pituitary-adrenal (HPA) axis has been shown to occur during cholestatic liver injury. Furthermore, we have demonstrated that in a model of cholestasis, serum bile acids gain entry into the brain via a leaky blood brain barrier and that hypothalamic bile acid content is increased. Therefore, the aim of the current study was to determine the effects of bile acid signaling on the HPA axis. The data presented show that HPA axis suppression during cholestatic liver injury, specifically circulating corticosterone levels and hypothalamic corticotropin releasing hormone (CRH) expression, can be attenuated by administration of the bile acid sequestrant cholestyramine. Secondly, treatment of hypothalamic neurons with various bile acids suppressed CRH expression and secretion in vitro. However, in vivo HPA axis suppression was only evident after the central injection of the bile acids taurocholic acid or glycochenodeoxycholic acid but not the other bile acids studied. Furthermore, we demonstrate that taurocholic acid and glycochenodeoxycholic acid are exerting their effects on hypothalamic CRH expression after their uptake through the apical sodium-dependent bile acid transporter and subsequent activation of the glucocorticoid receptor. Taken together with previous studies, our data support the hypothesis that during cholestatic liver injury, bile acids gain entry into the brain, are transported into neurons through the apical sodium-dependent bile acid transporter and can activate the glucocorticoid receptor to suppress the HPA axis. These data also lend themselves to the broader hypothesis that bile acids may act as central modulators of hypothalamic peptides that may be altered during liver disease.
C1 [McMillin, Matthew; Frampton, Gabriel; Grant, Stephanie; DeMorrow, Sharon] Texas A&M Hlth Sci Ctr, Coll Med, Cent Texas Vet Hlth Care Syst 76504, Temple, TX 76508 USA.
   [McMillin, Matthew; Frampton, Gabriel; Grant, Stephanie; Patel, Nisha; DeMorrow, Sharon] Texas A&M Hlth Sci Ctr, Coll Med, Dept Internal Med, Temple, TX 76508 USA.
   [McMillin, Matthew; Frampton, Gabriel; Grant, Stephanie; DeMorrow, Sharon] Digest Dis Res Ctr, Temple, TX 76508 USA.
   [Divan, Ali; Newell-Rogers, Karen] Baylor Scott & White Hlth, Dept Surg, Temple, TX 76508 USA.
   [Quinn, Matthew] NIEHS, Signal Transduct Lab, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
RP DeMorrow, S (reprint author), Baylor Scott & White Hlth, Dept Internal Med, Bldg 205,1901 South 1st St, Temple, TX 76504 USA.
EM demorrow@medicine.tamhsc.edu
OI McMillin, Matthew/0000-0002-5980-0921
FU National Institutes of Health [DK082435, DK078532]; United States
   Department of Veterans Affairs Merit Award from the United States
   Department of Veterans Affairs Biomedical Laboratory Research and
   Development Service [BX002638-01]; Texas A&M Health Science Center
   College of Medicine summer research program scholarship
FX This work was supported by a National Institutes of Health R01 Award
   DK082435, a National Institutes of Health K01 Award DK078532, a United
   States Department of Veterans Affairs Merit Award BX002638-01 from the
   United States Department of Veterans Affairs Biomedical Laboratory
   Research and Development Service (to S.D.) and by a Texas A&M Health
   Science Center College of Medicine summer research program scholarship
   (to N.P.).
NR 43
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PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0888-8809
J9 MOL ENDOCRINOL
JI Mol. Endocrinol.
PD DEC
PY 2015
VL 29
IS 12
BP 1720
EP 1730
DI 10.1210/me.2015-1087
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CY6IC
UT WOS:000366511400006
PM 26431088
ER

PT J
AU Kavarthapu, R
   Dufau, ML
AF Kavarthapu, Raghuveer
   Dufau, Maria L.
TI Germ Cell Nuclear Factor (GCNF/RTR) Regulates Transcription of
   Gonadotropin-Regulated Testicular RNA Helicase (GRTH/DDX25) in
   Testicular Germ Cells-The Androgen Connection
SO MOLECULAR ENDOCRINOLOGY
LA English
DT Article
ID ACTIVATED PROTEIN-KINASE; RAT SEMINIFEROUS TUBULES; ORPHAN RECEPTOR;
   SERTOLI-CELLS; RESPONSE ELEMENT; RESEARCH RESOURCE; GENE-EXPRESSION;
   KNOCKOUT MICE; DNA-BINDING; SPERMATOGENESIS
AB Gonadotropin-regulated testicular RNA helicase (GRTH) (GRTH/DDX25), is a testis-specific protein essential for completion of spermatogenesis. Transgenic mice carrying 5'-flanking regions of the GRTH gene/green fluorescence protein (GFP) reporter revealed a region (-6.4/-3.6 kb) which directs its expression in germ cells (GCs) via androgen action. This study identifies a functional cis-binding element on the GRTH gene for GC nuclear factor (GCNF) (GCNF/RTR) required to regulate GRTH gene expression in postmeiotic testis GCs and explore the action of androgen on GCNF and GRTH transcription/expression. GCNF expression decreased in mice testis upon flutamide (androgen receptor antagonist) treatment, indicating the presence of an androgen/GCNF network to direct GRTH expression in GC. Binding studies and chromatin immunoprecipitation demonstrated specific association of GCNF to a consensus half-site (-5270/-5252) of the GRTH gene in both round spermatids and spermatocytes, which was abolished by flutamide treatment in round spermatids. Moreover, flutamide treatment of wild-type mice caused selective reduction of GCNF and GRTH in round spermatids. GCNF knock-down in seminiferous tubules from GRTH-transgenic mice (dark zone, round spermatid rich) caused decreased GFP expression. Exposure of tubules to flutamide caused decrease in GCNF and GFP expression, whereas androgen exposure induced significant increase. Our studies provide evidence for actions of androgen on GCNF cell-specific regulation of GRTH expression in GC. GRTH associates with GCNF mRNA, its absence caused increase on GCNF expression and mRNA stability indicative of a negative autocrine regulation of GCNF by GRTH. These in vivo/in vitro models link androgen actions to GC through GCNF, as regulated transfactor that controls transcription/expression of GRTH.
C1 [Kavarthapu, Raghuveer; Dufau, Maria L.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Mol Endocrinol, Program Dev Endocrinol & Genet, NIH, Bethesda, MD 20892 USA.
RP Dufau, ML (reprint author), NICHD, Sect Mol Endocrinol, NIH, Bldg 49,Rm 6A28, Bethesda, MD 20892 USA.
EM dufaum@mail.nih.gov
OI kavarthapu, raghuveer/0000-0002-2198-2029
FU National Institutes of Health Intramural Research Program through the
   Eunice Kennedy Shriver National Institute of Child Health and Human
   Development
FX This work was supported by the National Institutes of Health Intramural
   Research Program through the Eunice Kennedy Shriver National Institute
   of Child Health and Human Development. R.K. was recipient of a
   Presidential Poster Award.
NR 50
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U1 0
U2 3
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0888-8809
J9 MOL ENDOCRINOL
JI Mol. Endocrinol.
PD DEC
PY 2015
VL 29
IS 12
BP 1792
EP 1804
DI 10.1210/me.2015-1198
PG 13
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CY6IC
UT WOS:000366511400012
PM 26484580
ER

PT J
AU Arafeh, R
   Qutob, N
   Emmanuel, R
   Keren-Paz, A
   Madore, J
   Elkahloun, A
   Wilmott, JS
   Gartner, JJ
   Di Pizio, A
   Winograd-Katz, S
   Sindiri, S
   Rotkopf, R
   Dutton-Regester, K
   Johansson, P
   Pritchard, AL
   Waddell, N
   Hill, VK
   Lin, JC
   Hevroni, Y
   Rosenberg, SA
   Khan, J
   Ben-Dor, S
   Niv, MY
   Ulitsky, I
   Mann, GJ
   Scolyer, RA
   Hayward, NK
   Samuels, Y
AF Arafeh, Rand
   Qutob, Nouar
   Emmanuel, Rafi
   Keren-Paz, Alona
   Madore, Jason
   Elkahloun, Abdel
   Wilmott, James S.
   Gartner, Jared J.
   Di Pizio, Antonella
   Winograd-Katz, Sabina
   Sindiri, Sivasish
   Rotkopf, Ron
   Dutton-Regester, Ken
   Johansson, Peter
   Pritchard, Antonia L.
   Waddell, Nicola
   Hill, Victoria K.
   Lin, Jimmy C.
   Hevroni, Yael
   Rosenberg, Steven A.
   Khan, Javed
   Ben-Dor, Shifra
   Niv, Masha Y.
   Ulitsky, Igor
   Mann, Graham J.
   Scolyer, Richard A.
   Hayward, Nicholas K.
   Samuels, Yardena
TI Recurrent inactivating RASA2 mutations in melanoma
SO NATURE GENETICS
LA English
DT Article
ID METASTATIC MELANOMA; CANCER; BRAF; INTEGRATION; MUTANTS; REVEALS
AB Analysis of 501 melanoma exomes identified RASA2, encoding a RasGAP, as a tumor-suppressor gene mutated in 5% of melanomas. Recurrent loss-of-function mutations in RASA2 were found to increase RAS activation, melanoma cell growth and migration. RASA2 expression was lost in >= 30% of human melanomas and was associated with reduced patient survival. These findings identify RASA2 inactivation as a melanoma driver and highlight the importance of RasGAPs in cancer.
C1 [Arafeh, Rand; Qutob, Nouar; Emmanuel, Rafi; Keren-Paz, Alona; Winograd-Katz, Sabina; Hevroni, Yael; Samuels, Yardena] Weizmann Inst Sci, Mol Cell Biol Dept, IL-76100 Rehovot, Israel.
   [Madore, Jason; Wilmott, James S.; Mann, Graham J.; Scolyer, Richard A.] Melanoma Inst Australia, Sydney, NSW, Australia.
   [Madore, Jason; Wilmott, James S.; Mann, Graham J.; Scolyer, Richard A.] Univ Sydney, Sydney Med Sch, Discipline Pathol, Sydney, NSW 2006, Australia.
   [Elkahloun, Abdel; Hill, Victoria K.] NHGRI, US NIH, Bethesda, MD 20892 USA.
   [Gartner, Jared J.; Sindiri, Sivasish; Lin, Jimmy C.; Rosenberg, Steven A.; Khan, Javed] NCI, US NIH, Bethesda, MD 20892 USA.
   [Di Pizio, Antonella; Niv, Masha Y.] Hebrew Univ Jerusalem, Inst Biochem Food Sci & Nutr, IL-76100 Rehovot, Israel.
   [Rotkopf, Ron; Ben-Dor, Shifra] Weizmann Inst Sci, Dept Biol Serv, IL-76100 Rehovot, Israel.
   [Dutton-Regester, Ken; Johansson, Peter; Pritchard, Antonia L.; Waddell, Nicola; Hayward, Nicholas K.] QIMR Berghofer Med Res Inst, Brisbane, Qld, Australia.
   [Ulitsky, Igor] Weizmann Inst Sci, Dept Regulat Biol, IL-76100 Rehovot, Israel.
   [Mann, Graham J.] Univ Sydney, Westmead Millennium Inst Med Res, Ctr Canc Res, Sydney, NSW 2006, Australia.
   [Scolyer, Richard A.] Royal Prince Alfred Hosp, Tissue Pathol & Diagnost Oncol, Sydney, NSW, Australia.
RP Samuels, Y (reprint author), Weizmann Inst Sci, Mol Cell Biol Dept, IL-76100 Rehovot, Israel.
EM yardena.samuels@weizmann.ac.il
RI Johansson, Peter/K-1053-2014; hayward, nicholas/C-1367-2015; Waddell,
   Nic/H-4929-2015; 
OI sindiri, sivasish/0000-0003-2516-969X; Scolyer,
   Richard/0000-0002-8991-0013; Johansson, Peter/0000-0001-7015-5452;
   hayward, nicholas/0000-0003-4760-1033; Ulitsky,
   Igor/0000-0003-0555-6561; Pritchard, Antonia/0000-0001-5336-0454
FU Intramural Research Programs of the National Human Genome Research
   Institute; National Cancer Institute; Australian National Health and
   Medical Research Council (NHMRC); Cancer Institute NSW; Israel Science
   Foundation [1604/13, 877/13]; European Research Council (ERC)
   [StG-335377]; ERC under the European Union's Horizon research and
   innovation program [677645]; Henry Chanoch Krenter Institute for
   Biomedical Imaging and Genomics; estate of Alice Schwarz-Gardos; estate
   of John Hunter; Knell Family; Peter and Patricia Gruber Award; Hamburger
   Family; Rising Tide Foundation; NHMRC; Cure Cancer Australia; Melanoma
   Institute Australia
FX We thank T. Wiesel for graphical assistance. This work was supported by
   the Intramural Research Programs of the National Human Genome Research
   Institute and the National Cancer Institute, as well as by program
   grants of the Australian National Health and Medical Research Council
   (NHMRC) and Cancer Institute NSW. Y.S. is supported by the Israel
   Science Foundation through grants 1604/13 and 877/13, the European
   Research Council (ERC; StG-335377), the ERC under the European Union's
   Horizon 2020 research and innovation program (grant agreement 677645),
   the Henry Chanoch Krenter Institute for Biomedical Imaging and Genomics,
   the estate of Alice Schwarz-Gardos, the estate of John Hunter, the Knell
   Family, the Peter and Patricia Gruber Award and the Hamburger Family.
   I.U. is supported by a grant from the Rising Tide Foundation. N.K.H.,
   K.D.-R. and R.A.S. are supported by fellowships from the NHMRC. A.L.P.
   is supported by Cure Cancer Australia. Support from the Melanoma
   Institute Australia is also gratefully acknowledged. We thank the TCGA
   Research Network for generating some of the data sets.
NR 24
TC 10
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U1 2
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD DEC
PY 2015
VL 47
IS 12
BP 1408
EP +
DI 10.1038/ng.3427
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA CX6LT
UT WOS:000365813200011
PM 26502337
ER

PT J
AU Gaulton, KJ
   Ferreira, T
   Lee, Y
   Raimondo, A
   Maegi, R
   Reschen, ME
   Mahajan, A
   Locke, A
   Rayner, NW
   Robertson, N
   Scott, RA
   Prokopenko, I
   Scott, LJ
   Green, T
   Sparso, T
   Thuillier, D
   Yengo, L
   Grallert, H
   Wahl, S
   Franberg, M
   Strawbridge, RJ
   Kestler, H
   Chheda, H
   Eisele, L
   Gustafsson, S
   Steinthorsdottir, V
   Thorleifsson, G
   Qi, L
   Karssen, LC
   van Leeuwen, EM
   Willems, SM
   Li, M
   Chen, H
   Fuchsberger, C
   Kwan, P
   Ma, C
   Linderman, M
   Lu, YC
   Thomsen, SK
   Rundle, JK
   Beer, NL
   van de Bunt, M
   Chalisey, A
   Kang, HM
   Voight, BF
   Abecasis, GR
   Almgren, P
   Baldassarre, D
   Balkau, B
   Benediktsson, R
   Bluher, M
   Boeing, H
   Bonnycastle, LL
   Bottinger, EP
   Burtt, NP
   Carey, J
   Charpentier, G
   Chines, PS
   Cornelis, MC
   Couper, DJ
   Crenshaw, AT
   van Dam, RM
   Doney, ASF
   Dorkhan, M
   Edkins, S
   Eriksson, JG
   Esko, T
   Eury, E
   Fadista, J
   Flannick, J
   Fontanillas, P
   Fox, C
   Franks, PW
   Gertow, K
   Gieger, C
   Gigante, B
   Gottesman, O
   Grant, GB
   Grarup, N
   Groves, CJ
   Hassinen, M
   Have, CT
   Herder, C
   Holmen, OL
   Hreidarsson, AB
   Humphries, SE
   Hunter, DJ
   Jackson, AU
   Jonsson, A
   Jorgensen, ME
   Jorgensen, T
   Kao, WHL
   Kerrison, ND
   Kinnunen, L
   Klopp, N
   Kong, A
   Kovacs, P
   Kraft, P
   Kravic, J
   Langford, C
   Leander, K
   Liang, L
   Lichtner, P
   Lindgren, CM
   Lindholm, E
   Linneberg, A
   Liu, CT
   Lobbens, S
   Luan, J
   Lyssenko, V
   Mannisto, S
   McLeod, O
   Meyer, J
   Mihailov, E
   Mirza, G
   Muhleisen, TW
   Muller-Nurasyid, M
   Navarro, C
   Nothen, MM
   Oskolkov, NN
   Owen, KR
   Palli, D
   Pechlivanis, S
   Peltonen, L
   Perry, JRB
   Platou, CGP
   Roden, M
   Ruderfer, D
   Rybin, D
   van der Schouw, YT
   Sennblad, B
   Sigurdsson, G
   Stancakova, A
   Steinbach, G
   Storm, P
   Strauch, K
   Stringham, HM
   Sun, Q
   Thorand, B
   Tikkanen, E
   Tonjes, A
   Trakalo, J
   Tremoli, E
   Tuomi, T
   Wennauer, R
   Wiltshire, S
   Wood, AR
   Zeggini, E
   Dunham, I
   Birney, E
   Pasquali, L
   Ferrer, J
   Loos, RJF
   Dupuis, J
   Florez, JC
   Boerwinkle, E
   Pankow, JS
   van Duijn, C
   Sijbrands, E
   Meigs, JB
   Hu, FB
   Thorsteinsdottir, U
   Stefansson, K
   Lakka, TA
   Rauramaa, R
   Stumvoll, M
   Pedersen, NL
   Lind, L
   Keinanen-Kiukaanniemi, SM
   Korpi-Hyovalti, E
   Saaristo, TE
   Saltevo, J
   Kuusisto, J
   Laakso, M
   Metspalu, A
   Erbel, R
   Jocke, KH
   Moebus, S
   Ripatti, S
   Salomaa, V
   Ingelsson, E
   Boehm, BO
   Bergman, RN
   Collins, FS
   Mohlke, KL
   Koistinen, H
   Tuomilehto, J
   Hveem, K
   Njolstad, I
   Deloukas, P
   Donnelly, PJ
   Frayling, TM
   Hattersley, AT
   de Faire, U
   Hamsten, A
   Illig, T
   Peters, A
   Cauchi, S
   Sladek, R
   Froguel, P
   Hansen, T
   Pedersen, O
   Morris, AD
   Palmer, CNA
   Kathiresan, S
   Melander, O
   Nilsson, PM
   Groop, LC
   Barroso, I
   Langenberg, C
   Wareham, NJ
   O'Callaghan, CA
   Gloyn, AL
   Altshuler, D
   Boehnke, M
   Teslovich, TM
   McCarthy, MI
   Morris, AP
AF Gaulton, Kyle J.
   Ferreira, Teresa
   Lee, Yeji
   Raimondo, Anne
   Maegi, Reedik
   Reschen, Michael E.
   Mahajan, Anubha
   Locke, Adam
   Rayner, N. William
   Robertson, Neil
   Scott, Robert A.
   Prokopenko, Inga
   Scott, Laura J.
   Green, Todd
   Sparso, Thomas
   Thuillier, Dorothee
   Yengo, Loic
   Grallert, Harald
   Wahl, Simone
   Franberg, Mattias
   Strawbridge, Rona J.
   Kestler, Hans
   Chheda, Himanshu
   Eisele, Lewin
   Gustafsson, Stefan
   Steinthorsdottir, Valgerdur
   Thorleifsson, Gudmar
   Qi, Lu
   Karssen, Lennart C.
   van Leeuwen, Elisabeth M.
   Willems, Sara M.
   Li, Man
   Chen, Han
   Fuchsberger, Christian
   Kwan, Phoenix
   Ma, Clement
   Linderman, Michael
   Lu, Yingchang
   Thomsen, Soren K.
   Rundle, Jana K.
   Beer, Nicola L.
   van de Bunt, Martijn
   Chalisey, Anil
   Kang, Hyun Min
   Voight, Benjamin F.
   Abecasis, Goncalo R.
   Almgren, Peter
   Baldassarre, Damiano
   Balkau, Beverley
   Benediktsson, Rafn
   Blueher, Matthias
   Boeing, Heiner
   Bonnycastle, Lori L.
   Bottinger, Erwin P.
   Burtt, Noel P.
   Carey, Jason
   Charpentier, Guillaume
   Chines, Peter S.
   Cornelis, Marilyn C.
   Couper, David J.
   Crenshaw, Andrew T.
   van Dam, Rob M.
   Doney, Alex S. F.
   Dorkhan, Mozhgan
   Edkins, Sarah
   Eriksson, Johan G.
   Esko, Tonu
   Eury, Elodie
   Fadista, Joao
   Flannick, Jason
   Fontanillas, Pierre
   Fox, Caroline
   Franks, Paul W.
   Gertow, Karl
   Gieger, Christian
   Gigante, Bruna
   Gottesman, Omri
   Grant, George B.
   Grarup, Niels
   Groves, Christopher J.
   Hassinen, Maija
   Have, Christian T.
   Herder, Christian
   Holmen, Oddgeir L.
   Hreidarsson, Astradur B.
   Humphries, Steve E.
   Hunter, David J.
   Jackson, Anne U.
   Jonsson, Anna
   Jorgensen, Marit E.
   Jorgensen, Torben
   Kao, Wen-Hong L.
   Kerrison, Nicola D.
   Kinnunen, Leena
   Klopp, Norman
   Kong, Augustine
   Kovacs, Peter
   Kraft, Peter
   Kravic, Jasmina
   Langford, Cordelia
   Leander, Karin
   Liang, Liming
   Lichtner, Peter
   Lindgren, Cecilia M.
   Lindholm, Eero
   Linneberg, Allan
   Liu, Ching-Ti
   Lobbens, Stephane
   Luan, Jian'an
   Lyssenko, Valeriya
   Mannisto, Satu
   McLeod, Olga
   Meyer, Julia
   Mihailov, Evelin
   Mirza, Ghazala
   Muehleisen, Thomas W.
   Mueller-Nurasyid, Martina
   Navarro, Carmen
   Noethen, Markus M.
   Oskolkov, Nikolay N.
   Owen, Katharine R.
   Palli, Domenico
   Pechlivanis, Sonali
   Peltonen, Leena
   Perry, John R. B.
   Platou, Carl G. P.
   Roden, Michael
   Ruderfer, Douglas
   Rybin, Denis
   van der Schouw, Yvonne T.
   Sennblad, Bengt
   Sigurdsson, Gunnar
   Stancakova, Alena
   Steinbach, Gerald
   Storm, Petter
   Strauch, Konstantin
   Stringham, Heather M.
   Sun, Qi
   Thorand, Barbara
   Tikkanen, Emmi
   Tonjes, Anke
   Trakalo, Joseph
   Tremoli, Elena
   Tuomi, Tiinamaija
   Wennauer, Roman
   Wiltshire, Steven
   Wood, Andrew R.
   Zeggini, Eleftheria
   Dunham, Ian
   Birney, Ewan
   Pasquali, Lorenzo
   Ferrer, Jorge
   Loos, Ruth J. F.
   Dupuis, Josee
   Florez, Jose C.
   Boerwinkle, Eric
   Pankow, James S.
   van Duijn, Cornelia
   Sijbrands, Eric
   Meigs, James B.
   Hu, Frank B.
   Thorsteinsdottir, Unnur
   Stefansson, Kari
   Lakka, Timo A.
   Rauramaa, Rainer
   Stumvoll, Michael
   Pedersen, Nancy L.
   Lind, Lars
   Keinanen-Kiukaanniemi, Sirkka M.
   Korpi-Hyovalti, Eeva
   Saaristo, Timo E.
   Saltevo, Juha
   Kuusisto, Johanna
   Laakso, Markku
   Metspalu, Andres
   Erbel, Raimund
   Joecke, Karl-Heinz
   Moebus, Susanne
   Ripatti, Samuli
   Salomaa, Veikko
   Ingelsson, Erik
   Boehm, Bernhard O.
   Bergman, Richard N.
   Collins, Francis S.
   Mohlke, Karen L.
   Koistinen, Heikki
   Tuomilehto, Jaakko
   Hveem, Kristian
   Njolstad, Inger
   Deloukas, Panagiotis
   Donnelly, Peter J.
   Frayling, Timothy M.
   Hattersley, Andrew T.
   de Faire, Ulf
   Hamsten, Anders
   Illig, Thomas
   Peters, Annette
   Cauchi, Stephane
   Sladek, Rob
   Froguel, Philippe
   Hansen, Torben
   Pedersen, Oluf
   Morris, Andrew D.
   Palmer, Collin N. A.
   Kathiresan, Sekar
   Melander, Olle
   Nilsson, Peter M.
   Groop, Leif C.
   Barroso, Ines
   Langenberg, Claudia
   Wareham, Nicholas J.
   O'Callaghan, Christopher A.
   Gloyn, Anna L.
   Altshuler, David
   Boehnke, Michael
   Teslovich, Tanya M.
   McCarthy, Mark I.
   Morris, Andrew P.
CA DIAbet Genetics Replication Meta-A
TI Genetic fine mapping and genomic annotation defines causal mechanisms at
   type 2 diabetes susceptibility loci
SO NATURE GENETICS
LA English
DT Article
ID LARGE-SCALE ASSOCIATION; HUMAN PANCREATIC-ISLETS; WIDE ASSOCIATION;
   BETA-CELL; TRANSCRIPTION FACTORS; GLUCOSE-HOMEOSTASIS; GENOTYPE
   IMPUTATION; INSULIN-SECRETION; COMMON VARIANTS; GLYCEMIC TRAITS
AB We performed fine mapping of 39 established type 2 diabetes (T2D) loci in 27,206 cases and 57,574 controls of European ancestry. We identified 49 distinct association signals at these loci, including five mapping in or near KCNQ1. 'Credible sets' of the variants most likely to drive each distinct signal mapped predominantly to noncoding sequence, implying that association with T2D is mediated through gene regulation. Credible set variants were enriched for overlap with FOXA2 chromatin immunoprecipitation binding sites in human islet and liver cells, including at MTNR1B, where fine mapping implicated rs10830963 as driving T2D association. We confirmed that the T2D risk allele for this SNP increases FOXA2-bound enhancer activity in islet- and liver-derived cells. We observed allele-specific differences in NEUROD1 binding in islet-derived cells, consistent with evidence that the T2D risk allele increases islet MTNR1B expression. Our study demonstrates how integration of genetic and genomic information can define molecular mechanisms through which variants underlying association signals exert their effects on disease.
C1 [Gaulton, Kyle J.; Ferreira, Teresa; Mahajan, Anubha; Rayner, N. William; Robertson, Neil; Beer, Nicola L.; van de Bunt, Martijn; Lindgren, Cecilia M.; Steinbach, Gerald; Trakalo, Joseph; Wiltshire, Steven; Ingelsson, Erik; Donnelly, Peter J.; Gloyn, Anna L.; McCarthy, Mark I.; Morris, Andrew P.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
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   [Erbel, Raimund] Univ Duisdurg Essen, Univ Hosp Essen, West German Heart Ctr, Clin Cardiol, Essen, Germany.
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   [Boehm, Bernhard O.] Univ Med Ctr Ulm, Dept Internal Med, Div Endocrinol & Diabet, Ulm, Germany.
   [Boehm, Bernhard O.] Univ London Imperial Coll Sci Technol & Med, Lee Kong Chian Sch Med, London SW7 2AZ, England.
   [Boehm, Bernhard O.] Nanyang Technol Univ, Singapore 639798, Singapore.
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   [Koistinen, Heikki] Univ Helsinki, Cent Hosp, Dept Med, Div Endocrinol, Helsinki, Finland.
   [Koistinen, Heikki] Minerva Fdn, Helsinki, Finland.
   [Tuomilehto, Jaakko] Hosp Univ La Paz, Inst Invest Sanitaria, Madrid, Spain.
   [Tuomilehto, Jaakko] Danube Univ Krems, Ctr Vasc Prevent, Krems, Austria.
   [Tuomilehto, Jaakko] King Abdulaziz Univ, Diabet Res Grp, Jeddah 21413, Saudi Arabia.
   [Njolstad, Inger] Univ Tromso, Fac Hlth Sci, Dept Community Med, Tromso, Norway.
   [Deloukas, Panagiotis] Queen Mary Univ London, Barts & London Sch Med & Dent, William Harvey Res Inst, London, England.
   [Donnelly, Peter J.] Univ Oxford, Dept Stat, Oxford OX1 3TG, England.
   [Hattersley, Andrew T.] Univ Exeter, Sch Med, Inst Biomed & Clin Sci, Exeter, Devon, England.
   [Sladek, Rob] Ctr Hosp Univ Montreal, Ctr Rech, Montreal Diabet Res Ctr, Montreal, PQ, Canada.
   [Sladek, Rob] McGill Univ, Montreal, PQ, Canada.
   [Sladek, Rob] Genome Quebec Innovat Ctr, Montreal, PQ, Canada.
   [Hansen, Torben] Univ Southern Denmark, Fac Hlth Sci, Odense, Denmark.
   [Morris, Andrew D.] Univ Edinburgh, Usher Inst Populat Hlth Sci & Informat, Edinburgh, Midlothian, Scotland.
   [Kathiresan, Sekar] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
   [Barroso, Ines] Univ Cambridge, Metab Res Labs, Wellcome Trust MRC Inst Metab Sci, Cambridge, England.
   [Barroso, Ines] Cambridge Biomed Res Ctr, Natl Inst Hlth Res, Cambridge, England.
   [Altshuler, David] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA.
   [Altshuler, David] Harvard Univ, Sch Med, Dept Mol Biol, Boston, MA USA.
   Univ Liverpool, Dept Biostat, Liverpool L69 3BX, Merseyside, England.
   [Morris, Andrew P.] Univ Liverpool, Dept Mol & Clin Pharmacol, Liverpool L69 3BX, Merseyside, England.
RP Gaulton, KJ (reprint author), Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
EM kgaulton@gmail.com; mark.mccarthy@drl.ox.ac.uk; apmorris@liverpool.ac.uk
RI Leander, Karin/C-7261-2017; Yengo, Loic/D-2692-2017; Johnson,
   Andrew/G-6520-2013; Ferrer, Jorge/A-3176-2012; Deloukas,
   Panos/B-2922-2013; Thorand, Barbara/B-5349-2014; Peters,
   Annette/A-6117-2011; Grallert, Harald/B-3424-2013; Veglia,
   Fabrizio/K-1958-2016; kinnunen, leena/B-7059-2012; Palmer,
   Colin/C-7053-2008; Study, GoDARTS/K-9448-2016; Grarup,
   Niels/K-2807-2015; van der Schouw, Yvonne/F-8327-2014; Ruderfer,
   Douglas/M-5795-2016
OI Nothen, Markus/0000-0002-8770-2464; Chen, Han/0000-0002-9510-4923;
   Tuomi, Tiinamaija/0000-0002-8306-6202; Have, Christian
   Theil/0000-0002-8634-4781; Jorgensen, Torben/0000-0001-9453-2830;
   Eriksson, Johan/0000-0002-2516-2060; Pankow, James/0000-0001-7076-483X;
   Karssen, Lennart C./0000-0002-1959-342X; Hattersley,
   Andrew/0000-0001-5620-473X; Linneberg, Allan/0000-0002-0994-0184;
   Peters, Annette/0000-0001-6645-0985; Gieger,
   Christian/0000-0001-6986-9554; PALLI, Domenico/0000-0002-5558-2437; van
   de Bunt, Martijn/0000-0002-6744-6125; Mannisto,
   Satu/0000-0002-8668-3046; Lakka, Timo/0000-0002-9199-2871; Gigante,
   Bruna/0000-0003-4508-7990; Koistinen, Heikki/0000-0001-7870-070X;
   Dunham, Ian/0000-0003-2525-5598; Birney, Ewan/0000-0001-8314-8497;
   Thomsen, Soren Krogsgaard/0000-0001-8894-2868; Forouhi,
   Nita/0000-0002-5041-248X; Leander, Karin/0000-0002-1404-9222; Yengo,
   Loic/0000-0002-4272-9305; Pasquali, Lorenzo/0000-0003-2423-1826; Rybin,
   Denis/0000-0002-3657-4829; Gaulton, Kyle/0000-0003-1318-7161; Sijbrands,
   Eric/0000-0001-8857-7389; TREMOLI, ELENA/0000-0002-0929-6106; Magi,
   Reedik/0000-0002-2964-6011; Fuchsberger, Christian/0000-0002-5918-8947;
   Humphries, Stephen E/0000-0002-8221-6547; Locke,
   Adam/0000-0001-6227-198X; Deloukas, Panos/0000-0001-9251-070X; Thorand,
   Barbara/0000-0002-8416-6440; Veglia, Fabrizio/0000-0002-9378-8874;
   kinnunen, leena/0000-0001-8739-4812; Palmer, Colin/0000-0002-6415-6560;
   Grarup, Niels/0000-0001-5526-1070; van der Schouw,
   Yvonne/0000-0002-4605-435X; Ruderfer, Douglas/0000-0002-2365-386X
FU Academy of Finland [77299, 102318, 10493, 118065, 123885, 124243,
   129293, 129680, 136895, 139635, 211119, 213506, 251217, 263836]; Agence
   National de la Recherche; Association de Langue Francaise pour l'Etude
   du Diabete et des Maladies Metaboliques; Association Diabeete Risque
   Vasculaire; Association Francaise des Diabetiques; Association of Danish
   Pharmacies; Augustinus Foundation; Becket Foundation; British Diabetes
   Association (BDA) Research; British Heart Foundation; Central Norway
   Health Authority; Central Finland Hospital District; Center for
   Inherited Disease Research (CIDR); City of Kuopio; City of Leutkirch;
   Copenhagen County; Danish Centre for Evaluation and Health Technology
   Assessment; Danish Council for Independent Research; Danish Heart
   Foundation; Danish Research Councils; Deutsche Forschungsgemeinschaft
   [ER 155/6-2]; Diabetes Research Foundation; Diabetes UK; Doris Duke
   Charitable Foundation; Erasmus Medical Center; Erasmus University;
   Estonian government [SF0180142s08]; European Commission [ENGAGE
   HEALTH-F4-2007-201413, FP7-201413, FP7-245536, EXGENESIS
   LSHM-CT-2004-005272, FP6 LSHM_CT_2006_037197, LSHM-CT-2007-037273,
   C-Public Health 2004310]; European Regional Development Fund; Federal
   Ministry of Education and Research, Germany [FKZ 01GI1128, FKZ
   01EO1001]; Federal Ministry of Health, Germany; Finnish Diabetes
   Association; Finnish Diabetes Research Foundation; Finnish Foundation
   for Cardiovascular Research; Finnish Medical Society; Folkhalsan
   Research Foundation; Foundation for Life and Health in Finland;
   Foundation for Old Servants; Fredrick och Ingrid Thuring Foundation;
   French region of Nord-Pas-de-Calais (Contrat de Projets Etat-Region);
   German Center for Diabetes Research; German Research Council [GRK1041];
   German National Genome Research Network; Groupe d'Etude des Maladies
   Metaboliques et Systemiques; Health Care Centers in Vasa, Narpes and
   Korsholm, Finland; Health Foundation; Heinz Nixdorf Foundation;
   Helmholtz Zentrum Munchen; Helsinki University Central Hospital Research
   Foundation; Hospital District of Southwest Finland; Ib Henriksens
   Foundation; IngaBritt and Arne Lundberg's Research Foundation [359];
   Karolinska Institutet; Knut and Alice Wallenberg Foundation [KAW
   2009.0243]; Kuopio University Hospital; Lundbeck Foundation; Magnus
   Bergvall Foundation; Medical Faculty of University Duisburg-Essen;
   Medical Research Council, UK [G0000649, G0601261]; Ministry for Health,
   Welfare and Sports, the Netherlands; Ministry of Education and Culture,
   Finland [722, 627]; Ministry of Education, Culture and Science, the
   Netherlands; Ministry of Health and Prevention, Denmark; Ministry of
   Social Affairs and Health, Finland; Ministry of Innovation, Science,
   Research and Technology of North Rhine-Westphalia, Germany; Munich
   Center of Health Sciences; Municipal Health Care Center and Hospital in
   Jakobstad, Finland; municipality of Rotterdam, the Netherlands; Narpes
   Health Care Foundation; National Health Screening Service of Norway;
   National Heart, Lung, and Blood Institute, USA [HHSN268201100005C,
   HHSN268201100006C, HHSN268201100007C, HHSN268201100008C,
   HHSN268201100009C, HHSN268201100010C, HHSN268201100011C,
   HHSN268201100012C, N01HC25195, N02HL64278, R01HL087641, R01HL59367,
   R01HL086694]; National Human Genome Research Institute, USA
   [U01HG004402, N01HG65403]; National Institute for Diabetes and Digestive
   and Kidney Diseases, USA [R01DK078616, U01DK085526, K24DK080140,
   R01DK073490]; National Institute for Health and Welfare, Finland;
   National Institutes of Health, USA [HHSN268200625226C, UL1RR025005,
   R01DK062370, R01DK072193, 1Z01HG000024, AG028555, AG08724, AG04563,
   AG10175, AG08861, U01HG004399, DK58845, CA055075, DK085545, DK098032];
   Netherlands Genomics Initiative; Netherlands Organisation for Health
   Research and Development; Netherlands Organisation of Scientific
   Research NOW Investments [175.010.2005.011, 911-03-012, 050-060-810];
   Nord-Trondelag County Council; Nordic Center of Excellence in Disease
   Genetics; Norwegian Institute of Public Health; Norwegian Research
   Council; Novo Nordisk Foundation; Ollquist Foundation; Oxford National
   Institute for Health Research (NIHR) Biomedical Research Centre; Paavo
   Nurmi Foundation; Paivikki and Sakari Sohlberg Foundation; Perklen
   Foundation; Pirkanmaa Hospital District, Finland; Programme Hospitalier
   de Recherche Clinique; Programme National de Recherche sur la Diabete;
   Research Institute for Diseases in the Elderly [014-93-015]; Robert
   Dawson Evans Endowment, Department of Medicine, Boston University School
   of Medicine and Boston Medical Center; Royal Swedish Academy of
   Sciences; Sarstedt, Germany; Signe and Ane Gyllenberg Foundation; Sigrid
   Juselius Foundation; Slottery Machine Association, Finland; Social
   Insurance Institution of Finland; South OstroBothnia Hospital District;
   state of Baden-Wurttemberg, Germany; Stockholm County Council [560183];
   Swedish Cultural Foundation, Finland; Swedish Diabetes Foundation;
   Swedish e-science Research Center; Swedish Foundation for Strategic
   Research; Swedish Heart-Lung Foundation; Swedish Research Council [SFO
   EXODIAB 2009-1039, 521-2010-3490, 521-2007-4037, 521-2008-2974, ANDIS
   825-2010-5983, LUDC 349-2008-6589, 8691]; Swedish Society of Medicine;
   Tore Nilsson Foundation; Torsten and Ragnar Soderbergs Stiftelser
   [MT33/09]; University Hospital Essen; University of Tromso; University
   College London NIHR Biomedical Research Centre; UK NIHR Cambridge
   Biomedical Research Centre; Uppsala University; Uppsala University
   Hospital; Vaasa Hospital District; Velux Foundation; Wellcome Trust
   [GR072960, 076113, 083948, 090367, 090532, 083270, 086596, 098017,
   095101, 098051, 098381]
FX Funding for the research undertaken in this study has been received from
   the Academy of Finland (including grants 77299, 102318, 10493, 118065,
   123885, 124243, 129293, 129680, 136895, 139635, 211119, 213506, 251217
   and 263836); Agence National de la Recherche; Association de Langue
   Francaise pour l'Etude du Diabete et des Maladies Metaboliques;
   Association Diabeete Risque Vasculaire; Association Francaise des
   Diabetiques; the Association of Danish Pharmacies; the Augustinus
   Foundation; the Becket Foundation; the British Diabetes Association
   (BDA) Research; the British Heart Foundation; the Central Norway Health
   Authority; the Central Finland Hospital District; the Center for
   Inherited Disease Research (CIDR); the City of Kuopio; the City of
   Leutkirch; Copenhagen County; the Danish Centre for Evaluation and
   Health Technology Assessment; the Danish Council for Independent
   Research; the Danish Heart Foundation; the Danish Research Councils;
   Deutsche Forschungsgemeinschaft (including project ER 155/6-2); the
   Diabetes Research Foundation; Diabetes UK; the Doris Duke Charitable
   Foundation; Erasmus Medical Center; Erasmus University; the Estonian
   government (SF0180142s08); the European Commission (including ENGAGE
   HEALTH-F4-2007-201413, FP7-201413, FP7-245536, EXGENESIS
   LSHM-CT-2004-005272, FP6 LSHM_CT_2006_037197, LSHM-CT-2007-037273,
   Directorate C-Public Health 2004310, DG XII); the European Regional
   Development Fund; the Federal Ministry of Education and Research,
   Germany (including FKZ 01GI1128 and FKZ 01EO1001); the Federal Ministry
   of Health, Germany; the Finnish Diabetes Association; the Finnish
   Diabetes Research Foundation; the Finnish Foundation for Cardiovascular
   Research; the Finnish Medical Society; the Folkhalsan Research
   Foundation; the Foundation for Life and Health in Finland; the
   Foundation for Old Servants; the Fredrick och Ingrid Thuring Foundation;
   the French region of Nord-Pas-de-Calais (Contrat de Projets
   Etat-Region); the German Center for Diabetes Research; the German
   Research Council (including grant GRK1041); the German National Genome
   Research Network; Groupe d'Etude des Maladies Metaboliques et
   Systemiques; the Health Care Centers in Vasa, Narpes and Korsholm,
   Finland; the Health Foundation; the Heinz Nixdorf Foundation; Helmholtz
   Zentrum Munchen; the Helsinki University Central Hospital Research
   Foundation; the Hospital District of Southwest Finland; the Ib
   Henriksens Foundation; IngaBritt and Arne Lundberg's Research Foundation
   (including grant 359); Karolinska Institutet; the Knut and Alice
   Wallenberg Foundation (including grant KAW 2009.; 0243); Kuopio
   University Hospital; the Lundbeck Foundation; the Magnus Bergvall
   Foundation; the Medical Faculty of University Duisburg-Essen; the
   Medical Research Council, UK (including grants G0000649 and G0601261);
   the Ministry for Health, Welfare and Sports, the Netherlands; the
   Ministry of Education and Culture, Finland (including grants 722 and
   627; 2004-2011); the Ministry of Education, Culture and Science, the
   Netherlands; the Ministry of Health and Prevention, Denmark; the
   Ministry of Social Affairs and Health, Finland; the Ministry of
   Innovation, Science, Research and Technology of North Rhine-Westphalia,
   Germany; the Munich Center of Health Sciences; the Municipal Health Care
   Center and Hospital in Jakobstad, Finland; the municipality of
   Rotterdam, the Netherlands; the Narpes Health Care Foundation; the
   National Health Screening Service of Norway; the National Heart, Lung,
   and Blood Institute, USA (including grant numbers/contracts
   HHSN268201100005C, HHSN268201100006C, HHSN268201100007C,
   HHSN268201100008C, HHSN268201100009C, HHSN268201100010C,
   HHSN268201100011C, HHSN268201100012C, N01HC25195, N02HL64278,
   R01HL087641, R01HL59367 and R01HL086694); the National Human Genome
   Research Institute, USA (including grant numbers/contracts U01HG004402
   and N01HG65403); the National Institute for Diabetes and Digestive and
   Kidney Diseases, USA (including grants R01DK078616, U01DK085526,
   K24DK080140 and R01DK073490); the National Institute for Health and
   Welfare, Finland; the National Institutes of Health, USA (including
   grant numbers/contracts HHSN268200625226C, UL1RR025005, R01DK062370,
   R01DK072193, 1Z01HG000024, AG028555, AG08724, AG04563, AG10175, AG08861,
   U01HG004399, DK58845, CA055075, DK085545 and DK098032); the Netherlands
   Genomics Initiative; the Netherlands Organisation for Health Research
   and Development; the Netherlands Organisation of Scientific Research NOW
   Investments (including grants 175.010.2005.; 011, 911-03-012 and
   050-060-810); the Nord-Trondelag County Council; the Nordic Center of
   Excellence in Disease Genetics; the Norwegian Institute of Public
   Health; the Norwegian Research Council; the Novo Nordisk Foundation; the
   Ollquist Foundation; the Oxford National Institute for Health Research
   (NIHR) Biomedical Research Centre; the Paavo Nurmi Foundation; the
   Paivikki and Sakari Sohlberg Foundation; the Perklen Foundation; the
   Pirkanmaa Hospital District, Finland; Programme Hospitalier de Recherche
   Clinique; Programme National de Recherche sur la Diabete; the Research
   Institute for Diseases in the Elderly (including grant 014-93-015); the
   Robert Dawson Evans Endowment, Department of Medicine, Boston University
   School of Medicine and Boston Medical Center; the Royal Swedish Academy
   of Sciences; Sarstedt, Germany; the Signe and Ane Gyllenberg Foundation;
   the Sigrid Juselius Foundation; the Slottery Machine Association,
   Finland; the Social Insurance Institution of Finland; the South
   OstroBothnia Hospital District; the state of Baden-Wurttemberg, Germany;
   the Stockholm County Council (including grant 560183); the Swedish
   Cultural Foundation, Finland; the Swedish Diabetes Foundation; the
   Swedish e-science Research Center; the Swedish Foundation for Strategic
   Research; the Swedish Heart-Lung Foundation; the Swedish Research
   Council (including grants SFO EXODIAB 2009-1039, 521-2010-3490,
   521-2007-4037, 521-2008-2974, ANDIS 825-2010-5983, LUDC 349-2008-6589
   and 8691); the Swedish Society of Medicine; the Tore Nilsson Foundation;
   the Torsten and Ragnar Soderbergs Stiftelser (including grant MT33/09);
   University Hospital Essen; University of Tromso; the University College
   London NIHR Biomedical Research Centre; the UK NIHR Cambridge Biomedical
   Research Centre; Uppsala University; Uppsala University Hospital; the
   Vaasa Hospital District; the Velux Foundation; and the Wellcome Trust
   (including the Biomedical Collections Grant GR072960 and grants 076113,
   083948, 090367, 090532, 083270, 086596, 098017, 095101, 098051 and
   098381). We are grateful to R. Scharfmann (INSERM U1016, Cochin
   Institute Paris) for the gift of EndoC beta H1 cells and for providing
   technical support with their maintenance. We thank P. Johnson and the
   Oxford NIHR Biomedical Research Centre-funded Islet Isolation facility
   for providing human islets for this study. Detailed acknowledgments are
   provided in the Supplementary Note.
NR 75
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PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD DEC
PY 2015
VL 47
IS 12
BP 1415
EP +
DI 10.1038/ng.3437
PG 14
WC Genetics & Heredity
SC Genetics & Heredity
GA CX6LT
UT WOS:000365813200013
PM 26551672
ER

PT J
AU Smedley, D
   Jacobsen, JOB
   Jager, M
   Kohler, S
   Holtgrewe, M
   Schubach, M
   Siragusa, E
   Zemojtel, T
   Buske, OJ
   Washington, NL
   Bone, WP
   Haendel, MA
   Robinson, PN
AF Smedley, Damian
   Jacobsen, Julius O. B.
   Jaeger, Marten
   Koehler, Sebastian
   Holtgrewe, Manuel
   Schubach, Max
   Siragusa, Enrico
   Zemojtel, Tomasz
   Buske, Orion J.
   Washington, Nicole L.
   Bone, William P.
   Haendel, Melissa A.
   Robinson, Peter N.
TI Next-generation diagnostics and disease-gene discovery with the Exomiser
SO NATURE PROTOCOLS
LA English
DT Article
ID HUMAN PHENOTYPE ONTOLOGY; MENDELIAN DISEASES; SEQUENCE DATA; SEMANTIC
   SIMILARITY; CANDIDATE GENES; NATIONAL CENTER; RARE DISEASES; EXOME;
   VARIANTS; PRIORITIZATION
AB Exomiser is an application that prioritizes genes and variants in next-generation sequencing (NGS) projects for novel disease-gene discovery or differential diagnostics of Mendelian disease. Exomiser comprises a suite of algorithms for prioritizing exome sequences using random-walk analysis of protein interaction networks, clinical relevance and cross-species phenotype comparisons, as well as a wide range of other computational filters for variant frequency, predicted pathogenicity and pedigree analysis. In this protocol, we provide a detailed explanation of how to install Exomiser and use it to prioritize exome sequences in a number of scenarios. Exomiser requires similar to 3 GB of RAM and roughly 15-90 s of computing time on a standard desktop computer to analyze a variant call format (VCF) file. Exomiser is freely available for academic use from http://www.sanger.ac.uk/science/tools/exomiser.
C1 [Smedley, Damian; Jacobsen, Julius O. B.] Wellcome Trust Sanger Inst, Skarnes Fac Grp, Hinxton, England.
   [Jaeger, Marten; Koehler, Sebastian; Holtgrewe, Manuel; Schubach, Max; Siragusa, Enrico; Zemojtel, Tomasz; Robinson, Peter N.] Charite, Inst Med & Human Genet, D-13353 Berlin, Germany.
   [Jaeger, Marten; Robinson, Peter N.] Charite, Berlin Brandenburg Ctr Regenerat Therapies BCRT, D-13353 Berlin, Germany.
   [Holtgrewe, Manuel; Siragusa, Enrico] Berlin Inst Hlth, Berlin, Germany.
   [Siragusa, Enrico; Robinson, Peter N.] Max Planck Inst Mol Genet, D-14195 Berlin, Germany.
   [Zemojtel, Tomasz] Polish Acad Sci, Inst Bioorgan Chem, Poznan, Poland.
   [Zemojtel, Tomasz] Lab Berlin Charite Vivantes, Humangenet, Berlin, Germany.
   [Buske, Orion J.] Univ Toronto, Dept Comp Sci, Toronto, ON, Canada.
   [Buske, Orion J.] Hosp Sick Children, Genet & Genome Biol, Toronto, ON M5G 1X8, Canada.
   [Washington, Nicole L.] Univ Calif Berkeley, Lawrence Berkeley Natl Lab, Div Environm Genom & Syst Biol, Berkeley, CA 94720 USA.
   [Bone, William P.] NIH, Undiagnosed Dis Program, Common Fund, Off Director, Bethesda, MD 20892 USA.
   [Haendel, Melissa A.] Oregon Hlth & Sci Univ, Dept Med Informat & Clin Epidemiol, Portland, OR 97201 USA.
   [Robinson, Peter N.] Free Univ Berlin, Inst Bioinformat, Dept Math & Comp Sci, Berlin, Germany.
RP Robinson, PN (reprint author), Charite, Inst Med & Human Genet, D-13353 Berlin, Germany.
EM peter.robinson@charite.de
OI Jacobsen, Julius/0000-0002-3265-1591; Kohler,
   Sebastian/0000-0002-5316-1399
FU Bundesministerium fur Bildung und Forschung (BMBF) [0313911]; European
   Community's Seventh Framework Programme [602300]; NIH [5R240D011883]
FX This project was supported by the Bundesministerium fur Bildung und
   Forschung (BMBF; project no. 0313911), the European Community's Seventh
   Framework Programme (grant agreement no. 602300; SYBIL) and NIH grant
   no. 5R240D011883 (Monarch Initiative).
NR 78
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U1 3
U2 15
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 DEC
PY 2015
VL 10
IS 12
BP 2004
EP 2015
DI 10.1038/nprot.2015.124
PG 12
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA CY0UR
UT WOS:000366122600008
PM 26562621
ER

PT J
AU Germain, RN
AF Germain, Ronald N.
TI Journal club TRACKING THE T CELL REPERTOIRE
SO NATURE REVIEWS IMMUNOLOGY
LA English
DT News Item
C1 [Germain, Ronald N.] NIAID, Lab Syst Biol, NIH, Bethesda, MD 20892 USA.
RP Germain, RN (reprint author), NIAID, Lab Syst Biol, NIH, Bethesda, MD 20892 USA.
EM rgermain@niaid.nih.gov
NR 0
TC 0
Z9 0
U1 2
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1733
EI 1474-1741
J9 NAT REV IMMUNOL
JI Nat. Rev. Immunol.
PD DEC
PY 2015
VL 15
IS 12
BP 730
EP 730
PG 1
WC Immunology
SC Immunology
GA CY1FS
UT WOS:000366152700008
PM 26515079
ER

PT J
AU Schank, JR
   Nelson, BS
   Damadzic, R
   Tapocik, JD
   Yao, M
   King, CE
   Rowe, KE
   Cheng, K
   Rice, KC
   Heilig, M
AF Schank, J. R.
   Nelson, B. S.
   Damadzic, R.
   Tapocik, J. D.
   Yao, M.
   King, C. E.
   Rowe, K. E.
   Cheng, K.
   Rice, K. C.
   Heilig, M.
TI Neurokinin-1 receptor antagonism attenuates neuronal activity triggered
   by stress-induced reinstatement of alcohol seeking
SO NEUROPHARMACOLOGY
LA English
DT Article
DE Stress; Alcohol; Reinstatement; Neurokinin-1; Substance P; Nucleus
   accumbens
ID DORSAL RAPHE NUCLEUS; P-CONTAINING NEURONS; LATERAL HABENULA;
   LOCUS-COERULEUS; RAT; SEROTONIN; BRAIN; ONDANSETRON; PROJECTIONS;
   ACCUMBENS
AB Substance P (SP) and its cognate neurokinin-1 receptor (NK1R) are involved in alcohol-related behaviors. We have previously reported that NK1R antagonism attenuates stress-induced reinstatement of alcohol seeking and suppresses escalated alcohol self-administration, but does not affect primary reinforcement or cue-induced reinstatement. Here, we administered an NK1R antagonist or vehicle prior to footshock-induced reinstatement of alcohol seeking, and mapped the resulting neuronal activation using Fos immunohistochemistry. As expected, vehicle treated animals exposed to footshock showed induction of Fos immunoreactivity in several regions of the brain stress circuitry, including the amygdala (AMG), nucleus accumbens (NAC), dorsal raphe nucleus (DR), prefrontal cortex (PFC), and bed nucleus of the stria terminalis (BNST). NK1R antagonism selectively suppressed the stress-induced increase in Fos in the DR and NAC shell. In the DR, Fos-induction by stress largely overlapped with tryptophan hydroxylase (TrpH), indicating activation of serotonergic neurons. Of NAC shell neurons activated during stress-induced reinstatement of alcohol seeking, about 30% co-expressed dynorphin (DYN), while 70% co-expressed enkephalin (ENK). Few (<1%) activated NAC shell neurons coexpressed choline acetyltransferase (ChAT), which labels the cholinergic interneurons of this region. Infusion of the NK1R antagonist L822429 into the NAC shell blocked stress-induced reinstatement of alcohol seeking. In contrast, L822429 infusion into the DR had no effect, suggesting that the influence of NK1R signaling on neuronal activity in the DR is indirect. Taken together, our results outline a potential pathway through which endogenous NK1R activation mediates stress-induced alcohol seeking. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Schank, J. R.; Nelson, B. S.] Univ Georgia, Dept Physiol & Pharmacol, Coll Vet Med, Athens, GA 30602 USA.
   [Damadzic, R.; Tapocik, J. D.; Yao, M.; King, C. E.; Rowe, K. E.; Heilig, M.] NIAAA, Lab Clin & Translat Studies, Bethesda, MD 20892 USA.
   [Cheng, K.; Rice, K. C.] NIDA, Chem Biol Res Branch, Bethesda, MD 20892 USA.
   [Cheng, K.; Rice, K. C.] NIAAA, Bethesda, MD 20892 USA.
RP Schank, JR (reprint author), Univ Georgia, Dept Physiol & Pharmacol, 501 DW Brooks Dr, Athens, GA 30602 USA.
EM jschank@uga.edu
FU National Institute on Alcohol Abuse and Alcoholism; National Institute
   on Drug Abuse Intramural Research Programs; University of Georgia
FX This work supported by the National Institute on Alcohol Abuse and
   Alcoholism and the National Institute on Drug Abuse Intramural Research
   Programs, and the University of Georgia. The authors declare no
   competing financial interests.
NR 35
TC 2
Z9 3
U1 0
U2 6
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 DEC
PY 2015
VL 99
BP 106
EP 114
DI 10.1016/j.neuropharm.2015.07.009
PG 9
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA CY0AA
UT WOS:000366066800011
PM 26188146
ER

PT J
AU Lucas, SJ
   Armstrong, DL
AF Lucas, Sarah J.
   Armstrong, David L.
TI Protein phosphatase modulation of somatostatin receptor signaling in the
   mouse hippocampus
SO NEUROPHARMACOLOGY
LA English
DT Article
DE Somatostatin; Neuronal excitability; Protein phosphatases; Hippocampus;
   K+ channels
ID CENTRAL-NERVOUS-SYSTEM; DOMAIN K+ CHANNELS; NEURONAL EXCITABILITY;
   POTASSIUM CURRENTS; ENTORHINAL CORTEX; ARACHIDONIC-ACID; IN-VITRO;
   INHIBITION; PHOSPHORYLATION; BRAIN
AB Many inhibitory interneurones in the hippocampus release the neuropeptide somatostatin (SST) which inhibits neuronal excitability through G(i)/G(o)-coupled receptors. To investigate the signaling pathways underlying the SST inhibition of neuronal excitability in the hippocampus, we performed perforated patch-clamp recordings from CA1 pyramidal neurones in acute brain slices from P14-P18 mice. Bath application of I mu M SST reversibly reduces the frequency of action potential firing in response to depolarising current steps, and is associated with neuronal hyperpolarisation and a reduction in membrane resistance. This effect is mediated by potassium channels with KCNK-like pharmacology. In addition, in slices that have been cultured in vitro for seven days or more, SST also produces a hyperpolarisation independent reduction in action potential firing, which can be also observed in acute slices when the Ser/Thr protein phosphatases PP2A and PP4 are inhibited selectively with fostriecin. This hyperpolarisation independent effect of SST appears to be mediated by G-protein-activated inwardly rectifying K+ (GIRK) channels. Knockdown of protein phosphatase 5, by Cre recombinase mediated deletion of the foxed Ppp5c gene, blocks the hyperpolarisation independent effect of SST, and reduces the hyperpolarisation dependent effect in a manner consistent with increased SST receptor desensitisation. Thus, reversible protein phosphorylation provides a mechanism to enhance or diminish the inhibitory effect of SST, which could allow system level regulation of circuit excitability in the hippocampus. Published by Elsevier Ltd.
C1 [Lucas, Sarah J.; Armstrong, David L.] NIEHS, Neurobiol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Lucas, SJ (reprint author), Univ Leicester, Dept Cell Physiol & Pharmacol, Med Sci Bldg,Univ Rd, Leicester LE1 9HN, Leics, England.
EM Sarah.Lucas@cantab.net
OI Lucas, Sarah/0000-0002-5577-763X
FU NIH [Z01-ES080043]
FX This work was supported by the NIH Intramural program award Z01-ES080043
   to D.L.A.
NR 50
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U1 0
U2 0
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 DEC
PY 2015
VL 99
BP 232
EP 241
DI 10.1016/j.neuropharm.2015.07.004
PG 10
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA CY0AA
UT WOS:000366066800022
PM 26196943
ER

PT J
AU Hong, J
   Lu, SY
   Xu, R
   Liow, JS
   Woock, AE
   Jenko, KJ
   Gladding, RL
   Zoghbi, SS
   Innis, RB
   Pike, VW
AF Hong, Jinsoo
   Lu, Shuiyu
   Xu, Rong
   Liow, Jeih-San
   Woock, Alicia E.
   Jenko, Kimberly J.
   Gladding, Robert L.
   Zoghbi, Sami S.
   Innis, Robert B.
   Pike, Victor W.
TI [carbonyl-C-11]4-Fluoro-N-methyl-N-(4-(6-(methylamino)pyrimidin-4-yl)thi
   azol-2-yl)benzamide ([C-11]FIMX) is an effective radioligand for PET
   imaging of metabotropic glutamate receptor 1 (mGluR1) in monkey brain
SO NUCLEAR MEDICINE AND BIOLOGY
LA English
DT Article
DE mGluR1; Radioligand; PET; Carbon-11; Monkey; Brain
ID IN-VIVO; FREE-FRACTION; LIGAND; RADIOTRACERS; MONOXIDE; ANTAGONISTS;
   DISORDERS; BINDING; PAIN; RAT
AB Introduction: Metabotropic glutamate subtype receptor 1 (mGluR1) is implicated in several neuropsychiatric disorders and is a target for drug development. [F-18]FIMX ([F-18]4-fluoro-N-methyl-N-(4-(6-(methylamino) pyrimidin-4-yl)thiazol-2-yl)benzamide) is an effective radioligand for imaging brain mGluR1 with PET. A similarly effective radioligand with a shorter half-life would usefully allow PET studies of mGluR1 at baseline and after pharmacological or other challenge on the same day. Here we describe the preparation of [C-11]FIMX for evaluation in monkey with PET.
   Methods: [C-11]FIMX was prepared via Pd-promoted carbonylation of 1-fluoro-4-iodobenzene with [C-11]carbon monoxide, aminolysis of the [C-11]acyl-palladium complex with the requisite Boc-protected amine, and deprotection with HCl in THF. PET scans of [C-11]FIMX injected into a monkey were performed at baseline and after preblock of mGluR1 with measurement of the arterial input function.
   Results: The radiosynthesis required 42 min and gave [C-11]FIMX in about 5% overall decay-corrected radiochemical yield and with a specific activity of about 100 GBq/mu mol. PET in rhesus monkey at baseline showed that radioactivity peaked high in receptor-rich cerebellum and much lower in receptor-poor occipital cortex.
   Radioactivity in cerebellum declined to 32% of peak at 85 min. V-T at baseline appeared stable in all brain regions after 60 min. Under mGluR1 pre-blocked condition, radioactivity uptake in all regions declined more rapidly to a low level. Receptor pre-block reduced V-T from 13.0 to 1.5 in cerebellum and from 2.9 to 1.4 in occipital cortex. Conclusion: [C-11]FIMX is an effective radioligand for imaging mGluR1 in monkey with PET. Published by Elsevier Inc.
C1 [Hong, Jinsoo; Lu, Shuiyu; Xu, Rong; Liow, Jeih-San; Woock, Alicia E.; Jenko, Kimberly J.; Gladding, Robert L.; Zoghbi, Sami S.; Innis, Robert B.; Pike, Victor W.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
RP Pike, VW (reprint author), NIMH, Mol Imaging Branch, NIH, Bldg 10,Room B3 C346A,10 Ctr Dr, Bethesda, MD 20892 USA.
EM pikev@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health (NIMH)
   [ZIA-MH002793]
FX This work was supported by the Intramural Research Program of the
   National Institutes of Health (NIMH; ZIA-MH002793). The authors are
   grateful to the NIH Clinical PET Center (Chief: Dr. P. Herscovitch) for
   the production of carbon-11.
NR 46
TC 2
Z9 2
U1 1
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0969-8051
EI 1872-9614
J9 NUCL MED BIOL
JI Nucl. Med. Biol.
PD DEC
PY 2015
VL 42
IS 12
BP 967
EP 974
DI 10.1016/j.nucmedbio.2015.07.006
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CY1EM
UT WOS:000366149500009
PM 26320813
ER

PT J
AU Kassis, JA
   Muller, J
AF Kassis, Judith A.
   Mueller, Juerg
TI Transcription through Polycomb response elements does not induce a
   switch from repression to activation
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Editorial Material
ID DROSOPHILA BITHORAX COMPLEX; ULTRABITHORAX DOMAIN; PROTEINS; STATES;
   GENE
C1 [Kassis, Judith A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Gene Express, NIH, Bethesda, MD 20892 USA.
   [Mueller, Juerg] Max Planck Inst Biochem, Lab Chromatin Biol, D-82152 Martinsried, Germany.
RP Kassis, JA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Gene Express, NIH, Bethesda, MD 20892 USA.
EM jkassis@mail.nih.gov
OI Kassis, Judith/0000-0001-9268-3213
NR 15
TC 0
Z9 0
U1 1
U2 5
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD DEC 1
PY 2015
VL 112
IS 48
BP 14755
EP 14756
DI 10.1073/pnas.1520102112
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA CX8XR
UT WOS:000365988900028
PM 26567151
ER

PT J
AU Mesquita, RD
   Vionette-Amaral, RJ
   Lowenberger, C
   Rivera-Pomar, R
   Monteiro, FA
   Minx, P
   Spieth, J
   Carvalho, AB
   Panzera, F
   Lawson, D
   Torres, AQ
   Ribeiro, JMC
   Sorgine, MHF
   Waterhouse, RM
   Montague, MJ
   Abad-Franch, F
   Alves-Bezerra, M
   Amaral, LR
   Araujo, HM
   Araujo, RN
   Aravind, L
   Atella, GC
   Azambuja, P
   Berni, M
   Bittencourt-Cunha, PR
   Braz, GRC
   Calderon-Fernandez, G
   Carareto, CMA
   Christensen, MB
   Costa, IR
   Costa, SG
   Dansa, M
   Daumas, CRO
   De-Paula, IF
   Dias, FA
   Dimopoulos, G
   Emrich, SJ
   Esponda-Behrens, N
   Fampa, P
   Fernandez-Medina, RD
   da Fonseca, RN
   Fontenele, M
   Fronick, C
   Fulton, LA
   Gandara, AC
   Garcia, ES
   Genta, FA
   Giraldo-Calderon, GI
   Gomes, B
   Gondim, KC
   Granzotto, A
   Guarneri, AA
   Guigo, R
   Harry, M
   Hughes, DST
   Jablonka, W
   Jacquin-Joly, E
   Juarez, MP
   Koerich, LB
   Latorre-Estivalis, JM
   Lavore, A
   Lawrence, GG
   Lazoski, C
   Lazzari, CR
   Lopes, RR
   Lorenzo, MG
   Lugon, MD
   Majerowicz, D
   Marcet, PL
   Mariotti, M
   Masuda, H
   Megy, K
   Melo, ACA
   Missirlis, F
   Mota, T
   Noriega, FG
   Nouzova, M
   Nunes, RD
   Oliveira, RLL
   Oliveira-Silveira, G
   Ons, S
   Pagola, L
   Paiva-Silva, GO
   Pascual, A
   Pavan, MG
   Pedrini, N
   Peixoto, AA
   Pereira, MH
   Pike, A
   Polycarpo, C
   Prosdocimi, F
   Ribeiro-Rodrigues, R
   Robertson, HM
   Salerno, AP
   Salmon, D
   Santesmasses, D
   Schama, R
   Seabra, ES
   Silva-Cardoso, L
   Silva-Neto, MAC
   Souza-Gomes, M
   Sterkel, M
   Taracena, ML
   Tojo, M
   Tu, ZJ
   Tubio, JMC
   Ursic-Bedoya, R
   Venancio, TM
   Walter-Nuno, AB
   Wilson, D
   Warren, WC
   Wilson, RK
   Huebner, E
   Dotson, EM
   Oliveira, PL
AF Mesquita, Rafael D.
   Vionette-Amaral, Raquel J.
   Lowenberger, Carl
   Rivera-Pomar, Rolando
   Monteiro, Fernando A.
   Minx, Patrick
   Spieth, John
   Bernardo Carvalho, A.
   Panzera, Francisco
   Lawson, Daniel
   Torres, Andre Q.
   Ribeiro, Jose M. C.
   Sorgine, Marcos H. F.
   Waterhouse, Robert M.
   Montague, Michael J.
   Abad-Franch, Fernando
   Alves-Bezerra, Michele
   Amaral, Laurence R.
   Araujo, Helena M.
   Araujo, Ricardo N.
   Aravind, L.
   Atella, Georgia C.
   Azambuja, Patricia
   Berni, Mateus
   Bittencourt-Cunha, Paula R.
   Braz, Gloria R. C.
   Calderon-Fernandez, Gustavo
   Carareto, Claudia M. A.
   Christensen, Mikkel B.
   Costa, Igor R.
   Costa, Samara G.
   Dansa, Marilvia
   Daumas-Filho, Carlos R. O.
   De-Paula, Iron F.
   Dias, Felipe A.
   Dimopoulos, George
   Emrich, Scott J.
   Esponda-Behrens, Natalia
   Fampa, Patricia
   Fernandez-Medina, Rita D.
   da Fonseca, Rodrigo N.
   Fontenele, Marcio
   Fronick, Catrina
   Fulton, Lucinda A.
   Gandara, Ana Caroline
   Garcia, Eloi S.
   Genta, Fernando A.
   Giraldo-Calderon, Gloria I.
   Gomes, Bruno
   Gondim, Katia C.
   Granzotto, Adriana
   Guarneri, Alessandra A.
   Guigo, Roderic
   Harry, Myriam
   Hughes, Daniel S. T.
   Jablonka, Willy
   Jacquin-Joly, Emmanuelle
   Patricia Juarez, M.
   Koerich, Leonardo B.
   Latorre-Estivalis, Jose Manuel
   Lavore, Andres
   Lawrence, Gena G.
   Lazoski, Cristiano
   Lazzari, Claudio R.
   Lopes, Raphael R.
   Lorenzo, Marcelo G.
   Lugon, Magda D.
   Majerowicz, David
   Marcet, Paula L.
   Mariotti, Marco
   Masuda, Hatisaburo
   Megy, Karine
   Melo, Ana C. A.
   Missirlis, Fanis
   Mota, Theo
   Noriega, Fernando G.
   Nouzova, Marcela
   Nunes, Rodrigo D.
   Oliveira, Raquel L. L.
   Oliveira-Silveira, Gilbert
   Ons, Sheila
   Pagola, Lucia
   Paiva-Silva, Gabriela O.
   Pascual, Agustina
   Pavan, Marcio G.
   Pedrini, Nicolas
   Peixoto, Alexandre A.
   Pereira, Marcos H.
   Pike, Andrew
   Polycarpo, Carla
   Prosdocimi, Francisco
   Ribeiro-Rodrigues, Rodrigo
   Robertson, Hugh M.
   Salerno, Ana Paula
   Salmon, Didier
   Santesmasses, Didac
   Schama, Renata
   Seabra-Junior, Eloy S.
   Silva-Cardoso, Livia
   Silva-Neto, Mario A. C.
   Souza-Gomes, Matheus
   Sterkel, Marcos
   Taracena, Mabel L.
   Tojo, Marta
   Tu, Zhijian Jake
   Tubio, Jose M. C.
   Ursic-Bedoya, Raul
   Venancio, Thiago M.
   Walter-Nuno, Ana Beatriz
   Wilson, Derek
   Warren, Wesley C.
   Wilson, Richard K.
   Huebner, Erwin
   Dotson, Ellen M.
   Oliveira, Pedro L.
TI Genome of Rhodnius prolixus, an insect vector of Chagas disease, reveals
   unique adaptations to hematophagy and parasite infection
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE Rhodnius prolixus; genome; hematophagy; immunity; Chagas disease
ID HEME-BINDING PROTEIN; ANOPHELES-GAMBIAE; CAENORHABDITIS-ELEGANS;
   BLOODSUCKING INSECT; TRIATOMA-INFESTANS; CARBON-DIOXIDE; GRAN CHACO;
   EVOLUTION; REDUVIIDAE; HEMIPTERA
AB Rhodnius prolixus not only has served as a model organism for the study of insect physiology, but also is a major vector of Chagas disease, an illness that affects approximately seven million people worldwide. We sequenced the genome of R. prolixus, generated assembled sequences covering 95% of the genome (similar to 702 Mb), including 15,456 putative protein-coding genes, and completed comprehensive genomic analyses of this obligate blood-feeding insect. Although immune-deficiency (IMD)-mediated immune responses were observed, R. prolixus putatively lacks key components of the IMD pathway, suggesting a reorganization of the canonical immune signaling network. Although both Toll and IMD effectors controlled intestinal microbiota, neither affected Trypanosoma cruzi, the causal agent of Chagas disease, implying the existence of evasion or tolerance mechanisms. R. prolixus has experienced an extensive loss of selenoprotein genes, with its repertoire reduced to only two proteins, one of which is a selenocysteine-based glutathione peroxidase, the first found in insects. The genome contained actively transcribed, horizontally transferred genes from Wolbachia sp., which showed evidence of codon use evolution toward the insect use pattern. Comparative protein analyses revealed many lineage-specific expansions and putative gene absences in R. prolixus, including tandem expansions of genes related to chemoreception, feeding, and digestion that possibly contributed to the evolution of a blood-feeding lifestyle. The genome assembly and these associated analyses provide critical information on the physiology and evolution of this important vector species and should be instrumental for the development of innovative disease control methods.
C1 [Mesquita, Rafael D.; Torres, Andre Q.; Braz, Gloria R. C.; Melo, Ana C. A.; Oliveira, Raquel L. L.] Univ Fed Rio de Janeiro, Inst Quim, Dept Bioquim, BR-21941909 Rio De Janeiro, Brazil.
   [Mesquita, Rafael D.; Monteiro, Fernando A.; Bernardo Carvalho, A.; Sorgine, Marcos H. F.; Araujo, Helena M.; Araujo, Ricardo N.; Atella, Georgia C.; Azambuja, Patricia; Braz, Gloria R. C.; Dias, Felipe A.; da Fonseca, Rodrigo N.; Fontenele, Marcio; Gandara, Ana Caroline; Garcia, Eloi S.; Genta, Fernando A.; Gomes, Bruno; Gondim, Katia C.; Guarneri, Alessandra A.; Koerich, Leonardo B.; Latorre-Estivalis, Jose Manuel; Lazoski, Cristiano; Lorenzo, Marcelo G.; Masuda, Hatisaburo; Melo, Ana C. A.; Nunes, Rodrigo D.; Paiva-Silva, Gabriela O.; Peixoto, Alexandre A.; Pereira, Marcos H.; Polycarpo, Carla; Schama, Renata; Silva-Neto, Mario A. C.; Venancio, Thiago M.; Oliveira, Pedro L.] Inst Nacl Ciencia & Tecnol Entomol Mol, BR-21941591 Rio De Janeiro, Brazil.
   [Vionette-Amaral, Raquel J.; Sorgine, Marcos H. F.; Alves-Bezerra, Michele; Atella, Georgia C.; Bittencourt-Cunha, Paula R.; Costa, Igor R.; Daumas-Filho, Carlos R. O.; De-Paula, Iron F.; Dias, Felipe A.; Gandara, Ana Caroline; Gondim, Katia C.; Jablonka, Willy; Lopes, Raphael R.; Majerowicz, David; Masuda, Hatisaburo; Nunes, Rodrigo D.; Oliveira-Silveira, Gilbert; Paiva-Silva, Gabriela O.; Polycarpo, Carla; Prosdocimi, Francisco; Salmon, Didier; Silva-Cardoso, Livia; Silva-Neto, Mario A. C.; Sterkel, Marcos; Taracena, Mabel L.; Walter-Nuno, Ana Beatriz; Oliveira, Pedro L.] Univ Fed Rio de Janeiro, Inst Bioquim Med Leopoldo Meis, Programa Biol Mol & Biotecnol, BR-21941591 Rio De Janeiro, Brazil.
   [Lowenberger, Carl; Ursic-Bedoya, Raul] Simon Fraser Univ, Biol Sci, Burnaby, BC V5A 1S6, Canada.
   [Rivera-Pomar, Rolando; Esponda-Behrens, Natalia; Lavore, Andres; Ons, Sheila; Pagola, Lucia; Pascual, Agustina] Univ Nacl La Plata, Ctr Reg Estudios Genom, RA-1900 La Plata, Argentina.
   [Rivera-Pomar, Rolando] Univ Nacl Noroeste Buenos Aires, Ctr Bioinvest, RA-2700 Pergamino, Argentina.
   [Monteiro, Fernando A.; Torres, Andre Q.; Azambuja, Patricia; Costa, Samara G.; Garcia, Eloi S.; Genta, Fernando A.; Gomes, Bruno; Pavan, Marcio G.; Peixoto, Alexandre A.; Schama, Renata] Fundacao Oswaldo Cruz, Inst Oswaldo Cruz, BR-21040900 Rio De Janeiro, Brazil.
   [Minx, Patrick; Spieth, John; Montague, Michael J.; Fronick, Catrina; Fulton, Lucinda A.; Warren, Wesley C.; Wilson, Richard K.] Washington Univ, Sch Med, McDonnell Genome Inst, St Louis, MO 63108 USA.
   [Bernardo Carvalho, A.; Koerich, Leonardo B.; Lazoski, Cristiano] Univ Fed Rio de Janeiro, Dept Genet, Inst Biol, BR-21941590 Rio De Janeiro, Brazil.
   [Panzera, Francisco] Univ Republica, Secc Genet Evolutiva, Fac Ciencias, Montevideo 11400, Uruguay.
   [Lawson, Daniel; Christensen, Mikkel B.; Hughes, Daniel S. T.; Megy, Karine; Wilson, Derek] Welcome Trust Genome Campus, European Mol Biol Lab, European Bioinformat Inst, Hinxton, Cambs CB10 1SD, England.
   [Ribeiro, Jose M. C.] NIAID, Sect Vector Biol, NIH, Rockville, MD 20852 USA.
   [Waterhouse, Robert M.] Univ Geneva, Sch Med, Dept Genet Med & Dev, CH-1211 Geneva, Switzerland.
   [Waterhouse, Robert M.] Swiss Inst Bioinformat, CH-1211 Geneva, Switzerland.
   [Waterhouse, Robert M.] MIT, Comp Sci & Artificial Intelligence Lab, Cambridge, MA 02139 USA.
   [Waterhouse, Robert M.] Broad Inst MIT & Harvard, Cambridge, MA 02142 USA.
   [Abad-Franch, Fernando] Fundacao Oswaldo Cruz, Grp Pesquisa Ecol Doencas Transmissiveis Amazonia, Inst Leonidas & Maria Deane, BR-69057070 Amazonas, Brazil.
   [Robertson, Hugh M.] Univ Fed Uberlandia, Lab Bioinformat & Analises Mol, Inst Genet & Bioquim, Fac Comp, BR-38700002 Minas Gerais, Brazil.
   [Araujo, Helena M.; Berni, Mateus; Fontenele, Marcio] Univ Fed Rio de Janeiro, Inst Ciencias Biomed, BR-21941591 Rio De Janeiro, Brazil.
   [Araujo, Ricardo N.; Pereira, Marcos H.] Univ Fed Minas Gerais, Dept Parasitol, Inst Ciencias Biol, BR-31270901 Minas Gerais, Brazil.
   [Aravind, L.] Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Rockville, MD 20894 USA.
   [Calderon-Fernandez, Gustavo; Patricia Juarez, M.; Pedrini, Nicolas] Univ Nacl La Plata, Inst Invest Bioquim La Plata, Fac Ciencias Med, CONICET, RA-1900 La Plata, Buenos Aires, Argentina.
   [Carareto, Claudia M. A.; Granzotto, Adriana] Univ Estadual Paulista, Dept Biol, BR-15054000 Sao Paulo, Brazil.
   [Dansa, Marilvia; Lugon, Magda D.; Venancio, Thiago M.] Univ Estadual Norte Fluminense, Ctr Biociencias & Biotecnol, Lab Quim & Funcao Proteinas Peptideos, BR-28013602 Rio De Janeiro, Brazil.
   [Dimopoulos, George; Pike, Andrew] Johns Hopkins Univ, Dept Mol Microbiol & Immunol, Bloomberg Sch Publ Hlth, Baltimore, MD 21205 USA.
   [Emrich, Scott J.] Univ Notre Dame, Dept Comp Sci & Engn, Notre Dame, IN 46556 USA.
   [Fampa, Patricia] Univ Fed Rio de Janeiro, Dept Biol Anim, Inst Ciencias Biol & Saude, BR-23897000 Rio De Janeiro, Brazil.
   [Fernandez-Medina, Rita D.] Fundacao Oswaldo Cruz, Escola Nacl Saude Publ, BR-21040360 Rio De Janeiro, Brazil.
   [da Fonseca, Rodrigo N.] Univ Fed Rio de Janeiro, Nucl Pesquisas Ecol Macae, BR-27910970 Rio De Janeiro, Brazil.
   [Giraldo-Calderon, Gloria I.] Univ Notre Dame, Dept Biol Sci, Notre Dame, IN 46556 USA.
   [Guarneri, Alessandra A.; Latorre-Estivalis, Jose Manuel; Lorenzo, Marcelo G.] Fundacao Oswaldo Cruz, Ctr Pesquisas Rene Rachou, BR-30190002 Minas Gerais, Brazil.
   [Guigo, Roderic; Mariotti, Marco; Santesmasses, Didac] Barcelona Inst Sci & Technol, Ctr Genom Regulat, Barcelona 08003, Catalonia, Spain.
   [Guigo, Roderic; Mariotti, Marco; Santesmasses, Didac] Univ Pompeu Fabra, Barcelona 08003, Catalonia, Spain.
   [Harry, Myriam] CNRS, Lab Evolut Genome & Speciat, Inst Rech Dev, UPR9034,UR 072, F-91198 Gif Sur Yvette, France.
   [Harry, Myriam] Univ Paris 11, F-91400 Orsay, France.
   [Jacquin-Joly, Emmanuelle] French Natl Inst Agr Res, Inst Ecol & Environm Sci Paris, F-78000 Versailles, France.
   [Lawrence, Gena G.; Marcet, Paula L.; Dotson, Ellen M.] Ctr Dis Control & Prevent, Entomol Branch, Div Parasit Dis & Malaria, Atlanta, GA 30329 USA.
   [Lazzari, Claudio R.] Univ Tours, Inst Rech Biol Insecte, UMR7261, Ctr Natl Rech Scientif, F-37200 Tours, France.
   [Majerowicz, David] Univ Fed Rio de Janeiro, Fac Farm, Dept Biotecnol Farma, BR-21941902 Rio De Janeiro, Brazil.
   [Missirlis, Fanis] Inst Politecn Nacl, Ctr Invest & Estudios Avanzados, Dept Physiol Biophys & Neurosci, Mexico City 03760, DF, Mexico.
   [Mota, Theo] Univ Fed Minas Gerais, Dept Fisiol & Biofis, Inst Ciencias Biol, BR-31270901 Minas Gerais, Brazil.
   [Noriega, Fernando G.; Nouzova, Marcela] Florida Int Univ, Dept Biol Sci, Miami, FL 11200 USA.
   [Ribeiro-Rodrigues, Rodrigo] Univ Fed Espirito Santo, Nucl Doencas Infecciosas, BR-29043900 Espirito Santo, Brazil.
   [Robertson, Hugh M.] Univ Illinois, Dept Entomol, Urbana, IL 61801 USA.
   [Salerno, Ana Paula; Seabra-Junior, Eloy S.] Inst Fed Edu Ciencia & Tecnol Rio De Janeriro, BR-20270021 Rio De Janeiro, Brazil.
   [Tojo, Marta] Univ Santiago Compostela, Inst Invest Sanitarias, Dept Physiol, Sch Med,Ctr Res Mol Med & Chron Dis, Santiago De Compostela 15782, Spain.
   [Tu, Zhijian Jake] Virginia Polytech Inst & State Univ, Dept Biochem, Blacksburg, VA 24061 USA.
   [Tubio, Jose M. C.] Univ Cambridge, Dept Vet Med, Cambridge CB3 0ES, England.
   [Huebner, Erwin] Univ Manitoba, Dept Biol Sci, Winnipeg, MB R3T 2N2, Canada.
RP Mesquita, RD (reprint author), Univ Fed Rio de Janeiro, Inst Quim, Dept Bioquim, BR-21941909 Rio De Janeiro, Brazil.
EM rdmesquita@iq.ufrj.br; edotson@cdc.gov; pedro@bioqmed.ufrj.br
RI Alves-Bezerra, Michele/B-4662-2014; Nunes, Rodrigo/J-6859-2012; Pavan,
   Marcio/F-3270-2015; Venancio, Thiago/B-5003-2011; Jablonka,
   Willy/D-2333-2017; Carareto, Claudia/D-2814-2012; Araujo,
   Helena/D-7149-2013; de Souza Gomes, Matheus/G-3480-2012; Missirlis,
   Fanis/C-1137-2011; Majerowicz, David/B-5361-2016; Costa,
   Igor/B-4698-2016; Amaral, Laurence/G-5905-2012; Melo, Ana C.
   A./K-1048-2013; Waterhouse, Robert/A-1858-2010; Lazoski,
   Cristiano/H-6192-2013; Carvalho, A. Bernardo/D-5402-2013; Pereira,
   Marcos/A-3774-2012; Prosdocimi, Francisco/F-6847-2012; Guigo,
   Roderic/D-1303-2010
OI Fontenele, Marcio/0000-0001-8828-3671; Marcet,
   Paula/0000-0002-0676-3020; Jablonka, Willy/0000-0001-5380-7797; Ribeiro,
   Jose/0000-0002-9107-0818; Oliveira, Pedro/0000-0003-0307-354X;
   Calderon-Fernandez, Gustavo/0000-0003-2279-6209; Alves-Bezerra,
   Michele/0000-0003-4430-6434; Nunes, Rodrigo/0000-0003-1346-291X; Pavan,
   Marcio/0000-0002-5699-242X; Araujo, Helena/0000-0003-0371-9523; Lawson,
   Daniel/0000-0001-7765-983X; Panzera, Francisco/0000-0001-5148-957X; de
   Souza Gomes, Matheus/0000-0001-7352-3089; Missirlis,
   Fanis/0000-0003-0467-8444; Majerowicz, David/0000-0001-7916-5315; Costa,
   Igor/0000-0003-0957-9461; Amaral, Laurence/0000-0003-4681-5451; Melo,
   Ana C. A./0000-0003-0686-7089; Waterhouse, Robert/0000-0003-4199-9052;
   Carvalho, A. Bernardo/0000-0001-8959-6469; Prosdocimi,
   Francisco/0000-0002-6761-3069; Guigo, Roderic/0000-0002-5738-4477
FU National Institutes of Health Grant [NHGRI-HG003079]; National
   Institutes of Health National Institute of Allergy and Infectious
   Diseases Grant [HHSN272200900039C]; Conselho Nacional de Desenvolvimento
   Cientifico e Tecnologico; Fundacao de Amparo a Pesquisa do Estado do Rio
   de Janeiro (FAPERJ); Fundacao de Amparo a Pesquisa do Estado de Sao
   Paulo; Fundacao de Amparo a Pesquisa do Estado de Minas Gerais; Consejo
   Nacional de Investigaciones Cientificas y Tecnicas de Argentina; Agencia
   Nacional de Promocion de Ciencia y Tecnologia; Fundacion Bunge y Born;
   Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior/FAPERJ; 
   [PIOF-GA-2011-303312]
FX We thank Charles B. Beard for the Rhodnius prolixus picture. Genome
   sequencing was funded by National Institutes of Health Grant
   NHGRI-HG003079; VectorBase was supported by National Institutes of
   Health National Institute of Allergy and Infectious Diseases Grant
   HHSN272200900039C; Brazilian groups were funded by Conselho Nacional de
   Desenvolvimento Cientifico e Tecnologico, Fundacao de Amparo a Pesquisa
   do Estado do Rio de Janeiro (FAPERJ), Fundacao de Amparo a Pesquisa do
   Estado de Sao Paulo, and Fundacao de Amparo a Pesquisa do Estado de
   Minas Gerais; R.R.-P. was supported by Consejo Nacional de
   Investigaciones Cientificas y Tecnicas de Argentina, Agencia Nacional de
   Promocion de Ciencia y Tecnologia, and Fundacion Bunge y Born; R.D.F.-M.
   was funded by Coordenacao de Aperfeicoamento de Pessoal de Nivel
   Superior/FAPERJ; and R.M.W. was supported by Marie Curie
   PIOF-GA-2011-303312.
NR 61
TC 37
Z9 37
U1 7
U2 35
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 DEC 1
PY 2015
VL 112
IS 48
BP 14936
EP 14941
DI 10.1073/pnas.1506226112
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA CX8XR
UT WOS:000365988900059
PM 26627243
ER

PT J
AU Plitt, M
   Barnes, KA
   Wallace, GL
   Kenworthy, L
   Martin, A
AF Plitt, Mark
   Barnes, Kelly Anne
   Wallace, Gregory L.
   Kenworthy, Lauren
   Martin, Alex
TI Resting-state functional connectivity predicts longitudinal change in
   autistic traits and adaptive functioning in autism
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE rs-fMRI; autism; machine learning; ASD; adaptive behavior
ID RECEPTIVE LANGUAGE DISORDER; DEFAULT MODE NETWORK; EARLY ADULT LIFE;
   SPECTRUM DISORDERS; ASPERGER-SYNDROME; EARLY-CHILDHOOD; DEVELOPMENTAL
   TRAJECTORIES; MALADAPTIVE BEHAVIORS; DIAGNOSTIC INTERVIEW;
   COGNITIVE-ABILITIES
AB Although typically identified in early childhood, the social communication symptoms and adaptive behavior deficits that are characteristic of autism spectrum disorder (ASD) persist throughout the lifespan. Despite this persistence, even individuals without cooccurring intellectual disability show substantial heterogeneity in outcomes. Previous studies have found various behavioral assessments [ such as intelligence quotient (IQ), early language ability, and baseline autistic traits and adaptive behavior scores] to be predictive of outcome, but most of the variance in functioning remains unexplained by such factors. In this study, we investigated to what extent functional brain connectivity measures obtained from resting-state functional connectivity MRI (rs-fcMRI) could predict the variance left unexplained by age and behavior (follow-up latency and baseline autistic traits and adaptive behavior scores) in two measures of outcome-adaptive behaviors and autistic traits at least 1 y postscan (mean follow-up latency = 2 y, 10 mo). We found that connectivity involving the so-called salience network (SN), default-mode network (DMN), and frontoparietal task control network (FPTCN) was highly predictive of future autistic traits and the change in autistic traits and adaptive behavior over the same time period. Furthermore, functional connectivity involving the SN, which is predominantly composed of the anterior insula and the dorsal anterior cingulate, predicted reliable improvement in adaptive behaviors with 100% sensitivity and 70.59% precision. From rs-fcMRI data, our study successfully predicted heterogeneity in outcomes for individuals with ASD that was unaccounted for by simple behavioral metrics and provides unique evidence for networks underlying long-term symptom abatement.
C1 [Plitt, Mark; Barnes, Kelly Anne; Wallace, Gregory L.; Kenworthy, Lauren; Martin, Alex] NIMH, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
   [Wallace, Gregory L.] George Washington Univ, Dept Speech & Hearing Sci, Washington, DC 20052 USA.
   [Kenworthy, Lauren] Childrens Natl Hlth Syst, Ctr Autism Spectrum Disorders, Washington, DC 20010 USA.
RP Plitt, M (reprint author), NIMH, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
EM mplitt@stanford.edu; alexmartin@mail.nih.gov
OI Wallace, Gregory/0000-0003-0329-5054
FU National Alliance for Research on Schizophrenia and Depression; Attias
   Family Foundation Young Investigator Grant from Brain & Behavior
   Research Foundation; Intramural Research Program, National Institute of
   Mental Health/NIH [ZIAMH002920]
FX We thank Bako Orionzi and Ian Eisenberg for efforts obtaining follow-up
   behavioral assessments and Gustavo Sudre, Jonathan Power, and Steve
   Gotts for helpful discussions regarding methods and statistics. This
   work was supported by a National Alliance for Research on Schizophrenia
   and Depression and Attias Family Foundation Young Investigator Grant
   from the Brain & Behavior Research Foundation (to K.A.B.) and by the
   Intramural Research Program, National Institute of Mental Health/NIH
   (ZIAMH002920).
NR 69
TC 5
Z9 5
U1 10
U2 29
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 DEC 1
PY 2015
VL 112
IS 48
BP E6699
EP E6706
DI 10.1073/pnas.1510098112
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA CX8XR
UT WOS:000365988900016
PM 26627261
ER

PT J
AU Saber, R
   Liu, K
   Ferrucci, L
   Criqui, MH
   Zhao, LH
   Tian, L
   Guralnik, JM
   Liao, YH
   Domanchuk, K
   Kibbe, MR
   Green, D
   Perlman, H
   McDermott, MM
AF Saber, Rana
   Liu, Kiang
   Ferrucci, Luigi
   Criqui, Michael H.
   Zhao, Lihui
   Tian, Lu
   Guralnik, Jack M.
   Liao, Yihua
   Domanchuk, Kathryn
   Kibbe, Melina R.
   Green, David
   Perlman, Harris
   McDermott, Mary M.
TI Ischemia-related changes in circulating stem and progenitor cells and
   associated clinical characteristics in peripheral artery disease
SO VASCULAR MEDICINE
LA English
DT Article
DE ischemia; peripheral artery disease; stem and progenitor cells;
   treadmill exercise
ID ANKLE BRACHIAL INDEX; FUNCTIONAL PERFORMANCE; CARDIOVASCULAR EVENTS;
   PHYSICAL-ACTIVITY; VASCULAR REPAIR; LEG SYMPTOMS; EXERCISE;
   MOBILIZATION; BLOOD; PREDICTS
AB The extent and clinical significance of stem and progenitor cell (SPC) increases in response to lower-extremity ischemia in people with peripheral artery disease (PAD) are unclear. We compared changes in SPC levels immediately following a treadmill exercise test between individuals with and without PAD. Among participants with PAD, we determined whether more severe PAD was associated with greater increases in SPCs following treadmill exercise-induced lower-extremity ischemia. We measured SPC levels in 25 participants with PAD and 20 without PAD before and immediately after a treadmill exercise test. Participants with PAD, compared to participants without PAD, had greater increases in CD34(+)CD45(dim) (+0.08 +/- 0.03 vs -0.06 +/- 0.04, p=0.008), CD34(+)CD45(dim)CD133(+) (+0.08 +/- 0.05 vs -0.08 +/- 0.04, p=0.014), CD34(+)CD45(dim)CD31(+) (+0.10 +/- 0.03 vs -0.07 +/- 0.04, p=0.002), and CD34(+)CD45(dim)ALDH(+) SPCs (+0.18 +/- 0.07 vs -0.05 +/- 0.08, p=0.054) measured as a percentage of all white blood cells. Among participants with PAD, those with any increases in the percent of SPCs immediately after the treadmill exercise test compared to those with no change or a decrease in SPCs had lower baseline ankle-brachial index values (0.65 +/- 0.17 vs 0.90 +/- 0.19, p=0.004) and shorter treadmill times to onset of ischemic leg symptoms (2.17 +/- 1.54 vs 5.25 +/- 3.72 minutes, p=0.012). In conclusion, treadmill exercise-induced lower-extremity ischemia is associated with acute increases in circulating SPCs among people with PAD. More severe PAD is associated with a higher prevalence of SPC increases in response to lower-extremity ischemia. Further prospective study is needed to establish the prognostic significance of ischemia-related increases in SPCs among patients with PAD.
C1 [Saber, Rana; Domanchuk, Kathryn; Green, David; Perlman, Harris; McDermott, Mary M.] Northwestern Univ, Feinberg Sch Med, Dept Med, Chicago, IL 60611 USA.
   [Liu, Kiang; Zhao, Lihui; Liao, Yihua; McDermott, Mary M.] Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
   [Ferrucci, Luigi] NIA, Bethesda, MD 20892 USA.
   [Criqui, Michael H.] Univ Calif San Diego, Dept Family & Prevent Med, La Jolla, CA 92093 USA.
   [Tian, Lu] Stanford Univ, Dept Hlth Res & Policy, Stanford, CA 94305 USA.
   [Guralnik, Jack M.] Univ Maryland, Sch Med, Dept Epidemiol & Publ Hlth, Baltimore, MD 21201 USA.
   [Kibbe, Melina R.] Northwestern Univ, Feinberg Sch Med, Dept Surg, Chicago, IL 60611 USA.
   [Kibbe, Melina R.] Jesse Brown Vet Affairs Med Ctr, Chicago, IL USA.
RP McDermott, MM (reprint author), Northwestern Univ, Feinberg Sch Med, Dept Med & Prevent Med, 750 N Lake Shore Dr,10th Floor, Chicago, IL 60611 USA.
EM mdm608@northwestern.edu
FU National Heart, Lung, and Blood Institute [R01-HL107510]; National
   Institute of Health's Intramural Program of the National Institute on
   Aging
FX The study was funded by the National Heart, Lung, and Blood Institute
   (R01-HL107510) and the National Institute of Health's Intramural Program
   of the National Institute on Aging.
NR 30
TC 1
Z9 1
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1358-863X
EI 1477-0377
J9 VASC MED
JI Vasc. Med.
PD DEC
PY 2015
VL 20
IS 6
BP 534
EP 543
DI 10.1177/1358863X15600255
PG 10
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA CY0JV
UT WOS:000366093300005
PM 26324152
ER

PT J
AU Lakdawala, SS
   Shih, AR
   Jayaraman, A
   Lamirande, EW
   Moore, I
   Paskel, M
   Sasisekharan, R
   Subbarao, K
AF Lakdawala, Seema S.
   Shih, Angela R.
   Jayaraman, Akila
   Lamirande, Elaine W.
   Moore, Ian
   Paskel, Myeisha
   Sasisekharan, Ram
   Subbarao, Kanta
TI Receptor specificity does not affect replication or virulence of the
   2009 pandemic H1N1 influenza virus in mice and ferrets (vol 446, pg 349,
   2013)
SO VIROLOGY
LA English
DT Correction
C1 [Lakdawala, Seema S.; Shih, Angela R.; Lamirande, Elaine W.; Moore, Ian; Paskel, Myeisha; Subbarao, Kanta] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
   [Jayaraman, Akila; Sasisekharan, Ram] MIT, Singapore MIT Alliance Res & Technol, Koch Inst Integrat Canc Res, Dept Biol Engn, Cambridge, MA 02139 USA.
RP Sasisekharan, R (reprint author), MIT, Singapore MIT Alliance Res & Technol, Koch Inst Integrat Canc Res, Dept Biol Engn, 77 Massachusetts Ave, Cambridge, MA 02139 USA.
EM rams@MIT.edu; ksubbarao@niaid.nih.gov
NR 1
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD DEC
PY 2015
VL 486
BP 321
EP 321
DI 10.1016/j.virol.2015.11.010
PG 1
WC Virology
SC Virology
GA CY2HQ
UT WOS:000366229800036
ER

PT J
AU Yu, L
   Laeyendecker, O
   Wendel, SK
   Liang, FX
   Liu, W
   Wang, XY
   Wang, L
   Pang, XW
   Fang, ZL
AF Yu, Li
   Laeyendecker, Oliver
   Wendel, Sarah K.
   Liang, Fuxiong
   Liu, Wei
   Wang, Xueyan
   Wang, Lu
   Pang, Xianwu
   Fang, Zhongliao
TI Short Communication: Low False Recent Rate of Limiting-Antigen Avidity
   Assay Among Long-Term Infected Subjects from Guangxi, China
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Article
AB Assays used for HIV cross-sectional incidence testing can misclassify some individuals with nonrecent HIV infection as recently infected, overestimating HIV incidence. We analyzed the frequency and factors associated with false-recent misclassification on subjects from Quangxi, China known to have long-term infection using the limited antigen-avidity assay (LAg-Avidity). Stored samples from treatment-naive individuals from Guangxi, China were tested using the LAg-Avidity. A total of 362 samples from individuals known to be infected 2 to 13.5 years were tested and the false-recent rate (FRR), the frequency of samples with a positive result, was determined at different cutoff values of the assay. Additionally, factors associated with misclassification were determined. The FRR of the LAg-Avidity was 1.1% (4/362) using a cutoff of 1.5 normalized optical density units (OD-n). All four samples had viral loads >1,000 copies/ml. Using a cutoff of 3.0 OD-n the FRR was 5.5% (20/362), with four samples having viral loads <1,000 copies/ml. Factors associated with a higher odds of misclassification were female gender (OR 7.7, 95% CI 1.0-56.4) and being a female sex worker (OR 31.3, 95% CI 4.0-242). At the higher cutoff, being of Zhuang decent, relative to Han, had higher odds of misclassification (OR 6.2, 95% CI 1.99-19.0). The LAg-Avidity assay had a low FRR in this Chinese population. Further investigations of the higher frequency of low LAg-Avidity results seen in female sex workers and individuals of Zhuang descent should be explored in a larger study.
C1 [Yu, Li; Liang, Fuxiong; Liu, Wei; Wang, Xueyan; Wang, Lu; Pang, Xianwu; Fang, Zhongliao] Guangxi Ctr Dis Prevent & Control, Nanning, Peoples R China.
   [Laeyendecker, Oliver; Wendel, Sarah K.] NIAID, NIH, Baltimore, MD 21205 USA.
   [Laeyendecker, Oliver] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
RP Laeyendecker, O (reprint author), NIAID, LIR, NIH, 855 North Wolfe St,Room 538A, Baltimore, MD 21205 USA.
EM olaeyen1@jhmi.edu
FU Division of Intramural Research of National Institute of Allergy and
   Infectious Diseases, National Institutes of Health
FX This study was funded in part by the Division of Intramural Research of
   the National Institute of Allergy and Infectious Diseases, National
   Institutes of Health.
NR 10
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 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD DEC 1
PY 2015
VL 31
IS 12
BP 1247
EP 1249
DI 10.1089/aid.2015.0097
PG 3
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA CX3EH
UT WOS:000365578100009
PM 26331573
ER

PT J
AU Huded, C
   Prasad, V
AF Huded, Chetan
   Prasad, Vinay
TI Meta-Analyses of Statin Therapy for Primary Prevention Do Not Answer Key
   Questions: An Empirical Appraisal of 5 Years of Statin Meta-Analyses
SO AMERICAN JOURNAL OF CARDIOVASCULAR DRUGS
LA English
DT Article
ID CORONARY-HEART-DISEASE; DENSITY-LIPOPROTEIN CHOLESTEROL; RANDOMIZED
   CONTROLLED-TRIAL; PLACEBO-CONTROLLED TRIAL; CARDIOVASCULAR-DISEASE;
   UPDATED METAANALYSIS; STROKE PREVENTION; LDL CHOLESTEROL; LOW-RISK;
   EVENTS
AB Although meta-analyses of statins in primary prevention are designed to provide doctors and patients with better evidence about the risks and potential benefits of treatment, they may ignore important patient-centered outcomes and concerns. We examined all meta-analyses of statins for primary prevention over the last 5 years. We assessed whether each meta-analysis addressed five key points: whether authors examined endpoints based on the use of statin therapy, and not stratified by low-density lipoprotein reduction; whether authors included only studies of statin versus placebo, and not varying doses or brands of statin; whether authors considered commonly cited harms; whether secondary prevention patients were excluded; and, whether overall mortality was examined. We examined 189 articles to identify 24 meta-analyses of statins that made claims regarding primary prevention. Six studies (25 %) reported outcomes as a function of reduction in serum lipid levels rather than treatment received. Seven studies (29 %) included trials of high-dose versus low-dose statin in their analysis. Five studies (21 %) did not examine all-cause mortality. The majority of studies (n = 21, 88 %) failed to exclude patients with known cardiovascular disease, and 22 (92 %) studies failed to assess two of three common safety concerns. Nevertheless, most (n = 20, 83 %) meta-analyses supported the use of statins in primary prevention. Based on our findings, we conclude that most recent meta-analyses of statins for primary prevention do not adequately address the question they seek to answer.
C1 [Huded, Chetan] Northwestern Univ, Dept Med, Chicago, IL 60611 USA.
   [Prasad, Vinay] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Prasad, V (reprint author), NCI, Med Oncol Branch, NIH, 10 Ctr Dr 10-12N226, Bethesda, MD 20892 USA.
EM vinayak.prasad@nih.gov
OI Prasad, Vinay/0000-0002-6110-8221
NR 60
TC 0
Z9 0
U1 0
U2 5
PU ADIS INT LTD
PI NORTHCOTE
PA 5 THE WAREHOUSE WAY, NORTHCOTE 0627, AUCKLAND, NEW ZEALAND
SN 1175-3277
EI 1179-187X
J9 AM J CARDIOVASC DRUG
JI Am. J. Cardiovasc. Drugs
PD DEC
PY 2015
VL 15
IS 6
BP 379
EP 386
DI 10.1007/s40256-015-0139-y
PG 8
WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy
SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy
GA CX7GB
UT WOS:000365869100001
PM 26141958
ER

PT J
AU Rabassa, M
   Zamora-Ros, R
   Urpi-Sarda, M
   Bandinelli, S
   Ferrucci, L
   Andres-Lacueva, C
   Cherubini, A
AF Rabassa, Montserrat
   Zamora-Ros, Raul
   Urpi-Sarda, Mireia
   Bandinelli, Stefania
   Ferrucci, Luigi
   Andres-Lacueva, Cristina
   Cherubini, Antonio
TI Association of habitual dietary resveratrol exposure with the
   development of frailty in older age: the Invecchiare in Chianti study
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
DE aging; biomarker; diet; epidemiology; frailty; InCHIANTI; resveratrol
ID ALL-CAUSE MORTALITY; TRANS-RESVERATROL; METABOLIC PROFILE; RED WINE;
   ADULTS; HUMANS; INDEX; SUPPLEMENTATION; CONSUMPTION; RESTRICTION
AB Background: Resveratrol may play a protective role against the frailty syndrome (FS) because of its antioxidant and anti-inflammatory properties.
   Objective: We prospectively evaluated the association between habitual dietary resveratrol exposure and the development of FS after 3-, 6-, and 9-y follow-up periods in a community-dwelling older population.
   Design: We conducted a longitudinal analysis with the use of data from 769 participants aged >= 65 y from the Invecchiare in Chianti (Aging in Chianti) study. Total dietary resveratrol (TDR) intake was estimated at baseline with the use of a validated food-frequency questionnaire, which was developed to assess participants' usual food intakes over the previous year, and an ad hoc resveratrol database. Total urinary resveratrol (TUR) was analyzed with the use of liquid chromatography-tandem mass spectrometry with a previous solid-phase extraction at baseline. The combination of both measures [total dietary resveratrol plus total urinary resveratrol (TDR + TUR)] was computed with the use of the Howe's method. FS was assessed at baseline and at 3-, 6-, and 9-y of follow-up and was defined as the presence of >= 3 of the following 5 criteria: shrinking, exhaustion, sedentariness, slowness, and weakness.
   Results: TDR+TUR concentrations were inversely associated with FS risk over 3-y of follow-up (OR for comparison of extreme tertiles: 0.11; 95% CI: 0.03, 0.45; P-trend = 0.002) but not after 6-and 9-y of follow-up in multinomial logistic regression models adjusted for baseline frailty status and potential confounders. These results did not differ when analyses were further adjusted for inflammatory markers.
   Conclusion: Higher habitual dietary resveratrol exposure was associated with lower risk of older community dwellers developing FS during the first 3 y of follow-up but not after longer follow-up periods.
C1 [Rabassa, Montserrat; Urpi-Sarda, Mireia; Andres-Lacueva, Cristina] Univ Barcelona, Inst Res Nutr & Food Safety INSA UB, Catalonian Reference Network Food Technol XaRTA, Biomarkers & Nutrimetab Lab,Nutr & Food Sci Dept, Barcelona, Spain.
   [Zamora-Ros, Raul] IARC, Nutr & Metab Sect, Biomarkers Grp, Lyon, France.
   [Bandinelli, Stefania] Azienda Sanit Firenze, Geriatr Rehabil Unit, Florence, Italy.
   [Ferrucci, Luigi] NIA, Clin Res Branch, NIH, Baltimore, MD 21224 USA.
   [Cherubini, Antonio] Italian Natl Res Ctr Aging, Geriatr & Geriatr Emergency Care, Ancona, Italy.
RP Andres-Lacueva, C (reprint author), Univ Barcelona, Inst Res Nutr & Food Safety INSA UB, Catalonian Reference Network Food Technol XaRTA, Biomarkers & Nutrimetab Lab,Nutr & Food Sci Dept, Campus Torribera, Barcelona, Spain.
EM candres@ub.edu
RI Andres-Lacueva, Cristina/J-3377-2012; 
OI Andres-Lacueva, Cristina/0000-0002-8494-4978; urpi,
   mireia/0000-0002-4064-5175
FU Spanish government grants from the Ministry of Economy and
   Competitiveness (MINECO); JPI HDHL FOODBALL project
   [PCIN-2014-133-MINECO-Spain]; Generalitat de Catalunya's Agency AGAUR
   [2014SGR1566]; Plan N de I+D+i [PI13/01172]; Italian Ministry of Health;
   United States National Institute on Aging; MINECO [RYC-2011-09677];
   Fondo Social Europeo; CONSOLIDER-INGENIO program; FUN-C-FOOD
   [CSD2007-063]; Fondo Europeo de Desarrollo Regional
FX Supported by the Spanish government grants from the Ministry of Economy
   and Competitiveness (MINECO) and cofounded by the Fondo Europeo de
   Desarrollo Regional (FEDER): AGL2009-13906-C02-01, CONSOLIDER-INGENIO
   2010 program, FUN-C-FOOD (CSD2007-063), and JPI HDHL FOODBALL project
   (PCIN-2014-133-MINECO-Spain). This research was also supported by the
   award (2014SGR1566) from the Generalitat de Catalunya's Agency AGAUR,
   and the PI13/01172 project (Plan N de I+D+i 2013-2016), cofounded by the
   ISCII-Subdireccion General de Evaluacion y Fomento de la Investigacion,
   and the Fondo Europeo de Desarrollo Regional. In the framework of the
   COST Action POSITIVE FA1403. The Invecchiare in Chianti study is
   supported in part by the Italian Ministry of Health and by the United
   States National Institute on Aging. MU-S received support for the "Ramon
   y Cajal" program (RYC-2011-09677) from MINECO and the Fondo Social
   Europeo.
NR 47
TC 4
Z9 4
U1 9
U2 15
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
EI 1938-3207
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD DEC
PY 2015
VL 102
IS 6
BP 1534
EP 1542
DI 10.3945/ajcn.115.118976
PG 9
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA CX5BY
UT WOS:000365717300029
PM 26490492
ER

PT J
AU Conde-Agudelo, A
   Romero, R
AF Conde-Agudelo, Agustin
   Romero, Roberto
TI Predictive accuracy of changes in transvaginal sonographic cervical
   length over time for preterm birth: a systematic review and metaanalysis
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Review
DE longitudinal studies; prematurity; predictive value of test; screening;
   shortening in cervical length; singleton gestation; twin gestation
ID DIAGNOSTIC-TEST ACCURACY; ASYMPTOMATIC TWIN PREGNANCIES; WEEKS
   GESTATION; HIGH-RISK; ULTRASONOGRAPHIC MEASUREMENT; LIKELIHOOD RATIOS;
   DELIVERY; WOMEN; ULTRASOUND; TESTS
AB OBJECTIVE: To determine the accuracy of changes in transvaginal sonographic cervical length over time in predicting preterm birth in women with singleton and twin gestations.
   DATA SOURCES: PubMed, Embase, Cinahl, Lilacs, and Medion (all from inception to June 30, 2015), bibliographies, Google scholar, and conference proceedings. Cohort or cross-sectional studies reporting on the predictive accuracy for preterm birth of changes in cervical length over time.
   STUDY APPRAISAL AND SYNTHESIS METHODS: Two reviewers independently selected studies, assessed the risk of bias, and extracted the data. Summary receiver-operating characteristic curves, pooled sensitivities and specificities, and summary likelihood ratios were generated.
   RESULTS: Fourteen studies met the inclusion criteria, of which 7 provided data on singleton gestations (3374 women) and 8 on twin gestations (1024 women). Among women with singleton gestations, the shortening of cervical length over time had a low predictive accuracy for preterm birth at < 37 and < 35 weeks of gestation with pooled sensitivities and specificities, and summary positive and negative likelihood ratios ranging from 49% to 74%, 44% to 85%, 1.3 to 4.1, and 0.3 to 0.7, respectively. In women with twin gestations, the shortening of cervical length over time had a low to moderate predictive accuracy for preterm birth at < 34, < 32, < 30, and < 28 weeks of gestation with pooled sensitivities and specificities, and summary positive and negative likelihood ratios ranging from 47% to 73%, 84% to 89%, 3.8 to 5.3, and 0.3 to 0.6, respectively. There were no statistically significant differences between the predictive accuracies for preterm birth of cervical length shortening over time and the single initial and/or final cervical length measurement in 8 of 11 studies that provided data for making these comparisons. In the largest and highest-quality study, a single measurement of cervical length obtained at 24 or 28 weeks of gestation was significantly more predictive of preterm birth than any decrease in cervical length between these gestational ages.
   CONCLUSIONS: Change in transvaginal sonographic cervical length over time is not a clinically useful test to predict preterm birth in women with singleton or twin gestations. A single cervical length measurement obtained between 18 and 24 weeks of gestation appears to be a better test to predict preterm birth than changes in cervical length over time.
C1 [Conde-Agudelo, Agustin; Romero, Roberto] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
   [Romero, Roberto] Univ Michigan, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA.
   [Romero, Roberto] Michigan State Univ, Dept Epidemiol & Biostat, E Lansing, MI 48824 USA.
   [Romero, Roberto] Wayne State Univ, Dept Mol Obstet & Genet, Detroit, MI USA.
RP Conde-Agudelo, A (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
EM romeror@mail.nih.gov
FU Intramural Research Program of the Eunice Kennedy Shriver National
   Institute of Child Health and Human Development, National Institutes of
   Health, Department of Health and Human Services
FX This study was supported by the Intramural Research Program of the
   Eunice Kennedy Shriver National Institute of Child Health and Human
   Development, National Institutes of Health, Department of Health and
   Human Services.
NR 61
TC 10
Z9 10
U1 0
U2 4
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
EI 1097-6868
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD DEC
PY 2015
VL 213
IS 6
BP 789
EP 801
DI 10.1016/j.ajog.2015.06.015
PG 13
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA CX5TH
UT WOS:000365764900005
PM 26070703
ER

PT J
AU Furcron, AE
   Romero, R
   Plazyo, O
   Unkel, R
   Xu, Y
   Hassan, SS
   Chaemsaithong, P
   Mahajan, A
   Gomez-Lopez, N
AF Furcron, Amy-Eunice
   Romero, Roberto
   Plazyo, Olesya
   Unkel, Ronald
   Xu, Yi
   Hassan, Sonia S.
   Chaemsaithong, Piya
   Mahajan, Arushi
   Gomez-Lopez, Nardhy
TI Vaginal progesterone, but not 17 alpha-hydroxyprogesterone caproate, has
   antiinflammatory effects at the murine maternal-fetal interface
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE decidua; endotoxin; interleukin-1 beta; macrophages; matrix
   metalloproteinase-9; myometrium; neutrophils; preterm birth; preterm
   labor; regulatory T cells
ID REGULATORY T-CELLS; SPONTANEOUS PRETERM BIRTH; UTERINE CERVICAL
   FIBROBLASTS; PLACEBO-CONTROLLED TRIAL; AMNIOTIC-FLUID INTERLEUKIN-6;
   TRANSCRIPTION FACTOR FOXP3; PRODUCE INTERFERON-GAMMA; HUMAN MYOMETRIAL
   CELLS; DOUBLE-BLIND; CLINICAL-SIGNIFICANCE
AB OBJECTIVE: Progestogen (vaginal progesterone or 17-alpha-hydroxyprogesterone caproate [17OHP-C]) administration to patients at risk for preterm delivery is widely used for the prevention of preterm birth (PTB). The mechanisms by which these agents prevent PTB are poorly understood. Progestogens have immunomodulatory functions; therefore, we investigated the local effects of vaginal progesterone and 17OHP-C on adaptive and innate immune cells implicated in the process of parturition.
   STUDY DESIGN: Pregnant C57BL/6 mice received vaginal progesterone (1 mg per 200 mu L, n = 10) or Replens (control, 200 mL, n = 10) from 13 to 17 days postcoitum (dpc) or were subcutaneously injected with 17OHP-C (2 mg per 100 mL, n = 10) or castor oil (control, 100 mL, n = 10) on 13, 15, and 17 dpc. Decidual and myometrial leukocytes were isolated prior to term delivery (18.5 dpc) for immunophenotyping by flow cytometry. Cervical tissue samples were collected to determine matrix metalloproteinase (MMP)-9 activity by in situ zymography and visualization of collagen content by Masson's trichrome staining. Plasma concentrations of progesterone, estradiol, and cytokines (interferon [IFN]gamma, interleukin (IL)-1 beta, IL-2, IL-4, IL-5, IL6, IL-10, IL-12p70, keratinocyte-activated chemokine/growth-related oncogene, and tumor necrosis factor-alpha) were quantified by enzyme-linked immunosorbent assays. Pregnant mice pretreated with vaginal progesterone or Replens were injected with 10 mg of an endotoxin on 16.5 dpc (n = 10 each) and monitored via infrared camera until delivery to determine the effect of vaginal progesterone on the rate of PTB.
   RESULTS: The following results were found: (1) vaginal progesterone, but not 17OHP-C, increased the proportion of decidual CD4+ regulatory T cells; (2) vaginal progesterone, but not 17OHP-C, decreased the proportion of decidual CD8+CD25+Foxp3+ T cells and macrophages; (3) vaginal progesterone did not result in M1/M2 macrophage polarization but reduced the proportion of myometrial IFN gamma+ neutrophils and cervical active MMP-9-positive neutrophils and monocytes; (4) 17OHP-C did not reduce the proportion of myometrial IFN gamma+ neutrophils; however, it increased the abundance of cervical active MMP-9-positive neutrophils and monocytes; (5) vaginal progesterone immune effects were associated with reduced systemic concentrations of IL-1 beta but not with alterations in progesterone or estradiol concentrations; and (6) vaginal progesterone pretreatment protected against endotoxin-induced PTB (effect size 50%, P = 0.011).
   CONCLUSION: Vaginal progesterone, but not 17OHP-C, has local antiinflammatory effects at the maternal-fetal interface and the cervix and protects against endotoxin-induced PTB.
C1 [Furcron, Amy-Eunice; Romero, Roberto; Plazyo, Olesya; Unkel, Ronald; Xu, Yi; Hassan, Sonia S.; Chaemsaithong, Piya; Gomez-Lopez, Nardhy] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Dept Hlth & Human Serv,Div Intramural Res, Perinatol Res Branch,Program Perinatal Res & Obst, Bethesda, MD USA.
   [Furcron, Amy-Eunice; Romero, Roberto; Plazyo, Olesya; Unkel, Ronald; Xu, Yi; Hassan, Sonia S.; Chaemsaithong, Piya; Gomez-Lopez, Nardhy] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Dept Hlth & Human Serv,Div Intramural Res, Perinatol Res Branch,Program Perinatal Res & Obst, Detroit, MI USA.
   [Furcron, Amy-Eunice; Hassan, Sonia S.; Chaemsaithong, Piya; Mahajan, Arushi; Gomez-Lopez, Nardhy] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA.
   [Gomez-Lopez, Nardhy] Wayne State Univ, Sch Med, Dept Immunol & Microbiol, Detroit, MI 48201 USA.
   [Romero, Roberto] Univ Michigan, Sch Med, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA.
   [Romero, Roberto] Michigan State Univ, Coll Human Med, Dept Epidemiol & Biostat, E Lansing, MI 48824 USA.
   [Romero, Roberto] Wayne State Univ, Ctr Mol Med & Genet, Detroit, MI USA.
RP Gomez-Lopez, N (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Dept Hlth & Human Serv,Div Intramural Res, Perinatol Res Branch,Program Perinatal Res & Obst, Bethesda, MD USA.
EM romeror@mail.nih.gov; nardhy.gomez-lopez@wayne.edu
RI Gomez-Lopez, Nardhy/R-7664-2016
OI Gomez-Lopez, Nardhy/0000-0002-3406-5262
FU Wayne State University Perinatal Initiative in Maternal, Perinatal, and
   Child Health; Perinatology Research Branch, Division of Intramural
   Research, Eunice Kennedy Shriver National Institute of Child Health and
   Human Development, National Institutes of Health, US Department of
   Health and Human Services
FX This study was supported by the Wayne State University Perinatal
   Initiative in Maternal, Perinatal, and Child Health and by the
   Perinatology Research Branch, Division of Intramural Research, Eunice
   Kennedy Shriver National Institute of Child Health and Human
   Development, National Institutes of Health, US Department of Health and
   Human Services.
NR 223
TC 5
Z9 5
U1 1
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
EI 1097-6868
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD DEC
PY 2015
VL 213
IS 6
AR 846.e1
DI 10.1016/j.ajog.2015.08.010
PG 19
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA CX5TH
UT WOS:000365764900019
PM 26264823
ER

PT J
AU Romero, R
   Grivel, JC
   Tarca, AL
   Chaemsaithong, P
   Xu, ZH
   Fitzgerald, W
   Hassan, SS
   Chaiworapongsa, T
   Margolis, L
AF Romero, Roberto
   Grivel, Jean-Charles
   Tarca, Adi L.
   Chaemsaithong, Piya
   Xu, Zhonghui
   Fitzgerald, Wendy
   Hassan, Sonia S.
   Chaiworapongsa, Tinnakorn
   Margolis, Leonid
TI Evidence of perturbations of the cytokine network in preterm labor
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE chemokine; chorioamnionitis; correlation network intra-amniotic
   infection; interactome; network analysis; sterile inflammation
ID MACROPHAGE INFLAMMATORY PROTEIN-1-ALPHA; FLUID MATRIX
   METALLOPROTEINASE-8; TUMOR-NECROSIS-FACTOR; MONOCYTE CHEMOTACTIC
   PROTEIN-1; MMP-8 BEDSIDE TEST; ACTIVATING PEPTIDE-1 INTERLEUKIN-8;
   MIDTRIMESTER GENETIC AMNIOCENTESIS; MATERNAL ANTIFETAL REJECTION; HUMAN
   AMNIOTIC-FLUID; BLOOD-CELL COUNT
AB OBJECTIVE: Intraamniotic inflammation/infection is the only mechanism of disease with persuasive evidence of causality for spontaneous preterm labor/delivery. Previous studies about the behavior of cytokines in preterm labor have been largely based on the analysis of the behavior of each protein independently. Emerging evidence indicates that the study of biologic networks can provide insight into the pathobiology of disease and improve biomarker discovery. The goal of this study was to characterize the inflammatory-related protein network in the amniotic fluid of patients with preterm labor.
   STUDY DESIGN: A retrospective cohort study was conducted that included women with singleton pregnancies who had spontaneous preterm labor and intact membranes (n = 135). These patients were classified according to the results of amniotic fluid culture, broad-range polymerase chain reaction coupled with electrospray ionization mass spectrometry, and amniotic fluid concentration of interleukin (IL)-6 into the following groups: (1) those without intraamniotic inflammation (n = 85), (2) those with microbial-associated intraamniotic inflammation (n = 15), and (3) those with intraamniotic inflammation without detectable bacteria (n = 35). Amniotic fluid concentrations of 33 inflammatory-related proteins were determined with the use of a multiplex bead array assay.
   RESULTS: Patients with preterm labor and intact membranes who had microbial-associated intraamniotic inflammation had a higher amniotic fluid inflammatory-related protein concentration correlation than those without intraamniotic inflammation (113 perturbed correlations). IL-1 beta, IL-6, macrophage inflammatory protein (MIP)-1 alpha, and IL-1 alpha were the most connected nodes (highest degree) in this differential correlation network (degrees of 20, 16, 12, and 12, respectively). Patients with sterile intraamniotic inflammation had correlation patterns of inflammatory-related proteins, both increased and decreased, when compared to those without intraamniotic inflammation (50 perturbed correlations). IL-1 alpha, MIP-1 alpha, and IL-1 beta were the most connected nodes in this differential correlation network (degrees of 12, 10, and 7, respectively). There were more coordinated inflammatory-related protein concentrations in the amniotic fluid of women with microbial-associated intraamniotic inflammation than in those with sterile intraamniotic inflammation (60 perturbed correlations), with IL-4 and IL-33 having the largest number of perturbed correlations (degrees of 15 and 13, respectively).
   CONCLUSIONS: We report for the first time an analysis of the inflammatory-related protein network in spontaneous preterm labor. Patients with preterm labor and microbial-associated intraamniotic inflammation had more coordinated amniotic fluid inflammatory-related proteins than either those with sterile intraamniotic inflammation or those without intraamniotic inflammation. The correlations were also stronger in patients with sterile intraamniotic inflammation than in those without intraamniotic inflammation. The findings herein could be of value in the development of biomarkers of preterm labor.
C1 [Romero, Roberto; Tarca, Adi L.; Chaemsaithong, Piya; Xu, Zhonghui; Hassan, Sonia S.; Chaiworapongsa, Tinnakorn] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, Program Perinatal Res & Obstet, Div Intramural Res,NIH, Bethesda, MD USA.
   [Romero, Roberto; Tarca, Adi L.; Chaemsaithong, Piya; Xu, Zhonghui; Hassan, Sonia S.; Chaiworapongsa, Tinnakorn] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, Program Perinatal Res & Obstet, Div Intramural Res,NIH, Detroit, MI USA.
   Univ Michigan, Sch Med, Dept Obstet & Gynecol, Ann Arbor, MI USA.
   Michigan State Univ, Dept Epidemiol & Biostat, E Lansing, MI 48824 USA.
   [Romero, Roberto] Wayne State Univ, Ctr Mol Med & Genet, Detroit, MI USA.
   [Tarca, Adi L.; Chaemsaithong, Piya; Hassan, Sonia S.; Chaiworapongsa, Tinnakorn] Wayne State Univ, Dept Obstet & Gynecol, Detroit, MI USA.
   [Grivel, Jean-Charles; Fitzgerald, Wendy; Margolis, Leonid] Eunice Kennedy Shriver NICHD, Sect Intercellular Interact, Program Phys Biol, NIH, Bethesda, MD USA.
   [Grivel, Jean-Charles] Sidra Med & Res Ctr, Div Translat Med, Doha, Qatar.
RP Romero, R (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, Program Perinatal Res & Obstet, Div Intramural Res,NIH, Bethesda, MD USA.
EM romeror@mail.nih.gov
FU Perinatology Research Branch, Division of Intramural Research, Eunice
   Kennedy Shriver National Institute of Child Health and Human
   Development, National Institutes of Health, Department of Health and
   Human Services (NICHD/NIH); NICHD/NIH [HHSN275201300006C]
FX Supported, in part, by the Perinatology Research Branch, Division of
   Intramural Research, Eunice Kennedy Shriver National Institute of Child
   Health and Human Development, National Institutes of Health, Department
   of Health and Human Services (NICHD/NIH), and in part, with federal
   funds from NICHD/NIH, under contract number HHSN275201300006C.
NR 279
TC 1
Z9 1
U1 1
U2 6
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
EI 1097-6868
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD DEC
PY 2015
VL 213
IS 6
AR 836.e1
DI 10.1016/j.ajog.2015.07.037
PG 18
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA CX5TH
UT WOS:000365764900015
PM 26232508
ER

PT J
AU Lee, MR
   Leggio, L
AF Lee, Mary R.
   Leggio, Lorenzo
TI Management of Alcohol Use Disorder in Patients Requiring Liver
   Transplant
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID LONG-TERM SURVIVAL; HEPATIC-ENCEPHALOPATHY; AMERICAN ASSOCIATION;
   PRACTICE GUIDELINE; UNITED-STATES; MELD SCORE; DISEASE; CIRRHOSIS;
   CONSUMPTION; OUTCOMES
C1 [Leggio, Lorenzo] NIAAA, Sect Clin Psychoneuroendocrinol & Neuropsychophar, Bethesda, MD 20892 USA.
   Natl Inst Drug Abuse, Bethesda, MD USA.
   Brown Univ, Dept Behav & Social Sci, Ctr Alcohol & Addict Studies, Providence, RI 02912 USA.
RP Leggio, L (reprint author), NIAAA, Sect Clin Psychoneuroendocrinol & Neuropsychophar, Bethesda, MD 20892 USA.
EM lorenzo.leggio@nih.gov
RI Leggio, Lorenzo/M-2972-2016
FU NIH [ZIA-AA000218]; Division of Intramural Clinical and Biological
   Research of the National Institute on Alcohol Abuse and Alcoholism;
   Intramural Research Program of the National Institute on Drug Abuse
FX Supported by NIH intramural funding ZIA-AA000218 (Section on Clinical
   Psychoneuroendocrinology and Neuropsychopharmacology; principal
   investigator, Dr. Leggio), jointly supported by the Division of
   Intramural Clinical and Biological Research of the National Institute on
   Alcohol Abuse and Alcoholism and the Intramural Research Program of the
   National Institute on Drug Abuse.
NR 54
TC 4
Z9 4
U1 0
U2 1
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
EI 1535-7228
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD DEC
PY 2015
VL 172
IS 12
BP 1182
EP 1189
DI 10.1176/appi.ajp.2015.15040567
PG 8
WC Psychiatry
SC Psychiatry
GA CX6UJ
UT WOS:000365836900005
PM 26619772
ER

PT J
AU Badura-Brack, AS
   Naim, R
   Ryan, TJ
   Levy, O
   Abend, R
   Khanna, MM
   McDermott, TJ
   Pine, DS
   Bar-Haim, Y
AF Badura-Brack, Amy S.
   Naim, Reut
   Ryan, Tara J.
   Levy, Ofir
   Abend, Rany
   Khanna, Maya M.
   McDermott, Timothy J.
   Pine, Daniel S.
   Bar-Haim, Yair
TI Effect of Attention Training on Attention Bias Variability and PTSD
   Symptoms: Randomized Controlled Trials in Israeli and US Combat Veterans
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID POSTTRAUMATIC-STRESS-DISORDER; MODIFICATION PROGRAM; ANXIETY DISORDERS;
   LONGITUDINAL DATA; DEPRESSION; THREAT; INDIVIDUALS; PHQ-9; METAANALYSIS;
   INFORMATION
AB Objective: Attention allocation to threat is perturbed in patients with posttraumatic stress disorder (PTSD), with some studies indicating excess attention to threat and others indicating fluctuations between threat vigilance and threat avoidance. The authors tested the efficacy of two alternative computerized protocols, attention bias modification and attention control training, for rectifying threat attendance patterns and reducing PTSD symptoms.
   Method: Two randomized controlled trials compared the efficacy of attention bias modification and attention control training for PTSD: one in Israel Defense Forces veterans and one in U.S. military veterans. Both utilized variants of the dot-probe task, with attention bias modification designed to shift attention away from threat and attention control training balancing attention allocation between threat and neutral stimuli. PTSD symptoms, attention bias, and attention bias variability were measured before and after treatment.
   Results: Both studies indicated significant symptom improvement after treatment, favoring attention control training. Additionally, both studies found that attention control training, but not attention bias modification, significantly reduced attention bias variability. Finally, a combined analysis of the two samples suggested that reductions in attention bias variability partially mediated improvement in PTSD symptoms.
   Conclusions: Attention control training may address aberrant fluctuations in attention allocation in PTSD, thereby reducing PTSD symptoms. Further study of treatment efficacy and its underlying neurocognitive mechanisms is warranted.
C1 [Badura-Brack, Amy S.] Creighton Univ, Dept Psychol, Omaha, NE 68178 USA.
   Tel Aviv Univ, Sch Psychol Sci, IL-69978 Tel Aviv, Israel.
   Tel Aviv Univ, Sagol Sch Neurosci, IL-69978 Tel Aviv, Israel.
   Simon Fraser Univ, Dept Psychol, Burnaby, BC V5A 1S6, Canada.
   Israel Def Forces, Med Corps, Div Mental Hlth, Jerusalem, Israel.
   NIMH, Intramural Res Program, Bethesda, MD 20892 USA.
RP Badura-Brack, AS (reprint author), Creighton Univ, Dept Psychol, Omaha, NE 68178 USA.
EM abadura@creighton.edu
OI McDermott, Timothy/0000-0002-8860-0646
FU At Ease USA
FX Partially supported by a grant from the nonprofit organization At Ease
   USA. The funders had no rote in study design, data collection and
   analysis, decision to publish, or preparation of the manuscript.
NR 53
TC 13
Z9 13
U1 11
U2 27
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
EI 1535-7228
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD DEC
PY 2015
VL 172
IS 12
BP 1233
EP 1241
DI 10.1176/appi.ajp.2015.14121578
PG 9
WC Psychiatry
SC Psychiatry
GA CX6UJ
UT WOS:000365836900011
PM 26206075
ER

PT J
AU Naim, R
   Abend, R
   Wald, I
   Eldar, S
   Levi, O
   Fruchter, E
   Ginat, K
   Halpern, P
   Sipos, ML
   Adler, AB
   Bliese, PD
   Quartana, PJ
   Pine, DS
   Bar-Haim, Y
AF Naim, Reut
   Abend, Rany
   Wald, Ilan
   Eldar, Sharon
   Levi, Ofir
   Fruchter, Eyal
   Ginat, Karen
   Halpern, Pinchas
   Sipos, Maurice L.
   Adler, Amy B.
   Bliese, Paul D.
   Quartana, Phillip J.
   Pine, Daniel S.
   Bar-Haim, Yair
TI Threat-Related Attention Bias Variability and Posttraumatic Stress
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID ANXIETY DISORDERS; PTSD; AMYGDALA; CHILDREN; METAANALYSIS; SYMPTOMS;
   FEAR; ADOLESCENTS; SPECIFICITY; DYSFUNCTION
AB Objective: Threat monitoring facilitates survival by allowing one to efficiently and accurately detect potential threats. Traumatic events can disrupt healthy threat monitoring, inducing biased and unstable threat-related attention deployment. Recent research suggests that greater attention bias variability, that is, attention fluctuations alternating toward and away from threat, occurs in participants with PTSD relative to healthy comparison subjects who were either exposed or not exposed to traumatic events. The current study extends findings on attention bias variability in PTSD
   Method: Previous measurement of attention bias variability was refined by employing a moving average technique. Analyses were conducted across seven independent data sets; in each, data on attention bias variability were collected by using variants of the dot-probe task. Trauma-related and anxiety symptoms were evaluated across samples by using structured psychiatric interviews and widely used self-report questionnaires, as specified for each sample.
   Results: Analyses revealed consistent evidence of greater attention bias variability in patients with PTSD following various types of traumatic events than in healthy participants, participants with social anxiety disorder, and participants with acute stress disorder. Moreover, threat-related, and not positive, attention bias variability was correlated with PTSD severity.
   Conclusions: These findings carry possibilities for using attention bias variability as a specific cognitive marker of PTSD and for tailoring protocols for attention bias modification for this disorder.
C1 [Naim, Reut] Tel Aviv Univ, Sagol Sch Neurosci, Sch Psychol Sci, IL-69978 Tel Aviv, Israel.
   Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel.
   Israel Def Forces, Med Corps, Div Mental Hlth, Jerusalem, Israel.
   Tel Aviv Med Ctr & Sch Med, Emergency Dept, Tel Aviv, Israel.
   US Army Med Res & Mat Command, Ctr Mil Psychiat & Neurosci, Walter Reed Army Inst Res, Silver Spring, MD USA.
   Univ S Carolina, Darla Moore Sch Business, Columbia, SC 29208 USA.
   NIMH, Intramural Res Program, Bethesda, MD 20892 USA.
RP Naim, R (reprint author), Tel Aviv Univ, Sagol Sch Neurosci, Sch Psychol Sci, IL-69978 Tel Aviv, Israel.
EM reutnaim@post.tau.ac.il
NR 50
TC 13
Z9 13
U1 9
U2 25
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
EI 1535-7228
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD DEC
PY 2015
VL 172
IS 12
BP 1242
EP 1250
DI 10.1176/appi.ajp.2015.14121579
PG 9
WC Psychiatry
SC Psychiatry
GA CX6UJ
UT WOS:000365836900012
PM 26206076
ER

PT J
AU Menon, MP
   Nicolae, A
   Meeker, H
   Raffeld, M
   Xi, LQ
   Jegalian, AG
   Miller, DC
   Pittaluga, S
   Jaffe, ES
AF Menon, Madhu P.
   Nicolae, Alina
   Meeker, Hillary
   Raffeld, Mark
   Xi, Liqiang
   Jegalian, Armin G.
   Miller, Douglas C.
   Pittaluga, Stefania
   Jaffe, Elaine S.
TI Primary CNS T-cell Lymphomas A Clinical, Morphologic, Immunophenotypic,
   and Molecular Analysis
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE T-cell lymphoma; central nervous system; next-generation sequencing; T
   cells; T-cell clonality; molecular diagnostics
ID CENTRAL-NERVOUS-SYSTEM; OF-THE-LITERATURE; NON-HODGKINS-LYMPHOMA; BRAIN
   CASE-REPORT; GAMMA-DELTA-T; STAT3 MUTATIONS; SPINAL-CORD; NK CELLS;
   CHILD; ADULT
AB Primary central nervous system (CNS) lymphomas are relatively rare with the most common subtype being diffuse large B-cell lymphoma. Primary CNS T-cell lymphomas (PCNSTL) account for <5% of CNS lymphomas. We report the clinical, morphologic, immunophenotypic, and molecular characteristics of 18 PCNSTLs. Fifteen cases were classified as peripheral T-cell lymphoma, not otherwise specified, 2 of which were of T-cell derivation and 1 was TCR silent; there was 1 anaplastic large cell lymphoma, ALK-positive and 2 anaplastic large cell lymphoma, ALK-negative. Median age was 58.5 years (range, 21 to 81 y), with an M:F ratio of 11:7. Imaging results showed that 15 patients had supratentorial lesions. Regardless of subtype, necrosis and perivascular cuffing of tumor cells were frequently observed (11/18 cases). CD3 was positive in all cases but 1; 10/17 were CD8-positive, and 5/17 were CD4-positive. Most cases studied had a cytotoxic phenotype with expression of TIA1 (13/15) and granzyme-B (9/13). Polymerase chain reaction analysis of T-cell receptor rearrangement confirmed a T-cell clone in 14 cases with adequate DNA quality. Next-generation sequencing showed somatic mutations in 36% of cases studied; 2 had >1 mutation, and none showed overlapping mutations. These included mutations in DNMT3A, KRAS, JAK3, STAT3, STAT5B, GNB1, and TET2 genes, genes implicated previously in other T-cell neoplasms. The outcome was heterogenous; 2 patients are alive without disease, 4 are alive with disease, and 6 died of disease. In conclusion, PCNSTLs are histologically and genomically heterogenous with frequent phenotypic aberrancy and a cytotoxic phenotype in most cases.
C1 [Menon, Madhu P.; Nicolae, Alina; Meeker, Hillary; Raffeld, Mark; Xi, Liqiang; Jegalian, Armin G.; Pittaluga, Stefania; Jaffe, Elaine S.] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Miller, Douglas C.] Univ Missouri, Sch Med, Dept Pathol & Anat Sci, Columbia, MO USA.
RP Jaffe, ES (reprint author), NCI, Pathol Lab, Ctr Canc Res, NIH, 10 Ctr Dr,Bldg 10,MSC 1500, Bethesda, MD 20892 USA.
EM elainejaffe@nih.gov
FU Center for Cancer Research, National Cancer Institute, National
   Institutes of Health
FX Supported by the intramural research program of the Center for Cancer
   Research, National Cancer Institute, National Institutes of Health.
   D.C.M. has reported financial relationships with outside parties that
   have no direct bearing on the work reported in this manuscript. The
   authors have disclosed that they have no significant relationships with,
   or financial interest in, any commercial companies pertaining to this
   article.
NR 64
TC 5
Z9 5
U1 1
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0147-5185
EI 1532-0979
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD DEC
PY 2015
VL 39
IS 12
BP 1719
EP 1729
DI 10.1097/PAS.0000000000000503
PG 11
WC Pathology; Surgery
SC Pathology; Surgery
GA CX3VI
UT WOS:000365627200014
PM 26379152
ER

PT J
AU Hricik, DE
   Augustine, J
   Nickerson, P
   Formica, RN
   Poggio, ED
   Rush, D
   Newell, KA
   Goebel, J
   Gibson, IW
   Fairchild, RL
   Spain, K
   Ikle, D
   Bridges, ND
   Heeger, PS
AF Hricik, D. E.
   Augustine, J.
   Nickerson, P.
   Formica, R. N.
   Poggio, E. D.
   Rush, D.
   Newell, K. A.
   Goebel, J.
   Gibson, I. W.
   Fairchild, R. L.
   Spain, K.
   Ikle, D.
   Bridges, N. D.
   Heeger, P. S.
CA CTOT-01 Consortium
TI Interferon Gamma ELISPOT Testing as a Risk-Stratifying Biomarker for
   Kidney Transplant Injury: Results From the CTOT-01 Multicenter Study
SO AMERICAN JOURNAL OF TRANSPLANTATION
LA English
DT Article
DE Clinical research; practice; glomerular filtration rate (GFR);
   immunobiology; kidney transplantation; nephrology; rejection: acute;
   risk assessment; risk stratification; T cell biology; translational
   research; science
ID RABBIT ANTITHYMOCYTE GLOBULIN; IMMUNOSORBENT SPOT ASSAY; ACUTE
   REJECTION; GRAFT FUNCTION; T-CELL; ALLOGRAFT SURVIVAL; RENAL-FUNCTION;
   RECIPIENTS; ALLOREACTIVITY; FREQUENCIES
AB Previous studies suggest that quantifying donor-reactive memory T cells prior to kidney transplantation by interferon gamma enzyme-linked immunosorbent spot assay (IFNELISPOT) can assist in assessing risk of posttransplant allograft injury. Herein, we report an analysis of IFNELISPOT results from the multicenter, Clinical Trials in Organ Transplantation-01 observational study of primary kidney transplant recipients treated with heterogeneous immunosuppression. Within the subset of 176 subjects with available IFNELISPOT results, pretransplant IFNELISPOT positivity surprisingly did not correlate with either the incidence of acute rejection (AR) or estimated glomerular filtration rate (eGFR) at 6- or 12-month. These unanticipated results prompted us to examine potential effect modifiers, including the use of T cell-depleting, rabbit anti-thymocyte globulin (ATG). Within the no-ATG subset, IFNELISPOTneg subjects had higher 6- and 12-month eGFRs than IFNELISPOTpos subjects, independent of biopsy-proven AR, peak PRA, human leukocyte antigen mismatches, African-American race, donor source, and recipient age or gender. In contrast, IFNELISPOT status did not correlate with posttransplant eGFR in subjects given ATG. Our data confirm an association between pretransplant IFNELISPOT positivity and lower posttransplant eGFR, but only in patients who do not receive ATG induction. Controlled studies are needed to test the hypothesis that ATG induction is preferentially beneficial to transplant candidates with high frequencies of donor-reactive memory T cells.
C1 [Hricik, D. E.; Augustine, J.] Univ Hosp Case Med Ctr, Dept Med, Cleveland, OH 44106 USA.
   [Nickerson, P.; Rush, D.] Univ Manitoba, Dept Med, Winnipeg, MB, Canada.
   [Formica, R. N.] Yale Univ, Sch Med, Dept Med, New Haven, CT 06510 USA.
   [Poggio, E. D.] Cleveland Clin, Dept Med, Cleveland, OH 44106 USA.
   [Newell, K. A.] Emory Univ, Dept Surg, Med Ctr, Atlanta, GA USA.
   [Goebel, J.] Cincinnati Childrens Hosp Med Ctr, Dept Pediat, Cincinnati, OH 45229 USA.
   [Gibson, I. W.] Univ Manitoba, Dept Pathol, Winnipeg, MB R3T 2N2, Canada.
   [Fairchild, R. L.] Cleveland Clin, Dept Immunol, Cleveland, OH 44106 USA.
   [Spain, K.; Ikle, D.] Rho, Chapel Hill, NC USA.
   [Bridges, N. D.] NIAID, Transplantat Branch, NIH, Bethesda, MD 20892 USA.
   [Heeger, P. S.] Mt Sinai Sch Med, Dept Med, New York, NY USA.
RP Hricik, DE (reprint author), Univ Hosp Case Med Ctr, Dept Med, Cleveland, OH 44106 USA.
EM donald.hricik@UHhospitals.org
FU National Institute of Allergy and Infectious Diseases of the National
   Institutes of Health [U01-AI063594]
FX The work was supported by the National Institute of Allergy and
   Infectious Diseases of the National Institutes of Health under Award
   Number U01-AI063594 (to P.S.H.). The content is solely the
   responsibility of the authors and does not necessarily represent the
   official views of the National Institutes of Health.
NR 23
TC 6
Z9 6
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1600-6135
EI 1600-6143
J9 AM J TRANSPLANT
JI Am. J. Transplant.
PD DEC
PY 2015
VL 15
IS 12
BP 3166
EP 3173
DI 10.1111/ajt.13401
PG 8
WC Surgery; Transplantation
SC Surgery; Transplantation
GA CX2NP
UT WOS:000365534100016
PM 26226830
ER

PT J
AU Fuchs, MCP
   Tambarussi, EV
   Lourencao, JC
   Nogueira, LM
   Bortoloto, TM
   Gonzalez, ER
   Oda, S
   Marino, CL
AF Fuchs, Maria C. P.
   Tambarussi, Evandro V.
   Lourencao, Juliana C.
   Nogueira, Leticia M.
   Bortoloto, Tania M.
   Gonzalez, Esteban R.
   Oda, Shinitiro
   Marino, Celso L.
TI Molecular marker associated with a deleterious recessive anomaly in
   Eucalyptus grandis seedlings
SO ANNALS OF FOREST SCIENCE
LA English
DT Article
DE Eucalypt anomaly; Molecular marker; Deleterious recessive alleles;
   Eucalypt development
ID BULKED SEGREGANT ANALYSIS; PATHOGENESIS-RELATED PROTEINS;
   DISEASE-RESISTANCE GENES; BIRCH POLLEN ALLERGEN; IN-SITU HYBRIDIZATION;
   INBREEDING DEPRESSION; ASSISTED SELECTION; GENOMIC REGIONS; PLANTS; SEED
AB The identification of an anomaly with deleterious effect and Mendelian segregation (3 normal: 1 abnormal) allowed the detection of a marker linked to a locus for the anomalous phenotype. This marker could be useful in marker-assisted breeding programs and for understanding this anomaly.
   Due to the mixed mating systems in Eucalyptus genera, outcrossing populations exhibit low inbreeding depression (abnormalities). In this study, we identified a developmental anomaly in a controlled cross of Eucalyptus grandis, with Mendelian segregation. The anomaly was characterized by branching, reduced height, smaller individual leaf area, and asymmetrical leaf shape.
   To investigate and evaluate the anomaly detected, we performed morphological and molecular analysis. The genitors and bulks of normal and abnormal individuals were screened with random primers. The polymorphic markers that co-segregated with the anomalous phenotype were selected, validated, converted into SCAR markers and analyzed in silico.
   Morphological analysis showed significant differences between normal and abnormal phenotypes. The co-segregating marker was present in one genitor, in all abnormal individuals, and in 31 % of normal individuals (recombinants). In silico analyses revealed a mutation of two base pairs between the contrasting phenotypes and identified the marker in an intergenic region presenting partial identity with an expressed sequence tag (EST) of Bet v1-like genes.
   A marker was developed to identify the recessive allele for the anomaly in E. grandis. This will be important for management of crosses in eucalypt breeding programs and in anomaly studies.
C1 [Fuchs, Maria C. P.; Lourencao, Juliana C.; Bortoloto, Tania M.; Marino, Celso L.] Univ Estadual Paulista, UNESP, Inst Biociencias, Dept Genet, BR-18618970 Botucatu, SP, Brazil.
   [Tambarussi, Evandro V.] Univ Fed Sao Carlos UFSCar, Dept Biol, BR-18052780 Sorocaba, SP, Brazil.
   [Nogueira, Leticia M.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Gonzalez, Esteban R.; Oda, Shinitiro] Empresa Suzano & Papel Celulose SA, BR-18207780 Itapetininga, SP, Brazil.
RP Fuchs, MCP (reprint author), Univ Estadual Paulista, UNESP, Inst Biociencias, Dept Genet, Distrito Rubiao Jr S-N, BR-18618970 Botucatu, SP, Brazil.
EM mceciliapf@yahoo.com.br
RI Tambarussi, Evandro/E-5695-2016
OI Tambarussi, Evandro/0000-0001-9478-5379
FU Fundacao de Amparo a Pesquisa do Estado de Sao Paulo [08/52266-6];
   Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
FX Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (Fapesp grant
   08/52266-6), and Coordenacao de Aperfeicoamento de Pessoal de Nivel
   Superior (CAPES).
NR 61
TC 0
Z9 0
U1 1
U2 8
PU SPRINGER FRANCE
PI PARIS
PA 22 RUE DE PALESTRO, PARIS, 75002, FRANCE
SN 1286-4560
EI 1297-966X
J9 ANN FOREST SCI
JI Ann. For. Sci.
PD DEC
PY 2015
VL 72
IS 8
BP 1043
EP 1052
DI 10.1007/s13595-015-0502-9
PG 10
WC Forestry
SC Forestry
GA CX6IV
UT WOS:000365805300006
ER

PT J
AU Naik, HB
   Natarajan, B
   Stansky, E
   Ahlman, MA
   Teague, H
   Salahuddin, T
   Ng, QM
   Joshi, AA
   Krishnamoorthy, P
   Dave, J
   Rose, SM
   Doveikis, J
   Playford, MP
   Prussick, RB
   Ehrlich, A
   Kaplan, MJ
   Lockshin, BN
   Gelfand, JM
   Mehta, NN
AF Naik, Haley B.
   Natarajan, Balaji
   Stansky, Elena
   Ahlman, Mark A.
   Teague, Heather
   Salahuddin, Taufiq
   Ng, Qimin
   Joshi, Aditya A.
   Krishnamoorthy, Parasuram
   Dave, Jenny
   Rose, Shawn M.
   Doveikis, Julia
   Playford, Martin P.
   Prussick, Ronald B.
   Ehrlich, Alison
   Kaplan, Mariana J.
   Lockshin, Benjamin N.
   Gelfand, Joel M.
   Mehta, Nehal N.
TI Severity of Psoriasis Associates With Aortic Vascular Inflammation
   Detected by FDG PET/CT and Neutrophil Activation in a Prospective
   Observational Study
SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
LA English
DT Article
DE inflammation; neutrophils; PET; CT; psoriasis; vascular inflammation
ID POSITRON-EMISSION-TOMOGRAPHY; POPULATION-BASED COHORT; PLAQUE
   INFLAMMATION; MYOCARDIAL-INFARCTION; CORONARY-ARTERY; RISK-FACTORS;
   IN-VIVO; ATHEROSCLEROSIS; PREVALENCE; MORTALITY
AB Objective To understand whether directly measured psoriasis severity is associated with vascular inflammation assessed by F-18-fluorodeoxyglucose positron emission tomography computed tomography.
   Approach In-depth cardiovascular and metabolic phenotyping was performed in adult psoriasis patients (n=60) and controls (n=20). Psoriasis severity was measured using psoriasis area severity index. Vascular inflammation was measured using average aortic target-to-background ratio using F-18-fluorodeoxyglucose positron emission tomography computed tomography.
   Results Both the psoriasis patients (28 men and 32 women, mean age 47 years) and controls (13 men and 7 women, mean age 41 years) were young with low cardiovascular risk. Psoriasis area severity index scores (median 5.4; interquartile range 2.8-8.3) were consistent with mild-to-moderate skin disease severity. Increasing psoriasis area severity index score was associated with an increase in aortic target-to-background ratio (=0.41, P=0.001), an association that changed little after adjustment for age, sex, and Framingham risk score. We observed evidence of increased neutrophil frequency (mean psoriasis, 3.71.2 versus 2.9 +/- 1.2; P=0.02) and activation by lower neutrophil surface CD16 and CD62L in blood. Serum levels of S100A8/A9 (745.1 +/- 53.3 versus 195.4 +/- 157.8 ng/mL; P<0.01) and neutrophil elastase-1 (43.0 +/- 2.4 versus 30.8 +/- 6.7 ng/mL; P<0.001) were elevated in psoriasis. Finally, S100A8/A9 protein was related to both psoriasis skin disease severity (=0.53; P=0.02) and vascular inflammation (=0.48; P=0.02).
   Conclusions Psoriasis severity is associated with vascular inflammation beyond cardiovascular risk factors. Psoriasis increased neutrophil activation and neutrophil markers, and S100A8/A9 was related to both skin disease severity and vascular inflammation.
C1 [Naik, Haley B.; Natarajan, Balaji; Stansky, Elena; Teague, Heather; Salahuddin, Taufiq; Ng, Qimin; Joshi, Aditya A.; Dave, Jenny; Rose, Shawn M.; Doveikis, Julia; Playford, Martin P.; Mehta, Nehal N.] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
   [Naik, Haley B.] NCI, Dermatol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Ahlman, Mark A.] NIAMSD, Mol Biomed Imaging Lab, NIH, Bethesda, MD 20892 USA.
   [Kaplan, Mariana J.] NIAMSD, System Autoimmun Branch, NIH, Bethesda, MD 20892 USA.
   [Krishnamoorthy, Parasuram] Englewood Hosp, Englewood, NJ USA.
   [Prussick, Ronald B.] Washington Dermatol Ctr, Rockville, MD USA.
   [Prussick, Ronald B.; Ehrlich, Alison] George Washington Hosp, Dept Dermatol, Washington, DC USA.
   [Lockshin, Benjamin N.] DermAssociates, Silver Spring, MD USA.
   [Gelfand, Joel M.] Univ Penn, Dept Dermatol, Dept Epidemiol & Biostat, Philadelphia, PA 19104 USA.
   [Gelfand, Joel M.] Univ Penn, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
RP Mehta, NN (reprint author), NHLBI, Cardiovasc & Pulm Branch, CRC, 10 Ctr Dr,Room 5-5140, Bethesda, MD 20892 USA.
EM nehal.mehta@nih.gov
OI Krishnamoorthy, Parasuram/0000-0002-4560-7346
FU National Heart, Lung and Blood Institute (NHLBI) Intramural Research
   Program [HL006193-01]; National Psoriasis Foundation Discovery Grant; 
   [R01-HL111293];  [K24 AR064310]
FX This study was supported by the National Heart, Lung and Blood Institute
   (NHLBI) Intramural Research Program (HL006193-01), R01-HL111293, and K24
   AR064310 and National Psoriasis Foundation Discovery Grant.
NR 52
TC 13
Z9 13
U1 0
U2 4
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 DEC
PY 2015
VL 35
IS 12
BP 2667
EP 2676
DI 10.1161/ATVBAHA.115.306460
PG 10
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA CX3JE
UT WOS:000365594100021
PM 26449753
ER

PT J
AU Edwan, JH
   Goldbach-Mansky, R
   Colbert, RA
AF Edwan, Jehad H.
   Goldbach-Mansky, Raphaela
   Colbert, Robert A.
TI Identification of Interleukin-1 beta-Producing Monocytes That Are
   Susceptible to Pyronecrotic Cell Death in Patients With Neonatal-Onset
   Multisystem Inflammatory Disease
SO ARTHRITIS & RHEUMATOLOGY
LA English
DT Article
ID INTERLEUKIN-1 INDUCES INTERLEUKIN-1; DENDRITIC CELLS; NALP3
   INFLAMMASOME; AUTOINFLAMMATORY DISEASE; SUSTAINED RESPONSE; NLRP3
   INFLAMMASOME; CIAS1 MUTATIONS; CD83; ASC; ACTIVATION
AB Objective. Spontaneous inflammatory responses initiated by NLRP3 mutations promote inflammasome-mediated interleukin-1 beta (IL-1 beta) processing and release and can induce rapid necrotic cell death. The cells that produce IL-1 beta in neonatal-onset multisystem inflammatory disease (NOMID) have not been clearly identified, nor have the mechanisms mediating IL-1 beta release and cell death been completely elucidated.
   Methods. Whole blood cells were stimulated with lipopolysaccharide (LPS) in the presence of cathepsin B and caspase 1 inhibitors, followed by ATP treatment. Supernatants were collected and incubated with IL-1 beta-capturing beads. Cells were fixed, permeabilized, and stained for a combination of cell surface and intracellular markers, and a novel flow cytometry bead-based assay was used to measure secreted IL-1 beta. LPS-stimulated cells were also evaluated using immunofluorescence microscopy.
   Results. Monocytes characterized by CD14(high) - CD16(low) expression and intracellular CD83 were increased in NOMID patients and were responsible for the majority of IL-1 beta production in response to LPS stimulation. This population of monocytes also underwent a rapid death response with LPS alone that is temporally associated with IL-1 beta and ASC release and has characteristic features of pyronecrotic but not pyroptotic cell death. Inhibition of cell death reduced IL-1 beta production from NOMID patient cells. In addition, IL-1 triggered cell death in monocytes from NOMID patients.
   Conclusion. Our findings indicate that monocytes are the predominant IL-1 beta-producing cell population in the peripheral blood of NOMID patients. Furthermore, they suggest that IL-1 receptor blockade may work in part by preventing pyronecrotic cell death, which may be an important target in NOMID and other forms of cryopyrin-associated periodic syndromes.
C1 [Edwan, Jehad H.; Goldbach-Mansky, Raphaela; Colbert, Robert A.] NIAMSD, NIH, Bethesda, MD 20892 USA.
RP Colbert, RA (reprint author), NIAMSD, Pediat Translat Res Branch, NIH, CRC, Bldg 10,Room 1-5142,10 Ctr Dr,MSC 1102, Bethesda, MD 20892 USA.
EM colbertr@mail.nih.gov
FU NIH (National Institute of Arthritis and Musculoskeletal and Skin
   Diseases Intramural Research Program) [Z01-AR-041184, ZIA-AR-041138];
   Sobi; Regeneron; Novartis; Eli Lilly
FX Supported by the NIH (National Institute of Arthritis and
   Musculoskeletal and Skin Diseases Intramural Research Program grants
   Z01-AR-041184 and ZIA-AR-041138).; Dr. Goldbach-Mansky has received
   study drugs and grant support from Sobi, Regeneron, Novartis, and Eli
   Lilly.
NR 47
TC 3
Z9 3
U1 1
U2 5
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 DEC
PY 2015
VL 67
IS 12
BP 3286
EP 3297
DI 10.1002/art.39307
PG 12
WC Rheumatology
SC Rheumatology
GA CX4SV
UT WOS:000365691500024
PM 26245468
ER

PT J
AU Fitzgerald, D
AF Fitzgerald, Dan
TI Mediating the Apocalypse: The Potential Semiotic Effects of Translating
   for Spoken and Sung Performance
SO BIBLE TRANSLATOR
LA English
DT Article
DE performance; narrative; song; orality; poetics; semiotics; sign; effect;
   icon; index
AB From the perspective of Peircean semiotics, people who experience a performed discoursefor example, one that is spoken, sung, and gesturedexperience that discourse as a more direct, real, and affective experience than when they experience that same discourse by reading it. This distinction is so because performed discourse typically engages many more iconic and indexical sign-object semioses than does read discourse. Therefore, Bible translators who translate written biblical discourse for the express purpose of making that discourse accessible through cultural performance are obliged, first, to discover the distinct, genre-specific, iconic, and indexical performance features of their receptor language and second, champion the inclusion of those performance features in their translation. As a case study of this kind of translation, this article describes the manner in which translators of the Baka Bible translation project in Cameroon translated select passages from the book of Revelation for spoken and sung narrative performance.
C1 [Fitzgerald, Dan] Amer Bible Soc, Nida Inst Bibl Scholarship, New York, NY USA.
RP Fitzgerald, D (reprint author), 9837 Seymour St, Houghton, NY 14744 USA.
EM dlfitzgerald@americanbible.org
NR 13
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 2051-6770
EI 2051-6789
J9 BIBLE TRANSL
JI Bible Transl.
PD DEC
PY 2015
VL 66
IS 3
BP 231
EP 245
DI 10.1177/2051677015608618
PG 15
WC Religion
SC Religion
GA CX4LK
UT WOS:000365672200004
ER

PT J
AU Chen, J
   Liu, J
AF Chen, Jing
   Liu, Jian
TI Erroneous Silencing of the Mitotic Checkpoint by Aberrant Spindle
   Pole-Kinetochore Coordination
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID ANAPHASE-PROMOTING COMPLEX; AURORA-B KINASE; ASSEMBLY CHECKPOINT; MOUSE
   OOCYTES; CHROMOSOMAL INSTABILITY; UNATTACHED KINETOCHORES; MICROTUBULE
   ATTACHMENT; CYTOPLASMIC DYNEIN; EXTRA CENTROSOMES; MAMMALIAN OOCYTES
AB To segregate chromosomes during cell division, microtubules that form the bipolar spindle attach to and pull on paired chromosome kinetochores. The spindle assembly checkpoint (SAC) is activated at unattached and misattached kinetochores to prevent further mitotic progression. The SAC is silenced after all the kinetochores establish proper and stable attachment to the spindle. Robust timing of SAC silencing after the last kinetochore-spindle attachment herein dictates the fidelity of chromosome segregation. Chromosome missegregation is rare in typical somatic cell mitosis, but frequent in cancer cell mitosis and in meiosis I of mammalian oocytes. In the latter cases, SAC is normally activated in response to disruptions of kinetochore-spindle attachments, suggesting that frequent chromosome missegregation ensues from faulty SAC silencing. In-depth understanding of how SAC silencing malfunctions in these cases is yet missing, but is believed to hold promise for treatment of cancer and prevention of human miscarriage and birth defects. We previously established a spatiotemporal model that, to the best of our knowledge, explained the robustness of SAC silencing in normal mitosis for the first time. In this article, we take advantage of the whole-cell perspective of the spatiotemporal model to identify possible causes of chromosome missegregation out of the distinct features of spindle assembly exhibited by cancer cells and mammalian oocytes. The model results explain why multipolar spindle could inhibit SAC silencing and spindle pole clustering could promote it albeit accompanied by more kinetochore attachment errors. The model also eliminates geometric factors as the cause for nonrobust SAC silencing in oocyte meiosis, and instead, suggests atypical kinetochore-spindle attachment in meiosis as a potential culprit. Overall, the model shows that abnormal spindle-pole formation and its aberrant coordination with atypical kinetochore-spindle attachments could compromise the robustness of SAC silencing. Our model highlights systems-level coupling between kinetochore-spindle attachment and spindle-pole formation in SAC silencing.
C1 [Chen, Jing; Liu, Jian] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Liu, J (reprint author), NHLBI, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM liuj7@nhlbi.nih.gov
RI Chen, Jing/D-4845-2016
OI Chen, Jing/0000-0001-6321-0505
FU Intramural Research Program of the National Heart, Lung, and Blood
   Institute at the National Institutes of Health
FX This work was supported by the Intramural Research Program of the
   National Heart, Lung, and Blood Institute at the National Institutes of
   Health.
NR 121
TC 3
Z9 3
U1 0
U2 5
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
EI 1542-0086
J9 BIOPHYS J
JI Biophys. J.
PD DEC 1
PY 2015
VL 109
IS 11
BP 2418
EP 2435
DI 10.1016/j.bpj.2015.10.024
PG 18
WC Biophysics
SC Biophysics
GA CX8CG
UT WOS:000365929500021
PM 26636952
ER

PT J
AU Li, ZY
   Mewawalla, P
   Stratton, P
   Yong, ASM
   Shaw, BE
   Hashmi, S
   Jagasia, M
   Mohty, M
   Majhail, NS
   Savani, BN
   Rovo, A
AF Li, Zhuoyan
   Mewawalla, Prerna
   Stratton, Pamela
   Yong, Agnes S. M.
   Shaw, Bronwen E.
   Hashmi, Shahrukh
   Jagasia, Madan
   Mohty, Mohamad
   Majhail, Navneet S.
   Savani, Bipin N.
   Rovo, Alicia
TI Sexual health in hematopoietic stem cell transplant recipients
SO CANCER
LA English
DT Article
DE late effects; sexual health; survivorship; toxicity; transplantation
ID BONE-MARROW-TRANSPLANTATION; VERSUS-HOST-DISEASE; LONG-TERM SURVIVORS;
   PREMATURE OVARIAN FAILURE; CASE-MATCHED CONTROLS; HEMATOLOGICAL
   MALIGNANCIES; UNITED-STATES; ERECTILE DYSFUNCTION; PREVENTIVE PRACTICES;
   GONADAL DAMAGE
AB Hematopoietic stem cell transplantation (HSCT) plays a central role in patients with malignant and, increasingly, nonmalignant conditions. As the number of transplants increases and the survival rate improves, long-term complications are important to recognize and treat to maintain quality of life. Sexual dysfunction is a commonly described but relatively often underestimated complication after HSCT. Conditioning regimens, generalized or genital graft-versus-host disease, medications, and cardiovascular complications as well as psychosocial problems are known to contribute significantly to physical and psychological sexual dysfunction. Moreover, it is often a difficult topic for patients, their significant others, and health care providers to discuss. Early recognition and management of sexual dysfunction after HSCT can lead to improved quality of life and outcomes for patients and their partners. This review focuses on the risk factors for and treatment of sexual dysfunction after transplantation and provides guidance concerning how to approach and manage a patient with sexual dysfunction after HSCT. Cancer 2015;121:4124-4131. (c) 2015 American Cancer Society.
   Sexual dysfunction is an often-described complication after hematopoietic stem cell transplantation that is difficult for patients and their health care providers to discuss. Through review of the available literature, guidance in the early recognition and management of sexual dysfunction will lead to improved quality of life outcomes.
C1 [Li, Zhuoyan] Vanderbilt Univ, Med Ctr, Dept Med, Nashville, TN USA.
   [Mewawalla, Prerna] Western Penn Canc Inst, Dept Hematol, Pittsburgh, PA USA.
   [Stratton, Pamela] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
   [Yong, Agnes S. M.] Univ Adelaide, Dept Hematol, SA Pathol, Adelaide, SA, Australia.
   [Yong, Agnes S. M.] Univ Adelaide, Sch Med, Adelaide, SA, Australia.
   [Shaw, Bronwen E.] Froedtert & Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI USA.
   [Hashmi, Shahrukh] Mayo Clin, Div Hematol, Rochester, MN USA.
   [Jagasia, Madan; Savani, Bipin N.] Vanderbilt Univ, Med Ctr, Hematol & Stem Cell Transplantat Sect, Div Hematol Oncol,Dept Med, Nashville, TN USA.
   [Jagasia, Madan; Savani, Bipin N.] Vet Affairs Med Ctr, Nashville, TN 37212 USA.
   [Mohty, Mohamad] INSERM 938, Paris, France.
   [Majhail, Navneet S.] Cleveland Clin, Blood & Marrow Transplant Program, Cleveland, OH 44106 USA.
   [Rovo, Alicia] Univ Hosp Bern, Dept Hematol, CH-3010 Bern, Switzerland.
RP Savani, BN (reprint author), Vanderbilt Univ, Med Ctr, Dept Med, Hematol & Stem Cell Transplantat Sect,Div Hematol, 1301 Med Ctr Dr,3927 TVC, Nashville, TN 37235 USA.
EM Bipin.Savani@Vanderbilt.Edu
FU Intramural Program of the National Institutes of Health
FX No specific funding was disclosed. Dr. Stratton is funded by the
   Intramural Program of the National Institutes of Health.
NR 59
TC 0
Z9 0
U1 3
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
EI 1097-0142
J9 CANCER-AM CANCER SOC
JI Cancer
PD DEC 1
PY 2015
VL 121
IS 23
BP 4124
EP 4131
DI 10.1002/cncr.29675
PG 8
WC Oncology
SC Oncology
GA CX3TJ
UT WOS:000365621900006
PM 26372459
ER

PT J
AU Ghazarian, AA
   Trabert, B
   Graubard, BI
   Schwartz, SM
   Altekruse, SF
   McGlynn, KA
AF Ghazarian, Armen A.
   Trabert, Britton
   Graubard, Barry I.
   Schwartz, Stephen M.
   Altekruse, Sean F.
   McGlynn, Katherine A.
TI Incidence of testicular germ cell tumors among US men by census region
SO CANCER
LA English
DT Article
DE ethnic groups; incidence; North American Association of Central Cancer
   Registries (NAACCR); testicular cancer; testicular germ cell tumor
   (TGCT); trends
ID UNITED-STATES; CANCER; SUSCEPTIBILITY; LOCI; VARIANTS; TRENDS; RISKS
AB BACKGROUNDThe incidence of testicular germ cell tumors (TGCTs) in the United States is notably higher among white men versus other men. Previously, however, it was reported that rates were rising among Hispanics in certain areas. To determine whether this finding was evident in a wider area of the United States, data from 39 US cancer registries were examined.
   METHODSRacial/ethnic-specific incidence rates per 100,000 man-years were calculated overall and by census region for the period of 1998-2011. Annual percentage changes (APCs) were estimated, and joinpoint models were fit. Differences in incidence by region were examined with the Wald test.
   RESULTSFrom 1998 to 2011, 88,993 TGCTs were recorded. The TGCT incidence was highest among non-Hispanic whites (6.57 per 100,000), who were followed by Hispanics (3.88), American Indians/Alaska Natives (2.88), Asians/Pacific Islanders (A/PIs; 1.60), and non-Hispanic blacks (1.20). The incidence significantly increased among Hispanics (APC, 2.31; P<.0001), with rates rising in all regions except the South. Rates rose slightly among non-Hispanic whites (APC, 0.51; P=.0076). Significant differences in rates by region were seen for Hispanics (P=.0001), non-Hispanic whites (P<.0001), and A/PIs (P<.0001), with the highest rates among Hispanics in the West and with the highest rates among non-Hispanic whites and A/PIs in the Northeast.
   CONCLUSIONSAlthough the incidence of TGCTs remained highest among non-Hispanic whites between 1998 and 2011, the greatest increase was experienced by Hispanics. Rising rates of TGCTs among Hispanics in the United States suggest that future attention is warranted. Reasons for the increase may include variability in birthplace, changing exposures, genetic susceptibility, and the length of US residence. Cancer 2015;121:4181-4189. (c) 2015 American Cancer Society.
   Between 1998 and 2011, although the incidence of testicular germ cell tumors in the United States remained highest among non-Hispanic white men, the greatest increase in incidence was experienced by Hispanic men. Significant differences in incidence rates by census region are observed for Hispanics, non-Hispanic whites, and Asian/Pacific Islanders, with the highest rates noted among Hispanics in the West and among non-Hispanic whites and Asian/Pacific Islanders in the Northeast.
C1 [Ghazarian, Armen A.; Trabert, Britton; Graubard, Barry I.; McGlynn, Katherine A.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Schwartz, Stephen M.] Fred Hutchinson Canc Res Ctr, Program Epidemiol, Div Publ Hlth Sci, Seattle, WA 98104 USA.
   [Schwartz, Stephen M.] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA.
   [Altekruse, Sean F.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP McGlynn, KA (reprint author), NCI, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Room 7-E104, Bethesda, MD 20892 USA.
EM mcglynnk@mail.nih.gov
RI Trabert, Britton/F-8051-2015
FU Intramural Research Program of the National Cancer Institute
FX This work was supported by the Intramural Research Program of the
   National Cancer Institute.
NR 27
TC 5
Z9 5
U1 2
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
EI 1097-0142
J9 CANCER-AM CANCER SOC
JI Cancer
PD DEC 1
PY 2015
VL 121
IS 23
BP 4181
EP 4189
DI 10.1002/cncr.29643
PG 9
WC Oncology
SC Oncology
GA CX3TJ
UT WOS:000365621900013
PM 26280359
ER

PT J
AU Ko, RH
   Jones, TL
   Radvinsky, D
   Robison, N
   Gaynon, PS
   Panosyan, EH
   Avramis, IA
   Avramis, VI
   Rubin, J
   Ettinger, LJ
   Seibel, NL
   Dhall, G
AF Ko, Richard H.
   Jones, Tamekia L.
   Radvinsky, David
   Robison, Nathan
   Gaynon, Paul S.
   Panosyan, Eduard H.
   Avramis, Ioannis A.
   Avramis, Vassilios I.
   Rubin, Joan
   Ettinger, Lawrence J.
   Seibel, Nita L.
   Dhall, Girish
TI Allergic reactions and antiasparaginase antibodies in children with
   high-risk acute lymphoblastic leukemia: A children's oncology group
   report
SO CANCER
LA English
DT Article
DE asparaginase; childhood acute lymphoblastic leukemia; drug
   hypersensitivity; survival
ID ESCHERICHIA-COLI-ASPARAGINASE; ERWINIA-ASPARAGINASE; HYPERSENSITIVITY;
   CANCER; LYMPHOMA; THERAPY; TRIAL
AB BACKGROUNDThe objectives of this study were to assess the incidence of clinical allergy and end-induction antiasparaginase (anti-ASNase) antibodies in children with high-risk acute lymphoblastic leukemia treated with pegylated (PEG) Escherichia coli ASNase and to determine whether they carry any prognostic significance.
   METHODSOf 2057 eligible patients, 1155 were allocated to augmented arms in which PEG ASNase replaced native ASNase postinduction. Erwinia chrysanthemi (Erwinia) ASNase could be used to replace native ASNase after allergy, if available. Allergy and survival data were complete for 990 patients. End-induction antibody titers were available for 600 patients.
   RESULTSDuring the consolidation phase, 289 of 990 patients (29.2%) had an allergic reaction. There were fewer allergic reactions to Erwinia ASNase than to native ASNase (odds ratio, 4.33; P<.0001) or PEG ASNase (odds ratio, 3.08; P<.0001) only during phase 1 of interim maintenance. There was no significant difference in 5-year event-free survival (EFS) between patients who received PEG ASNase throughout the entire study postinduction versus those who developed an allergic reaction to PEG ASNase during consolidation phase and subsequently received Erwinia ASNase (80.8%2.8% and 81.6%3.8%, respectively; P=.66). Patients who had positive antibody titers postinduction were more likely to have an allergic reaction to PEG ASNase (odds ratio, 2.4; P<.001). The 5-year EFS rate between patients who had negative versus positive antibody titers (80%+/- 2.6% and 77.7%+/- 4.3%, respectively; P=.68) and between patients who did not receive any ASNase postconsolidation and those who received PEG ASNase throughout the study (P=.22) were significantly different.
   CONCLUSIONSThe current results demonstrate differences in the incidence rates of toxicity between ASNase preparations but not in EFS. The presence of anti-ASNase antibodies did not affect EFS. Cancer 2015;121:4205-4211. (c) 2015 American Cancer Society.
   Different preparations of asparaginase are used in the treatment of pediatric acute lymphoblastic leukemia, and the optimal use of this agent has yet to be elucidated. The authors observe differences in the incidence of toxicity with various asparaginase preparations and demonstrate that antiasparaginase antibodies do not affect event-free survival.
C1 [Ko, Richard H.; Robison, Nathan; Gaynon, Paul S.; Avramis, Ioannis A.; Avramis, Vassilios I.; Dhall, Girish] Childrens Hosp Los Angeles, Childrens Ctr Canc & Blood, Los Angeles, CA 90027 USA.
   [Ko, Richard H.; Robison, Nathan; Gaynon, Paul S.; Avramis, Vassilios I.; Dhall, Girish] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
   [Jones, Tamekia L.] Univ Tennessee, Hlth Sci Ctr, Dept Prevent Med, Memphis, TN USA.
   [Radvinsky, David] Suny Downstate Med Ctr, Brooklyn, NY 11203 USA.
   [Panosyan, Eduard H.] Harbor Univ Calif Los Angeles Med Ctr, Div Pediat Hematol & Oncol, Torrance, CA USA.
   [Rubin, Joan] St Peters Univ Hosp, Dept Pediat, New Brunswick, NJ USA.
   [Ettinger, Lawrence J.] Childrens Oncol Grp, Monrovia, CA USA.
   [Seibel, Nita L.] NCI, Canc Therapy Evaluat Program, Bethesda, MD USA.
RP Ko, RH (reprint author), Childrens Hosp Los Angeles, Childrens Ctr Canc & Blood, Pediat Clin, 4650 Sunset Blvd,Mailstop 54, Los Angeles, CA 90027 USA.
EM rko@chla.usc.edu
FU Children's Oncology Group (COG) Chair's grant [U10 CA98543-08];
   Children's Oncology Group National Clinical Trials Network (COG NCTN)
   [U10 CA180886, U10 CA98413-08, U10 CA180899]
FX This research was supported by Children's Oncology Group (COG) Chair's
   grant U10 CA98543-08, Children's Oncology Group National Clinical Trials
   Network (COG NCTN) Group Operations Center grant U10 CA180886,
   Statistics and Data Center grant U10 CA98413-08, and COG NCTN Statistics
   and Data Center grant U10 CA180899.
NR 27
TC 5
Z9 5
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
EI 1097-0142
J9 CANCER-AM CANCER SOC
JI Cancer
PD DEC 1
PY 2015
VL 121
IS 23
BP 4205
EP 4211
DI 10.1002/cncr.29641
PG 7
WC Oncology
SC Oncology
GA CX3TJ
UT WOS:000365621900016
PM 26308766
ER

PT J
AU Gibbs, KD
   McGready, J
   Griffin, K
AF Gibbs, Kenneth D., Jr.
   McGready, John
   Griffin, Kimberly
TI Career Development among American Biomedical Postdocs
SO CBE-LIFE SCIENCES EDUCATION
LA English
DT Article
ID COLLEGE-STUDENTS; SELF-EFFICACY; SCIENCE; PERCEPTIONS; WOMEN;
   ENVIRONMENT; GENERATION; TRANSITION; INTERESTS; CHOICE
AB Recent biomedical workforce policy efforts have centered on enhancing career preparation for trainees, and increasing diversity in the research workforce. Postdoctoral scientists, or postdocs, are among those most directly impacted by such initiatives, yet their career development remains understudied. This study reports results from a 2012 national survey of 1002 American biomedical postdocs. On average, postdocs reported increased knowledge about career options but lower clarity about their career goals relative to PhD entry. The majority of postdocs were offered structured career development at their postdoctoral institutions, but less than one-third received this from their graduate departments. Postdocs from all social backgrounds reported significant declines in interest in faculty careers at research-intensive universities and increased interest in nonresearch careers; however, there were differences in the magnitude and period of training during which these changes occurred across gender and race/ethnicity. Group differences in interest in faculty careers were explained by career interest differences formed during graduate school but not by differences in research productivity, research self-efficacy, or advisor relationships. These findings point to the need for enhanced career development earlier in the training process, and interventions sensitive to distinctive patterns of interest development across social identity groups.
C1 [Gibbs, Kenneth D., Jr.] NCI, Canc Prevent Fellowship Program, Canc Prevent Div, Rockville, MD 20850 USA.
   [Gibbs, Kenneth D., Jr.] NCI, Sci Res & Technol Branch, Behav Res Program, Div Canc Control & Populat Sci, Rockville, MD 20850 USA.
   [McGready, John] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Biostat, Baltimore, MD 21205 USA.
   [Griffin, Kimberly] Univ Maryland, Dept Counseling Higher Educ & Special Educ, College Pk, MD 20742 USA.
RP Gibbs, KD (reprint author), NCI, Canc Prevent Fellowship Program, Canc Prevent Div, Rockville, MD 20850 USA.
EM kgibbsjr@gmail.com
OI Gibbs, Kenneth/0000-0002-3532-5396
FU Burroughs Wellcome Fund [1011798]
FX We thank Keith Micoli, Chris Pickett, and Sibby Anderson-Thompkins for
   their thoughtful feedback before submission. This work was supported, in
   part, by a generous grant from the Burroughs Wellcome Fund (Grant Number
   1011798). The funders had no role in study design, data collection and
   analysis, decision to publish, or preparation of the manuscript. K.D.G.
   is a member of the board of directors for the National Postdoctoral
   Association. Findings and views expressed in this work are those of the
   authors alone and do not necessarily reflect the views of any
   organization with which they are affiliated.
NR 40
TC 9
Z9 9
U1 11
U2 20
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1931-7913
J9 CBE-LIFE SCI EDUC
JI CBE-Life Sci. Educ.
PD DEC 1
PY 2015
VL 14
IS 4
AR ar44
DI 10.1187/cbe.15-03-0075
PG 12
WC Education, Scientific Disciplines
SC Education & Educational Research
GA CX7OW
UT WOS:000365892700007
PM 26582238
ER

PT J
AU Omeir, R
   Thomas, R
   Teferedegne, B
   Williams, C
   Foseh, G
   Macauley, J
   Brinster, L
   Beren, J
   Peden, K
   Breen, M
   Lewis, AM
AF Omeir, R.
   Thomas, R.
   Teferedegne, B.
   Williams, C.
   Foseh, G.
   Macauley, J.
   Brinster, L.
   Beren, J.
   Peden, K.
   Breen, M.
   Lewis, A. M., Jr.
TI A novel canine kidney cell line model for the evaluation of neoplastic
   development: karyotype evolution associated with spontaneous
   immortalization and tumorigenicity
SO CHROMOSOME RESEARCH
LA English
DT Article
DE Neoplastic transformation; Tumorigenicity; Canine chromosomes;
   Comparative genomic hybridization (CGH); Fluorescence in situ
   hybridization (FISH); Madin-Darby canine kidney (MDCK) cell line;
   CKB1-3T7 cell line
ID COPY NUMBER ABERRATIONS; CHINESE-HAMSTER CELLS; NEWBORN NUDE-MICE;
   IN-VITRO; DOMESTIC DOG; CYTOGENETIC CHARACTERIZATION; DIFFERENTIATED
   PROPERTIES; EMBRYO CELLS; ARRAY CGH; CHROMOSOME
AB The molecular mechanisms underlying spontaneous neoplastic transformation in cultured mammalian cells remain poorly understood, confounding recognition of parallels with the biology of naturally occurring cancer. The broad use of tumorigenic canine cell lines as research tools, coupled with the accumulation of cytogenomic data from naturally occurring canine cancers, makes the domestic dog an ideal system in which to investigate these relationships. We developed a canine kidney cell line, CKB1-3T7, which allows prospective examination of the onset of spontaneous immortalization and tumorigenicity. We documented the accumulation of cytogenomic aberrations in CKB1-3T7 over 24 months in continuous culture. The majority of aberrations emerged in parallel with key phenotypic changes in cell morphology, growth kinetics, and tumor incidence and latency. Focal deletion of CDKN2A/B emerged first, preceding the onset and progression of tumorigenic potential, and progressed to a homozygous deletion across the cell population during extended culture. Interestingly, CKB1-3T7 demonstrated a tumorigenic phenotype in vivo prior to exhibiting loss of contact inhibition in vitro. We also performed the first genome-wide characterization of the canine tumorigenic cell line MDCK, which also exhibited CDKN2A/B deletion. MDCK and CKB1-3T7 cells shared several additional aberrations that we have reported previously as being highly recurrent in spontaneous canine cancers, many of which, as with CDKN2A/B deletion, are evolutionarily conserved in their human counterparts. The conservation of these molecular events across multiple species, in vitro and in vivo, despite their contrasting karyotypic architecture, is a powerful indicator of a common mechanism underlying emerging neoplastic activity. Through integrated cytogenomic and phenotypic characterization of serial passages of CKB1-3T7 from initiation to development of a tumorigenic phenotype, we present a robust and readily accessible model (to be made available through the American Type Culture Collection) of spontaneous neoplastic transformation that overcomes many of the limitations of earlier studies.
C1 [Omeir, R.; Teferedegne, B.; Foseh, G.; Macauley, J.; Beren, J.; Lewis, A. M., Jr.] US FDA, Lab DNA Viruses, Div Viral Prod, Off Vaccines Res & Review,Ctr Biol Evaluat & Res, Silver Spring, MD 20993 USA.
   [Thomas, R.; Williams, C.; Breen, M.] N Carolina State Univ, Coll Vet Med, Dept Mol Biomed Sci, Raleigh, NC 27607 USA.
   [Thomas, R.; Breen, M.] N Carolina State Univ, Ctr Comparat Med & Translat Res, Raleigh, NC 27607 USA.
   [Brinster, L.] NIH, Div Vet Resources, Bethesda, MD 20892 USA.
   [Beren, J.] US FDA, Off Counter Terrorism & Emergency Coordinat, Ctr Drug Evaluat & Res, Silver Spring, MD 20993 USA.
   [Breen, M.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Canc Genet Program, Chapel Hill, NC 27599 USA.
   [Breen, M.] N Carolina State Univ, Ctr Human Hlth & Environm, Raleigh, NC 27607 USA.
RP Lewis, AM (reprint author), US FDA, Lab DNA Viruses, Div Viral Prod, Off Vaccines Res & Review,Ctr Biol Evaluat & Res, 10903 New Hampshire Ave, Silver Spring, MD 20993 USA.
EM matthew_breen@ncsu.edu; andrew.lewis@fda.hhs.gov
FU Division of Microbiology and Infectious Diseases of the National
   Institute of Allergy and Infectious Diseases [YI-AI-4893-02NIAID];
   Medical Counter Measures Initiative Grant; CBER Pandemic Influenza
   Counter Measures Grant; NCSU Cancer Genomics Fund
FX This study was supported in part by a contract from the Division of
   Microbiology and Infectious Diseases of the National Institute of
   Allergy and Infectious Diseases through an Interagency Agreement with
   CBER/FDA (contract number YI-AI-4893-02NIAID), Medical Counter Measures
   Initiative Grant, and a CBER Pandemic Influenza Counter Measures Grant.
   The molecular cytogenetics work was funded in part by the NCSU Cancer
   Genomics Fund (MB). The CKB1-3T7 cell line was developed and its
   biological properties characterized in LDNAV, CBER, FDA. Cytogenomic
   evaluation of the CKB1-3T7 and MDCK cell lines was performed at North
   Carolina State University. We thank Barry Falgout, Arifa Khan, Kari
   Irvine, and Melissa Savage for critical review of the manuscript. All
   authors contributed in the development of the manuscript for
   publication.
NR 72
TC 1
Z9 1
U1 2
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0967-3849
EI 1573-6849
J9 CHROMOSOME RES
JI Chromosome Res.
PD DEC
PY 2015
VL 23
IS 4
BP 663
EP 680
DI 10.1007/s10577-015-9474-8
PG 18
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA CX5OI
UT WOS:000365751100003
PM 25957863
ER

PT J
AU Chakrabarti, KR
   Hessler, L
   Bhandary, L
   Martin, SS
AF Chakrabarti, Kristi R.
   Hessler, Lindsay
   Bhandary, Lekhana
   Martin, Stuart S.
TI Molecular Pathways: New Signaling Considerations When Targeting
   Cytoskeletal Balance to Reduce Tumor Growth
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID BREAST-CANCER METASTASIS; PROMOTES MICROTENTACLE FORMATION; EMBRYONIC
   STEM-CELLS; ALPHA-TUBULIN; NEOADJUVANT CHEMOTHERAPY; EPITHELIAL-CELLS;
   ROCK INHIBITOR; OVARIAN-CANCER; REATTACHMENT; INVASION
AB The dynamic balance between microtubule extension and actin contraction regulates mammalian cell shape, division, and motility, which has made the cytoskeleton an attractive and very successful target for cancer drugs. Numerous compounds in clinical use to reduce tumor growth cause microtubule breakdown (vinca alkaloids, colchicine-site, and halichondrins) or hyperstabilization of microtubules (taxanes and epothilones). However, both of these strategies indiscriminately alter the assembly and dynamics of all microtubules, which causes significant dose-limiting toxicities on normal tissues. Emerging data are revealing that posttranslational modifications of tubulin (detyrosination, acetylation) or microtubule-associated proteins (Tau, Aurora kinase) may allow for more specific targeting of microtubule subsets, thereby avoiding the broad disruption of all microtubule polymerization. Developing approaches to reduce tumor cell migration and invasion focus on disrupting actin regulation by the kinases SRC and ROCK. Because the dynamic balance between microtubule extension and actin contraction also regulates cell fate decisions and stem cell characteristics, disrupting this cytoskeletal balance could yield unexpected effects beyond tumor growth. This review will examine recent data demonstrating that cytoskeletal cancer drugs affect wound-healing responses, microtentacle-dependent reattachment efficiency, and stem cell characteristics in ways that could affect the metastatic potential of tumor cells, both beneficially and detrimentally. (C) 2015 AACR.
C1 [Chakrabarti, Kristi R.; Hessler, Lindsay; Bhandary, Lekhana; Martin, Stuart S.] Univ Maryland, Sch Med, Marlene & Stewart Greenebaum NCI Canc Ctr, Baltimore, MD 21201 USA.
   [Chakrabarti, Kristi R.; Bhandary, Lekhana; Martin, Stuart S.] Univ Maryland, Sch Med, Program Mol Med, Baltimore, MD 21201 USA.
   [Hessler, Lindsay] Univ Maryland, Med Ctr, Gen Surg Residency Program, Baltimore, MD 21201 USA.
   [Martin, Stuart S.] Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA.
RP Martin, SS (reprint author), Univ Maryland, Sch Med, 655 West Baltimore St,Bressler Bldg,Room 10-29, Baltimore, MD 21201 USA.
EM ssmartin@som.umaryland.edu
FU NCI of the NIH [F30CA196075, T32CA154274, R01CA154624, R01CA124704];
   U.S. Department of Defense [BC100675]
FX This work was supported by the NCI of the NIH under award numbers
   F30CA196075 (to K.R. Chakrabarti), T32CA154274 (to K.R. Chakrabarti and
   L. Hessler), and R01CA154624 and R01CA124704 (to L. Bhandary and S.S.
   Martin), and an Era of Hope Scholar Award (BC100675) from the U.S.
   Department of Defense (to S.S. Martin).
NR 61
TC 0
Z9 0
U1 4
U2 14
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD DEC 1
PY 2015
VL 21
IS 23
BP 5209
EP 5214
DI 10.1158/1078-0432.CCR-15-0328
PG 6
WC Oncology
SC Oncology
GA CX3MT
UT WOS:000365603800006
PM 26463706
ER

PT J
AU Johnatty, SE
   Tyrer, JP
   Kar, S
   Beesley, J
   Lu, Y
   Gao, B
   Fasching, PA
   Hein, A
   Ekici, AB
   Beckmann, MW
   Lambrechts, D
   Van Nieuwenhuysen, E
   Vergote, I
   Lambrechts, S
   Rossing, MA
   Doherty, JA
   Chang-Claude, J
   Modugno, F
   Ness, RB
   Moysich, KB
   Levine, DA
   Kiemeney, LA
   Massuger, LFAG
   Gronwald, J
   Lubinski, J
   Jakubowska, A
   Cybulski, C
   Brinton, L
   Lissowska, J
   Wentzensen, N
   Song, H
   Rhenius, V
   Campbell, I
   Eccles, D
   Sieh, W
   Whittemore, AS
   McGuire, V
   Rothstein, JH
   Sutphen, R
   Anton-Culver, H
   Ziogas, A
   Gayther, SA
   Gentry-Maharaj, A
   Menon, U
   Ramus, SJ
   Pearce, CL
   Pike, MC
   Stram, DO
   Wu, AH
   Kupryjanczyk, J
   Dansonka-Mieszkowska, A
   Rzepecka, IK
   Spiewankiewicz, B
   Goodman, MT
   Wilkens, LR
   Carney, ME
   Thompson, PJ
   Heitz, F
   du Bois, A
   Schwaab, I
   Harter, P
   Pisterer, J
   Hillemanns, P
   Karlan, BY
   Walsh, C
   Lester, J
   Orsulic, S
   Winham, SJ
   Earp, M
   Larson, MC
   Fogarty, ZC
   Hogdall, E
   Jensen, A
   Kjaer, SK
   Fridley, BL
   Cunningham, JM
   Vierkant, RA
   Schildkraut, JM
   Iversen, ES
   Terry, KL
   Cramer, DW
   Bandera, EV
   Orlow, I
   Pejovic, T
   Bean, Y
   Hogdall, C
   Lundvall, L
   McNeish, I
   Paul, J
   Carty, K
   Siddiqui, N
   Glasspool, R
   Sellers, T
   Kennedy, C
   Chiew, YE
   Berchuck, A
   MacGregor, S
   Pharoah, PDP
   Goode, EL
   deFazio, A
   Webb, PM
   Chenevix-Trench, G
AF Johnatty, Sharon E.
   Tyrer, Jonathan P.
   Kar, Siddhartha
   Beesley, Jonathan
   Lu, Yi
   Gao, Bo
   Fasching, Peter A.
   Hein, Alexander
   Ekici, Arif B.
   Beckmann, Matthias W.
   Lambrechts, Diether
   Van Nieuwenhuysen, Els
   Vergote, Ignace
   Lambrechts, Sandrina
   Rossing, Mary Anne
   Doherty, Jennifer A.
   Chang-Claude, Jenny
   Modugno, Francesmary
   Ness, Roberta B.
   Moysich, Kirsten B.
   Levine, Douglas A.
   Kiemeney, Lambertus A.
   Massuger, Leon F. A. G.
   Gronwald, Jacek
   Lubinski, Jan
   Jakubowska, Anna
   Cybulski, Cezary
   Brinton, Louise
   Lissowska, Jolanta
   Wentzensen, Nicolas
   Song, Honglin
   Rhenius, Valerie
   Campbell, Ian
   Eccles, Diana
   Sieh, Weiva
   Whittemore, Alice S.
   McGuire, Valerie
   Rothstein, Joseph H.
   Sutphen, Rebecca
   Anton-Culver, Hoda
   Ziogas, Argyrios
   Gayther, Simon A.
   Gentry-Maharaj, Aleksandra
   Menon, Usha
   Ramus, Susan J.
   Pearce, Celeste L.
   Pike, Malcolm C.
   Stram, Daniel O.
   Wu, Anna H.
   Kupryjanczyk, Jolanta
   Dansonka-Mieszkowska, Agnieszka
   Rzepecka, Iwona K.
   Spiewankiewicz, Beata
   Goodman, Marc T.
   Wilkens, Lynne R.
   Carney, Michael E.
   Thompson, Pamela J.
   Heitz, Florian
   du Bois, Andreas
   Schwaab, Ira
   Harter, Philipp
   Pisterer, Jacobus
   Hillemanns, Peter
   Karlan, Beth Y.
   Walsh, Christine
   Lester, Jenny
   Orsulic, Sandra
   Winham, Stacey J.
   Earp, Madalene
   Larson, Melissa C.
   Fogarty, Zachary C.
   Hogdall, Estrid
   Jensen, Allan
   Kjaer, Susanne Kruger
   Fridley, Brooke L.
   Cunningham, Julie M.
   Vierkant, Robert A.
   Schildkraut, Joellen M.
   Iversen, Edwin S.
   Terry, Kathryn L.
   Cramer, Daniel W.
   Bandera, Elisa V.
   Orlow, Irene
   Pejovic, Tanja
   Bean, Yukie
   Hogdall, Claus
   Lundvall, Lene
   McNeish, Ian
   Paul, James
   Carty, Karen
   Siddiqui, Nadeem
   Glasspool, Rosalind
   Sellers, Thomas
   Kennedy, Catherine
   Chiew, Yoke-Eng
   Berchuck, Andrew
   MacGregor, Stuart
   Pharoah, Paul D. P.
   Goode, Ellen L.
   deFazio, Anna
   Webb, Penelope M.
   Chenevix-Trench, Georgia
CA AGO Study Grp
   Australian Ovarian Canc Study Grp
TI Genome-wide Analysis Identifies Novel Loci Associated with Ovarian
   Cancer Outcomes: Findings from the Ovarian Cancer Association Consortium
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID SURVIVAL; POLYMORPHISMS; CHEMOTHERAPY; PROGRESSION; THERAPY; WOMEN;
   YAP1; SUSCEPTIBILITY; PERSPECTIVES; METAANALYSIS
AB Purpose: Chemotherapy resistance remains a major challenge in the treatment of ovarian cancer. We hypothesize that germline polymorphisms might be associated with clinical outcome.
   Experimental Design: We analyzed approximately 2.8 million genotyped and imputed SNPs from the iCOGS experiment for progression-free survival (PFS) and overall survival (OS) in 2,901 European epithelial ovarian cancer (EOC) patients who underwent first-line treatment of cytoreductive surgery and chemotherapy regardless of regimen, and in a subset of 1,098 patients treated with >= 4 cycles of paclitaxel and carboplatin at standard doses. We evaluated the top SNPs in 4,434 EOC patients, including patients from The Cancer Genome Atlas. In addition, we conducted pathway analysis of all intragenic SNPs and tested their association with PFS and OS using gene set enrichment analysis.
   Results: Five SNPs were significantly associated (P >= 1.0 x 10(-5)) with poorer outcomes in at least one of the four analyses, three of which, rs4910232 (11p15.3), rs2549714 (16q23), and rs6674079 (1q22), were located in long noncoding RNAs (lncRNAs) RP11-179A10.1, RP11-314O13.1, and RP11-284F21.8, respectively (P >= 7.1 x 10(-6)). ENCODE ChIP-seq data at 1q22 for normal ovary show evidence of histone modification around RP11-284F21.8, and rs6674079 is perfectly correlated with another SNP within the super-enhancer MEF2D, expression levels of which were reportedly associated with prognosis in another solid tumor. YAP1- and WWTR1 (TAZ)-stimulated gene expression and high-density lipoprotein (HDL)-mediated lipid transport pathways were associated with PFS and OS, respectively, in the cohort who had standard chemotherapy (pGSEA <= 6 x 10(-3)).
   Conclusions: We have identified SNPs in three lncRNAs that might be important targets for novel EOC therapies. Clin Cancer Res; 21(23); 5264-76. 2015 AACR.
C1 [Johnatty, Sharon E.; Beesley, Jonathan; Lu, Yi; MacGregor, Stuart; Chenevix-Trench, Georgia] QIMR Berghofer Med Res Inst, Dept Genet & Computat Biol, Brisbane, Qld, Australia.
   [Tyrer, Jonathan P.; Kar, Siddhartha; Pharoah, Paul D. P.] Univ Cambridge, Dept Oncol, Dept Publ Hlth & Primary Care, Strangeways Res Lab, Cambridge, England.
   [Gao, Bo; Kennedy, Catherine; Chiew, Yoke-Eng; deFazio, Anna] Westmead Hosp, Dept Gynaecol Oncol, Sydney, NSW, Australia.
   [Gao, Bo; Kennedy, Catherine; Chiew, Yoke-Eng; deFazio, Anna] Univ Sydney, Ctr Canc Res, Westmead Millennium Inst, Sydney, NSW 2006, Australia.
   [Fasching, Peter A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Hematol & Oncol, Los Angeles, CA 90095 USA.
   [Fasching, Peter A.; Ekici, Arif B.] Univ Erlangen Nurnberg, Inst Human Genet, Univ Hosp Erlangen, Erlangen, Germany.
   [Hein, Alexander; Beckmann, Matthias W.] Univ Erlangen Nurnberg, Dept Gynecol & Obstet, Univ Hosp Erlangen, Comprehens Canc Ctr Erlangen EMN, D-91054 Erlangen, Germany.
   [Lambrechts, Diether] VIB, Vesalius Res Ctr, Leuven, Belgium.
   [Lambrechts, Diether] Univ Leuven, Dept Oncol, Lab Translat Genet, Leuven, Belgium.
   [Van Nieuwenhuysen, Els; Vergote, Ignace; Lambrechts, Sandrina] Univ Leuven, Leuven Canc Inst, Dept Gynecol Oncol, Leuven, Belgium.
   [Rossing, Mary Anne] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Program Epidemiol, Seattle, WA 98104 USA.
   [Rossing, Mary Anne] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
   [Doherty, Jennifer A.] Geisel Sch Med Dartmouth, Sect Biostat & Epidemiol, Dept Community & Family Med, Lebanon, NH USA.
   [Chang-Claude, Jenny] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
   [Modugno, Francesmary] Univ Pittsburgh, Sch Med, Dept Obstet Gynecol & Reprod Sci, Pittsburgh, PA USA.
   [Modugno, Francesmary] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
   [Modugno, Francesmary] Magee Womens Res Inst, Womens Canc Res Program, Pittsburgh, PA USA.
   [Modugno, Francesmary] Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
   [Ness, Roberta B.] Univ Texas Sch Publ Hlth, Houston, TX USA.
   [Moysich, Kirsten B.] Roswell Pk Canc Inst, Dept Canc Prevent & Control, Buffalo, NY 14263 USA.
   [Levine, Douglas A.] Mem Sloan Kettering Canc Ctr, Dept Surg, Gynecol Serv, New York, NY 10021 USA.
   [Kiemeney, Lambertus A.] Radboud Univ Nijmegen, Med Ctr, Radboud Inst Hlth Sci, NL-6525 ED Nijmegen, Netherlands.
   [Massuger, Leon F. A. G.] Radboud Univ Nijmegen, Med Ctr, Radboud Inst Mol Sci, NL-6525 ED Nijmegen, Netherlands.
   [Gronwald, Jacek; Lubinski, Jan; Jakubowska, Anna; Cybulski, Cezary] Pomeranian Med Univ, Dept Genet & Pathol, Int Hereditary Canc Ctr, Szczecin, Poland.
   [Brinton, Louise; Wentzensen, Nicolas] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Lissowska, Jolanta] Maria Sklodowska Curie Mem Canc Ctr, Dept Canc Epidemiol & Prevent, Warsaw, Poland.
   [Lissowska, Jolanta; Kupryjanczyk, Jolanta; Dansonka-Mieszkowska, Agnieszka; Rzepecka, Iwona K.; Spiewankiewicz, Beata] Inst Oncol, Warsaw, Poland.
   [Song, Honglin; Rhenius, Valerie] Univ Cambridge, Strangeways Res Lab, Dept Oncol, Cambridge, England.
   [Campbell, Ian] Peter MacCallum Canc Ctr, Div Res, Canc Genet Lab, Melbourne, Vic, Australia.
   [Campbell, Ian] Univ Melbourne, Dept Oncol, Melbourne, Vic, Australia.
   [Eccles, Diana] Univ Southampton, Southampton Univ Hosp, Fac Med, Southampton, Hants, England.
   [Sieh, Weiva; Whittemore, Alice S.; McGuire, Valerie; Rothstein, Joseph H.] Stanford Univ, Sch Med, Dept Hlth Res & Policy Epidemiol, Stanford, CA 94305 USA.
   [Sutphen, Rebecca] Univ S Florida, Coll Med, Epidemiol Ctr, Tampa, FL USA.
   [Anton-Culver, Hoda] Univ Calif Irvine, Sch Med, Ctr Canc Genet Res & Prevent, Dept Epidemiol, Irvine, CA 92717 USA.
   [Ziogas, Argyrios] Univ Calif Irvine, Dept Epidemiol, Irvine, CA USA.
   [Gayther, Simon A.; Ramus, Susan J.; Pearce, Celeste L.; Pike, Malcolm C.; Stram, Daniel O.; Wu, Anna H.] Univ So Calif, Keck Sch Med, Norris Comprehens Canc Ctr, Dept Prevent Med, Los Angeles, CA 90033 USA.
   [Gentry-Maharaj, Aleksandra; Menon, Usha] UCL EGA Inst Womens Hlth, Womens Canc, London, England.
   [Pearce, Celeste L.] Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA.
   [Pike, Malcolm C.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
   [Kupryjanczyk, Jolanta; Dansonka-Mieszkowska, Agnieszka; Rzepecka, Iwona K.] Maria Sklodowska Curie Mem Canc Ctr, Dept Pathol & Lab Diagnost, Warsaw, Poland.
   [Spiewankiewicz, Beata] Maria Sklodowska Curie Mem Canc Ctr, Dept Gynecol Oncol, Warsaw, Poland.
   [Goodman, Marc T.; Thompson, Pamela J.] Cedars Sinai Med Ctr, Samuel Oschin Comprehens Canc Inst, Canc Prevent & Control, Los Angeles, CA 90048 USA.
   [Goodman, Marc T.; Thompson, Pamela J.] Cedars Sinai Med Ctr, Dept Biomed Sci, Community & Populat Hlth Res Inst, Los Angeles, CA 90048 USA.
   [Wilkens, Lynne R.; Carney, Michael E.] Univ Hawaii, Ctr Canc, Canc Epidemiol Program, Honolulu, HI 96822 USA.
   [Heitz, Florian; du Bois, Andreas; Harter, Philipp] Kliniken Essen Mitte, Dept Gynecol & Gynecol Oncol, Essen, Germany.
   [Heitz, Florian; du Bois, Andreas; Harter, Philipp] Dr Horst Schmidt Kliniken Wiesbaden, Dept Gynecol & Gynecol Oncol, Wiesbaden, Germany.
   [Schwaab, Ira] Inst Humangenet Wiesbaden, Wiesbaden, Germany.
   [Pisterer, Jacobus] Zentrum Gynakol Onkol, Kiel, Germany.
   [Hillemanns, Peter] Hannover Med Sch, Dept Obstet & Gynaecol, Hannover, Germany.
   [Karlan, Beth Y.; Walsh, Christine; Lester, Jenny; Orsulic, Sandra] Cedars Sinai Med Ctr, Samuel Oschin Comprehens Canc Inst, Womens Canc Program, Los Angeles, CA 90048 USA.
   [Winham, Stacey J.; Earp, Madalene; Larson, Melissa C.; Fogarty, Zachary C.; Vierkant, Robert A.; Goode, Ellen L.] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
   [Hogdall, Estrid; Jensen, Allan; Kjaer, Susanne Kruger] Danish Canc Soc, Res Ctr, Dept Virus Lifestyle & Genes, Copenhagen, Denmark.
   [Hogdall, Estrid] Univ Copenhagen, Herlev Hosp, Dept Pathol, Mol Unit, Copenhagen, Denmark.
   [Kjaer, Susanne Kruger] Univ Copenhagen, Rigshosp, Dept Gynecol, DK-2100 Copenhagen, Denmark.
   [Fridley, Brooke L.] Univ Kansas, Med Ctr, Biostat & Informat Shared Resource, Kansas City, KS 66103 USA.
   [Cunningham, Julie M.] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA.
   [Schildkraut, Joellen M.] Duke Univ, Med Ctr, Dept Community & Family Med, Durham, NC 27710 USA.
   [Schildkraut, Joellen M.] Duke Canc Inst, Canc Control & Populat Sci, Durham, NC USA.
   [Iversen, Edwin S.] Duke Univ, Dept Stat Sci, Durham, NC USA.
   [Terry, Kathryn L.; Cramer, Daniel W.] Brigham & Womens Hosp, Obstet & Gynecol Epidemiol Ctr, Boston, MA 02115 USA.
   [Terry, Kathryn L.; Cramer, Daniel W.] Harvard Univ, Sch Med, Boston, MA USA.
   [Terry, Kathryn L.; Cramer, Daniel W.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
   [Bandera, Elisa V.] Rutgers State Univ, Canc Prevent & Control Program, Rutgers Canc Inst New Jersey, New Brunswick, NJ 08903 USA.
   [Orlow, Irene] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, Epidemiol Serv, New York, NY 10021 USA.
   [Pejovic, Tanja; Bean, Yukie] Oregon Hlth & Sci Univ, Dept Obstet & Gynecol, Portland, OR 97201 USA.
   [Pejovic, Tanja; Bean, Yukie] Knight Canc Inst, Portland, OR USA.
   [Hogdall, Claus; Lundvall, Lene] Univ Copenhagen, Rigshosp, Juliane Marie Ctr, Dept Gynaecol, DK-2100 Copenhagen, Denmark.
   [McNeish, Ian] Univ Glasgow, Beatson Inst Canc Res, Wolfson Wohl Canc Res Ctr, Inst Canc Sci, Glasgow, Lanark, Scotland.
   [Paul, James; Carty, Karen; Glasspool, Rosalind] Beatson West Scotland Canc Ctr, Canc Res UK Clin Trials Unit, Glasgow, Lanark, Scotland.
   [Siddiqui, Nadeem] Glasgow Royal Infirm, Dept Gynaecol Oncol, Glasgow G4 0SF, Lanark, Scotland.
   [Sellers, Thomas] Univ S Florida, H Lee Moffitt Canc Ctr, Dept Canc Epidemiol, Tampa, FL 33682 USA.
   [Berchuck, Andrew] Duke Univ, Med Ctr, Dept Obstet & Gynecol, Durham, NC 27710 USA.
   [Webb, Penelope M.] QIMR Berghofer Med Res Inst, Dept Populat Hlth, Brisbane, Qld, Australia.
RP Chenevix-Trench, G (reprint author), QIMR Berghofer Med Res Inst, 300 Herston Rd, Herston, Qld 4006, Australia.
EM georgia.trench@qimrberghofer.edu.au
RI Macgregor, Stuart/C-6442-2009; Bowtell, David/H-1007-2016; Hein,
   Alexander/F-6999-2010; Johnatty, Sharon/R-8890-2016; Gronwald,
   Jacek/A-4576-2017; 
OI Macgregor, Stuart/0000-0001-6731-8142; Bowtell,
   David/0000-0001-9089-7525; Hein, Alexander/0000-0003-2601-3398;
   Johnatty, Sharon/0000-0002-7888-1966; Gronwald,
   Jacek/0000-0002-3643-2871; Ramus, Susan/0000-0003-0005-7798; McNeish,
   Iain/0000-0002-9387-7586; Orlow, Irene/0000-0001-6234-6961; Winham,
   Stacey/0000-0002-8492-9102
FU Army Medical Research and Materiel Command [DAMD17-01-1-0729]; National
   Health St Medical Research Council of Australia; Cancer Council of New
   South Wales; Cancer Council of Victoria; Cancer Council of Queensland;
   Cancer Council of South Australia; Cancer Council of Tasmania; Cancer
   Foundation of Western Australia; National Health and Medical Research
   Council of Australia [199600, 400281]; AOCS Cancer Council [191, 211,
   182]; Fl AN Funds of the University of Erlangen Nuremberg; Nationaal
   Kankerplan; NIH [R01-CA112523, R01-CA87538, P30-CA15083, P50-CA136393,
   R01-CA122443, R01-CA76016, R01 CA 054419-10, P50 CA105009]; German
   Federal Ministry of Education and Research of Germany, Programme of
   Clinical Biomedical Research [01 GB 9401]; German Cancer Research
   Center; U.S. National Cancer Institute [K07-CA80668, R01CA095023,
   P50-CA159981, R01-CA126841]; US Army Medical Research and Materiel
   Command [DAMD17-02-1-0669]; NIH/National Center for Research Resources/
   General Clinical Research Center grant [MO1- RR000056]; American Cancer
   Society [120950-SIOP-06-258-06-COUN, SIOP-06-258-01-COUN]; National
   Center for Advancing Translational Sciences (NCATS) [UL1TR000124,
   ULITR000124.I]; European Communitys Seventh Framework Programme
   [223175223175 (HEALTH F2-2009-223175)]; Cancer Research UK
   [CI287/A10118, CI287/A10710, C12292/AI1174, C1281/AI2014, C5047/A8384,
   C5047/AI5007, C5047/AI0692, C8197/AI6565, C490/A8339, C490/A10119,
   C490/A10124, C490/A16561, C536/A13086, C536/A6689]; National institutes
   of Health [CA128978]; Post-Cancer GWAS initiative [1U19 CA148537, 1U19
   CA148065, 1U119 CA148112]; Department of Defence [W81XWH-10-1-0341];
   Canadian Institutes of Health Research (CIHR) for the CIHR Team in
   Familial Risks of Breast Cancer, Komen Foundation for the Cure; Breast
   Cancer Research Foundation; Ovarian Cancer Research Fund; University of
   Sydney Cancer Research Fund; Cancer institute NSW through the Sydney
   West Translational Cancer Research Centre; NCI CCSG award
   [P30-CA008748]; Mayo Foundation; Minnesota Ovarian Cancer Alliance; Fred
   C. and Katherine B. Andersen Foundation; National Cancer Institute [R01
   -CA 61107]; Danish Cancer Society [94-22252]; Mermaid I project;
   Department of Defense [DAMD17-02-1-0666]; Department of Defense CDMRP
   [W81XWH-10-1-0280]; NCI [NIH-K07 CA095666, R01-CA83918,
   NIH-K22-CA138563, P30-CA072720]; Cancer Institute of New Jersey; Sherie
   Hildreth Ovarian Cancer Research Fund; OHSU Foundation; Intramural
   Research Program of the NCI; UK National Institute for Health Research
   Biomedical Research Centre at the University, of Cambridge; Imperial
   Experimental Cancer Research Centre [C1312/A15589]; Australian National
   Health and Medical Research Council [310670, 628903]; Cancer Institute
   NSW [12/RIG/I-17]; Eve Appeal (The Oak Foundation); National Institute
   for Health Research University College London Hospitals Biomedical
   Research Centre; California Cancer Research Program [00-01389V-20170,
   2II0200];  [R01 CA 058598]
FX AUS studies (Australian Ovarian Cancer Study and the Australian Cancer
   Study) were funded by Army Medical Research and Materiel Command
   (DAMD17-01-1-0729); National Health St Medical Research Council of
   Australia; Cancer Councils of New South Wales, Victoria, Queensland,
   South Australia, and Tasmania; Cancer Foundation of Western Australia;
   and National Health and Medical Research Council of Australia (199600
   and 400281). The grant numbers for AOCS Cancer Council funding are as
   follows: Multi State Application Numbers 191, 211, and 182. The Bavarian
   study (BAY) WaS supported by Fl AN Funds of the University of Erlangen
   Nuremberg. The Belgian study (BEL) was funded by Nationaal Kankerplan.
   The Diseases of the Ovary and their Evaluation (DOV) study was funded by
   NIH R01-CA112523 and R01-CA87538. The German Ovarian Cancer Study (GER)
   was supported by the German Federal Ministry of Education and Research
   of Germany, Programme of Clinical Biomedical Research (01 GB 9401), and
   the German Cancer Research Center (DKFZ). The Hawaii Ovarian Cancer
   Study (HAW) was supported by R01 CA 058598. The Hormones and Ovarian
   Cancer Prediction study (HOP) was supported by U.S. National Cancer
   Institute: K07-CA80668, R01CA095023, P50-CA159981, 1101-CAl26841; US
   Army Medical Research and Materiel Command: DAMD17-02-1-0669; and
   NIH/National Center for Research Resources/ General Clinical Research
   Center grant MO1- RR000056. The Women's Cancer Program (LAX) was
   supported by the American Cancer Society Early Detection Professorship
   (120950-SIOP-06-258-06-COUN) and the National Center for Advancing
   Translational Sciences (NCATS), Grant UL1TR000124. The Mayo Clinic
   Case-Only Ovarian Cancer Study (MAC) was funded by the NIH
   (R01-CA122443, P30-CA15083, P50-CA136393). The Mayo Clinic Ovarian
   Cancer Case Control Study (MAY) was supported by NIH (R01-CA122443,
   P30-CA15083, P50-CA136393); Mayo Foundation; Minnesota Ovarian Cancer
   Alliance; Fred C. and Katherine B. Andersen Foundation. The MALOVA study
   (MAL) was funded by the National Cancer Institute (grant R01-CA 61107),
   the Danish Cancer Society (grant 94-22252), and the Mermaid I project.
   The North Carolina Ovarian Cancer Study (NCO) was supported by NIH
   (R01-CA76016) and the Department of Defense (DAMD17-02-1-0666). The New
   England based Case Control Study of Ovarian Cancer (NEC) was supported
   by NIH grants R01 CA 054419-10 and P50 CA105009, and Department of
   Defense CDMRP grant W81XWH-10-1-0280. The New Jersey Ovarian Cancer
   Study (NJO) was funded by the NCI (NIH-K07 CA095666, R01-CA83918,
   NIH-K22-CA138563, and P30-CA072720) and the Cancer Institute of New
   Jersey. The Oregon study (ORE) Was funded hy the Sherie Hildreth Ovarian
   Cancer Research Fund and the OHSU Foundation. The Polish Ovarian Cancer
   Case Control Study (POL) was funded by Intramural Research Program of
   the NCI. The SEARCH study (SEA) was supported by Cancer Research UK
   (C490/A8339, C490/A10119, C490/A10124, and C490/A16561) and UK National
   Institute for Health Research Biomedical Research Centre at the
   University, of Cambridge. The Scottish Randomised Trial in Ovarian
   Cancer (SRO) was funded by Cancer Research UK (C536/A13086, C536/A6689)
   and Imperial Experimental Cancer Research Centre (C1312/A15589). The
   Gynaecological Oncology Biobank at Westmead (WHMH) is a member of the
   Australasian Biospecimen Network-Oncology group, funded by the
   Australian National Health and Medical Research Council Enabling Grants
   ID 310670 and ID 628903 and the Cancer Institute NSW Grant ID
   12/RIG/I-17.; The United Kingdom Ovarian cancer Population Study (LIKO)
   was funded by The Eve Appeal (The Oak Foundation) and supported by the
   National Institute for Health Research University College London
   Hospitals Biomedical Research Centre. The UK Familial Ovarian Cancer
   Registry (LIKO) Cancer Research UK (C490/A6187); UK National Institute
   for Health Research Biomedical Research Centers kit the University of
   Cambridge. The Los Angeles County Case Control Studies of Ovarian
   Cancer-3 (USC) P01CA17054, P30CA14089, R01CA61132, N01PC67010,
   R03CA113148, R03CA115195, N01CN025403, and California Cancer Research
   Program (00-01389V-20170, 2II0200). The Warsaw Ovarian Cancer Study
   (WOC) Polish Ministry of Science and Higher Education (4 PO5C 028 14, 2
   PO5A 068 27), The Maria Sklodowska Curie Memorial Cancer Center and
   Institute of Oncology, Warsaw, Poland.; Anna deFazio was funded by the
   University of Sydney Cancer Research Fund and the Cancer institute NSW
   through the Sydney West Translational Cancer Research Centre. Dr. RV.
   Marian was supported hy American Cancer Society Early Detection
   Professorship (SIOP-06-258-01-COUN) and the National Center for
   Advancing Translational Sciences (NCATS), Grant ULITR000124.I. Orlow was
   supported by NCI CCSG award (P30-CA008748).; Funding for the iCOGS
   infrastructure came from the European Communitys Seventh Framework
   Programme under grant agreement no 223175 (HEALTH F2-2009-223175; COGS),
   Cancer Research UK (CI287/A10118, CI287/A 10710, C12292/AI1174,
   C1281/AI2014, C5047/A8384, C5047/AI5007, C5047/AI0692, C8197/AI6565),
   the National institutes of Health (CA128978) and Post-Cancer GWAS
   initiative (1U19 CA148537, 1U19 CA148065, and 1U119 CA148112 - the
   GAME-ON initiative), the Department of Defence (W81XWH-10-1-0341), the
   Canadian Institutes of Health Research (CIHR) for the CIHR Team in
   Familial Risks of Breast Cancer, Komen Foundation for the Cure, the
   Breast Cancer Research Foundation and the Ovarian Cancer Research Fund.
NR 50
TC 5
Z9 5
U1 2
U2 8
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD DEC 1
PY 2015
VL 21
IS 23
BP 5264
EP 5276
DI 10.1158/1078-0432.CCR-15-0632
PG 13
WC Oncology
SC Oncology
GA CX3MT
UT WOS:000365603800012
PM 26152742
ER

PT J
AU Lou, H
   Villagran, G
   Boland, JF
   Im, KM
   Polo, S
   Zhou, WY
   Odey, U
   Juarez-Torres, E
   Medina-Martinez, I
   Roman-Basaure, E
   Mitchell, J
   Roberson, D
   Sawitzke, J
   Garland, L
   Rodriguez-Herrera, M
   Wells, D
   Troyer, J
   Pinto, FC
   Bass, S
   Zhang, XJ
   Castillo, M
   Gold, B
   Morales, H
   Yeager, M
   Berumen, J
   Alvirez, E
   Gharzouzi, E
   Dean, M
AF Lou, Hong
   Villagran, Guillermo
   Boland, Joseph F.
   Im, Kate M.
   Polo, Sarita
   Zhou, Weiyin
   Odey, Ushie
   Juarez-Torres, Eligia
   Medina-Martinez, Ingrid
   Roman-Basaure, Edgar
   Mitchell, Jason
   Roberson, David
   Sawitzke, Julie
   Garland, Lisa
   Rodriguez-Herrera, Maria
   Wells, David
   Troyer, Jennifer
   Castillo Pinto, Francisco
   Bass, Sara
   Zhang, Xijun
   Castillo, Miriam
   Gold, Bert
   Morales, Hesler
   Yeager, Meredith
   Berumen, Jaime
   Alvirez, Enrique
   Gharzouzi, Eduardo
   Dean, Michael
TI Genome Analysis of Latin American Cervical Cancer: Frequent Activation
   of the PIK3CA Pathway
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID DNA-SEQUENCING DATA; HUMAN-PAPILLOMAVIRUS; ONCOGENIC MUTATIONS; DOMAIN
   MUTATIONS; HPV INTEGRATION; HELICAL DOMAIN; RISK-FACTOR; P110-ALPHA;
   CARCINOMA; WOMEN
AB Purpose: Cervical cancer is one of the most common causes of cancer mortality for women living in poverty, causing more than 28,000 deaths annually in Latin America and 266,000 worldwide. To better understand the molecular basis of the disease, we ascertained blood and tumor samples from Guatemala and Venezuela and performed genomic characterization.
   Experimental Design: We performed human papillomavirus (HPV) typing and identified somatically mutated genes using exome and ultra-deep targeted sequencing with confirmation in samples from Mexico. Copy number changes were also assessed in the exome sequence.
   Results: Cervical cancer cases in Guatemala and Venezuela have an average age of diagnosis of 50 years and 5.6 children. Analysis of 675 tumors revealed activation of PIK3CA and other PI3K/AKT pathway genes in 31% of squamous carcinomas and 24% of adeno-and adenosquamous tumors, predominantly at two sites (E542K, E545K) in the helical domain of the PIK3CA gene. This distribution of PIK3CA mutations is distinct from most other cancer types and does not result in the in vitro phosphorylation of AKT. Somatic mutations were more frequent in squamous carcinomas diagnosed after the age of 50 years. Frequent gain of chromosome 3q was found, and low PIK3CA mutation fractions in many tumors suggest that PI3K mutation can be a late event in tumor progression.
   Conclusions: PI3K pathway mutation is important to cervical carcinogenesis in Latin America. Therapeutic agents that directly target PI3K could play a role in the therapy of this common malignancy. (C) 2015 AACR.
C1 [Lou, Hong; Sawitzke, Julie; Garland, Lisa; Wells, David; Troyer, Jennifer] Leidos Biomed Res Inc, Basic Sci Program, Frederick, MD USA.
   [Villagran, Guillermo; Polo, Sarita; Castillo Pinto, Francisco; Castillo, Miriam; Morales, Hesler; Gharzouzi, Eduardo] Inst Cancerol, Guatemala City, Guatemala.
   [Boland, Joseph F.; Zhou, Weiyin; Mitchell, Jason; Roberson, David; Bass, Sara; Zhang, Xijun; Yeager, Meredith] Leidos Biomed Res Inc, Div Canc Epidemiol & Genet, Canc Genet Res Lab, Frederick, MD USA.
   [Boland, Joseph F.; Zhou, Weiyin; Mitchell, Jason; Roberson, David; Bass, Sara; Zhang, Xijun; Yeager, Meredith] Natl Lab Canc Res, Gaithersburg, MD USA.
   [Im, Kate M.; Rodriguez-Herrera, Maria; Gold, Bert; Dean, Michael] NCI, Expt Immunol Lab, Frederick, MD 21701 USA.
   [Odey, Ushie; Alvirez, Enrique] Hosp Cent Univ Dr Antonio M Pineda, Barquisimeto, Lara State, Venezuela.
   [Juarez-Torres, Eligia; Medina-Martinez, Ingrid; Berumen, Jaime] Univ Nacl Autonoma Mexico, Fac Med, Hosp Gen Mexico, Unidad Med Genom, Mexico City 04510, DF, Mexico.
   [Roman-Basaure, Edgar] Hosp Gen Mexico City, Serv Oncol, Mexico City, DF, Mexico.
RP Dean, M (reprint author), NCI, Expt Immunol Lab, Bldg 560,Room 21-89b, Frederick, MD 21702 USA.
EM deanm@mail.nih.gov
FU Intramural Research Program of the NIH, National Cancer Institute,
   Center for Cancer Research; Leidos Biomedical Research, Inc.
   [HHSN261200800001E]; National University of Mexico [SDI.PTID.05.2]
FX The work was supported in part by the Intramural Research Program of the
   NIH, National Cancer Institute, Center for Cancer Research, and by
   Leidos Biomedical Research, Inc., under contract #HHSN261200800001E and
   the National University of Mexico (www.unam.mx), grant number
   SDI.PTID.05.2 (to J. Berumen).
NR 50
TC 4
Z9 4
U1 1
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD DEC 1
PY 2015
VL 21
IS 23
BP 5360
EP 5370
DI 10.1158/1078-0432.CCR-14-1837
PG 11
WC Oncology
SC Oncology
GA CX3MT
UT WOS:000365603800021
PM 26080840
ER

PT J
AU Deng, W
   Chen, WW
   Zhang, ZY
   Huang, SS
   Kong, W
   Sun, Y
   Tang, XJ
   Yao, GH
   Feng, XB
   Chen, WJ
   Sun, LY
AF Deng, Wei
   Chen, Weiwei
   Zhang, Zhuoya
   Huang, Saisai
   Kong, Wei
   Sun, Yue
   Tang, Xiaojun
   Yao, Genhong
   Feng, Xuebing
   Chen, WanJun
   Sun, Lingyun
TI Mesenchymal stem cells promote CD206 expression and phagocytic activity
   of macrophages through IL-6 in systemic lupus erythematosus
SO CLINICAL IMMUNOLOGY
LA English
DT Article
DE Umbilical cord-derived mesenchymal stem cells; Systemic lupus
   erythematosus; Macrophage; IL-6
ID M2 MACROPHAGES; TRANSPLANTATION; MICE; NEPHRITIS; CLASSIFICATION;
   POLARIZATION; PHENOTYPE; CRITERIA; COLITIS; BIOLOGY
AB Human umbilical cord-derived mesenchymal stem cells (UCMSCs) show therapeutic effects on systemic lupus erythematosus (SLE). Deficiency in functional polarization and phagocytosis in macrophages has been suggested in the pathogenesis of SLE. We found that macrophages from B6.MRL-Fas(lpr) mice exhibited lower level of CD206, the marker for alternatively activated macrophage (AAM, also called M2). In addition, the phagocytic activity of B6.MRL-Fas(lpr) macrophages was also decreased. UCMSC transplantation improved the proportion of CD206(+) macrophages and their phagocytic activity in B6.MRL-Fas(lpr) mice. Importantly, macrophages from SLE patients also showed lower expression of CD206 and reduced phagocytic activity, which were corrected by being co-cultured with UCMSCs in vitro and in SLE patients receiving UCMSC transplantation. Mechanistically, we demonstrated that IL-6 was required for the up-regulation of CD206 expression and phagocytic activity of UCMSC-treated SLE macrophages. Our results indicate that UCMSCs alleviate SLE through promoting CD206 expression and phagocytic activity of macrophages in an IL-6 dependent manner. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Deng, Wei; Chen, Weiwei; Zhang, Zhuoya; Huang, Saisai; Kong, Wei; Sun, Yue; Tang, Xiaojun; Yao, Genhong; Feng, Xuebing; Sun, Lingyun] Nanjing Univ, Sch Med, Affiliated Drum Tower Hosp, Dept Rheumatol & Immunol, Nanjing 210008, Jiangsu, Peoples R China.
   [Chen, WanJun] Natl Inst Dent & Craniofacial Res, Mucosal Immunol Sect, OPCB, NIH, Bethesda, MD 20892 USA.
RP Sun, LY (reprint author), Nanjing Univ, Sch Med, Affiliated Drum Tower Hosp, Dept Rheumatol & Immunol, 321 Zhongshan Rd, Nanjing 210008, Jiangsu, Peoples R China.
EM lingyunsun@nju.edu.cn
FU Major International (Regional) Joint Research Project of China
   [81120108021]; National Natural Science Foundation of China [81273304,
   81401349]; Fundamental Research Funds for the Central Universities of
   China [021414340284]; Intramural Research Program of NIH, NIDCR
FX This work was funded by grants from the Major International (Regional)
   Joint Research Project of China (No. 81120108021), the National Natural
   Science Foundation of China (No. 81273304, 81401349) and the Fundamental
   Research Funds for the Central Universities of China (No. 021414340284).
   W.J.C. was supported by the Intramural Research Program of NIH, NIDCR.
NR 46
TC 4
Z9 4
U1 1
U2 10
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1521-6616
EI 1521-7035
J9 CLIN IMMUNOL
JI Clin. Immunol.
PD DEC
PY 2015
VL 161
IS 2
BP 209
EP 216
DI 10.1016/j.clim.2015.07.011
PG 8
WC Immunology
SC Immunology
GA CX6SL
UT WOS:000365831600022
PM 26209923
ER

PT J
AU Lawson, BR
   Gonzalez-Quintial, R
   Eleftheriadis, T
   Farrar, MA
   Miller, SD
   Sauer, K
   McGavern, DB
   Kono, DH
   Baccala, R
   Theofilopoulos, AN
AF Lawson, Brian R.
   Gonzalez-Quintial, Rosana
   Eleftheriadis, Theodoros
   Farrar, Michael A.
   Miller, Stephen D.
   Sauer, Karsten
   McGavern, Dorian B.
   Kono, Dwight H.
   Baccala, Roberto
   Theofilopoulos, Argyrios N.
TI Interleukin-7 is required for CD4(+) T cell activation and autoimmune
   neuroinflammation
SO CLINICAL IMMUNOLOGY
LA English
DT Article
DE IL-7; T cells; EAE; Signaling pathways
ID RECEPTOR-DEFICIENT MICE; CENTRAL-NERVOUS-SYSTEM; MULTIPLE-SCLEROSIS;
   IL-7; PROLIFERATION; SURVIVAL; NAIVE; HOMEOSTASIS; EXPRESSION; MEMORY
AB IL-7 is known to be vital for T cell homeostasis but has previously been presumed to be dispensable for TCR-induced activation. Here, we show that IL-7 is critical for the initial activation of CD4(+) T cells in that it provides some of the necessary early signaling components, such as activated STAT5 and Akt. Accordingly, short-term in vivo IL-7R alpha blockade inhibited the activation and expansion of autoantigen-specific CD4(+) T cells and, when used to treat experimental autoimmune encephalomyelitis (EAE), prevented and ameliorated disease. Our studies demonstrate that IL-7 signaling is a prerequisite for optimal CD4(+) T cell activation and that IL-7R antagonism may be effective in treating CD4(+) T cell-mediated neuroinflammation and other autoimmune inflammatory conditions. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Lawson, Brian R.; Gonzalez-Quintial, Rosana; Eleftheriadis, Theodoros; Sauer, Karsten; Kono, Dwight H.; Baccala, Roberto; Theofilopoulos, Argyrios N.] Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
   [Farrar, Michael A.] Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55414 USA.
   [Miller, Stephen D.] Northwestern Univ, Sch Med, Dept Microbiol Immunol, Chicago, IL 60611 USA.
   [McGavern, Dorian B.] NINDS, NIH, Bethesda, MD 20892 USA.
RP Theofilopoulos, AN (reprint author), Scripps Res Inst, Dept Immunol & Microbial Sci, IMM 3,10550 North Torrey Pines Rd, La Jolla, CA 92037 USA.
EM argyrio@scripps.edu
OI Farrar, Michael/0000-0002-5569-0366; Eleftheriadis,
   Theodoros/0000-0001-9302-1633
FU NIH National Institute of Arthritis and Musculoskeletal and Skin
   Diseases [AR065919]
FX This is manuscript number 29180 from the Department of Immunology and
   Microbial Science of The Scripps Research Institute. We would like to
   thank M. Kat Occhipinti for editorial assistance, and John Scatizzi,
   Dilki Wichramarachchi, and Tannaz Hasnat for excellent technical
   assistance. This work was supported by grant AR065919 from the NIH
   National Institute of Arthritis and Musculoskeletal and Skin Diseases.
NR 56
TC 4
Z9 4
U1 1
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1521-6616
EI 1521-7035
J9 CLIN IMMUNOL
JI Clin. Immunol.
PD DEC
PY 2015
VL 161
IS 2
BP 260
EP 269
DI 10.1016/j.clim.2015.08.007
PG 10
WC Immunology
SC Immunology
GA CX6SL
UT WOS:000365831600027
PM 26319414
ER

PT J
AU Chung, ST
   Chacko, SK
   Sunehag, AL
   Haymond, MW
AF Chung, Stephanie T.
   Chacko, Shaji K.
   Sunehag, Agneta L.
   Haymond, Morey W.
TI Measurements of Gluconeogenesis and Glycogenolysis: A Methodological
   Review
SO DIABETES
LA English
DT Review
ID HEPATIC GLUCOSE-PRODUCTION; ISOTOPOMER DISTRIBUTION ANALYSIS;
   NUCLEAR-MAGNETIC-RESONANCE; DOSE-RESPONSE CHARACTERISTICS; DEPENDENT
   DIABETES-MELLITUS; TOTAL PARENTERAL-NUTRITION; IMPAIRED FASTING GLUCOSE;
   MASS ISOTOPOMER; LIVER-GLYCOGEN; C-13 NMR
AB Gluconeogenesis is a complex metabolic process that involves multiple enzymatic steps regulated by myriad factors, including substrate concentrations, the redox state, activation and inhibition of specific enzyme steps, and hormonal modulation. At present, the most widely accepted technique to determine gluconeogenesis is by measuring the incorporation of deuterium from the body water pool into newly formed glucose. However, several techniques using radioactive and stable-labeled isotopes have been used to quantitate the contribution and regulation of gluconeogenesis in humans. Each method has its advantages, methodological assumptions, and set of propagated errors. In this review, we examine the strengths and weaknesses of the most commonly used stable isotopes methods to measure gluconeogenesis in vivo. We discuss the advantages and limitations of each method and summarize the applicability of these measurements in understanding normal and pathophysiological conditions.
C1 [Chung, Stephanie T.] NIDDKD, NIH, Bethesda, MD USA.
   [Chacko, Shaji K.; Sunehag, Agneta L.; Haymond, Morey W.] Baylor Coll Med, USDA ARS, Childrens Nutr Res Ctr, Dept Pediat, Houston, TX 77030 USA.
RP Haymond, MW (reprint author), Baylor Coll Med, USDA ARS, Childrens Nutr Res Ctr, Dept Pediat, Houston, TX 77030 USA.
EM mhaymond@bcm.edu
FU U.S. Department of Agriculture/Agricultural Research Service Children's
   Nutrition Research Center, Department of Pediatrics, Baylor College of
   Medicine; intramural department at the National Institute of Diabetes
   and Digestive and Kidney Diseases at the National Inititutes of Health;
   Marilyn Fishman Endocrine Fellows Foundation [2R01-HD-037957,
   1R01-HD-044609, 5T32-DK-063873, 5R01-DK-055478]; U.S. Department of
   Agriculture [CRIS 6250-51000]
FX This work is a publication of the U.S. Department of
   Agriculture/Agricultural Research Service Children's Nutrition Research
   Center, Department of Pediatrics, Baylor College of Medicine. S.T.C. is
   supported by the intramural department at the National Institute of
   Diabetes and Digestive and Kidney Diseases at the National Inititutes of
   Health. The authors' studies reported in this review were supported by
   the Marilyn Fishman Endocrine Fellows Foundation (grant to S.T.C.),
   2R01-HD-037957 (A.L.S.), 1R01-HD-044609 (A.L.S.), 5T32-DK-063873
   (M.W.H.), 5R01-DK-055478 (M.W.H.), and the U.S. Department of
   Agriculture (CRIS 6250-51000 to M.W.H.).
NR 123
TC 2
Z9 2
U1 2
U2 14
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 DEC
PY 2015
VL 64
IS 12
BP 3996
EP 4010
DI 10.2337/db15-0640
PG 15
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CX8DN
UT WOS:000365932900008
PM 26604176
ER

PT J
AU Padgett, LE
   Anderson, B
   Liu, C
   Ganini, D
   Mason, RP
   Piganelli, JD
   Mathews, CE
   Tse, HM
AF Padgett, Lindsey E.
   Anderson, Brian
   Liu, Chao
   Ganini, Douglas
   Mason, Ronald P.
   Piganelli, Jon D.
   Mathews, Clayton E.
   Tse, Hubert M.
TI Loss of NOX-Derived Superoxide Exacerbates Diabetogenic CD4 T-Cell
   Effector Responses in Type 1 Diabetes
SO DIABETES
LA English
DT Article
ID CHRONIC GRANULOMATOUS-DISEASE; NADPH OXIDASE; RECEPTOR STIMULATION;
   OXIDATIVE BURST; BETA-CELLS; MACROPHAGES; ACTIVATION; ARTHRITIS; MICE;
   AUTOIMMUNITY
AB Reactive oxygen species (ROS) play prominent roles in numerous biological systems. While classically expressed by neutrophils and macrophages, CD4 T cells also express NADPH oxidase (NOX), the superoxide-generating multisubunit enzyme. Our laboratory recently demonstrated that superoxide-deficient nonobese diabetic (NOD. Ncf1(m1J)) mice exhibited a delay in type 1 diabetes (T1D) partially due to blunted IFN-gamma synthesis by CD4 T cells. For further investigation of the roles of superoxide on CD4 T-cell diabetogenicity, the NOD.BDC-2.5.Ncf(m1J) (BDC-2.5.Ncf1(m1J)) mouse strain was generated, possessing autoreactive CD4 T cells deficient in NOX-derived superoxide. Unlike NOD.Ncfr(m1J), stimulated BDC-2.5.Ncf1(m1J) CD4 T cells and splenocytes displayed elevated synthesis of Th1 cytokines and chemokines. Superoxide-deficient BDC-2.5 mice developed spontaneous T1D, and CD4 T cells were more diabetogenic upon adoptive transfer into NOD.Rag recipients due to a skewing toward impaired Treg suppression. Exogenous superoxide blunted exacerbated Th1 cytokines and proinflammatory chemokines to approximately wild-type levels, concomitant with reduced IL-12R beta 2 signaling and P-STAT4 (Y693) activation. These results highlight the importance of NOX-derived superoxide in curbing autoreactivity due, in part, to control of Treg function and as a redox-dependent checkpoint of effector T-cell responses. Ultimately, our studies reveal the complexities of free radicals in CD4 T-cell responses.
C1 [Padgett, Lindsey E.; Anderson, Brian; Tse, Hubert M.] Univ Alabama Birmingham, Sch Med, Dept Microbiol, Comprehens Diabet Ctr, Birmingham, AL 35294 USA.
   [Liu, Chao; Mathews, Clayton E.] Univ Florida, Coll Med, Dept Pathol Immunol & Lab Med, Gainesville, FL USA.
   [Ganini, Douglas; Mason, Ronald P.] NIH, Free Rad Metabolites Immun Inflammat & Dis Lab, Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
   [Piganelli, Jon D.] Univ Pittsburgh, Sch Med, Dept Surg Immunol & Pathol, Pittsburgh, PA USA.
RP Tse, HM (reprint author), Univ Alabama Birmingham, Sch Med, Dept Microbiol, Comprehens Diabet Ctr, Birmingham, AL 35294 USA.
EM htse@uab.edu
FU National Institutes of Health (NIH)/National Institute of Diabetes and
   Digestive and Kidney Diseases (NIDDK) R01 award [DK-099550]; American
   Diabetes Association Career Development Award [7-12-CD-11]; P30 Pilot
   Feasibility award from the UAB Comprehensive Diabetes Center/Diabetes
   Research Training Center; NIH National Institute of Allergy and
   Infectious Diseases [5T32AI007051-35]; Immunologic Diseases and Basic
   Immunology T32 training grant; Travel for Techniques Program Award from
   the American Association for Immunologists, Inc.; NIH/NIDDK R01 award
   [DK-074656]; JDRF; Intramural Research Program of the National Institute
   of Environmental Health Sciences/NIH; Animal Resources Program
   [G20RR025858]; Comprehensive Arthritis, Musculoskeletal, and
   Autoimmunity Center: Analytic and Preparative Cytometry Facility [P30
   AR48311]; Comprehensive Arthritis, Musculoskeletal, and Autoimmunity
   Center: Epitope Recognition Immunoreagent Core [P30 AR48311]
FX This work was supported by a National Institutes of Health
   (NIH)/National Institute of Diabetes and Digestive and Kidney Diseases
   (NIDDK) R01 award (DK-099550), an American Diabetes Association Career
   Development Award (7-12-CD-11), a P30 Pilot Feasibility award from the
   UAB Comprehensive Diabetes Center/Diabetes Research Training Center, an
   NIH National Institute of Allergy and Infectious Diseases
   (5T32AI007051-35) Immunologic Diseases and Basic Immunology T32 training
   grant (to L.E.P.), and a Travel for Techniques Program Award from the
   American Association for Immunologists, Inc. (to H.M.T.). Further
   support was provided by an NIH/NIDDK R01 award (DK-074656) and a grant
   from the JDRF (to C.E.M.). This research was partially supported by the
   Intramural Research Program of the National Institute of Environmental
   Health Sciences/NIH. The following core facilities of UAB were used to
   generate data for the manuscript: Animal Resources Program (G20RR025858,
   Sam Cartner); the Comprehensive Arthritis, Musculoskeletal, and
   Autoimmunity Center: Analytic and Preparative Cytometry Facility (P30
   AR48311, John D. Mountz); and the Comprehensive Arthritis,
   Musculoskeletal, and Autoimmunity Center: Epitope Recognition
   Immunoreagent Core (P30 AR48311, Mary Ann Accavitti-Loper).
NR 47
TC 3
Z9 3
U1 0
U2 3
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 DEC
PY 2015
VL 64
IS 12
BP 4171
EP 4183
DI 10.2337/db15-0546
PG 13
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CX8DN
UT WOS:000365932900022
PM 26269022
ER

PT J
AU Papandonatos, GD
   Pan, Q
   Pajewski, NM
   Delahanty, LM
   Peter, I
   Erar, B
   Ahmad, S
   Harden, M
   Chen, L
   Fontanillas, P
   Wagenknecht, LE
   Kahn, SE
   Wing, RR
   Jablonski, KA
   Huggins, GS
   Knowler, WC
   Florez, JC
   McCaffery, JM
   Franks, PW
AF Papandonatos, George D.
   Pan, Qing
   Pajewski, Nicholas M.
   Delahanty, Linda M.
   Peter, Inga
   Erar, Bahar
   Ahmad, Shafqat
   Harden, Maegan
   Chen, Ling
   Fontanillas, Pierre
   Wagenknecht, Lynne E.
   Kahn, Steven E.
   Wing, Rena R.
   Jablonski, Kathleen A.
   Huggins, Gordon S.
   Knowler, William C.
   Florez, Jose C.
   McCaffery, Jeanne M.
   Franks, Paul W.
CA Giant Consortium
   Diabetes Prevention Program & The
TI Genetic Predisposition to Weight Loss and Regain With Lifestyle
   Intervention: Analyses From the Diabetes Prevention Program and the Look
   AHEAD Randomized Controlled Trials
SO DIABETES
LA English
DT Article
ID BODY-MASS INDEX; HEAT-SHOCK-PROTEIN; CARDIOVASCULAR-DISEASE;
   CLINICAL-TRIAL; RISK-FACTORS; OBESITY; INDIVIDUALS; LOCI; ASSOCIATION;
   TRANSLATION
AB Clinically relevant weight loss is achievable through lifestyle modification, but unintentional weight regain is common. We investigated whether recently discovered genetic variants affect weight loss and/or weight regain during behavioral intervention. Participants at high-risk of type 2 diabetes (Diabetes Prevention Program [DPP]; N = 917/907 intervention/comparison) or with type 2 diabetes (Look AHEAD [Action for Health in Diabetes]; N = 2,014/1,892 intervention/comparison) were from two parallel arm (lifestyle vs. comparison) randomized controlled trials. The associations of 91 established obesity-predisposing loci with weight loss across 4 years and with weight regain across years 2-4 after a minimum of 3% weight loss were tested. Each copy of the minor G allele of MTIF3 rs1885988 was consistently associated with greater weight loss following lifestyle intervention over 4 years across the DPP and Look AHEAD. No such effect was observed across comparison arms, leading to a nominally significant single nucleotide polymorphism x treatment interaction (P = 4.3 x 10(-3)). However, this effect was not significant at a study-wise significance level (Bonferroni threshold P < 5.8 x 10(-4)). Most obesity-predisposing gene variants were not associated with weight loss or regain within the DPP and Look AHEAD trials, directly or via interactions with lifestyle.
C1 [Papandonatos, George D.; Erar, Bahar] Brown Univ, Ctr Stat Sci, Providence, RI 02912 USA.
   [Pan, Qing; Jablonski, Kathleen A.] George Washington Univ, Ctr Biostat, Rockville, MD USA.
   [Pajewski, Nicholas M.] Wake Forest Sch Med, Div Publ Hlth Sci, Dept Biostat Sci, Winston Salem, NC USA.
   [Delahanty, Linda M.; Florez, Jose C.] Massachusetts Gen Hosp, Diabet Res Ctr, Diabet Unit, Boston, MA 02114 USA.
   [Delahanty, Linda M.; Florez, Jose C.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
   [Peter, Inga] Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, New York, NY 10029 USA.
   [Ahmad, Shafqat; Franks, Paul W.] Skane Univ, Univ Lund, Dept Clin Sci, Genet & Mol Epidemiol Unit,Hosp Malmo, Malmo, Sweden.
   [Harden, Maegan] Broad Inst, Genom Platform, Cambridge, MA USA.
   [Chen, Ling; Fontanillas, Pierre; Florez, Jose C.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
   [Chen, Ling; Fontanillas, Pierre; Florez, Jose C.] Broad Inst, Program Med & Populat Genet, Cambridge, MA USA.
   [Wagenknecht, Lynne E.] Wake Forest Sch Med, Div Publ Hlth Sci, Look AHEAD Coordinating Ctr, Winston Salem, NC USA.
   [Kahn, Steven E.] VA Puget Sound Hlth Care Syst, Dept Med, Div Metab Endocrinol & Nutr, Seattle, WA USA.
   [Kahn, Steven E.] Univ Washington, Seattle, WA 98195 USA.
   [Wing, Rena R.; McCaffery, Jeanne M.] Miriam Hosp, Weight Control & Diabet Res Ctr, Providence, RI 02906 USA.
   [Wing, Rena R.; McCaffery, Jeanne M.] Brown Univ, Warren Alpert Med Sch, Providence, RI 02912 USA.
   [Huggins, Gordon S.] Tufts Med Ctr, Mol Cardiol Res Inst, Ctr Translat Genom, Boston, MA USA.
   [Knowler, William C.] NIDDK, Phoenix, AZ USA.
   [Franks, Paul W.] Umea Univ, Dept Publ Hlth & Clin Med, Umea, Sweden.
   [Franks, Paul W.] Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA.
RP Franks, PW (reprint author), Skane Univ, Univ Lund, Dept Clin Sci, Genet & Mol Epidemiol Unit,Hosp Malmo, Malmo, Sweden.
EM jeanne_mccaffery@brown.edu; paul.franks@med.lu.se
OI Papandonatos, George/0000-0001-6770-932X; Kahn,
   Steven/0000-0001-7307-9002
FU National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
   [R01 DK072041-02, DK056992-14S1]; Department of Veterans Affairs; Doris
   Duke Charitable Foundation Clinical Scientist Development Award; Swedish
   Heart-Lung Foundation; Novo Nordisk Foundation; Swedish Research
   Council; EXODIAB; Swedish Diabetes Association; NIDDK of the National
   Institutes of Health (NIH); NIDDK; Indian Health Service; NIH Office of
   Research on Minority Health; Eunice Kennedy Shriver National Institute
   of Child Health and Human Development; National Institute on Aging;
   Centers for Disease Control and Prevention; NIH Office of Research on
   Women's Health; American Diabetes Association; Intramural Research
   Program of the NIDDK
FX The DPP and Look AHEAD analyses were funded by the National Institute of
   Diabetes and Digestive and Kidney Diseases (NIDDK) grants R01
   DK072041-02 (to K.A.J. and J.C.F. [W.C.K. and P.W.F. are
   co-nvestigators]) and DK056992-14S1, respectively. S.E.K. is supported
   in part by the Department of Veterans Affairs. J.C.F. is supported by a
   Doris Duke Charitable Foundation Clinical Scientist Development Award.
   P.W.F. was supported by grants from the Swedish Heart-Lung Foundation,
   the Novo Nordisk Foundation, the Swedish Research Council, EXODIAB, and
   the Swedish Diabetes Association.; DPP: The NIDDK of the National
   Institutes of Health (NIH) provided funding to the clinical centers and
   the coordinating center for the design and conduct of the study and
   collection, management, analysis, and interpretation of the data. The
   Southwestern American Indian Centers were supported directly by the
   NIDDK and the Indian Health Service. The General Clinical Research
   Center Program of the National Center for Research Resources supported
   data collection at many of the clinical centers. Funding for data
   collection and participant support was also provided by the NIH Office
   of Research on Minority Health, the Eunice Kennedy Shriver National
   Institute of Child Health and Human Development, the National Institute
   on Aging, the Centers for Disease Control and Prevention, the NIH Office
   of Research on Women's Health, the Department of Veterans Affairs, and
   the American Diabetes Association. Bristol-Myers Squibb and Parke-Davis
   provided medication. This research was also supported, in part, by the
   Intramural Research Program of the NIDDK. LifeScan, Health O Meter,
   Hoechst Marion Roussel Inc., Merck-Medco Managed Care, LLC, Merck & Co.,
   Inc., Nike Sports Marketing, SlimFast Foods Co., and Quaker Oats Co.
   donated materials, equipment, or medicines for concomitant conditions.
   McKesson BioServices, Matthews Media Group, Inc., and the Henry M.
   Jackson Foundation for the Advancement of Military Medicine, Inc.
   provided support services under subcontract with the coordinating
   center.
NR 32
TC 7
Z9 7
U1 2
U2 10
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 DEC
PY 2015
VL 64
IS 12
BP 4312
EP 4321
DI 10.2337/db15-0441
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CX8DN
UT WOS:000365932900034
PM 26253612
ER

PT J
AU Baier, LJ
   Muller, YL
   Remedi, MS
   Traurig, M
   Piaggi, P
   Wiessner, G
   Huang, K
   Stacy, A
   Kobes, S
   Krakoff, J
   Bennett, PH
   Nelson, RG
   Knowler, WC
   Hanson, RL
   Nichols, CG
   Bogardus, C
AF Baier, Leslie J.
   Muller, Yunhua Li
   Remedi, Maria Sara
   Traurig, Michael
   Piaggi, Paolo
   Wiessner, Gregory
   Huang, Ke
   Stacy, Alyssa
   Kobes, Sayuko
   Krakoff, Jonathan
   Bennett, Peter H.
   Nelson, Robert G.
   Knowler, William C.
   Hanson, Robert L.
   Nichols, Colin G.
   Bogardus, Clifton
TI ABCC8 R1420H Loss-of-Function Variant in a Southwest American Indian
   Community: Association With Increased Birth Weight and Doubled Risk of
   Type 2 Diabetes
SO DIABETES
LA English
DT Article
ID PERSISTENT HYPERINSULINEMIC HYPOGLYCEMIA; SULFONYLUREA RECEPTOR SUR1;
   GENOME-WIDE ASSOCIATION; SENSITIVE K+ CHANNELS; PIMA-INDIANS; CONGENITAL
   HYPERINSULINISM; INSULIN-SECRETION; GLUCOSE-INTOLERANCE;
   ENERGY-EXPENDITURE; GENETIC-VARIATION
AB Missense variants in KCNJ11 and ABCC8, which encode the KIR6.2 and SUR1 subunits of the beta-cell K-ATP channel, have previously been implicated in type 2 diabetes, neonatal diabetes, and hyperinsulinemic hypoglycemia of infancy (HHI). To determine whether variation in these genes affects risk for type 2 diabetes or increased birth weight as a consequence of fetal hyperinsulinemia in Pima Indians, missense and common noncoding variants were analyzed in individuals living in the Gila River Indian Community. A R1420H variant in SUR1 (ABCC8) was identified in 3.3% of the population (N = 7,710). R1420H carriers had higher mean birth weights and a twofold increased risk for type 2 diabetes with a 7-year earlier onset age despite being leaner than noncarriers. One individual homozygous for R1420H was identified; retrospective review of his medical records was consistent with HHI and a diagnosis of diabetes at age 3.5 years. In vitro studies showed that the R1420H substitution decreases K-ATP channel activity. Identification of this loss-of-function variant in ABCC8 with a carrier frequency of 3.3% affects clinical care as homozygous inheritance and potential HHI will occur in 1/3,600 births in this American Indian population.
C1 [Baier, Leslie J.; Muller, Yunhua Li; Traurig, Michael; Piaggi, Paolo; Wiessner, Gregory; Huang, Ke; Stacy, Alyssa; Kobes, Sayuko; Krakoff, Jonathan; Bennett, Peter H.; Nelson, Robert G.; Knowler, William C.; Hanson, Robert L.; Bogardus, Clifton] NIH, Phoenix Epidemiol & Clin Res Branch, NIDDK, Phoenix, AZ 85007 USA.
   [Remedi, Maria Sara; Nichols, Colin G.] Washington Univ, Dept Cell Biol & Physiol, St Louis, MO USA.
RP Baier, LJ (reprint author), NIH, Phoenix Epidemiol & Clin Res Branch, NIDDK, Phoenix, AZ 85007 USA.
EM lbaier@phx.niddk.nih.gov
FU Intramural Research Program of the National Institute of Diabetes and
   Digestive and Kidney Diseases, National Institutes of Health
FX This research was supported by the Intramural Research Program of the
   National Institute of Diabetes and Digestive and Kidney Diseases,
   National Institutes of Health.
NR 66
TC 5
Z9 5
U1 2
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 DEC
PY 2015
VL 64
IS 12
BP 4322
EP 4332
DI 10.2337/db15-0459
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CX8DN
UT WOS:000365932900035
PM 26246406
ER

PT J
AU Thavikulwat, AT
   Lopez, P
   Caruso, RC
   Jeffrey, BG
AF Thavikulwat, Alisa T.
   Lopez, Patrick
   Caruso, Rafael C.
   Jeffrey, Brett G.
TI The effects of gender and age on the range of the normal human
   electro-oculogram
SO DOCUMENTA OPHTHALMOLOGICA
LA English
DT Article
DE EOG; Electro-oculogram; Fast oscillation; Arden ratio; Clinical
   electrophysiology; Retinal pigment epithelium
ID CLINICAL ELECTROOCULOGRAPHY; NORMAL VALUES; EOG; OSCILLATIONS; LIGHT;
   PARAMETERS; RESPONSES; ALCOHOL
AB To define the normal ranges for the slow oscillations (SO) and fast oscillations (FO) of the electro-oculogram (EOG) recorded to International Society for Clinical Electrophysiology of Vision (ISCEV) standards. The effects of age and gender on the EOG ranges were examined.
   ISCEV standard SOs and FOs were recorded from 121 subjects (51 % male) aged from 7 to 72 years. Study variables for the SO were dark trough (DT) and light peak (LP) amplitudes (A mu V), times to DT and LP (min), and the Arden ratio (LP/DT amplitude). The FO was fit by a sine wave and peak-to-peak amplitude (A mu V), phase (A degrees), and peak-to-trough (PT) ratios derived. The effects of age, gender and pupil size on EOG parameters were examined by multiple regression analysis.
   The average Arden ratio was 2.5. Arden ratio decreased with age at a rate of 0.13 per decade of age (R (2) = 0.14, P < 0.0001). The 5th percentile of the Arden ratio decreased from 2.0 to 1.7 between 10 and 60 years of age. Median time to LP was 9 min (interquartile range 8-9 min). Time to LP was age-dependent and increased by 2 min for subjects over 55 years of age compared with those less than 25 years. EOG amplitudes were greater in women than in men (P < 0.005). The average PT ratio was 1.18, which was not affected by age or gender. Time to reach the light trough of the FO was 40 s, which increased with age (1.1 s/decade). No correlation was observed between Arden ratio and PT ratio.
   The major strength of this study is the definition of the normal range and associated lower limits of ISCEV standard EOGs based on recordings from 121 subjects balanced by gender and spanning the 1st through 8th decades of life. Decreased Arden ratio and increased time to LP are associated with aging, which is likely due to the intricate mechanisms involved in generation of the light rise. Differences between the FO and SO with respect to the effects of aging are consistent with separate generation of these two EOG signals.
C1 [Thavikulwat, Alisa T.; Lopez, Patrick; Jeffrey, Brett G.] NEI, NIH, Bethesda, MD 20892 USA.
   [Caruso, Rafael C.] Princeton Univ, Dept Psychol, Princeton, NJ 08544 USA.
   [Jeffrey, Brett G.] NEI, Ophthalm Genet & Visual Funct Branch, Bethesda, MD 20892 USA.
RP Jeffrey, BG (reprint author), NEI, Ophthalm Genet & Visual Funct Branch, 10 Ctr Dr,Room 10N226, Bethesda, MD 20892 USA.
EM jeffreybg@nei.nih.gov
FU National Institutes of Health (NIH) Intramural Research Program
   [97-EI-0080, 08-EI-N014]; NIH Medical Research Scholars Program; NIH
FX The National Institutes of Health (NIH) Intramural Research Program
   provided financial support in the form of human Protocols 97-EI-0080 and
   08-EI-N014. Alisa Thavikulwat was funded by 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 Newport Foundation, The
   American Association for Dental Research, The Howard Hughes Medical
   Institute, and the Colgate-Palmolive Company, as well as other private
   donors. The sponsors had no role in the design or conduct of this
   research.
NR 29
TC 0
Z9 0
U1 2
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0012-4486
EI 1573-2622
J9 DOC OPHTHALMOL
JI Doc. Ophthalmol.
PD DEC
PY 2015
VL 131
IS 3
BP 177
EP 188
DI 10.1007/s10633-015-9514-x
PG 12
WC Ophthalmology
SC Ophthalmology
GA CX5QM
UT WOS:000365757200003
PM 26474906
ER

PT J
AU Hanley, PW
   Barnhart, KF
   Abee, CR
   Lambeth, SR
   Weese, JS
AF Hanley, Patrick W.
   Barnhart, Kirstin F.
   Abee, Christian R.
   Lambeth, Susan R.
   Weese, J. Scott
TI Methicillin-Resistant Staphylococcus aureus Prevalence among Captive
   Chimpanzees, Texas, USA, 2012
SO EMERGING INFECTIOUS DISEASES
LA English
DT Article
ID STRAINS; ANIMALS
AB Methicillin-resistant Staphylococcus aureus (MRSA) infection in humans and animals is concerning. In 2012, our evaluation of a captive chimpanzee colony in Texas revealed MRSA prevalence of 69%. Animal care staff should be aware of possible zoonotic MRSA transmission resulting from high prevalence among captive chimpanzees.
C1 [Hanley, Patrick W.] NIH, Rocky Mt Vet Branch, Hamilton, MT USA.
   [Barnhart, Kirstin F.] AbbVie Inc, N Chicago, IL USA.
   [Abee, Christian R.; Lambeth, Susan R.] Univ Texas MD Anderson Canc Ctr, Bastrop, TX USA.
   [Weese, J. Scott] Univ Guelph, Guelph, ON N1G 2W1, Canada.
RP Hanley, PW (reprint author), NIAID, Rocky Mt Vet Branch, Rocky Mt Labs, NIH, 903 S 4th St, Hamilton, MT 59840 USA.
EM patrick.hanley@nih.gov
NR 15
TC 1
Z9 1
U1 3
U2 6
PU CENTERS  DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1080-6040
EI 1080-6059
J9 EMERG INFECT DIS
JI Emerg. Infect. Dis
PD DEC
PY 2015
VL 21
IS 12
BP 2158
EP 2160
DI 10.3201/eid2112.142004
PG 3
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA CX1MT
UT WOS:000365461000008
PM 26583847
ER

PT J
AU Ferrer, RA
   Grenen, EG
   Taber, JM
AF Ferrer, Rebecca A.
   Grenen, Emily G.
   Taber, Jennifer M.
TI Effectiveness of Internet-Based Affect Induction Procedures: A
   Systematic Review and Meta-Analysis
SO EMOTION
LA English
DT Article
DE emotion induction; mood induction; Internet experiments; meta-analysis
ID MECHANICAL TURK; MOOD-INDUCTION; FUNNEL-PLOT; EMOTION; ONLINE; ANGER;
   BIAS; FEAR; COMMITMENT; EXPRESSION
AB Procedures used to induce affect in a laboratory are effective and well-validated. Given recent methodological and technological advances in Internet research, it is important to determine whether affect can be effectively induced using Internet methodology. We conducted a meta-analysis and systematic review of prior research that has used Internet-based affect induction procedures, and examined potential moderators of the effectiveness of affect induction procedures. Twenty-six studies were included in final analyses, with 89 independent effect sizes. Affect induction procedures effectively induced general positive affect, general negative affect, fear, disgust, anger, sadness, and guilt, but did not significantly induce happiness. Contamination of other nontarget affect did not appear to be a major concern. Video inductions resulted in greater effect sizes. Overall, results indicate that affect can be effectively induced in Internet studies, suggesting an important venue for the acceleration of affective science.
C1 [Ferrer, Rebecca A.] NCI, Basic Biobehav & Psychol Sci Branch, Behav Res Program, Div Canc Control & Populat Sci,NIH, Rockville, MD 20850 USA.
   [Grenen, Emily G.; Taber, Jennifer M.] NCI, Behav Res Program, Div Canc Control & Populat Sci, NIH, Rockville, MD 20850 USA.
RP Ferrer, RA (reprint author), NCI, Basic Biobehav & Psychol Sci Branch, Behav Res Program, Div Canc Control & Populat Sci,NIH, Rockville, MD 20850 USA.
EM ferrerra@mail.nih.gov
NR 73
TC 6
Z9 6
U1 10
U2 22
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 1528-3542
EI 1931-1516
J9 EMOTION
JI Emotion
PD DEC
PY 2015
VL 15
IS 6
BP 752
EP 762
DI 10.1037/emo0000035
PG 11
WC Psychology, Experimental
SC Psychology
GA CX4WS
UT WOS:000365701700011
PM 25938613
ER

PT J
AU Goodman, MT
   Saraiya, M
   Thompson, TD
   Steinau, M
   Hernandez, BY
   Lynch, CF
   Lyu, CW
   Wilkinson, EJ
   Tucker, T
   Copeland, G
   Peters, ES
   Altekruse, S
   Unger, ER
AF Goodman, Marc T.
   Saraiya, Mona
   Thompson, Trevor D.
   Steinau, Martin
   Hernandez, Brenda Y.
   Lynch, Charles F.
   Lyu, Christopher W.
   Wilkinson, Edward J.
   Tucker, Thomas
   Copeland, Glenn
   Peters, Edward S.
   Altekruse, Sean
   Unger, Elizabeth R.
TI Human papillomavirus genotype and oropharynx cancer survival in the
   United States of America
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Cancer of the oropharynx; Human papillomavirus; Archived tissue; Cancer
   registry; Survival
ID SQUAMOUS-CELL CARCINOMA; PHASE-III TRIAL; NECK-CANCER;
   PROGNOSTIC-SIGNIFICANCE; VACCINE INTRODUCTION; ORAL-CAVITY; HPV STATUS;
   HEAD; PREVALENCE; WORLDWIDE
AB Background: The presence of human papillomavirus (HPV) DNA in oropharyngeal squamous cell cancer (OPSCC) tissue appears to be a strong predictor of improved prognosis, but this observation has not been explored in a population-based sample with generalisable findings.
   Methods: Follow-up data from a large sample of OPSCC patients identified through six population-based cancer registries in the United States of America (USA) were used to characterise the association of tumour HPV status with survival.
   Results: HPV DNA was detected in tumour tissue from 71% (378 in 529) of the OPSCC patients. A total of 65% of patients with HPV16-associated tumours survived 5 years compared to 46% of patients with other HPV types and 28% of patients with HPV-negative tumours (p log-rank test < 0.0001). The OPSCC patients with detectable HPV16 DNA had a 62% reduced hazard of death at 5 years, and patients with other HPV types had a 42% reduced hazard of death at 5 years compared to HPV-negative patients. Compared to non-Hispanic Whites, Blacks with OPSCC had a 2.6-fold greater risk of death at 5 years after adjustment for HPV status and other prognostic variables. Both surgery and radiation therapy were associated with a reduced 5-year risk of death, but no evidence was found for an interaction between HPV status and radiotherapy or surgery on survival time.
   Conclusions: Data from this US study suggest that HPV16-positive OPSCC patients survive longer than HPV-negative patients regardless of treatment, highlighting the prognostic importance of HPV status for this malignancy. Optimal treatment regimens for OPSCC could be tailored to each patient's HPV status and prognostic profile. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Goodman, Marc T.] Cedars Sinai Med Ctr, Canc Prevent & Control Program, Samuel Oschin Comprehens Canc Inst, Los Angeles, CA 90048 USA.
   [Saraiya, Mona; Thompson, Trevor D.] Ctr Dis Control & Prevent, Div Canc Prevent & Control, Natl Ctr Chron Dis Prevent & Hlth Promot, Atlanta, GA USA.
   [Steinau, Martin; Unger, Elizabeth R.] Ctr Dis Control & Prevent, Div High Consequence Pathogens & Pathol, Natl Ctr Emerging & Zoonot Infect Dis, Atlanta, GA USA.
   [Hernandez, Brenda Y.] Univ Hawaii, Ctr Canc, Honolulu, HI 96822 USA.
   [Lynch, Charles F.] Univ Iowa, Coll Publ Hlth, Dept Epidemiol, Iowa City, IA USA.
   [Lyu, Christopher W.] Battelle Mem Inst, Durham, NC USA.
   [Wilkinson, Edward J.] Univ Florida, Coll Med, Dept Pathol Immunol & Lab Med, Gainesville, FL USA.
   [Tucker, Thomas] Univ Kentucky, Coll Publ Hlth, Dept Epidemiol, Lexington, KY USA.
   [Copeland, Glenn] Michigan Dept Community Hlth, Lansing, MI USA.
   [Peters, Edward S.] Louisiana State Univ, Hlth Sci Ctr, Sch Publ Hlth, Dept Epidemiol, New Orleans, LA USA.
   [Altekruse, Sean] NCI, Div Canc Control & Populat Sci, Rockville, MD USA.
RP Goodman, MT (reprint author), Cedars Sinai Med Ctr, 8700 Beverly Blvd,Suite 1S37, Los Angeles, CA 90048 USA.
EM marc.goodman@cshs.org; msaraiya@cdc.gov
OI /0000-0003-4928-6532
FU Intramural NIH HHS; NCCDPHP CDC HHS [U58 DP000810, 5U58DP000812-5, U58
   DP000769, 5U58DP000810-5, 5U58DP000844-5, U58 DP000812, U58 DP000844,
   5U58DP000769-5]; NCI NIH HHS [N01-PC-35137, N01-PC-35143, N01PC35137,
   R01 CA077318, P30 CA071789, P30 CA086862, N01 PC035137, N01PC35143]
NR 40
TC 6
Z9 6
U1 0
U2 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0959-8049
EI 1879-0852
J9 EUR J CANCER
JI Eur. J. Cancer
PD DEC
PY 2015
VL 51
IS 18
BP 2759
EP 2767
DI 10.1016/j.ejca.2015.09.005
PG 9
WC Oncology
SC Oncology
GA CX3UI
UT WOS:000365624500005
PM 26602016
ER

PT J
AU Tacke, F
   Wynn, TA
AF Tacke, Frank
   Wynn, Thomas A.
TI Biomarker and Therapeutic Potential of CSF1 in Acute Liver Failure
SO GASTROENTEROLOGY
LA English
DT Editorial Material
ID COLONY-STIMULATING FACTOR; KUPFFER CELLS; FIBROSIS; INJURY; MACROPHAGES;
   CIRRHOSIS; SPECTRUM
C1 [Tacke, Frank] Univ Hosp Aachen, Dept Med 3, D-52074 Aachen, Germany.
   [Wynn, Thomas A.] NIAID, Immunopathogenesis Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Tacke, F (reprint author), Univ Hosp Aachen, Dept Med 3, Pauwelsstr 30, D-52074 Aachen, Germany.
EM frank.tacke@gmx.net
FU Intramural NIH HHS [Z01 AI000829-11]
NR 16
TC 0
Z9 0
U1 1
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
EI 1528-0012
J9 GASTROENTEROLOGY
JI Gastroenterology
PD DEC
PY 2015
VL 149
IS 7
BP 1675
EP 1678
DI 10.1053/j.gastro.2015.10.024
PG 5
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CX6JX
UT WOS:000365808100016
PM 26505816
ER

PT J
AU Pasricha, PJ
   Yates, KP
   Nguyen, L
   Clarke, J
   Abell, TL
   Farrugia, G
   Hasler, WL
   Koch, KL
   Snape, WJ
   McCallum, RW
   Sarosiek, I
   Tonascia, J
   Miriel, LA
   Lee, L
   Hamilton, F
   Parkman, HP
AF Pasricha, Pankaj J.
   Yates, Katherine P.
   Nguyen, Linda
   Clarke, John
   Abell, Thomas L.
   Farrugia, Gianrico
   Hasler, William L.
   Koch, Kenneth L.
   Snape, William J.
   McCallum, Richard W.
   Sarosiek, Irene
   Tonascia, James
   Miriel, Laura A.
   Lee, Linda
   Hamilton, Frank
   Parkman, Henry P.
TI Outcomes and Factors Associated With Reduced Symptoms in Patients With
   Gastroparesis
SO GASTROENTEROLOGY
LA English
DT Article
DE GpCRC; Improvement; Predictors; Etiology
ID QUALITY-OF-LIFE; UPPER GASTROINTESTINAL DISORDERS; HIGH-FAT DIET;
   IDIOPATHIC GASTROPARESIS; CLINICAL CHARACTERISTICS; DIABETIC
   GASTROPARESIS; POSTOPERATIVE NAUSEA; DISEASE; SEVERITY; INDEX
AB BACKGROUND & AIMS: Gastroparesis is a chronic clinical syndrome characterized by delayed gastric emptying. However, little is known about patient outcomes or factors associated with reduction of symptoms. METHODS: We studied adult patients with gastroparesis (of diabetic or idiopathic type) enrolled in the National Institute of Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium Gastroparesis Registry, seen every 16 weeks and treated according to the standard of care with prescribed medications or other therapies at 7 tertiary care centers. Characteristics associated with reduced symptoms, based on a decrease of 1 or more in the gastroparesis cardinal symptom index (GCSI) score after 48 weeks of care, were determined from logistic regression models. Data were collected from patients for up to 4 years (median, 2.1 y). RESULTS: Of 262 patients, 28% had reductions in GCSI scores of 1 or more at 48 weeks. However, there were no significant reductions in GCSI score from weeks 48 through 192. Factors independently associated with reduced symptoms at 48 weeks included male sex, age 50 years and older, initial infectious prodrome, antidepressant use, and 4-hour gastric retention greater than 20%. Factors associated with no reduction in symptoms included overweight or obesity, a history of smoking, use of pain modulators, moderate to severe abdominal pain, a severe gastroesophageal reflex, and moderate to severe depression. CONCLUSIONS: Over a median follow-up period of 2.1 years, 28% of patients treated for gastroparesis at centers of expertise had reductions in GCSI scores of 1 or greater, regardless of diabetes. These findings indicate the chronic nature of gastroparesis. We identified factors associated with reduced symptoms that might be used to guide treatment.
C1 [Pasricha, Pankaj J.; Yates, Katherine P.; Clarke, John; Tonascia, James; Miriel, Laura A.; Lee, Linda] Johns Hopkins Univ, Sch Med, Div Gastroenterol, Baltimore, MD USA.
   [Pasricha, Pankaj J.; Yates, Katherine P.; Clarke, John; Tonascia, James; Miriel, Laura A.; Lee, Linda] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA.
   [Nguyen, Linda] Stanford Univ, Div Gastroenterol & Hepatol, Palo Alto, CA 94304 USA.
   [Abell, Thomas L.] Univ Louisville, Div Gastroenterol, Louisville, KY 40292 USA.
   [Farrugia, Gianrico] Mayo Clin, Rochester, MN USA.
   [Hasler, William L.] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
   [Koch, Kenneth L.] Wake Forest Univ, Dept Internal Med Gastroenterol, Winston Salem, NC 27109 USA.
   [Snape, William J.] Calif Pacific Med Ctr, Ctr Neurogastroenterol & Motil, San Francisco, CA USA.
   [McCallum, Richard W.; Sarosiek, Irene] Texas Tech Univ, Dept Internal Med, El Paso, TX USA.
   [Hamilton, Frank] NIDDK, Digest Dis Branch, Bethesda, MD 20892 USA.
   [Parkman, Henry P.] Temple Univ, Dept Med, Gastroenterol Sect, Philadelphia, PA 19122 USA.
RP Pasricha, PJ (reprint author), Johns Hopkins Carey Sch Business, Johns Hopkins Sch Med, Johns Hopkins Ctr Neurogastroenterol, 720 Rutland St,Ross 958, Baltimore, MD 21205 USA.
EM Ppasric1@jhmi.edu
FU National Institute of Diabetes and Digestive and Kidney Diseases
   [U01DK073983, U01DK073975, U01DK073985, U01DK074007, U01DK073974,
   U01DK074008]
FX The Gastroparesis Clinical Research Consortium is supported by the
   National Institute of Diabetes and Digestive and Kidney Diseases
   (U01DK073983, U01DK073975, U01DK073985, U01DK074007, U01DK073974, and
   U01DK074008).
NR 56
TC 12
Z9 12
U1 3
U2 10
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
EI 1528-0012
J9 GASTROENTEROLOGY
JI Gastroenterology
PD DEC
PY 2015
VL 149
IS 7
BP 1762
EP +
DI 10.1053/j.gastro.2015.08.008
PG 17
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CX6JX
UT WOS:000365808100030
PM 26299414
ER

PT J
AU Carapito, R
   Poustchi, H
   Kwemou, M
   Untrau, M
   Sharifi, AH
   Merat, S
   Haj-Sheykholeslami, A
   Jabbari, H
   Esmaili, S
   Michel, S
   Toussaint, J
   Le Gentil, M
   Ansari-Moghaddam, A
   Radosavljevic, M
   Etemadi, A
   Georgel, P
   Malekzadeh, R
   Bahram, S
AF Carapito, R.
   Poustchi, H.
   Kwemou, M.
   Untrau, M.
   Sharifi, A. H.
   Merat, S.
   Haj-Sheykholeslami, A.
   Jabbari, H.
   Esmaili, S.
   Michel, S.
   Toussaint, J.
   Le Gentil, M.
   Ansari-Moghaddam, A.
   Radosavljevic, M.
   Etemadi, A.
   Georgel, P.
   Malekzadeh, R.
   Bahram, S.
TI Polymorphisms in EGFR and IL28B are associated with spontaneous
   clearance in an HCV-infected iranian population
SO GENES AND IMMUNITY
LA English
DT Article
ID HEPATITIS-C VIRUS; HOST GENETIC-DETERMINANTS; VIRAL CLEARANCE; CANCER;
   COHORT
AB Although most hepatitis C virus (HCV)-infected individuals develop chronic infection, about 25% of them are able to clear the virus spontaneously without any therapeutic intervention. The aim of the present study was to identify genes associated with spontaneous HCV clearance in a population of Iranian patients. We genotyped 110 single-nucleotide polymorphisms (SNPs) in 59 selected-candidate-genes in a cohort of 107 HCV-infected participants who spontaneously cleared the infection and 176 participants whose infection persisted. Three out of the 110 SNPs were found to be associated with HCV outcome (P-values < 0.03). rs11506105 in EGFR (epidermal growth factor receptor gene), and rs11881222 and rs12979860 in IL28B (interferon-lambda 3 gene). Multivariate logistic regression of the three markers showed that the A/A genotypes in both rs11506105 (EFGR) and rs11881222 (IL28B), and the C/C genotype in rs12979860 (IL28B) are associated with HCV clearance (recessive model: odds ratio (OR) = 2.06, 95% confidence interval (95% CI) = 1.09-3.88, P = 0.025; OR = 2.09, 95% CI = 1.23-3.60, P = 0.007; and OR = 1.95, 95% CI = 1.15-3.35, P = 0.014 for rs11506105, rs12979860 and rs11881222, respectively). In conclusion, EGFR and IL28B SNPs are strong independent predictive markers of spontaneous viral clearance.
C1 [Carapito, R.; Kwemou, M.; Untrau, M.; Michel, S.; Toussaint, J.; Le Gentil, M.; Radosavljevic, M.; Georgel, P.; Bahram, S.] Univ Strasbourg, Federat Hosp Univ FHU OMICARE,Fac Med,LabEx Trans, Ctr Rech Immunol & Hematol,Plateforme GENOMAX, Lab ImmunoRhumatol Mol,INSERM,UMR S1109,FMTS, F-67085 Strasbourg, France.
   [Poustchi, H.; Sharifi, A. H.; Merat, S.; Haj-Sheykholeslami, A.; Jabbari, H.; Esmaili, S.; Etemadi, A.; Malekzadeh, R.] Univ Tehran Med Sci, Liver & Pancreatobiliary Dis Res Ctr, Digest Dis Res Inst, Tehran 14117, Iran.
   [Merat, S.; Malekzadeh, R.] Univ Tehran Med Sci, Shariati Hosp, Digest Dis Res Inst, Digest Dis Res Ctr, Tehran 14117, Iran.
   [Ansari-Moghaddam, A.] Zahedan Univ Med Sci, Hlth Promot Res Ctr, Zahedan, Iran.
   [Etemadi, A.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
RP Malekzadeh, R (reprint author), Univ Tehran Med Sci, Shariati Hosp, Digest Dis Res Inst, Digest Dis Res Ctr, Kargar Shomali Ave, Tehran 14117, Iran.
EM malek@tums.ac.ir; siamak@unistra.fr
RI Etemadi, Arash/C-1386-2016; georgel, philippe/P-5676-2016; Carapito,
   Raphael/O-5317-2016; 
OI Etemadi, Arash/0000-0002-3458-1072; georgel,
   philippe/0000-0001-6853-7080; Carapito, Raphael/0000-0002-7036-442X;
   Ansari Moghaddam, Alireza/0000-0002-3267-7193
FU Strasbourg High Throughput Next Generation Sequencing facility
   (GENOMAX), INSERM [UMR_S 1109]; Agence Nationale de la Recherche,
   Programme Blanc entitled GENHEPC [ANR-07-BLAN-0108]; Institut de
   Recherche pour le Developpement (IRD); Institut Universitaire de France
   (IUF); Partenariat Hubert Curien GUNDISHAPUR, ministeres des Affaires
   etrangeres et du developpement international (MAEDI); Enseignement
   superieur et de la Recherche (MESR); Centre National pour la Recherche
   Scientifique (CNRS); Tehran University of Medical Sciences; intramural
   research program of the Division of Cancer Epidemiology and Genetics,
   National Cancer Institute
FX This work was supported by funds from the Strasbourg High Throughput
   Next Generation Sequencing facility (GENOMAX), INSERM UMR_S 1109 and
   Agence Nationale de la Recherche, Programme Blanc ANR-07-BLAN-0108
   entitled GENHEPC and Institut de Recherche pour le Developpement (IRD).
   Our laboratory was further supported by the Institut Universitaire de
   France (IUF), the Partenariat Hubert Curien GUNDISHAPUR by the
   ministeres des Affaires etrangeres et du developpement international
   (MAEDI) and Enseignement superieur et de la Recherche (MESR), the
   Institut de Recherche pour le developpement (IRD) and the Centre
   National pour la Recherche Scientifique (CNRS). This work was
   additionally supported by Tehran University of Medical Sciences and in
   part by the intramural research program of the Division of Cancer
   Epidemiology and Genetics, National Cancer Institute.
NR 27
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PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1466-4879
EI 1476-5470
J9 GENES IMMUN
JI Genes Immun.
PD DEC
PY 2015
VL 16
IS 8
BP 514
EP 518
DI 10.1038/gene.2015.38
PG 5
WC Genetics & Heredity; Immunology
SC Genetics & Heredity; Immunology
GA CX8TD
UT WOS:000365976200002
PM 26378651
ER

PT J
AU Sung, H
   Camargo, MC
   Yu, K
   Weinstein, SJ
   Morgan, DR
   Albanes, D
   Rabkin, CS
AF Sung, H.
   Camargo, M. C.
   Yu, K.
   Weinstein, S. J.
   Morgan, D. R.
   Albanes, D.
   Rabkin, C. S.
TI Association of 4p14 TLR locus with antibodies to Helicobacter pylori
SO GENES AND IMMUNITY
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; TOLL-LIKE RECEPTORS; PANCREATIC-CANCER;
   GASTRIC-CANCER; HIGH-RISK; SUSCEPTIBILITY; SEROPOSITIVITY; VARIANTS;
   POLYMORPHISMS; PEPSINOGEN
AB A genome-wide association study among Europeans related polymorphisms of the Toll-like receptor (TLR) locus at 4p14 and the Fc gamma receptor 2a locus at 1q23.3 to Helicobacter pylori serologic status. We replicated associations of 4p14 but not 1q23.3 with anti-Helicobacter pylori antibodies in 1402 Finnish males. Importantly, our analysis clarified that the phenotype affected by 4p14 is quantitative level of these antibodies rather than association with seropositivity per se. In addition, we annotated variants at 4p14 as expression quantitative trait loci (eQTL) associated with TLR6/10 and FAM114A1. Our findings suggest that 4p14 polymorphisms are linked to host immune response to H. pylori infection but not to its acquisition.
C1 [Sung, H.; Camargo, M. C.; Yu, K.; Weinstein, S. J.; Albanes, D.; Rabkin, C. S.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Morgan, D. R.] Vanderbilt Univ, Div Gastroenterol, Nashville, TN 37235 USA.
RP Sung, H (reprint author), NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,6E512, Bethesda, MD 20892 USA.
EM hyuna.sung@nih.gov
RI Camargo, M. Constanza/R-9891-2016
FU Intramural Research Program of the National Institutes of Health,
   National Cancer Institute, Division of Cancer Epidemiology and Genetics;
   National Cancer Institute, Department of Health and Human Services
   [N01-CN-45165, N01-RC-45035, N01-RC-37004, HHSN261201000006C]
FX We thank the principal investigators of the ATBC trial and its multiple
   substudies for access to the genotyping and serology data on study
   participants. This research was supported by the Intramural Research
   Program of the National Institutes of Health, National Cancer Institute,
   Division of Cancer Epidemiology and Genetics. In addition, this research
   was supported by US Public Health Service contracts N01-CN-45165,
   N01-RC-45035, N01-RC-37004 and HHSN261201000006C from the National
   Cancer Institute, Department of Health and Human Services.
NR 29
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U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1466-4879
EI 1476-5470
J9 GENES IMMUN
JI Genes Immun.
PD DEC
PY 2015
VL 16
IS 8
BP 567
EP 570
DI 10.1038/gene.2015.33
PG 4
WC Genetics & Heredity; Immunology
SC Genetics & Heredity; Immunology
GA CX8TD
UT WOS:000365976200008
PM 26312625
ER

PT J
AU Walcott, FL
   Dunn, BK
AF Walcott, Farzana L.
   Dunn, Barbara K.
TI Legislation in the genomic era: the Affordable Care Act and genetic
   testing for cancer risk assessment
SO GENETICS IN MEDICINE
LA English
DT Editorial Material
C1 [Walcott, Farzana L.; Dunn, Barbara K.] NCI, Chemoprevent Agents Res Dev Grp, Canc Prevent Div, Rockville, MD 20852 USA.
   [Walcott, Farzana L.] NCI, Canc Prevent Fellowship Program, Canc Prevent Div, Rockville, MD USA.
RP Walcott, FL (reprint author), NCI, Chemoprevent Agents Res Dev Grp, Canc Prevent Div, Rockville, MD 20852 USA.
EM farzana.walcott@nih.gov
NR 6
TC 2
Z9 2
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD DEC
PY 2015
VL 17
IS 12
BP 962
EP 964
DI 10.1038/gim.2015.18
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA CX8TP
UT WOS:000365977400003
PM 25741860
ER

PT J
AU Yu, P
   Cui, Y
   Cai, WS
   Wu, HH
   Xiao, XQ
   Shao, QZ
   Ma, L
   Guo, S
   Wu, NN
   Jin, ZB
   Wang, YJ
   Cai, T
   Sun, ZS
   Qu, J
AF Yu, Ping
   Cui, Yun
   Cai, Wanshi
   Wu, Honghu
   Xiao, Xiaoqiang
   Shao, Qianzhi
   Ma, Liang
   Guo, Sen
   Wu, Nana
   Jin, Zi-Bing
   Wang, Yongjin
   Cai, Tao
   Sun, Zhong Sheng
   Qu, Jia
TI Lysosomal storage disease in the brain: mutations of the
   beta-mannosidase gene identified in autosomal dominant nystagmus
SO GENETICS IN MEDICINE
LA English
DT Article
DE lysosomal storage diseases; MANBA; neuronal ceroid lipofuscinoses;
   nystagmus; whole-exome sequencing
ID NEURONAL CEROID-LIPOFUSCINOSIS; INFANTILE NYSTAGMUS; MULTIPLE-SCLEROSIS;
   PENDULAR NYSTAGMUS; OPTIC-NERVE; ABNORMALITIES; PREVALENCE; MECHANISM;
   FEATURES; FORM
AB Purpose: Genetic etiology of congenital/infantile nystagmus remains largely unknown. This study aimed to identify genomic mutations in patients with infantile nystagmus and an associated disease network.
   Methods: Patients with inherited and sporadic infantile nystagmus were recruited for whole-exome and Sanger sequencing. beta-Mannosidase activities were measured. Gene expression, proteinprotein interaction, and nystagmus-associated lysosomal storage disease (LSD) genes were analyzed.
   Results: A novel heterozygous mutation (c.2013G>A; p.R638H) of MANBA, which encodes lysosomal beta-mannosidase, was identified in patients with autosomal-dominant nystagmus. An additional mutation (c.2346T > A; p.L749H) in MANBA was found by screening patients with sporadic nystagmus. MANBA was expressed in the pretectal nucleus of the developing midbrain, known to be involved in oculomotor and optokinetic nystagmus. Functional validation of these mutations demonstrated a significant decrease of beta-mannosidase activities in the patients as well as in mutant-transfected HEK293T cells. Further analysis revealed that nystagmus is present in at least 24 different LSDs involving the brain.
   Conclusion: This is the first identification of MANBA mutations in patients with autosomal-dominant nystagmus, suggesting a new clinical entity. Because a-mannosidase activities are required for development of the oculomotor nervous system, our findings shed new light on the role of LSD-associated genes in the pathogenesis of infantile nystagmus.
C1 [Yu, Ping; Wu, Honghu; Xiao, Xiaoqiang; Shao, Qianzhi; Guo, Sen; Wu, Nana; Sun, Zhong Sheng] Wenzhou Med Univ, Inst Genom Med, Wenzhou, Zhejiang, Peoples R China.
   [Cui, Yun; Ma, Liang; Wang, Yongjin] Heping Hosp, Changzhi Med Coll, Dept Ophthalmol, Changzhi, Shanxi, Peoples R China.
   [Cai, Wanshi; Sun, Zhong Sheng] Chinese Acad Sci, Beijing Inst Life Sci, Beijing, Peoples R China.
   [Jin, Zi-Bing; Qu, Jia] State Key Lab Cultivat Base, Wenzhou, Zhejiang, Peoples R China.
   [Jin, Zi-Bing; Qu, Jia] Key Lab Vis Sci, Wenzhou, Zhejiang, Peoples R China.
   NIH, Expt Med Sect, Natl Inst Dent & Craniofacial Res, Bethesda, MD 20892 USA.
RP Yu, P (reprint author), Wenzhou Med Univ, Inst Genom Med, Wenzhou, Zhejiang, Peoples R China.
EM jyzwzyu@gmail.com; tcai@mail.nih.gov; jqu@mail.eye.ac.cn
RI Jin, Zi-Bing/J-6810-2014
OI Jin, Zi-Bing/0000-0003-0515-698X
FU Wenzhou Medical University and Zhejiang Province Nature Science
   Research; National Natural Science Foundation of China; Natural Science
   Foundation of Zhejiang Province [81110114, Z2110521]; Foundation of
   Shanxi Province Health Bureau [201302017]; National Key Basic Research
   Program [2013CB967502, 2011CB504600]
FX This work was supported by research funding from Wenzhou Medical
   University and Zhejiang Province Nature Science Research (to P.Y.), the
   National Natural Science Foundation of China and the Natural Science
   Foundation of Zhejiang Province (81110114 and Z2110521, respectively, to
   Z.S.S.), the Foundation of Shanxi Province Health Bureau (201302017 to
   Y.C.), and by the National Key Basic Research Program (2013CB967502 to
   Z.-B.J. and 2011CB504600 to J.Q.). The authors thank the patients and
   their families for their participation in this study as well as Jinyu Wu
   and Qianzhi Shao and all other co-workers involved in the WES analysis.
NR 40
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U1 2
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD DEC
PY 2015
VL 17
IS 12
BP 971
EP 979
DI 10.1038/gim.2015.10
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA CX8TP
UT WOS:000365977400005
PM 25741867
ER

PT J
AU De Castro, M
   Johnston, J
   Biesecker, L
AF De Castro, Mauricio
   Johnston, Jennifer
   Biesecker, Leslie
TI Determining the prevalence of McArdle disease from gene frequency by
   analysis of next-generation sequencing data
SO GENETICS IN MEDICINE
LA English
DT Article
DE allele frequency; McArdle disease; next-generation sequencing;
   prevalence; PYGM
ID DEFICIENCY; EXPRESSION; VARIANTS; MEDICINE; BLOOD
AB ` Purpose: McArdle disease is one of the most common glycogen storage disorders. Although the exact prevalence is not known, it has been estimated to be 1 in 100,000 patients in the United States. More than 100 mutations in PYGM have been associated with this disorder. McArdle disease has significant clinical variability: Some patients present with severe muscle pain and weakness; others have only mild, exercise-related symptoms.
   Methods: Next-generation sequencing data allow estimation of disease prevalence with minimal ascertainment bias. We analyzed gene frequencies in two cohorts of patients based on exome sequencing results. We categorized variants into three groups: a curated set of published mutations, variants of uncertain significance, and likely benign variants.
   Results: An initial estimate based on the frequency of six common mutations predicts a disease prevalence of 1/7,650 (95% confidence interval (CI) 1/5,362-1/11,108), which greatly deviates from published estimates. A second method using the two most common mutations predicts a prevalence of 1/42,355 (95% CI 1/24,536-1/76,310) in Caucasians.
   Conclusions: These results suggest that the currently accepted prevalence of McArdle disease is an underestimate and that some of the currently considered pathogenic variants are likely benign.
C1 [De Castro, Mauricio; Johnston, Jennifer; Biesecker, Leslie] NHGRI, NIH, Bethesda, MD 20892 USA.
RP De Castro, M (reprint author), NHGRI, NIH, Bethesda, MD 20892 USA.
EM Mauricio.decastro-pretelt@nih.gov
FU Intramural NIH HHS [ZIA HG200387-02]
NR 20
TC 5
Z9 5
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD DEC
PY 2015
VL 17
IS 12
BP 1002
EP 1006
DI 10.1038/gim.2015.9
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA CX8TP
UT WOS:000365977400009
PM 25741863
ER

PT J
AU Warren, WC
   Jasinska, AJ
   Garcia-Perez, R
   Svarda, H
   Tomlinson, C
   Rocchi, M
   Archidiacono, N
   Capozzi, O
   Minx, P
   Montague, MJ
   Kyung, K
   Hillier, LW
   Kremitzki, M
   Graves, T
   Chiang, C
   Hughes, J
   Tran, N
   Huang, Y
   Ramensky, V
   Choi, OW
   Jung, YJ
   Schmitt, CA
   Juretic, N
   Wasserscheid, J
   Turner, TR
   Wiseman, RW
   Tuscher, JJ
   Kar, JA
   Schmitz, JE
   Zahn, R
   O'Connor, DH
   Redmond, E
   Nisbett, A
   Jacquelin, B
   Muller-Trutwin, MC
   Brenchley, JM
   Dione, M
   Antonio, M
   Schroth, GP
   Kaplan, JR
   Jorgensen, MJ
   Thomas, GWC
   Hahn, MW
   Raney, BJ
   Aken, B
   Nag, R
   Schmitz, J
   Churakov, G
   No, A
   Stanyon, R
   Webb, D
   Thibaud-Nissen, F
   Nordborg, M
   Marques-Bonet, T
   Dewar, K
   Weinstock, GM
   Wilson, RK
   Freimer, NB
AF Warren, Wesley C.
   Jasinska, Anna J.
   Garcia-Perez, Raquel
   Svarda, Hannes
   Tomlinson, Chad
   Rocchi, Mariano
   Archidiacono, Nicoletta
   Capozzi, Oronzo
   Minx, Patrick
   Montague, Michael J.
   Kyung, Kim
   Hillier, LaDeana W.
   Kremitzki, Milinn
   Graves, Tina
   Chiang, Colby
   Hughes, Jennifer
   Tran, Nam
   Huang, Yu
   Ramensky, Vasily
   Choi, Oi-wa
   Jung, Yoon J.
   Schmitt, Christopher A.
   Juretic, Nikoleta
   Wasserscheid, Jessica
   Turner, Trudy R.
   Wiseman, Roger W.
   Tuscher, Jennifer J.
   Kar, Julie A.
   Schmitz, Joern E.
   Zahn, Roland
   O'Connor, David H.
   Redmond, Eugene
   Nisbett, Alex
   Jacquelin, Beatrice
   Mueller-Trutwin, Michaela C.
   Brenchley, Jason M.
   Dione, Michel
   Antonio, Martin
   Schroth, Gary P.
   Kaplan, Jay R.
   Jorgensen, Matthew J.
   Thomas, Gregg W. C.
   Hahn, Matthew W.
   Raney, Brian J.
   Aken, Bronwen
   Nag, Rishi
   Schmitz, Juergen
   Churakov, Gennady
   Noll, Angela
   Stanyon, Roscoe
   Webb, David
   Thibaud-Nissen, Francoise
   Nordborg, Magnus
   Marques-Bonet, Tomas
   Dewar, Ken
   Weinstock, George M.
   Wilson, Richard K.
   Freimer, Nelson B.
TI The genome of the vervet (Chlorocebus aethiops sabaeus)
SO GENOME RESEARCH
LA English
DT Article
ID AFRICAN-GREEN MONKEYS; MAJOR HISTOCOMPATIBILITY COMPLEX; SIMIAN
   IMMUNODEFICIENCY VIRUS; COPY NUMBER VARIATION; GENETIC DIVERSITY;
   ANALYSIS TOOLKIT; PRIMATE; MACAQUE; EVOLUTIONARY; MAP
AB We describe a genome reference of the African green monkey or vervet (Chlorocebus aethiops). This member of the Old World monkey (OWM) superfamily is uniquely valuable for genetic investigations of simian immunodeficiency virus (Sly), for which it is the most abundant natural host species, and of a wide range of health-related phenotypes assessed in Caribbean vervets (C. a. sabaeus), whose numbers have expanded dramatically since Europeans introduced small numbers of their ancestors from West Africa during the colonial era. We use the reference to characterize the genomic relationship between vervets and other primates, the intra-generic phylogeny of vervet subspecies, and genome-wide structural variations of a pedigreed C.a. sabaeuspopulation. Through comparative analyses with human and rhesus macaque, we characterize at high resolution the unique chromosomal fission events that differentiate the vervets and their close relatives from most other catarrhine primates, in whom karyotype is highly conserved. We also provide a summary of transposable elements and contrast these with the rhesus macaque and human. Analysis of sequenced genomes representing each of the main vervet subspecies supports previously hypothesized relationships between these populations, which range across most of sub-Saharan Africa, while uncovering high levels of genetic diversity within each. Sequence-based analyses of major histocompatibility complex alFig polymorphisms reveal extremely low diversity in Caribbean C.a. sabaeusvervets, compared to vervets from putatively ancestral West African regions. In the C.a. sabaeus research population, we discover the first structural variations that are, in some cases, predicted to have a deleterious effect; future studies will determine the phenotypic impact of these variations.
C1 [Warren, Wesley C.; Tomlinson, Chad; Minx, Patrick; Montague, Michael J.; Kyung, Kim; Hillier, LaDeana W.; Kremitzki, Milinn; Graves, Tina; Chiang, Colby; Wilson, Richard K.] Washington Univ, Sch Med, Genome Inst, St Louis, MO 63108 USA.
   [Jasinska, Anna J.; Tran, Nam; Huang, Yu; Ramensky, Vasily; Choi, Oi-wa; Jung, Yoon J.; Schmitt, Christopher A.; Freimer, Nelson B.] Univ Calif Los Angeles, Ctr Neurobehav Genet, Semel Inst Neurosci & Human Behav, Los Angeles, CA 90095 USA.
   [Jasinska, Anna J.] Polish Acad Sci, Inst Bioorgan Chem, PL-61704 Poznan, Poland.
   [Garcia-Perez, Raquel; Marques-Bonet, Tomas] UPF CSIC, Inst Biol Evolut, ICREA, Barcelona 08003, Spain.
   [Garcia-Perez, Raquel; Marques-Bonet, Tomas] PRBB PCB, CNAG, Barcelona 08003, Spain.
   [Svarda, Hannes; Nordborg, Magnus] Austrian Acad Sci, Vienna Bioctr VBC, Gregor Mendel Inst, A-1030 Vienna, Austria.
   [Rocchi, Mariano; Archidiacono, Nicoletta; Capozzi, Oronzo] Univ Bari, Dept Biol, I-70126 Bari, Italy.
   [Hughes, Jennifer] Whitehead Inst, Cambridge, MA 02142 USA.
   [Juretic, Nikoleta; Wasserscheid, Jessica; Dewar, Ken] McGill Univ, Dept Human Genet, Montreal, PQ H3A 1B1, Canada.
   [Turner, Trudy R.] Univ Wisconsin, Dept Anthropol, Madison, WI 53705 USA.
   [Turner, Trudy R.] Univ Orange Free State, Fac Nat & Agr Sci, Dept Genet, ZA-9300 Bloemfontein, South Africa.
   [Wiseman, Roger W.; Tuscher, Jennifer J.; Kar, Julie A.; O'Connor, David H.] Univ Wisconsin, Dept Lab Med & Pathol, Madison, WI 53705 USA.
   [Schmitz, Joern E.] Beth Israel Deaconess Med Ctr, Ctr Virol & Vaccine Res, Boston, MA 02115 USA.
   [Zahn, Roland] Crucell Holland BV, NL-2333 CN Leiden, Netherlands.
   [Jacquelin, Beatrice; Mueller-Trutwin, Michaela C.] Inst Pasteur, Unite Regulat Infect Retrovirales, F-75015 Paris, France.
   [Brenchley, Jason M.] NIAID, NIH, Bethesda, MD 20892 USA.
   [Dione, Michel; Antonio, Martin] MRC, Fajara, Gambia.
   [Schroth, Gary P.] Illumina Inc, San Diego, CA 92722 USA.
   [Kaplan, Jay R.; Jorgensen, Matthew J.] Wake Forest Sch Med, Ctr Comparat Med Res, Winston Salem, NC 27157 USA.
   [Thomas, Gregg W. C.; Hahn, Matthew W.] Indiana Univ, Dept Biol, Bloomington, IN 47405 USA.
   [Raney, Brian J.] Univ Calif Santa Cruz, Santa Cruz, CA 95060 USA.
   [Aken, Bronwen; Nag, Rishi] European Bioinformat Inst, European Mol Biol Lab, Cambridge CB10 1SD, England.
   [Schmitz, Juergen; Churakov, Gennady; Noll, Angela] Univ Munster, Inst Expt Pathol ZMBE, D-48149 Munster, Germany.
   [Churakov, Gennady] Univ Munster, Inst Evolut & Biodivers, D-48149 Munster, Germany.
   [Stanyon, Roscoe] Univ Florence, Dept Biol, I-50122 Florence, Italy.
   [Webb, David; Thibaud-Nissen, Francoise] Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
   [Weinstock, George M.] Jackson Lab Genom Med, Farmington, CT 06001 USA.
RP Warren, WC (reprint author), Washington Univ, Sch Med, Genome Inst, St Louis, MO 63108 USA.
EM wwarren@genome.wustl.edu
RI Schmitt, Christopher/F-7251-2013; 
OI Schmitt, Christopher/0000-0003-2143-9226; archidiacono,
   nicoletta/0000-0002-1439-9521; Rocchi, Mariano/0000-0002-9451-5616;
   Aken, Bronwen/0000-0002-3032-4095; Marques-Bonet,
   Tomas/0000-0002-5597-3075; Chiang, Colby/0000-0002-4113-6065; Nag,
   Rishi/0000-0001-6399-3773; Svardal, Hannes/0000-0001-7866-7313
FU NIH-NHGRI [5U54HG00307907]; NIH [RR019963/OD010965, R01RR016300,
   R01OD010980]; French National Agency for Research on AIDS and Viral
   Hepatitis (ANRS); Ministero della Universita e della Ricerca; Genome
   Canada; Genome Quebec; Wellcome Trust [WT095908]; European Molecular
   Biology Laboratory
FX Funding to R.K.W. was provided by NIH-NHGRI grant 5U54HG00307907.
   Support for the Vervet Research Colony was provided by NIH grant
   RR019963/OD010965 to J.R.K. Funding to N.B.F. was provided by NIH grants
   R01RR016300 and R01OD010980. The French National Agency for Research on
   AIDS and Viral Hepatitis (ANRS) provided funding to M.C.M.-T. Funding to
   M.R. and R.S. was provided by the Ministero della Universita e della
   Ricerca. Funding to K.D. was provided by Genome Canada and Genome
   Quebec. B.A. and R.N. acknowledge support from the Wellcome Trust (grant
   number WT095908) and the European Molecular Biology Laboratory. We thank
   the following organizations for providing sampling permits and
   permissions: Ethiopian Wildlife Conservation Authority; Zambia Wildlife
   Authority; Wildlife Division, Forestry Commission, Republic of Ghana;
   and Gambia Department of Parks and Wildlife Management. We thank Dr.
   James L. Blanchard and Dr. Ivona Pandrea for vervet samples used to
   characterize MHC. We thank Josh McMichael and Josh Peck for figure
   assistance. We thank Joanne Nelson and Barbara Gillam for data
   submission. We thank the members of the library production group led by
   Catrina Fronick and sequencing led by Matt Cordes. We also thank the
   Medical Research Council Unit (MRC), The Gambia for their assistance, as
   well as all the veterinarians who worked with us to safely obtain
   samples.
NR 71
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U1 1
U2 15
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1088-9051
EI 1549-5469
J9 GENOME RES
JI Genome Res.
PD DEC
PY 2015
VL 25
IS 12
BP 1921
EP 1933
DI 10.1101/gr.192922.115
PG 13
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Genetics & Heredity
GA CX6RZ
UT WOS:000365830400014
PM 26377836
ER

PT J
AU Gong, SY
   Auer, I
   Duggal, R
   Pittaluga, S
   Raffeld, M
   Jaffe, ES
AF Gong, Shunyou
   Auer, Iwona
   Duggal, Rajan
   Pittaluga, Stefania
   Raffeld, Mark
   Jaffe, Elaine S.
TI Epstein-Barr virus-associated inflammatory pseudotumor presenting as a
   colonic mass
SO HUMAN PATHOLOGY
LA English
DT Article
DE Inflammatory pseudotumor; Epstein-Ban virus; Inflammatory
   pseudotumor-like follicular dendritic cell tumor; Gastrointestinal
   tract; Myofibroblasts
ID DENDRITIC CELL TUMOR; PROLIFERATION; LIVER
AB Epstein-Barr virus (EBV) positive inflammatory pseudotumor (IPT) commonly involves spleen and liver and has only rarely been reported in the gastrointestinal (GI) tract. The spindle cells may express myofibroblastic or follicular dendritic cell markers. We report a challenging case of EBV-positive IPT arising in the ascending colon. The lesion was composed of spindle cells positive for smooth muscle actin but negative for all follicular dendritic cell markers tested and was associated with an exuberant lymphoid proliferation containing reactive follicles, abundant plasma cells, and small lymphocytes. We further discuss pitfalls for possible misdiagnosis as ALK-positive inflammatory myofibroblastic tumor, IgG4-related disease, and peripheral T-cell lymphoma. Our case represents the first EBV-positive inflammatory pseudotumor of the GI tract in the Western literature. Awareness of this rare entity in GI tract is essential for correct diagnosis and appropriate patient management. Published by Elsevier Inc.
C1 [Gong, Shunyou; Pittaluga, Stefania; Raffeld, Mark; Jaffe, Elaine S.] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Auer, Iwona] Univ Calgary, Dept Pathol & Lab Med, Div Hematopathol, Calgary, AB T2N 2T9, Canada.
   [Auer, Iwona] Calgary Lab Serv, Calgary, AB T2N 2T9, Canada.
   [Duggal, Rajan] Medanta, Dept Pathol, Gurgaon 122001, Delhi Ncr, India.
RP Jaffe, ES (reprint author), NCI, Hematopathol Sect, Pathol Lab, Ctr Canc Res,NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM ejaffe@mail.nih.gov
FU Intramural Research Program of the Center for Cancer Research, National
   Cancer Institute, National Institutes of Health [ZIA SC 000550]; Visitor
   Training Programme of the American Society of Hematology
FX This work was supported through the Intramural Research Program of the
   Center for Cancer Research, National Cancer Institute, National
   Institutes of Health (intramural NIH funding no. ZIA SC 000550). Dr
   Rajan Duggal was supported by a grant from the Visitor Training
   Programme of the American Society of Hematology.
NR 16
TC 4
Z9 4
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 0046-8177
EI 1532-8392
J9 HUM PATHOL
JI Hum. Pathol.
PD DEC
PY 2015
VL 46
IS 12
BP 1956
EP 1961
DI 10.1016/j.humpath.2015.08.011
PG 6
WC Pathology
SC Pathology
GA CX6UG
UT WOS:000365836600021
PM 26477709
ER

PT J
AU Pugliese, C
   Kenworthy, L
   Bal, VH
   Wallace, GL
   Yerys, BE
   Maddox, BB
   White, SW
   Popal, H
   Armour, AC
   Miller, J
   Herrington, JD
   Schultz, RT
   Martin, A
   Anthony, LG
AF Pugliese, Cara E.
   Kenworthy, Lauren
   Bal, Vanessa Hus
   Wallace, Gregory L.
   Yerys, Benjamin E.
   Maddox, Brenna B.
   White, Susan W.
   Popal, Haroon
   Armour, Anna Chelsea
   Miller, Judith
   Herrington, John D.
   Schultz, Robert T.
   Martin, Alex
   Anthony, Laura Gutermuth
TI Replication and Comparison of the Newly Proposed ADOS-2, Module 4
   Algorithm in ASD Without ID: A Multi-site Study
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism spectrum disorder; Adults; Adolescents; Diagnosis; Autism
   diagnostic observation schedule; Sensitivity; Specificity
ID DIAGNOSTIC OBSERVATION SCHEDULE; AUTISM SPECTRUM DISORDERS; INTERVIEW;
   SYMPTOMS; CHILDREN; SCORES; ADULTS; INDIVIDUALS; ADOLESCENCE; ABILITIES
AB Recent updates have been proposed to the Autism Diagnostic Observation Schedule-2 Module 4 diagnostic algorithm. This new algorithm, however, has not yet been validated in an independent sample without intellectual disability (ID). This multi-site study compared the original and revised algorithms in individuals with ASD without ID. The revised algorithm demonstrated increased sensitivity, but lower specificity in the overall sample. Estimates were highest for females, individuals with a verbal IQ below 85 or above 115, and ages 16 and older. Best practice diagnostic procedures should include the Module 4 in conjunction with other assessment tools. Balancing needs for sensitivity and specificity depending on the purpose of assessment (e.g., clinical vs. research) and demographic characteristics mentioned above will enhance its utility.
C1 [Pugliese, Cara E.; Kenworthy, Lauren; Armour, Anna Chelsea; Anthony, Laura Gutermuth] Childrens Natl Hlth Syst, Ctr Autism Spectrum Disorders, Washington, DC 20010 USA.
   [Pugliese, Cara E.; Kenworthy, Lauren; Armour, Anna Chelsea; Anthony, Laura Gutermuth] Childrens Natl Hlth Syst, Childrens Natl Res Inst, Washington, DC USA.
   [Bal, Vanessa Hus] Univ Calif San Francisco, Sch Med, Dept Psychiat, San Francisco, CA 94143 USA.
   [Wallace, Gregory L.] George Washington Univ, Dept Speech & Hearing Sci, Washington, DC USA.
   [Yerys, Benjamin E.; Maddox, Brenna B.; Miller, Judith; Herrington, John D.; Schultz, Robert T.] Childrens Hosp Philadelphia, Ctr Autism Res, Philadelphia, PA 19104 USA.
   [Yerys, Benjamin E.; Miller, Judith; Herrington, John D.] Univ Penn, Dept Psychiat, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Maddox, Brenna B.; White, Susan W.] Virginia Tech, Dept Psychol, Blacksburg, VA USA.
   [Popal, Haroon; Martin, Alex] NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA.
   [Schultz, Robert T.] Univ Penn, Dept Pediat, Philadelphia, PA 19104 USA.
RP Pugliese, C (reprint author), Childrens Natl Hlth Syst, Ctr Autism Spectrum Disorders, Washington, DC 20010 USA.
EM CPuglies@ChildrensNational.org
OI Wallace, Gregory/0000-0003-0329-5054
FU Isadore and Bertha Gudelsky Family Foundation; Fredrick and Elizabeth
   Singer Foundation; Organization for Autism Research; Autism Speaks
   (Dennis Weatherstone Predoctoral Fellowship); Philadelphia Foundation;
   Pfizer; Shire Pharmaceuticals; Robert Wood Johnson Foundation [6672];
   Pennsylvania Department of Health (SAP) [4100042728, 4100047863];
   National Institutes of Health and the Intramural Research Program at
   NIMH [1-ZIA-MH002920-05, P30HD040677, T32 HD046388-01A2,
   1K01MH079945-01, K23MH086111, R21MH092615, RC1MH088791, P30HD026979]; 
   [R01MH081873]
FX This work was supported in part by an award from the Isadore and Bertha
   Gudelsky Family Foundation and the Fredrick and Elizabeth Singer
   Foundation, and grants by the Organization for Autism Research, Autism
   Speaks (Dennis Weatherstone Predoctoral Fellowship), the Philadelphia
   Foundation, Pfizer, Shire Pharmaceuticals, Robert Wood Johnson
   Foundation (#6672), the Pennsylvania Department of Health (SAP
   #4100042728, SAP #4100047863), and the National Institutes of Health and
   the Intramural Research Program at NIMH (1-ZIA-MH002920-05, P30HD040677,
   T32 HD046388-01A2, 1K01MH079945-01, K23MH086111, R21MH092615,
   RC1MH088791, and P30HD026979). We gratefully acknowledge Catherine Lord,
   PhD for contributing data for comparative analyses; those data were
   funded by R01MH081873 to CL.
NR 40
TC 5
Z9 5
U1 5
U2 16
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD DEC
PY 2015
VL 45
IS 12
SI SI
BP 3919
EP 3931
DI 10.1007/s10803-015-2586-3
PG 13
WC Psychology, Developmental
SC Psychology
GA CX0WD
UT WOS:000365417100016
PM 26385796
ER

PT J
AU Zerbo, O
   Qian, YG
   Yoshida, C
   Grether, JK
   Van de Water, J
   Croen, LA
AF Zerbo, Ousseny
   Qian, Yinge
   Yoshida, Cathleen
   Grether, Judith K.
   Van de Water, Judy
   Croen, Lisa A.
TI Maternal Infection During Pregnancy and Autism Spectrum Disorders
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Maternal infection; Pregnancy; Autism spectrum disorder
ID BRAIN-DEVELOPMENT; PREVALENCE; ACTIVATION; CYTOKINES; RISK; ASSOCIATION;
   ADOLESCENTS; CHEMOKINES
AB We conducted a nested case-control study including 407 cases and 2,075 frequency matched controls to investigate the association between maternal infections during pregnancy and risk of autism spectrum disorders (ASD). Cases, controls, and maternal infections were ascertained from Kaiser Permanente Northern California clinical databases. No overall association between diagnoses of any maternal infection during pregnancy and ASD was observed [adjusted odds ratio (ORadj) = 1.15, 95 % confidence interval (CI) 0.92-1.43]. However, women with infections diagnosed during a hospital admission (ORadj = 1.48, 95 % CI 1.07-2.04), particularly bacterial infections (ORadj = 1.58, 95 % CI 1.06-2.37), were at increased risk of delivering a child with ASD. Multiple infections during pregnancy were associated with ASD (ORadj = 1.36, 95 % CI 1.05-1.78).
C1 [Zerbo, Ousseny; Qian, Yinge; Yoshida, Cathleen; Croen, Lisa A.] Kaiser Permanente No Calif, Div Res, Oakland, CA 94612 USA.
   [Van de Water, Judy] Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
   [Van de Water, Judy] Univ Calif Davis, MIND Inst, Davis, CA 95616 USA.
   [Van de Water, Judy] Univ Calif Davis, NIEHS, Ctr Childrens Environm Hlth, Davis, CA 95616 USA.
RP Zerbo, O (reprint author), Kaiser Permanente No Calif, Div Res, 2000 Broadway, Oakland, CA 94612 USA.
EM Ousseny.x.zerbo@kp.org
FU Centers for Disease Control and Prevention [U10/CCU920392]; Kaiser
   Foundation Research Institute; Autism Speaks
FX The authors would like to thank Dr. Kaht Dorward, MD, from the
   department of Obstetrics and Gynecology at Kaiser Permanente San
   Francisco for her input on maternal infections during pregnancy. This
   study was funded by grants from the Centers for Disease Control and
   Prevention, (U10/CCU920392), the Kaiser Foundation Research Institute,
   and Autism Speaks.
NR 47
TC 18
Z9 18
U1 4
U2 16
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD DEC
PY 2015
VL 45
IS 12
SI SI
BP 4015
EP 4025
DI 10.1007/s10803-013-2016-3
PG 11
WC Psychology, Developmental
SC Psychology
GA CX0WD
UT WOS:000365417100025
PM 24366406
ER

PT J
AU Fearon, KCH
   Argiles, JM
   Baracos, VE
   Bernabei, R
   Coats, AJS
   Crawford, J
   Deutz, NE
   Doehner, W
   Evans, WJ
   Ferrucci, L
   Garcia, JM
   Gralla, RJ
   Jatoi, A
   Kalantar-Zadeh, K
   Lainscak, M
   Morley, JE
   Muscaritoli, M
   Polkey, MI
   Rosano, G
   Rossi-Fanelli, F
   Schols, AM
   Strasser, F
   Vellas, B
   von Haehling, S
   Anker, SD
AF Fearon, K. C. H.
   Argiles, J. M.
   Baracos, V. E.
   Bernabei, R.
   Coats, A. J. S.
   Crawford, J.
   Deutz, N. E.
   Doehner, W.
   Evans, W. J.
   Ferrucci, L.
   Garcia, J. M.
   Gralla, R. J.
   Jatoi, A.
   Kalantar-Zadeh, K.
   Lainscak, M.
   Morley, J. E.
   Muscaritoli, M.
   Polkey, M. I.
   Rosano, G.
   Rossi-Fanelli, F.
   Schols, A. M.
   Strasser, F.
   Vellas, B.
   von Haehling, S.
   Anker, S. D.
TI Request for regulatory guidance for cancer cachexia intervention trials
SO JOURNAL OF CACHEXIA SARCOPENIA AND MUSCLE
LA English
DT Editorial Material
ID MUSCLE STRENGTH; HEART-FAILURE; REHABILITATION; SARCOPENIA; EXERCISE;
   MASS; CARE
C1 [Fearon, K. C. H.] Univ Edinburgh, Royal Infirm, Sch Clin Sci & Community Hlth, Clin & Surg Sci, Edinburgh EH3 9YW, Midlothian, Scotland.
   [Argiles, J. M.] Univ Barcelona, Fac Biol, Biochem & Mol Biol Canc, Barcelona, Spain.
   [Baracos, V. E.] Univ Alberta, Dept Oncol, Edmonton, AB, Canada.
   [Bernabei, R.] Univ Cattolica Sacro Cuore, Dept Geriatr Neurosci & Orthoped, I-00168 Rome, Italy.
   [Coats, A. J. S.] Monash Univ, Clayton, Vic 3800, Australia.
   [Coats, A. J. S.] Univ Warwick, Coventry CV4 7AL, W Midlands, England.
   [Crawford, J.] Duke Canc Inst, Durham, NC USA.
   [Deutz, N. E.] Texas A&M Univ, Dept Hlth & Kinesiol, Ctr Translat Res Aging & Longev, College Stn, TX 77843 USA.
   [Doehner, W.] Charite, CSB, D-13353 Berlin, Germany.
   [Evans, W. J.] KineMed Inc, Emeryville, CA 94608 USA.
   [Evans, W. J.] Duke Med Ctr, Div Geriatr, Durham, NC 27710 USA.
   [Ferrucci, L.] NIA, Intramural Res Program, NIH, Baltimore, MD 20892 USA.
   [Garcia, J. M.] Michael E DeBakey VA Med Ctr, Ctr Translat Res Inflammatory Dis, Div Endocrinol Diabet & Metab, Houston, TX 77030 USA.
   [Garcia, J. M.] Baylor Coll Med, Houston, TX 77030 USA.
   [Gralla, R. J.] Albert Einstein Coll Med, Jacobi Med Ctr, Bronx, NY 10461 USA.
   [Jatoi, A.] Mayo Clin, Dept Oncol, Rochester, MN 55905 USA.
   [Kalantar-Zadeh, K.] Univ Calif Irvine, Med Ctr, Div Nephrol & Hypertens, Orange, CA 92868 USA.
   [Lainscak, M.] Gen Hosp Celje, Dept Cardiol, Celje, Slovenia.
   [Lainscak, M.] Gen Hosp Celje, Dept Res & Educ, Celje, Slovenia.
   [Morley, J. E.] St Louis Univ, Sch Med, Div Geriatr Med, St Louis, MO 63103 USA.
   [Morley, J. E.] St Louis Univ, Sch Med, Div Endocrinol, St Louis, MO 63103 USA.
   [Muscaritoli, M.; Rossi-Fanelli, F.] Univ Roma La Sapienza, Dept Clin Med, I-00185 Rome, Italy.
   [Polkey, M. I.] Royal Brompton & NHS Fdn Trust, NIHR Resp Biomed Res Unit, London, England.
   [Polkey, M. I.] Univ London Imperial Coll Sci Technol & Med, London, England.
   [Rosano, G.] IRCCS San Raffaele Roma Nutramed Consortium, Dept Med Sci, Rome, Italy.
   [Schols, A. M.] Maastricht Univ, Med Ctr, Dept Resp Med, NUTRIM Sch Nutr & Translat Res Metab, NL-6200 MD Maastricht, Netherlands.
   [Strasser, F.] Cantonal Hosp St Gallen, Dept Internal Med, Clin Oncol Hematol, Oncol Palliat Med, St Gallen, Switzerland.
   [Strasser, F.] Cantonal Hosp St Gallen, Palliat Ctr, St Gallen, Switzerland.
   [Vellas, B.] CHU Toulouse, Dept Geriatr, Toulouse, France.
   [von Haehling, S.; Anker, S. D.] Univ Med Ctr Gottingen UMG, Dept Cardiol & Pneumol, Innovat Clin Trials, Gottingen, Germany.
RP Fearon, KCH (reprint author), Univ Edinburgh, Royal Infirm, Sch Clin Sci & Community Hlth, Clin & Surg Sci, Edinburgh EH3 9YW, Midlothian, Scotland.
OI Kalantar-Zadeh, Kamyar/0000-0002-8666-0725
NR 14
TC 17
Z9 17
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2190-5991
EI 2190-6009
J9 J CACHEXIA SARCOPENI
JI J. Caxhexia Sarcopenia Muscle
PD DEC
PY 2015
VL 6
IS 4
BP 272
EP 274
DI 10.1002/jcsm.12083
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA CX2OP
UT WOS:000365536800002
PM 26675232
ER

PT J
AU Micci, L
   Ryan, ES
   Fromentin, R
   Bosinger, SE
   Harper, JL
   He, TY
   Paganini, S
   Easley, KA
   Chahroudi, A
   Benne, C
   Gumber, S
   McGary, CS
   Rogers, KA
   Deleage, C
   Lucero, C
   Byrareddy, SN
   Apetrei, C
   Estes, JD
   Lifson, JD
   Piatak, M
   Chomont, N
   Villinger, F
   Silvestri, G
   Brenchley, JM
   Paiardini, M
AF Micci, Luca
   Ryan, Emily S.
   Fromentin, Remi
   Bosinger, Steven E.
   Harper, Justin L.
   He, Tianyu
   Paganini, Sara
   Easley, Kirk A.
   Chahroudi, Ann
   Benne, Clarisse
   Gumber, Sanjeev
   McGary, Colleen S.
   Rogers, Kenneth A.
   Deleage, Claire
   Lucero, Carissa
   Byrareddy, Siddappa N.
   Apetrei, Cristian
   Estes, Jacob D.
   Lifson, Jeffrey D.
   Piatak, Michael, Jr.
   Chomont, Nicolas
   Villinger, Francois
   Silvestri, Guido
   Brenchley, Jason M.
   Paiardini, Mirko
TI Interleukin-21 combined with ART reduces inflammation and viral
   reservoir in SIV-infected macaques
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID CD4(+) T-CELLS; CHRONIC HIV-INFECTION; ACTIVE ANTIRETROVIRAL THERAPY;
   PHASE-I TRIAL; RHESUS MACAQUES; METASTATIC MELANOMA; IMMUNE ACTIVATION;
   SOOTY MANGABEY; T(H)17 CELLS; PLASMA-CELLS
AB Despite successful control of viremia, many HIV-infected individuals given antiretroviral therapy (ART) exhibit residual inflammation, which is associated with non-AIDS-related morbidity and mortality and may contribute to virus persistence during ART. Here, we investigated the effects of IL-21 administration on both inflammation and virus persistence in ART-treated, SIV-infected rhesus macaques (RMs). Compared with SIV-infected animals only given ART, SIV-Infected RMs given both ART and IL-21 showed improved restoration of intestinal Th17 and Th22 cells and a more effective reduction of immune activation in blood and intestinal mucosa, with the latter maintained through 8 months after ART interruption. Additionally, IL-21, in combination with ART, was associated with reduced levels of Sly RNA in plasma and decreased CD4(+) T cell levels harboring replication-competent virus during ART. At the latest experimental time points, which were up to 8 months after ART interruption, plasma viremia and cell-associated SIV DNA levels remained substantially lower than those before ART initiation in IL-21-treated animals but not in controls. Together, these data suggest that IL-21 supplementation of ART reduces residual inflammation and virus persistence in a relevant model of lentiviral disease and warrants further investigation as a potential intervention for HIV infection.
C1 [Micci, Luca; Ryan, Emily S.; Bosinger, Steven E.; Harper, Justin L.; Paganini, Sara; Chahroudi, Ann; McGary, Colleen S.; Rogers, Kenneth A.; Villinger, Francois; Silvestri, Guido; Paiardini, Mirko] Emory Univ, Sch Med, Yerkes Natl Primate Res Ctr, Div Microbiol & Immunol, Atlanta, GA 30329 USA.
   [Fromentin, Remi; Chomont, Nicolas] Univ Montreal, Fac Med, Dept Microbiol Infectiol & Immunol, Montreal, PQ H3C 3J7, Canada.
   [Fromentin, Remi; Chomont, Nicolas] CHUM, Ctr Rech, Montreal, PQ, Canada.
   [Bosinger, Steven E.] Emory Univ, Yerkes Nonhuman Primate Genom Core, Atlanta, GA 30329 USA.
   [He, Tianyu; Apetrei, Cristian] Univ Pittsburgh, Ctr Vaccine Res, Pittsburgh, PA USA.
   [Easley, Kirk A.] Emory Univ, Sch Med, Dept Biostat & Bioinformat, Rollins Sch Publ Hlth, Atlanta, GA 30329 USA.
   [Chahroudi, Ann] Emory Univ, Sch Med, Dept Pediat, Atlanta, GA 30329 USA.
   [Benne, Clarisse] Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44106 USA.
   [Gumber, Sanjeev] Yerkes Natl Primate Res Ctr, Div Pathol, Atlanta, GA USA.
   [Gumber, Sanjeev; Byrareddy, Siddappa N.; Villinger, Francois; Silvestri, Guido; Paiardini, Mirko] Emory Univ, Sch Med, Dept Pathol & Lab Med, Atlanta, GA 30322 USA.
   [Deleage, Claire; Lucero, Carissa; Estes, Jacob D.; Lifson, Jeffrey D.; Piatak, Michael, Jr.] Leidos Biomed Res Inc, AIDS Canc Virus Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
RP Paiardini, M (reprint author), Emory Univ, Sch Med, Yerkes Natl Primate Res Ctr, Div Microbiol & Immunol, 954 Gatewood Rd, Atlanta, GA 30329 USA.
EM mirko.paiardini@emory.edu
RI Easley, Kirk/K-6910-2015; 
OI Easley, Kirk/0000-0003-4419-2617; Gumber, Sanjeev/0000-0001-9048-2717
FU NIAID, NIH [R01AI116379, R01AI110334, R33AI104278, ORIP/OD P51OD011132,
   ORIP/OD 5R24RR016988, P30AI50409]; amfAR grant [109109-57-RGRL];
   National Cancer Institute, NIH [HHSN261200800001E]; Division of
   Intramural Research, NIAID, NIH [A1001029]
FX We gratefully acknowledge Gilead (Romas Geleziunas), Johnson & Johnson
   (Guenter Kraus), and Merck (Dania Hazuda) for supplying the
   antiretroviral drugs. The authors also thank Sherrie Jean, Stephanie
   Ehnert, Christopher Souder, and all the animal care and veterinary staff
   at the YNPRC; Barbara Cervasi and Kiran Gill at the Emory University
   Flow Cytometry Core; Thomas Vanderford, Benton Lawson, and Melon T. Nega
   at the Emory Center for AIDS Research (CFAR) Virology and Molecular
   Biomarkers Core; Nirav Patel and Gregory Tharp at the Yerkes Nonhuman
   Primate Genomics Core; Guofu Fang and Balwan Singh at the Resource for
   Nonhuman Primate Immune Reagents of Emory University for producing
   rMamuIL-21-IgFc; and Kristina T. Ortiz of Emory University. Finally, we
   thank Afam Okoye and Yoshinori Fukazawa at Oregon Health & Science
   University for their technical advice on the VOA. Research reported in
   this publication was supported by the NIAID, NIH under award numbers
   R01AI116379, R01AI110334, and R33AI104278 (to M. Paiardini), ORIP/OD
   P51OD011132 (formerly NCRR P51RR000165, to the YNPRC), ORIP/OD
   5R24RR016988 and P30AI50409 (to the Emory Center for AIDS Research), as
   well as by amfAR grant 109109-57-RGRL (to M. Paiardini). This project
   has been supported in part by federal funds from the National Cancer
   Institute, NIH, under contract HHSN261200800001E, as well as by the
   Division of Intramural Research, NIAID, NIH (A1001029). The content is
   solely the responsibility of the authors and does not necessarily
   represent the official views of the NIH, nor does mention of trade
   names, commercial products, or organizations imply endorsement by the
   U.S. Government.
NR 71
TC 17
Z9 17
U1 0
U2 4
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD DEC
PY 2015
VL 125
IS 12
BP 4497
EP 4513
DI 10.1172/JCI81400
PG 17
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA CX6SI
UT WOS:000365831300017
PM 26551680
ER

PT J
AU Traba, J
   Kwarteng-Siaw, M
   Okoll, TC
   Li, J
   Huffstutler, RD
   Bray, A
   Waclawiw, MA
   Han, K
   Pelletier, M
   Sauve, AA
   Siegel, RM
   Sack, MN
AF Traba, Javier
   Kwarteng-Siaw, Miriam
   Okoll, Tracy C.
   Li, Jessica
   Huffstutler, Rebecca D.
   Bray, Amanda
   Waclawiw, Myron A.
   Han, Kim
   Pelletier, Martin
   Sauve, Anthony A.
   Siegel, Richard M.
   Sack, Michael N.
TI Fasting and refeeding differentially regulate NLRP3 inflammasome
   activation in human subjects
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID INNATE IMMUNE-RESPONSE; INSULIN-RESISTANCE; CALORIE RESTRICTION;
   OXIDATIVE STRESS; PLASMA-LEVELS; DISEASE; OBESITY; SIRT3; METABOLISM;
   DEACETYLATION
AB BACKGROUND. Activation of the NLRP3 inflammasome is associated with metabolic dysfunction, and intermittent fasting has been shown to improve clinical presentation of NLRP3 inflammasome-linked diseases. As mitochondrial perturbations, which function as a damage-associated molecular pattern, exacerbate NLRP3 inflammasome activation, we investigated whether fasting blunts inflammasome activation via sirtuin-mediated augmentation of mitochondria! integrity.
   METHODS. We performed a clinical study of 19 healthy volunteers. Each subject underwent a 24-hour fast and then was fed a fixed-calorie meal. Blood was drawn during the fasted and fed states and analyzed for NRLP3 inflammasome activation. We enrolled an additional group of 8 healthy volunteers to assess the effects of the sirtuin activator, nicotinamide riboside, on NLRP3 inflammasome activation.
   RESULTS. In the fasting/refeeding study, individuals showed less NLRP3 inflammasome activation in the fasted state compared with that in refed conditions. In a human macrophage line, depletion of the mitochondrial-enriched sirtuin deacetylase SIRT3 increased NLRP3 inflammasome activation in association with excessive mitochondrial ROS production. Furthermore, genetic and pharmacologic SIRT3 activation blunted NLRP3 activity in parallel with enhanced mitochondrial function in cultured cells and in leukocytes extracted from healthy volunteers and from refed individuals but not in those collected during fasting.
   CONCLUSIONS. Together, our data indicate that nutrient levels regulate the NLRP3 inflammasome, in part through SIRT3-mediated mitochondrial homeostatic control. Moreover, these results suggest that deacetylase-dependent inflammasome attenuation may be amenable to targeting in human disease.
C1 [Traba, Javier; Kwarteng-Siaw, Miriam; Okoll, Tracy C.; Li, Jessica; Huffstutler, Rebecca D.; Bray, Amanda; Han, Kim; Sack, Michael N.] NHLBI, Cardiovasc & Pulm Branch, Bethesda, MD 20892 USA.
   [Waclawiw, Myron A.] NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
   [Pelletier, Martin; Siegel, Richard M.] NIAMSD, Autoimmun Branch, NIH, Bethesda, MD 20892 USA.
   [Sauve, Anthony A.] Weill Cornell Med Coll, Dept Pharmacol, New York, NY USA.
RP Sack, MN (reprint author), NHLBI, Lab Mitochondrial Biol & Metab, Bid 10-CRC,Room 5-3150,10 Ctr Dr,MSC 1454, Bethesda, MD 20892 USA.
EM sackm@nih.gov
FU Division of Intramural Research, NHLBI, NIH [HL005102-11]; NIH
   Biomedical Research Training Program of Underrepresented Minority Groups
FX This study was supported by the Division of Intramural Research, NHLBI,
   NIH (to M.N. Sack -HL005102-11). M. Kwarteng-Siaw was funded through the
   NIH Biomedical Research Training Program of Underrepresented Minority
   Groups. A.A. Sauve has intellectual property related to methods of
   production of NR and receives royalties from a commercial license to
   ChromaDex Inc. of this intellectual property. Furthermore, A.A. Sauve is
   a consultant and cofounder of Metro Mid-Atlantic Biotech LLC. We thank
   Shahin Hassanzadeh and Kinneret Broder for coordinating blood
   collections, Jamie Grimes for clinical protocol administration, and Neal
   Young of the NHLBI for including M.N. Sack as an Associate Investigator
   on his blood collection protocol. We thank David Gius from Northwestern
   University for supplying antibodies to measure SOD2 and IDH2 protein
   acetylation.
NR 47
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U1 6
U2 16
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD DEC
PY 2015
VL 125
IS 12
BP 4592
EP 4600
DI 10.1172/JCI83260
PG 9
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA CX6SI
UT WOS:000365831300024
PM 26529255
ER

PT J
AU Ilyas, S
   Yang, JC
AF Ilyas, Sadia
   Yang, James C.
TI Landscape of Tumor Antigens in T Cell Immunotherapy
SO JOURNAL OF IMMUNOLOGY
LA English
DT Review
ID AUTOLOGOUS HUMAN-MELANOMA; LONG-TERM SAFETY; LUNG-CANCER; RECEIVING
   NIVOLUMAB; IMMUNE-RESPONSES; PD-1 BLOCKADE; LYMPHOCYTES; ANTIBODY;
   IDENTIFICATION; CARCINOMA
AB Cancer immunotherapy is a rapidly evolving field that exploits T cell responses to tumor-associated Ags to induce tumor rejection. Molecular identification of tumor rejection Ags has helped define several classes of Ags, including tissue differentiation and tumor germline Ags. The ability to genetically engineer Ag-specific receptors into T cells provides an opportunity to translate these findings into therapies. New immunotherapy agents, notably checkpoint inhibitors, have demonstrated unprecedented efficacy in certain cancers. However, the nature of the Ags driving those beneficial immune responses remains unclear. New evidence suggests that tumors express immunogenic, tumor-specific epitopes generated from the same mutations that drive cancer development. Correlations between cancer types responding to immunotherapies and the frequency of somatic mutations may clarify what drives natural antitumor immune responses. This fusion of tumor immunology and genetics is leading to new ways to target this class of ideal tumor-specific Ags and could allow the application of immunotherapy to many cancers.
C1 [Ilyas, Sadia; Yang, James C.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
RP Yang, JC (reprint author), NCI, Surg Branch, NIH, Bldg 10A CRC,Room 3-5952, Bethesda, MD 20892 USA.
EM JamesYang@mail.nih.gov
FU Intramural NIH HHS [ZIA BC011337-01, ZIA BC011337-05, Z99 CA999999, Z01
   SC006660-23]
NR 47
TC 4
Z9 5
U1 2
U2 15
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD DEC 1
PY 2015
VL 195
IS 11
BP 5117
EP 5122
DI 10.4049/jimmunol.1501657
PG 6
WC Immunology
SC Immunology
GA CX3NP
UT WOS:000365606100008
PM 26589749
ER

PT J
AU Chang, TH
   Yoshimi, R
   Ozato, K
AF Chang, Tsung-Hsien
   Yoshimi, Ryusuke
   Ozato, Keiko
TI Tripartite Motif (TRIM) 12c, a Mouse Homolog of TRIM5, Is a Ubiquitin
   Ligase That Stimulates Type I IFN and NF-kappa B Pathways along with
   TNFR-Associated Factor 6
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID TOLL-LIKE RECEPTORS; RESTRICTION FACTOR TRIM5-ALPHA; RETROVIRAL
   RESTRICTION; REGULATORY FACTOR-8; CYTOKINE EXPRESSION; IMMUNE-RESPONSES;
   GENE-EXPRESSION; FAMILY PROTEINS; INNATE IMMUNITY; PRYSPRY DOMAIN
AB Tripartite motif (TRIM) protein TRIM5 of the primate species restricts replication of HIV and other retroviruses. Whereas primates have a single TRIM5 gene, the corresponding locus in the mouse has expanded during evolution, now containing more than eight related genes. Owing to the complexity of the genomic organization, a mouse homolog of TRIM5 has not been fully studied thus far. In the present study, we report that Trim12c (formerly Trim12-2) encodes a TRIM5-like protein with a ubiquitin ligase activity. Similar to the primate TRIM5, TRIM12c is expressed in the cytoplasm as a punctate structure and induced upon IFN and pathogen stimulation in macrophages and dendritic cells. We show that TRIM12c interacts with TRAF6, a key protein in the pathogen recognition receptor signaling, and reciprocally enhances their ubiquitination, leading to cooperative activation of IFN and NF-kappa B pathways. This study identifies TRIM12c as a mouse TRIM5 equivalent, critical for host innate immunity.
C1 [Chang, Tsung-Hsien; Yoshimi, Ryusuke; Ozato, Keiko] NICHHD, NIH, Program Genom Differentiat, Bethesda, MD 20892 USA.
   [Chang, Tsung-Hsien] Kaohsiung Vet Gen Hosp, Dept Med Educ & Res, Kaohsiung 81362, Taiwan.
RP Ozato, K (reprint author), NICHHD, NIH, Program Genom Differentiat, 6 Ctr Dr,Bldg 6,Room 2A01, Bethesda, MD 20892 USA.
EM ozatok@nih.gov
OI Yoshimi, Ryusuke/0000-0002-3945-307X
FU Kaohsiung Veterans General Hospital [VGHKS102-004]; Ministry of Science
   and Technology, Taiwan [NSC 99-2320-B-075B-005, MOST
   104-2320-B-075B-005]
FX This work was supported in part by Kaohsiung Veterans General Hospital
   Grant VGHKS102-004 and by Ministry of Science and Technology, Taiwan
   Grants NSC 99-2320-B-075B-005 and MOST 104-2320-B-075B-005.
NR 55
TC 2
Z9 3
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 DEC 1
PY 2015
VL 195
IS 11
BP 5367
EP 5379
DI 10.4049/jimmunol.1402064
PG 13
WC Immunology
SC Immunology
GA CX3NP
UT WOS:000365606100031
PM 26503954
ER

PT J
AU Raz, N
   Bick, AS
   Klistorner, A
   Spektor, S
   Reich, DS
   Ben-Hur, T
   Levin, N
AF Raz, Noa
   Bick, Atira S.
   Klistorner, Alexander
   Spektor, Sergey
   Reich, Daniel S.
   Ben-Hur, Tamir
   Levin, Netta
TI Physiological Correlates and Predictors of Functional Recovery After
   Chiasmal Decompression
SO JOURNAL OF NEURO-OPHTHALMOLOGY
LA English
DT Article
ID OPTICAL COHERENCE TOMOGRAPHY; PITUITARY-ADENOMA; COMPRESSION; NEURITIS;
   PATTERN; FIELD
AB Background:The intrinsic abilities and limits of the nervous system to repair itself after damage may be assessed using a model of optic chiasmal compression, before and after a corrective surgical procedure.Methods:Visual fields (VFs), multifocal visual evoked potentials (mfVEP), retinal nerve fiber layer (RNFL) thickness, and diffusion tensor imaging were used to evaluate a patient before and after removal of a meningioma compressing the chiasm. Normally sighted individuals served as controls. The advantage of each modality to document visual function and predict postoperative outcome (2-year follow-up) was evaluated.Results:Postsurgery visual recovery was best explained by critical mass of normally conducting fibers and not associated with average conduction amplitudes. Recovered VF was observed in quadrants in which more than 50% of fibers were identified, characterized by intact mfVEP latencies, but severely reduced amplitudes. Recovery was evident despite additional reduction of RNFL thickness and abnormal optic tract diffusivity. The critical mass of normally conducting fibers was also the best prognostic indicator for functional outcome 2 years later.Conclusions:Our results highlight the ability of the remaining normally conductive axons to predict visual recovery after decompression of the optic chiasm. The redundancy in anterior visual pathways may be explained, neuroanatomically, by overlapping receptive fields.
C1 [Raz, Noa; Bick, Atira S.; Ben-Hur, Tamir; Levin, Netta] Hadassah Hebrew Univ, Med Ctr, Dept Neurol, Agnes Ginges Ctr Human Neurogenet, IL-91120 Jerusalem, Israel.
   [Spektor, Sergey] Hadassah Hebrew Univ, Med Ctr, Dept Neurosurg, IL-91120 Jerusalem, Israel.
   [Klistorner, Alexander] Univ Sydney, Dept Ophthalmol, Sydney, NSW 2006, Australia.
   [Reich, Daniel S.] NINDS, Translat Neuroradiol Unit, NIH, Bethesda, MD 20892 USA.
RP Levin, N (reprint author), Hadassah Hebrew Univ, Med Ctr, Dept Neurol, fMRI Unit, POB 12,000, IL-91120 Jerusalem, Israel.
EM netta@hadassah.org.il
RI Reich, Daniel/E-5701-2010
OI Reich, Daniel/0000-0002-2628-4334
FU Sidney and Judy Swartz fund for research in multiple sclerosis;
   Intramural Research Program of the National Institute of Neurological
   Disorders and Stroke, USA
FX Supported in part by the Sidney and Judy Swartz fund for research in
   multiple sclerosis and by the Intramural Research Program of the
   National Institute of Neurological Disorders and Stroke, USA.
NR 15
TC 2
Z9 2
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1070-8022
EI 1536-5166
J9 J NEURO-OPHTHALMOL
JI J. Neuro-Ophthal.
PD DEC
PY 2015
VL 35
IS 4
BP 348
EP 352
DI 10.1097/WNO.0000000000000266
PG 5
WC Clinical Neurology; Ophthalmology
SC Neurosciences & Neurology; Ophthalmology
GA CX3OE
UT WOS:000365607700004
PM 25996300
ER

PT J
AU Zheng, K
   Liang, NX
   Zhang, JJ
   Lang, LX
   Zhang, W
   Li, SQ
   Zhao, J
   Niu, G
   Li, F
   Zhu, ZH
   Chen, XY
AF Zheng, Kun
   Liang, Naixin
   Zhang, Jingjing
   Lang, Lixin
   Zhang, Wei
   Li, Shanqing
   Zhao, Jun
   Niu, Gang
   Li, Fang
   Zhu, Zhaohui
   Chen, Xiaoyuan
TI Ga-68-NOTA-PRGD2 PET/CT for Integrin Imaging in Patients with Lung
   Cancer
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE integrin; Ga-68-NOTA-PRGD2; PET/CT; lung cancer; lymph node metastasis
ID POSITRON-EMISSION-TOMOGRAPHY; IN-111-LABELED RGD-PEPTIDE;
   ALPHA(V)BETA(3) EXPRESSION; ALPHA-V-BETA-3 EXPRESSION;
   RADIATION-DOSIMETRY; FDG-PET; ANGIOGENESIS; ACCURACY; AGENT;
   BIODISTRIBUTION
AB This study was designed to assess the diagnostic value of 68Ga-NOTA-PRGD2 (NOTA-PRGD2 is NOTA-PEG4-E[c(RGDfK)](2)) PET/CT in lung cancer. Methods: Ninety-one patients (48 men and 43 women; age, 22-82 y) with suspected lung lesions on CT were enrolled with informed consent. Immediately after intravenous injection of 117.7 +/- 37.7 MBq of Ga-68-NOTA-PRGD2, 15 patients underwent dynamic whole-body PET/CT scans for 1-2 h, and the remaining 76 patients underwent whole-body PET/CT scans at 30 +/- 10 min after bolus injection. Each patient also underwent standard F-18-FDG PET/CT for comparison. Results: No side effect was found after Ga-68-NOTA-PRGD2 injection. Ga-68-NOTA-PRGD2 was rapidly cleared from the blood pool and primarily excreted through the urinary system. The standardized uptake values of proven malignancies were significantly higher than those of the benign ones. With an average standardized uptake value of greater than 1.3 being considered malignant, the sensitivity, specificity, and accuracy of Ga-68-NOTA-PRGD2 PET/CT in diagnosing lung cancer were 83.8% (57/68), 91.3%(21/23), and 85.7%(78/91), respectively. The diagnostic value of Ga-68-NOTA-PRGD2 for lung cancer is comparable to that of F-18-FDG PET/CT. However, Ga-68-NOTA-PRGD2 PET/CT is more specific than F-18-FDG PET/CT in assessing lymph node metastasis, with positive and negative predictive values of 90.0% (27/30) and 93.8% (121/129), respectively, whereas those of F-18-FDG PET/CT were 30.2% (29/96) and 90.5% (57/63), respectively. Conclusion: This study indicates the efficacy of Ga-68-NOTA-PRGD2 PET/CT in lung cancer diagnosis. 68Ga-NOTA-PRGD2 PET/CT shows significant advantage over F-18-FDG PET/CT in judging metastatic lymph nodes with higher specificity.
C1 [Zheng, Kun; Zhang, Jingjing; Zhang, Wei; Li, Fang; Zhu, Zhaohui] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Nucl Med, Beijing 100730, Peoples R China.
   [Zheng, Kun; Liang, Naixin; Zhang, Jingjing; Zhang, Wei; Li, Shanqing; Zhao, Jun; Li, Fang; Zhu, Zhaohui] Peking Union Med Coll, Beijing, Peoples R China.
   [Liang, Naixin; Li, Shanqing] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Thorac Surg, Beijing 100730, Peoples R China.
   [Lang, Lixin; Niu, Gang; Chen, Xiaoyuan] Natl Inst Biomed Imaging & Bioengn, LOMIN, NIH, Bethesda, MD USA.
   [Zhao, Jun] Chinese Acad Med Sci, Canc Hosp, Dept Thorac Surg, Beijing 100730, Peoples R China.
RP Chen, XY (reprint author), NIH, 35A Convent Dr,GD937, Bethesda, MD 20892 USA.
EM zhuzhh@pumch.cn; shawn.chen@nih.gov
FU Capital Special Project for Featured Clinical Application
   [Z121107001012119]; National Natural Science Foundation of China project
   [81171369, 81171370, 81371596, 81271614]; Ministry of Education of China
   [311037]; Young Scientist Research Funding of Peking Union Medical
   College Hospital [PUMCH2013]; Intramural Research Program (IRP) of the
   National Institute of Biomedical Imaging and Bioengineering (NIBIB),
   National Institutes of Health (NIH)
FX The costs of publication of this article were defrayed in part by the
   payment of page charges. Therefore, and solely to indicate this fact,
   this article is hereby marked "advertisement" in accordance with 18 USC
   section 1734. This work was supported in part by the Capital Special
   Project for Featured Clinical Application (Z121107001012119), the
   National Natural Science Foundation of China projects (81171369,
   81171370, 81371596, and 81271614), the Ministry of Education of China
   (311037), Young Scientist Research Funding of Peking Union Medical
   College Hospital (PUMCH2013), and the Intramural Research Program (IRP)
   of the National Institute of Biomedical Imaging and Bioengineering
   (NIBIB), National Institutes of Health (NIH). No other potential
   conflict of interest relevant to this article was reported.
NR 36
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U1 8
U2 12
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 DEC
PY 2015
VL 56
IS 12
BP 1823
EP 1827
DI 10.2967/jnumed.115.160648
PG 5
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CX5EL
UT WOS:000365724800005
PM 26429958
ER

PT J
AU Blanchet, EM
   Taieb, D
   Millo, C
   Martucci, V
   Chen, CC
   Merino, M
   Herscovitch, P
   Pacak, K
AF Blanchet, Elise M.
   Taieb, David
   Millo, Corina
   Martucci, Victoria
   Chen, Clara C.
   Merino, Maria
   Herscovitch, Peter
   Pacak, Karel
TI F-18-FLT PET/CT in the Evaluation of Pheochromocytomas and
   Paragangliomas: A Pilot Study
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE pheochromocytoma and paraganglioma; F-18-fluorothymidine;
   F-18-fluorodeoxyglucose; positron emission tomography; proliferation;
   glycolysis
ID POSITRON-EMISSION-TOMOGRAPHY; IMMUNOHISTOCHEMICAL MARKERS; MALIGNANT
   PHEOCHROMOCYTOMAS; METASTATIC PHEOCHROMOCYTOMA;
   FUNCTIONAL-CHARACTERIZATION; ENDOCRINE TUMORS; DIAGNOSIS; PROLIFERATION;
   MUTATIONS; SURVIVAL
AB F-18-FDG PET/CT has been proven to be a highly sensitive method for pheochromocytomas/paragangliomas (PHEOs/PGLs) associated with succinate dehydrogenase (SDH) mutations. This finding has been attributed to altered tumor cell metabolism resulting from these mutations and does not provide additional prognostic information to genotype. Therefore, identification of new biomarkers for aggressiveness is needed. A high Ki-67 index was proposed to be an additional prognostic factor. This pilot study aimed to evaluate 3'-deoxy-3'-F-18-fluorothymidine (F-18-FLT) PET/CT, a PET proliferation tracer, as a potential imaging agent in a series of 12 PHEO/PGL patients with different genetic backgrounds, to compare F-18-FLT uptake with F-18-FDG PET/CT, and to evaluate classic factors of aggressiveness. Methods: Twelve patients (7 metastatic and 5 nonmetastatic) were prospectively evaluated with F-18-FDG and F-18-FLT and followed for at least 2 y after the initial imaging work-up. Uptake was assessed at a lesion level, visually and quantitatively by maximum standardized uptake values (SUVmax) for both tracers. F-18-FLT uptake was compared with risk factors known to be linked with a poor prognosis in PGLs (SDHB-mutated status, lesion size, dopaminergic phenotype) and with F-18-FDG uptake. Results: In 12 patients, 77 lesions were assessed. All lesions had low F-18-FLT uptake (median SUVmax, 2.25; range, 0.7-4.5). There was no apparent superiority of F-18-FLT uptake in progressive lesions, and most of the lesions showed a mismatch, with high F-18-FDG uptake (median SUVmax, 10.8; range, 1.1-79.0) contrasting with low F-18-FLT uptake. Conclusion: This study suggests that PHEOs/PGLs-even those that progress-do not exhibit intense F-18-FLT uptake. It provides the first in vivo demonstration that proliferation may not be a major determinant of F-18-FDG uptake in these tumors. These findings provide new insight into the biologic behavior of PGL and suggest that antiproliferative agents may be suboptimal for treatment of these tumors.
C1 [Blanchet, Elise M.; Martucci, Victoria; Pacak, Karel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
   [Taieb, David] Aix Marseille Univ, La Timone Univ Hosp, European Ctr Res Med Imaging, Marseille, France.
   [Millo, Corina; Herscovitch, Peter] NIH, Positron Emiss Tomog Dept, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA.
   [Chen, Clara C.] NIH, Dept Nucl Med, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA.
   [Merino, Maria] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
RP Pacak, K (reprint author), NICHD, Sect Med Neuroendocrinol, Program Reprod & Adult Endocrinol, NIH,CRC, Bldg 10,1 East,Rm 1-3140,10 Ctr Dr,MSC 1109, Bethesda, MD 20892 USA.
EM karel@mail.nih.gov
FU Intramural Research Program of the Eunice Kennedy Shriver National
   Institute of Child Health and Human Development, National Institutes of
   Health
FX The costs of publication of this article were defrayed in part by the
   payment of page charges. Therefore, and solely to indicate this fact,
   this article is hereby marked "advertisement" in accordance with 18 USC
   section 1734. This work was supported by the Intramural Research Program
   of the Eunice Kennedy Shriver National Institute of Child Health and
   Human Development, National Institutes of Health. No other potential
   conflict of interest relevant to this article was reported.
NR 32
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Z9 2
U1 0
U2 1
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD DEC
PY 2015
VL 56
IS 12
BP 1849
EP 1854
DI 10.2967/jnumed.115.159061
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CX5EL
UT WOS:000365724800009
PM 26359261
ER

PT J
AU Subar, AF
   Freedman, LS
   Tooze, JA
   Kirkpatrick, SI
   Boushey, C
   Neuhouser, ML
   Thompson, FE
   Potischman, N
   Guenther, PM
   Tarasuk, V
   Reedy, J
   Krebs-Smith, SM
AF Subar, Amy F.
   Freedman, Laurence S.
   Tooze, Janet A.
   Kirkpatrick, Sharon I.
   Boushey, Carol
   Neuhouser, Marian L.
   Thompson, Frances E.
   Potischman, Nancy
   Guenther, Patricia M.
   Tarasuk, Valerie
   Reedy, Jill
   Krebs-Smith, Susan M.
TI Addressing Current Criticism Regarding the Value of Self-Report Dietary
   Data
SO JOURNAL OF NUTRITION
LA English
DT Article
DE dietary assessment; dietary surveillance; measurement error;
   underreporting; nutritional epidemiology; energy intake
ID DOUBLY LABELED WATER; COVARIANCE STRUCTURE MODELS; LOW-ENERGY REPORTERS;
   MEASUREMENT-ERROR; NUTRITIONAL EPIDEMIOLOGY; RECOVERY BIOMARKERS;
   BREAST-CANCER; ASSESSMENT INSTRUMENTS; FUNDAMENTAL PRINCIPLES; 24-HOUR
   RECALLS
AB Recent reports have asserted that, because of energy underreporting, dietary self-report data suffer from measurement error so great that findings that rely on them are of no value. This commentary considers the amassed evidence that shows that self-report dietary intake data can successfully be used to inform dietary guidance and public health policy. Topics discussed include what is known and what can be done about the measurement error inherent in data collected by using self-report dietary assessment instruments and the extent and magnitude of underreporting energy compared with other nutrients and food groups. Also discussed is the overall impact of energy underreporting on dietary surveillance and nutritional epidemiology. In conclusion, 7 specific recommendations for collecting, analyzing, and interpreting self-report dietary data are provided: 1) continue to collect self-report dietary intake data because they contain valuable, rich, and critical information about foods and beverages consumed by populations that can be used to inform nutrition policy and assess diet-disease associations; 2) do not use self-reported energy intake as a measure of true energy intake; 3) do use self-reported energy intake for energy adjustment of other self-reported dietary constituents to improve risk estimation in studies of diet-health associations; 4) acknowledge the limitations of self-report dietary data and analyze and interpret them appropriately; 5) design studies and conduct analyses that allow adjustment for measurement error; 6) design new epidemiologic studies to collect dietary data from both short-term (recalls or food records) and long-term (food-frequency questionnaires) instruments on the entire study population to allow for maximizing the strengths of each instrument; and 7) continue to develop, evaluate, and further expand methods of dietary assessment, including dietary biomarkers and methods using new technologies.
C1 [Subar, Amy F.; Thompson, Frances E.; Reedy, Jill; Krebs-Smith, Susan M.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
   [Potischman, Nancy] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Freedman, Laurence S.] Gertner Inst Epidemiol & Hlth Policy Res, Biostat Unit, Tel Hashomer, Israel.
   [Tooze, Janet A.] Wake Forest Sch Med, Winston Salem, NC USA.
   [Kirkpatrick, Sharon I.] Univ Waterloo, Sch Publ Hlth & Hlth Syst, Waterloo, ON N2L 3G1, Canada.
   [Boushey, Carol] Univ Hawaii, Ctr Canc, Canc Epidemiol Program, Honolulu, HI 96822 USA.
   [Neuhouser, Marian L.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.
   [Guenther, Patricia M.] Univ Utah, Dept Nutr & Integrat Physiol, Salt Lake City, UT USA.
   [Tarasuk, Valerie] Univ Toronto, Dept Nutr Sci, Toronto, ON, Canada.
RP Subar, AF (reprint author), NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
EM subara@mail.nih.gov
OI Kirkpatrick, Sharon/0000-0001-9896-5975
FU NCI NIH HHS [R01 CA119171]
NR 102
TC 25
Z9 25
U1 8
U2 21
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-3166
EI 1541-6100
J9 J NUTR
JI J. Nutr.
PD DEC
PY 2015
VL 145
IS 12
BP 2639
EP 2645
DI 10.3945/jn.115.219634
PG 7
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA CX5DY
UT WOS:000365723300001
PM 26468491
ER

PT J
AU Salpekar, JA
   Joshi, PT
   Axelson, DA
   Reinblatt, SP
   Yenokyan, G
   Sanyal, A
   Walkup, JT
   Vitiello, B
   Luby, JL
   Wagner, KD
   Nusrat, N
   Riddle, MA
AF Salpekar, Jay A.
   Joshi, Paramjit T.
   Axelson, David A.
   Reinblatt, Shauna P.
   Yenokyan, Gayane
   Sanyal, Abanti
   Walkup, John T.
   Vitiello, Benedetto
   Luby, Joan L.
   Wagner, Karen Dineen
   Nusrat, Nasima
   Riddle, Mark A.
TI Depression and Suicidality Outcomes in the Treatment of Early Age Mania
   Study
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE bipolar; depression; pediatrics; treatment; clinical trial
ID PEDIATRIC BIPOLAR DISORDER; ANTIDEPRESSANT TREATMENT; CONTROLLED-TRIAL;
   ADOLESCENTS; CHILDREN; RISPERIDONE; METAANALYSIS; LAMOTRIGINE;
   COMBINATION; PREVALENCE
AB Objective: To assess the efficacy of mood-stabilizing medications for depression and suicidality in pediatric bipolar disorder.
   Method: The Treatment of Early Age Mania (TEAM) study is a multicenter, prospective, randomized, masked comparison of divalproex sodium (VAL), lithium carbonate (LI), and risperidone (RISP) in an 8-week parallel clinical trial. A total of 279 children and adolescents with DSM-IV diagnoses of bipolar I disorder, mixed or manic, aged 6 to 15 years were enrolled. The primary outcome measure was improvement on the Clinical Global Impression scale for depression (CGI-BP-I-D). Secondary outcome measures included the Children's Depression Rating Scale (CDRS-R) and suicidality status. Statistics included longitudinal analysis of outcomes using generalized linear mixed models with random intercept both for the complete data set and by using last observation carried forward.
   Results: CGI-BP-I-D ratings were better in the RISP group (60.7%) as compared to the LI (42.2%; p = .03) or VAL (35.0%; p = .003) groups from baseline to the end of the study. CDRS scores in all treatment groups improved equally by study end. In week 1, scores were lower with RISP compared to VAL (mean = 4.72,95% CI = 2.67, 6.78), and compared to LI (mean = 3.63, 95% CI = 1.51, 5.74), although group differences were not present by the end of the study. Suicidality was infrequent, and there was no overall effect of treatment on suicidality ratings.
   Conclusion: Depressive symptoms, present in the acutely manic or mixed phase of pediatric bipolar disorder, improved with all 3 medications, though RISP appeared to yield more rapid improvement than LI or VAL and was superior using a global categorical outcome.
C1 [Salpekar, Jay A.] Kennedy Krieger Inst, Baltimore, MD 21205 USA.
   [Salpekar, Jay A.; Reinblatt, Shauna P.; Riddle, Mark A.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
   [Joshi, Paramjit T.; Nusrat, Nasima] Childrens Natl Med Ctr, Washington, DC 20010 USA.
   [Joshi, Paramjit T.; Nusrat, Nasima] George Washington Univ, Washington, DC USA.
   [Yenokyan, Gayane; Sanyal, Abanti] Johns Hopkins Bloomberg Sch Publ Hlth, Johns Hopkins Biostat Ctr, Baltimore, MD USA.
   [Axelson, David A.] Nationwide Childrens Hosp, Columbus, OH USA.
   [Axelson, David A.] Ohio State Univ, Columbus, OH 43210 USA.
   [Wagner, Karen Dineen] Univ Texas Med Branch, Galveston, TX 77555 USA.
   [Walkup, John T.] Weill Cornell Med Coll, New York Presbyterian Hosp, New York, NY USA.
   [Luby, Joan L.] Washington Univ, St Louis, MO USA.
   [Vitiello, Benedetto] NIMH, Bethesda, MD 20892 USA.
RP Salpekar, JA (reprint author), Kennedy Krieger Inst, 716 N Broadway, Baltimore, MD 21205 USA.
EM Salpekar@kennedykrieger.org
OI Sanyal, Abanti/0000-0003-0674-3617; Yenokyan, Gayane/0000-0003-1482-5612
FU NIMH [U01 MH064846, U01 MH064850, U01 MH064851, U01 MH064868, U01
   MH064869, U01 MH064887, U01 MH064911]; National Center for Research
   Resources; National Center for Advancing Translational Sciences of the
   National Institutes of Health (NIH) [1UL1TR001079]
FX This study received funding from NIMH cooperative agreement grants U01
   MH064846 (Geller/WU), U01 MH064850 (Wagner/UTMB), U01 MH064851
   (Axelson/Pitt), U01 MH064868 (Luby/WU), U01 MH064869 (Walkup/JHU), U01
   MH064887 (Joshi/CNMC), and U01 MH064911 (discontinued site/reallocated).
   Partial support for statistical work was also received from the National
   Center for Research Resources and the National Center for Advancing
   Translational Sciences of the National Institutes of Health (NIH,
   1UL1TR001079).
NR 28
TC 2
Z9 2
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0890-8567
EI 1527-5418
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD DEC
PY 2015
VL 54
IS 12
BP 999
EP 1007
DI 10.1016/j.jaac.2015.09.016
PG 9
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA CX6SS
UT WOS:000365832400007
PM 26598475
ER

PT J
AU Walkup, JT
   Wagner, KD
   Miller, L
   Yenokyan, G
   Luby, JL
   Joshi, PT
   Axelson, DA
   Robb, A
   Salpekar, JA
   Wolf, D
   Sanyal, A
   Birmaher, B
   Vitiello, B
   Riddle, MA
AF Walkup, John T.
   Wagner, Karen Dineen
   Miller, Leslie
   Yenokyan, Gayane
   Luby, Joan L.
   Joshi, Paramjit T.
   Axelson, David A.
   Robb, Adelaide
   Salpekar, Jay A.
   Wolf, Dwight
   Sanyal, Abanti
   Birmaher, Boris
   Vitiello, Benedetto
   Riddle, Mark A.
TI Treatment of Early-Age Mania: Outcomes for Partial and Non responders to
   Initial Treatment
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE mania; bipolar; treatment; pharmacology; nonresponders
ID BIPOLAR-I DISORDER; PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; DIVALPROEX
   SODIUM; KIDDIE SCHEDULE; ADOLESCENTS; CHILDREN; RISPERIDONE; PREDICTORS;
   EFFICACY
AB Objective: The Treatment of Early Age Mania (TEAM) study evaluated lithium, risperidone, and divalproex sodium (divalproex) in children with bipolar I disorder who were naive to antimanic medication, or were partial or nonresponders to 1 of 3 study medications. This report evaluates the benefit of either an add-on or a switch of antimanic medications for an 8-week trial period in partial responders and nonresponders, respectively.
   Method: TEAM is a randomized, controlled trial of individuals (N = 379) aged 6 to 15 years (mean +/- SD = 10.2 +/- 2.7 years) with DSM-IV bipolar I disorder (mixed or manic phase). Participants (n = 154) in this report were either nonresponders or partial responders to 1 of the 3 study medications. Nonresponders (n = 89) were randomly assigned to 1 of the other 2 antimanic medications and cross-tapered. Partial responders (n = 65) were randomly assigned to 1 of 2 other antimanic medications as an add-on to their initial medication. Adverse event (AE) rates are reported only for the add-on group.
   Results: Response rate for children switched to risperidone (47.6%) was higher than for those switched to either lithium (12.8%; p = .005; number needed to treat [NNT] = 3; 95% CI = 1.71-9.09) or divalproex (17.2%; p = .03; NNT = 3; 95% CI = 1.79-20.10); response rate for partial responders who added risperidone (53.3%) was higher than for those who added divalproex (0%; p = .0002; NNT = 2; 95% CI = 1.27-3.56) and trended higher for lithium (26.7%; p = .07; NNT = 4). Reported AEs in the add-on group were largely consistent with the known AE profile for the second medication. Weight gain (kg) was observed for all add-on medications: lithium add-on (n = 29 of 30) = 1.66 +/- 1.97; risperidone add-on (n = 15 of 15) = 2.8 +/- 1.34; divalproex add-on (n = 19 of 20) = 1.42 +/- 1.96. There was no evidence at the 5% significance level that the average weight gain was different by study medication for partial responders (p = .07, 1-way analysis of variance).
   Conclusion: Risperidone appears to be more useful than lithium or divalproex for children with bipolar I disorder and other comorbid conditions who are nonresponders or partial responders to an initial antimanic medication trial.
C1 [Walkup, John T.] Weill Cornell Med Coll, New York Presbyterian Hosp, New York, NY USA.
   [Wagner, Karen Dineen; Wolf, Dwight] Univ Texas Med Branch, Galveston, TX 77555 USA.
   [Miller, Leslie; Riddle, Mark A.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
   [Yenokyan, Gayane; Sanyal, Abanti] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
   [Luby, Joan L.] Washington Univ, St Louis, MO USA.
   [Joshi, Paramjit T.; Robb, Adelaide; Salpekar, Jay A.] George Washington Univ, Childrens Natl Med Ctr, Sch Med, Washington, DC USA.
   [Axelson, David A.] Nationwide Childrens Hosp, Columbus, OH USA.
   [Axelson, David A.] Ohio State Univ, Wexner Med Ctr, Columbus, OH USA.
   [Birmaher, Boris] Univ Pittsburgh, Med Ctr, Western Psychiat Inst & Clin, Pittsburgh, PA USA.
   [Vitiello, Benedetto] NIMH, Bethesda, MD USA.
RP Walkup, JT (reprint author), Weill Cornell Med Coll, 525 E 68th St,Box 140, New York, NY 10065 USA.
EM jtw9001@med.cornell.edu
OI Sanyal, Abanti/0000-0003-0674-3617; Yenokyan, Gayane/0000-0003-1482-5612
FU NIMH [U01 MH064846, U01 MH064850, U01 MH064851, U01 MH064868, U01
   MH064869, U01 MH064887, U01 MH064911]; National Center for Research
   Resources; National Center for Advancing Translational Sciences of the
   National Institutes of Health (NIH) [1UL1TR001079]
FX This study received funding from NIMH cooperative agreement grants U01
   MH064846 (Geller/WU), U01 MH064850 (Wagner/UTMB), U01 MH064851
   (Axelson/Pitt), U01 MH064868 (Luby/WU), U01 MH064869 (Walkup/JHU), U01
   MH064887 (Joshi/CNMC), and U01 MH064911 (discontinued site/reallocated).
   Partial support for statistical work was also received from the National
   Center for Research Resources and the National Center for Advancing
   Translational Sciences of the National Institutes of Health (NIH;
   1UL1TR001079).
NR 34
TC 2
Z9 2
U1 5
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0890-8567
EI 1527-5418
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD DEC
PY 2015
VL 54
IS 12
BP 1008
EP 1019
DI 10.1016/j.jaac.2015.09.015
PG 12
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA CX6SS
UT WOS:000365832400008
PM 26598476
ER

PT J
AU Hricik, DE
   Formica, RN
   Nickerson, P
   Rush, D
   Fairchild, RL
   Poggio, ED
   Gibson, LW
   Wiebe, C
   Tinckam, K
   Bunnapradist, S
   Samaniego-Picota, M
   Brennan, DC
   Schroppel, B
   Gaber, O
   Armstrong, B
   Ikle, D
   Diop, H
   Bridges, ND
   Heeger, PS
AF Hricik, Donald E.
   Formica, Richard N.
   Nickerson, Peter
   Rush, David
   Fairchild, Robert L.
   Poggio, Emilio D.
   Gibson, Ian W.
   Wiebe, Chris
   Tinckam, Kathryn
   Bunnapradist, Suphamai
   Samaniego-Picota, Milagros
   Brennan, Daniel C.
   Schroeppel, Bernd
   Gaber, Osama
   Armstrong, Brian
   Ikle, David
   Diop, Helena
   Bridges, Nancy D.
   Heeger, Peter S.
CA Clin Trials Organ Transplantation
TI Adverse Outcomes of Tacrolimus Withdrawal in Immune-Quiescent Kidney
   Transplant Recipients
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID RENAL-ALLOGRAFT SURVIVAL; MYCOPHENOLATE-MOFETIL; CYCLOSPORINE
   WITHDRAWAL; CALCINEURIN INHIBITORS; ACUTE REJECTION; FOLLOW-UP;
   MULTICENTER; TRIAL; IMMUNOSUPPRESSION; IDENTIFICATION
AB Concerns about adverse effects of calcineurin inhibitors (CNIs) have prompted development of protocols that minimize their use. Whereas previous CNI withdrawal trials in heterogeneous cohorts showed unacceptable rates of acute rejection (AR), we hypothesized that we could identify individuals capable of tolerating CNI withdrawal by targeting immunologically quiescent kidney transplant recipients. The Clinical Trials in Organ Transplantation-09 Trial was a randomized, prospective study of nonsensitized primary recipients of living donor kidney transplants. Subjects received rabbit antithymocyte globulin, tacrolimus, nnycophenolate mofetil, and prednisone. Six months post-transplantation, subjects without de novo donor-specific antibodies (DSAs), AR, or inflammation at protocol biopsy were randomized to wean off or remain on tacrolimus. The intended primary end point was the change in interstitial fibrosis/tubular atrophy score between implantation and 24-month protocol biopsies. Serially collected urine CXCL9 ELISA results were correlated with outcomes. The study was terminated prematurely because of unacceptable rates of AR (4 of 14) and/or de novo DSAs (5 of 14) in the tacrolimus withdrawal arm. Positive urinary CXCL9 predated clinical detection of AR by a median of 15 days. Analyses showed that >16 HLA-DQ epitope mismatches and pretransplant, peripheral blood, donor reactive IFN-gamma ELISPOT assay results correlated with development Of DSAs and/or AR on tacrolimus withdrawal. Although data indicate that urinary CXCL9 monitoring, epitope mismatches, and ELISPOT assays are potentially informative, complete CNI withdrawal must be strongly discouraged in kidney transplant recipients who are receiving standard-of-care imnnunosuppression, including those who are deemed to be immunologically quiescent on the basis of current clinical and laboratory criteria.
C1 [Hricik, Donald E.] Univ Hosp Case Med Ctr, Dept Med, Cleveland, OH USA.
   [Formica, Richard N.] Yale Univ, Sch Med, Dept Med, New Haven, CT 06510 USA.
   [Formica, Richard N.] Yale Univ, Sch Med, Dept Surg, New Haven, CT 06510 USA.
   [Nickerson, Peter; Rush, David; Gibson, Ian W.; Wiebe, Chris] Univ Manitoba, Coll Med, Winnipeg, MB, Canada.
   [Fairchild, Robert L.; Poggio, Emilio D.] Cleveland Clin, Dept Immunol, Cleveland, OH 44106 USA.
   [Fairchild, Robert L.; Poggio, Emilio D.] Cleveland Clin, Glickman Urol Inst, Cleveland, OH 44106 USA.
   [Tinckam, Kathryn] Univ Toronto, Dept Med, Toronto, ON, Canada.
   [Bunnapradist, Suphamai] Univ Calif Los Angeles, Med Ctr, Dept Med, Los Angeles, CA 90024 USA.
   [Samaniego-Picota, Milagros] Univ Michigan, Med Ctr, Dept Med, Ann Arbor, MI 48109 USA.
   [Brennan, Daniel C.] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA.
   [Schroeppel, Bernd; Heeger, Peter S.] Icahn Sch Med Mt Sinai, Dept Med, New York, NY 10029 USA.
   [Schroeppel, Bernd; Heeger, Peter S.] Icahn Sch Med Mt Sinai, Recanati Miller Transplant Inst, New York, NY 10029 USA.
   [Gaber, Osama] Houston Methodist Hosp, Dept Surg, Houston, TX USA.
   [Gaber, Osama] Weill Cornell Med Coll, New York, NY USA.
   [Armstrong, Brian; Ikle, David] Rho, Chapel Hill, NC USA.
   [Diop, Helena; Bridges, Nancy D.] NIAID, Transplantat Branch, NIH, Bethesda, MD 20892 USA.
RP Heeger, PS (reprint author), Icahn Sch Med Mt Sinai, One Gustave Levy Pl,Box 1243, New York, NY 10029 USA.
EM peter.heeger@mssm.edu
FU National Institute of Allergy and Infectious Diseases of the National
   Institutes of Health [U01-AI063594]
FX The work was supported by the National Institute of Allergy and
   Infectious Diseases of the National Institutes of Health under Award
   Number U01-AI063594 (to P.S.H.). The content is solely the
   responsibility of the authors and does not necessarily represent the
   official views of the National Institutes of Health.
NR 31
TC 21
Z9 21
U1 1
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 DEC
PY 2015
VL 26
IS 12
BP 3114
EP 3122
DI 10.1681/ASN.2014121234
PG 9
WC Urology & Nephrology
SC Urology & Nephrology
GA CX1OR
UT WOS:000365466000025
PM 25925687
ER

PT J
AU Hoy, WE
   Hughson, MD
   Kopp, JB
   Mott, SA
   Bertram, JF
   Winkler, CA
AF Hoy, Wendy E.
   Hughson, Michael D.
   Kopp, Jeffrey B.
   Mott, Susan A.
   Bertram, John F.
   Winkler, Cheryl A.
TI APOL1 Risk Alleles Are Associated with Exaggerated Age-Related Changes
   in Glomerular Number and Volume in African-American Adults: An Autopsy
   Study
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID HIV-ASSOCIATED NEPHROPATHY; GENE VARIANTS ASSOCIATE; CHRONIC
   KIDNEY-DISEASE; CARDIOVASCULAR-DISEASE; BLOOD-PRESSURE; RENAL-DISEASE;
   HYPERTENSION; WEIGHT; RACE
AB APOL1 genetic variants contribute to kidney disease in African Americans. We assessed correlations between APOL1 profiles and renal histological features in subjects without renal disease. Glomerular number (N-glom,) and mean glomerular volume (V-glom,) were measured by the dissector/fractionator method in kidneys of African-American and non-African-American adults without renal disease, undergoing autopsies in Jackson, Mississippi. APOL1 risk alleles were genotyped and the kidney findings were evaluated in the context of those profiles. The proportions of African Americans with none, one, and two APOL1 risk alleles were 38%, 43%, and 19%, respectively; 38% of African Americans had G1 allele variants and 31% of African Americans had G2 allele variants. Only APOL1-positive African Americans had significant reductions in N-glom and increases in V-glom with increasing age. Regression analysis predicted an annual average loss of 8834 (P=0.03, sex adjusted) glomeruli per single kidney over the first 38 years of adult life in African Americans with two risk alleles. Body mass index above the group medians, but below the obesity definition of >= 30 kg/m(2), enhanced the expression of age-related changes in N-glom in African Americans with either one or two APOL1 risk alleles. These findings indicate that APOL1 risk alleles are associated with exaggerated age-related nephron loss, probably decaying from a larger pool of smaller glomeruli in early adult life, along with enlargement of the remaining glomeruli. These phenomena might mark mechanisms of accentuated susceptibility to kidney disease in APOL1-positive African Americans.
C1 [Hoy, Wendy E.; Mott, Susan A.] Univ Queensland, Ctr Chron Dis, Brisbane, Qld, Australia.
   [Hughson, Michael D.] Univ Mississippi, Med Ctr, Dept Pathol, Jackson, MS 39216 USA.
   [Kopp, Jeffrey B.] NIDDK, Kidney Dis Sect, NIH, Bethesda, MD 20892 USA.
   [Bertram, John F.] Monash Univ, Sch Biomed Sci, Dept Anat & Dev Biol, Melbourne, Vic 3004, Australia.
   [Winkler, Cheryl A.] NCI, Basic Res Lab, Ctr Canc Res, Lidos Biomed Inc,Frederick Natl Lab, Frederick, MD 21701 USA.
RP Hoy, WE (reprint author), Univ Queensland, Ctr Chron Dis, Brisbane, Qld, Australia.
EM w.hoy@uq.edu
RI Bertram, John/I-2588-2014; Hoy, Wendy/A-7325-2010; 
OI Bertram, John/0000-0001-5863-6464; Hoy, Wendy/0000-0002-8405-1539;
   hughson, michael/0000-0003-1310-707X
FU National Health and Medical Research Council (NHMRC) of Australia
   [I94276]; Colonial Foundation of Australia; NHMRC Australia Fellowship
   [511081]; National Institutes of Health (NIH) NIDDK [RO1-DK065970-01];
   American Heart Association, South-eastern affiliate; Intramural Research
   Program of the National Cancer Institute; NIDDK; federal funds from the
   National Cancer Institute, NIH [HHSN26120080001E]
FX The autopsy study has been supported by a project grant from the
   National Health and Medical Research Council (NHMRC) of Australia,
   (#I94276), by an untied grant from the Colonial Foundation of Australia
   (Hoy, 2001-2011), an NHMRC Australia Fellowship (Hoy, 2008-2012,
   #511081), by the National Institutes of Health (NIH) NIDDK
   (RO1-DK065970-01, Hughson, 2004-2007), and a grant from the American
   Heart Association, South-eastern affiliate (Hughson, 2001-2003). This
   work was also supported in part by the Intramural Research Program of
   the National Cancer Institute and the NIDDK, NIH. This project has been
   funded in whole or in part with federal funds from the National Cancer
   Institute, NIH, under contract HHSN26120080001E.
NR 31
TC 5
Z9 5
U1 1
U2 3
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1046-6673
EI 1533-3450
J9 J AM SOC NEPHROL
JI J. Am. Soc. Nephrol.
PD DEC
PY 2015
VL 26
IS 12
BP 3179
EP 3189
DI 10.1681/ASN.2014080768
PG 11
WC Urology & Nephrology
SC Urology & Nephrology
GA CX1OR
UT WOS:000365466000031
PM 26038529
ER

PT J
AU Lin, J
   Carter, CA
   McGlynn, KA
   Zahm, SH
   Nations, JA
   Anderson, WF
   Shriver, CD
   Zhu, KM
AF Lin, Jie
   Carter, Corey A.
   McGlynn, Katherine A.
   Zahm, Shelia H.
   Nations, Joel A.
   Anderson, William F.
   Shriver, Craig D.
   Zhu, Kangmin
TI A Prognostic Model to Predict Mortality among Non-Small-Cell Lung Cancer
   Patients in the US Military Health System
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Article
DE Model; Military health system; Mortality; Non-small-cell lung cancer;
   Risk prediction
ID OF-DEFENSE BENEFICIARIES; CARE-SYSTEM; SURVIVAL; VALIDATION; STAGE;
   OUTCOMES; COMORBIDITIES; CHEMOTHERAPY; DESIGN; PEOPLE
AB Introduction: Accurate prognosis assessment after non-small-cell lung cancer (NSCLC) diagnosis is an essential step for making effective clinical decisions. This study is aimed to develop a prediction model with routinely available variables to assess prognosis in patients with NSCLC in the U.S. Military Health System.
   Methods: We used the linked database from the Department of Defense's Central Cancer Registry and the Military Health System Data Repository. The data set was randomly and equally split into a training set to guide model development and a testing set to validate the model prediction. Stepwise Cox regression was used to identify predictors of survival. Model performance was assessed by calculating area under the receiver operating curves and construction of calibration plots. A simple risk scoring system was developed to aid quick risk score calculation and risk estimation for NSCLC clinical management.
   Results: The study subjects were 5054 patients diagnosed with NSCLC between 1998 and 2007. Age, sex, tobacco use, tumor stage, histology, surgery, chemotherapy, peripheral vascular disease, cerebrovascular disease, and diabetes mellitus were identified as significant predictors of survival. Calibration showed high agreement between predicted and observed event rates. The area under the receiver operating curves reached 0.841, 0.849, 0.848, and 0.838 during 1, 2, 3, and 5 years, respectively.
   Conclusions: This is the first NSCLC prognosis model for quick risk assessment within the Military Health System. After external validation, the model can be translated into clinical use both as a web-based tool and through mobile applications easily accessible to physicians, patients, and researchers.
C1 [Lin, Jie; Carter, Corey A.; Nations, Joel A.; Shriver, Craig D.; Zhu, Kangmin] Walter Reed Natl Mil Med Ctr, John P Murtha Canc Ctr, Bethesda, MD USA.
   [Carter, Corey A.; Nations, Joel A.] Walter Reed Natl Mil Med Ctr, Dept Med, Bethesda, MD USA.
   [McGlynn, Katherine A.; Zahm, Shelia H.; Anderson, William F.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Shriver, Craig D.] Uniformed Serv Univ Hlth Sci, Dept Surg, Bethesda, MD 20814 USA.
   [Zhu, Kangmin] Uniformed Serv Univ Hlth Sci, Dept Preventat Med & Biostat, Bethesda, MD 20814 USA.
RP Zhu, KM (reprint author), Walter Reed Natl Mil Med Ctr, Div Mil Epidemiol & Populat Sci, John P Murtha Canc Ctr, 11300 Rockville Pike,Suite 1120, Rockville, MD 20852 USA.
EM kzhu@murthacancercenter.org
FU John P. Murtha Cancer Center; Walter Reed National Military Medical
   Center through Uniformed Services University of the Health Sciences
   under Henry M. Jackson Foundation for Advancement of Military Medicine;
   intramural research program of the National Cancer Institute; United
   States Military Cancer Institute and Division of Cancer Epidemiology and
   Genetics, National Cancer Institute
FX This project was supported by John P. Murtha Cancer Center, Walter Reed
   National Military Medical Center through the Uniformed Services
   University of the Health Sciences under the auspices of the Henry M.
   Jackson Foundation for the Advancement of Military Medicine and by the
   intramural research program of the National Cancer Institute. The
   original data linkage was supported by the United States Military Cancer
   Institute and Division of Cancer Epidemiology and Genetics, National
   Cancer Institute.
NR 42
TC 1
Z9 1
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1556-0864
EI 1556-1380
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD DEC
PY 2015
VL 10
IS 12
BP 1694
EP 1702
DI 10.1097/JTO.0000000000000691
PG 9
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA CX3DG
UT WOS:000365575100007
PM 26473644
ER

PT J
AU Liu, Y
   deSouza, NM
   Shankar, LK
   Kauczor, HU
   Trattnig, S
   Collette, S
   Chiti, A
AF Liu, Yan
   deSouza, Nandita M.
   Shankar, Lalitha K.
   Kauczor, Hans-Ulrich
   Trattnig, Siegfried
   Collette, Sandra
   Chiti, Arturo
TI A risk management approach for imaging biomarker-driven clinical trials
   in oncology
SO LANCET ONCOLOGY
LA English
DT Article
ID POSITRON-EMISSION-TOMOGRAPHY; RESPONSE EVALUATION CRITERIA; HODGKIN
   LYMPHOMA; F-18-FDG PET; SOLID TUMORS; LUNG-CANCER; METAANALYSIS;
   PROGRESSION; REPRODUCIBILITY; REPEATABILITY
AB Imaging has steadily evolved in clinical cancer research as a result of improved conventional imaging methods and the innovation of new functional and molecular imaging techniques. Despite this evolution, the design and data quality derived from imaging within clinical trials are not ideal and gaps exist with paucity of optimised methods, constraints of trial operational support, and scarce resources. Difficulties associated with integrating imaging biomarkers into trials have been neglected compared with inclusion of tissue and blood biomarkers, largely because of inherent challenges in the complexity of imaging technologies, safety issues related to new imaging contrast media, standardisation of image acquisition across multivendor platforms, and various postprocessing options available with advanced software. Ignorance of these pitfalls directly affects the quality of the imaging read-out, leading to trial failure, particularly when imaging is a primary endpoint. Therefore, we propose a practical risk-based framework and recommendations for trials driven by imaging biomarkers, which allow identification of risks at trial initiation to better allocate resources and prioritise key tasks.
C1 [Liu, Yan; Collette, Sandra] European Org Res & Treatment Canc Headquarters, B-1200 Brussels, Belgium.
   [deSouza, Nandita M.] Inst Canc Res, Canc Res UK Canc Imaging Ctr, MRI Unit, Sutton, Surrey, England.
   [deSouza, Nandita M.] Royal Marsden NHS Fdn Trust, Sutton, Surrey, England.
   [Shankar, Lalitha K.] NCI, Clin Trial Branch, Canc Imaging Program, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
   [Kauczor, Hans-Ulrich] Univ Heidelberg Hosp, Dept Diagnost & Intervent Radiol, Heidelberg, Germany.
   [Trattnig, Siegfried] Med Univ Vienna, Dept Biomed Imaging & Image Guided Therapy, Ctr Excellence High Field MR, Vienna, Austria.
   [Chiti, Arturo] Humanitas Univ, Milan, Italy.
   [Chiti, Arturo] Humanitas Res Hosp, Dept Nucl Med, Milan, Italy.
RP Liu, Y (reprint author), European Org Res & Treatment Canc Headquarters, B-1200 Brussels, Belgium.
EM yan.liu@eortc.be
FU Innovative Medicines Initiative Joint Undertaking [115151]; European
   Union; EFPIA companies
FX The research leading to these results has received support from the
   Innovative Medicines Initiative Joint Undertaking under grant agreement
   number 115151, resources of which are composed of financial contribution
   from the European Union's Seventh Framework Programme (FP7/2007-2013)
   and EFPIA companies' in kind contribution.
NR 38
TC 1
Z9 1
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
EI 1474-5488
J9 LANCET ONCOL
JI Lancet Oncol.
PD DEC
PY 2015
VL 16
IS 16
BP E622
EP E628
PG 7
WC Oncology
SC Oncology
GA CX6IF
UT WOS:000365803700032
PM 26678215
ER

PT J
AU Yang, ZH
   Inoue, S
   Taniguchi, Y
   Miyahara, H
   Iwasaki, Y
   Takeo, J
   Sakaue, H
   Nakaya, Y
AF Yang, Zhi-Hong
   Inoue, Seika
   Taniguchi, Yasuko
   Miyahara, Hiroko
   Iwasaki, Yusuke
   Takeo, Jiro
   Sakaue, Hiroshi
   Nakaya, Yutaka
TI Long-term dietary supplementation with saury oil attenuates metabolic
   abnormalities in mice fed a high-fat diet: combined beneficial effect of
   omega-3 fatty acids and long-chain monounsaturated fatty acids
SO LIPIDS IN HEALTH AND DISEASE
LA English
DT Article
ID INSULIN-RESISTANCE; EICOSAPENTAENOIC ACID; HDL-CHOLESTEROL; C57BL/6J
   MICE; RISK-FACTORS; OBESITY; DISEASE; EXPRESSION; ADIPOSITY; TISSUE
AB Background: Pacific saury is a common dietary component in East Asia. Saury oil contains considerable levels of n-3 unsaturated fatty acids (PUFA) and long-chain monounsaturated fatty acids (LCMUFA) with aliphatic tails longer than 18 carbons. In our previous study, consumption of saury oil for 4 to 6 wk improved insulin sensitivity and the plasma lipid profile in mice. However, the long-term effects of saury oil on metabolic syndrome (MetS) risk factors remain to be demonstrated. In the current study, we examined the long-term effects of saury oil on mice fed a high-fat diet, and compared the effect of n-3 PUFA EPA and LCMUFA on MetS risk factor in diet-induced obese mice.
   Methods and Results: In Experiment 1, male C57BL/6 J mice were fed either a 32 % lard diet (control) or a diet containing 22 % lard plus 10 % saury oil (saury oil group) for 18 weeks. Although no differences were found in body weight and energy expenditure between the control and saury oil groups, the saury oil diet decreased plasma insulin, non-HDL cholesterol, hepatic steatosis, and adipocyte size, and altered levels of mRNA transcribed from genes involved in insulin signaling and inflammation in adipose tissue. Organ and plasma fatty acid profile analysis revealed that consumption of saury oil increased n-3 PUFA and LCMUFA (especially n-11 LCMUFA) levels in multiple organs, and decreased the fatty acid desaturation index (C16:1/C16:0; C18:1/C18:0) in liver and adipose tissue. In Experiment 2, male C57BL/6 J mice were fed a 32 % lard diet (control), a diet containing 28 % lard plus 4 % EPA (EPA group), or a diet containing 20 % lard plus 12 % LCMUFA concentrate (LCMUFA group) for 8 weeks. EPA or LCMUFA intake increased organ levels of EPA and LCMUFA, respectively. Consumption of EPA reduced plasma lipid levels and hepatic lipid deposition, and decreased the fatty acid desaturation index in liver and adipose tissue. Consumption of LCMUFA decreased plasma non-HDL cholesterol, improved hyperinsulinemia, and decreased the fatty acid desaturation index in adipose tissue. EPA accumulated mainly in liver, and LCMUFA (especially n-11 LCMUFA) accumulated mainly in white adipose tissue, suggesting their possible individual biological effects for improving MetS.
   Conclusion: Our results suggest that saury oil-mediated improvement of metabolic syndrome in diet-induced obese mice may possibly be due to a combined effect of n-3 PUFA and LCMUFA.
C1 [Yang, Zhi-Hong; Miyahara, Hiroko; Iwasaki, Yusuke; Takeo, Jiro] Nippon Suisan Kaisha, Cent Res Lab, Hachioji, Tokyo 1920991, Japan.
   [Yang, Zhi-Hong] NHLBI, Lipoprot Metab Sect, Cardiopulm Branch, NIH, Bethesda, MD 20892 USA.
   [Inoue, Seika; Taniguchi, Yasuko; Sakaue, Hiroshi; Nakaya, Yutaka] Univ Tokushima, Grad Sch Hlth Biosci, Dept Nutr & Metab, Tokushima 770, Japan.
RP Yang, ZH (reprint author), Nippon Suisan Kaisha, Cent Res Lab, 32-3 Nanakuni 1 Chome, Hachioji, Tokyo 1920991, Japan.
EM zhihong.yang@nih.gov
NR 38
TC 3
Z9 3
U1 3
U2 7
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1476-511X
J9 LIPIDS HEALTH DIS
JI Lipids Health Dis.
PD DEC 1
PY 2015
VL 14
AR 155
DI 10.1186/s12944-015-0161-8
PG 13
WC Biochemistry & Molecular Biology; Nutrition & Dietetics
SC Biochemistry & Molecular Biology; Nutrition & Dietetics
GA CX2ZB
UT WOS:000365564200001
PM 26627187
ER

PT J
AU Qing, Z
   Dong, ZY
   Li, SF
   Zang, YF
   Liu, DQ
AF Qing, Zhao
   Dong, Zhangye
   Li, Sufang
   Zang, Yufeng
   Liu, Dongqiang
TI Global signal regression has complex effects on regional homogeneity of
   resting state fMRI signal
SO MAGNETIC RESONANCE IMAGING
LA English
DT Article
DE Resting state fMRI; Regional homogeneity; Global signal regression; Eyes
   open; Eyes closed
ID ABNORMAL NEURAL ACTIVITY; DEFAULT MODE NETWORK; FUNCTIONAL CONNECTIVITY;
   BASAL GANGLIA; HUMAN BRAIN; MOTOR; MRI; DISEASE; CORTEX; FLUCTUATIONS
AB Regional homogeneity (ReHo) quantifies spatially local synchronization of resting state fMRI signal and has been applied to lots of clinic studies. Accumulating evidences demonstrated that the synchronization between spatially distinct brain regions, i.e. functional connectivity, can be remarkably influenced if the global mean time course is regressed out, namely global signal regression (GSR). Very recently, it was reported GSR reduces the test-retest reliability of ReHo, and reduces the positive correlation between ReHo and head motion. In this study, we were interested in two questions: 1) how GSR affects the raw ReHo values and its spatial distribution over the brain; 2) how GSR affects the differences of ReHo between two resting states, eyes open (EO) and eyes closed (EC), in healthy individuals. We found that the ReHo values were reduced by GSR but the spatial distribution of ReHo was not changed remarkably. In addition, split-half reproducibility analysis showed reproducible ReHo difference between EO and EC in some areas (e.g., thalamus and caudate) only with GSR, but showed reproducible ReHo difference in some other area (right temporal pole) only without GSR. The effects of GSR were almost independent of regression of other nuisance covariates. Our results suggest that the influences of GSR on ReHo are remarkable, reliable and complex. For the between-condition comparison, the GSR effects are region specific. We suggest that, for application studies using ReHo approach, it would be helpful to report results both with and without GSR. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Qing, Zhao; Dong, Zhangye] Beijing Normal Univ, Natl Key Lab Cognit Neurosci & Learning, Beijing 100875, Peoples R China.
   [Li, Sufang] NIDA, Neuroimage Res Branch, NIH, Baltimore, MD USA.
   [Zang, Yufeng; Liu, Dongqiang] Hangzhou Normal Univ, Ctr Cognit & Brain Disorders, Hangzhou 310015, Zhejiang, Peoples R China.
   [Zang, Yufeng; Liu, Dongqiang] Zhejiang Key Lab Res Assessment Cognit Impairment, Hangzhou, Zhejiang, Peoples R China.
RP Liu, DQ (reprint author), Hangzhou Normal Univ, Ctr Cognit & Brain Disorders, Hangzhou 310015, Zhejiang, Peoples R China.
EM charlesliu116@gmail.com
RI Li, Sufang/N-5697-2016
OI Li, Sufang/0000-0002-4716-4761
FU National Natural Science Foundation of China [81020108022, 81271652,
   81201083, 31471084]; "Qian Jiang Distinguished Professor" program
FX Financial support for the data used in this project was provided by
   grants from the National Natural Science Foundation of China:
   81020108022, 81271652, 81201083, 31471084. Dr. Zang is partly supported
   by "Qian Jiang Distinguished Professor" program.
NR 55
TC 3
Z9 3
U1 2
U2 6
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 DEC
PY 2015
VL 33
IS 10
BP 1306
EP 1313
DI 10.1016/j.mri.2015.07.011
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CX8EG
UT WOS:000365934800015
PM 26234499
ER

PT J
AU Anstey, NM
   Auburn, S
   Baird, JK
   Battle, KE
   Bobogare, A
   Chancellor, A
   Chasombat, S
   Cheng, Q
   Domingo, GJ
   Drakeley, CJ
   Drukpa, T
   Dysoley, L
   Espino, FE
   Gething, PW
   Ghimire, P
   Gosling, RD
   Grewal-Daumerie, P
   Hay, SI
   Howes, RE
   Hwang, J
   Karim, J
   Khan, WA
   Kim, JY
   Ley, B
   Mannion, K
   McCarthy, J
   Keong, WM
   Mueller, I
   Namgay, R
   Price, RN
   Qi, G
   Rebueno, M
   Reeder, J
   Richards, J
   Sattabongkot-Prachumsri, J
   Shanks, GD
   Sibley, CH
   Surya, A
   Taleo, G
   Thang, D
   Thongpaseuth, V
   Thriemer, K
   Trimarsanto, H
   Vestergaard, LS
   von Seidelein, L
   Whittaker, M
AF Anstey, Nicholas M.
   Auburn, Sarah
   Baird, J. Kevin
   Battle, Katherine E.
   Bobogare, Albino
   Chancellor, Arna
   Chasombat, Sanchai
   Cheng, Qin
   Domingo, Gonzalo J.
   Drakeley, Christopher J.
   Drukpa, Tobgyel
   Dysoley, Lek
   Esperanza Espino, Fe
   Gething, Peter W.
   Ghimire, Prakash
   Gosling, Roly D.
   Grewal-Daumerie, Penny
   Hay, Simon I.
   Howes, Rosalind E.
   Hwang, Jimee
   Karim, Jahirul
   Khan, Wasif Ali
   Kim, Jung-Yeon
   Ley, Benedikt
   Mannion, Kylie
   McCarthy, James
   Keong, Wan Ming
   Mueller, Ivo
   Namgay, Rinzin
   Price, Ric N.
   Qi, Gao
   Rebueno, Marvi
   Reeder, John
   Richards, Jack
   Sattabongkot-Prachumsri, Jetsumon
   Shanks, G. Dennis
   Sibley, Carol Hopkins
   Surya, Asik
   Taleo, George
   Ngo Duc Thang
   Thongpaseuth, Vonethalom
   Thriemer, Kamala
   Trimarsanto, Hidayat
   Vestergaard, Lasse S.
   von Seidelein, Lorenz
   Whittaker, Maxine
CA Vivax Working Grp
TI Targeting vivax malaria in the Asia Pacific: The Asia Pacific Malaria
   Elimination Network Vivax Working Group
SO MALARIA JOURNAL
LA English
DT Article
DE Malaria; Plasmodium vivax; APMEN; Asia-Pacific; Elimination
ID RESISTANT PLASMODIUM-VIVAX; GLUCOSE-6-PHOSPHATE-DEHYDROGENASE
   DEFICIENCY; FALCIPARUM; INFECTIONS; TESTS; HYPNOZOITES; MORBIDITY;
   DIVERSITY; PREGNANCY; INDONESIA
AB The Asia Pacific Malaria Elimination Network (APMEN) is a collaboration of 18 country partners committed to eliminating malaria from within their borders. Over the past 5 years, APMEN has helped to build the knowledge, tools and in-country technical expertise required to attain this goal. At its inaugural meeting in Brisbane in 2009, Plasmodium vivax infections were identified across the region as a common threat to this ambitious programme; the APMEN Vivax Working Group was established to tackle specifically this issue. The Working Group developed a four-stage strategy to identify knowledge gaps, build regional consensus on shared priorities, generate evidence and change practice to optimize malaria elimination activities. This case study describes the issues faced and the solutions found in developing this robust strategic partnership between national programmes and research partners within the Working Group. The success of the approach adopted by the group may facilitate similar applications in other regions seeking to deploy evidence-based policy and practice.
C1 [Anstey, Nicholas M.; Auburn, Sarah; Ley, Benedikt; Mannion, Kylie; Price, Ric N.; Thriemer, Kamala] Menzies Sch Hlth Res, Global & Trop Hlth Div, Darwin, NT, Australia.
   [Anstey, Nicholas M.; Auburn, Sarah; Ley, Benedikt; Mannion, Kylie; Price, Ric N.; Thriemer, Kamala] Charles Darwin Univ, Darwin, NT 0909, Australia.
   [Baird, J. Kevin] Eijkman Oxford Clin Res Unit, Jakarta, Indonesia.
   [Baird, J. Kevin; Price, Ric N.] Univ Oxford, Nuffield Dept Clin Med, Ctr Trop Med, Oxford, England.
   [Battle, Katherine E.] Univ Oxford, Dept Zool, Spatial Ecol & Epidemiol Grp, Oxford, England.
   [Chancellor, Arna; Whittaker, Maxine] Univ Queensland, Sch Publ Hlth, Brisbane, Qld, Australia.
   [Cheng, Qin] Australian Army Malaria Inst, Enoggera, Qld, Australia.
   [Drakeley, Christopher J.] London Sch Hyg & Trop Med, Dept Immunol & Infect, Fac Infect & Trop Dis, London WC1, England.
   [Dysoley, Lek] Natl Ctr Parasitol Entomol & Malaria Control, Phnom Penh, Cambodia.
   [Dysoley, Lek] Natl Inst Publ Hlth, Sch Publ Hlth, Phnom Penh, Cambodia.
   [Esperanza Espino, Fe] Res Inst Trop Med, Dept Hlth, Manila, Philippines.
   [Gething, Peter W.] Univ Oxford, Dept Zool, Spatial Ecol & Epidemiol Grp, Oxford, England.
   [Ghimire, Prakash] Tribhuvan Univ, Kathmandu, Nepal.
   [Ghimire, Prakash] WHO, Country Off Nepal, Kathmandu, Nepal.
   [Gosling, Roly D.] Univ Calif San Francisco, Global Hlth Sci, San Francisco, CA 94143 USA.
   [Grewal-Daumerie, Penny] Med Malaria Venture, Geneva, Switzerland.
   [Hay, Simon I.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
   [Hay, Simon I.] Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
   [Hay, Simon I.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
   [Howes, Rosalind E.] Univ Oxford, Dept Zool, Spatial Ecol & Epidemiol Grp, Oxford, England.
   [Howes, Rosalind E.] Case Western Reserve Univ, Ctr Global Hlth & Dis, Cleveland, OH 44106 USA.
   [Hwang, Jimee] Ctr Dis Control & Prevent, Presidents Malaria Initiat, Malaria Branch, Atlanta, GA USA.
   [Hwang, Jimee] Univ Calif San Francisco, Global Hlth Grp, San Francisco, CA 94143 USA.
   [Karim, Jahirul] Directorate Gen Hlth Serv, Dhaka, Bangladesh.
   [Khan, Wasif Ali] Int Ctr Diarrhoeal Dis Res, Ctr Vaccine Sci, Dhaka, Bangladesh.
   [McCarthy, James] QIMR Berghofer Med Res Inst, Herston, Qld, Australia.
   [McCarthy, James] Univ Queensland, Australia Sch Med, Herston, Qld, Australia.
   [Mueller, Ivo] Walter Eliza Hall Inst, Populat Hlth Immun Div, Parkville, Vic, Australia.
   [Mueller, Ivo] Barcelona Inst Global Hlth ISGLOBAL, Barcelona, Spain.
   [Namgay, Rinzin] Dept Publ Hlth, Vector Borne Dis Control Programme, Gelephu, Bhutan.
   [Qi, Gao] Jiangsu Inst Parasit Dis, Wuxi, Jiangsu, Peoples R China.
   [Rebueno, Marvi] Pilipinas Shell Fdn Inc, Movement Malaria, Manila, Philippines.
   [Reeder, John] Burnet Inst, Ctr Populat Hlth, Melbourne, Vic, Australia.
   [Reeder, John] Monash Univ, Dept Epidemiol & Preventat Med, Melbourne, Vic 3004, Australia.
   [Richards, Jack] Burnet Inst, Ctr Biomed Res, Melbourne, Vic, Australia.
   [Richards, Jack] Univ Melbourne, Dept Med, Royal Melbourne Hosp, Parkville, Vic 3052, Australia.
   [Richards, Jack] Univ Melbourne, Victorian Infect Dis Serv, Peter Doherty Inst, Parkville, Vic 3052, Australia.
   [Sattabongkot-Prachumsri, Jetsumon] Mahidol Univ, Fac Trop Med, Mahidol Vivax Res Unit, Bangkok, Thailand.
   [Shanks, G. Dennis] Australian Army Malaria Inst, Enoggera, Qld, Australia.
   [Shanks, G. Dennis] Univ Queensland, Sch Populat Hlth, Herston, Qld, Australia.
   [Sibley, Carol Hopkins] WWARN, Oxford, England.
   [Sibley, Carol Hopkins] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA.
   [Surya, Asik] Minist Hlth Republ Indonesia, Natl Malaria Control Program, Jakarta, Indonesia.
   [Ngo Duc Thang] Natl Inst Malariol Parasitol & Entomol, Hanoi, Vietnam.
   [Thongpaseuth, Vonethalom] Ctr Malariol Parasitol & Entomol, Dept Communicable Dis Control, Viangchan, Laos.
   [Trimarsanto, Hidayat] Eijkman Inst Mol Biol, Jakarta, Indonesia.
   [Vestergaard, Lasse S.] WHO, Reg Off Western Pacific, Manila, Philippines.
   [von Seidelein, Lorenz] Mahidol Univ, Mahidol Oxford Trop Med Res Unit, Bangkok 10700, Thailand.
RP Anstey, NM (reprint author), Menzies Sch Hlth Res, Global & Trop Hlth Div, Darwin, NT, Australia.
EM Nicholas.Anstey@menzies.edu.au; sarah.auburn@menzies.edu.au;
   kevin.baird@ndm.ox.ac.uk; katherine.battle@zoo.ox.ac.uk;
   Albino.Bobogare@simtri.gov.sb; a.chancellor@uq.edu.au;
   drsanchai@gmail.com; Qin.Cheng@defence.gov.au; gdomingo@path.org;
   Chris.Drakeley@lshtm.ac.uk; dtobgyel@gmail.com; soleycnm@gmail.com;
   fe.espino2012@gmail.com; peter.gething@zoo.ox.ac.uk;
   prakashghimire@hotmail.com; Roly.Gosling@ucsf.edu; grewalp@mmv.org;
   sihay@uw.edu; rosalind.howes@zoo.ox.ac.uk; Jimee.Hwang@ucsf.edu;
   jahirulkarim@gmail.com; wakhan@icddrb.org; creative-kim@daum.net;
   benedikt.ley@menzies.edu.au; kylie.mannion@menzies.edu.au;
   James.McCarthy@qimr.edu.au; wming@moh.gov.my; ivomueller@fastmail.fm;
   rinzin69@yahoo.com; rprice@menzies.edu.au; gaoqi54@hotmail.com;
   marvi_rebueno@yahoo.com; reederj@who.int; richards@burnet.edu.au;
   jetsumon.pra@mahidol.ac.th; Dennis.SHANKS@defence.gov.au;
   carol.sibley@wwarn.org; asiksurya@yahoo.com; gtaleo@vanuatu.gov.vu;
   thangnimpevn@yahoo.com; t.vonethalom@gmail.com;
   kamala.ley-thriemer@menzies.edu.au; anto@eijkman.go.id;
   vestergaardl@wpro.who.int; Lorenz@tropmedres.ac;
   m.whittaker@sph.uq.edu.au
RI Hay, Simon/F-8967-2015; 
OI Hay, Simon/0000-0002-0611-7272; Price, Richard/0000-0003-2000-2874;
   Thriemer, Kamala/0000-0001-7536-7497; Trimarsanto,
   Hidayat/0000-0003-2436-8283; Gething, Peter/0000-0001-6759-5449
FU Australian Government Department of Foreign Affairs and Trade from the
   Bill and Melinda Gates Foundation; Malaria for Medicine Venture (MMV)
FX Major funding for the Asia Pacific Malaria Elimination Network (APMEN)
   Vivax Working Group (VxWG) is provided by the Australian Government
   Department of Foreign Affairs and Trade alongside funds received from
   the Bill and Melinda Gates Foundation and the Malaria for Medicine
   Venture (MMV).
NR 67
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Z9 0
U1 1
U2 7
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 DEC 1
PY 2015
VL 14
AR 484
DI 10.1186/s12936-015-0958-y
PG 11
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA CX6FB
UT WOS:000365795500011
ER

PT J
AU Khadka, P
   Hsu, JK
   Veith, S
   Tadokoro, T
   Shamanna, RA
   Mangerich, A
   Croteau, DL
   Bohr, VA
AF Khadka, Prabhat
   Hsu, Joseph K.
   Veith, Sebastian
   Tadokoro, Takashi
   Shamanna, Raghavendra A.
   Mangerich, Aswin
   Croteau, Deborah L.
   Bohr, Vilhelm A.
TI Differential and Concordant Roles for Poly(ADP-Ribose) Polymerase 1 and
   Poly(ADP-Ribose) in Regulating WRN and RECQL5 Activities
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID WERNER-SYNDROME PROTEIN; DNA-DAMAGE RESPONSE; DOUBLE-STRAND BREAKS;
   ADP-RIBOSYLATION; HOMOLOGOUS RECOMBINATION; GENOME STABILIZATION; PARG
   REVEALS; REPAIR; HELICASE; CANCER
AB Poly(ADP-ribose) (PAR) polymerase I (PARP1) catalyzes the poly(ADP-ribosyl)ation (PARylation) of proteins, a posttranslational modification which forms the nucleic acid-like polymer PAR. PARP1 and PAR are integral players in the early DNA damage response, since PARylation orchestrates the recruitment of repair proteins to sites of damage. Human RecQ helicases are DNA unwinding proteins that are critical responders to DNA damage, but how their recruitment and activities are regulated by PARPs and PAR is poorly understood. Here we report that all human RecQ helicases interact with PAR noncovalently. Furthermore, we define the effects that PARP1, PARylated PARP1, and PAR have on RECQL5 and WRN, using both in vitro and in vivo assays. We show that PARylation is involved in the recruitment of RECQL5 and WRN to laser-induced DNA damage and that RECQL5 and WRN have differential responses to PARylated PARP1 and PAR. Furthermore, we show that the loss of RECQL5 or WRN resulted in increased sensitivity to PARP inhibition. In conclusion, our results demonstrate that PARP1 and PAR actively, and in some instances differentially, regulate the activities and cellular localization of RECQL5 and WRN, suggesting that PARylation acts as a fine-tuning mechanism to coordinate their functions in time and space during the genotoxic stress response.
C1 [Khadka, Prabhat; Hsu, Joseph K.; Tadokoro, Takashi; Shamanna, Raghavendra A.; Croteau, Deborah L.; Bohr, Vilhelm A.] NIA, Lab Mol Gerontol, Biomed Res Ctr, NIH, Baltimore, MD 21224 USA.
   [Veith, Sebastian; Mangerich, Aswin] Univ Konstanz, Dept Biol, Mol Toxicol Grp, Constance, Germany.
RP Bohr, VA (reprint author), NIA, Lab Mol Gerontol, Biomed Res Ctr, NIH, Baltimore, MD 21224 USA.
EM vbohr@nih.gov
FU Intramural Research Program of the National Institutes of Health,
   National Institute on Aging; DFG-funded research training group 1331
FX This work was supported in part by the Intramural Research Program of
   the National Institutes of Health, National Institute on Aging. S.V. was
   supported by a fellowship of DFG-funded research training group 1331.
NR 58
TC 3
Z9 3
U1 1
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
EI 1098-5549
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD DEC
PY 2015
VL 35
IS 23
BP 3974
EP 3989
DI 10.1128/MCB.00427-15
PG 16
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA CX5BF
UT WOS:000365714900004
PM 26391948
ER

PT J
AU Xing, JY
   Yi, J
   Cai, XY
   Tang, H
   Liu, ZY
   Zhang, XT
   Martindale, JL
   Yang, XL
   Jiang, B
   Gorospe, M
   Wang, WG
AF Xing, Junyue
   Yi, Jie
   Cai, Xiaoyu
   Tang, Hao
   Liu, Zhenyun
   Zhang, Xiaotian
   Martindale, Jennifer L.
   Yang, Xiaoling
   Jiang, Bin
   Gorospe, Myriam
   Wang, Wengong
TI NSun2 Promotes Cell Growth via Elevating Cyclin-Dependent Kinase 1
   Translation
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID RNA METHYLTRANSFERASE NSUN2; MESSENGER-RNA; BINDING PROTEIN; CDK1;
   ACTIVATION; MITOSIS; PHOSPHORYLATION; METHYLATION; PROLIFERATION;
   TRANSITIONS
AB The tRNA methytransfera se NSun2 promotes cell proliferation, but the molecular mechanism has not been elucidated. Here, we report that NSun2 regulates cyclin-dependent kinase 1 (CDK1) expression in a cell cycle-dependent manner. Knockdown of NSun2 decreased the CDK1 protein level, while overexpression of NSun2 elevated it without altering CDK1 mRNA levels. Further studies revealed that NSun2 methylated CDK1 mRNA in vitro and in cells and that methylation by NSun2 enhanced CDK1 translation. Importantly, NSun2-mediated regulation of CDK1 expression had an impact on the cell division cycle. These results provide new insight into the regulation of CDK1 during the cell division cycle.
C1 [Xing, Junyue; Cai, Xiaoyu; Tang, Hao; Liu, Zhenyun; Zhang, Xiaotian; Jiang, Bin; Wang, Wengong] Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Dept Biochem & Mol Biol,Beijing Key Lab Prot Post, Beijing 100871, Peoples R China.
   [Martindale, Jennifer L.; Yang, Xiaoling; Gorospe, Myriam] NIA, Genet Lab, NIH, Baltimore, MD 21224 USA.
   [Yi, Jie] Beijing Union Med Coll Hosp, Dept Clin Lab, Beijing, Peoples R China.
RP Wang, WG (reprint author), Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Dept Biochem & Mol Biol,Beijing Key Lab Prot Post, Beijing 100871, Peoples R China.
EM wwg@bjmu.edu.cn
FU National Science Foundation of China [81230008, 81420108016, 91339114];
   Ministry of Education of People's Republic of China [B07001]
FX This work was supported by grants 81230008, 81420108016, and 91339114
   from the National Science Foundation of China and by grant B07001 (111
   project) from the Ministry of Education of People's Republic of China.
NR 41
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U1 1
U2 5
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
EI 1098-5549
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD DEC
PY 2015
VL 35
IS 23
BP 4043
EP 4052
DI 10.1128/MCB.00742-15
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA CX5BF
UT WOS:000365714900009
PM 26391950
ER

PT J
AU Fukuda, T
   Mishina, Y
   Walker, MP
   DiAugustine, RP
AF Fukuda, Tomokazu
   Mishina, Yuji
   Walker, Michael P.
   DiAugustine, Richard P.
TI Conditional Transgenic System for Mouse Aurora A Kinase: Degradation by
   the Ubiquitin Proteasome Pathway Controls the Level of the Transgenic
   Protein (vol 25, pg 5270, 2005)
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Correction
C1 [Fukuda, Tomokazu; Walker, Michael P.; DiAugustine, Richard P.] NIEHS, Hormones & Canc Grp, Lab Mol Carcinogenesis, Res Triangle Pk, NC 27709 USA.
   [Mishina, Yuji] NIEHS, Reprod & Dev Toxicol Lab, Res Triangle Pk, NC 27709 USA.
RP Fukuda, T (reprint author), NIEHS, Hormones & Canc Grp, Lab Mol Carcinogenesis, POB 12233, Res Triangle Pk, NC 27709 USA.
NR 1
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PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
EI 1098-5549
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD DEC
PY 2015
VL 35
IS 23
BP 4094
EP 4094
DI 10.1128/MCB.00735-15
PG 1
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA CX5BF
UT WOS:000365714900014
PM 26518639
ER

PT J
AU Kim, Y
   Hooten, NN
   Dluzen, DF
   Martindale, JL
   Gorospe, M
   Evans, MK
AF Kim, Yoonseo
   Hooten, Nicole Noren
   Dluzen, Douglas F.
   Martindale, Jennifer L.
   Gorospe, Myriam
   Evans, Michele K.
TI Posttranscriptional Regulation of the Inflammatory Marker C-Reactive
   Protein by the RNA-Binding Protein HuR and MicroRNA 637
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID NF-KAPPA-B; MESSENGER-RNA; GENE-EXPRESSION; CELLULAR SENESCENCE; SIGNAL
   TRANSDUCER; C/EBP-BETA; INTERLEUKIN-6; CANCER; STABILITY; PROMOTER
AB C-reactive protein (CRP), an acute-phase plasma protein, is a major component of inflammatory reactions functioning as a mediator of innate immunity. It has been widely used as a validated clinical biomarker of the inflammatory state in trauma, infection, and age-associated chronic diseases, including cancer and cardiovascular disease (CVD). Despite this, the molecular mechanisms that regulate CRP expression are not well understood. Given that the CRP3' untranslated region (UTR) is long and AU rich, we hypothesized that CRP may be regulated posttranscriptionally by RNA-binding proteins (RBPs) and by microRNAs. Here, we found that the RBP HuR bound directly to the CRP3' UTR and affected CRP mRNA levels. Through this interaction, HuR selectively increased CRP mRNA stability and promoted CRP translation. Interestingly, treatment with the age-associated inflammatory cytokine interleukin-6 (IL-6) increased binding of HuR to CRP mRNA, and conversely, HuR was required for IL-6-mediated upregulation of CRP expression. In addition, we identified microRNA 637 (miR-637) as a microRNA that potently inhibited CRP expression in competition with HuR. Taken together, we have uncovered an important posttranscriptional mechanism that modulates the expression of the inflammatory marker CRP, which may be utilized in the development of treatments for inflammatory processes that cause CVD and age-related diseases.
C1 [Kim, Yoonseo; Hooten, Nicole Noren; Dluzen, Douglas F.; Evans, Michele K.] NIA, Lab Epidemiol & Populat Sci, NIH, Baltimore, MD 21224 USA.
   [Martindale, Jennifer L.; Gorospe, Myriam] NIA, Genet Lab, NIH, Baltimore, MD 21224 USA.
RP Evans, MK (reprint author), NIA, Lab Epidemiol & Populat Sci, NIH, Baltimore, MD 21224 USA.
EM me42v@nih.gov
OI Dluzen, Douglas/0000-0002-9426-5071
FU Intramural Research Program of the National Institutes of Health
   National Institute on Aging
FX This study was supported by the Intramural Research Program of the
   National Institutes of Health National Institute on Aging.
NR 47
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PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
EI 1098-5549
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD DEC
PY 2015
VL 35
IS 24
BP 4212
EP 4221
DI 10.1128/MCB.00645-15
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA CX5BL
UT WOS:000365715500010
PM 26438598
ER

PT J
AU Gordon, SM
   McKenzie, B
   Kemeh, G
   Sampson, M
   Perl, S
   Young, NS
   Fessler, MB
   Remaley, AT
AF Gordon, Scott M.
   McKenzie, Benjamin
   Kemeh, Georgina
   Sampson, Maureen
   Perl, Shira
   Young, Neal S.
   Fessler, Michael B.
   Remaley, Alan T.
TI Rosuvastatin Alters the Proteome of High Density Lipoproteins:
   Generation of alpha-1-antitrypsin Enriched Particles with
   Anti-inflammatory Properties
SO MOLECULAR & CELLULAR PROTEOMICS
LA English
DT Article
ID 2-DIMENSIONAL GEL-ELECTROPHORESIS; INDUCED PULMONARY-EMPHYSEMA;
   NEUTROPHIL ELASTASE; MASS-SPECTROMETRY; CHOLESTEROL; STATINS;
   ALPHA(1)-ANTITRYPSIN; MACROPHAGES; PROTEINS; THERAPY
AB Statins lower plasma cholesterol by as much as 50%, thus reducing future cardiovascular events. However, the physiological effects of statins are diverse and not all are related to low density lipoprotein cholesterol (LDL-C) lowering. We performed a small clinical pilot study to assess the impact of statins on lipoprotein-associated proteins in healthy individuals (n = 10) with normal LDL-C (<130 mg/dL), who were treated with rosuvastatin (20 mg/day) for 28 days. Proteomic analysis of size-exclusion chromatography isolated LDL, large high density lipoprotein (HDL-L), and small HDL (HDL-S) fractions and spectral counting was used to compare relative protein detection before and after statin therapy. Significant protein changes were found in each lipoprotein pool and included both increases and decreases in several proteins involved in lipoprotein metabolism, complement regulation and acute phase response. The most dramatic effect of the rosuvastatin treatment was an increase in alpha-1-antirypsin (A1AT) spectral counts associated with HDL-L particles. Quantitative measurement by ELISA confirmed an average 5.7-fold increase in HDL-L associated A1AT. Molecular modeling predictions indicated that the hydrophobic reactive center loop of A1AT, the functional domain responsible for its protease inhibitor activity, is likely involved in lipid binding and association with HDL was found to protect A1AT against oxidative inactivation. Cell culture experiments, using J774 macrophages, demonstrated that the association of A1AT with HDL enhances its antiprotease activity, preventing elastase induced production of tumor necrosis factor . In conclusion, we show that statins can significantly alter the protein composition of both LDL and HDL and our studies reveal a novel functional relationship between A1AT and HDL. The up-regulation of A1AT on HDL enhances its anti-inflammatory functionality, which may contribute to the non-lipid lowering beneficial effects of statins.
C1 [Gordon, Scott M.; McKenzie, Benjamin; Kemeh, Georgina; Sampson, Maureen; Remaley, Alan T.] NHLBI, Lipoprotein Metab Sect, NIH, Bethesda, MD 20892 USA.
   [Perl, Shira; Young, Neal S.] NHLBI, Cell Biol Sect, NIH, Bethesda, MD 20892 USA.
   [Fessler, Michael B.] Natl Inst Environm Hlth Sci, Inflammat & Dis Lab, Immun, NIH, Res Triangle Pk, NC USA.
RP Gordon, SM (reprint author), NHLBI, Lipoprotein Metab Sect, 9000 Rockville Pike,Bldg 10 Room 8N224, Bethesda, MD 20892 USA.
EM scott.gordon@nih.gov
FU National Institutes of Health, National Heart Lung and Blood Institute
FX This work was supported by the National Institutes of Health, National
   Heart Lung and Blood Institute. Intramural Research Program. The content
   is solely the responsibility of the authors and does not necessarily
   represent the official views of the National Institutes of Health.
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PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 1535-9476
EI 1535-9484
J9 MOL CELL PROTEOMICS
JI Mol. Cell. Proteomics
PD DEC
PY 2015
VL 14
IS 12
BP 3247
EP 3257
DI 10.1074/mcp.M115.054031
PG 11
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA CX3ZN
UT WOS:000365638100012
PM 26483418
ER

PT J
AU Armanios, M
   de Cabo, R
   Mannick, J
   Partridge, L
   van Deursen, J
   Villeda, S
AF Armanios, Mary
   de Cabo, Rafael
   Mannick, Joan
   Partridge, Linda
   van Deursen, Jan
   Villeda, Saul
TI Translational strategies in aging and age-related disease
SO NATURE MEDICINE
LA English
DT Editorial Material
ID RESTRICTION MIMETICS; CALORIE RESTRICTION; LIFE; INTERVENTIONS; RISK;
   GENE
AB Aging is a risk factor for several of the world's most prevalent diseases, including neurodegenerative disorders, cancer, cardiovascular disease and metabolic disease. Although our understanding of the molecular pathways that contribute to the aging process and age-related disease is progressing through the use of model organisms, how to apply this knowledge in the clinic is less clear. In September, Nature Medicine, in collaboration with the Volkswagen Foundation, hosted a conference at the beautiful Herrenhausen Palace in Hannover, Germany with the goal of broadening our understanding of the aging process and its meaning as a 'risk factor' in disease. Here, several of the speakers at that conference answer questions posed by Nature Medicine.
C1 [Armanios, Mary] Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21205 USA.
   [de Cabo, Rafael] NIA, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
   [Mannick, Joan] Novartis Inst BioMed Res, Cambridge, MA USA.
   [Partridge, Linda] UCL, Dept Genet Evolut & Environm, Inst Hlth Ageing, London, England.
   [van Deursen, Jan] Max Planck Inst Biol Ageing, Cologne, Germany.
   [van Deursen, Jan] Mayo Clin, Dept Pediat & Adolescent Med, Rochester, MN USA.
   [van Deursen, Jan] Mayo Clin, Dept Biochem & Mol Biol, Rochester, MN USA.
   [Villeda, Saul] Univ Calif San Francisco, Dept Anat, San Francisco, CA 94143 USA.
   [Villeda, Saul] Eli & Edythe Broad Ctr Regenerat Med & Stem Cell, San Francisco, CA USA.
RP Armanios, M (reprint author), Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21205 USA.
RI de Cabo, Rafael/J-5230-2016; 
OI de Cabo, Rafael/0000-0002-3354-2442; , rafael/0000-0003-2830-5693
FU NCI NIH HHS [R01 CA096985]; NIA NIH HHS [R37 AG013925]; Wellcome Trust
   [098565]
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PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD DEC
PY 2015
VL 21
IS 12
BP 1395
EP 1399
DI 10.1038/nm.4004
PG 5
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
   Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
   Medicine
GA CX9EV
UT WOS:000366008700009
PM 26646495
ER

PT J
AU Finkel, T
AF Finkel, Toren
TI The metabolic regulation of aging
SO NATURE MEDICINE
LA English
DT Review
ID EXTENDS LIFE-SPAN; RANDOMIZED CONTROLLED-TRIAL; LONG-LIVED MICE;
   HIGH-FAT DIET; CALORIC RESTRICTION; CAENORHABDITIS-ELEGANS; OXIDATIVE
   STRESS; C-ELEGANS; MITOCHONDRIAL-FUNCTION; RHESUS-MONKEYS
AB Here we review the environmental and genetic manipulations that link cellular and organismal metabolism to aging. In particular, we explore how nutrients are sensed and how various intracellular energy nodes seem to coordinate distinct metabolic alterations linked to extended longevity. In addition, the role of mitochondria as both a metabolic and signaling organelle is discussed. Finally, we review a host of new targeted pharmacological approaches that attempt to exploit the connection between aging and metabolism to treat a wide range of age-related diseases. Together, these insights are beginning to reveal answers to century-old mysteries and are providing a future road map for the rational extension of lifespan.
C1 [Finkel, Toren] NHLBI, Ctr Mol Med, NIH, Bethesda, MD 20892 USA.
RP Finkel, T (reprint author), NHLBI, Ctr Mol Med, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM finkelt@nih.gov
FU US National Institutes of Health Intramural Program; Leducq Foundation
FX I am grateful to members of my laboratory for their helpful suggestions,
   and in particular to I. Rovira for help with the manuscript. This work
   is supported by funds from the US National Institutes of Health
   Intramural Program and from The Leducq Foundation.
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PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD DEC
PY 2015
VL 21
IS 12
BP 1416
EP 1423
DI 10.1038/nm.3998
PG 8
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
   Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
   Medicine
GA CX9EV
UT WOS:000366008700012
PM 26646498
ER

PT J
AU Bremner, KE
   Krahn, MD
   Warren, JL
   Hoch, JS
   Barrett, MJ
   Liu, N
   Barbera, L
   Yabroff, KR
AF Bremner, Karen E.
   Krahn, Murray D.
   Warren, Joan L.
   Hoch, Jeffrey S.
   Barrett, Michael J.
   Liu, Ning
   Barbera, Lisa
   Yabroff, K. Robin
TI An international comparison of costs of end-of-life care for advanced
   lung cancer patients using health administrative data
SO PALLIATIVE MEDICINE
LA English
DT Article
DE Terminal care; costs and cost analysis; nonsmall cell lung carcinoma;
   health services; comparative study
ID SEER-MEDICARE DATA; UNITED-STATES; PALLIATIVE CARE; PROSTATE-CANCER;
   BREAST-CANCER; CANADA; ONTARIO; INDICATORS; POPULATION; QUALITY
AB Background: Patterns of end-of-life cancer care differ in Canada and the United States; yet little is known about differences in service-specific and overall costs.
   Aim: The aim of this study was to compare end-of-life costs in Ontario, Canada, and the United States, using administrative health data.
   Design: Advanced-stage nonsmall cell lung cancer patients who died from cancer at age 65.5years in 2001-2005 were selected from the US Surveillance, Epidemiology, and End Results-Medicare database (N=16,858) and the Ontario Cancer Registry (N=8643). We estimated total and service-specific costs (2009US dollars) in each of the last 6months of life from the public payer perspectives for short-term and long-term survivors (lived<180 and 180days post-diagnosis, respectively). Services were defined for comparisons between systems.
   Results: Mean monthly costs increased as death approached, were higher in short-term than long-term survivors, and were generally higher in the United States than in Ontario until the month before death, when they were similar (long-term survivors: US$10,464 and US$10,094 (p=0.53), short-term survivors US$14,455 and US$12,836 (p=0.11), in Surveillance, Epidemiology, and End Results-Medicare and Ontario, respectively). Costs for Medicare hospice and Ontario's palliative care components were similar and increased closer to death. Inpatient hospitalization was the main cost driver with similar costs in both cohorts, despite lower utilization in the United States. The compositions of many services and costs differed.
   Conclusion: Costs for nonsmall cell lung cancer patients were slightly higher in the United States than Ontario until 1month before death. Administrative data allow exploration and international comparisons of reimbursement policies, health-care delivery, and costs at the end of life.
C1 [Bremner, Karen E.; Krahn, Murray D.] Univ Hlth Network, Toronto Gen Res Inst, Toronto, ON, Canada.
   [Krahn, Murray D.; Hoch, Jeffrey S.] Univ Toronto, Fac Pharm, Inst Hlth Policy Management & Evaluat, Toronto Hlth Econ & Technol Assessment Collaborat, Toronto, ON, Canada.
   [Krahn, Murray D.; Hoch, Jeffrey S.; Liu, Ning] Inst Clin Evaluat Sci, Toronto, ON, Canada.
   [Warren, Joan L.; Yabroff, K. Robin] Natl Canc Inst, Div Canc Control & Populat Sci, Rockville, MD USA.
   [Hoch, Jeffrey S.] St Michaels Hosp, Li Ka Shing Knowledge Inst, Canadian Ctr Appl Res Canc Control, Toronto, ON M5B 1W8, Canada.
   [Hoch, Jeffrey S.] Canc Care Ontario, Pharmacoecon Res Unit, Toronto, ON, Canada.
   [Barrett, Michael J.] Informat Management Serv Inc, Calverton, MD USA.
   [Barbera, Lisa] Univ Toronto, Dept Radiat Oncol, Toronto, ON, Canada.
RP Bremner, KE (reprint author), Toronto Gen Hosp, Room EN13-222A,200 Elizabeth St, Toronto, ON M5G 2C4, Canada.
EM kbremner@uhnresearch.ca
OI Krahn, Murray/0000-0001-5836-397X; Hoch, Jeffrey/0000-0002-4880-4281
FU Cancer Care Ontario; Ontario Institute for Cancer Research; Canadian
   Centre for Applied Research in Cancer Control (ARCC) - Canadian Cancer
   Society Research Institute; F Norman Hughes Chair in Pharmacoeconomics,
   Faculty of Pharmacy, University of Toronto
FX The Ontario portion of this work was supported by research grants from
   Cancer Care Ontario, the Ontario Institute for Cancer Research, and the
   Canadian Centre for Applied Research in Cancer Control (ARCC) which is
   funded by the Canadian Cancer Society Research Institute. Dr Krahn was
   supported by a career support award through the F Norman Hughes Chair in
   Pharmacoeconomics, Faculty of Pharmacy, University of Toronto. The
   SEER-Medicare portion of the study was performed by federal researchers
   at the US National Cancer Institute. There was no external funding for
   the SEER-Medicare work.
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PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0269-2163
EI 1477-030X
J9 PALLIATIVE MED
JI Palliat. Med.
PD DEC
PY 2015
VL 29
IS 10
BP 918
EP 928
DI 10.1177/0269216315596505
PG 11
WC Health Care Sciences & Services; Public, Environmental & Occupational
   Health; Medicine, General & Internal
SC Health Care Sciences & Services; Public, Environmental & Occupational
   Health; General & Internal Medicine
GA CX5GK
UT WOS:000365729900006
PM 26330452
ER

PT J
AU Meeske, KA
   Ji, LY
   Freyer, DR
   Gaynon, P
   Ruccione, K
   Butturini, A
   Avramis, VI
   Siegel, S
   Matloub, Y
   Seibel, NL
   Sposto, R
AF Meeske, Kathleen A.
   Ji, Lingyun
   Freyer, David R.
   Gaynon, Paul
   Ruccione, Kathleen
   Butturini, Anna
   Avramis, Vassilios I.
   Siegel, Stuart
   Matloub, Yousif
   Seibel, Nita L.
   Sposto, Richard
TI Comparative Toxicity by Sex Among Children Treated for Acute
   Lymphoblastic Leukemia: A Report From the Children's Oncology Group
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE acute lymphoblastic leukemia; acute toxicities; disparities; pediatric
   oncology; sex
ID LEAN BODY-MASS; CHILDHOOD-CANCER; GENDER-DIFFERENCES; PHARMACOLOGICAL
   RESPONSE; 5-YEAR SURVIVORS; LATE MORTALITY; 1ST REMISSION;
   PHARMACOKINETICS; PHARMACODYNAMICS; CLEARANCE
AB Background. Epidemiologic studies find sex-based differences in incidence, survival, and long-term outcomes for children with cancer. The purpose of this study was to determine whether male and female patients differ with regard to acute treatment-related toxicities. Procedures. We reviewed data collected on the Children's cancer group (CCG) high-risk acute lymphoblastic leukemia (ALL-HR) study (CCG-1961), and compared male and female patients' toxicity incidence and related variables in the first four phases of treatment. Similar analyses were performed with standard-risk ALL (ALL-SR) patients enrolled in CCG-1991. Results. Among ALL-HR patients, females had significantly more hospital days, delays in therapy, grade 3 or 4 toxicities (e.g., gastrointestinal, liver), and supportive care interventions (e.g., transfusions, intravenous antibiotics) than males. Females were significantly more likely to have died of treatment-related causes than males (Hazard ratio = 2.8, 95% CI = 1.5-5.3, P = 0.002). Five months after beginning treatment, the cumulative incidence of treatment-related deaths was 2.6% for females and 1.2% for males. Similar disparities were found among ALL-SR patients, with females experiencing significantly more hospital days and treatment-related toxicities than males. Conclusions. This study complements cancer survivorship studies that also report an increase in treatment-related late effects among females. Risk profiles appear to be different for male and female patients, with females having greater risk of developing both acute and long-term treatment-related toxicities. The underlying biological mechanisms for these sex differences are poorly understood and warrant further study in order to determine how sex-based outcome disparities can be addressed in future clinical trials and practice. Pediatr Blood (C) 2015 Wiley Periodicals, Inc.
C1 [Meeske, Kathleen A.; Freyer, David R.; Gaynon, Paul; Ruccione, Kathleen; Avramis, Vassilios I.; Siegel, Stuart; Sposto, Richard] Childrens Hosp Los Angeles, Childrens Ctr Canc & Blood Dis, Los Angeles, CA 90027 USA.
   [Meeske, Kathleen A.; Freyer, David R.; Gaynon, Paul; Ruccione, Kathleen; Avramis, Vassilios I.; Siegel, Stuart] Univ So Calif, Keck Sch Med, Dept Pediat, Los Angeles, CA 90033 USA.
   [Ji, Lingyun; Sposto, Richard] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
   [Butturini, Anna] Agensys Inc, Santa Monica, CA USA.
   [Matloub, Yousif] Case Western Reserve Univ, Rainbow Babies & Childrens Hosp, Div Hematol Oncol, Cleveland, OH 44106 USA.
   [Seibel, Nita L.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Meeske, KA (reprint author), Childrens Hosp Los Angeles, Childrens Ctr Canc & Blood Dis, 4650 Sunset Blvd,MS 54, Los Angeles, CA 90027 USA.
EM kmeeske@chla.usc.edu
FU Concern Foundation for Cancer Research; Children's Center for Cancer and
   Blood Diseases; Children's Hospital Los Angeles; National Cancer
   Institute, National Institutes of Health (Children's Oncology Group
   Chair) [U10 CA098453]
FX Grant sponsor: Concern Foundation for Cancer Research; Grant sponsor:
   Children's Center for Cancer and Blood Diseases; Grant sponsor:
   Children's Hospital Los Angeles; Grant sponsor: National Cancer
   Institute, National Institutes of Health (Children's Oncology Group
   Chair); Grant number: U10 CA098453
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U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1545-5009
EI 1545-5017
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD DEC
PY 2015
VL 62
IS 12
BP 2140
EP 2149
DI 10.1002/pbc.25628
PG 10
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA CX0UN
UT WOS:000365412600015
PM 26173904
ER

PT J
AU Horkay, F
   Basser, PJ
   Hecht, AM
   Geissler, E
AF Horkay, Ferenc
   Basser, Peter J.
   Hecht, Anne-Marie
   Geissler, Erik
TI Effect of calcium/sodium ion exchange on the osmotic properties and
   structure of polyelectrolyte gels
SO PROCEEDINGS OF THE INSTITUTION OF MECHANICAL ENGINEERS PART H-JOURNAL OF
   ENGINEERING IN MEDICINE
LA English
DT Article
DE Polymer gel; biomimetics; ions; osmotic pressure; small-angle
   scattering; DNA; polyacrylic acid
ID PHYSIOLOGICAL SALT-SOLUTIONS; DISCONTINUOUS VOLUME TRANSITIONS;
   EQUILIBRIUM SWELLING BEHAVIOR; POLYACRYLATE HYDROGELS;
   PHASE-TRANSITIONS; POLYANIONIC GELS; ADSORPTION; SCATTERING; DNA
AB We discuss the main findings of a long-term research program exploring the consequences of sodium/calcium ion exchange on the macroscopic osmotic and elastic properties, and the microscopic structure of representative synthetic polyelectrolyte (sodium polyacrylate, (polyacrylic acid)) and biopolymer gels (DNA). A common feature of these gels is that above a threshold calcium ion concentration, they exhibit a reversible volume phase transition. At the macroscopic level, the concentration dependence of the osmotic pressure shows that calcium ions influence primarily the third-order interaction term in the Flory-Huggins model of polymer solutions. Mechanical tests reveal that the elastic modulus is practically unaffected by the presence of calcium ions, indicating that ion bridging does not create permanent cross-links. At the microscopic level, small-angle neutron scattering shows that polyacrylic acid and DNA gels exhibit qualitatively similar structural features in spite of important differences (e.g. chain flexibility and chemical composition) between the two polymers. The main effect of calcium ions is that the neutron scattering intensity increases due to the decrease in the osmotic modulus. At the level of the counterion cloud around dissolved macroions, anomalous small-angle X-ray scattering measurements made on DNA indicate that divalent ions form a cylindrical sheath enveloping the chain, but they are not localized. Small-angle neutron scattering and small-angle X-ray scattering provide complementary information on the structure and interactions in polymer solutions and gels.
C1 [Horkay, Ferenc; Basser, Peter J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Tissue Biophys & Biomimet, NIH, Bethesda, MD 20892 USA.
   [Hecht, Anne-Marie; Geissler, Erik] Univ Grenoble Alpes, CNRS, Lab Interdisciplinaire Phys LIPhy, Grenoble, France.
RP Horkay, F (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Tissue Biophys & Biomimet, NIH, Bldg 13,Room 3W16,13 South Dr, Bethesda, MD 20892 USA.
EM horkayf@helix.nih.gov
FU NICHD/NIH; National Institute of Standards and Technology, US Department
   of Commerce; National Science Foundation [DMR-0944772]
FX The author(s) disclosed receipt of the following financial support for
   the research, authorship, and/or publication of this article: This work
   was supported by the intramural research program of the NICHD/NIH. This
   work was also supported by the National Institute of Standards and
   Technology, US Department of Commerce, by providing the neutron research
   facilities used in this work. This work utilized facilities supported by
   the National Science Foundation under Agreement No. DMR-0944772.
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PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0954-4119
EI 2041-3033
J9 P I MECH ENG H
JI Proc. Inst. Mech. Eng. Part H-J. Eng. Med.
PD DEC
PY 2015
VL 229
IS 12
SI SI
BP 895
EP 904
DI 10.1177/0954411915602915
PG 10
WC Engineering, Biomedical
SC Engineering
GA CX4MM
UT WOS:000365675000008
PM 26614803
ER

PT J
AU Teff, KL
   Silva, CM
AF Teff, Karen L.
   Silva, Corinne M.
TI Waking Up to the Importance of Sleep and Circadian Rhythms for Metabolic
   Health: The Need for In-Depth Phenotyping
SO SLEEP
LA English
DT Editorial Material
C1 [Teff, Karen L.; Silva, Corinne M.] NIDDK, Div Diabet Endocrinol & Metab Dis, NIH, Bethesda, MD 20892 USA.
RP Teff, KL (reprint author), NIDDK, NIH, Bldg 2DEM,Room 685,6707 Democracy Blvd, Bethesda, MD 20892 USA.
EM teffk@niddk.nih.gov
NR 1
TC 0
Z9 0
U1 1
U2 2
PU AMER ACAD SLEEP MEDICINE
PI WESTCHESTER
PA ONE WESTBROOK CORPORATE CTR, STE 920, WESTCHESTER, IL 60154 USA
SN 0161-8105
EI 1550-9109
J9 SLEEP
JI Sleep
PD DEC 1
PY 2015
VL 38
IS 12
BP 1847
EP 1848
DI 10.5665/sleep.5224
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA CX3RH
UT WOS:000365616300007
PM 26564132
ER

PT J
AU Mysliwiec, V
   Gill, J
   Matsangas, P
   Baxter, T
   Barr, T
   Roth, BJ
AF Mysliwiec, Vincent
   Gill, Jessica
   Matsangas, Panagiotis
   Baxter, Tristin
   Barr, Taura
   Roth, Bernard J.
TI IGF-1: a potential biomarker for efficacy of sleep improvement with
   automatic airway pressure therapy for obstructive sleep apnea?
SO SLEEP AND BREATHING
LA English
DT Article
DE Obstructive sleep apnea; Insulin-like growth factor (IGF-1); Positive
   airway pressure (PAP); Adherence
ID GROWTH-FACTOR 1; DAYTIME SLEEPINESS; BINDING PROTEIN-3; CPAP;
   ASSOCIATION; POPULATION; MORTALITY; SERUM; MEN; RESISTANCE
AB Background Positive airway pressure (PAP) reverses obstructive sleep apnea (OSA)-related hypoxia and restores slow wave sleep (SWS). Insulin-like growth factor 1 (IGF-1) is a neuropeptide that facilitates the repair of neurons from hypoxia and improves sleep regulation. IGF-1 concentrations are lower in OSA, and likely increase following PAP treatment; however, this relationship has not yet been determined in a younger cohort of OSA patients.
   Methods This was a prospective, observational pilot study of 58 young men, who were diagnosed with OSA and provided PAP as an intervention. Adherence to PAP treatment over 3 months was objectively measured, as well as changes in the apnea-hypopnea index (AHI). Serum concentrations of IGF-1and C-reactive protein (CRP) were measured and correlated with PAP adherence.
   Results IGF-1 concentrations at baseline were similar between PAP adherent 55.5 +/- 34.4 ng/ml and PAP nonadherent participants 61.2 +/- 27.1 ng/ml (p = 0.4), with the overall mean IGF-1 concentration of 59.0 +/- 29.9 ng/ml. At follow-up, adherent participants had concentrations of IGF-1 that were significantly higher 128 +/- 59.5 ng/ml compared to nonadherent participants 86.0 +/- 47.4 ng/ml (p < 0.01). Increases in IGF-1 concentrations were significantly associated with reductions in AHI (Spearman's rho = -0.409, p = 0.015). Conversely, CRP concentrations did not differ between baseline and follow-up measurements in either group.
   Conclusions Adherence to PAP treatment leads to significant increases in IGF-1 concentrations in young men with OSA. While an objective measure of adherence exists, PAP usage does not allow for measure of sleep improvement. IGF-1 may serve as a potential biomarker for the efficacy of PAP therapy on improved sleep.
C1 [Mysliwiec, Vincent] 121st Gen Hosp, Med Specialties Clin, Unit 15281, APO AP, Seoul 962055281, South Korea.
   [Gill, Jessica] NINR, NIH, Bethesda, MD 20892 USA.
   [Matsangas, Panagiotis] Naval Postgrad Sch, Dept Operat Res, Monterey, CA 93943 USA.
   [Baxter, Tristin; Roth, Bernard J.] Madigan Army Med Ctr, Dept Pulm, Crit Care, Sleep Med, Tacoma, WA 98431 USA.
   [Barr, Taura] W Virginia Univ, Morgantown, WV 26506 USA.
RP Roth, BJ (reprint author), Madigan Army Med Ctr, Dept Pulm, Crit Care, Sleep Med, 9040A Fitzsimmons Ave, Tacoma, WA 98431 USA.
EM bernard.j.roth.civ@mail.mil
NR 38
TC 1
Z9 1
U1 2
U2 5
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1520-9512
EI 1522-1709
J9 SLEEP BREATH
JI Sleep Breath.
PD DEC
PY 2015
VL 19
IS 4
BP 1221
EP 1228
DI 10.1007/s11325-015-1142-x
PG 8
WC Clinical Neurology; Respiratory System
SC Neurosciences & Neurology; Respiratory System
GA CX5LZ
UT WOS:000365744500015
PM 25724553
ER

PT J
AU Broderick, JP
   Berkhemer, OA
   Palesch, YY
   Dippel, DWJ
   Foster, LD
   Roos, YBWEM
   van der Lugt, A
   Tomsick, TA
   Majoie, CBLM
   van Zwam, WH
   Demchuk, AM
   van Oostenbrugge, RJ
   Khatri, P
   Lingsma, HF
   Hill, MD
   Roozenbeek, B
   Jauch, EC
   Jovin, TG
   Yan, B
   von Kummer, R
   Molina, CA
   Goyal, M
   Schonewille, WJ
   Mazighi, M
   Engelter, ST
   Anderson, CS
   Spilker, J
   Carrozzella, J
   Ryckborst, KJ
   Janis, LS
   Simpson, KN
AF Broderick, Joseph P.
   Berkhemer, Olvert A.
   Palesch, Yuko Y.
   Dippel, Diederik W. J.
   Foster, Lydia D.
   Roos, Yvo B. W. E. M.
   van der Lugt, Aad
   Tomsick, Thomas A.
   Majoie, Charles B. L. M.
   van Zwam, Wim H.
   Demchuk, Andrew M.
   van Oostenbrugge, Robert J.
   Khatri, Pooja
   Lingsma, Hester F.
   Hill, Michael D.
   Roozenbeek, Bob
   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 S.
   Spilker, Judith
   Carrozzella, Janice
   Ryckborst, Karla J.
   Janis, L. Scott
   Simpson, Kit N.
CA IMS II
   MR CLEAN Investigators
TI Endovascular Therapy Is Effective and Safe for Patients With Severe
   Ischemic Stroke
SO STROKE
LA English
DT Article
DE clinical trial; endovascular procedures; stroke; tissue-type plasminogen
   activator
ID COMPUTED-TOMOGRAPHY SCORE; INTRAVENOUS T-PA; INTERVENTIONAL MANAGEMENT;
   III TRIAL; THROMBECTOMY; TIME; REPERFUSION; OUTCOMES; ONSET
AB Background and Purpose-We assessed the effect of endovascular treatment in acute ischemic stroke patients with severe neurological deficit (National Institutes of Health Stroke Scale score, >= 20) after a prespecified analysis plan.
   Methods-The pooled analysis of the Interventional Management of Stroke III (IMS III) and Multicenter Randomized Clinical Trial of Endovascular Therapy for Acute Ischemic Stroke in the Netherlands (MR CLEAN) trials included participants with an National Institutes of Health Stroke Scale score of >= 20 before intravenous tissue-type plasminogen activator (tPA) treatment (IMS III) or randomization (MR CLEAN) who were treated with intravenous tPA <= 3 hours of stroke onset. Our hypothesis was that participants with severe stroke randomized to endovascular therapy after intravenous tPA would have improved 90-day outcome (distribution of modified Rankin Scale scores), when compared with those who received intravenous tPA alone.
   Results-Among 342 participants in the pooled analysis (194 from IMS III and 148 from MR CLEAN), an ordinal logistic regression model showed that the endovascular group had superior 90-day outcome compared with the intravenous tPA group (adjusted odds ratio, 1.78; 95% confidence interval, 1.20-2.66). In the logistic regression model of the dichotomous outcome (modified Rankin Scale score, 0-2, or functional independence), the endovascular group had superior outcomes (adjusted odds ratio, 1.97; 95% confidence interval, 1.09-3.56). Functional independence (modified Rankin Scale score, <= 2) at 90 days was 25% in the endovascular group when compared with 14% in the intravenous tPA group.
   Conclusions-Endovascular therapy after intravenous tPA within 3 hours of symptom onset improves functional outcome at 90 days after severe ischemic stroke.
C1 [Broderick, Joseph P.; Tomsick, Thomas A.; Khatri, Pooja; Spilker, Judith; Carrozzella, Janice] Univ Cincinnati, Inst Neurosci, Acad Hlth Ctr, Dept Neurol & Rehabil Med, Cincinnati, OH 45267 USA.
   [Broderick, Joseph P.; Tomsick, Thomas A.; Khatri, Pooja; Spilker, Judith; Carrozzella, Janice] Univ Cincinnati, Inst Neurosci, Acad Hlth Ctr, Dept Radiol, Cincinnati, OH 45267 USA.
   [Jauch, Edward C.] Med Univ S Carolina, Div Emergency Med, Charleston, SC USA.
   [Palesch, Yuko Y.; Foster, Lydia D.] Med Univ S Carolina, Dept Publ Hlth Sci, Charleston, SC USA.
   [Simpson, Kit N.] Med Univ S Carolina, Dept Healthcare Management & Leadership, Charleston, SC USA.
   [Demchuk, Andrew M.; Hill, Michael D.; Goyal, Mayank; Ryckborst, Karla J.] Univ Calgary, Hotchkiss Brain Inst, Dept Clin Neurosci, Seaman Family MR Res Ctr,Calgary Stroke Program, Calgary, AB, Canada.
   [Demchuk, Andrew M.; Hill, Michael D.; Goyal, Mayank; Ryckborst, Karla J.] Univ Calgary, Hotchkiss Brain Inst, Dept Radiol, Calgary, AB, Canada.
   [Jovin, Tudor G.] Univ Pittsburgh, Med Ctr, Stroke Inst, Pittsburgh, PA 15260 USA.
   [Yan, Bernard] Univ Melbourne, Royal Melbourne Hosp, Melbourne Brain Ctr, Melbourne, Vic 3050, Australia.
   [von Kummer, Ruediger] Dresden Univ, Univ Hosp, Stroke Ctr, Dept Neuroradiol, Dresden, Germany.
   [Molina, Carlos A.] Hosp Univ Vall dHebron, Dept Neurol, Neurovasc Unit, Barcelona, Spain.
   [Schonewille, Wouter J.] Univ Med Ctr Utrecht, Dept Neurol, Utrecht, Netherlands.
   [Schonewille, Wouter J.] Rudolph Magnus Inst Neurosci, 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 S.] Univ Sydney, Royal Prince Alfred Hosp, George Inst Global Hlth, Sydney, NSW 2006, Australia.
   [Janis, L. Scott] NINDS, NIH, Bethesda, MD 20892 USA.
   [Berkhemer, Olvert A.; Majoie, Charles B. L. M.] Univ Amsterdam, Acad Med Ctr, Dept Radiol, NL-1105 AZ Amsterdam, Netherlands.
   [Roos, Yvo B. W. E. M.] Univ Amsterdam, Acad Med Ctr, Dept Neurol, NL-1105 AZ Amsterdam, Netherlands.
   [Dippel, Diederik W. J.; Roozenbeek, Bob] Erasmus MC Univ, Med Ctr, Dept Neurol, Rotterdam, Netherlands.
   [van der Lugt, Aad] Erasmus MC Univ, Med Ctr, Dept Radiol, Rotterdam, Netherlands.
   [Dippel, Diederik W. J.; Roozenbeek, Bob] Erasmus MC Univ, Med Ctr, Dept Publ Hlth, Rotterdam, Netherlands.
   [van Zwam, Wim H.] Maastricht Univ, Med Ctr, Cardiovasc Res Inst Maastricht CARIM, Dept Radiol, Maastricht, Netherlands.
   [van Oostenbrugge, Robert J.] Maastricht Univ, Med Ctr, Cardiovasc Res Inst Maastricht CARIM, Dept Neurol, Maastricht, Netherlands.
RP Broderick, JP (reprint author), Univ Cincinnati, Inst Neurosci, Dept Neurol, 260 Stetson St,Suite 2300,POB 670525, Cincinnati, OH 45267 USA.
EM joseph.broderick@uc.edu
FU National Institutes of Health/National Institute of Neurological
   Disorders and Stroke [U01NS052220, U01NS054630, U01NS077304]; Dutch
   Heart Foundation; AngioCare BV; Covidien/EV3R; MEDAC Gmbh/LAMEPRO;
   Penumbra Inc.
FX The Interventional Management of Stroke III (IMS III) trial was funded
   by National Institutes of Health/National Institute of Neurological
   Disorders and Stroke grant numbers: University of Cincinnati
   (U01NS052220) and Medical University of South Carolina (U01NS054630 and
   U01NS077304). Genentech Inc supplied study drug used for intra-arterial
   tissue-type plasminogen activator treatment in the Endovascular group.
   EKOS Corp, Concentric Inc, and Cordis Neurovascular Inc supplied study
   catheters during Protocol Versions 1 to 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. The Multicenter
   Randomized Clinical Trial of Endovascular Therapy for Acute Ischemic
   Stroke in the Netherlands (MR CLEAN) trial was funded by the Dutch Heart
   Foundation and through unrestricted grants from AngioCare BV,
   Covidien/EV3R, MEDAC Gmbh/LAMEPRO, and Penumbra Inc.
NR 27
TC 6
Z9 6
U1 0
U2 6
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 DEC
PY 2015
VL 46
IS 12
BP 3416
EP 3422
DI 10.1161/STROKEAHA.115.011397
PG 7
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA CX2NS
UT WOS:000365534400012
PM 26486865
ER

PT J
AU Sheth, KN
   Martini, SR
   Moomaw, CJ
   Koch, S
   Elkind, MS
   Sung, G
   Kittner, SJ
   Frankel, M
   Rosand, J
   Langefeld, CD
   Comeau, ME
   Waddy, SP
   Osborne, J
   Woo, D
AF Sheth, Kevin N.
   Martini, Sharyl R.
   Moomaw, Charles J.
   Koch, Sebastian
   Elkind, Mitchell S. V.
   Sung, Gene
   Kittner, Steven J.
   Frankel, Michael
   Rosand, Jonathan
   Langefeld, Carl D.
   Comeau, Mary E.
   Waddy, Salina P.
   Osborne, Jennifer
   Woo, Daniel
CA ERICH Investigators
TI Prophylactic Antiepileptic Drug Use and Outcome in the Ethnic/Racial
   Variations of Intracerebral Hemorrhage Study
SO STROKE
LA English
DT Article
DE cerebral hemorrhage; critical care; hematoma; seizures; stroke
ID STROKE-ASSOCIATION; GUIDELINES; MANAGEMENT; ICH
AB Background and Purpose-The role of antiepileptic drug (AED) prophylaxis after intracerebral hemorrhage (ICH) remains unclear. This analysis describes prevalence of prophylactic AED use, as directed by treating clinicians, in a prospective ICH cohort and tests the hypothesis that it is associated with poor outcome.
   Methods-Analysis included 744 patients with ICH enrolled in the Ethnic/Racial Variations of Intracerebral Hemorrhage (ERICH) study before November 2012. Baseline clinical characteristics and AED use were recorded in standardized fashion. ICH location and volume were recorded from baseline neuroimaging. We analyzed differences in patient characteristics by AED prophylaxis, and we used logistic regression to test whether AED prophylaxis was associated with poor outcome. The primary outcome was 3-month modified Rankin Scale score, with 4 to 6 considered poor outcome.
   Results-AEDs were used for prophylaxis in 289 (39%) of the 744 subjects; of these, levetiracetam was used in 89%. Patients with lobar ICH, craniotomy, or larger hematomas were more likely to receive prophlyaxis. Although prophylactic AED use was associated with poor outcome in an unadjusted model (odds ratio, 1.40; 95% confidence interval, 1.04-1.88; P=0.03), this association was no longer significant after adjusting for clinical and demographic characteristics (odds ratio, 1.11; 95% confidence interval, 0.74-1.65; P=0.62).
   Conclusions-We found no evidence that AED use (predominantly levetiracetam) is independently associated with poor outcome. A prospective study is required to assess for a more modest effect of AED use on outcome after ICH.
C1 [Sheth, Kevin N.] Yale Univ, Sch Med, Dept Neurol, New Haven, CT 06510 USA.
   [Martini, Sharyl R.] Baylor Coll Med, Dept Neurol, Houston, TX 77030 USA.
   [Moomaw, Charles J.; Osborne, Jennifer; Woo, Daniel] Univ Cincinnati, Dept Neurol & Rehabil Med, Cincinnati, OH 45221 USA.
   [Koch, Sebastian] Univ Miami, Sch Med, Dept Neurol, Miami, FL USA.
   [Elkind, Mitchell S. V.] Columbia Univ Coll Phys & Surg, Dept Neurol, New York, NY 10032 USA.
   [Sung, Gene] Univ So Calif, Dept Neurol, Los Angeles, CA USA.
   [Kittner, Steven J.] Univ Maryland, Sch Med, Dept Neurol, Baltimore, MD 21201 USA.
   [Frankel, Michael] Emory Univ, Sch Med, Dept Neurol, Atlanta, GA 30322 USA.
   [Rosand, Jonathan] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
   [Langefeld, Carl D.; Comeau, Mary E.] Wake Forest Sch Med, Dept Biostat Sci, Winston Salem, NC USA.
   [Langefeld, Carl D.; Comeau, Mary E.] Wake Forest Sch Med, Ctr Publ Hlth Genom, Winston Salem, NC USA.
   [Waddy, Salina P.] NINDS, Off Clin Res, Bethesda, MD 20892 USA.
RP Sheth, KN (reprint author), 15 York St,LCI 1003, New Haven, CT 06510 USA.
EM kevin.sheth@yale.edu
FU National Institute of Neurological Disorders and Stroke [NINDS:
   U-01-NS069763]
FX This study was supported by a grant from the National Institute of
   Neurological Disorders and Stroke (NINDS: U-01-NS069763).
NR 13
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 0039-2499
EI 1524-4628
J9 STROKE
JI Stroke
PD DEC
PY 2015
VL 46
IS 12
BP 3532
EP 3535
DI 10.1161/STROKEAHA.115.010875
PG 4
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA CX2NS
UT WOS:000365534400026
PM 26470777
ER

PT J
AU Battal, D
   Barnes, AJ
   Castaneto, MS
   Martin, TM
   Klette, KL
   Huestis, MA
AF Battal, Dilek
   Barnes, Allan J.
   Castaneto, Marisol S.
   Martin, Thomas M.
   Klette, Kevin L.
   Huestis, Marilyn A.
TI Urine Mescaline Screening With a Biochip Array Immunoassay and
   Quantification by Gas Chromatography-Mass Spectrometry
SO THERAPEUTIC DRUG MONITORING
LA English
DT Article
DE mescaline; peyote; GC; MS; herbal drugs; urine
ID HUMAN BLOOD-PLASMA; VALIDATED QUANTIFICATION; HALLUCINOGENS; DRUGS;
   RATS; TECHNOLOGY; DERIVATIVES; AGGRESSION; PSILOCYBIN; LSD-25
AB Mescaline, the primary psychoactive chemical in peyote cactus, has been consumed for thousands of years in ancient religious ceremonies. The US military wanted to determine if mescaline intake was a problem for personnel readiness. Twenty thousand seventeen urine specimens negative for cannabinoids, cocaine, opiates, and amphetamines were tested for mescaline with the Randox Drugs of Abuse V (DOA-V) biochip array immunoassay at the manufacturer's recommended cutoff of 6 mcg/L. A sensitive and specific method for mescaline quantification in urine was developed and fully validated. Extracted analytes were derivatized with pentafluoropropionic anhydride and pentafluoropropanol and quantified by gas chromatography-mass spectrometry (GC/MS) with electron impact ionization. Standard curves, using linear least squares regression with 1/x(2) weighting, were linear from 1 to 250 mcg/L with coefficients of determination >0.994. Intra- and inter-assay imprecision was <4.4 coefficient of variation (%CV), with accuracies >90.4%. Mean extraction efficiencies were >92.0% across the linear range. This fully validated method was applied for the confirmation of urinary mescaline in 526 presumptive-positive specimens and 198 randomly selected presumptive-negative specimens at the manufacturer's 6 mcg/L cutoff. No specimen confirmed positive at the GC/MS limit of quantification of 1 mcg/L. Results indicated that during this time frame, there was insufficient mescaline drug use in the military to warrant routine screening in the drug testing program. However, mescaline stability, although assessed, could have contributed to lower prevalence. We also present a validated GC/MS method for mescaline quantification in urine for reliable confirmation of suspected mescaline intake.
C1 [Battal, Dilek] Mersin Univ, Fac Pharm, Dept Toxicol, Mersin, Turkey.
   [Barnes, Allan J.; Castaneto, Marisol S.; Huestis, Marilyn A.] NIDA, Chem & Drug Metab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
   [Martin, Thomas M.; Klette, Kevin L.] Off Secretary Def Operat Readiness & Safety, Drug Testing & Program Policy, Washington, DC USA.
RP Huestis, MA (reprint author), NIDA, Chem & Drug Metab, IRP, Biomed Res Ctr,NIH, 251 Bayview Blvd,Suite 200,Room 05A-721, Baltimore, MD 21224 USA.
EM mhuestis@intra.nida.nih.gov
NR 40
TC 0
Z9 0
U1 5
U2 12
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0163-4356
EI 1536-3694
J9 THER DRUG MONIT
JI Ther. Drug Monit.
PD DEC
PY 2015
VL 37
IS 6
BP 805
EP 811
DI 10.1097/FTD.0000000000000220
PG 7
WC Medical Laboratory Technology; Pharmacology & Pharmacy; Toxicology
SC Medical Laboratory Technology; Pharmacology & Pharmacy; Toxicology
GA CX3JI
UT WOS:000365594600016
PM 25992796
ER

PT J
AU Keane, KA
   Parker, GA
   Regan, KS
   Picut, C
   Dixon, D
   Creasy, D
   Giri, D
   Hukkanen, RR
AF Keane, Kevin A.
   Parker, George A.
   Regan, Karen S.
   Picut, Catherine
   Dixon, Darlene
   Creasy, Dianne
   Giri, Dipak
   Hukkanen, Renee R.
TI Scientific and Regulatory Policy Committee (SRPC) Points to Consider:
   Histopathology Evaluation of the Pubertal Development and Thyroid
   Function Assay (OPPTS 890.1450, OPPTS 890.1500) in Rats to Screen for
   Endocrine Disruptors
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE EPA; endocrine disruptor screening program; pubertal development;
   thyroid function; OPPTS 890; 1450; OPPTS 890; 1500
ID MAMMARY-GLAND DEVELOPMENT; EDSTAC RECOMMENDATIONS; REPRODUCTIVE
   HORMONES; PREPUBERTAL EXPOSURES; TOXICOLOGIC PATHOLOGY; CIRCULATING
   HORMONES; JOINT PUBLICATION; SEXUAL-MATURATION; REVISED GUIDES; 1ST
   OVULATION
AB The U.S. Environmental Protection Agency Endocrine Disruptor Screening Program (EDSP) is a multitiered approach to determine the potential for environmental chemicals to alter the endocrine system. The Pubertal Development and Thyroid Function in Intact Juvenile/Peripubertal Female and Male Rats (OPPTS 890.1450, 890.1500) are 2 of the 9 EDSP tier 1 test Guidelines, which assess upstream mechanistic pathways along with downstream morphological end points including histological evaluation of the kidneys, thyroid, and select male/female reproductive tissues (ovaries, uterus, testes, and epididymides). These assays are part of a battery of in vivo and in vitro screens used for initial detection of test article endocrine activity. In this Points to Consider article, we describe tissue processing, evaluation, and nomenclature to aid in standardization of assay results across laboratories. Pubertal assay end points addressed include organ weights, estrous cyclicity, clinical pathology, hormonal assays, and histological evaluation. Potential treatment-related findings that may indicate endocrine disruption are reviewed. Additional tissues that may be useful in assessment of endocrine disruption (vagina, mammary glands, and liver) are discussed. This Points to Consider article is intended to provide information for evaluating peripubertal tissues within the context of individual assay end points, the overall pubertal assay, and tier I assays of the EDSP program.
C1 [Keane, Kevin A.] Novo Nordisk, Beijing, Peoples R China.
   [Parker, George A.; Picut, Catherine] WIL Res, Hillsborough, NC 27278 USA.
   [Regan, Karen S.] Regan Path Tox Serv Inc, Ashland, OH USA.
   [Dixon, Darlene] NIEHS, Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
   [Creasy, Dianne] Dianne Creasy Consulting LLC, Pipersville, PA USA.
   [Giri, Dipak] Integrated Syst Lab, Raleigh, NC USA.
   [Hukkanen, Renee R.] Dow Chem Co USA, Midland, MI 48674 USA.
   [Hukkanen, Renee R.] Univ Washington, Dept Comparat Med, Seattle, WA 98195 USA.
RP Parker, GA (reprint author), WIL Res, 310 Millstone Dr, Hillsborough, NC 27278 USA.
EM george.parker@wilresearch.com
FU Intramural NIH HHS [Z01 ES021196-15]
NR 79
TC 4
Z9 4
U1 1
U2 5
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
EI 1533-1601
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD DEC
PY 2015
VL 43
IS 8
BP 1047
EP 1063
DI 10.1177/0192623315579943
PG 17
WC Pathology; Toxicology
SC Pathology; Toxicology
GA CX5JT
UT WOS:000365738600002
PM 25948506
ER

PT J
AU Harvey, JB
   Osborne, TS
   Hong, HHL
   Bhusari, S
   Ton, TV
   Pandiri, AR
   Masinde, T
   Dunnick, J
   Peddada, S
   Elmore, S
   Hoenerhoff, MJ
AF Harvey, Janice B.
   Osborne, Tanasa S.
   Hong, Hue-Hua L.
   Bhusari, Sachin
   Ton, Tai-Vu
   Pandiri, Arun R.
   Masinde, Tiwanda
   Dunnick, June
   Peddada, Shyamal
   Elmore, Susan
   Hoenerhoff, Mark J.
TI Uterine Carcinomas in Tetrabromobisphenol A-exposed Wistar Han Rats
   Harbor Increased Tp53 Mutations and Mimic High-grade Type I Endometrial
   Carcinomas in Women
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE tetrabromobisphenol A; dometrial carcinoma; Tp53; Ctnnb1; Kras; Ccnd1;
   Her2; Cdh1; Wistar Han rats
ID MOLECULAR PATHOLOGY; ALLELIC IMBALANCE; P53 GENE; CANCER;
   ADENOCARCINOMA; CLASSIFICATION; CARCINOGENICITY; HYPERPLASIA;
   EXPRESSION; PROFILES
AB Endometrial carcinoma is the most common gynecologic malignancy is the United States and accounts for 6% of all cancers in women. The disease is classified as type I or type II based on clinicopathologic and molecular features. It is a multifactorial disease with a number of risk factors, including environmental exposures. How environmental exposures, such as flame retardants, may affect the incidence of endometrial cancer is a topic of current and ongoing interest. Tetrabromobisphenol A (TBBPA) is a widely used brominated flame retardant found in a variety of household products. A recent 2-year National Toxicology Program carcinogenicity study found that exposure to TBBPA was associated with a marked increase in the development of uterine tumors, specifically uterine carcinomas, in Wistar Han rats. Molecularly, TBBPA-induced uterine carcinomas in Wistar Han rats were characterized by a marked increase in tumor protein 53 mutation compared to spontaneous uterine carcinomas, as well as overexpression of human epidermal growth factor receptor 2. Similar to spontaneous carcinomas, tumors in TBBPA-exposed rats were estrogen receptor-alpha positive and progesterone receptor negative by immunohistochemistry. The morphologic and molecular features of uterine carcinomas in TBBPA-exposed rats resemble those of high-grade type I tumors in women, and these data suggest that exposure to TBBPA may pose an increased cancer risk.
C1 [Harvey, Janice B.; Osborne, Tanasa S.; Hong, Hue-Hua L.; Bhusari, Sachin; Ton, Tai-Vu; Masinde, Tiwanda; Elmore, Susan; Hoenerhoff, Mark J.] NIEHS, Div Natl Toxicol Program, Cellular & Mol Pathol Branch, Res Triangle Pk, NC 27709 USA.
   [Harvey, Janice B.] N Carolina State Univ, Coll Vet Med, Raleigh, NC USA.
   [Pandiri, Arun R.] Expt Pathol Labs, Res Triangle Pk, NC USA.
   [Dunnick, June] NIEHS, Expt Toxicol Branch, Div Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
   [Peddada, Shyamal] NIEHS, Biostat Branch, Div Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
RP Osborne, TS (reprint author), NIEHS, Natl Toxicol Program, B361 Rall Bldg, Res Triangle Pk, NC 27709 USA.
EM osbornet@niehs.nih.gov
FU National Institutes of Environmental Health Sciences (NIEHS), National
   Institutes of Health (NIH); Division of the National Toxicology Program
   (DNTP)
FX The author(s) disclosed receipt of the following financial support for
   the research, authorship, and/or publication of this article: This work
   was supported by the National Institutes of Environmental Health
   Sciences (NIEHS), National Institutes of Health (NIH), and the Division
   of the National Toxicology Program (DNTP).
NR 39
TC 3
Z9 3
U1 2
U2 11
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
EI 1533-1601
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD DEC
PY 2015
VL 43
IS 8
BP 1103
EP 1113
DI 10.1177/0192623315599256
PG 11
WC Pathology; Toxicology
SC Pathology; Toxicology
GA CX5JT
UT WOS:000365738600006
PM 26353976
ER

PT J
AU Bhusari, S
   Pandiri, AR
   Nagai, H
   Wang, Y
   Foley, J
   Hong, HHL
   Ton, TV
   DeVito, M
   Shockley, KR
   Peddada, SD
   Gerrish, KE
   Malarkey, DE
   Hooth, MJ
   Sills, RC
   Hoenerhoff, MJ
AF Bhusari, Sachin
   Pandiri, Arun R.
   Nagai, Hiroaki
   Wang, Yu
   Foley, Julie
   Hong, Hue-Hua L.
   Ton, Thai-Vu
   DeVito, Michael
   Shockley, Keith R.
   Peddada, Shyamal D.
   Gerrish, Kevin E.
   Malarkey, David E.
   Hooth, Michelle J.
   Sills, Robert C.
   Hoenerhoff, Mark J.
TI Genomic Profiling Reveals Unique Molecular Alterations in
   Hepatoblastomas and Adjacent Hepatocellular Carcinomas in B6C3F1 Mice
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE carcinogenesis; liver; genomics; microarray; molecular pathology; rodent
   pathology; toxicologic pathology
ID HEDGEHOG SIGNALING PATHWAY; WNT/BETA-CATENIN; LIVER-TUMORS;
   PROSTATE-CANCER; STEM-CELLS; GENE; MUTATIONS; EXPRESSION; MOUSE;
   CARCINOGENESIS
AB The cell of origin of hepatoblastoma (HB) in humans and mice is unknown; it is hypothesized to be a transformed hepatocyte, oval cell, or hepatic progenitor cell. In mice, current dogma is that HBs arise from preexisting hepatocellular neoplasms as a result of further neoplastic transformation. However, there is little evidence supporting this direct relationship. To better understand the relationship between hepatocellular carcinoma (HCC) and HB and determine molecular similarities between mouse and human HB, global gene expression analysis and targeted mutation analysis were performed using HB, HCC, and adjacent liver from the same animals in a recent National Toxicology Program bioassay. There were significant differences in Hras and Ctnnb1 mutation spectra, and by microarray, HBs showed dysregulation of embryonic development, stem cell pluripotency, and genomic imprinting compared to HCC. Meta-analysis showed similarities between HB, early mouse embryonic liver, and hepatocyte-derived stem/progenitor cells compared to HCC. Our data show that there are striking differences between HB and HCC and suggest that HB is a significantly different entity that may arise from a hepatic precursor cell. Furthermore, mouse HB is similar to the human disease at the pathway level and therefore is likely a relevant model for evaluating human cancer hazard.
C1 [Bhusari, Sachin; Pandiri, Arun R.; Nagai, Hiroaki; Wang, Yu; Foley, Julie; Hong, Hue-Hua L.; Ton, Thai-Vu; Malarkey, David E.; Sills, Robert C.; Hoenerhoff, Mark J.] NIEHS, Cellular & Mol Pathol Branch, Res Triangle Pk, NC 27709 USA.
   [Pandiri, Arun R.] Expt Pathol Labs, Res Triangle Pk, NC USA.
   [DeVito, Michael] NIEHS, Toxicol Branch, Div Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
   [Shockley, Keith R.; Peddada, Shyamal D.] NIEHS, Biostat & Computat Biol Branch, Res Triangle Pk, NC 27709 USA.
   [Gerrish, Kevin E.] NIEHS, Mol Genom Core, Res Triangle Pk, NC 27709 USA.
   [Hooth, Michelle J.] Div Natl Toxicol Program, Program Operat Branch, Res Triangle Pk, NC USA.
RP Hoenerhoff, MJ (reprint author), Univ Michigan, Sch Med, Unit Lab Anim Med, Vivo Anim Core, North Campus Res Complex,2800 Plymouth Rd,Bldg 36, Ann Arbor, MI 48103 USA.
EM hoenerho@med.umich.edu
FU Intramural NIH HHS [Z99 ES999999]
NR 49
TC 1
Z9 1
U1 0
U2 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
EI 1533-1601
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD DEC
PY 2015
VL 43
IS 8
BP 1114
EP 1126
DI 10.1177/0192623315599853
PG 13
WC Pathology; Toxicology
SC Pathology; Toxicology
GA CX5JT
UT WOS:000365738600007
PM 26289556
ER

PT J
AU Malarkey, DE
   Willson, GA
   Willson, CJ
   Adams, ET
   Olson, GR
   Witt, WM
   Elmore, SA
   Hardisty, JF
   Boyle, MC
   Crabbs, TA
   Miller, RA
AF Malarkey, David E.
   Willson, Gabrielle A.
   Willson, Cynthia J.
   Adams, E. Terence
   Olson, Greg R.
   Witt, William M.
   Elmore, Susan A.
   Hardisty, Jerry F.
   Boyle, Michael C.
   Crabbs, Torrie A.
   Miller, Rodney A.
TI Utilizing Whole Slide Images for Pathology Peer Review and Working
   Groups
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE digital images; digital pathology; digital slides; pathology working
   group; peer review; whole slide images; whole slide imaging
AB This article describes the results of comparisons of digitally scanned whole slide images (WSIs) and glass microscope slides for diagnosis of tissues under peer review by the National Toxicology Program. Findings in this article were developed as a result of the data collected from 6 pathology working groups (PWGs), 1 pathology peer review, and survey comments from over 25 participating pathologists. For each PWG, 6-14 pathologists examined 10-143 tissues per study from 6- and 9-month perinatal studies and 2-year carcinogenicity studies. Overall it was found that evaluation of WSIs is generally equivalent to using glass slides. Concordance of PWG consensus diagnoses based upon review of WSIs versus glass slides ranged from 74% to 100% (median 86%). The intra- and interobserver diagnostic variation did not appear to influence the conclusions of any study. Based upon user opinions collected from surveys, WSIs may be less optimal than glass slides for evaluation of subtle lesions, large complex lesions, small lesions in a large section of tissue, and foci of altered hepatocytes. These results indicate that, although there may be some limitations, the use of WSIs can effectively accomplish the objectives of a conventional glass slide review and definitely serves as a useful adjunct to the conduct of PWGs.
C1 [Malarkey, David E.; Elmore, Susan A.] NIEHS, Natl Toxicol Program, Cellular & Mol Pathol Branch, Res Triangle Pk, NC 27709 USA.
   [Willson, Gabrielle A.; Hardisty, Jerry F.; Crabbs, Torrie A.; Miller, Rodney A.] Expt Pathol Labs Inc, Res Triangle Pk, NC USA.
   [Willson, Cynthia J.; Adams, E. Terence] Integrated Lab Syst Inc, Res Triangle Pk, NC USA.
   [Olson, Greg R.; Witt, William M.] Toxicol Pathol Associates, Jefferson, AR USA.
   [Boyle, Michael C.] Amgen Inc, Thousand Oaks, CA 91320 USA.
RP Malarkey, DE (reprint author), NIEHS, MD B3-06,POB 12233, Res Triangle Pk, NC 27709 USA.
EM malarkey@niehs.nih.gov
FU NIH, National Institute of Environmental Health Sciences
FX The author(s) disclosed receipt of the following financial support for
   the research, authorship, and/or publication of this article: This work
   was supported by the NIH, National Institute of Environmental Health
   Sciences.
NR 6
TC 0
Z9 0
U1 1
U2 3
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
EI 1533-1601
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD DEC
PY 2015
VL 43
IS 8
BP 1149
EP 1157
DI 10.1177/0192623315605933
PG 9
WC Pathology; Toxicology
SC Pathology; Toxicology
GA CX5JT
UT WOS:000365738600010
PM 26511845
ER

PT J
AU Remick, AK
   Catlin, NR
   Quist, EM
   Steinbach, TJ
   Dixon, D
AF Remick, Amera K.
   Catlin, Natasha R.
   Quist, Erin M.
   Steinbach, Thomas J.
   Dixon, Darlene
TI Juvenile Toxicology: Relevance and Challenges for Toxicologists and
   Pathologists
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE developmental pathology; pediatrics; pharmaceutical development;
   products; preclinical safety assessment; risk management; toxicologic
   pathology; drug development
ID PEDIATRIC DRUG DEVELOPMENT; NONHUMAN-PRIMATES; DEVELOPMENTAL TOXICITY;
   BISPHENOL-A; NEUROENDOCRINE PARAMETERS; POSTNATAL-DEVELOPMENT;
   REPRODUCTIVE-SYSTEM; IMMUNE-RESPONSES; MACACA-MULATTA; NERVOUS-SYSTEM
AB The Society of Toxicologic Pathology (STP) Education Committee and the STP Reproductive Special Interest Group held a North Carolina regional meeting entitled, Juvenile Toxicology: Relevance and Challenges for Toxicologists and Pathologists on March 13, 2015, at the National Institute of Environmental Health Sciences/National Toxicology Program in Research Triangle Park, North Carolina. The purpose of this regional meeting was to familiarize attendees with the topic of juvenile toxicity testing and discuss its relevance to clinical pediatric medicine, regulatory perspectives, challenges of appropriate study design confronted by toxicologists, and challenges of histopathologic examination and interpretation of juvenile tissues faced by pathologists. The 1-day meeting was a success with over 60 attendees representing industry, government, research organizations, and academia.
C1 [Remick, Amera K.] WIL Res, Hillsborough, NC USA.
   [Catlin, Natasha R.] Natl Inst Environm Hlth Sci, Toxicol Branch, Dev & Reprod Toxicol Grp, Natl Toxicol Program NTP Div, Res Triangle Pk, NC USA.
   [Quist, Erin M.] Natl Inst Environm Hlth Sci, Reprod Endocrinol Grp, NTPL, Res Triangle Pk, NC USA.
   [Quist, Erin M.] Natl Inst Environm Hlth Sci, Cellular & Mol Pathol Branch, NTP Div, NTP Pathol Grp, Res Triangle Pk, NC USA.
   [Steinbach, Thomas J.] Expt Pathol Labs Inc, Durham, NC USA.
   [Dixon, Darlene] Natl Inst Environm Hlth Sci, Mol Pathogenesis Grp, NTPL, Res Triangle Pk, NC USA.
RP Remick, AK (reprint author), WIL Res Pathol, 310 Millstone Dr, Hillsborough, NC 27278 USA.
EM amera.remick@wilresearch.com
FU Intramural NIH HHS [ZIA ES021196-16, Z01 ES021196-15]
NR 72
TC 0
Z9 0
U1 1
U2 7
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
EI 1533-1601
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD DEC
PY 2015
VL 43
IS 8
BP 1166
EP 1171
DI 10.1177/0192623315595883
PG 6
WC Pathology; Toxicology
SC Pathology; Toxicology
GA CX5JT
UT WOS:000365738600013
PM 26220944
ER

PT J
AU Knudsen, GA
   Hughes, MF
   McIntosh, KL
   Sanders, JM
   Birnbaum, LS
AF Knudsen, Gabriel A.
   Hughes, Michael F.
   McIntosh, Katelyn L.
   Sanders, J. Michael
   Birnbaum, Linda S.
TI Estimation of tetrabromobisphenol A (TBBPA) percutaneous uptake in
   humans using the parallelogram method
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE Dermal bioavailability; Brominated flame retardant; Tetrabromobisphenol
   A; Parallelogram method; Persistent organic pollutant
ID VITRO DERMAL ABSORPTION; SPRAGUE-DAWLEY RATS; IN-VITRO; FLAME
   RETARDANTS; BISPHENOL-A; HOUSE-DUST; EXPOSURE; SKIN; DISPOSITION; VIVO
AB Tetrabromobisphenol A (TBBPA) is currently the world's highest production volume brominated flame retardant. Humans are frequently exposed to TBBPA by the dermal route. In the present study, a parallelogram approach was used to make predictions of internal dose in exposed humans. Human and rat skin samples received 100 nmol of TBBPA/cm(2) skin and absorption and penetrance were determined using a flow-through in vitro system. TBBPA-derived [C-14]-radioactivity was determined at 6 h intervals in the media and at 24 h post-dosing in the skin. The human skin and media contained an average of 3.4% and 0.2% of the total dose at the terminal time point respectively, while the rat skin and media contained 9.3% and 3.5%, respectively. In the intact rat, 14% of a dermally-administered dose of similar to 100 nmol/cm(2) remained in the skin at the dosing site, with an additional 8% reaching systemic circulation by 24 h post-dosing. Relative absorption and penetrance were less (10% total) at 24 h following dermal administration of a ten-fold higher dose (similar to 1000 nmol/cm(2)) to rats. However, by 72 h, 70% of this dose was either absorbed into the dosing-site skin or had reached systemic circulation. It is clear from these results that TBBPA can be absorbed by the skin and dermal contact with TBBPA may represent a small but important route of exposure. Together, these in vitro data in human and rat skin and in vivo data from rats may be used to predict TBBPA absorption in humans following dermal exposure. Based on this parallelogram calculation, up to 6% of dermally applied TBBPA may be bioavailable to humans exposed to TBBPA. Published by Elsevier Inc.
C1 [Knudsen, Gabriel A.; McIntosh, Katelyn L.; Sanders, J. Michael; Birnbaum, Linda S.] NIEHS, NCI, Res Triangle Pk, NC 27709 USA.
   [Hughes, Michael F.] US EPA, Integrated Syst Toxicol Div, Natl Hlth & Environm Effects Res Lab, Off Res & Dev, Res Triangle Pk, NC 27711 USA.
RP Knudsen, GA (reprint author), 111 T W Alexander Dr,BG 101 C202A, Res Triangle Pk, NC 27709 USA.
EM gabriel.knudsen@nih.gov
OI Knudsen, Gabriel/0000-0002-7208-6451
FU NIH/NCI [ZIA BC 011476]
FX The authors would like to thank Ms. Brenda Edwards, Mr. Vivek Miyani,
   Mr. Rohil Chekuri, Mr. Ethan Hull, and Mr. Abdella Sadik for technical
   assistance. This article has been reviewed in accordance with the policy
   of the National Health and Environmental Effects Research Laboratory,
   U.S. Environmental Protection Agency, and approved publication. Approval
   does not signify that the contents necessarily reflect the views and
   policies of the Agency, nor does mention of trade names or commercial
   products constitute endorsement or recommendation for use. This research
   was supported in part by the Intramural Research Program of NIH/NCI (ZIA
   BC 011476).
NR 49
TC 1
Z9 1
U1 3
U2 19
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0041-008X
EI 1096-0333
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD DEC 1
PY 2015
VL 289
IS 2
BP 323
EP 329
DI 10.1016/j.taap.2015.09.012
PG 7
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA CX1NC
UT WOS:000365461900019
PM 26387765
ER

PT J
AU George, PJ
   Kumar, NP
   Jaganathan, J
   Dolla, C
   Kumaran, P
   Nair, D
   Banurekha, VV
   Shen, K
   Nutman, TB
   Babu, S
AF George, Parakkal Jovvian
   Kumar, Nathella Pavan
   Jaganathan, Jeeva
   Dolla, Chandrakumar
   Kumaran, Paul
   Nair, Dina
   Banurekha, Vaithilingam V.
   Shen, Kui
   Nutman, Thomas B.
   Babu, Subash
TI Modulation of pro- and anti-inflammatory cytokines in active and latent
   tuberculosis by coexistent Strongyloides stercoralis infection
SO TUBERCULOSIS
LA English
DT Article
DE Tuberculosis; Strongyloides; Helminths; Cytokines
ID MYCOBACTERIUM-TUBERCULOSIS; COINCIDENT FILARIAL; HELMINTH-PARASITES;
   IMMUNITY; TB; MECHANISMS; BIOMARKERS; PATHOGENS; RESPONSES; THERAPY
AB Helminth infections are known to induce modulation of both innate and adaptive immune responses in active and latent tuberculosis (TB). However, the role of helminth infections in modulating systemic cytokine responses in active and latent tuberculosis (LTB) is not known. To define the systemic cytokine levels in helminth-TB coinfection, we measured the circulating plasma levels of Type 1, Type 2, Type 17, other pro-inflammatory and regulatory cytokines in individuals with active TB (ATB) with or without coexistent Strongyloides stercoralis (Ss) infection by multiplex ELISA. Similarly, we also measured the same cytokine levels in individuals with LTB with or without concomitant Ss infection in a cross-sectional study. Our data reveal that individuals with ATB or LTB and coexistent Ss infection have significantly lower levels of Type 1 (IFN gamma, TNF alpha and IL-2) and Type 17 (IL-17A and IL-17F) cytokines compared to those without Ss infection. In contrast, those with ATB and LTB with Ss infection have significantly higher levels of the regulatory cytokines (IL-10 and TGF beta), and those with LTB and Ss infection also have significantly higher levels of Type 2 cytokines (IL-4, IL-5 and IL-13) as well. Finally, those with LTB (but not ATB) exhibit significantly lower levels of other pro-inflammatory cytokines (IFN alpha, IFN beta, IL-6, IL-12 and GM-CSF). Our data therefore reveal a profound effect of Ss infection on the systemic cytokine responses in ATB and LTB and indicate that coincident helminth infections might influence pathogenesis of TB infection and disease. Published by Elsevier Ltd.
C1 [George, Parakkal Jovvian; Kumar, Nathella Pavan; Jaganathan, Jeeva; Babu, Subash] Natl Inst Res TB, ICER, NIH, Chennai 600031, Tamil Nadu, India.
   [Dolla, Chandrakumar; Kumaran, Paul; Nair, Dina; Banurekha, Vaithilingam V.] Natl Inst Res TB, Chennai 600031, Tamil Nadu, India.
   [Shen, Kui] NIAID, Bioinformat & Computat Biosci Branch, NIH, Bethesda, MD 20892 USA.
   [Nutman, Thomas B.; Babu, Subash] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Babu, S (reprint author), Natl Inst Res TB, ICER, NIH, Chennai 600031, Tamil Nadu, India.
EM sbabu@mail.nih.gov
FU Intramural NIH HHS [Z99 AI999999]
NR 34
TC 3
Z9 3
U1 2
U2 4
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
   LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 1472-9792
J9 TUBERCULOSIS
JI Tuberculosis
PD DEC
PY 2015
VL 95
IS 6
BP 822
EP 828
DI 10.1016/j.tube.2015.09.009
PG 7
WC Immunology; Microbiology; Respiratory System
SC Immunology; Microbiology; Respiratory System
GA CX3UZ
UT WOS:000365626300026
PM 26542223
ER

PT J
AU Keadle, SK
   Moore, SC
   Sampson, JN
   Xiao, Q
   Albanes, D
   Matthews, CE
AF Keadle, Sarah K.
   Moore, Steven C.
   Sampson, Joshua N.
   Xiao, Qian
   Albanes, Demetrius
   Matthews, Charles E.
TI Causes of Death Associated With Prolonged TV Viewing NIH-AARP Diet and
   Health Study
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID RETIRED-PERSONS DIET; ALL-CAUSE MORTALITY; SEDENTARY BEHAVIOR;
   PHYSICAL-ACTIVITY; DIABETES-MELLITUS; CARDIOVASCULAR-DISEASE;
   AMERICAN-ASSOCIATION; NATIONAL-INSTITUTES; ENERGY-INTAKE; OLDER WOMEN
AB Introduction: TV viewing is the most prevalent sedentary behavior and is associated with increased risk of cardiovascular disease and cancer mortality, but the association with other leading causes of death is unknown. This study examined the association between TV viewing and leading causes of death in the U.S.
   Methods: A prospective cohort of 221,426 individuals (57% male) aged 50-71 years who were free of chronic disease at baseline (1995-1996), 93% white, with an average BMI of 26.7 (SD=4.4) kg/m(2) were included. Participants self-reported TV viewing at baseline and were followed until death or December 31, 2011. Hazard ratios (HRs) and 95% CIs for TV viewing and cause-specific mortality were estimated using Cox proportional hazards regression. Analyses were conducted in 2014-2015.
   Results: After an average follow-up of 14.1 years, adjusted mortality risk for a 2-hour/day increase in TV viewing was significantly higher for the following causes of death (HR [95% CI]): cancer (1.07 [1.03, 1.11]); heart disease (1.23 [1.17, 1.29]); chronic obstructive pulmonary disease (1.28 [1.14, 1.43]); diabetes (1.56 [1.33, 1.83]); influenza/pneumonia (1.24 [1.02, 1.50]); Parkinson disease (1.35 [1.11, 1.65]); liver disease (1.33 [1.05, 1.67]); and suicide (1.43 [1.10, 1.85]. Mortality associations persisted in stratified analyses with important potential confounders, reducing causation concerns.
   Conclusions: This study shows the breadth of mortality outcomes associated with prolonged TV viewing, and identifies novel associations for several leading causes of death. TV viewing is a prevalent discretionary behavior that may be a more important target for public health intervention than previously recognized.
C1 [Keadle, Sarah K.; Moore, Steven C.; Xiao, Qian; Albanes, Demetrius; Matthews, Charles E.] NCI, Div Canc Epidemiol & Genet, Nutrit Epidemiol Branch, Bethesda, MD 20892 USA.
   [Keadle, Sarah K.; Xiao, Qian] NCI, Canc Prevent Div, Canc Prevent Fellowship Program, Bethesda, MD 20892 USA.
   [Sampson, Joshua N.] NCI, Div Canc Epidemiol & Genet, Biostat Branch, Bethesda, MD 20892 USA.
RP Keadle, SK (reprint author), NCI, Div Canc Epidemiol & Genet, Nutrit Epidemiol Branch, 9609 Med Ctr Dr 6E-318, Bethesda, MD 20892 USA.
EM sarah.keadle@nih.gov
RI Moore, Steven/D-8760-2016; Dey, Kamalesh/E-6568-2017; 
OI Moore, Steven/0000-0002-8169-1661; Keadle, Sarah/0000-0002-9569-9306
FU Intramural Research Program of the NIH, National Cancer Institute
FX We are indebted to the participants in the NIH-AARP Diet and Health
   Study for their outstanding cooperation. This research was supported in
   part by the Intramural Research Program of the NIH, National Cancer
   Institute. The funder did not play any role in study design; collection,
   analysis, and interpretation of data; writing the report; or the
   decision to submit the report for publication.
NR 49
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 0749-3797
EI 1873-2607
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD DEC
PY 2015
VL 49
IS 6
BP 811
EP 821
DI 10.1016/j.amepre.2015.05.023
PG 11
WC Public, Environmental & Occupational Health; Medicine, General &
   Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA CW5UK
UT WOS:000365061900001
PM 26215832
ER

PT J
AU Nansel, TR
   Thomas, DM
   Liu, AY
AF Nansel, Tonja R.
   Thomas, Dexter M.
   Liu, Aiyi
TI Efficacy of a Behavioral Intervention for Pediatric Type 1 Diabetes
   Across Income
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID METABOLIC-CONTROL; GLYCEMIC CONTROL; YOUTH; ADOLESCENTS; HEALTH;
   MELLITUS; CHILDREN; EQUITY; LIFE
AB Introduction: Youth with Type 1 diabetes and lower family income typically have poorer glycemic control. This post hoc analysis examines whether a family-oriented behavioral intervention for this population is differentially effective across income levels.
   Methods: Families of youth aged 9-15 years with Type 1 diabetes (N=390; 49.2% female; age, 12.4 [1.7] years; hemoglobin Alc [HbA1c], 8.4 [1.2]; pump, 33.8%) at four U.S. pediatric endocrinology clinics participated in a 2-year RCT (data collected 2006-2011) of a clinic-integrated behavioral intervention designed to improve diabetes management by facilitating problem-solving skills, communication skills, and responsibility sharing. HbA1c was analyzed centrally. Family income was categorized as <$50,000 (low); $50,000 to <$100,000 (middle); and >=$100,000 (high). Treatment effect was defined as the change in HbAlc from baseline to 2-year follow-up. A linear model tested the interaction of treatment effect with family income, controlling for race, insulin regimen, and site (analyzed in 2014).
   Results: Baseline HbA1c was significantly poorer (p=0.004) in the low-income group. There was a significant overall effect of treatment group on change in HbA1c from baseline to follow-up (p=0.04). The interaction term for treatment by income group was not significant (p=0.44). Within each income category, a smaller deterioration in glycemic control was observed for the treatment group relative to controls.
   Conclusions: This clinic-integrated behavioral intervention was similarly effective in improving glycemic control among youth with Type 1 diabetes across income levels. This family-oriented problem-solving approach offers flexibility in addressing families' needs and may optimize impact on health outcomes across income groups. Published by Elsevier Inc. on behalf of American Journal of Preventive Medicine
C1 [Nansel, Tonja R.; Thomas, Dexter M.; Liu, Aiyi] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, Bethesda, MD USA.
RP Nansel, TR (reprint author), 6100 Execut Blvd,Room 7B13R,MSC 7510, Bethesda, MD 20892 USA.
EM nanselt@mail.nih.gov
OI Nansel, Tonja/0000-0002-8298-7595; Liu, Aiyi/0000-0002-6618-5082
FU NIH, Eunice Kennedy Shriver National Institute of Child Health and Human
   Development [N01-HD-4-3364, N01-HD-4-3361, N01-HD-4-3362, N01-HD-4-3363,
   N01-HD-3-3360]
FX This research was supported by the intramural research program of the
   NIH, Eunice Kennedy Shriver National Institute of Child Health and Human
   Development, contract numbers N01-HD-4-3364, N01-HD-4-3361,
   N01-HD-4-3362, N01-HD-4-3363, and N01-HD-3-3360. The authors wish to
   acknowledge the contributions of the research staff at the participating
   clinical sites and the families who participated in the study.
NR 22
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PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
EI 1873-2607
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD DEC
PY 2015
VL 49
IS 6
BP 930
EP 934
DI 10.1016/j.amepre.2015.05.006
PG 5
WC Public, Environmental & Occupational Health; Medicine, General &
   Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA CW5UK
UT WOS:000365061900013
PM 26231856
ER

PT J
AU Buchanan, ND
   Dasari, S
   Rodriguez, JL
   Smith, JL
   Hodgson, ME
   Weinberg, CR
   Sandler, DP
AF Buchanan, Natasha D.
   Dasari, Sabitha
   Rodriguez, Juan L.
   Smith, Judith Lee
   Hodgson, M. Elizabeth
   Weinberg, Clarice R.
   Sandler, Dale P.
TI Post-treatment Neurocognition and Psychosocial Care Among Breast Cancer
   Survivors
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID COGNITIVE IMPAIRMENT; CHEMOTHERAPY; TAMOXIFEN; WOMEN; AGE; EXEMESTANE;
   EXPOSURES; ATTITUDES; SIDE
AB Introduction: Chemotherapy for breast cancer has been associated with cognitive problems; however, the impact of adjuvant hormone therapy is less clear. No studies have explored provider discussions about cognitive concerns or factors associated with neurocognitive treatment. This study examined cognitive problems, factors associated with having a provider discussion, and receipt of neurocognitive treatment.
   Methods: Female breast cancer survivors (N=2,537) from the Sister Study and the Two Sister Study who were at least 1 year post-treatment were surveyed in 2012 about their cancer therapies (confirmed by medical records); cognitive concerns; related provider discussions; and neurocognitive treatment. A total of 2,296 women were included in the current 2014 analysis. Extensive covariate information was also ascertained for predictive multivariate models.
   Results: The prevalence of self-reported cognitive problems after treatment was 60%. Of those reporting cognitive problems, only 37% had discussed those concerns with a provider and 15% had been treated for cognitive symptoms. The odds of reported cognitive concerns that started during and after treatment were elevated for those who received only hormone therapy and no chemotherapy (OR=1.64, 95% CI=1.15, 2.33); chemotherapy and no hormone therapy (OR=5.63, 95% CI=3.52, 9.00); or both (OR=6.33, 95% CI=4.21, 9.54) compared with those reporting neither treatment.
   Conclusions: The high prevalence of cognitive concerns underscores the importance of monitoring breast cancer survivors for potential neurocognitive effects of hormone and chemotherapy, discussions with survivors about those concerns, and treatment referrals. Monitoring changes over time can help to evaluate both psychosocial and neurocognitive care provided for survivors. Published by Elsevier Inc. on behalf of American Journal of Preventive Medicine.
C1 [Buchanan, Natasha D.; Rodriguez, Juan L.; Smith, Judith Lee] CDC, Div Canc Prevent & Control, Epidemiol & Appl Res Branch, Atlanta, GA 30341 USA.
   [Dasari, Sabitha] Northrop Grumman Corp, Informat Syst, Atlanta, GA USA.
   [Hodgson, M. Elizabeth] Social & Sci Syst Inc, Durham, NC USA.
   [Weinberg, Clarice R.] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
   [Sandler, Dale P.] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
RP Buchanan, ND (reprint author), CDC, 4770 Buford Highway NE,MS F-76, Atlanta, GA 30341 USA.
EM nbuchanan@cdc.gov
OI Sandler, Dale/0000-0002-6776-0018
FU Centers for Disease Control and Prevention, Division of Cancer
   Prevention and Control; Intramural Research Program of the NIH, National
   Institute of Environmental Health Sciences [Z01 ES044005, Z01
   ES0102245]; Susan G. Komen for the Cure FAS [0703856]; CDC, Division of
   Cancer Prevention and Control
FX Publication of this article was supported by the Centers for Disease
   Control and Prevention, Division of Cancer Prevention and Control.; This
   research was supported in part by the Intramural Research Program of the
   NIH, National Institute of Environmental Health Sciences (Z01 ES044005
   and Z01 ES0102245); Susan G. Komen for the Cure FAS 0703856 (the Two
   Sister Study); and by CDC, Division of Cancer Prevention and Control
   (Survivorship Survey).
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PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
EI 1873-2607
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD DEC
PY 2015
VL 49
IS 6
SU 5
BP S498
EP S508
DI 10.1016/j.amepre.2015.08.013
PG 11
WC Public, Environmental & Occupational Health; Medicine, General &
   Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA CW5UH
UT WOS:000365061600006
PM 26590645
ER

PT J
AU Guy, GP
   Yabroff, KR
   Ekwueme, DU
   Virgo, KS
   Han, XS
   Banegas, MP
   Soni, A
   Zheng, ZY
   Chawla, N
   Geiger, AM
AF Guy, Gery P., Jr.
   Yabroff, K. Robin
   Ekwueme, Donatus U.
   Virgo, Katherine S.
   Han, Xuesong
   Banegas, Matthew P.
   Soni, Anita
   Zheng, Zhiyuan
   Chawla, Neetu
   Geiger, Ann M.
TI Healthcare Expenditure Burden Among Non-elderly Cancer Survivors,
   2008-2012
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID 2ND PRIMARY CANCERS; BREAST-CANCER; UNITED-STATES; NATIONAL-SURVEY;
   MEDICAL-CARE; COST; THERAPY; ADULTS; ONCOLOGISTS; MAMMOGRAPHY
AB Introduction: There is increasing concern regarding the financial burden of cancer on patients and their families. This study presents nationally representative estimates of annual out-of-pocket (OOP) burden among non-elderly cancer survivors and assesses the association between high OOP burden and access to care and preventive service utilization.
   Methods: Using the 2008-2012 Medical Expenditure Panel Survey, 4,271 cancer survivors and 96,780 individuals without a history of cancer were identified, all aged 18-64 years. High annual OOP burden was defined as spending >20% of annual family income on OOP healthcare costs. Associations between high OOP burden and access to care were evaluated with multivariable logistic regression. Analyses were conducted in 2015.
   Results: Compared with individuals without a cancer history, cancer survivors were more likely to report a high OOP burden (4.3% vs 3.4%, p=0.009) in adjusted analyses. High OOP burden was more common among cancer survivors who were poor (18.4%), with either public insurance (7.9%) or uninsured (5.7%), and not working (10.2%). Among cancer survivors, high OOP burden was associated with being unable to obtain necessary medical care (19.2% vs 12.5%, p=0.002), delaying necessary medical care (21.6% vs 13.8%, p=0.002), and lower breast cancer screening rates among age-appropriate women (63.2% vs 75.9%, p=0.02).
   Conclusions: High OOP burden is more common among adults with a cancer history than those without a cancer history. High OOP burden was associated with being unable to obtain necessary medical care, delaying necessary medical care, and lower breast cancer screening rates among women. Published by Elsevier Inc. on behalf of American Journal of Preventive Medicine.
C1 [Guy, Gery P., Jr.; Ekwueme, Donatus U.] CDC, Div Canc Prevent & Control, Natl Ctr Chron Dis Prevent & Hlth Promot, Atlanta, GA 30341 USA.
   [Yabroff, K. Robin; Geiger, Ann M.] NCI, Healthcare Delivery Res Program, Div Canc Control & Populat Sci, Rockville, MD USA.
   [Virgo, Katherine S.] Emory Univ, Dept Hlth Policy & Management, Rollins Sch Publ Hlth, Atlanta, GA 30322 USA.
   [Han, Xuesong; Zheng, Zhiyuan] Amer Canc Soc, Surveillance & Hlth Serv Res Program, Atlanta, GA 30329 USA.
   [Banegas, Matthew P.] Kaiser Permanente Northwest, Ctr Hlth Res, Portland, OR USA.
   [Soni, Anita] Ctr Financing Access & Cost Trends, Agcy Healthcare Res & Qual, Rockville, MD USA.
   [Chawla, Neetu] Kaiser Permanente No Calif, Div Res, Oakland, CA USA.
RP Guy, GP (reprint author), CDC, Div Canc Prevent & Control, 4770 Buford Highway NE,MS K-76, Atlanta, GA 30341 USA.
EM irm2@cdc.gov
FU Centers for Disease Control and Prevention, Division of Cancer
   Prevention and Control
FX Publication of this article was supported by the Centers for Disease
   Control and Prevention, Division of Cancer Prevention and Control.
NR 36
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U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
EI 1873-2607
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD DEC
PY 2015
VL 49
IS 6
SU 5
BP S489
EP S497
DI 10.1016/j.amepre.2015.09.002
PG 9
WC Public, Environmental & Occupational Health; Medicine, General &
   Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA CW5UH
UT WOS:000365061600005
PM 26590644
ER

PT J
AU Hoffman, SL
   Vekemans, J
   Richie, TL
   Duffy, PE
AF Hoffman, Stephen L.
   Vekemans, Johan
   Richie, Thomas L.
   Duffy, Patrick E.
TI The March Toward Malaria Vaccines
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID PLASMODIUM-FALCIPARUM SPOROZOITES; TRANSMISSION-BLOCKING VACCINE; T-CELL
   IMMUNITY; CIRCUMSPOROZOITE PROTEIN VACCINE; DIRECT VENOUS INOCULATION;
   IN-ADJUVANT VACCINES; DNA VACCINE; ANTIBODY-RESPONSES; SEQUENTIAL
   IMMUNIZATION; LISTERIA-MONOCYTOGENES
AB In 2013 there were an estimated 584,000 deaths and 198 million clinical illnesses due to malaria, the majority in sub-Saharan Africa. Vaccines would be the ideal addition to the existing armamentarium of anti-malaria tools. However, malaria is caused by parasites, and parasites are much more complex in terms of their biology than the viruses and bacteria for which we have vaccines, passing through multiple stages of development in the human host, each stage expressing hundreds of unique antigens. This complexity makes it more difficult to develop a vaccine for parasites than for viruses and bacteria, since an immune response targeting one stage may not offer protection against a later stage, because different antigens are the targets of protective immunity at different stages. Furthermore, depending on the life cycle stage and whether the parasite is extra- or intra-cellular, antibody and/or cellular immune responses provide protection. It is thus not surprising that there is no vaccine on the market for prevention of malaria, or any human parasitic infection. In fact, no vaccine for any disease with this breadth of targets and immune responses exists. In this limited review, we focus on four approaches to malaria vaccines, (1) a recombinant protein with adjuvant vaccine aimed at Plasmodium falciparum (Pf) pre-erythrocytic stages of the parasite cycle (RTS,S/AS01), (2) whole sporozoite vaccines aimed at Pf pre-erythrocytic stages (PfSPZ Vaccine and PfSPZ-CVac), (3) prime boost vaccines that include recombinant DNA, viruses and bacteria, and protein with adjuvant aimed primarily at Pf pre-erythrocytic, but also asexual erythrocytic stages, and (4) recombinant protein with adjuvant vaccines aimed at Pf and Plasmodium vivax sexual erythrocytic and mosquito stages. We recognize that we are not covering all approaches to malaria vaccine development, or most of the critically important work on development of vaccines against P. vivax, the second most important cause of malaria. Progress during the last few years has been significant, and a first generation malaria candidate vaccine, RTS,S/AS01, is under review by the European Medicines Agency (EMA) for its quality, safety and efficacy under article 58, which allows the EMA to give a scientific opinion about products intended exclusively for markets outside of the European Union. However, much work is in progress to optimize malaria vaccines in regard to magnitude and durability of protective efficacy and the financing and practicality of delivery. Thus, we are hopeful that anti-malaria vaccines will soon be important tools in the battle against malaria. (C) 2015 by American Journal of Preventive Medicine and Elsevier Ltd. All rights reserved.
C1 [Hoffman, Stephen L.; Richie, Thomas L.] Sanaria Inc, Rockville, MD 20850 USA.
   [Vekemans, Johan] GSK Vaccines, Rixensart, Belgium.
   [Duffy, Patrick E.] NIAID, Lab Malaria Immunol & Vaccinol, NIH, Rockville, MD 20852 USA.
RP Hoffman, SL (reprint author), Sanaria Inc, Rockville, MD 20850 USA.
EM slhoffman@sanaria.com
FU Merck; Novartis; Sanaria Inc.; GSK Vaccines; Intramural Research Program
   of NIAID, NIH
FX This article is being published concurrently in the American Journal of
   Preventive Medicine and Vaccine. The articles are identical except for
   stylistic changes in keeping with each journal's style. Either of these
   versions may be used in citing this article. Publication of this article
   was supported by Merck and Novartis.; SLH and TLR are supported by
   Sanaria Inc., JV by GSK Vaccines, and PED by the Intramural Research
   Program of NIAID, NIH.
NR 110
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U1 1
U2 26
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
EI 1873-2607
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD DEC
PY 2015
VL 49
IS 6
SU 4
BP S319
EP S333
DI 10.1016/j.amepre.2015.09.011
PG 15
WC Public, Environmental & Occupational Health; Medicine, General &
   Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA CW5UI
UT WOS:000365061700003
PM 26590432
ER

PT J
AU Pholphirul, P
AF Pholphirul, Piriya
TI Happiness from Giving: Quantitative Investigation of Thai Buddhists
SO APPLIED RESEARCH IN QUALITY OF LIFE
LA English
DT Article
DE Happiness; Religious giving; Nonreligious giving; Buddhism
ID IMPURE ALTRUISM; WARM-GLOW; BENEVOLENCE; BEHAVIOR; CHARITY
AB According to Buddhist teachings, giving without condition leads to a higher level of happiness. Even though there are a number of studies examining factors that determine happiness, none quantitatively examine happiness from the perspective of a "giving" relationship. Using a household dataset from Thailand, where Buddhism is the main religion, this paper suggests that religious and nonreligious giving leads to a higher happiness level than not giving at all. Moreover, for nonreligious giving, it is found that charitable giving in terms of money and goods gives a donor more happiness than does volunteer work, but that both types of giving enhance one's happiness. Religious giving (offering food and dedicating other offerings to Buddhist monks) is also found to increase happiness, more so for respondents who regularly give for religious purposes. In particular, regularly giving to monks leads to the highest happiness level, perhaps since Buddhism permeates Thai society and dedicating offerings to monks is believed to provide great merit. In addition, when making offerings to monks, donors usually do it randomly, at a temple, which suggests that making merit at a temple also leads to higher level of happiness.
C1 [Pholphirul, Piriya] NIDA, Grad Sch Dev Econ, Bangkok 10240, Thailand.
   [Pholphirul, Piriya] NIDA, Int Coll Natl Inst Dev Adm ICO NIDA, Bangkok 10240, Thailand.
RP Pholphirul, P (reprint author), NIDA, Grad Sch Dev Econ, Serithai Rd, Bangkok 10240, Thailand.
EM piriya@nida.ac.th
FU Thailand Research Fund; National Institute of Development Administration
FX The author would like to thank the Thailand Research Fund and the
   National Institute of Development Administration for support grants and
   Nattawan Santipong and Thananut Singhathep for their able research
   assistance.
NR 26
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U2 20
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1871-2584
EI 1871-2576
J9 APPL RES QUAL LIFE
JI Appl. Res. Qual. Life
PD DEC
PY 2015
VL 10
IS 4
BP 703
EP 720
DI 10.1007/s11482-014-9349-8
PG 18
WC Social Sciences, Interdisciplinary
SC Social Sciences - Other Topics
GA CW3YG
UT WOS:000364927700010
ER

PT J
AU Kalra, S
   Burbelo, PD
   Bayat, A
   Ching, KH
   Thurm, A
   Iadarola, MJ
   Swedo, SE
AF Kalra, Simran
   Burbelo, Peter D.
   Bayat, Ahmad
   Ching, Kathryn H.
   Thurm, Audrey
   Iadarola, Michael J.
   Swedo, Susan E.
TI No evidence of antibodies against GAD65 and other specific antigens in
   children with autism
SO BBA CLINICAL
LA English
DT Article
DE Autism spectrum disorders; Autoantibodies; Glutamic acid decarboxylase;
   Virus
ID SPECTRUM DISORDERS; LUCIFERASE IMMUNOPRECIPITATION; AUTOANTIBODIES;
   AUTOIMMUNE; DISEASE; PROTEIN; PLASMA; CELLS; SERUM; XMRV
AB Background: The presence of autoantibodies has been proposed as evidence for a role of autoimmunity in autism. This report investigates the prevalence of autoantibodies in children with autism using the luciferase immuno-precipitation systems (LIPS) immunoassay technology. A panel of autoantibody targets against several known and candidate neurological autoantigens, autoimmune-associated autoantigens and viruses was employed.
   Methods: Serological analysis was performed on typically developing children (n = 55), developmentally delayed children without autism (n = 24) and children diagnosed with autism(n = 104). Autoantibodies were measured against glutamic acid decarboxylase-65 (GAD65), a CNS autoantigen proposed to be associated with autism and against Ro52, glial fibrillary acidic protein, tyrosine hydroxylase, aquaporin-4, and gamma-enolase, the mouse mammary tumor virus and the xenotropic murine leukemia virus. Antibody levels and seropositivity prevalence were analyzed for statistically significant differences between the three groups.
   Results: The majority of the children (98%) were seronegative for all targets in the antigen panel. No GAD65 seropositive children were detected in the cohort. Several low level seropositive sera against several of the protein targets were identified in isolated children in each of the three groups, but there was no difference in prevalence.
   Conclusion: Using this panel of antigens and a sensitive, robust assay, no evidence of unusual immunoreactivity was detected in children with autism, providing evidence against a role of autoimmunity against several previously implicated proteins in autism spectrum disorder pathogenesis. General significance: The idea that autoantibodies represent an underlying cause or are biomarkers for autism pathophysiology is not supported by this report. 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 [Kalra, Simran; Thurm, Audrey; Swedo, Susan E.] NIMH, NIH, Pediat & Dev Neurosci Branch, Bethesda, MD 20892 USA.
   [Burbelo, Peter D.] Natl Inst Dent & Craniofacial Res, NIH, Dent Clin Res Core, Bethesda, MD 20892 USA.
   [Bayat, Ahmad; Ching, Kathryn H.; Iadarola, Michael J.] NIH, Ctr Clin, Dept Perioperat Med, Bethesda, MD 20892 USA.
RP Burbelo, PD (reprint author), Natl Inst Dent & Craniofacial Res, NIH, Dent Clin Res Core, Bethesda, MD 20892 USA.
EM burbelop@nidcr.nih.gov
FU Intramural NIH HHS [Z01 DE000724-01, Z01 MH002868-02]
NR 40
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U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 2214-6474
J9 BBA CLIN
JI BBA Clin.
PD DEC
PY 2015
VL 4
BP 81
EP 84
DI 10.1016/j.bbacli.2015.08.001
PG 4
WC Medicine, General & Internal
SC General & Internal Medicine
GA CW7VF
UT WOS:000365206800013
PM 26366376
ER

PT J
AU Burke, MJ
   Verneris, MR
   Le Rademacher, J
   He, WS
   Abdel-Azim, H
   Abraham, AA
   Auletta, JJ
   Ayas, M
   Brown, VI
   Cairo, MS
   Chan, KW
   Perez, MAD
   Dvorak, CC
   Egeler, RM
   Eldjerou, L
   Frangoul, H
   Guilcher, GMT
   Hayashi, RJ
   Ibrahim, A
   Kasow, KA
   Leung, WH
   Olsson, RF
   Pulsipher, MA
   Shah, N
   Shah, NN
   Thiel, E
   Talano, JA
   Kitko, CL
AF Burke, Michael J.
   Verneris, Michael R.
   Le Rademacher, Jennifer
   He, Wensheng
   Abdel-Azim, Hisham
   Abraham, Allistair A.
   Auletta, Jeffery J.
   Ayas, Mouhab
   Brown, Valerie I.
   Cairo, Mitchell S.
   Chan, Ka Wah
   Diaz Perez, Miguel A.
   Dvorak, Christopher C.
   Egeler, R. Maarten
   Eldjerou, Lamis
   Frangoul, Haydar
   Guilcher, Gregory M. T.
   Hayashi, Robert J.
   Ibrahim, Ahmed
   Kasow, Kimberly A.
   Leung, Wing H.
   Olsson, Richard F.
   Pulsipher, Michael A.
   Shah, Niketa
   Shah, Nirali N.
   Thiel, Elizabeth
   Talano, Julie-An
   Kitko, Carrie L.
TI Transplant Outcomes for Children with T Cell Acute Lymphoblastic
   Leukemia in Second Remission: A Report from the Center for International
   Blood and Marrow Transplant Research
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE Pediatric; T-cell ALL; Relapse; Acute lymphoblastic leukemia;
   Transplantation
ID VERSUS-HOST-DISEASE; ONCOLOGY-GROUP POG; PROGNOSTIC-FACTORS; IMPROVED
   SURVIVAL; CHILDHOOD; RELAPSE; THERAPY; TRIAL; RISK; ADOLESCENTS
AB Survival for children with relapsed T cell acute lymphoblastic leukemia (T-ALL) is poor when treated with chemotherapy alone, and outcomes after allogeneic hematopoietic cell transplantation (HCT) is not well described. Two hundred twenty-nine children with T-ALL in second complete remission (CR2) received an HCT after myeloablative conditioning between 2000 and 2011 and were reported to the Center for International Blood and Marrow Transplant Research. Median age was 10 years (range, 2 to 18). Donor source was umbilical cord blood (26%), matched sibling bone marrow (38%), or unrelated bone marrow/peripheral blood (36%). Acute (grades II to IV) and chronic graft-versus-host disease occurred in, respectively, 35% (95% confidence interval [CI], 27% to 45%) and 26% (95% CI, 20% to 33%) of patients. Transplant-related mortality at day 100 and 3-year relapse rates were 13% (95% CI, 9% to 18%) and 30% (95% CI, 24% to 37%), respectively. Three-year overall survival and disease-free survival rates were 48% (95% CI, 41% to 55%) and 46% (95% CI, 39% to 52%), respectively. In multivariate analysis, patients with bone marrow relapse, with or without concurrent extramedullary relapse before HCT, were most likely to relapse (hazard ratio, 3.94; P =.005) as compared with isolated extramedullary disease. In conclusion, HCT for pediatric T-ALL in CR2 demonstrates reasonable and durable outcomes, and consideration for HCT is warranted. (c) 2015 American Society for Blood and Marrow Transplantation.
C1 [Burke, Michael J.; Talano, Julie-An] Med Coll Wisconsin, Dept Pediat, Div Hematol Oncol Blood & Marrow Transplant, Milwaukee, WI 53226 USA.
   [Burke, Michael J.; Talano, Julie-An] Childrens Hosp Wisconsin, Milwaukee, WI 53226 USA.
   [Verneris, Michael R.] Univ Minnesota, Dept Pediat, Minneapolis, MN 55455 USA.
   [Le Rademacher, Jennifer; He, Wensheng; Thiel, Elizabeth] Med Coll Wisconsin, Dept Med, CIBMTR, Milwaukee, WI 53226 USA.
   [Le Rademacher, Jennifer] Med Coll Wisconsin, Div Biostat, Inst Hlth & Soc, Milwaukee, WI 53226 USA.
   [Abdel-Azim, Hisham; Pulsipher, Michael A.] Univ So Calif, Keck Sch Med, Childrens Hosp Los Angeles, Div Hematol Oncol & Blood & Marrow Transplantat, Los Angeles, CA 90033 USA.
   [Abraham, Allistair A.] Childrens Natl Med Ctr, Ctr Canc & Blood Disorders, Div Blood & Marrow Transplantat, Washington, DC 20010 USA.
   [Auletta, Jeffery J.] Nationwide Childrens Hosp, Div Hematol Oncol Bone Marrow Transplantat & Infe, Columbus, OH USA.
   [Ayas, Mouhab] King Faisal Specialist Hosp & Res Ctr, Dept Pediat Hematol Oncol, Riyadh, Saudi Arabia.
   [Brown, Valerie I.] Penn State Hershey Childrens Hosp, Dept Pediat, Div Pediat Oncol Hematol, Hershey, PA USA.
   [Brown, Valerie I.] Penn State Univ, Milton S Hershey Med Ctr, Coll Med, Hershey, PA 17033 USA.
   [Cairo, Mitchell S.] New York Med Coll, Dept Pediat, Valhalla, NY 10595 USA.
   [Chan, Ka Wah] Texas Transplant Inst, Dept Pediat, San Antonio, TX USA.
   [Diaz Perez, Miguel A.] Hosp Infantil Univ Nino Jesus, Dept Hematol Oncol, Madrid, Spain.
   [Dvorak, Christopher C.] Univ Calif San Francisco, Dept Pediat, Med Ctr, San Francisco, CA USA.
   [Egeler, R. Maarten] Hosp Sick Children, Dept Hematol Oncol, Toronto, ON M5G 1X8, Canada.
   [Eldjerou, Lamis] Univ Florida, Dept Pediat, Gainesville, FL USA.
   [Frangoul, Haydar] Vanderbilt Univ, Dept Pediat, Div Hematol Oncol, Sch Med, Nashville, TN USA.
   [Guilcher, Gregory M. T.] Alberta Childrens Prov Gen Hosp, Sect Paediat Oncol & Blood & Marrow Transplant, Calgary, AB, Canada.
   [Hayashi, Robert J.] Washington Univ, Sch Med, Dept Pediat, Div Pediat Hematol Oncol, St Louis, MO 63110 USA.
   [Ibrahim, Ahmed] Makassed Gen Hosp, Dept Hematol Oncol, Beiruit, Lebanon.
   [Kasow, Kimberly A.] Univ N Carolina, Dept Pediat, Div Hematol Oncol, Chapel Hill, NC USA.
   [Leung, Wing H.] St Jude Childrens Res Hosp, Div Bone Marrow Transplantat, Memphis, TN 38105 USA.
   [Olsson, Richard F.] Karolinska Inst, Dept Lab Med, Div Therapeut Immunol, Stockholm, Sweden.
   [Olsson, Richard F.] Uppsala Univ, Ctr Clin Res Sormland, Uppsala, Sweden.
   [Shah, Niketa] Mayo Clin Arizona, Dept Pediat, Div Hematol Oncol, Phoenix, AZ USA.
   [Shah, Niketa] Phoenix Childrens Hosp, Phoenix, AZ USA.
   [Shah, Nirali N.] Natl Canc Inst NIH, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD USA.
   [Kitko, Carrie L.] Vanderbilt Univ, Dept Pediat, Stem Cell Transplant Program, Nashville, TN USA.
RP Burke, MJ (reprint author), Childrens Hosp Wisconsin, Dept Pediat, Med Coll Wisconsin, Div Hematol Oncol Blood & Marrow Transplant,MACC, 8701 Watertown Plank Rd, Milwaukee, WI 53226 USA.
EM mmburke@mcw.edu
FU Public Health Service Grant from the National Cancer Institute (NCI)
   [U24-CA076518]; National Heart, Lung and Blood Institute (NHLBI);
   National Institute of Allergy and Infectious Diseases; NHLBI
   [5U10HL069294]; NCI [5U10HL069294]; Health Resources and Services
   Administration [HHSH250201200016 C]; Office of Naval Research
   [N00014-13-1-0039, N00014-14-1-0028]; Actinium Pharmaceuticals; Allos
   Therapeutics, Inc.; Amgen, Inc.
FX The CIBMTR is supported by Public Health Service Grant/Cooperative
   Agreement U24-CA076518 from the National Cancer Institute (NCI), the
   National Heart, Lung and Blood Institute (NHLBI), and the National
   Institute of Allergy and Infectious Diseases; Grant/Cooperative
   Agreement 5U10HL069294 from the NHLBI and NCI; a contract
   (HHSH250201200016 C) with Health Resources and Services Administration;
   2 grants (N00014-13-1-0039 and N00014-14-1-0028) from the Office of
   Naval Research; and grants from Actinium Pharmaceuticals; Allos
   Therapeutics, Inc.; Amgen, Inc.; anonymous donation to the Medical
   College of Wisconsin; Ariad; Be the Match Foundation; Blue Cross and
   Blue Shield Association; Celgene Corporation; Chimerix, Inc.; Fred
   Hutchinson Cancer Research Center; Fresenius-Biotech North America,
   Inc.; Gamida Cell Teva Joint Venture Ltd.; Genentech, Inc.; Gentium SpA;
   Genzyme Corporation; GlaxoSmithKline; Health Research, Inc. Roswell Park
   Cancer Institute; HistoGenetics, Inc.; Incyte Corporation; Jeff Gordon
   Children's Foundation; Kiadis Pharma; The Leukemia & Lymphoma Society;
   Medac GmbH; The Medical College of Wisconsin; Merck & Co, Inc.;
   Millennium: The Takeda Oncology Co.; Milliman USA, Inc.; Miltenyi
   Biotec, Inc.; National Marrow Donor Program; Onyx Pharmaceuticals; Optum
   Healthcare Solutions, Inc.; Osiris Therapeutics, Inc.; Otsuka America
   Pharmaceutical, Inc.; Perkin Elmer, Inc.; Remedy Informatics; Sanofi US;
   Seattle Genetics; Sigma-Tau Pharmaceuticals; Soligenix, Inc.; St.
   Baldrick's Foundation; StemCyte, A Global Cord Blood Therapeutics Co.;
   Stemsoft Software, Inc.; Swedish Orphan Biovitrum; Tarix
   Pharmaceuticals; TerumoBCT; Teva Neuroscience, Inc.; THERAKOS, Inc.;
   University of Minnesota; University of Utah; and Wellpoint, Inc. The
   views expressed in this article do not reflect the official policy or
   position of the National Institutes of Health, the Department of the
   Navy, the Department of Defense, the Health Resources and Services
   Administration, or any other agency of the U.S. Government.
NR 30
TC 2
Z9 4
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
EI 1523-6536
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD DEC
PY 2015
VL 21
IS 12
BP 2154
EP 2159
DI 10.1016/j.bbmt.2015.08.023
PG 6
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA CW4SF
UT WOS:000364981700018
PM 26327632
ER

PT J
AU Fox, E
   Widemann, BC
   Pastakia, D
   Chen, CC
   Yang, SX
   Cole, D
   Balis, FM
AF Fox, Elizabeth
   Widemann, Brigitte C.
   Pastakia, Devang
   Chen, Clara C.
   Yang, Sherry X.
   Cole, Diane
   Balis, Frank M.
TI Pharmacokinetic and pharmacodynamic study of tariquidar (XR9576), a
   P-glycoprotein inhibitor, in combination with doxorubicin, vinorelbine,
   or docetaxel in children and adolescents with refractory solid tumors
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE Multidrug resistance; P-glycoprotein; Pediatric cancer; Phase I;
   Pharmacokinetics
ID PHASE-I TRIAL; CANCER RESISTANCE PROTEIN; MULTIDRUG-RESISTANCE; DRUG
   EFFLUX; PSC 833; EXPRESSION; REVERSAL; BLOOD; GENE; CHEMOTHERAPY
AB P-glycoprotein (Pgp), an ATP-dependent transport protein, confers multidrug resistance in cancer cells. Tariquidar binds and inhibits Pgp. To assess the toxicity, pharmacokinetics (PK), and pharmacodynamics of tariquidar, we conducted a phase I trial of tariquidar in combination with doxorubicin, docetaxel, or vinorelbine in children and adolescents with recurrent or refractory solid tumors.
   Patients less than 19 years of age with refractory or recurrent solid tumors were eligible. Tariquidar (1, 1.5, or 2 mg/kg) was administered alone and in combination with doxorubicin, docetaxel, or vinorelbine. PK of tariquidar and cytotoxic drugs was performed. Pgp function was assessed by a rhodamine efflux assay and Tc-99m-sestamibi scintigraphy. Tumor Pgp expression was assessed by immunohistochemistry. Response was assessed using Response Evaluation Criteria in Solid Tumors.
   Twenty-nine subjects were enrolled. No tariquidar-related dose-limiting toxicity (DLT) was observed. DLT related to cytotoxic drugs occurred in 12 % of subjects receiving tariquidar 2 mg/kg. When administered in combination with tariquidar, the clearance of docetaxel and vinorelbine was reduced compared to prior studies. Inhibition of rhodamine efflux was dose dependent. After tariquidar administration, Tc-99m-sestamibi accumulation in tumor increased by 22 %. Objective responses (1 complete, 2 partial) were observed. There was no association between tumor Pgp expression and response.
   A tolerable and biologically active dose of tariquidar was established in children and adolescents. This trial demonstrates that modulators of resistance can be evaluated in combination with chemotherapy, and pharmacokinetic and pharmacodynamic endpoints can be useful in determination of recommended dose in children and adolescents.
C1 [Fox, Elizabeth; Balis, Frank M.] Univ Penn, Childrens Hosp Philadelphia, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Widemann, Brigitte C.; Cole, Diane] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
   [Pastakia, Devang] Vanderbilt Univ Sch Med, Dept Pediat, Nashville, TN USA.
   [Chen, Clara C.] NIH, Dept Nucl Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Yang, Sherry X.] NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
RP Fox, E (reprint author), Univ Penn, Childrens Hosp Philadelphia, Perelman Sch Med, CTRB 4016,3501 Civic Ctr Blvd, Philadelphia, PA 19104 USA.
EM foxe@email.chop.edu
FU Intramural Research Program of the NIH, National Cancer Institute,
   Center for Cancer Research
FX The research was supported by the Intramural Research Program of the
   NIH, National Cancer Institute, Center for Cancer Research.
NR 35
TC 3
Z9 3
U1 3
U2 13
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
EI 1432-0843
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD DEC
PY 2015
VL 76
IS 6
BP 1273
EP 1283
DI 10.1007/s00280-015-2845-1
PG 11
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA CW7ZJ
UT WOS:000365217800018
PM 26486517
ER

PT J
AU Lederman, RJ
   Babaliaros, VC
   Greenbaum, AB
AF Lederman, Robert J.
   Babaliaros, Vasilis C.
   Greenbaum, Adam B.
TI How to perform transcaval access and closure for transcatheter aortic
   valve implantation
SO CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS
LA English
DT Article
DE structural heart disease; alternative access routes; caval-aortic
   access; nontransfemoral access
ID REPLACEMENT
AB Transcaval, or caval-aortic, access is a promising approach for fully percutaneous transcatheter aortic valve implantation in patients without good conventional access options. This tutorial review provides step-by-step guidance to planning and executing the procedure, along with approaches to remedy complications. (c) 2015 Wiley Periodicals, Inc.
C1 [Lederman, Robert J.] NHLBI, Cardiovasc & Pulm Branch, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
   [Babaliaros, Vasilis C.] Emory Univ Hosp, Struct Heart & Valve Ctr, Atlanta, GA 30322 USA.
   [Greenbaum, Adam B.] Henry Ford Hlth Syst, Inst Struct Heart Dis, Div Cardiol, Detroit, MI USA.
RP Lederman, RJ (reprint author), NHLBI, Cardiovasc & Pulm Branch, Div Intramural Res, NIH, Bldg 10,Room 2c713,MSC 1538, Bethesda, MD 20892 USA.
EM lederman@nih.gov
OI lederman, robert/0000-0003-1202-6673
FU Division of Intramural Research [Z01-HL006040]
FX Contract grant sponsor: Division of Intramural Research; Contract grant
   number: Z01-HL006040.
NR 6
TC 4
Z9 4
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1522-1946
EI 1522-726X
J9 CATHETER CARDIO INTE
JI Catheter. Cardiovasc. Interv.
PD DEC 1
PY 2015
VL 86
IS 7
BP 1242
EP 1254
DI 10.1002/ccd.26141
PG 13
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA CW9MS
UT WOS:000365323400016
PM 26356244
ER

PT J
AU Monzack, EL
   May, LA
   Roy, S
   Gale, JE
   Cunningham, LL
AF Monzack, E. L.
   May, L. A.
   Roy, S.
   Gale, J. E.
   Cunningham, L. L.
TI Live imaging the phagocytic activity of inner ear supporting cells in
   response to hair cell death
SO CELL DEATH AND DIFFERENTIATION
LA English
DT Article
ID HEARING-LOSS; ACOUSTIC TRAUMA; CISPLATIN OTOTOXICITY; SENSORY EPITHELIA;
   NOISE EXPOSURE; CHICK COCHLEA; MYOSIN VIIA; IN-VITRO; F-ACTIN;
   REGENERATION
AB Hearing loss and balance disorders affect millions of people worldwide. Sensory transduction in the inner ear requires both mechanosensory hair cells (HCs) and surrounding glia-like supporting cells (SCs). HCs are susceptible to death from aging, noise overexposure, and treatment with therapeutic drugs that have ototoxic side effects; these ototoxic drugs include the aminoglycoside antibiotics and the antineoplastic drug cisplatin. Although both classes of drugs are known to kill HCs, their effects on SCs are less well understood. Recent data indicate that SCs sense and respond to HC stress, and that their responses can influence HC death, survival, and phagocytosis. These responses to HC stress and death are critical to the health of the inner ear. Here we have used live confocal imaging of the adult mouse utricle, to examine the SC responses to HC death caused by aminoglycosides or cisplatin. Our data indicate that when HCs are killed by aminoglycosides, SCs efficiently remove HC corpses from the sensory epithelium in a process that includes constricting the apical portion of the HC after loss of membrane integrity. SCs then form a phagosome, which can completely engulf the remaining HC body, a phenomenon not previously reported in mammals. In contrast, cisplatin treatment results in accumulation of dead HCs in the sensory epithelium, accompanied by an increase in SC death. The surviving SCs constrict fewer HCs and display impaired phagocytosis. These data are supported by in vivo experiments, in which cochlear SCs show reduced capacity for scar formation in cisplatin-treated mice compared with those treated with aminoglycosides. Together, these data point to a broader defect in the ability of the cisplatin-treated SCs, to preserve tissue health in the mature mammalian inner ear.
C1 [Monzack, E. L.; May, L. A.; Roy, S.; Cunningham, L. L.] Natl Inst Deafness & Other Commun Disorders, NIH, Bethesda, MD 20892 USA.
   [Gale, J. E.] UCL, UCL Ear Inst, London WC1X 8EE, England.
RP Cunningham, LL (reprint author), Natl Inst Deafness & Other Commun Disorders, NIH, Bldg 35A Room ID971,35A Convent Dr, Bethesda, MD 20892 USA.
EM lisa.cunningham@nih.gov
FU NIDCD Division of Intramural Research [ZIA DC000079]; Flexigrant from
   Action on Hearing Loss
FX We thank Dr Joseph Burns and Dr Jonathan Bird for their insightful
   comments on this manuscript. We also thank the NIDCD/NINDS animal care
   staff for their support during the cisplatin injection protocol, as well
   as Dr Jane Johnson at the University of Texas Southwestern Medical
   Center for generously providing the Atoh1-nGFP mice. This work was
   supported by the NIDCD Division of Intramural Research (ZIA DC000079)
   and a Flexigrant from Action on Hearing Loss.
NR 48
TC 3
Z9 3
U1 1
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1350-9047
EI 1476-5403
J9 CELL DEATH DIFFER
JI Cell Death Differ.
PD DEC
PY 2015
VL 22
IS 12
BP 1995
EP 2005
DI 10.1038/cdd.2015.48
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA CW2UU
UT WOS:000364849400010
PM 25929858
ER

PT J
AU Lee, M
   Williams, K
   Hu, Y
   Andreas, J
   Patel, S
   Zhang, SY
   Crawford, N
AF Lee, Minnkyong
   Williams, Kendra A.
   Hu, Ying
   Andreas, Jonathan
   Patel, Shashank J.
   Zhang, Suiyuan
   Crawford, Nigel P. S.
TI GNL3 and SKA3 are novel prostate cancer metastasis susceptibility genes
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Article
DE Prostate cancer; Metastasis; Mouse models; TRAMP; Genetic susceptibility
ID NEUROENDOCRINE CARCINOMA; CELL-PROLIFERATION; TRAMP MODEL; PROGRESSION;
   MOUSE; NUCLEOSTEMIN; EXPRESSION; COMPONENT; COMPLEX; RRP1B
AB Prostate cancer (PC) is very common in developed countries. However, the molecular determinants of PC metastasis are unclear. Previously, we reported that germline variation influences metastasis in the C57BL/6-Tg(TRAMP)8247Ng/J (TRAMP) mouse model of PC. These mice develop prostate tumors similar to a subset of poor outcome, treatment-associated human PC tumors. Here, we used TRAMP mice to nominate candidate genes and validate their role in aggressive human PC in PC datasets and cell lines. Candidate metastasis susceptibility genes were identified through quantitative trait locus (QTL) mapping in 201 (TRAMP x PWK/PhJ) F2 males. Two metastasis-associated QTLs were identified; one on chromosome 12 (LOD = 5.86), and one on chromosome 14 (LOD = 4.41). Correlation analysis using microarray data from (TRAMP x PWK/PhJ) F2 prostate tumors identified 35 metastasis-associated transcripts within the two loci. The role of these genes in susceptibility to aggressive human PC was determined through in silico analysis using multiple datasets. First, analysis of candidate gene expression in two human PC datasets demonstrated that five candidate genes were associated with an increased risk of aggressive disease and lower disease-free survival. Second, four of these genes (GNL3, MAT1A, SKA3, and ZMYM5) harbored SNPs associated with aggressive tumorigenesis in the PLCO/CGEMS GWAS of 1172 PC patients. Finally, over-expression of GNL3 and SKA3 in the PC-3 human PC cell line decreased in vitro cell migration and invasion. This novel approach demonstrates how mouse models can be used to identify metastasis susceptibility genes, and gives new insight into the molecular mechanisms of fatal PC.
C1 [Lee, Minnkyong; Williams, Kendra A.; Andreas, Jonathan; Patel, Shashank J.; Crawford, Nigel P. S.] NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
   [Hu, Ying] NCI, Ctr Biomed Informat & Informat Technol, NIH, Rockville, MD 20850 USA.
   [Zhang, Suiyuan] NHGRI, Computat & Stat Genom Branch, NIH, Bethesda, MD 20892 USA.
RP Crawford, N (reprint author), NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
EM crawforn@mail.nih.gov
FU National Human Genome Research Institute, National Institutes of Health
   [HG200366-05]
FX 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). This research was supported by
   the Intramural Research Program of the National Human Genome Research
   Institute, National Institutes of Health [HG200366-05].
NR 45
TC 3
Z9 3
U1 1
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
EI 1573-7276
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD DEC
PY 2015
VL 32
IS 8
BP 769
EP 782
DI 10.1007/s10585-015-9745-y
PG 14
WC Oncology
SC Oncology
GA CW8EV
UT WOS:000365233200002
PM 26429724
ER

PT J
AU Salem, B
   Miner, S
   Hensel, NF
   Battiwalla, M
   Keyvanfar, K
   Stroncek, DF
   Gee, AP
   Hanley, PJ
   Bollard, CM
   Ito, S
   Barrett, AJ
AF Salem, Bahey
   Miner, Samantha
   Hensel, Nancy F.
   Battiwalla, Minoo
   Keyvanfar, Keyvan
   Stroncek, David F.
   Gee, Adrian P.
   Hanley, Patrick J.
   Bollard, Catherine M.
   Ito, Sawa
   Barrett, A. John
TI Quantitative activation suppression assay to evaluate human bone
   marrow-derived mesenchymal stromal cell potency
SO CYTOTHERAPY
LA English
DT Article
DE immunosuppression; suppression potency assay; mesenchymal stromal cells;
   K299
ID REGULATORY T-CELL; VERSUS-HOST-DISEASE; STEM-CELLS; MEMORY CELLS;
   EXPANSION; TRANSPLANTATION; KARPAS-299; PHENOTYPE; EFFECTOR; RECEPTOR
AB Background aims. With the increasing use of cell therapies involving immune modulatory cells, there is a need for a simple standardized method to evaluate and compare the suppressive potency of different cell products. We used the Karpas 299 (K299) cell line as the reference suppressor cell to develop a standardized suppression assay to quantify the immune-modulatory capacity of bone marrow derived mesenchymal stromal cells (BM-MSCs). Methods. Healthy donor CD4 T cells were co-cultured with the K299 cell line or with third-party BM-MSCs. After stimulation with anti-CD3/CD28 beads, CD 154 activation and proliferation of CD4 T cells were measured to calculate suppression. Results. The K299 cell line reproducibly suppressed both the activation and proliferation of healthy donor CD4 T cells in a dose-dependent manner. A rapid (16-h) assay that was based on activation-suppression was selected for development. In replicate testing, there was an inherent variability of suppression of 11% coefficient of variation between different responder T cells. Suppression by BM-MSCs on different responders correlated with suppression by K299. We therefore used K299 suppression as the reference to define suppression potency of BM-MSCs in K299 Suppression Units. We found that inter-donor variability, passage number, method of manufacture and exposure of BM-MSCs to steroids or interferon-gamma all affected BM-MSC potency of suppression. Conclusions. This method provides a platform for standardizing suppressor function to facilitate comparisons between laboratories and for use as a cell product release assay.
C1 [Salem, Bahey; Miner, Samantha; Hensel, Nancy F.; Battiwalla, Minoo; Keyvanfar, Keyvan; Ito, Sawa; Barrett, A. John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Stroncek, David F.] NIH, Dept Transfus Med, Bethesda, MD USA.
   [Salem, Bahey; Gee, Adrian P.] Houston Methodist Hosp, Texas Childrens Hosp, Ctr Cell & Gene Therapy, Houston, TX USA.
   [Salem, Bahey; Gee, Adrian P.] Baylor Coll Med, Houston, TX 77030 USA.
   [Hanley, Patrick J.; Bollard, Catherine M.] Childrens Natl Hlth Syst, Program Cell Enhancement & Technol Immunotherapy, Ctr Canc & Immunol Res, Sheikh Zayed Inst Pediat Surg Innovat, Washington, DC USA.
   [Hanley, Patrick J.; Bollard, Catherine M.] Childrens Natl Hlth Syst, Div Blood & Marrow Transplantat, Washington, DC USA.
RP Ito, S (reprint author), 10 Ctr Dr,Bldg 10,CRC Room 5-3581, Bethesda, MD 20892 USA.
EM itos2@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health, at the
   National Heart, Lung, and Blood Institute; Children's National Health
   System
FX This study was supported by the Intramural Research Program of the
   National Institutes of Health, at the National Heart, Lung, and Blood
   Institute. A Board of Visitors Grant was awarded to C.M.B. and P.J.H. at
   Children's National Health System.
NR 31
TC 5
Z9 5
U1 0
U2 0
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 DEC
PY 2015
VL 17
IS 12
BP 1675
EP 1686
DI 10.1016/j.jcyt.2015.08.008
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 CW8JU
UT WOS:000365246500003
PM 26422657
ER

PT J
AU Myers, MF
   Fernandes, SL
   Arduser, L
   Hopper, JL
   Koehly, LM
AF Myers, Melanie F.
   Fernandes, Sara L.
   Arduser, Lora
   Hopper, Jennifer L.
   Koehly, Laura M.
TI Talking About Type 2 Diabetes Family Communication From the Perspective
   of At-Risk Relatives
SO DIABETES EDUCATOR
LA English
DT Article
ID NONPOLYPOSIS COLORECTAL-CANCER; RANDOMIZED CONTROLLED-TRIAL; 1ST DEGREE
   RELATIVES; PHYSICAL-ACTIVITY; QUALITATIVE DESCRIPTION;
   CARDIOVASCULAR-DISEASE; HEALTH-RISK; PREVENTION; HISTORY; ADULTS
AB Purpose
   The purpose of this study was to describe type 2 diabetes (T2DM) communication and risk reduction recommendations from the perspective of family members at risk for T2DM based on family history.
   Methods
   Semistructured qualitative interviews were conducted with 33 individuals with a first-degree relative with T2DM. Participants were recruited from the community and a previous pharmacogenetics study. Deductive and inductive codes were applied to the transcripts.
   Results
   Conversations with family members with and without T2DM focused on symptoms and disease management of the family member with T2DM. With at-risk relatives, conversations also focused on prevention. Lack of perceived relevance to family members without T2DM was a barrier to communication. Recommendations to facilitate communication included education of an at-risk family member to increase awareness of risk, followed by sharing of learned information with others.
   Conclusion
   Efforts are needed to increase awareness and improve communication about T2DM risk factors, familial risk, and risk reduction behaviors within families with a family history of T2DM. Family members with and without T2DM should be encouraged to communicate with their relatives about T2DM and the risk to family members. Identification of family members who can facilitate communication, education, and modeling of healthy behaviors may increase awareness and motivate at-risk individuals to engage in risk-reducing behaviors.
C1 [Myers, Melanie F.; Fernandes, Sara L.; Hopper, Jennifer L.] Cincinnati Childrens Hosp Med Ctr, Dept Pediat, Cincinnati, OH 45229 USA.
   [Myers, Melanie F.; Fernandes, Sara L.; Hopper, Jennifer L.] Univ Cincinnati, Coll Med, Cincinnati, OH 45229 USA.
   [Fernandes, Sara L.] LabCorp Integrated Genet, Monrovia, CA USA.
   [Arduser, Lora] Univ Cincinnati, Coll Arts & Sci, Cincinnati, OH USA.
   [Koehly, Laura M.] NHGRI, Social & Behav Res Branch, Bethesda, MD 20892 USA.
RP Myers, MF (reprint author), Cincinnati Childrens Hosp Med Ctr, 3333 Burnet Ave,MLC 4006, Cincinnati, OH 45229 USA.
EM Melanie.Myers@cchmc.org
FU National Institute of Diabetes and Digestive and Kidney Diseases
   [DK095473]; National Human Genome Research Institute's Intramural
   Research Program [Z01HG200335]
FX This study was supported by a National Institute of Diabetes and
   Digestive and Kidney Diseases grant (DK095473 to M.F.M.) and the
   National Human Genome Research Institute's Intramural Research Program
   (Z01HG200335 to L.M.K.).
NR 51
TC 1
Z9 1
U1 0
U2 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0145-7217
EI 1554-6063
J9 DIABETES EDUCATOR
JI Diabetes Educ.
PD DEC
PY 2015
VL 41
IS 6
BP 716
EP 728
DI 10.1177/0145721715604367
PG 13
WC Endocrinology & Metabolism; Public, Environmental & Occupational Health
SC Endocrinology & Metabolism; Public, Environmental & Occupational Health
GA CW8LS
UT WOS:000365251700006
PM 26323720
ER

PT J
AU Wang, YF
   Wei, YY
   Gaborieau, V
   Shi, JX
   Han, YH
   Timofeeva, MN
   Su, L
   Li, YF
   Eisen, T
   Amos, CI
   Landi, MT
   Christiani, DC
   Mckay, JD
   Houlston, RS
AF Wang, Yufei
   Wei, Yongyue
   Gaborieau, Valerie
   Shi, Jianxin
   Han, Younghun
   Timofeeva, Maria N.
   Su, Li
   Li, Yafang
   Eisen, Timothy
   Amos, Christopher I.
   Landi, Maria Teresa
   Christiani, David C.
   McKay, James D.
   Houlston, Richard S.
TI Deciphering associations for lung cancer risk through imputation and
   analysis of 12 316 cases and 16 831 controls
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; COMMON GENETIC-VARIATION; CLASSICAL HLA
   ALLELES; SUSCEPTIBILITY LOCUS; GENOTYPE IMPUTATION; TELOMERE LENGTH;
   LARGE-SCALE; VARIANTS; ADENOCARCINOMA; METAANALYSIS
AB Recent genome-wide association studies have identified common variants at multiple loci influencing lung cancer risk. To decipher the genetic basis of the association signals at 3q28, 5p15.33, 6p21.33, 9p21 and 12p13.33, we performed a meta-analysis of data from five genome-wide association studies in populations of European ancestry totalling 12 316 lung cancer cases and 16 831 controls using imputation to recover untyped genotypes. For four of the regions, it was possible to refine the association signal identifying a smaller region of interest likely to harbour the functional variant. Our analysis did not provide evidence that any of the associations at the loci being a consequence of synthetic associations rather than linkage disequilibrium with a common risk variant at these risk loci.
C1 [Wang, Yufei; Houlston, Richard S.] Inst Canc Res, Div Genet & Epidemiol, Sutton SM2 5NG, Surrey, England.
   [Wei, Yongyue; Su, Li; Christiani, David C.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
   [Gaborieau, Valerie; Timofeeva, Maria N.; McKay, James D.] WHO, IARC, Lyon, France.
   [Shi, Jianxin] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
   [Han, Younghun; Li, Yafang; Amos, Christopher I.] Ctr Genom Med, Geisel Sch Med, Dept Community & Family Med, Lebanon, NH USA.
   [Timofeeva, Maria N.] Univ Edinburgh, Inst Genet & Mol Med, Edinburgh, Midlothian, Scotland.
   [Eisen, Timothy] Addenbrookes Hosp, Cambridge, England.
   [Landi, Maria Teresa] NCI, Dept Hlth & Human Serv, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
RP Houlston, RS (reprint author), Inst Canc Res, Div Genet & Epidemiol, 15 Cotswold Rd, Sutton SM2 5NG, Surrey, England.
EM richard.houlston@icr.ac.uk
OI Houlston, Richard/0000-0002-5268-0242
FU National Institute of Health (NIH) [U19CA148127, 5R01CA055769,
   5R01CA127219, 5R01CA133996, 5R01CA121197, R01 CA111703, UO1 CA63673, R01
   CA092039, CA074386, CA092824, CA090578]; Cancer Research UK
   [C1298/A8780, C1298/A8362]; HEAL; Sanofi-Aventis; Institut National du
   Cancer; European Community (Integrated Project DNA repair)
   [LSHG-CT-2005-512113]; Norwegian Cancer Association; Czech Republic
   (RECAMO) [CZ.1.05/2.1.00/03.0101]; Fred Hutchinson Cancer Research
   Center, an FP7 grant [REGPOT 245536]; Estonian Government
   [SF0180142s08]; EU; TCGA [3230]
FX This study was supported by grants from the National Institute of Health
   (NIH) (U19CA148127, 5R01CA055769, 5R01CA127219, 5R01CA133996, and
   5R01CA121197, R01 CA111703 and UO1 CA63673, R01 CA092039, CA074386,
   CA092824, CA090578), Cancer Research UK (C1298/A8780, C1298/A8362),
   HEAL, Sanofi-Aventis, Institut National du Cancer, the European
   Community (Integrated Project DNA repair, LSHG-CT-2005-512113), the
   Norwegian Cancer Association, the Czech Republic (RECAMO,
   CZ.1.05/2.1.00/03.0101), the Fred Hutchinson Cancer Research Center, an
   FP7 grant (REGPOT 245536), the Estonian Government (SF0180142s08), by EU
   RDF in the frame of Centre of Excellence in Genomics and Estoinian
   Research Infrastructure's Roadmap. We thank all individuals who
   participated in this study. The ICR study made use of data from the
   WTCCCII (http: //www.wtccc.org.uk). We acknowledge the TCGA for their
   contribution of lung cancer genomic data to this study (Project Number
   3230).
NR 44
TC 5
Z9 5
U1 1
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1018-4813
EI 1476-5438
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD DEC
PY 2015
VL 23
IS 12
BP 1723
EP 1728
DI 10.1038/ejhg.2015.48
PG 6
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA CW6TC
UT WOS:000365129700023
PM 25804397
ER

PT J
AU Shapiro, GI
   McCallum, S
   Adams, LM
   Sherman, L
   Weller, S
   Swann, S
   Keer, H
   Miles, D
   Muller, T
   Rabe, DC
   Cecchi, F
   Bottaro, DP
   LoRusso, P
AF Shapiro, Geoffrey I.
   McCallum, Stewart
   Adams, Laurel M.
   Sherman, Laurie
   Weller, Steve
   Swann, Suzanne
   Keer, Harold
   Miles, Dale
   Mueller, Thomas
   Rabe, Daniel C.
   Cecchi, Fabiola
   Bottaro, Donald P.
   LoRusso, Patricia
TI A Phase 1 dose-escalation study of the safety and pharmacokinetics of
   once-daily oral foretinib, a multi-kinase inhibitor, in patients with
   solid tumors (vol 31, pg 742, 2013)
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Correction
C1 [Adams, Laurel M.; Weller, Steve] GlaxoSmithKline, Oncol Res & Dev, Durham, NC USA.
   [Swann, Suzanne] CSL Behring, King Of Prussia, PA USA.
   [Keer, Harold; Miles, Dale; Mueller, Thomas] Exelixis, San Francisco, CA USA.
   [LoRusso, Patricia] Wayne State Univ, Barbara Ann Karmanos Canc Inst, Detroit, MI USA.
   [Rabe, Daniel C.; Cecchi, Fabiola] NCI, Urol Oncol Branch, Ctr Canc Res, Collegeville, PA USA.
RP Adams, LM (reprint author), Medimmune, Gaithersburg, MD 20878 USA.
EM adamsla@medimmune.com
NR 1
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-6997
EI 1573-0646
J9 INVEST NEW DRUG
JI Invest. New Drugs
PD DEC
PY 2015
VL 33
IS 6
BP 1292
EP 1292
DI 10.1007/s10637-015-0287-6
PG 1
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA CW7PR
UT WOS:000365192100017
PM 26407571
ER

PT J
AU Shellman, YG
   Lambert, KA
   Brauweiler, A
   Fain, P
   Spritz, RA
   Martini, M
   Janssen, KP
   Box, NF
   Terzian, T
   Rewers, M
   Horvath, A
   Stratakis, CA
   Robinson, WA
   Robinson, SE
   Norris, DA
   Artinger, KB
   Pacheco, TR
AF Shellman, Yiqun G.
   Lambert, Karoline A.
   Brauweiler, Anne
   Fain, Pamela
   Spritz, Richard A.
   Martini, Melanie
   Janssen, Klaus-Peter
   Box, Neil F.
   Terzian, Tamara
   Rewers, Marian
   Horvath, Anelia
   Stratakis, Constantine A.
   Robinson, William A.
   Robinson, Steven E.
   Norris, David A.
   Artinger, Kristin B.
   Pacheco, Theresa R.
TI SASH1 Is Involved in an Autosomal Dominant Lentiginous Phenotype
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Letter
ID TUMOR-SUPPRESSOR GENE; CELL; PROLIFERATION; APOPTOSIS; CANCER
C1 [Shellman, Yiqun G.; Lambert, Karoline A.; Brauweiler, Anne; Norris, David A.; Pacheco, Theresa R.] Univ Colorado, Dept Dermatol, Sch Med, Aurora, CO 80045 USA.
   [Fain, Pamela; Spritz, Richard A.] Univ Colorado, Sch Med, Human Med Genet & Genom Program, Aurora, CO USA.
   [Fain, Pamela; Rewers, Marian] Univ Colorado, Sch Med, Barbara Davis Ctr Childhood Diabet, Aurora, CO USA.
   [Martini, Melanie; Janssen, Klaus-Peter] Tech Univ Munich, Klinikum Rechts Isar, Dept Surg, D-80290 Munich, Germany.
   [Box, Neil F.; Terzian, Tamara] Univ Colorado, Sch Med, Dept Dermatol, Charles C Gates Regenerat Med & Stem Cell Biol Pr, Aurora, CO USA.
   [Horvath, Anelia; Stratakis, Constantine A.] Eunice Kenney Shriver Natl Inst Child Hlth & Huma, Sect Endocrinol & Genet, Program Dev Endocrinol & Genet, NIH, Bethesda, MD USA.
   [Robinson, William A.; Robinson, Steven E.] Univ Colorado, Sch Med, Div Med Oncol, Aurora, CO USA.
   [Artinger, Kristin B.] Univ Colorado, Sch Dent Med, Department Craniofacial Biol, Aurora, CO USA.
RP Shellman, YG (reprint author), Univ Colorado, Dept Dermatol, Sch Med, Anschutz Med Campus, Aurora, CO 80045 USA.
EM Yiqun.Shellman@ucdenver.edu; Theresa.Pacheco@ucdenver.edu
FU NCATS NIH HHS [UL1 TR001082]; NCI NIH HHS [P30CA046934, P30 CA046934];
   NIAMS NIH HHS [K01 AR063203, P30AR057212, R03AR064555, T32AR007411,
   K23AR49214, R03 AR064555, P30 AR057212, T32 AR007411, R03 AR066880, K23
   AR049214]
NR 15
TC 2
Z9 2
U1 1
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD DEC
PY 2015
VL 135
IS 12
BP 3192
EP 3194
DI 10.1038/jid.2015.292
PG 3
WC Dermatology
SC Dermatology
GA CW7LT
UT WOS:000365181100041
PM 26203640
ER

PT J
AU Ziu, M
   Kalkanis, SN
   Gilbert, M
   Ryken, TC
   Olson, JJ
AF Ziu, Mateo
   Kalkanis, Steven N.
   Gilbert, Mark
   Ryken, Timothy C.
   Olson, Jeffrey J.
TI The role of initial chemotherapy for the treatment of adults with
   diffuse low grade glioma A systematic review and evidence-based clinical
   practice guideline
SO JOURNAL OF NEURO-ONCOLOGY
LA English
DT Review
DE Low grade glioma; Guidelines; Chemotherapy; Treatment; Temozolomide; PCV
ID TEMOZOLOMIDE TREATMENT; PCV CHEMOTHERAPY; OLIGODENDROGLIOMA; TRIAL;
   ASTROCYTOMAS; PROCARBAZINE; VINCRISTINE; LOMUSTINE; EFFICACY; THERAPY
AB Adult patients (older than 18 years of age) with newly diagnosed World Health Organization (WHO) Grade II gliomas (Oligodendroglioma, astrocytoma, mixed oligoastrocytoma).
   Is there a role for chemotherapy as adjuvant therapy of choice in treatment of patients with newly diagnosed low-grade gliomas?
   Chemotherapy is recommended as a treatment option to postpone the use of radiotherapy, to slow tumor growth and to improve progression free survival (PFS), overall survival (OS) and clinical symptoms in adult patients with newly diagnosed LGG.
   Who are the patients with newly diagnosed LGG that would benefit the most from chemotherapy?
   Chemotherapy is recommended as an optional component alone or in combination with radiation as the initial adjuvant therapy for all patients who cannot undergo gross total resection (GTR) of a newly diagnosed LGG. Patient with residual tumor > 1 cm on post-operative MRI, presenting diameter of > 4 cm or older than 40 years of age should be considered for adjuvant therapy as well.
   Are there tumor markers that can predict which patients can benefit the most from initial treatment with chemotherapy?
   The addition of chemotherapy to standard RT is recommended in LGG patients that carry IDH mutation. In addition, temozolomide (TMZ) is recommended as a treatment option to slow tumor growth in patients who harbor the 1p/19q co-deletion.
   How soon should the chemotherapy be started once the diagnosis of LGG is confirmed?
   There is insufficient evidence to make a definitive recommendation on the timing of starting chemotherapy after surgical/pathological diagnosis of LGG has been made. However, using the 12 weeks mark as the latest timeframe to start adjuvant chemotherapy is suggested. It is recommended that patients be enrolled in properly designed clinical trials to assess the timing of chemotherapy initiation once diagnosis is confirmed for this target population.
   What chemotherapeutic agents should be used for treatment of newly diagnosed LGG?
   There is insufficient evidence to make a recommendation of one particular regimen. Enrollment of subjects in properly designed trials comparing the efficacy of these or other agents is recommended so as to determine which of these regimens is superior.
   What is the optimal duration and dosing of chemotherapy as initial treatment for LGG?
   Insufficient evidence exists regarding the duration of any specific cytotoxic drug regimen for treatment of newly diagnosed LGG. Enrollment of subjects in properly designed clinical investigations assessing the optimal duration of this therapy is recommended.
   Should chemotherapy be given alone or in conjunction with RT as initial therapy for LGG?
   Insufficient evidence exists to make recommendations in this regard. Hence, enrollment of patients in properly designed clinical trials assessing the difference between chemotherapy alone, RT alone or a combination of them is recommended.
   Should chemotherapy be given in addition to other type of adjuvant therapy to patients with newly diagnosed LGG?
   Level II: It is recommended that chemotherapy be added to the RT in patients with unfavorable LGG to improve their progression free survival.
C1 [Ziu, Mateo] Seton Brain & Spine Inst, Dept Neurosurg, Austin, TX 78701 USA.
   [Kalkanis, Steven N.] Henry Ford Hlth Syst, Dept Neurosurg, Detroit, MI USA.
   [Gilbert, Mark] NCI, Ctr Canc Res, Neurooncol Branch, Bethesda, MD 20892 USA.
   [Ryken, Timothy C.] Univ Kansas, Med Ctr, Dept Neurosurg, Kansas City, KS 66103 USA.
   [Olson, Jeffrey J.] Emory Univ, Sch Med, Dept Neurosurg, Atlanta, GA USA.
RP Ziu, M (reprint author), Seton Brain & Spine Inst, Dept Neurosurg, 1400 N IH-35,Suite 300, Austin, TX 78701 USA.
EM mziu@seton.org
OI Ziu, Mateo/0000-0002-3671-2638
FU National Cancer Institute; Genentech; Millennium
FX Dr. Kalkanis is a consultant for Arbor and Varian. Dr. Olson is a
   consultant for the American Cancer Society; has received research
   funding from the National Cancer Institute, Genentech, and Millennium;
   and has received investigational drug provision from Merck.
NR 21
TC 2
Z9 4
U1 5
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-594X
EI 1573-7373
J9 J NEURO-ONCOL
JI J. Neuro-Oncol.
PD DEC
PY 2015
VL 125
IS 3
SI SI
BP 585
EP 607
DI 10.1007/s11060-015-1931-x
PG 23
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA CX0XD
UT WOS:000365419800008
PM 26530261
ER

PT J
AU Tulipan, N
   Wellons, JC
   Thom, EA
   Gupta, N
   Sutton, LN
   Burrows, PK
   Farmer, D
   Walsh, W
   Johnson, MP
   Rand, L
   Tolivaisa, S
   D'Alton, ME
   Adzick, NS
AF Tulipan, Noel
   Wellons, John C., III
   Thom, Elizabeth A.
   Gupta, Nalin
   Sutton, Leslie N.
   Burrows, Pamela K.
   Farmer, Diana
   Walsh, William
   Johnson, Mark P.
   Rand, Larry
   Tolivaisa, Susan
   D'Alton, Mary E.
   Adzick, N. Scott
CA MOMS Investigators
TI Prenatal surgery for myelomeningocele and the need for cerebrospinal
   fluid shunt placement
SO JOURNAL OF NEUROSURGERY-PEDIATRICS
LA English
DT Article
DE myelomeningocele; spina bifida; hydrocephalus; hindbrain herniation;
   fetal surgery; cerebrospinal fluid shunt; congenital
ID ENDOSCOPIC 3RD VENTRICULOSTOMY; CHOROID-PLEXUS CAUTERIZATION;
   CLINICAL-RESEARCH NETWORK; HYDROCEPHALUS; INFANTS; ARTICLE
AB OBJECT The Management of Myelomeningocele Study (MOMS) was a multicenter randomized trial comparing the safety and efficacy of prenatal and postnatal closure of myelomeningocele. The trial was stopped early because of the demonstrated efficacy of prenatal surgery, and outcomes on 158 of 183 pregnancies were reported. Here, the authors update the 1-year outcomes for the complete trial, analyze the primary and related outcomes, and evaluate whether specific prerandomization risk factors are associated with prenatal surgery benefit.
   METHODS The primary outcome was a composite of fetal loss or any of the following: infant death, CSF shunt placement, or meeting the prespecified criteria for shunt placement. Primary outcome, actual shunt placement, and shunt revision rates for prenatal versus postnatal repair were compared. The shunt criteria were reassessed to determine which were most concordant with practice, and a new composite outcome was created from the primary outcome by replacing the original criteria for CSF shunt placement with the revised criteria. The authors used logistic regression to estimate whether there were interactions between the type of surgery and known prenatal risk factors,(lesion level, gestational age, degree of hindbrain herniation, and ventricle size) for shunt placement, and to determine which factors were associated with shunting among those infants who underwent prenatal surgery.
   RESULTS Ninety-one women were randomized to prenatal surgery and 92 to postnatal repair. The primary outcome occurred in 73% of infants in the prenatal surgery group and in 98% in the postnatal group (p < 0.0001). Actual rates of shunt placement were only 44% and 84% in the 2 groups, respectively (p < 0.0001). The authors revised the most commonly met criterion to require overt clinical signs of increased intracranial pressure, defined as split sutures, bulging fontanelle, or sunsetting eyes, in addition to increasing head circumference or hydrocephalus. Using these modified criteria, only 3 patients in each group met criteria but did not receive a shunt. For the revised composite outcome, there was a difference between the prenatal and postnatal surgery groups: 49.5% versus 87.0% (p < 0.0001). There was also a significant reduction in the number of children who had a shunt placed and then required a revision by 1 year of age in the prenatal group (15.4% vs 40.2%, relative risk 0.38 [95% CI 0.22-0.66]). In the prenatal surgery group, 20% of those with ventricle size < 10 mm at initial screening, 45.2% with ventricle size of 10 up to 15 mm, and 79.0% with ventricle size 15 mm received a shunt, whereas in the postnatal group, 79.4%, 86.0%, and 87.5%, respectively, received a shunt (p = 0.02). Lesion level and degree of hindbrain herniation appeared to have no effect on the eventual need for shunting (p = 0.19 and p = 0.13, respectively). Similar results were obtained for the revised outcome.
   CONCLUSIONS Larger ventricles at initial screening are associated with an increased need for shunting among those undergoing fetal surgery for myelomeningocele. During prenatal counseling, care should be exercised in recommending prenatal surgery when the ventricles are 15 mm or larger because prenatal surgery does not appear to improve outcome in this group. The revised criteria may be useful as guidelines for treating hydrocephalus in this group.
C1 [Tulipan, Noel; Wellons, John C., III] Vanderbilt Univ, Med Ctr, Dept Neurosurg, Nashville, TN 37232 USA.
   [Walsh, William] Vanderbilt Univ, Med Ctr, Dept Pediat, Nashville, TN 37232 USA.
   [Thom, Elizabeth A.; Burrows, Pamela K.] George Washington Univ, Ctr Biostat, Washington, DC USA.
   [Gupta, Nalin] Univ Calif San Francisco, Dept Neurol Surg, San Francisco, CA USA.
   [Farmer, Diana] Univ Calif San Francisco, Dept Surg, San Francisco, CA USA.
   [Rand, Larry] Univ Calif San Francisco, Dept Obstet & Gynecol, San Francisco, CA 94143 USA.
   [Sutton, Leslie N.] Childrens Hosp Philadelphia, Dept Neurosurg, Philadelphia, PA USA.
   [Johnson, Mark P.; Adzick, N. Scott] Childrens Hosp Philadelphia, Ctr Fetal Diag & Treatment, Philadelphia, PA USA.
   [Tolivaisa, Susan] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pregnancy & Perinatol Branch, Bethesda, MD USA.
   [D'Alton, Mary E.] Columbia Univ, Dept Obstet & Gynecol, New York, NY USA.
RP Wellons, JC (reprint author), Vanderbilt Univ, Med Ctr, Dept Neurosurg, Monroe Carell Jr Childrens Hosp Vanderbilt, 2200 Childrens Way,Rm 9226,9222 Doctors Off Tower, Nashville, TN 37232 USA.
EM jay.wellons@vanderbilt.edu
FU Eunice Kennedy Shriver National Institute of Child Health and Human
   Development (NICHD) [U10-HD041666, U10-HD041667, U10-HD041669,
   U01-HD041665]
FX Supported by grants from the Eunice Kennedy Shriver National Institute
   of Child Health and Human Development (NICHD): U10-HD041666 (Adzick),
   U10-HD041667 (Brock), U10-HD041669 (Farmer), and U01-HD041665 (Thom).
NR 13
TC 8
Z9 9
U1 2
U2 7
PU AMER ASSOC NEUROLOGICAL SURGEONS
PI ROLLING MEADOWS
PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA
SN 1933-0707
EI 1933-0715
J9 J NEUROSURG-PEDIATR
JI J. Neurosurg.-Pediatr.
PD DEC
PY 2015
VL 16
IS 6
BP 613
EP 620
DI 10.3171/2015.7.PEDS15336
PG 8
WC Clinical Neurology; Pediatrics; Surgery
SC Neurosciences & Neurology; Pediatrics; Surgery
GA CX0FM
UT WOS:000365372300001
PM 26369371
ER

PT J
AU Chang, MK
   Sears, C
   Huang, JC
   Miller, AJ
   Kushner, HW
   Lee, JS
AF Chang, Michael K.
   Sears, Chad
   Huang, John C.
   Miller, Arthur J.
   Kushner, Harvey W.
   Lee, Janice S.
TI Correlation of Airway Volume With Orthognathic Surgical Movement Using
   Cone-Beam Computed Tomography
SO JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY
LA English
DT Article
ID OBSTRUCTIVE SLEEP-APNEA; PHARYNGEAL AIRWAY; MANDIBULAR PROGNATHISM;
   SURGERY; RECONSTRUCTION; ADVANCEMENT; CT; UVULOPALATOPHARYNGOPLASTY;
   MORPHOLOGY; SEVERITY
AB Purpose: Orthognathic surgery can induce changes in airway volume. The aim of this study was to determine whether there is a correlation of surgical movement of the maxilla or mandible to airway volume changes.
   Materials and Methods: This was a prospective cohort study and the sample was composed of patients undergoing single-jaw orthognathic procedures from 2004 through 2007. Cone-beam computed tomograms were obtained before surgery (T0), immediately after surgery (T1), and at least 6 months after surgery (T2). The airway was segmented from 3-dimensional images and identified as the whole airway, consisting of the naso-, oro-, and hypopharynx. The volumetric percentage of change of the airway between time points was compared and correlated to the surgical movements using paired t test and cubic regression analysis. The level of statistical significance was set at a P value less than or equal to.05.
   Results: The sample was composed of 33 patients. Sixteen patients underwent maxillary advancement with mean advancement of 5.4mm (3 to 8mm), 13 underwent mandibular advancement with mean advancement of 8.0 mm(5 to 15mm), and 4 underwent mandibular setback of 4.0mm. For maxillary advancement at T1, volume percentages of change for the whole airway and the naso-, oro-, and hypopharynx were 18.4 (P <=.05), 53.8 (P <=.05), 26.3, and 5.5%, respectively, and at T2, the changes were 10.0, 46.7 (P <=.05), 6.8, and 1.0%, respectively. For mandibular advancement at T1, volume percentages of change were 34.6 (P <=.05), 26.1, 54.1 (P <=.05), and 17.4%, respectively, and at T2, the changes were 15.0 (P <=.05), -3.7, 23.5 (P <=.05), and 12.1%, respectively. There were no meaningful long-term airway changes with mandibular setback.
   Conclusion: The study results suggest that there might be an anatomic limit to pharyngeal airway expansion associated with single-jaw orthognathic surgery. Published by Elsevier Inc on behalf of the American Association of Oral and Maxillofacial Surgeons
C1 [Chang, Michael K.; Sears, Chad; Huang, John C.; Miller, Arthur J.] Univ Calif San Francisco, Div Orthodont, Dept Orofacial Sci, San Francisco, CA 94143 USA.
   [Kushner, Harvey W.] Biomed Comp Res Inst, Dept Biostat, Philadelphia, PA USA.
   [Lee, Janice S.] NIDCR, NIH, Bethesda, MD 20892 USA.
RP Lee, JS (reprint author), NIDCR, NIH, 10 Ctr Dr,Bldg 10,Room 5-2531 North East Atrium, Bethesda, MD 20892 USA.
EM Janice.lee@nih.gov
FU University of California-San Francisco Academic Senate Award
FX This study was supported by the University of California-San Francisco
   Academic Senate Award (to J.C.H. and J.S.L.). None of the other authors
   reported any disclosures.
NR 37
TC 0
Z9 0
U1 1
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0278-2391
EI 1531-5053
J9 J ORAL MAXIL SURG
JI J. Oral Maxillofac. Surg.
PD DEC
PY 2015
VL 73
IS 12
SU S
BP S67
EP S76
DI 10.1016/j.joms.2015.09.002
PG 10
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA CW9WA
UT WOS:000365347700010
PM 26608156
ER

PT J
AU Serafine, KM
   Rice, KC
   France, CP
AF Serafine, Katherine M.
   Rice, Kenner C.
   France, Charles P.
TI Directly Observable Behavioral Effects of Lorcaserin in Rats
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID 5-HT2C RECEPTOR AGONIST; HEAD-TWITCH BEHAVIOR; PHARMACOLOGICAL
   CHARACTERIZATION; FOOD RESTRICTION; D-FENFLURAMINE; COCAINE; DRUGS;
   OBESITY; 5-HYDROXYTRYPTAMINE; DISCRIMINATION
AB (1R)-8-chloro-1-methyl-2,3,4,5-tetrahydro-1H-3-benzazepine (lorcaserin) is approved by the United States Food and Drug Administration for treating obesity, and its therapeutic effects are thought to result from agonist activity at serotonin (5-HT)(2C) receptors. Lorcaserin has affinity for other 5-HT receptor subtypes, although its activity at those subtypes is not fully described. The current study compared the behavioral effects of lorcaserin (0.0032-32.0 mg/kg) to the effects of other 5-HT receptor selective agonists in rats (n = 8). The 5-HT2C receptor selective agonist 1-(3-chlorophenyl) piperazine (mCPP, 0.032-1.0 mg/kg) and lorcaserin induced yawning which was attenuated by the 5-HT2C receptor selective antagonist 6-chloro-5-methyl-N-(6-[(2-methylpyridin-3-yl)oxy]pydidin-3-yl)indoline-1-carboxamide (1.0 mg/kg). The 5-HT2A receptor selective agonist 2,5-dimethoxy-4-methylamphetamine (0.1-3.2 mg/kg) induced head twitching, which was attenuated by the 5-HT2A receptor selective antagonist R-(1)-2,3-dimethoxyphenyl-1-2-(4-piperidine)-methanol] (MDL 100907, 0.01 mg/kg), lorcaserin (3.2 mg/kg), and mCPP (3.2 mg/kg). In rats pretreated with MDL 100907 (1.0 mg/kg), lorcaserin also induced head twitching. At larger doses, lorcaserin produced forepaw treading, which was attenuated by the 5-HT1A receptor selective antagonist N-(2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl)-N-(2-pyridyl) cyclohexanecarboxamide (0.178 mg/kg). While the behavioral effects of lorcaserin in rats are consistent with it having agonist activity at 5-HT2C receptors, these data suggest that at larger doses it also has agonist activity at 5-HT2A and possibly 5-HT1A receptors. Mounting evidence suggests that 5-HT2C receptor agonists might be effective for treating drug abuse. A more complete description of the activity of lorcaserin at 5-HT receptor subtypes will facilitate a better understanding of the mechanisms that mediate its therapeutic effects.
C1 [Serafine, Katherine M.; France, Charles P.] Univ Texas Hlth Sci Ctr San Antonio, Dept Pharmacol, San Antonio, TX 78229 USA.
   [France, Charles P.] Univ Texas Hlth Sci Ctr San Antonio, Dept Psychiat, San Antonio, TX 78229 USA.
   [Rice, Kenner C.] NIDA, Chem Biol Res Lab, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
   [Rice, Kenner C.] NIAAA, NIH, Bethesda, MD USA.
RP France, CP (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Pharmacol, 7703 Floyd Curl Dr,Mail Code 7764, San Antonio, TX 78229 USA.
EM france@uthscsa.edu
OI Serafine, Katherine/0000-0002-5099-8505
FU National Institutes of Health National Institute on Drug Abuse
   [K05DA017918, T32DA031115]; National Institutes of Health Intramural
   Research Programs of the National Institute on Drug Abuse; National
   Institute of Alcohol Abuse and Alcoholism
FX This work was supported, in part, by grants from the National Institutes
   of Health National Institute on Drug Abuse [Grants K05DA017918 and
   T32DA031115]. A portion of this work was supported by the National
   Institutes of Health Intramural Research Programs of the National
   Institute on Drug Abuse and the National Institute of Alcohol Abuse and
   Alcoholism. The content is solely the responsibility of the authors and
   does not necessarily represent the official views of the National
   Institute on Drug Abuse, the National Institute of Alcohol Abuse and
   Alcoholism, or the National Institutes of Health. The authors have no
   conflict of interest.
NR 31
TC 2
Z9 2
U1 0
U2 2
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0022-3565
EI 1521-0103
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD DEC
PY 2015
VL 355
IS 3
BP 381
EP 385
DI 10.1124/jpet.115.228148
PG 5
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA CW7ID
UT WOS:000365170700005
PM 26384326
ER

PT J
AU Arons, E
   Zhou, H
   Edelman, DC
   Gomez, A
   Steinberg, SM
   Petersen, D
   Wang, YH
   Meltzer, PS
   Kreitman, RJ
AF Arons, Evgeny
   Zhou, Hong
   Edelman, Daniel C.
   Gomez, Allison
   Steinberg, Seth M.
   Petersen, David
   Wang, Yonghong
   Meltzer, Paul S.
   Kreitman, Robert J.
TI Impact of telomere length on survival in classic and variant hairy cell
   leukemia
SO LEUKEMIA RESEARCH
LA English
DT Article
DE Telomere; Hairy cell leukemia; Molecular marker; Chromosomes; DNA damage
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; LYMPHOPROLIFERATIVE DISORDERS;
   MYELOID-LEUKEMIA; FOLLOW-UP; DIAGNOSIS; CLADRIBINE; DYSFUNCTION;
   MUTATIONS; HISTOPATHOGENESIS; INSTABILITY
AB Telomeres, which protect the ends of chromosomes, are shortened in several hematologic malignancies, often with adverse prognostic implications, but their effect on prognosis of classic and variant hairy cell leukemia (HCL and HCLv) has not been reported. HCL/HCLv genomic DNA from 46 patients was studied by PCR to determine the ratio of telomere to single copy gene number (T/S). T/S was unrelated to diagnosis of HCL or HCLv (p = 0.27), but shorter T/S was associated with unmutated immunoglobulin rearrangements (p = 0.033) and age above the median at diagnosis (p = 0.017). Low T/S was associated with shorter overall survival from diagnosis (OS), particularly T/S <0.655 (p = 0.0064, adjusted p = 0.019). Shorter OS was also associated with presence of unmutated (p <0.0001) or IGHV4-34+ (p <0.0001) rearrangements, or increasing age (p = 0.0002). Multivariable analysis with Cox modeling showed that short T/S along with either unmutated or IGHV4-34+ rearrangements remained associated with reduced OS (p = 0.0071, p = 0.0024, respectively) after age adjustment. While T/S is relatively long in HCL and the disease usually indolent with excellent survival, shortened telomeres in HCL/HCLv are associated with decreased survival. Shortened T/S could represent a risk factor needing further investigation/intervention to determine if non-chemotherapy treatment options, in addition to or instead of chemotherapy, might be particularly useful. Published by Elsevier Ltd.
C1 [Arons, Evgeny; Zhou, Hong; Kreitman, Robert J.] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
   [Edelman, Daniel C.; Gomez, Allison; Petersen, David; Wang, Yonghong; Meltzer, Paul S.] NCI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA.
   [Steinberg, Seth M.] NCI, Biostat & Data Management Sect, Off Clin Director, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Kreitman, RJ (reprint author), NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM kreitman@mail.nih.gov
FU NCI; Hairy Cell Leukemia Foundation
FX The authors would like to recognize the contributions of our clinical
   staff for helping to obtain samples during the time they were collected,
   including Betty Maestri, Rita Mincemoyer, Barbara Debrah and Sonya Duke.
   NIH summer interns Paul Tran and Gabriella Canales contributed to the
   initial development of the MMQPCR TL assay at NCI. This study was
   supported in part by the Intramural Research Program, NCI, and the Hairy
   Cell Leukemia Foundation. Author contributions: DCE, EA, PSM and RJK
   designed the research study, EA, HZ, AG, and DP performed the research,
   EA, DCE, SMS, YW, PSM and RJK analyzed the data, and EA, DCE, SMS and
   RJK wrote the paper.
NR 46
TC 2
Z9 2
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0145-2126
EI 1873-5835
J9 LEUKEMIA RES
JI Leuk. Res.
PD DEC
PY 2015
VL 39
IS 12
BP 1360
EP 1366
DI 10.1016/j.leukres.2015.09.015
PG 7
WC Oncology; Hematology
SC Oncology; Hematology
GA CW9RF
UT WOS:000365335200009
PM 26520623
ER

PT J
AU Kemper, MF
   Srivastava, S
   King, MT
   Clarke, K
   Veech, RL
   Pawlosky, RJ
AF Kemper, Martin F.
   Srivastava, Shireesh
   King, M. Todd
   Clarke, Kieran
   Veech, Richard L.
   Pawlosky, Robert J.
TI An Ester of beta-Hydroxybutyrate Regulates Cholesterol Biosynthesis in
   Rats and a Cholesterol Biomarker in Humans
SO LIPIDS
LA English
DT Article
DE Cholesterol biosynthesis; beta-Hydroxybutyrate; Diabetes; Ketogenic
   diet; Mass spectrometry; Statins; Liver; Triglycerides; Human; Dietary
   supplement
ID ACETOACETYL-COA SYNTHETASE; FATTY-ACID SYNTHESIS; KETONE ESTER;
   (R)-3-HYDROXYBUTYL (R)-3-HYDROXYBUTYRATE; ALZHEIMERS-DISEASE; IN-VIVO;
   DIET; MITOCHONDRIAL; HOMEOSTASIS; MANAGEMENT
AB In response to carbohydrate deprivation or prolonged fasting the ketone bodies, beta-hydroxybutyrate (beta HB) and acetoacetate (AcAc), are produced from the incomplete beta-oxidation of fatty acids in the liver. Neither beta HB nor AcAc are well utilized for synthesis of sterols or fatty acids in human or rat liver. To study the effects of ketones on cholesterol homeostasis a novel beta HB ester (KE) ((R)-3-hydroxybutyl (R)-3-hydroxybutyrate) was synthesized and given orally to rats and humans as a partial dietary carbohydrate replacement. Rats maintained on a diet containing 30-energy % as KE with a concomitant reduction in carbohydrate had lower plasma cholesterol and mevalonate (-40 and -27 %, respectively) and in the liver had lower levels of the mevalonate precursors acetoacetyl-CoA and HMG-CoA (-33 and -54 %) compared to controls. Whole liver and membrane LDL-R as well as SREBP-2 protein levels were higher (+24, +67, and +91 %, respectively). When formulated into a beverage for human consumption subjects consuming a KE drink (30-energy %) had elevated plasma beta HB which correlated with decreased mevalonate, a liver cholesterol synthesis biomarker. Partial replacement of dietary carbohydrate with KE induced ketosis and altered cholesterol homeostasis in rats. In healthy individuals an elevated plasma beta HB correlated with lower plasma mevalonate.
C1 [Kemper, Martin F.; King, M. Todd; Veech, Richard L.; Pawlosky, Robert J.] NIAAA, Lab Metab Control, Rockville, MD 20852 USA.
   [Srivastava, Shireesh] DBT ICGEB Ctr Adv Bioenergy Res, New Delhi 110067, India.
   [Clarke, Kieran] Univ Oxford, Dept Physiol Anat & Genet, Oxford OX1 3PT, England.
RP Pawlosky, RJ (reprint author), NIAAA, Lab Metab Control, 5625 Fishers Ln 1S22, Rockville, MD 20852 USA.
EM bpawlosky@dicbr.niaaa.nih.gov
FU National Institutes of Health, NIH; Oxford University; Defense Advanced
   Research Projects Administration
FX This work was supported by The National Institutes of Health, NIH and
   Oxford University. Development of the Ketone Ester was supported by the
   Defense Advanced Research Projects Administration.
NR 28
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Z9 3
U1 3
U2 10
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0024-4201
EI 1558-9307
J9 LIPIDS
JI Lipids
PD DEC
PY 2015
VL 50
IS 12
BP 1185
EP 1193
DI 10.1007/s11745-015-4085-x
PG 9
WC Biochemistry & Molecular Biology; Nutrition & Dietetics
SC Biochemistry & Molecular Biology; Nutrition & Dietetics
GA CW6RO
UT WOS:000365125400003
PM 26498829
ER

PT J
AU Gunti, S
   Kampylafka, EI
   Tzioufas, AG
   Notkins, AL
AF Gunti, S.
   Kampylafka, E. I.
   Tzioufas, A. G.
   Notkins, A. L.
TI Polyreactive antibodies in the circulation of patients with systemic
   lupus erythematosus
SO LUPUS
LA English
DT Letter
ID AUTOANTIBODIES; DISEASE; CELLS
C1 [Gunti, S.; Notkins, A. L.] Natl Inst Dent & Craniofacial Res, Expt Med Sect, Lab Sensory Biol, NIH, Bethesda, MD 20892 USA.
   [Kampylafka, E. I.; Tzioufas, A. G.] Univ Athens, Sch Med, Dept Pathophysiol, Athens, Greece.
RP Notkins, AL (reprint author), Natl Inst Dent & Craniofacial Res, Expt Med Sect, Lab Sensory Biol, NIH, Bethesda, MD 20892 USA.
EM anotkins@mail.nih.gov
FU Intramural NIH HHS [Z99 DE999999]
NR 9
TC 0
Z9 0
U1 1
U2 1
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0961-2033
EI 1477-0962
J9 LUPUS
JI Lupus
PD DEC
PY 2015
VL 24
IS 14
BP 1567
EP 1569
DI 10.1177/0961203315603144
PG 3
WC Rheumatology
SC Rheumatology
GA CW7KT
UT WOS:000365178300014
PM 26385217
ER

PT J
AU Northcutt, AL
   Hutchinson, MR
   Wang, X
   Baratta, MV
   Hiranita, T
   Cochran, TA
   Pomrenze, MB
   Galer, EL
   Kopajtic, TA
   Li, CM
   Amat, J
   Larson, G
   Cooper, DC
   Huang, Y
   O'Neill, CE
   Yin, H
   Zahniser, NR
   Katz, JL
   Rice, KC
   Maier, SF
   Bachtell, RK
   Watkins, LR
AF Northcutt, A. L.
   Hutchinson, M. R.
   Wang, X.
   Baratta, M. V.
   Hiranita, T.
   Cochran, T. A.
   Pomrenze, M. B.
   Galer, E. L.
   Kopajtic, T. A.
   Li, C. M.
   Amat, J.
   Larson, G.
   Cooper, D. C.
   Huang, Y.
   O'Neill, C. E.
   Yin, H.
   Zahniser, N. R.
   Katz, J. L.
   Rice, K. C.
   Maier, S. F.
   Bachtell, R. K.
   Watkins, L. R.
TI DAT isn't all that: cocaine reward and reinforcement require Toll-like
   receptor 4 signaling
SO MOLECULAR PSYCHIATRY
LA English
DT Article
ID INCREASE EXTRACELLULAR DOPAMINE; NUCLEUS-ACCUMBENS; NEUROPATHIC PAIN;
   MOLECULAR-MECHANISMS; DRUG-DEPENDENCE; NERVOUS-SYSTEM; NITRIC-OXIDE;
   ACTIVATION; BRAIN; MICE
AB The initial reinforcing properties of drugs of abuse, such as cocaine, are largely attributed to their ability to activate the mesolimbic dopamine system. Resulting increases in extracellular dopamine in the nucleus accumbens (NAc) are traditionally thought to result from cocaine's ability to block dopamine transporters (DATs). Here we demonstrate that cocaine also interacts with the immunosurveillance receptor complex, Toll-like receptor 4 (TLR4), on microglial cells to initiate central innate immune signaling. Disruption of cocaine signaling at TLR4 suppresses cocaine-induced extracellular dopamine in the NAc, as well as cocaine conditioned place preference and cocaine self-administration. These results provide a novel understanding of the neurobiological mechanisms underlying cocaine reward/reinforcement that includes a critical role for central immune signaling, and offer a new target for medication development for cocaine abuse treatment.
C1 [Northcutt, A. L.; Wang, X.; Cochran, T. A.; Galer, E. L.; Amat, J.; O'Neill, C. E.; Maier, S. F.; Bachtell, R. K.; Watkins, L. R.] Univ Colorado, Ctr Neurosci, Dept Psychol & Neurosci, Boulder, CO 80309 USA.
   [Hutchinson, M. R.] Univ Adelaide, Sch Med Sci, Discipline Physiol, Adelaide, SA, Australia.
   [Wang, X.; Yin, H.] Univ Colorado, Ctr Neurosci, Biofrontiers Inst, Boulder, CO 80309 USA.
   [Baratta, M. V.; Pomrenze, M. B.; Cooper, D. C.; Bachtell, R. K.] Univ Colorado, Ctr Neurosci, Inst Behav Genet, Boulder, CO 80309 USA.
   [Hiranita, T.; Kopajtic, T. A.; Katz, J. L.] NIDA, Dept Hlth & Human Serv, Medicat Discovery Res Branch, NIH,Intramural Res Program,Biomed Res Ctr MDRB, Baltimore, MD USA.
   [Li, C. M.; Huang, Y.] Univ Calif San Francisco, Dept Bioengn & Therapeut Sci, Drug Studies Unit, San Francisco, CA 94143 USA.
   [Larson, G.; Zahniser, N. R.] Univ Colorado, Dept Pharmacol, Denver, CO 80202 USA.
   [Larson, G.; Zahniser, N. R.] Univ Colorado, Program Neurosci, Denver, CO 80202 USA.
   [Yin, H.] Univ Colorado, Ctr Neurosci, Dept Chem & Biochem, Boulder, CO 80309 USA.
   [Yin, H.] Tsinghua Univ, Ctr Basic Mol Sci, Beijing 100084, Peoples R China.
   [Yin, H.] Tsinghua Univ, Dept Chem, Beijing 100084, Peoples R China.
   [Rice, K. C.] NIDA, Chem Biol Res Branch, NIH, Rockville, MD USA.
   [Rice, K. C.] NIAAA, NIH, Rockville, MD 20852 USA.
RP Northcutt, AL (reprint author), Univ Colorado, Ctr Neurosci, Dept Psychol & Neurosci, Campus Box 345, Boulder, CO 80309 USA.
EM Alexis.Northcutt@Colorado.EDU
OI Hutchinson, Mark/0000-0003-2154-5950; Katz,
   Jonathan/0000-0002-1068-1159; YIN, HANG/0000-0002-9762-4818
FU intramural research programs of the National Institute on Drug Abuse;
   National Institute on Alcohol Abuse and Alcoholism; NIH [DA029420,
   DA033358, GM103843, GM101279]; NIDA [N01DA-9-8883]; DoD [PR110146];
   Australian Research Council [DP110100297]
FX We thank the NIDA Addiction Treatment Discovery Program (NIDA ATDP) for
   data generated through a contract with Caliper Life Sciences. A portion
   of this work was supported by the intramural research programs of the
   National Institute on Drug Abuse and the National Institute on Alcohol
   Abuse and Alcoholism. This work was supported by NIH Grants DA029420,
   DA033358, GM103843 and GM101279, NIDA Grant N01DA-9-8883 and DoD Grant
   PR110146. MRH is funded by an Australian Research Council Research
   Fellowship (DP110100297).
NR 62
TC 12
Z9 13
U1 5
U2 15
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 DEC
PY 2015
VL 20
IS 12
BP 1525
EP 1537
DI 10.1038/mp.2014.177
PG 13
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA CW7ZN
UT WOS:000365218200009
PM 25644383
ER

PT J
AU Desikan, RS
   Schork, AJ
   Wang, Y
   Witoelar, A
   Sharma, M
   McEvoy, LK
   Holland, D
   Brewer, JB
   Chen, CH
   Thompson, WK
   Harold, D
   Williams, J
   Owen, MJ
   O'Donovan, MC
   Pericak-Vance, MA
   Mayeux, R
   Haines, JL
   Farrer, LA
   Schellenberg, GD
   Heutink, P
   Singleton, AB
   Brice, A
   Wood, NW
   Hardy, J
   Martinez, M
   Choi, SH
   DeStefano, A
   Ikram, MA
   Bis, JC
   Smith, A
   Fitzpatrick, AL
   Launer, L
   van Duijn, C
   Seshadri, S
   Ulstein, ID
   Aarsland, D
   Fladby, T
   Djurovic, S
   Hyman, BT
   Snaedal, J
   Stefansson, H
   Stefansson, K
   Gasser, T
   Andreassen, OA
   Dale, AM
AF Desikan, R. S.
   Schork, A. J.
   Wang, Y.
   Witoelar, A.
   Sharma, M.
   McEvoy, L. K.
   Holland, D.
   Brewer, J. B.
   Chen, C-H
   Thompson, W. K.
   Harold, D.
   Williams, J.
   Owen, M. J.
   O'Donovan, M. C.
   Pericak-Vance, M. A.
   Mayeux, R.
   Haines, J. L.
   Farrer, L. A.
   Schellenberg, G. D.
   Heutink, P.
   Singleton, A. B.
   Brice, A.
   Wood, N. W.
   Hardy, J.
   Martinez, M.
   Choi, S. H.
   DeStefano, A.
   Ikram, M. A.
   Bis, J. C.
   Smith, A.
   Fitzpatrick, A. L.
   Launer, L.
   van Duijn, C.
   Seshadri, S.
   Ulstein, I. D.
   Aarsland, D.
   Fladby, T.
   Djurovic, S.
   Hyman, B. T.
   Snaedal, J.
   Stefansson, H.
   Stefansson, K.
   Gasser, T.
   Andreassen, O. A.
   Dale, A. M.
CA ADNI
   ADGC Investigator
   GERAD Investigator
   CHARGE Investigator
   IPDGC Investigator
TI Genetic overlap between Alzheimer's disease and Parkinson's disease at
   the MAPT locus
SO MOLECULAR PSYCHIATRY
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; MILD COGNITIVE IMPAIRMENT; COMMON VARIANTS;
   RISK-FACTORS; IDENTIFIES VARIANTS; EXPRESSION; HAPLOTYPE; TAU;
   METAANALYSIS; NEURODEGENERATION
AB We investigated the genetic overlap between Alzheimer's disease (AD) and Parkinson's disease (PD). Using summary statistics (P-values) from large recent genome-wide association studies (GWAS) (total n = 89 904 individuals), we sought to identify single nucleotide polymorphisms (SNPs) associating with both AD and PD. We found and replicated association of both AD and PD with the A allele of rs393152 within the extended MAPT region on chromosome 17 (meta analysis P-value across five independent AD cohorts = 1.65 x 10(-7)). In independent datasets, we found a dose-dependent effect of the A allele of rs393152 on intra-cerebral MAPT transcript levels and volume loss within the entorhinal cortex and hippocampus. Our findings identify the tau-associated MAPT locus as a site of genetic overlap between AD and PD, and extending prior work, we show that the MAPT region increases risk of Alzheimer's neurodegeneration.
C1 [Desikan, R. S.; McEvoy, L. K.; Brewer, J. B.; Chen, C-H; Dale, A. M.] Univ Calif San Diego, Dept Radiol, La Jolla, CA 92037 USA.
   [Schork, A. J.; Dale, A. M.] Univ Calif San Diego, Dept Cognit Sci, La Jolla, CA 92037 USA.
   [Wang, Y.; Holland, D.; Brewer, J. B.; Dale, A. M.] Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92037 USA.
   [Wang, Y.; Witoelar, A.; Djurovic, S.; Andreassen, O. A.] Univ Oslo, NORMENT, Oslo, Norway.
   [Wang, Y.; Witoelar, A.; Fladby, T.; Djurovic, S.; Andreassen, O. A.] Univ Oslo, Inst Clin Med, Oslo, Norway.
   [Wang, Y.; Witoelar, A.; Djurovic, S.; Andreassen, O. A.] Oslo Univ Hosp, Div Mental Hlth & Addict, N-0424 Oslo, Norway.
   [Sharma, M.; Gasser, T.] Univ Tubingen, Hertie Inst Clin Brain Res, Dept Neurodegenerat Dis, Tubingen, Germany.
   [Sharma, M.] Univ Tubingen, Inst Clin Epidemiol & Appl Biometry, Tubingen, Germany.
   [Chen, C-H; Thompson, W. K.; Andreassen, O. A.; Dale, A. M.] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92037 USA.
   [Harold, D.; Williams, J.; Owen, M. J.; O'Donovan, M. C.] Cardiff Univ, Sch Med, MRC, Ctr Neuropsychiat Genet & Genom,Inst Psychol Med, Cardiff CF10 3AX, S Glam, Wales.
   [Pericak-Vance, M. A.] Univ Miami, John P Hussman Inst Human Genom, Miami, FL USA.
   [Mayeux, R.] Columbia Univ, Dept Neurol, Taub Inst Alzheimers Dis & Aging Brain, New York, NY USA.
   [Mayeux, R.] Columbia Univ, Gertrude H Sergievsky Ctr, New York, NY 10027 USA.
   [Haines, J. L.] Vanderbilt Univ, Dept Mol Physiol & Biophys, Vanderbilt Ctr Human Genet Res, Nashville, TN 37232 USA.
   [Farrer, L. A.] Boston Univ, Sch Med, Dept Med Biomed Genet, Boston, MA 02118 USA.
   [Farrer, L. A.; Seshadri, S.] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
   [Farrer, L. A.] Boston Univ, Sch Med, Dept Ophthalmol, Boston, MA 02118 USA.
   [Farrer, L. A.] Boston Univ, Sch Med, Dept Biostat, Boston, MA 02118 USA.
   [Farrer, L. A.] Boston Univ, Sch Med, Dept Epidemiol, Boston, MA 02118 USA.
   [Farrer, L. A.] Boston Univ, Sch Publ Hlth, Dept Med Biomed Genet, Boston, MA USA.
   [Farrer, L. A.] Boston Univ, Sch Publ Hlth, Dept Neurol, Boston, MA USA.
   [Farrer, L. A.] Boston Univ, Sch Publ Hlth, Dept Ophthalmol, Boston, MA USA.
   [Farrer, L. A.; Choi, S. H.; DeStefano, A.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
   [Farrer, L. A.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
   [Schellenberg, G. D.] Univ Penn, Dept Pathol & Lab Med, Perelman Sch Med, Philadelphia, PA USA.
   [Heutink, P.] German Ctr Neurodegenerat Dis DZNE Tubingen, Tubingen, Germany.
   [Singleton, A. B.] NIA, Neurogenet Lab, Bethesda, MD 20892 USA.
   [Brice, A.] Univ Paris 06, Sorbonne Univ, Paris, France.
   [Wood, N. W.] UCL, Genet Inst, London, England.
   [Wood, N. W.; Hardy, J.] UCL, Dept Mol Neurosci, Inst Neurol, London, England.
   [Martinez, M.] CHU Purpan, CPTP, UMR1043, INSERM, Toulouse, France.
   [DeStefano, A.; Seshadri, S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
   [Ikram, M. A.; van Duijn, C.] Erasmus MC Univ, Med Ctr, Dept Epidemiol, Rotterdam, Netherlands.
   [Bis, J. C.] Univ Washington, Dept Internal Med, Seattle, WA 98195 USA.
   [Smith, A.] Iceland Heart Assoc, Kopavogur, Iceland.
   [Fitzpatrick, A. L.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
   [Launer, L.] NIA, Lab Epidemiol Demog & Biometry, Intramural Res Program, Washington, DC USA.
   [Ulstein, I. D.] Oslo Univ Hosp, Dept Old Age Psychiat, Norwegian Ctr Dementia Res, N-0450 Oslo, Norway.
   [Aarsland, D.] Akershus Univ Hosp, Dept Geriatr Psychiat, Oslo, Norway.
   [Aarsland, D.] Stavanger Univ Hosp, Ctr Age Related Med, Stavanger, Norway.
   [Aarsland, D.] Karolinska Inst, Dept Neurobiol Care Sci & Soc, Alzheimers Dis Res Ctr, Stockholm, Sweden.
   [Fladby, T.] Akershus Univ Hosp, Dept Neurol, Oslo, Norway.
   [Hyman, B. T.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
   [Snaedal, J.] Univ Hosp Reykjavik, Dept Geriatr Med, Reykjavik, Iceland.
   [Stefansson, H.; Stefansson, K.] deCODE Genet Amgen, Reykjavik, Iceland.
   [Stefansson, K.] Univ Iceland, Fac Med, Reykjavik, Iceland.
RP Desikan, RS (reprint author), Univ Calif San Diego, Dept Radiol, 8950 Villa La Jolla Dr,Suite C101, La Jolla, CA 92037 USA.
EM rdesikan@ucsd.edu; o.a.andreassen@medisin.uio.no; amdale@ucsd.edu
RI Hardy, John/C-2451-2009; Singleton, Andrew/C-3010-2009; Wood,
   Nicholas/C-2505-2009; 
OI Wood, Nicholas/0000-0002-9500-3348; Stefansson,
   Hreinn/0000-0002-9331-6666; Farrer, Lindsay/0000-0001-5533-4225;
   Seshadri, Sudha/0000-0001-6135-2622; Harold, Denise/0000-0001-5195-0143;
   Aarsland, Dag/0000-0001-6314-216X
FU National Institutes of Health [R01AG031224, K01AG029218, K02NS067427,
   T32 EB005970, UO1AG032984, U24-AG041689, R01 MH100351]; Research Council
   of Norway [213837, 225989, 223273, 237250/EU JPND]; South East Norway
   Health Authority [2013-123]; Norwegian Health Association; KG Jebsen
   Foundation; NIH [RC2DA029475, R01HD061414]; Robert J. Glushko and Pamela
   Samuelson Graduate Fellowship; ADGC; ADNI
FX We would like to thank Drs. Irene Litvan, Subhojit Roy and Marilyn
   Albert for helpful comments on an earlier version of this manuscript.
   This research was supported by grants from the National Institutes of
   Health (R01AG031224, K01AG029218, K02NS067427, T32 EB005970,
   UO1AG032984, U24-AG041689, and R01 MH100351), the Research Council of
   Norway (#213837, #225989, #223273, #237250/EU JPND), the South East
   Norway Health Authority (2013-123), the Norwegian Health Association and
   the KG Jebsen Foundation. AJS was supported by NIH grants RC2DA029475
   and R01HD061414 and the Robert J. Glushko and Pamela Samuelson Graduate
   Fellowship. Please see Supplementary Acknowledgements for ADGC and ADNI
   funding sources.
NR 47
TC 20
Z9 20
U1 0
U2 12
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 DEC
PY 2015
VL 20
IS 12
BP 1588
EP 1595
DI 10.1038/mp.2015.6
PG 8
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA CW7ZN
UT WOS:000365218200015
PM 25687773
ER

PT J
AU Shevach, EM
   Margulies, DH
AF Shevach, Ethan M.
   Margulies, David H.
TI William E. Paul 1936-2015 OBITUARY
SO NATURE IMMUNOLOGY
LA English
DT Biographical-Item
C1 [Shevach, Ethan M.; Margulies, David H.] NIAAA, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Shevach, EM (reprint author), NIAAA, Immunol Lab, NIH, Bethesda, MD 20892 USA.
EM eshevach@niaid.nih.gov
NR 1
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 1529-2908
EI 1529-2916
J9 NAT IMMUNOL
JI Nat. Immunol.
PD DEC
PY 2015
VL 16
IS 12
BP 1205
EP 1205
PG 1
WC Immunology
SC Immunology
GA CW5UM
UT WOS:000365062100001
PM 26580498
ER

PT J
AU Akbarian, S
   Liu, CY
   Knowles, JA
   Vaccarino, FM
   Farnham, PJ
   Crawford, GE
   Jaffe, AE
   Pinto, D
   Dracheva, S
   Geschwind, DH
   Mill, J
   Nairn, AC
   Abyzov, A
   Pochareddy, S
   Prabhakar, S
   Weissman, S
   Sullivan, PF
   State, MW
   Weng, ZP
   Peters, MA
   White, KP
   Gerstein, MB
   Amiri, A
   Armoskus, C
   Ashley-Koch, AE
   Bae, T
   Beckel-Mitchener, A
   Berman, BP
   Coetzee, GA
   Coppola, G
   Francoeur, N
   Fromer, M
   Gao, R
   Grennan, K
   Herstein, J
   Kavanagh, DH
   Ivanov, NA
   Jiang, Y
   Kitchen, RR
   Kozlenkov, A
   Kundakovic, M
   Li, MF
   Li, Z
   Liu, S
   Mangravite, LM
   Mattei, E
   Markenscoff-Papadimitriou, E
   Navarro, FCP
   North, N
   Omberg, L
   Panchision, D
   Parikshak, N
   Poschmann, J
   Price, AJ
   Purcaro, M
   Reddy, TE
   Roussos, P
   Schreiner, S
   Scuderri, S
   Sebra, R
   Shibata, M
   Shieh, AW
   Skarica, M
   Sun, WJ
   Swarup, V
   Thomas, A
   Tsuji, J
   van Bakel, H
   Wang, DF
   Wang, YJ
   Wang, K
   Werling, DM
   Willsey, AJ
   Witt, H
   Won, H
   Wong, CCY
   Wray, GA
   Wu, EY
   Xu, XM
   Yao, LJ
   Senthil, G
   Lehner, T
   Sklar, P
   Sestan, N
AF Akbarian, Schahram
   Liu, Chunyu
   Knowles, James A.
   Vaccarino, Flora M.
   Farnham, Peggy J.
   Crawford, Gregory E.
   Jaffe, Andrew E.
   Pinto, Dalila
   Dracheva, Stella
   Geschwind, Daniel H.
   Mill, Jonathan
   Nairn, Angus C.
   Abyzov, Alexej
   Pochareddy, Sirisha
   Prabhakar, Shyam
   Weissman, Sherman
   Sullivan, Patrick F.
   State, Matthew W.
   Weng, Zhiping
   Peters, Mette A.
   White, Kevin P.
   Gerstein, Mark B.
   Amiri, Anahita
   Armoskus, Chris
   Ashley-Koch, Allison E.
   Bae, Taejeong
   Beckel-Mitchener, Andrea
   Berman, Benjamin P.
   Coetzee, Gerhard A.
   Coppola, Gianfilippo
   Francoeur, Nancy
   Fromer, Menachem
   Gao, Robert
   Grennan, Kay
   Herstein, Jennifer
   Kavanagh, David H.
   Ivanov, Nikolay A.
   Jiang, Yan
   Kitchen, Robert R.
   Kozlenkov, Alexey
   Kundakovic, Marija
   Li, Mingfeng
   Li, Zhen
   Liu, Shuang
   Mangravite, Lara M.
   Mattei, Eugenio
   Markenscoff-Papadimitriou, Eirene
   Navarro, Fabio C. P.
   North, Nicole
   Omberg, Larsson
   Panchision, David
   Parikshak, Neelroop
   Poschmann, Jeremie
   Price, Amanda J.
   Purcaro, Michael
   Reddy, Timothy E.
   Roussos, Panos
   Schreiner, Shannon
   Scuderri, Soraya
   Sebra, Robert
   Shibata, Mikihito
   Shieh, Annie W.
   Skarica, Mario
   Sun, Wenjie
   Swarup, Vivek
   Thomas, Amber
   Tsuji, Junko
   van Bakel, Harm
   Wang, Daifeng
   Wang, Yongjun
   Wang, Kai
   Werling, Donna M.
   Willsey, A. Jeremy
   Witt, Heather
   Won, Hyejung
   Wong, Chloe C. Y.
   Wray, Gregory A.
   Wu, Emily Y.
   Xu, Xuming
   Yao, Lijing
   Senthil, Geetha
   Lehner, Thomas
   Sklar, Pamela
   Sestan, Nenad
CA PsychENCODE Consortium
TI The PsychENCODE project
SO NATURE NEUROSCIENCE
LA English
DT Article
ID NONCODING GENETIC-VARIATION; DE-NOVO MUTATIONS; HUMAN BRAIN;
   PSYCHIATRIC-DISORDERS; TRANSCRIPTIONAL REGULATION; EXPRESSION VARIATION;
   REGULATORY NETWORKS; DISEASE MECHANISMS; BIPOLAR DISORDER; DNA
   METHYLATION
AB Recent research on disparate psychiatric disorders has implicated rare variants in genes involved in global gene regulation and chromatin modification, as well as many common variants located primarily in regulatory regions of the genome. Understanding precisely how these variants contribute to disease will require a deeper appreciation for the mechanisms of gene regulation in the developing and adult human brain. The PsychENCODE project aims to produce a public resource of multidimensional genomic data using tissue- and cell type specific samples from approximately 1,000 phenotypically well-characterized, high-quality healthy and disease-affected human post-mortem brains, as well as functionally characterize disease-associated regulatory elements and variants in model systems. We are beginning with a focus on autism spectrum disorder, bipolar disorder and schizophrenia, and expect that this knowledge will apply to a wide variety of psychiatric disorders. This paper outlines the motivation and design of PsychENCODE.
C1 [Akbarian, Schahram; Pinto, Dalila; Dracheva, Stella; Francoeur, Nancy; Fromer, Menachem; Kavanagh, David H.; Jiang, Yan; Kozlenkov, Alexey; Kundakovic, Marija; Roussos, Panos; Sebra, Robert; van Bakel, Harm; Sklar, Pamela] Icahn Sch Med Mt Sinai, New York, NY 10029 USA.
   [Liu, Chunyu; Grennan, Kay; Shieh, Annie W.; Wang, Yongjun] Univ Illinois, Chicago, IL USA.
   [Knowles, James A.; Farnham, Peggy J.; Armoskus, Chris; Berman, Benjamin P.; Coetzee, Gerhard A.; Gao, Robert; Herstein, Jennifer; Schreiner, Shannon; Wang, Kai; Witt, Heather; Yao, Lijing] Univ So Calif, Los Angeles, CA USA.
   [Vaccarino, Flora M.; Nairn, Angus C.; Pochareddy, Sirisha; Weissman, Sherman; Gerstein, Mark B.; Amiri, Anahita; Coppola, Gianfilippo; Kitchen, Robert R.; Li, Mingfeng; Li, Zhen; Liu, Shuang; Navarro, Fabio C. P.; Scuderri, Soraya; Shibata, Mikihito; Skarica, Mario; Wang, Daifeng; Xu, Xuming; Sestan, Nenad] Yale Univ, New Haven, CT USA.
   [Crawford, Gregory E.; Ashley-Koch, Allison E.; Reddy, Timothy E.; Wray, Gregory A.] Duke Univ, Durham, NC USA.
   [Jaffe, Andrew E.; Ivanov, Nikolay A.; Price, Amanda J.] Lieber Inst Brain Dev, Baltimore, MD USA.
   [Geschwind, Daniel H.; Parikshak, Neelroop; Swarup, Vivek; Won, Hyejung; Wu, Emily Y.] Univ Calif Los Angeles, Los Angeles, CA USA.
   [Mill, Jonathan; Poschmann, Jeremie; Wong, Chloe C. Y.] Kings Coll London, London WC2R 2LS, England.
   [Mill, Jonathan; Poschmann, Jeremie; Wong, Chloe C. Y.] Univ Exeter, Exeter EX4 4QJ, Devon, England.
   [Abyzov, Alexej; Bae, Taejeong] Mayo Clin, Rochester, MN USA.
   [Prabhakar, Shyam; Sun, Wenjie] Genome Inst Singapore, Singapore, Singapore.
   [Sullivan, Patrick F.] Univ N Carolina, Chapel Hill, NC USA.
   [State, Matthew W.; Markenscoff-Papadimitriou, Eirene; Werling, Donna M.; Willsey, A. Jeremy] Univ Calif San Francisco, San Francisco, CA 94143 USA.
   [Weng, Zhiping; Mattei, Eugenio; Purcaro, Michael; Tsuji, Junko] Univ Massachusetts, Sch Med, Worcester, MA USA.
   [Peters, Mette A.; Mangravite, Lara M.; Omberg, Larsson] Sage Bionetworks, Seattle, WA USA.
   [White, Kevin P.; Thomas, Amber] Univ Chicago, Chicago, IL 60637 USA.
   [Beckel-Mitchener, Andrea; North, Nicole; Panchision, David; Senthil, Geetha; Lehner, Thomas] NIMH, Bethesda, MD 20892 USA.
RP Akbarian, S (reprint author), Icahn Sch Med Mt Sinai, New York, NY 10029 USA.
EM geetha.senthil2@nih.gov; tlehner@mail.nih.gov; pamela.sklar@mssm.edu;
   nenad.sestan@yale.edu
RI Jaffe, Andrew/L-3089-2016; Mill, Jonathan/B-3276-2010; Roussos,
   Panos/J-7090-2013; 
OI Jaffe, Andrew/0000-0001-6886-1454; Mill, Jonathan/0000-0003-1115-3224;
   Roussos, Panos/0000-0002-4640-6239; Abyzov, Alexej/0000-0001-5405-6729;
   Bae, Taejeong/0000-0002-4626-3725; Navarro, Fabio/0000-0002-5640-9070;
   Vaccarino, Flora/0000-0003-2167-981X; Ashley-Koch,
   Allison/0000-0001-5409-9155
FU US National Institute of Mental Health
FX The authors would like to acknowledge and thank the tissue donors and
   their families. We also thank all consortium members for discussions and
   feedback on this document. The PsychENCODE consortium projects are
   funded by the US National Institute of Mental Health.
NR 50
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U1 4
U2 16
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 DEC
PY 2015
VL 18
IS 12
BP 1707
EP 1712
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA CX1LV
UT WOS:000365458600005
ER

PT J
AU Baron, J
   Savendahl, L
   De Luca, F
   Dauber, A
   Phillip, M
   Wit, JM
   Nilsson, O
AF Baron, Jeffrey
   Saevendahl, Lars
   De Luca, Francesco
   Dauber, Andrew
   Phillip, Moshe
   Wit, Jan M.
   Nilsson, Ola
TI Short and tall stature: a new paradigm emerges
SO NATURE REVIEWS ENDOCRINOLOGY
LA English
DT Review
ID LONGITUDINAL BONE-GROWTH; IDIOPATHIC SHORT STATURE; RECEPTOR-B NPR2;
   PRO-INFLAMMATORY CYTOKINES; C-NATRIURETIC PEPTIDE; MEIER-GORLIN
   SYNDROME; COPY NUMBER VARIANTS; CHONDROCYTE PROLIFERATION; PLATE
   CHONDROCYTES; FACTOR-I
AB In the past, the growth hormone (GH)-insulin-like growth factor 1 (IGF-1) axis was often considered to be the main system that regulated childhood growth and, therefore, determined short stature and tall stature. However, findings have now revealed that the GH-IGF-1 axis is just one of many regulatory systems that control chondrogenesis in the growth plate, which is the biological process that drives height gain. Consequently, normal growth in children depends not only on GH and IGF-1 but also on multiple hormones, paracrine factors, extracellular matrix molecules and intracellular proteins that regulate the activity of growth plate chondrocytes. Mutations in the genes that encode many of these local proteins cause short stature or tall stature. Similarly, genome-wide association studies have revealed that the normal variation in height seems to be largely due to genes outside the GH-IGF-1 axis that affect growth at the growth plate through a wide variety of mechanisms. These findings point to a new conceptual framework for understanding short and tall stature that is centred not on two particular hormones but rather on the growth plate, which is the structure responsible for height gain.
C1 [Baron, Jeffrey] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Growth & Dev, NIH, Bethesda, MD 20892 USA.
   [Saevendahl, Lars; Nilsson, Ola] Karolinska Inst, Dept Womens & Childrens Hlth, Div Pediat Endocrinol, SE-17176 Stockholm, Sweden.
   [De Luca, Francesco] St Christophers Hosp Children, Sect Endocrinol & Diabet, Philadelphia, PA 19134 USA.
   [Dauber, Andrew] Cincinnati Childrens Hosp Med Ctr, Cincinnati Ctr Growth Disorders, Div Endocrinol, Cincinnati, OH 45229 USA.
   [Phillip, Moshe] Schneider Childrens Med Ctr Israel, Natl Ctr Childrens Diabet, Jesse Z & Sara Lea Shafer Inst Endocrinol & Diabe, IL-49202 Petah Tiqwa, Israel.
   [Wit, Jan M.] Leiden Univ, Med Ctr, Dept Pediat, NL-2300 RC Leiden, Netherlands.
RP Baron, J (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Growth & Dev, NIH, 10 Ctr Dr,MSC-1103, Bethesda, MD 20892 USA.
EM jeffrey.baron@nih.gov
FU Ferring; Merck Serono; Novo Nordisk; Pfizer; Ipsen; Sandoz; Teva;
   European Society for Paediatric Endocrinology research fellowship - Novo
   Nordisk
FX J.B. is listed as a co-inventor on a patent application by the NIH for
   targeted treatment of cartilage disorders. L.S. has received speakers'
   honoraria and/or research support from Ferring, Merck Serono, Novo
   Nordisk and Pfizer, and has submitted a patent application for novel
   peptides to treat bone or cartilage disorders and other diseases. A.D.
   has been a faculty speaker at continuing medical education symposia
   sponsored by Ipsen, Novo Nordisk and Sandoz. M.P. has received research
   support from Novo Nordisk, Pfizer and Teva, personal fees from Novo
   Nordisk and is a director of NG Solutions. J.M.W. has served as a
   consultant for Ammonett, Biopartners, Merck Serono, OPKO, Pfizer, Teva
   and Versartis, and has received speakers' honoraria from Lilly, Merck
   Serono, Pfizer, Sandoz and Versartis. O.N. has received a European
   Society for Paediatric Endocrinology research fellowship sponsored by
   Novo Nordisk and speaker's honoraria from Lilly. F.D.L. has no competing
   interests to declare.
NR 149
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U1 3
U2 8
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-5029
EI 1759-5037
J9 NAT REV ENDOCRINOL
JI Nat. Rev. Endocrinol.
PD DEC
PY 2015
VL 11
IS 12
BP 735
EP 746
DI 10.1038/nrendo.2015.165
PG 12
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CW8AK
UT WOS:000365220600004
PM 26437621
ER

PT J
AU Fields, RD
AF Fields, R. Douglas
TI A new mechanism of nervous system plasticity: activity-dependent
   myelination
SO NATURE REVIEWS NEUROSCIENCE
LA English
DT Review
ID AXON INITIAL SEGMENT; OLIGODENDROCYTE PRECURSOR CELLS; WHITE-MATTER
   MICROSTRUCTURE; ADHESION MOLECULE L1; ACTION-POTENTIALS; PROGENITOR
   CELLS; CNS MYELINATION; GLIAL-CELLS; INDIVIDUAL OLIGODENDROCYTES;
   SYNAPTIC PLASTICITY
AB The synapse is the focus of experimental research and theory on the cellular mechanisms of nervous system plasticity and learning, but recent research is expanding the consideration of plasticity into new mechanisms beyond the synapse, notably including the possibility that conduction velocity could be modifiable through changes in myelin to optimize the timing of information transmission through neural circuits. This concept emerges from a confluence of brain imaging that reveals changes in white matter in the human brain during learning, together with cellular studies showing that the process of myelination can be influenced by action potential firing in axons. This Opinion article summarizes the new research on activity-dependent myelination, explores the possible implications of these studies and outlines the potential for new research.
C1 [Fields, R. Douglas] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Nervous Syst Dev & Plast Sect, Bethesda, MD 20892 USA.
RP Fields, RD (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Nervous Syst Dev & Plast Sect, Bethesda, MD 20892 USA.
EM fieldsd@mail.nih.gov
FU Eunice Kennedy Shriver National Institute of Child Health and Human
   Development (NICHD)
FX This work was supported by funds for intramural research from the Eunice
   Kennedy Shriver National Institute of Child Health and Human Development
   (NICHD). Electron micrographs in Figure 2 are courtesy of Louis Dye,
   Microscopy Imaging Core, NICHD. 3D reconstruction is courtesy of Emily
   Benson and Grahame Kidd, Renovo, Inc.
NR 111
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U1 10
U2 32
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 DEC
PY 2015
VL 16
IS 12
BP 756
EP U77
DI 10.1038/nrn4023
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA CW8YO
UT WOS:000365285600010
PM 26585800
ER

PT J
AU MacDorman, MF
   Reddy, UM
   Silver, RM
AF MacDorman, Marian F.
   Reddy, Uma M.
   Silver, Robert M.
TI Trends in Stillbirth by Gestational Age in the United States, 2006-2012
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID DEATH; DELIVERY; FETAL; RISK
AB OBJECTIVE:To evaluate stillbirth trends by gestational age.METHODS:National Center for Health Statistics' fetal death and live birth data files were used to analyze the 2006 and 2012 cohorts of deliveries and compute gestational age-specific stillbirth rates at 20 weeks of gestation or greater using two methods: traditional (eg, stillbirths at 38 weeks of gestation/live births and stillbirths at 38 weeks of gestation) and prospective (stillbirths at 38 weeks of gestation/number of women still pregnant at 38 weeks of gestation). Changes in rates and in the percent distribution of stillbirths and live births were assessed.RESULTS:In 2006 and 2012, the stillbirth rate was 6.05 stillbirths per 1,000 deliveries. There was little change in the percent distribution of stillbirths by gestational age from 2006 to 2012. However, the percent distribution of live births by gestational age changed considerably: births at 34-38 weeks of gestation decreased by 10-16%, and births at 39 weeks of gestation increased by 17%. Traditionally computed stillbirth rates were unchanged at most gestational ages, but rose at 24-27, 34-36, 37, and 38 weeks of gestation. However, rates were influenced by decreases in births at those gestational ages; the pattern of stillbirths by gestational age was unchanged. In contrast, there were no differences in prospective stillbirth rates at 21-42 weeks of gestation.CONCLUSION:The lack of change in prospective stillbirth rates from 2006 to 2012 suggests that preventing nonmedically indicated deliveries before 39 weeks of gestation did not increase the U.S. stillbirth rate.LEVEL OF EVIDENCE:II
C1 [MacDorman, Marian F.] Univ Maryland, Maryland Populat Res Ctr, College Pk, MD 20742 USA.
   Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pregnancy & Perinatol Branch, NIH, Bethesda, MD USA.
   Univ Utah, Dept Obstet & Gynecol, Hlth Sci Ctr, Salt Lake City, UT USA.
RP MacDorman, MF (reprint author), Univ Maryland, Maryland Populat Res Ctr, 2015 Morrill Hall, College Pk, MD 20742 USA.
EM mmacdorm@umd.edu
FU Intramural NIH HHS [Z99 HD999999]
NR 19
TC 17
Z9 17
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD DEC
PY 2015
VL 126
IS 6
BP 1146
EP 1150
DI 10.1097/AOG.0000000000001152
PG 5
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA CW9EL
UT WOS:000365301300005
PM 26551188
ER

PT J
AU Halland, F
   Morken, NH
   Deroo, LA
   Klungsoyr, K
   Wilcox, AJ
   Skjaerven, R
AF Halland, Frode
   Morken, Nils-Halvdan
   DeRoo, Lisa A.
   Klungsoyr, Kari
   Wilcox, Allen J.
   Skjaerven, Rolv
TI Association of Women's Reproductive History With Long-term Mortality and
   Effect of Socioeconomic Factors
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID MATERNAL CARDIOVASCULAR-DISEASE; CORONARY-HEART-DISEASE; LATER-LIFE;
   BIRTH COHORT; RISK-FACTORS; PREGNANCY; HEALTH; NUMBER; CHILDBEARING;
   FERTILITY
AB OBJECTIVE:To assess the effects of socioeconomic factors on the association between parity and long-term maternal mortality.METHODS:This was a population-based cohort study of mothers with births registered in the Medical Birth Registry of Norway during the period 1967-2009. We estimated age-specific (40-69 years) cardiovascular and noncardiovascular mortality ratios by number of births using Cox proportional hazard models. To assess effect modification by mothers' attained education, we stratified on low (less than 11 years) and high (11 years or greater) educational level. We further evaluated fathers' mortality by number of births using the same analytical approach.RESULTS:Mothers with low education had higher mortality (cardiovascular: hazard ratio 2.62, 95% confidence interval [CI] 2.34-2.93, noncardiovascular: hazard ratio 1.67, 95% CI 1.62-1.73). Among mothers with low education, cardiovascular mortality increased linearly with each additional birth above one (P trend=.02). In contrast, among mothers with high education, cardiovascular mortality declined with added births (P trend=.045). For noncardiovascular mortality there was no association among mothers with low education, whereas mortality declined with increasing number of births among mothers with high education (P trend<.01). Father's mortality showed similar associations with number of births when stratified on maternal education.CONCLUSION:Women's long-term mortality rose with number of births only for cardiovascular causes of death and only among mothers with low education. Partners of women with low education had similar increasing risk with increasing number of births. Maternal educational level is a strong modifier of the association between parity and long-term mortality.LEVEL OF EVIDENCE:II
C1 Univ Bergen, Dept Global Publ Hlth & Primary Care, Dept Obstet & Gynaecol, Haukeland Univ Hosp,Med Birth Registry Norway, N-5018 Bergen, Norway.
   Univ Bergen, Dept Clin Sci, Dept Obstet & Gynaecol, Haukeland Univ Hosp,Med Birth Registry Norway, N-5018 Bergen, Norway.
   Norwegian Inst Publ Hlth, Bergen, Norway.
   NIEHS, Epidemiol Branch, NIH, Durham, NC USA.
RP Halland, F (reprint author), Univ Bergen, Dept Global Publ Hlth & Primary Care, Kalfarveien 31, N-5018 Bergen, Norway.
EM Frode.Halland@uib.no
OI Wilcox, Allen/0000-0002-3376-1311
FU Norwegian Research Council through University of Bergen; Intramural
   Program of the U.S. National Institute of Environmental Health Sciences,
   National Institutes of Health
FX Supported by the Norwegian Research Council through the University of
   Bergen and in part by the Intramural Program of the U.S. National
   Institute of Environmental Health Sciences, National Institutes of
   Health.
NR 27
TC 4
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U1 2
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD DEC
PY 2015
VL 126
IS 6
BP 1181
EP 1187
DI 10.1097/AOG.0000000000001155
PG 7
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA CW9EQ
UT WOS:000365301800004
PM 26551179
ER

PT J
AU Lee, T
   Sigurdson, AJ
   Preston, DL
   Cahoon, EK
   Freedman, DM
   Simon, SL
   Nelson, K
   Matanoski, G
   Kitahara, CM
   Liu, JJ
   Wang, T
   Alexander, BH
   Doody, MM
   Linet, MS
   Little, MP
AF Lee, Terrence
   Sigurdson, Alice J.
   Preston, Dale L.
   Cahoon, Elizabeth K.
   Freedman, D. Michal
   Simon, Steven L.
   Nelson, Kenrad
   Matanoski, Genevieve
   Kitahara, Cari M.
   Liu, Jason J.
   Wang, Timothy
   Alexander, Bruce H.
   Doody, Michele M.
   Linet, Martha S.
   Little, Mark P.
TI Occupational ionising radiation and risk of basal cell carcinoma in US
   radiologic technologists (1983-2005)
SO OCCUPATIONAL AND ENVIRONMENTAL MEDICINE
LA English
DT Article
ID ATOMIC-BOMB SURVIVORS; SKIN-CANCER INCIDENCE; AIRLINE CABIN CREW;
   UNITED-STATES; EXPOSURE; WORKERS; COHORT; CHILDHOOD; MORTALITY; RINGWORM
AB Objective To determine risk for incident basal cell carcinoma from cumulative low-dose ionising radiation in the US radiologic technologist cohort.
   Methods We analysed 65 719 Caucasian technologists who were cancer-free at baseline (1983-1989 or 1994-1998) and answered a follow-up questionnaire (2003-2005). Absorbed radiation dose to the skin in mGy for estimated cumulative occupational radiation exposure was reconstructed for each technologist based on badge dose measurements, questionnaire-derived work history and protection practices, and literature information. Radiation-associated risk was assessed using Poisson regression and included adjustment for several demographic, lifestyle, host and sun exposure factors.
   Results Cumulative mean absorbed skin dose (to head/neck/arms) was 55.8 mGy (range 0-1735 mGy). For lifetime cumulative dose, we did not observe an excess radiation-related risk (excess relative risk/Gy=-0.01 (95% CI -0.43 to 0.52). However, we observed that basal cell carcinoma risk was increased for radiation dose received before age 30 (excess relative risk/Gy=0.59, 95% CI -0.11 to 1.42) and before 1960 (excess relative risk/Gy= 2.92, 95% CI 1.39 to 4.45).
   Conclusions Basal cell carcinoma risk was unrelated to low-dose radiation exposure among radiologic technologists. Because of uncertainties in dosimetry and sensitivity to model specifications, both our null results and our findings of excess risk for dose received before age 30 and exposure before 1960 should be interpreted with caution.
C1 [Lee, Terrence; Sigurdson, Alice J.; Cahoon, Elizabeth K.; Freedman, D. Michal; Simon, Steven L.; Kitahara, Cari M.; Liu, Jason J.; Doody, Michele M.; Linet, Martha S.; Little, Mark P.] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Preston, Dale L.] Hirosoft Int, Eureka, CA USA.
   [Nelson, Kenrad; Matanoski, Genevieve] Johns Hopkins Univ, Dept Epidemiol, Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
   [Wang, Timothy] Johns Hopkins Univ, Dept Dermatol, Johns Hopkins Sch Med, Baltimore, MD 21218 USA.
   [Alexander, Bruce H.] Univ Minnesota, Sch Publ Hlth, Div Environm Hlth Sci, Minneapolis, MN USA.
RP Little, MP (reprint author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, DHHS,NIH, 9609 Med Ctr Dr,Room 7E546,MSC 9778, Bethesda, MD 20892 USA.
EM mark.little@nih.gov
RI Kitahara, Cari/R-8267-2016; 
OI Little, Mark/0000-0003-0980-7567
FU ARRT; National Institutes of Health, National Cancer Institute, Division
   of Cancer Epidemiology and Genetics
FX The authors thank Dr Elizabeth Platz and Dr Paul Strickland for their
   input in the design of the study and review of early results of the
   study, and for the detailed and helpful comments of the three referees.
   They also thank the radiologic technologists who participated in the
   USRT Study; Jerry Reid of the ARRT for continued support of this study
   and Diane Kampa, Allison Iwan and Richard Hoffbeck of the University of
   Minnesota for study management and data collection and management. This
   work was supported by the Intramural Research Program of the National
   Institutes of Health, National Cancer Institute, Division of Cancer
   Epidemiology and Genetics.
NR 40
TC 1
Z9 1
U1 4
U2 10
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1351-0711
EI 1470-7926
J9 OCCUP ENVIRON MED
JI Occup. Environ. Med.
PD DEC
PY 2015
VL 72
IS 12
BP 862
EP 869
DI 10.1136/oemed-2015-102880
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA CW6WF
UT WOS:000365138400007
PM 26350677
ER

PT J
AU Alonso, WJ
   Yu, C
   Viboud, C
   Richard, SA
   Schuck-Paim, C
   Simonsen, L
   Mello, WA
   Miller, MA
AF Alonso, Wladimir J.
   Yu, Christine
   Viboud, Cecile
   Richard, Stephanie A.
   Schuck-Paim, Cynthia
   Simonsen, Lone
   Mello, Wyller A.
   Miller, Mark A.
TI A global map of hemispheric influenza vaccine recommendations based on
   local patterns of viral circulation
SO SCIENTIFIC REPORTS
LA English
DT Article
ID SEASONALITY; VIRUSES; AFRICA; TOOL
AB Both the Northern and the Southern Hemisphere annual WHO influenza vaccine recommendations are designed to ensure vaccine delivery before the winter-time peak of viral circulation in each hemisphere. However, influenza seasonal patterns are highly diverse in tropical countries and may be out of phase with the WHO recommendations for their respective hemisphere. We modelled the peak timing of influenza activity for 125 countries using laboratory-based surveillance data from the WHO's FLUNET database and compared it with the influenza hemispheric recommendations in place. Influenza vaccine recommendations for respectively 25% and 39% of the Northern and Southern Hemisphere countries were out of phase with peak influenza circulation in their corresponding hemisphere (62% and 53%, respectively, when the analysis was limited to the 52 countries in the tropical belt). These results indicate that routine influenza immunization efforts should be closely tailored to local patterns of viral circulation, rather than a country's hemispheric position.
C1 [Alonso, Wladimir J.; Viboud, Cecile; Richard, Stephanie A.; Miller, Mark A.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
   [Schuck-Paim, Cynthia] Univ Oxford Wolfson Coll, Oxford OX2 6UD, England.
   [Yu, Christine; Simonsen, Lone] George Washington Univ, Milken Inst Sch Publ Hlth, Washington, DC 20052 USA.
RP Alonso, WJ (reprint author), NIH, Fogarty Int Ctr, Bldg 10, Bethesda, MD 20892 USA.
EM wladimir.alonso@nih.gov
OI Simonsen, Lone/0000-0003-1535-8526
FU Office of Pandemics and Emerging Threats of the Department of Health and
   Human Services; RAPIDD program of the Science & Technology Directorate;
   Department of Homeland Security US; Lundbeck Fundation, Denmark; Marie
   Sklodowska-Curie Senior Fellowship [H2020-MSCA-IF-2014, 6594]
FX Funding for this project comes from the Office of Pandemics and Emerging
   Threats of the Department of Health and Human Services (WJA, CV, MM) and
   from the RAPIDD program of the Science & Technology Directorate,
   Department of Homeland Security US, the Lundbeck Fundation, Denmark, and
   a Marie Sklodowska-Curie Senior Fellowship award (H2020-MSCA-IF-2014,
   project id 6594) (LS).
NR 28
TC 3
Z9 3
U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD DEC 1
PY 2015
VL 5
AR 17214
DI 10.1038/srep17214
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA CX1TN
UT WOS:000365478600001
PM 26621769
ER

PT J
AU Liu, QY
   Via, LE
   Luo, T
   Liang, LL
   Liu, X
   Wu, SF
   Shen, QY
   Wei, W
   Ruan, XL
   Yuan, X
   Zhang, GL
   Barry, CE
   Gao, Q
AF Liu, Qingyun
   Via, Laura E.
   Luo, Tao
   Liang, Lili
   Liu, Xin
   Wu, Sufang
   Shen, Qingyu
   Wei, Wang
   Ruan, Xianglin
   Yuan, Xing
   Zhang, Guolong
   Barry, Clifton E., III
   Gao, Qian
TI Within patient microevolution of Mycobacterium tuberculosis correlates
   with heterogeneous responses to treatment
SO SCIENTIFIC REPORTS
LA English
DT Article
ID MULTIDRUG-RESISTANT TUBERCULOSIS; CANCER EVOLUTION; DRUG-RESISTANCE;
   LUNG-CANCER; INFECTION; MUTATION; STRAIN; CHINA
AB Genetic heterogeneity of Mycobacterium tuberculosis (MTB) within a patient has caused great concern as it might complicate antibiotic treatment and cause treatment failure. But the extent of genetic heterogeneity has not been described in detail nor has its association with heterogeneous treatment response. During treatment of a subject with MDR-TB, serial computed tomography (CT) scans showed this subject had six anatomically discrete lesions and they responded to treatment with disparate kinetics, suggesting heterogeneous MTB population may exist. To investigate this heterogeneity, we applied deep whole genome sequencing of serial sputum isolates and discovered that the MTB population within this patient contained three dominant sub-clones differing by 10 similar to 14 single nucleotide polymorphisms (SNPs). Differential mutation patterns in known resistance alleles indicated these sub-clones had different drug-resistance patterns, which may explain the heterogeneous treatment responses between lesions. Our results showed clear evidence of branched microevolution of MTB in vivo, which led to a diverse bacterial community. These findings indicated that complex sub-populations of MTB might coexist within patient and contribute to lesions' disparate responses to antibiotic treatment.
C1 [Liu, Qingyun; Luo, Tao; Gao, Qian] Fudan Univ, Sch Basic Med Sci, Inst Biomed Sci, Key Lab Med Mol Virol,Minist Educ, Shanghai 200032, Peoples R China.
   [Liu, Qingyun; Luo, Tao; Gao, Qian] Fudan Univ, Sch Basic Med Sci, Inst Biomed Sci, Key Lab Med Mol Virol,Minist Hlth, Shanghai 200032, Peoples R China.
   [Liu, Qingyun; Luo, Tao; Gao, Qian] Fudan Univ, Sch Basic Med Sci, Inst Med Microbiol, Shanghai 200032, Peoples R China.
   [Liu, Qingyun; Via, Laura E.; Barry, Clifton E., III] NIAID, TB Res Sect, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
   [Via, Laura E.; Barry, Clifton E., III] Univ Cape Town, Fac Hlth Sci, Inst Infect Dis & Mol Med, ZA-7701 Rondebosch, South Africa.
   [Via, Laura E.; Barry, Clifton E., III] Univ Cape Town, Fac Hlth Sci, Dept Clin Lab Sci, ZA-7701 Rondebosch, South Africa.
   [Liang, Lili; Liu, Xin; Wu, Sufang; Wei, Wang; Ruan, Xianglin; Yuan, Xing] Henan Prov Chest Hosp, Zhengzhou 450003, Henan, Peoples R China.
   [Shen, Qingyu; Zhang, Guolong; Gao, Qian] Sino US Int Res Ctr TB, Zhengzhou 450003, Henan, Peoples R China.
RP Zhang, GL (reprint author), Sino US Int Res Ctr TB, Zhengzhou 450003, Henan, Peoples R China.
EM guolongzhang@hotmail.com; cbarry@niaid.nih.gov; qgao99@yahoo.com
RI Barry, III, Clifton/H-3839-2012
FU Intramural Research Program of the National Institute of Allergy and
   Infectious Diseases, NIH though the International Centers of Excellence
   in Research program; Ministry of Science and Technology of China
   [2014DFA30340]; Natural Science Foundation of China [91231115]
FX We thank the subjects who participated in the study and the doctors and
   nurses of the Henan Provincial Chest Hospital who gave their time and
   energy to conduct this study. Funding for this study was provided by the
   Intramural Research Program of the National Institute of Allergy and
   Infectious Diseases, NIH though the International Centers of Excellence
   in Research program to Henan Provincial Chest Hospital and Sino-US
   International Research Center of Tuberculosis; by the Ministry of
   Science and Technology of China (2014DFA30340) and by the Natural
   Science Foundation of China (91231115).
NR 38
TC 11
Z9 11
U1 13
U2 24
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD DEC 1
PY 2015
VL 5
AR 17507
DI 10.1038/srep17507
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA CX1XP
UT WOS:000365489300001
PM 26620446
ER

PT J
AU Glait-Santar, C
   Desmond, R
   Feng, XM
   Bat, T
   Chen, JC
   Heuston, E
   Mizukawa, B
   Mulloy, JC
   Bodine, DM
   Larochelle, A
   Dunbar, CE
AF Glait-Santar, Chen
   Desmond, Ronan
   Feng, Xingmin
   Bat, Taha
   Chen, Jichun
   Heuston, Elisabeth
   Mizukawa, Benjamin
   Mulloy, James C.
   Bodine, David M.
   Larochelle, Andre
   Dunbar, Cynthia E.
TI Functional Niche Competition Between Normal Hematopoietic Stem and
   Progenitor Cells and Myeloid Leukemia Cells
SO STEM CELLS
LA English
DT Article
DE Bone marrow; Niche; Hematopoietic stem cells; Acute myeloid leukemia;
   Murine; Competition
ID BONE-MARROW MICROENVIRONMENT; MURINE MARROW; TRANSPLANTATION;
   LOCALIZATION; REMISSION; PROTEINS; CAPACITY; SURVIVAL; THERAPY; SITES
AB Hematopoietic stem and progenitor cells (HSPCs) reside in a specialized niche that regulates their proliferative capacity and their fate. There is increasing evidence for similar roles of marrow niches on controlling the behavior of leukemic cells; however, whether normal hematopoietic stem cell (HSC) and leukemic cells reside in or functionally compete for the same marrow niche is unclear. We used the mixed lineage leukemia-AF9 (MLL-AF9) murine acute myeloid leukemia (AML) in a competitive repopulation model to investigate whether normal HSPC and leukemic cells functionally compete for the same marrow niches. Irradiated recipient mice were transplanted with fixed numbers of MLL-AF9 cells mixed with increasing doses of normal syngeneic whole bone marrow (WBM) or with purified HSPC (LSK). Survival was significantly increased and leukemic progression was delayed proportional to increasing doses of normal WBM or normal LSK cells in multiple independent experiments, with all doses of WBM or LSK cells studied above the threshold for rapid and complete hematopoietic reconstitution in the absence of leukemia. Confocal microscopy demonstrated nests of either leukemic cells or normal hematopoietic cells but not both in the marrow adjacent to endosteum. Early following transplantation, leukemic cells from animals receiving lower LSK doses were cycling more actively than in those receiving higher doses. These results suggest that normal HSPC and AML cells compete for the same functional niche. Manipulation of the niche could impact on response to antileukemic therapies, and the numbers of normal HSPC could impact on leukemia outcome, informing approaches to cell dose in the context of stem cell transplantation.
C1 [Glait-Santar, Chen; Desmond, Ronan; Feng, Xingmin; Bat, Taha; Chen, Jichun; Larochelle, Andre; Dunbar, Cynthia E.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Desmond, Ronan] Tallaght Hosp, Dept Haematol, Dublin, Ireland.
   [Heuston, Elisabeth; Bodine, David M.] NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
   [Mizukawa, Benjamin; Mulloy, James C.] Cincinnati Childrens Hosp Med Ctr, Div Expt Hematol & Canc Biol, Cincinnati, OH 45229 USA.
RP Dunbar, CE (reprint author), NHLBI, Hematol Branch, NIH, Bldg 10 CRC 4E-5132,10 Ctr Dr, Bethesda, MD 20892 USA.
EM dunbarc@nhlbi.nih.gov
OI Heuston, Elisabeth/0000-0002-1603-4083
FU National Heart, Lung, and Blood Institute; National Human Genome
   Research Institute
FX This work was funded by the intramural programs of the National Heart,
   Lung, and Blood Institute and the National Human Genome Research
   Institute. We thank the NHLBI Light Microscopy Core and the Hematology
   Branch flow cytometry facility, and Keyvan Keyvanfar for his valuable
   assistance.
NR 30
TC 6
Z9 6
U1 1
U2 6
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 DEC
PY 2015
VL 33
IS 12
SI SI
BP 3635
EP 3642
DI 10.1002/stem.2208
PG 8
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
   Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA CW8EL
UT WOS:000365232200007
PM 26388434
ER

PT J
AU Araki, T
   Nishino, M
   Gao, W
   Dupuis, J
   Putman, RK
   Washko, GR
   Hunninghake, GM
   O'Connor, GT
   Hatabu, H
AF Araki, Tetsuro
   Nishino, Mizuki
   Gao, Wei
   Dupuis, Josee
   Putman, Rachel K.
   Washko, George R.
   Hunninghake, Gary M.
   O'Connor, George T.
   Hatabu, Hiroto
TI Pulmonary cysts identified on chest CT: are they part of aging change or
   of clinical significance?
SO THORAX
LA English
DT Article
ID INTERSTITIAL LUNG ABNORMALITIES; HIGH-RESOLUTION CT; BODY-MASS INDEX;
   THIN-SECTION CT; COMPUTED-TOMOGRAPHY; ASYMPTOMATIC SUBJECTS; REFERENCE
   VALUES; SMOKING; AGE; POPULATION
AB Objective To investigate the prevalence and natural course of pulmonary cysts in a population-based cohort and to describe the CT image characteristics in association with participant demographics and pulmonary functions.
   Materials and methods Chest CT scans of 2633 participants (mean age 59.2 years; 50% female) of the Framingham Heart Study (FHS) were visually evaluated for the presence of pulmonary cysts and their image characteristics. These findings were correlated with participant demographics and results of pulmonary function tests as well as the presence of emphysema independently detected on CT. The interval change was investigated by comparison with previous CT scans (median interval 6.1 years).
   Results Pulmonary cysts were seen in 7.6% (95% CI 6.6% to 8.7%; 200/2633). They were not observed in participants younger than 40 years old, and the prevalence increased with age. Multiple cysts (at least five) were seen in 0.9% of all participants. Participants with pulmonary cysts showed significantly lower body mass index (BMI) (p<0.001). Pulmonary cysts were most likely to appear solitary in the peripheral area of the lower lobes and remain unchanged or slightly increase in size over time. Pulmonary cysts showed no significant influence on pulmonary functions (p=0.07-0.6) except for diffusing capacity of the lung for carbon monoxide (DLCO) (p=0.03)and no association with cigarette smoking (p=0.1-0.9) or emphysema (p=0.7).
   Conclusions Pulmonary cysts identified on chest CT may be a part of the aging changes of the lungs, occurring in asymptomatic individuals older than 40 years, and are associated with decreased BMI and DLCO. Multiple pulmonary cysts may need to be evaluated for the possibility of cystic lung diseases.
C1 [Araki, Tetsuro; Nishino, Mizuki; Hatabu, Hiroto] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Radiol,Ctr Pulm Funct Imaging, Boston, MA 02215 USA.
   [Dupuis, Josee; Putman, Rachel K.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02215 USA.
   [Dupuis, Josee; O'Connor, George T.] Natl Heart Lung & Blood Inst Framingham Heart Stu, Framingham, MA USA.
   [Putman, Rachel K.; Washko, George R.; Hunninghake, Gary M.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Pulm & Crit Care Div, Boston, MA 02215 USA.
   [O'Connor, George T.] Boston Univ, Sch Med, Ctr Pulm, Boston, MA 02215 USA.
   [O'Connor, George T.] Boston Univ, Sch Med, Dept Med, Boston, MA 02215 USA.
RP Araki, T (reprint author), Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Radiol,Ctr Pulm Funct Imaging, 75 Francis St, Boston, MA 02215 USA.
EM taraki@partners.org
FU NCI [1K23CA157631]; NHLBI [N01-HC-25195, R01 HL111024]; NIH [R01
   HL111024, R01 HL116473, R01 HL107246, P01 HL114501, K08 HL092222, U01
   HL105371, K25 HL104085]
FX MN is supported by NCI Grant Number: 1K23CA157631. GRW is supported by
   NIH Grant Number: R01 HL116473, R01 HL107246 and P01 HL114501. GMH is
   supported by NIH Grant Number: K08 HL092222, U01 HL105371, P01 HL114501
   and R01 HL111024. HH is supported by NIH Grant Number: K25 HL104085 and
   R01 HL116473. This work was partially supported by the NHLBI's
   Framingham Heart Study contract N01-HC-25195 and R01 HL111024.
NR 30
TC 2
Z9 2
U1 0
U2 1
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 DEC
PY 2015
VL 70
IS 12
BP 1156
EP 1162
DI 10.1136/thoraxjnl-2015-207653
PG 7
WC Respiratory System
SC Respiratory System
GA CW7ZP
UT WOS:000365218400011
PM 26514407
ER

PT J
AU Murphy, G
   Dawsey, SM
   Engels, EA
   Ricker, W
   Parsons, R
   Etemadi, A
   Lin, SW
   Abnet, CC
   Freedman, ND
AF Murphy, Gwen
   Dawsey, Sanford M.
   Engels, Eric A.
   Ricker, Winnie
   Parsons, Ruth
   Etemadi, Arash
   Lin, Shih-Wen
   Abnet, Christian C.
   Freedman, Neal D.
TI Cancer Risk After Pernicious Anemia in the US Elderly Population
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Chronic Atrophic Autoimmune Gastritis; Acid Secretion; Parietal Cells;
   Stomach Cancer
ID GASTRIC CARCINOID-TUMORS; SERUM PEPSINOGENS; COHORT; CARCINOGENESIS;
   ADENOCARCINOMA; PREVENTION; PREVALENCE; HISTOLOGY; STOMACH; DISEASE
AB BACKGROUND & AIMS: Pernicious anemia, a result of autoimmune gastritis, is the most common cause of vitamin B-12 deficiency, affecting 2% to 5% of the elderly population. Treatment with vitamin B-12 cures the anemia, but not the gastritis. Findings from small studies have indicated that patients with pernicious anemia could have an increased risk of cancer.
   METHODS: We performed a population-based, case-control study of individuals in the Surveillance, Epidemiology, and End Results-Medicare database, comparing 1,138,390 cancer cases (age, 66-99 y) with 100,000 matched individuals without cancer (controls). Individuals with pernicious anemia were identified based on their medical claims within the year before selection for the study. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using unconditional logistic regression, and models were adjusted for sex, age, and calendar year of diagnosis and selection.
   RESULTS: Compared with controls, we found individuals with pernicious anemia to be at increased risk for noncardia gastric adenocarcinoma (OR, 2.18; 95% CI, 1.94-2.45) and gastric carcinoid tumors (OR, 11.43; 95% CI, 8.90-14.69). In addition, people with pernicious anemia have an increased risk of developing tonsilar cancer (OR, 2.00; 95% CI, 1.40-2.85), hypopharyngeal cancer (OR, 1.92; 95% CI, 1.35-2.73), esophageal squamous cell carcinoma (OR, 2.12; 95% CI, 1.76-2.55), small intestinal cancer (OR, 1.63; 95% CI, 1.32-2.02), liver cancer (OR, 1.49; 95% CI, 1.28-1.73), myeloma (OR, 1.55; 95% CI, 1.37-1.75), acute myeloid leukemia (OR, 1.68; 95% CI, 1.46-1.93), and myelodysplastic syndrome (OR, 2.87; 95% CI, 2.53-3.26). People with pernicious anemia have a lower risk of rectal cancer than the general population (OR, 0.82; 95% CI, 0.74-0.92).
   CONCLUSIONS: In a population-based, case-control study of individuals in the Surveillance, Epidemiology, and End Results-Medicare database, we found individuals with pernicious anemia to have significantly increased risks of gastric carcinoid tumors, adenocarcinomas, and other cancers located throughout the body.
C1 [Murphy, Gwen; Dawsey, Sanford M.; Engels, Eric A.; Etemadi, Arash; Lin, Shih-Wen; Abnet, Christian C.; Freedman, Neal D.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Ricker, Winnie; Parsons, Ruth] Informat Management Serv Inc, Calverton, MD USA.
RP Murphy, G (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,6E314, Bethesda, MD 20892 USA.
EM murphygw@mail.nih.gov
RI Abnet, Christian/C-4111-2015; Etemadi, Arash/C-1386-2016
OI Abnet, Christian/0000-0002-3008-7843; Etemadi, Arash/0000-0002-3458-1072
FU National Cancer Institute at the US National Institutes of Health
FX This work was supported by the Intramural Research Program of the
   National Cancer Institute at the US National Institutes of Health.
NR 31
TC 13
Z9 13
U1 2
U2 11
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 DEC
PY 2015
VL 13
IS 13
BP 2282
EP +
DI 10.1016/j.cgh.2015.05.040
PG 12
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CW7PK
UT WOS:000365191300016
PM 26079040
ER

PT J
AU Kim, SYH
   Miller, FG
AF Kim, Scott Y. H.
   Miller, Franklin G.
TI Ethical complexities in standard of care randomized trials: A case study
   of morning versus nighttime dosing of blood pressure drugs
SO CLINICAL TRIALS
LA English
DT Article
DE Standard of care; research ethics; pragmatic trials; comparative
   effectiveness research; informed consent
ID REDUCES CARDIOVASCULAR RISK; INFORMED-CONSENT; ANTIHYPERTENSIVE THERAPY;
   HYPERTENSIVE PATIENTS; LOWERING TREATMENT; TIME; CHRONOTHERAPY;
   MEDICATIONS; OUTCOMES; SUPPORT
AB Background: Pragmatic trials comparing standard of care treatments provide comparative effectiveness data to make practice of medicine more evidence-based. With electronic health records, recruiting and conducting such trials can be relatively inexpensive. But some worry that the traditional research ethics framework poses unnecessary obstacles and is not appropriate for evaluating such clinical trials. This concern is based on the view (which we call the Standard of Care Principle) that such research is similar to usual clinical practice and therefore does not raise significant ethical issues since everyone in the research study will receive an accepted standard of care treatment.
   Methods: A case study of a pragmatic randomized clinical trial (Blood Pressure Medication Timing study) comparing morning versus nighttime dosing of antihypertensive medications. The Blood Pressure Medication Timing study has been proposed as a paradigm example of why the Standard of Care Principle obviates the need for traditional levels of ethical scrutiny and how the current regulatory framework poses unnecessary obstacles to research. We provide an ethical analysis of the Blood Pressure Medication Timing study, drawing on the empirical literature as well as on normative analysis.
   Results: The Standard of Care Principle is the main ethical rationale given by commentators for asserting that the Blood Pressure Medication Timing study does not require significant ethical debate and by investigators for the assertion that the Blood Pressure Medication Timing study is minimal risk and thus eligible for lessened regulatory requirements. However, the Blood Pressure Medication Timing study raises important ethical issues, including whether it is even necessary, given the considerable randomized clinical trial evidence in support of nighttime dosing, a much larger (N approximate to 17,000) confirmatory randomized clinical trial already in progress, evidence for safety of nighttime dosing, and the cost-free availability of the intervention. Furthermore, the Standard of Care Principle provides a misleading basis for analyzing the informed consent requirements, especially regarding the requirement to disclose alternative courses of treatment that might be advantageous to the subject.
   Conclusion: The Standard of Care Principle is ethically inadequate and misleading even when it is applied to the pragmatic randomized clinical trial proposed as a paradigm case for its application.
C1 [Kim, Scott Y. H.; Miller, Franklin G.] Natl Inst Hlth Clin Ctr, Dept Bioeth, Bethesda, MD 20892 USA.
   [Miller, Franklin G.] Weill Cornell Med Coll, New York, NY USA.
RP Kim, SYH (reprint author), Natl Inst Hlth Clin Ctr, Dept Bioeth, 10 Ctr Dr,Bldg. 10,Room IC118, Bethesda, MD 20892 USA.
EM scott.kim@nih.gov
FU Intramural Research Program; National Institutes of Health Clinical
   Center Department of Bioethics
FX This study was supported by Intramural Research Program and National
   Institutes of Health Clinical Center Department of Bioethics.
NR 33
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Z9 0
U1 1
U2 3
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
EI 1740-7753
J9 CLIN TRIALS
JI Clin. Trials
PD DEC
PY 2015
VL 12
IS 6
BP 557
EP 563
DI 10.1177/1740774515607213
PG 7
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA CW2MQ
UT WOS:000364826800001
PM 26400874
ER

PT J
AU Zuckerman, J
   van der Schalie, B
   Cahill, K
AF Zuckerman, Judith
   van der Schalie, Barbara
   Cahill, Kelly
TI Developing training for Data Safety Monitoring Board members: A National
   Institute of Allergy and Infectious Diseases case study
SO CLINICAL TRIALS
LA English
DT Article
DE DSMB training; publicly available DSMB member resources; web-based
   modules
AB Background: Data Safety Monitoring Boards primarily review accumulating data on clinical trials and provide recommendations to sponsors on whether a protocol should continue as planned, be modified, or be terminated. Data Safety Monitoring Boards often provide their recommendations based upon accumulating data to which only their members are given access. Despite the substantial responsibilities assumed by Data Safety Monitoring Board members, there is limited information in the literature about the unique knowledge they must possess and, consequently, the training content needs that are required in order for them to fulfill their obligations.
   Purpose: This article describes how the National Institute of Allergy and Infectious Diseases identified the knowledge that Data Safety Monitoring Board members should acquire and the computer-based training they developed to address the learning needs of the National Institute of Allergy and Infectious Diseases assembled Data Safety Monitoring Board members.
   Methods: The National Institute of Allergy and Infectious Diseases conducted a comprehensive literature search and interviewed Data Safety Monitoring Board subject matter experts, including Data Safety Monitoring Board members and chairs from academic institutions, pharmaceutical companies, and the National Institutes of Health to (1) assess whether Data Safety Monitoring Board training is an identified need, (2) evaluate whether Data Safety Monitoring Board training has been developed, and (3) formulate suitable learning objectives. Data Safety Monitoring Board training modules were developed based on the identified learning objectives identified from the interviews.
   Results: Three Data Safety Monitoring Board training modules were developed and formatted for web-based access, which is free of charge to the public at https://dsmblearningcenter.niaid.nih.gov. The modules include the following: an introduction to the objectives and purpose of Data Safety Monitoring Boards, the organization and responsibilities of Data Safety Monitoring Boards, and a review of statistical topics.
   Limitations: The complex concepts that Data Safety Monitoring Board members must apply to their deliberations and decisions require practice and application that come through hands-on experience. To build competency in the Data Safety Monitoring Board member role, not only does a member need to understand these complex concepts but also the member must have the opportunity to practice and apply this knowledge to real-life situations. Additional resources to facilitate practice and application of the complex issues that Data Safety Monitoring Boards deal with should be considered. The computer-based training is targeted to new and inexperienced Data Safety Monitoring Board members. Ongoing learning opportunities should be developed for experienced Data Safety Monitoring Board members. Non-English training must also be considered.
   Conclusion: The National Institute of Allergy and Infectious Diseases identified that training is not widely available for Data Safety Monitoring Board members to build the unique knowledge and skills necessary to serve on Data Safety Monitoring Boards. Consequently, National Institute of Allergy and Infectious Diseases developed publicly available web-based Data Safety Monitoring Board training modules for new or inexperienced members. Additional tools and resources are needed to help Data Safety Monitoring Board members acquire the knowledge and skills to serve their critical function in clinical research and to maximize research participant protections.
C1 [Zuckerman, Judith] NIAID, Off Strateg Planning & Assessment, Rockville, MD 20852 USA.
   [van der Schalie, Barbara] Leidos Biomedical Res Inc, Clin Res Directorate, Clin Monitoring Res Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
   [Cahill, Kelly] NIAID, Off Clin Res Policy & Regulatory Operat, Div Clin Res, Rockville, MD 20852 USA.
RP Zuckerman, J (reprint author), NIAID, Off Strateg Planning & Assessment, 5601 Fishers Lane,Rm 5C31, Rockville, MD 20852 USA.
EM jzuckerman@niaid.nih.gov
FU National Cancer Institute; National Institutes of Health
   [HHSN261200800001E]; National Institute of Allergy and Infectious
   Diseases
FX This project has been funded in whole or in part with federal funds from
   the National Cancer Institute and National Institutes of Health, under
   Contract No. HHSN261200800001E. This research was supported (in part) by
   the National Institute of Allergy and Infectious Diseases.
NR 7
TC 0
Z9 1
U1 0
U2 3
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
EI 1740-7753
J9 CLIN TRIALS
JI Clin. Trials
PD DEC
PY 2015
VL 12
IS 6
BP 688
EP 691
DI 10.1177/1740774515591498
PG 4
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA CW2MQ
UT WOS:000364826800016
PM 26152835
ER

PT J
AU Barker, TV
   Troller-Renfree, S
   Pine, DS
   Fox, NA
AF Barker, Tyson V.
   Troller-Renfree, Sonya
   Pine, Daniel S.
   Fox, Nathan A.
TI Individual differences in social anxiety affect the salience of errors
   in social contexts
SO COGNITIVE AFFECTIVE & BEHAVIORAL NEUROSCIENCE
LA English
DT Article
DE Error-related negativity; Social anxiety; ERP; Positive error
ID OBSESSIVE-COMPULSIVE DISORDER; ANTERIOR CINGULATE CORTEX; STATE WORRY
   QUESTIONNAIRE; BECK DEPRESSION INVENTORY; BRAIN ACTIVITY; PSYCHOMETRIC
   PROPERTIES; NEGATIVITY ERN; BEHAVIORAL-INHIBITION; STARTLE REACTIVITY;
   SELF-PRESENTATION
AB The error-related negativity (ERN) is an event-related potential that occurs approximately 50 ms after an erroneous response. The magnitude of the ERN is influenced by contextual factors, such as when errors are made during social evaluation. The ERN is also influenced by individual differences in anxiety, and it is elevated among anxious individuals. However, little research has examined how individual differences in anxiety interact with contextual factors to impact the ERN. Social anxiety involves fear and apprehension of social evaluation. In the present study, we explored how individual differences in social anxiety interact with social contexts to modulate the ERN. The ERN was measured in 43 young adults characterized as being either high or low in social anxiety, while they completed a flanker task in two contexts: alone and during social evaluation. The results revealed a significant interaction between social anxiety and context, such that the ERN was enhanced in a social relative to a nonsocial context only among highly socially anxious individuals. Furthermore, the degree of such enhancement significantly correlated with individual differences in social anxiety. These findings demonstrate that social anxiety is characterized by enhanced neural activity to errors in social-evaluative contexts.
C1 [Barker, Tyson V.; Troller-Renfree, Sonya; Fox, Nathan A.] Univ Maryland, Dept Human Dev & Quantitat Methodol, College Pk, MD 20742 USA.
   [Pine, Daniel S.] NIMH, Sect Dev & Affect Neurosci, Bethesda, MD 20892 USA.
RP Barker, TV (reprint author), Univ Maryland, Dept Human Dev & Quantitat Methodol, 3304 Benjamin Bldg, College Pk, MD 20742 USA.
EM tvbarker@umd.edu
OI Troller-Renfree, Sonya/0000-0001-9979-4696
FU Intramural NIH HHS; NICHD NIH HHS [5T32HD007542, T32 HD007542]; NIMH NIH
   HHS [R01 MH074454]; PHS HHS [HDR3717899]
NR 102
TC 3
Z9 3
U1 11
U2 28
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1530-7026
EI 1531-135X
J9 COGN AFFECT BEHAV NE
JI Cogn. Affect. Behav. Neurosci.
PD DEC
PY 2015
VL 15
IS 4
BP 723
EP 735
DI 10.3758/s13415-015-0360-9
PG 13
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA CW4IK
UT WOS:000364954700001
PM 25967929
ER

PT J
AU Radin, RM
   Tanofsky-Kraff, M
   Shomaker, LB
   Kelly, NR
   Pickworth, CK
   Shank, LM
   Altschul, AM
   Brady, SM
   Demidowich, AP
   Yanovski, SZ
   Hubbard, V
   Yanovski, JA
AF Radin, Rachel M.
   Tanofsky-Kraff, Marian
   Shomaker, Lauren B.
   Kelly, Nichole R.
   Pickworth, Courtney K.
   Shank, Lisa M.
   Altschul, Anne M.
   Brady, Sheila M.
   Demidowich, Andrew P.
   Yanovski, Susan Z.
   Hubbard, Van S.
   Yanovski, Jack A.
TI Metabolic characteristics of youth with loss of control eating
SO EATING BEHAVIORS
LA English
DT Article
DE Binge eating; Loss of control eating; Metabolic dysfunction; Adolescence
ID CHILDREN; ADOLESCENTS; RISK
AB Purpose: Preliminary data in adults suggest that binge eating is associated with greater prevalence of metabolic syndrome (MetS) components. However, there are limited data in youth, and little is known of the role of binge episode size in these relationships.
   Methods: We examined the relationship between loss of control eating and metabolic characteristics in a convenience sample of 329 treatment-seeking and non-treatment-seeking adolescent boys and girls. The sample was enriched by design with adolescents who were overweight or obese and with individuals who reported episodes of loss of control over their eating (either objectively large binge episodes, OBEs or subjectively large binge episodes, SBEs, in the past month), as assessed by clinical interview. MetS components (blood pressure, lipids, glucose, and waist circumference) were the primary variables of interest.
   Results: 46% of the cohort reported loss of control eating; among those, 53% reported SBEs only and 47% reported OBEs. Youth with loss of control eating had higher systolic blood pressure (p = .001) and higher low-density lipoprotein cholesterol (LDL-c) (p =. 002) compared to those without loss of control eating, in analyses adjusted for intervention-seeking status, fat mass and sociodemographic characteristics. Youth reporting OBEs had higher LDL-c (p = .013) compared to those reporting only SBEs.
   Conclusions: Adolescents reporting loss of control episodes had greater dysfunction in some components of the MetS compared to youth without loss of control; episode size may contribute to metabolic dysfunction. Published by Elsevier Ltd.
C1 [Radin, Rachel M.; Tanofsky-Kraff, Marian; Shomaker, Lauren B.; Kelly, Nichole R.; Pickworth, Courtney K.; Shank, Lisa M.; Altschul, Anne M.; Brady, Sheila M.; Demidowich, Andrew P.; Yanovski, Susan Z.; Yanovski, Jack A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Growth & Obes, Programin Dev Endocrinol & Genet, NIH,DHHS, Bethesda, MD 20892 USA.
   [Radin, Rachel M.; Tanofsky-Kraff, Marian; Kelly, Nichole R.; Shank, Lisa M.] Uniformed Serv Univ Hlth Sci, Dept Med & Clin Psychol, Bethesda, MD 20814 USA.
   [Radin, Rachel M.; Kelly, Nichole R.] Adv Mil Med Inc, Henry M Jackson Fdn, Bethesda, MD USA.
   [Shomaker, Lauren B.] Colorado State Univ, Ft Collins, CO 80523 USA.
   [Yanovski, Susan Z.; Hubbard, Van S.] NIDDK, Div Digest Dis & Nutr, NIH, Bethesda, MD USA.
   [Hubbard, Van S.] NIH, Div Nutr Res Coordinat, Bethesda, MD USA.
RP Yanovski, JA (reprint author), NICHD, Sect Growth & Obes, Programin Dev Endocrinol & Genet, NIH,Hatfield Clin Res Ctr, 10 Ctr Dr,Room 1E-3330,MSC 1103, Bethesda, MD 20892 USA.
EM jy15i@nih.gov
OI Shank, Lisa/0000-0002-6922-7946
FU NICHD [1ZIAHD000641, K99/R00HD069516, F32HD056762]; National Institute
   for Minority Health and Health Disparities (NIMHD) [1ZIAHD00641]; Office
   of Behavioral and Social Science Research, the Office of Disease
   Prevention, and the Division of Nutrition Research Coordination, NIH
   [1ZIAHD00641]; NIH; USUHS [R072IC]; NIDDK [R01DK080906-04]
FX Funding for this study was provided by the following sources: Intramural
   Research Program Grant 1ZIAHD000641 from the NICHD (to J.A.Y.) with
   supplemental funding from the National Institute for Minority Health and
   Health Disparities (NIMHD) (1ZIAHD00641), Office of Behavioral and
   Social Science Research, the Office of Disease Prevention, and the
   Division of Nutrition Research Coordination, NIH (1ZIAHD00641) (to
   J.A.Y.), NIH; K99/R00HD069516 from NICHD (to L.B.S.), and F32HD056762
   from NICHD (to L.B.S.); USUHS grant R072IC (to M.T.K.), and NIDDK grant
   R01DK080906-04 (to M.T.K.). The above funding sources and agencies
   (NICHD, NIMHD, NIDDK, and USUHS) had no role in the study design,
   collection, analysis or interpretation of the data, writing of the
   manuscript, or the decision to submit the paper for publication. The
   opinions and assertions expressed herein are those of the authors and
   are not to be construed as reflecting the views of the PHS, USUHS, or
   the U.S. Department of Defense.
NR 17
TC 3
Z9 3
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1471-0153
EI 1873-7358
J9 EAT BEHAV
JI Eat. Behav.
PD DEC
PY 2015
VL 19
BP 86
EP 89
DI 10.1016/j.eatbeh.2015.07.002
PG 4
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA CW4UP
UT WOS:000364992200019
PM 26210388
ER

PT J
AU Donfrancesco, R
   Marano, A
   Calderoni, D
   Mugnaini, D
   Thomas, F
   Di Trani, M
   Innocenzi, M
   Vitiello, B
AF Donfrancesco, R.
   Marano, A.
   Calderoni, D.
   Mugnaini, D.
   Thomas, F.
   Di Trani, M.
   Innocenzi, M.
   Vitiello, B.
TI Prevalence of severe ADHD: an epidemiological study in the Italian
   regions of Tuscany and Latium
SO EPIDEMIOLOGY AND PSYCHIATRIC SCIENCES
LA English
DT Article
DE Attention deficit; hyperactivity disorder; children; Italy; prevalence
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEFICIT HYPERACTIVITY
   DISORDER; HYPERKINETIC DISORDER; PSYCHIATRIC-DISORDERS; WORLDWIDE
   PREVALENCE; UNITED-STATES; CHILDREN; SAMPLE; METHYLPHENIDATE;
   ADOLESCENTS
AB Background. The rate with which attention deficit/hyperactivity disorder (ADHD) is diagnosed varies widely across countries, suggesting that cultural factors influence the clinical interpretation of child behaviour. This study estimated the point prevalence of severe ADHD among elementary and middle-school Italian children.
   Method. An epidemiological sample of 2016 children attending 2nd-8th grade in the Italian regions of Tuscany and Latium was selected based on census distribution of the school-age population. Teachers completed the Italian version of the ADHD Rating Scale for Teachers (SDAI). For children with at least six inattention symptoms and/or at least six hyperactivity/impulsivity symptoms rated 'very often' by the teachers, the parents completed the Italian ADHD Rating Scale for Parents (SDAG). Children with documented ADHD symptoms at both school and home received a complete psychiatric interview with the Kiddie Schedule for Affective Disorders and Schizophrenia-present and lifetime version (K-SADS-PL).
   Results. Of the 1887 assessed children, 4.45% (95% CI 3.58-5.51) met the ADHD cut-off on teacher ratings, 1.43% (0.96-2.12) had ADHD symptoms endorsed by both teacher and parent, and 1.32% (0.87-1.97) were further confirmed by the psychiatric evaluation. The male:female ratio was 7:1. The inattentive type accounted for about half of the ADHD cases.
   Conclusions. When applying stringent criteria for both severity and pervasiveness of symptoms, it is estimated that about 1.3% of the Italian elementary and middle-school children suffer from severe ADHD.
C1 [Donfrancesco, R.] Osped Sandro Pertini, I-00157 Rome, Italy.
   [Marano, A.] Univ Aquila, Dept Life Hlth & Environm Sci, I-67100 Laquila, Italy.
   [Calderoni, D.; Thomas, F.; Innocenzi, M.] Natl Hlth Syst ASL Roma B, Rome, Italy.
   [Mugnaini, D.] Local Hlth Serv Florence, Ctr Neuropsychol Assessment, Florence, Italy.
   [Di Trani, M.] Univ Roma La Sapienza, Dept Clin & Dynam Psychol, Rome, Italy.
   [Vitiello, B.] NIMH, Bethesda, MD 20892 USA.
RP Donfrancesco, R (reprint author), Osped Sandro Pertini, Via Monti Tiburtini, I-00157 Rome, Italy.
EM renato.donfrancesco@yahoo.it
NR 36
TC 0
Z9 0
U1 2
U2 7
PU CAMBRIDGE UNIV PRESS
PI CAMBRIDGE
PA EDINBURGH BLDG, SHAFTESBURY RD, CB2 8RU CAMBRIDGE, ENGLAND
SN 2045-7960
EI 2045-7979
J9 EPIDEMIOL PSYCH SCI
JI Epidemiol. Psychiatr. Sci.
PD DEC
PY 2015
VL 24
IS 6
BP 525
EP 533
DI 10.1017/S2045796014000523
PG 9
WC Psychiatry
SC Psychiatry
GA CW5FT
UT WOS:000365021700013
PM 25221947
ER

EF