FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU McLinden, RJ
   LaBranche, CC
   Chenine, AL
   Polonis, VR
   Eller, MA
   Wieczorek, L
   Ochsenbauer, C
   Kappes, JC
   Perfetto, S
   Montefiori, DC
   Michael, NL
   Kim, JH
AF McLinden, Robert J.
   LaBranche, Celia C.
   Chenine, Agnes-Laurence
   Polonis, Victoria R.
   Eller, Michael A.
   Wieczorek, Lindsay
   Ochsenbauer, Christina
   Kappes, John C.
   Perfetto, Stephen
   Montefiori, David C.
   Michael, Nelson L.
   Kim, Jerome H.
TI Detection of HIV-1 Neutralizing Antibodies in a Human
   CD4(+)/CXCR4(+)/CCR5(+) T-Lymphoblastoid Cell Assay System
SO PLOS ONE
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; HUMAN MONOCLONAL-ANTIBODIES; CROSS-CLADE
   NEUTRALIZATION; INFECTIOUS MOLECULAR CLONES; PROXIMAL EXTERNAL REGION;
   BLOOD MONONUCLEAR-CELLS; FUSION INHIBITOR T-20; SUBTYPE-C INFECTION; V3
   LOOP; EFFICACY TRIAL
AB Sensitive assays are needed to meaningfully assess low levels of neutralizing antibodies (NAbs) that may be important for protection against the acquisition of HIV-1 infection in vaccine recipients. The current assay of choice uses a non-lymphoid cell line (TZM-bl) that may lack sensitivity owing to over expression of CD4 and CCR5. We used transfection of a human CD4+/CXCR4+/alpha(4)beta(7)+ T-lymphoblastoid cell line (A3.01) with a CMV IE promoter-driven CCR5neo vector to stably express CCR5. The resulting line, designated A3R5, is permissive to a wide range of CCR5-tropic circulating strains of HIV-1, including HIV-1 molecular clones containing a Tat-inducible Renilla luciferase reporter gene and expressing multiple Env subtypes. Flow cytometric analysis found CCR5 surface expression on A3R5 cells to be markedly less than TZM-bl but similar to CD3.8 stimulated PBMC. More importantly, neutralization mediated by a diverse panel of monoclonal antibodies, HIV-1 positive polyclonal sera and sCD4 was consistently greater in A3R5 compared to TZM-bl cells. The A3R5 cell line provides a novel approach to guide the development and qualification of promising new HIV-1 vaccine immunogens.
C1 [McLinden, Robert J.; Chenine, Agnes-Laurence; Polonis, Victoria R.; Eller, Michael A.; Wieczorek, Lindsay; Michael, Nelson L.; Kim, Jerome H.] WRAIR, Mil HIV Res Program, Silver Spring, MD USA.
   [LaBranche, Celia C.; Montefiori, David C.] Duke U Med Ctr, Dept Surg, Durham, NC USA.
   [Ochsenbauer, Christina; Kappes, John C.] Univ Alabama Birmingham, Dept Med, Birmingham, AL 35294 USA.
   [Kappes, John C.] Birmingham Vet Affairs Med Ctr, Res Serv, Birmingham, AL USA.
   [Perfetto, Stephen] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
RP McLinden, RJ (reprint author), WRAIR, Mil HIV Res Program, Silver Spring, MD USA.
EM rmclinden@hivresearch.org
FU U.S. Army Medical Research and Material Command (USAMRMC)
   [Y1-AI-2642-12]; National Institute of Allergy and Infectious Diseases
   [Y1-AI-2642-12]; Henry M. Jackson Foundation for the Advancement of
   Military Medicine, Inc. [W81XWH-07-2-0067]; U.S. Department of Defense
   (DOD) [W81XWH-07-2-0067]; Bill & Melinda Gates Foundation's
   Collaboration for AIDS Vaccine Discovery (CAVD)/Comprehensive Antibody
   Vaccine Immune Monitoring Consortium (CA-VIMC) [38619, 1032144]; NIH
   Center for HIV/AIDS Vaccine Immunology (CHAVI) [UO1-AI067854]
FX This work was supported in part by an Interagency Agreement
   (Y1-AI-2642-12) between U.S. Army Medical Research and Material Command
   (USAMRMC) and the National Institute of Allergy and Infectious Diseases.
   This work was also supported by a cooperative agreement
   (W81XWH-07-2-0067) between the Henry M. Jackson Foundation for the
   Advancement of Military Medicine, Inc., and the U.S. Department of
   Defense (DOD). The contribution of DCM was supported by the Bill &
   Melinda Gates Foundation's Collaboration for AIDS Vaccine Discovery
   (CAVD)/Comprehensive Antibody Vaccine Immune Monitoring Consortium
   (CA-VIMC), grant numbers 38619 and 1032144. The contribution of CO and
   JCK was supported by NIH Center for HIV/AIDS Vaccine Immunology (CHAVI)
   grant, UO1-AI067854; the Bill & Melinda Gates Foundation's Collaboration
   for AIDS Vaccine Discovery (CAVD)/Comprehensive Antibody Vaccine Immune
   Monitoring Consortium (CA-VIMC), grant numbers 38619 and 1032144; and
   facilities of the Virology and Genetic Sequencing cores of the UAB
   Center for AIDS Research (P30-AI-27767). The funders had no role in
   study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
NR 103
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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 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 28
PY 2013
VL 8
IS 11
AR UNSP e77756
DI 10.1371/journal.pone.0077756
PG 13
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 261IJ
UT WOS:000327657900001
PM 24312168
ER

PT J
AU Rachmany, L
   Tweedie, D
   Rubovitch, V
   Yu, QS
   Li, YZ
   Wang, JY
   Pick, CG
   Greig, NH
AF Rachmany, Lital
   Tweedie, David
   Rubovitch, Vardit
   Yu, Qian-Sheng
   Li, Yazhou
   Wang, Jia-Yi
   Pick, Chaim G.
   Greig, Nigel H.
TI Cognitive Impairments Accompanying Rodent Mild Traumatic Brain Injury
   Involve p53-Dependent Neuronal Cell Death and Are Ameliorated by the
   Tetrahydrobenzothiazole PFT-alpha
SO PLOS ONE
LA English
DT Article
ID GLUCAGON-LIKE PEPTIDE-1; OBJECT RECOGNITION MEMORY; FLUORO-JADE-B;
   CEREBRAL-ISCHEMIA; HEAD-INJURY; IN-VITRO; P53-INDUCED APOPTOSIS;
   FUNCTIONAL OUTCOMES; GENE-EXPRESSION; P53
AB With parallels to concussive mild traumatic brain injury (mTBI) occurring in humans, anesthetized mice subjected to a single 30 g weight drop mTBI event to the right parietal cortex exhibited significant diffuse neuronal degeneration that was accompanied by delayed impairments in recognition and spatial memory. To elucidate the involvement of reversible p53-dependent apoptosis in this neuronal loss and associated cognitive deficits, mice were subjected to experimental mTBI followed by the systemic administration of the tetrahydrobenzothiazole p53 inactivator, PFT-alpha, or vehicle. Neuronal loss was quantified immunohistochemically at 72 hr. post-injury by the use of fluoro-Jade B and NeuN within the dentate gyrus on both sides of the brain, and recognition and spatial memory were assessed by novel object recognition and Y-maze paradigms at 7 and 30 days post injury. Systemic administration of a single dose of PFT-alpha 1 hr. post-injury significantly ameliorated both neuronal cell death and cognitive impairments, which were no different from sham control animals. Cellular studies on human SH-SY5Y cells and rat primary neurons challenged with glutamate excitotoxicity and H2O2 induced oxidative stress, confirmed the ability of PFT-alpha and a close analog to protect against these TBI associated mechanisms mediating neuronal loss. These studies suggest that p53-dependent apoptotic mechanisms underpin the neuronal and cognitive losses accompanying mTBI, and that these are potentially reversible by p53 inactivation.
C1 [Rachmany, Lital; Rubovitch, Vardit; Pick, Chaim G.] Tel Aviv Univ, Sackler Sch Med, Dept Anat & Anthropol, IL-69978 Tel Aviv, Israel.
   [Rachmany, Lital; Rubovitch, Vardit; Pick, Chaim G.] Tel Aviv Univ, Sagol Sch Neurosci, IL-69978 Tel Aviv, Israel.
   [Tweedie, David; Yu, Qian-Sheng; Li, Yazhou; Greig, Nigel H.] NIA, Drug Design & Dev Sect, Translat Gerontol Branch, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
   [Wang, Jia-Yi] Taipei Med Univ, Coll Med, Grad Inst Med Sci, Taipei, Taiwan.
RP Pick, CG (reprint author), Tel Aviv Univ, Sackler Sch Med, Dept Anat & Anthropol, IL-69978 Tel Aviv, Israel.
EM pickc@post.tau.ac.il; Greign@grc.nia.nih.gov
FU Intramural Research Program of the National Institute on Aging, National
   Institutes of Health; National Science Council, Taiwan [NSC
   101-2321-B-038-003, NSC 102-2321-B-038-003]; Sackler School of Medicine,
   Tel-Aviv University; Israeli 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 (DT,QSY,NHG); (ii) grants from the National Science Council (NSC
   101-2321-B-038-003 and NSC 102-2321-B-038-003), Taiwan (JYW); (iii) by
   the Sackler School of Medicine, Tel-Aviv University, and, in part, by a
   grant from the Israeli Science Foundation (grant no. 108/09)
   (LR,VR,CGP). The funders had no role in study design, data collection
   and analysis, decision to publish, or preparation of the manuscript.
NR 87
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U1 0
U2 13
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 28
PY 2013
VL 8
IS 11
AR UNSP e79837
DI 10.1371/journal.pone.0079837
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 261IJ
UT WOS:000327657900003
PM 24312187
ER

PT J
AU Vural, A
   McQuiston, TJ
   Blumer, JB
   Park, C
   Hwang, IY
   Williams-Bey, Y
   Shi, CS
   Ma, DZ
   Kehrl, JH
AF Vural, Ali
   McQuiston, Travis J.
   Blumer, Joe B.
   Park, Chung
   Hwang, Il-Young
   Williams-Bey, Yolanda
   Shi, Chong-Shan
   Ma, Dzwokai Zach
   Kehrl, John H.
TI Normal Autophagic Activity in Macrophages from Mice Lacking G alpha(i3),
   AGS3, or RGS19
SO PLOS ONE
LA English
DT Article
ID GUANINE-NUCLEOTIDE EXCHANGE; ALPHA-INTERACTING PROTEIN; HT-29 CELLS;
   ADAPTIVE IMMUNITY; SIGNALING COMPLEX; REGULATOR AGS3; MACROAUTOPHAGY;
   RECEPTOR; ACTIVATOR; INSULIN
AB In macrophages autophagy assists antigen presentation, affects cytokine release, and promotes intracellular pathogen elimination. In some cells autophagy is modulated by a signaling pathway that employs G alpha(i3), Activator of G-protein Signaling-3 (AGS3/GPSM1), and Regulator of G-protein Signaling 19 (RGS19). As macrophages express each of these proteins, we tested their importance in regulating macrophage autophagy. We assessed LC3 processing and the formation of LC3 puncta in bone marrow derived macrophages prepared from wild type, Gnai3(-/-), Gpsm1(-/-), or Rgs19(-/-) mice following amino acid starvation or Nigericin treatment. In addition, we evaluated rapamycin-induced autophagic proteolysis rates by long-lived protein degradation assays and anti-autophagic action after rapamycin induction in wild type, Gnai3(-/-), and Gpsm1(-/-) macrophages. In similar assays we compared macrophages treated or not with pertussis toxin, an inhibitor of GPCR (G-protein couple receptor) triggered G alpha(i) nucleotide exchange. Despite previous findings, the level of basal autophagy, autophagic induction, autophagic flux, autophagic degradation and the anti-autophagic action in macrophages that lacked G alpha(i3), AGS3, or RGS19; or had been treated with pertussis toxin, were similar to controls. These results indicate that while Gai signaling may impact autophagy in some cell types it does not in macrophages.
C1 [Vural, Ali; Park, Chung; Hwang, Il-Young; Williams-Bey, Yolanda; Shi, Chong-Shan; Kehrl, John H.] NIAID, B Cell Mol Immunol Sect, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
   [McQuiston, Travis J.] NIAID, Translat Mycol Unit, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
   [Blumer, Joe B.] Med Univ S Carolina, Dept Cell & Mol Pharmacol & Expt Therapeut, Charleston, SC 29425 USA.
   [Ma, Dzwokai Zach] Univ Calif Santa Barbara, Dept Mol Cellular & Dev Biol, Santa Barbara, CA 93106 USA.
RP Kehrl, JH (reprint author), NIAID, B Cell Mol Immunol Sect, Immunoregulat Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM jkehrl@niaid.nih.gov
FU National Institutes of Allergy and Infectious Diseases
FX This research was supported by the intramural program of the National
   Institutes of Allergy and Infectious Diseases. There was no other source
   of external funding. The funders had no role in study design, data
   collection and analysis, decision to publish, or preparation of the
   manuscript.
NR 47
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U1 0
U2 0
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 28
PY 2013
VL 8
IS 11
AR UNSP e81886
DI 10.1371/journal.pone.0081886
PG 13
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 261IJ
UT WOS:000327657900058
PM 24312373
ER

PT J
AU Karargyris, A
   Rondonotti, E
   Mandelli, G
   Koulaouzidis, A
AF Karargyris, Alexandros
   Rondonotti, Emanuele
   Mandelli, Giovanna
   Koulaouzidis, Anastasios
TI Evaluation of 4 three-dimensional representation algorithms in capsule
   endoscopy images
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Capsule endoscopy; Small-bowel; Three-dimensional; Software; Algorithm;
   Reconstruction; Technology; Advance
ID SMALL-BOWEL; SHAPE; RECONSTRUCTION
AB AIM: To evaluate the three-dimensional (3-D) representation performance of 4 publicly available Shape-from-Shading (SfS) algorithms in small-bowel capsule endoscopy (SBCE).
   METHODS: SfS techniques recover the shape of objects using the gradual variation of shading. There are 4 publicly available SfS algorithms. To the best of our knowledge, no comparative study with images obtained during clinical SBCE has been performed to date. Three experienced reviewers were asked to evaluate 54 two-dimensional (2-D) images (categories: protrusion/inflammation/vascular) transformed to 3-D by the aforementioned SfS 3-D algorithms. The best algorithm was selected and inter-rater agreement was calculated.
   RESULTS: Four publicly available SfS algorithms were compared. Tsai's SfS algorithm outperformed the rest (selected as best performing in 45/54 SBCE images), followed by Ciuti's algorithm (best performing in 7/54 images) and Torreao's (in 1/54 images). In 26/54 images; Tsai's algorithm was unanimously selected as the best performing 3-D representation SfS software. Tsai's 3-D algorithm superiority was independent of lesion category (protrusion/inflammatory/vascular; P = 0.678) and/or CE system used to obtain the 2-D images (MiroCam (R)/PillCam (R); P = 0.558). Lastly, the inter-observer agreement was good (kappa = 0.55).
   CONCLUSION: 3-D representation software offers a plausible alternative for 3-D representation of conventional capsule endoscopy images (until optics technology matures enough to allow hardware enabled-"real" 3-D reconstruction of the gastrointestinal tract). (C) 2013 Baishideng Publishing Group Co., Limited. All rights reserved.
C1 [Karargyris, Alexandros] NIH, Natl Lib Med, Bethesda, MD 20892 USA.
   [Rondonotti, Emanuele; Mandelli, Giovanna] Osped Valduce, Gastroenterol Unit, I-22100 Como, Italy.
   [Koulaouzidis, Anastasios] Royal Infirm Edinburgh NHS Trust, Ctr Liver & Digest Disorders, Edinburgh EH16 4SA, Midlothian, Scotland.
RP Koulaouzidis, A (reprint author), Royal Infirm Edinburgh NHS Trust, Ctr Liver & Digest Disorders, Endoscopy Unit, 51 Little France Crescent,Old Dalkeith Rd, Edinburgh EH16 4SA, Midlothian, Scotland.
EM akoulaouzidis@hotmail.com
NR 25
TC 8
Z9 8
U1 1
U2 4
PU BAISHIDENG PUBL GRP CO LTD
PI WANCHAI
PA ROOM 1701, 17-F, HENAN BUILDING, NO. 90, JAFFE RD, WANCHAI, HONG KONG
   100025, PEOPLES R CHINA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD NOV 28
PY 2013
VL 19
IS 44
BP 8028
EP 8033
DI 10.3748/wjg.v19.i44.8028
PG 6
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 259HZ
UT WOS:000327519300022
PM 24307796
ER

PT J
AU Suls, J
AF Suls, Jerry
TI Using "Cinema Verite" (truthful cinema) to facilitate replication and
   accountability in psychological research
SO FRONTIERS IN PSYCHOLOGY
LA English
DT Article
DE research practices; replication
ID SCIENCE; OCCUR
AB To increase replication and accountability, it is proposed that researchers make audio/video recordings of laboratory protocols using currently available technologies, such as smart-phones. A detailed record of the procedure representing each experimental condition of the study design with simulated participants could then be posted on the internet and made accessible to researchers wanting more information about the procedures described in the research publication. Making recordings of all research participants a standard practice would be a greater challenge because of threats to internal validity and ethical concerns, however it is feasible and merits a broad discussion among researchers, professional societies, IRB's and funding organizations.
C1 NCI, Behav Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Suls, J (reprint author), NCI, Behav Res Program, Div Canc Control & Populat Sci, 9609 Med Ctr Dr,Room 3E148,MSC 9761, Bethesda, MD 20892 USA.
EM jerry.suls@nih.gov
NR 18
TC 1
Z9 1
U1 0
U2 0
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1664-1078
J9 FRONT PSYCHOL
JI Front. Psychol.
PD NOV 27
PY 2013
VL 4
AR 872
DI 10.3389/fpsyg.2013.00872
PG 3
WC Psychology, Multidisciplinary
SC Psychology
GA AA6YN
UT WOS:000331244300001
PM 24348437
ER

PT J
AU Millum, J
   Wendler, D
   Emanuel, EJ
AF Millum, Joseph
   Wendler, David
   Emanuel, Ezekiel J.
TI The 50th Anniversary of the Declaration of Helsinki Progress but Many
   Remaining Challenges
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
ID CARE
C1 [Millum, Joseph; Wendler, David] NIH, Dept Bioeth, Ctr Clin, Bethesda, MD 20892 USA.
   [Millum, Joseph] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
   [Emanuel, Ezekiel J.] Univ Penn, Off Provost, Philadelphia, PA 19104 USA.
   [Emanuel, Ezekiel J.] Univ Penn, Dept Med Eth & Hlth Policy, Perelman Sch Med, Philadelphia, PA 19104 USA.
RP Emanuel, EJ (reprint author), Univ Penn, Dept Med Eth & Hlth Policy, 122 Coll Hall, Philadelphia, PA 19104 USA.
EM vp-global@upenn.edu
FU Intramural NIH HHS [Z99 CL999999]
NR 7
TC 24
Z9 27
U1 1
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 27
PY 2013
VL 310
IS 20
BP 2143
EP 2144
DI 10.1001/jama.2013.281632
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 257RS
UT WOS:000327404400018
PM 24141885
ER

PT J
AU Imperiale, A
   Moussallieh, FM
   Sebag, F
   Brunaud, L
   Barlier, A
   Elbayed, K
   Bachellier, P
   Goichot, B
   Pacak, K
   Namer, IJ
   Taieb, D
AF Imperiale, Alessio
   Moussallieh, Francois-Marie
   Sebag, Frederic
   Brunaud, Laurent
   Barlier, Anne
   Elbayed, Karim
   Bachellier, Philippe
   Goichot, Bernard
   Pacak, Karel
   Namer, Izzie-Jacques
   Taieb, David
TI A New Specific Succinate-Glutamate Metabolomic Hallmark in Sdhx-Related
   Paragangliomas
SO PLOS ONE
LA English
DT Article
ID ENDOCRINE NEOPLASIA TYPE-2; CROSS-VALIDATION; GENE-MUTATIONS;
   PHEOCHROMOCYTOMA; SPECTROSCOPY; PHENOTYPES; FUMARATE; DATABASE; DISEASE;
   KREBS
AB Paragangliomas (PGLs) are frequently associated with germline mutations in genes involved in energy metabolism. The purpose of the present study was to assess whether the tumor metabolomic profile of patients with hereditary and apparently sporadic PGLs enables the distinction of different subtypes of tumors. Twenty-eight unrelated patients with a histological diagnosis of PGLs were included in the present study. Twelve had germline mutations in SDHx genes (5 SDHB, 7 SDHD), 6 VHL, and 10 were apparently sporadic. Intact tumor samples from these patients (one per patient) were evaluated with H-1 high-resolution magic angle spinning (HRMAS) NMR spectroscopy. SDHx-related tumors were characterized by an increase in succinate levels in comparison to other tumor subtypes (p = 0.0001 vs VHL and p = 0.000003 vs apparently sporadic). Furthermore, we found significantly lower values of glutamate in SDHx-related tumors compared to other subtypes (p = 0.0007 vs VHL and p = 0.003 vs apparently sporadic). Moreover, SDHx-tumors also exhibited lower values of ATP/ADP/AMP (p = 0.01) compared to VHL. VHL tumors were found to have the highest values of glutathione (GSH) compared to other tumors. Based on 4 metabolites (succinate, glutamate, GSH, and ATP/ADP/AMP), tumors were accurately distinguished from the other ones on both 3- and 2-class PLS-DA models. The present study shows that HRMAS NMR spectroscopy is a very promising method for investigating the metabolomic profile of various PGLs. The present data suggest the existence of a specific succinate-glutamate hallmark of SDHx PGLs. The relevance of such a metabolomic hallmark is expected to be very useful in designing novel treatment options as well as improving the diagnosis and follow-up of these tumors, including metastatic ones.
C1 [Imperiale, Alessio; Moussallieh, Francois-Marie; Namer, Izzie-Jacques] Univ Hosp Strasbourg, Dept Biophys & Nucl Med, Strasbourg, France.
   [Imperiale, Alessio; Moussallieh, Francois-Marie; Elbayed, Karim; Namer, Izzie-Jacques] Univ Strasbourg, ICube, UMR 7357, CNRS, Strasbourg, France.
   [Imperiale, Alessio; Moussallieh, Francois-Marie; Elbayed, Karim; Namer, Izzie-Jacques] Fac Med Strasbourg, FMTS, Strasbourg, France.
   [Sebag, Frederic] Aix Marseille Univ, La Timone Univ Hosp, Dept Endocrine Surg, Marseille, France.
   [Brunaud, Laurent] Brabois Univ Hosp, Dept Digest Hepatobiliary & Endocrine Surg, Nancy, France.
   [Barlier, Anne] Aix Marseille Univ, Concept Hosp, Lab Biochem & Mol Biol, Marseille, France.
   [Bachellier, Philippe] Univ Hosp Strasbourg, Dept Visceral Surg & Transplantat, Strasbourg, France.
   [Goichot, Bernard] Univ Hosp Strasbourg, Dept Internal Med Diabet & Metab Disorders, Strasbourg, France.
   [Pacak, Karel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
   [Taieb, David] Aix Marseille Univ, Dept Biophys & Nucl Med, La Timone Univ Hosp, European Ctr Res Med Imaging, Marseille, France.
RP Imperiale, A (reprint author), Univ Hosp Strasbourg, Dept Biophys & Nucl Med, Strasbourg, France.
EM alessio.imperiale@chru-strasbourg.fr
OI Barlier, Anne/0000-0002-3740-6173
FU Region Alsace; Oseo; Communaute Urbaine de Strasbourg; Conseil
   Departemental du Bas-Rhin; Bruker BioSpin; University of Strasbourg;
   Strasbourg University Hospital
FX This work is part of the CARMeN project and was supported by grants from
   Region Alsace, Oseo, Communaute Urbaine de Strasbourg, Conseil
   Departemental du Bas-Rhin, Bruker BioSpin, University of Strasbourg and
   Strasbourg University Hospital. The funders had no role in study design,
   data collection and analysis, decision to publish, or preparation of the
   manuscript.
NR 36
TC 10
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U1 1
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 27
PY 2013
VL 8
IS 11
AR e80539
DI 10.1371/journal.pone.0080539
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 261GG
UT WOS:000327652100047
PM 24312232
ER

PT J
AU Root, DH
AF Root, David H.
TI The Ventromedial Ventral Pallidum Subregion Is Necessary for
   Outcome-Specific Pavlovian-Instrumental Transfer
SO JOURNAL OF NEUROSCIENCE
LA English
DT Editorial Material
ID AXONAL BRANCHING PATTERNS; PHASIC FIRING PATTERNS; NUCLEUS-ACCUMBENS
   CORE; BASOLATERAL AMYGDALA; NEURONS; SHELL; RAT; SEEKING
C1 NIDA, Neuronal Networks Sect, Integrat Neurosci Res Branch, Baltimore, MD 21224 USA.
RP Root, DH (reprint author), NIDA, Neuronal Networks Sect, Integrat Neurosci Res Branch, 251 Bayview Blvd,Suite 200, Baltimore, MD 21224 USA.
EM David.Root@nih.gov
OI Root, David/0000-0002-1927-2175
FU Intramural NIH HHS
NR 15
TC 1
Z9 1
U1 0
U2 2
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 27
PY 2013
VL 33
IS 48
BP 18707
EP 18709
DI 10.1523/JNEUROSCI.4021-13.2013
PG 3
WC Neurosciences
SC Neurosciences & Neurology
GA 262NE
UT WOS:000327741400001
PM 24285876
ER

PT J
AU Schmid, MC
   Schmiedt, JT
   Peters, AJ
   Saunders, RC
   Maier, A
   Leopold, DA
AF Schmid, Michael C.
   Schmiedt, Joscha T.
   Peters, Andrew J.
   Saunders, Richard C.
   Maier, Alexander
   Leopold, David A.
TI Motion-Sensitive Responses in Visual Area V4 in the Absence of Primary
   Visual Cortex
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID LATERAL GENICULATE-NUCLEUS; SUPERIOR COLLICULUS; STRIATE CORTEX; MACAQUE
   MONKEY; AFFERENT BASIS; MT; ORGANIZATION; NEURONS; PATHWAYS; INPUT
AB Neurons in cortical ventral-stream area V4 are thought to contribute to important aspects of visual processing by integrating information from primary visual cortex (V1). However, how V4 neurons respond to visual stimulation after V1 injury remains unclear: While electrophysiological investigation of V4 neurons during reversible V1 inactivation suggests that virtually all responses are eliminated (Girard et al., 1991), fMRI in humans and monkeys with permanent lesions shows reliable V1-independent activity (Baseler et al., 1999; Goebel et al., 2001; Schmid et al., 2010). To resolve this apparent discrepancy, we longitudinally assessed neuronal functions of macaque area V4 using chronically implanted electrode arrays before and after creating a permanent aspiration lesion in V1. During the month after lesioning, we observed weak yet significant spiking activity in response to stimuli presented to the lesion-affected part of the visual field. These V1-independent responses showed sensitivity for motion and likely reflect the effect of V1-bypassing geniculate input into extrastriate areas.
C1 [Schmid, Michael C.; Schmiedt, Joscha T.] Max Planck Gesell, Ernst Strungmann Inst Neurosci, D-60528 Frankfurt, Germany.
   [Peters, Andrew J.] Univ Calif San Diego, La Jolla, CA 92093 USA.
   [Maier, Alexander] Vanderbilt Univ, Dept Psychol, Nashville, TN 37240 USA.
   [Saunders, Richard C.; Leopold, David A.] NIMH, Lab Neuropsychol, Bethesda, MD 20892 USA.
   [Leopold, David A.] NIMH, Neurophysiol Imaging Facil, Natl Inst Neurol Disorders & Stroke, Bethesda, MD 20892 USA.
   [Leopold, David A.] NEI, Bethesda, MD 20892 USA.
RP Schmid, MC (reprint author), Max Planck Gesell, Ernst Strungmann Inst Neurosci, Deutschordenstr 46, D-60528 Frankfurt, Germany.
EM michael.schmid@esi-frankfurt.de
RI Maier, Alexander/B-7489-2009; Schmid, Michael/G-1867-2010; 
OI Maier, Alexander/0000-0002-7250-502X; Schmid,
   Michael/0000-0003-1424-130X; Schmiedt, Joscha
   Tapani/0000-0001-6233-1866; Peters, Andrew/0000-0001-9351-1456; Leopold,
   David/0000-0002-1345-6360
FU Intramural Research Program of the National Institute of Mental Health;
   Deutsche Forschungsgemeinschaft Emmy Noether grant
FX This work was supported by the Intramural Research Program of the
   National Institute of Mental Health (D. A. L.) and a Deutsche
   Forschungsgemeinschaft Emmy Noether grant (M. C. S.). The authors thank
   Alex Cummings, David Hu, Charles Zhu, Frank Ye, George Dold, Andy Mitz,
   Rachel Reoli, Katy Smith, and James Yu for technical assistance; Michele
   Cox for help with experiments and analysis; Georgios Spyropoulos for
   preliminary analysis; and Pascal Fries for support.
NR 27
TC 9
Z9 9
U1 0
U2 9
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 27
PY 2013
VL 33
IS 48
BP 18740
EP 18745
DI 10.1523/JNEUROSCI.3923-13.2013
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA 262NE
UT WOS:000327741400005
PM 24285880
ER

PT J
AU Quaia, C
   Optican, LM
   Cumming, BG
AF Quaia, Christian
   Optican, Lance M.
   Cumming, Bruce G.
TI Terminator Disparity Contributes to Stereo Matching for Eye Movements
   and Perception
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID PRIMARY VISUAL-CORTEX; MACAQUE V1 NEURONS; DEPTH-PERCEPTION; APERTURE
   PROBLEM; BINOCULAR DISPARITY; MOTION INTEGRATION; SURROUND SUPPRESSION;
   OCCLUSION JUNCTIONS; TEMPORAL DYNAMICS; RECEPTIVE-FIELDS
AB In the context of motion detection, the endings (or terminators) of 1-D features can be detected as 2-D features, affecting the perceived direction of motion of the 1-D features (the barber-pole illusion) and the direction of tracking eye movements. In the realm of binocular disparity processing, an equivalent role for the disparity of terminators has not been established. Here we explore the stereo analogy of the barber-pole stimulus, applying disparity to a 1-D noise stimulus seen through an elongated, zero-disparity, aperture. We found that, in human subjects, these stimuli induce robust short-latency reflexive vergence eye movements, initially in the direction orthogonal to the 1-D features, but shortly thereafter in the direction predicted by the disparity of the terminators. In addition, these same stimuli induce vivid depth percepts, which can only be attributed to the disparity of line terminators. When the 1-D noise patterns are given opposite contrast in the two eyes (anticorrelation), both components of the vergence response reverse sign. Finally, terminators drive vergence even when the aperture is defined by a texture (as opposed to a contrast) boundary. These findings prove that terminators contribute to stereo matching, and constrain the type of neuronal mechanisms that might be responsible for the detection of terminator disparity.
C1 [Quaia, Christian; Optican, Lance M.; Cumming, Bruce G.] NEI, Sensorimotor Res Lab, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Quaia, C (reprint author), NEI, Sensorimotor Res Lab, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
EM quaiac@nei.nih.gov
FU Intramural Research Program of the National Eye Institute, National
   Institutes of Health, Department of Health and Human Services
FX This work was supported by the Intramural Research Program of the
   National Eye Institute, National Institutes of Health, Department of
   Health and Human Services. We thank Dr. Boris Sheliga for assistance in
   running the experiments and for comments on the manuscript.
NR 68
TC 0
Z9 0
U1 0
U2 3
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 27
PY 2013
VL 33
IS 48
BP 18867
EP 18879
DI 10.1523/JNEUROSCI.3332-13.2013
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA 262NE
UT WOS:000327741400018
PM 24285893
ER

PT J
AU Agarwal, N
   Iyer, D
   Patel, SG
   Sekhar, RV
   Phillips, TM
   Schubert, U
   Oplt, T
   Buras, ED
   Samson, SL
   Couturier, J
   Lewis, DE
   Rodriguez-Barradas, MC
   Jahoor, F
   Kino, T
   Kopp, JB
   Balasubramanyam, A
AF Agarwal, Neeti
   Iyer, Dinakar
   Patel, Sanjeet G.
   Sekhar, Rajagopal V.
   Phillips, Terry M.
   Schubert, Ulrich
   Oplt, Toni
   Buras, Eric D.
   Samson, Susan L.
   Couturier, Jacob
   Lewis, Dorothy E.
   Rodriguez-Barradas, Maria C.
   Jahoor, Farook
   Kino, Tomoshige
   Kopp, Jeffrey B.
   Balasubramanyam, Ashok
TI HIV-1 Vpr Induces Adipose Dysfunction in Vivo Through Reciprocal Effects
   on PPAR/GR Co-Regulation
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; INHIBITOR-RELATED LIPODYSTROPHY;
   TRIGLYCERIDE TRANSFER PROTEIN; ACTIVATED-RECEPTOR-ALPHA; FATTY-ACID
   OXIDATION; CELL-CYCLE ARREST; ADIPOCYTE DIFFERENTIATION; ANTIRETROVIRAL
   THERAPY; SKELETAL-MUSCLE; GENE-EXPRESSION
AB Viral infections, such as HIV, have been linked to obesity, but mechanistic evidence that they cause adipose dysfunction in vivo is lacking. We investigated a pathogenic role for the HIV-1 accessory protein viral protein R (Vpr), which can coactivate the glucocorticoid receptor (GR) and co-repress peroxisome proliferator-activated receptor gamma (PPAR gamma) in vitro, in HIV-associated adipose dysfunction. Vpr circulated in the blood of most HIV-infected patients tested, including those on antiretroviral therapy (ART) with undetectable viral load. Vpr-mediated mechanisms were dissected in vivo using mouse models expressing the Vpr transgene in adipose tissues and liver (Vpr-Tg) or infused with synthetic Vpr. Both models demonstrated accelerated whole-body lipolysis, hyperglycemia and hypertriglyceridemia, and tissue-specific findings. Fat depots in these mice had diminished mass, macrophage infiltration, and blunted PPAR gamma target gene expression but increased GR target gene expression. In liver, we observed blunted PPAR alpha target gene expression, steatosis with decreased adenosine monophosphate-activated protein kinase activity, and insulin resistance. Similar to human HIV-infected patients, Vpr circulated in the serum of Vpr-Tg mice. Vpr blocked differentiation in preadipocytes through cell cycle arrest, whereas in mature adipocytes, it increased lipolysis with reciprocally altered association of PPAR gamma and GR with their target promoters. These results delineate a distinct pathogenic sequence: Vpr, released from HIV-1 in tissue reservoirs after ART, can disrupt PPAR/GR co-regulation and cell cycle control to produce adipose dysfunction and hepatosteatosis. Confirmation of these mechanisms in HIV patients could lead to targeted treatment of the metabolic complications with Vpr inhibitors, GR antagonists, or PPAR gamma/PPAR alpha agonists.
C1 [Agarwal, Neeti; Iyer, Dinakar; Patel, Sanjeet G.; Sekhar, Rajagopal V.; Oplt, Toni; Buras, Eric D.; Samson, Susan L.; Balasubramanyam, Ashok] Baylor Coll Med, Diabet Res Ctr, Div Diabet Endocrinol & Metab, Translat Metab Unit, Houston, TX 77030 USA.
   [Sekhar, Rajagopal V.; Samson, Susan L.; Balasubramanyam, Ashok] Ben Taub Gen Hosp, Endocrine Serv, Houston, TX 77030 USA.
   [Phillips, Terry M.; Kino, Tomoshige] NIH, Bethesda, MD 20892 USA.
   [Schubert, Ulrich] Univ Erlangen Nurnberg, D-91052 Erlangen, Germany.
   [Couturier, Jacob; Lewis, Dorothy E.] Univ Texas Hlth Sci Ctr Houston, Dept Med, Div Infect Dis, Houston, TX 77030 USA.
   [Rodriguez-Barradas, Maria C.] Baylor Coll Med, Vet Affairs Med Ctr, Sect Infect Dis, Houston, TX 77030 USA.
   [Jahoor, Farook] Baylor Coll Med, Childrens Nutr Res Ctr, Dept Pediat, Houston, TX 77030 USA.
   [Kopp, Jeffrey B.] NIDDK, Kidney Dis Sect, NIH, Bethesda, MD 20892 USA.
RP Balasubramanyam, A (reprint author), Baylor Coll Med, Diabet Res Ctr, Div Diabet Endocrinol & Metab, Translat Metab Unit, Houston, TX 77030 USA.
EM ashokb@bcm.edu
OI Kopp, Jeffrey/0000-0001-9052-186X
FU Baylor Center for AIDS Research [P30AI36211]; Seed award; P30DK079638;
   German Research Council [SFB 796, 643]; NIDDK Intramural Research
   Program; NIH Office of the Director;  [DK081553]
FX We thank H. Mersmann, L. A. Cowart, V. Yechoor, B. Chang, and H.J.
   Pownall for valuable discussions; J.W. Hsu, S. Hartig, P. Saha, and W.
   Chen for experimental help; and E. Davidson and D. Nguyen for technical
   assistance. We are grateful to the late P.J. Reeds for insights that
   guided this study. Funding: This work was supported by DK081553 and a
   Developmental Grant from the Baylor Center for AIDS Research P30AI36211
   (to A. B.), a Seed award (to R. V. S.), P30DK079638 (Diabetes Research
   Center at Baylor), German Research Council grants SFB 796 and 643 (to U.
   S.), the NIDDK Intramural Research Program, and the NIH Office of the
   Director.
NR 49
TC 11
Z9 11
U1 0
U2 2
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1946-6234
EI 1946-6242
J9 SCI TRANSL MED
JI Sci. Transl. Med.
PD NOV 27
PY 2013
VL 5
IS 213
AR 213ra164
DI 10.1126/scitranslmed.3007148
PG 12
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 258FI
UT WOS:000327444300002
PM 24285483
ER

PT J
AU Ahmet, I
   Yaniv, Y
   Sirenko, S
   Lakatta, EG
AF Ahmet, Ismayil
   Yaniv, Yael
   Sirenko, Syevda
   Lakatta, Edward G.
TI In Vivo Evidence that Adenylyl Cyclase and Sarcoplasmie Reticulum
   Pumping Regulate the Intrinsic Rate of Heart's Pacemaker
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Aging; Heart rate/Heart rate variability; Sinoatrial node
C1 [Ahmet, Ismayil; Yaniv, Yael; Sirenko, Syevda; Lakatta, Edward G.] NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD USA.
RI Yaniv, Yael/B-3311-2015
OI Yaniv, Yael/0000-0002-5183-6284
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 10978
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162901275
ER

PT J
AU AlGhatrif, M
   Strait, JB
   Morrell, C
   Canepa, M
   Wright, J
   Elango, P
   Scuteri, A
   Najjar, SS
   Ferrucci, L
   Lakatta, EG
AF AlGhatrif, Majd
   Strait, James B.
   Morrell, Chris
   Canepa, Marco
   Wright, Jeanette
   Elango, Palchamy
   Scuteri, Angelo
   Najjar, Samer S.
   Ferrucci, Luigi
   Lakatta, Edward G.
TI Attenuated Aortic Dilatation, Not Increased Wall Stiffness Best Explains
   the Rise in Pulse Pressure in Women With Aging: Results From the
   Baltimore Longitudinal Study of Aging
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Arteriosclerosis; Aorta; Hypertension; Aging
C1 [AlGhatrif, Majd; Strait, James B.; Morrell, Chris; Canepa, Marco; Wright, Jeanette; Elango, Palchamy; Scuteri, Angelo; Najjar, Samer S.; Ferrucci, Luigi; Lakatta, Edward G.] NIA, Cardiovasc Sci Lab, Baltimore, MD 21224 USA.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 18061
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162907199
ER

PT J
AU Allen, NB
   Ning, HY
   Huffman, MD
   Liu, K
   Reis, J
   Lloyd-Jones, D
AF Allen, Norrina B.
   Ning, Hongyan
   Huffman, Mark D.
   Liu, Klang
   Reis, Jared
   Lloyd-Jones, Donald
TI Maintenance of Ideal Cardiovascular Health Over 20 Years and Its Impact
   on Health Related Quality of Life: The Coronary Artery Risk Development
   in Young Adults (CARDIA) Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE 2020 Goals; Quality of life
C1 [Allen, Norrina B.; Ning, Hongyan; Huffman, Mark D.; Liu, Klang; Lloyd-Jones, Donald] Northwestern Univ, Dept Prevent Med, Chicago, IL 60611 USA.
   [Reis, Jared] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 15499
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162905037
ER

PT J
AU Alrob, OA
   Sankaralingam, S
   Masoud, W
   Sack, M
   Clanachan, A
   Lopaschuk, G
AF Alrob, Osama Abo
   Sankaralingam, Sowndramalingam
   Masoud, Waleed
   Sack, Michael
   Clanachan, Alexander
   Lopaschuk, Gary
TI Lysine Acetylation Enhances Cardiac Fatty Acid beta-Oxidation
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Obesity; Heart failure; Ischemia reperfusion; Energy metabolism
C1 [Alrob, Osama Abo; Sankaralingam, Sowndramalingam; Masoud, Waleed; Clanachan, Alexander; Lopaschuk, Gary] Univ Alberta, Edmonton, AB, Canada.
   [Sack, Michael] NIH, Lab Mitochondrial Biol & Metab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 11526
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162901482
ER

PT J
AU Aoyemang, P
   Ayers, C
   Barrington, D
   Suresh, V
   McClurkin, M
   Powell-Wiley, TM
AF Aoyemang, Priscilla
   Ayers, Colby
   Barrington, Debbie
   Suresh, Visakha
   McClurkin, Michael
   Powell-Wiley, Tiffany M.
TI Food Insecurity and Inadequate Health Insurance Coverage are Barriers to
   Ideal Cardiovascular Health for US Adults: Data From the National Health
   and Nutrition Examination Survey (NHANES)
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE 2020 Goals; Health factors; Disparities
C1 [Aoyemang, Priscilla; Suresh, Visakha; McClurkin, Michael] NHLBI, NIH, Bethesda, MD 20892 USA.
   [Ayers, Colby] Unv Southwestern Med Cntr, Dallas, TX USA.
   [Barrington, Debbie] Natl Inst Minor Hlth & Hlth Dispar, NIH, Bethesda, MD USA.
   [Powell-Wiley, Tiffany M.] NHLBI, NIH, Silver Spring, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 14135
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162903467
ER

PT J
AU Armstrong, AC
   Muller, M
   Ambale-Venkatesh, B
   Halstead, M
   Kishi, S
   Bryan, RN
   Sidney, S
   Correia, LC
   Gidding, S
   Launer, LJ
   Lima, JA
AF Armstrong, Anderson C.
   Muller, Majon
   Ambale-Venkatesh, Bharath
   Halstead, Michael
   Kishi, Satoru
   Bryan, R. Nick
   Sidney, Stephen
   Correia, Luis C.
   Gidding, Samuel
   Launer, Lenore J.
   Lima, Joao A.
TI Association of Cardiac Structure and Function With Advanced Magnetic
   Resonance Cerebral Measures: The Cardia Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Strain rate; Cerebrovascular disorders; Remodeling; Cardiovascular
   imaging
C1 [Armstrong, Anderson C.; Ambale-Venkatesh, Bharath; Kishi, Satoru; Lima, Joao A.] Johns Hopkins Univ, Baltimore, MD USA.
   [Muller, Majon; Halstead, Michael; Launer, Lenore J.] NIA, NIH, Bethesda, MD 20892 USA.
   [Bryan, R. Nick] Univ Penn Hlth Syst, Dept Radiol, Philadelphia, PA USA.
   [Sidney, Stephen] Kaiser Permanente, Div Rsch, Oakland, CA USA.
   [Correia, Luis C.] Escola Bahiana Med & Saude Publ, Sch Med, Salvador, BA, Brazil.
   [Gidding, Samuel] Alfred I duPont Hosp Children, Div Cardiol, Wilmington, DE USA.
RI Armstrong, Anderson/G-8407-2012; Ambale Venkatesh, Bharath/F-4941-2016
OI Armstrong, Anderson/0000-0003-3161-8922; Ambale Venkatesh,
   Bharath/0000-0002-2330-2373
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 15127
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162904408
ER

PT J
AU Babaev, V
   Ding, L
   Zhang, YM
   May, JM
   Lin, PC
   Fazio, S
   Linton, MF
AF Babaev, Vladimir
   Ding, Lei
   Zhang, Youmin
   May, James M.
   Lin, P. Charles
   Fazio, Sergio
   Linton, MacRae F.
TI Macrophage IKKalpha Deficiency Suppresses Akt Phosphorylation, Reduces
   Cell Survival and Decreases Early Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Arteriogenesis; Leukocytes; Apoptosis; Cell signaling; Signal
   transduction
C1 [Babaev, Vladimir; Ding, Lei; Zhang, Youmin; May, James M.; Fazio, Sergio; Linton, MacRae F.] Vanderbilt Univ, Nashville, TN 37235 USA.
   [Lin, P. Charles] NCI, Cntr Canc Rsch, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 15960
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162905291
ER

PT J
AU Barroso, MM
   Florindo, C
   Turanov, AA
   Carlson, BA
   Gladyshev, VN
   Hatfield, DL
   de Almeida, IT
   Castro, R
   Loscalzo, J
   Handy, DE
AF Barroso, Madalena M.
   Florindo, Cristina
   Turanov, Anton A.
   Carlson, Bradlev A.
   Gladyshev, Vadim N.
   Hatfield, Dolph L.
   de Almeida, Isabel Tavares
   Castro, Rita
   Loscalzo, Joseph
   Handy, Diane E.
TI Alteration of the Selenoproteome by Cellular Hypomethylation Promotes
   Endothelial Cell Activation
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Arteriosclerosis; Endothelial function; Inflammation; Leukocytes;
   Oxidative stress
C1 [Barroso, Madalena M.; Turanov, Anton A.; Gladyshev, Vadim N.; Loscalzo, Joseph; Handy, Diane E.] Brigham & Womens Hosp, Boston, MA 02115 USA.
   [Barroso, Madalena M.; Turanov, Anton A.; Gladyshev, Vadim N.; Loscalzo, Joseph; Handy, Diane E.] Harvard Univ, Sch Med, Boston, MA USA.
   [Florindo, Cristina; de Almeida, Isabel Tavares; Castro, Rita] Rsch Inst Med & Pharmaceut Sci, Lisbon, Portugal.
   [Carlson, Bradlev A.] NCI, NIH, Bethesda, MD 20892 USA.
   [Hatfield, Dolph L.] NIH, Bethesda, MD 20892 USA.
RI Tavares de Almeida, Isabel/F-8319-2014; Castro, Rita /G-7731-2011;
   iMed.ULisboa, iMed.ULisboa/C-6292-2014
OI Castro, Rita /0000-0002-4585-0741; 
NR 0
TC 0
Z9 0
U1 1
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 10272
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162901062
ER

PT J
AU Boden, WE
   Robinson, JG
   Miller, M
   Simmons, D
   Xu, P
   Abramson, B
   Elam, MB
   Nash, SD
   Brown, TM
   McBride, R
   Fleg, JL
   Desvignie-Nickens, PM
   Probstfield, JL
AF Boden, William E.
   Robinson, Jennifer G.
   Miller, Michael
   Simmons, Debra
   Xu, Ping
   Abramson, Beth
   Elam, Marshall B.
   Nash, Stephen D.
   Brown, Todd M.
   McBride, Ruth
   Fleg, Jerome L.
   Desvignie-Nickens, Patrice M.
   Probstfield, Jeffrey L.
TI Does the Metabolic Syndrome Cluster Provide Incremental Prognostic
   Information Over the Individual Components? Post Hoc Analysis of the
   AIM-HIGH Trial
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Metabolic syndrome; HDL elevating therapies; Risk factors; Clinical
   trials
C1 [Boden, William E.] Albany Stratton VA Med Cntr, Albany, NY USA.
   [Robinson, Jennifer G.] Univ Iowa, Sch Publ Hlth, Iowa City, IA USA.
   [Miller, Michael] Univ Maryland Med Syst, Baltimore, MD USA.
   [Simmons, Debra] Univ Utah, Salt Lake City, UT USA.
   [Xu, Ping] Axio Rsch, Biostat, Seattle, WA USA.
   [Abramson, Beth] St Michaels Hlth Cntr, Toronto, ON, Canada.
   [Elam, Marshall B.] Memphis VA Med Cntr, Memphis, VA USA.
   [Nash, Stephen D.] Syracuse Preventit Cardiol, Med, Syracuse, NY USA.
   [Brown, Todd M.] Univ Alabama Birmingham, Birmingham, AL USA.
   [McBride, Ruth] Axio Rsch LLC, Rsch, Seattle, WA USA.
   [Fleg, Jerome L.] Natl Naval Med Cntr, Bethesda, MD USA.
   [Desvignie-Nickens, Patrice M.] NHLBI, Silver Spring, MD USA.
   [Probstfield, Jeffrey L.] Univ Washington, Sch Publ Hlth, Clin Trials Serv Unit, Seattle, WA 98195 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 11553
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162901494
ER

PT J
AU Cao, J
   Thompson, E
   Abraham, NG
   Peterson, SJ
   Zeldin, DC
   Schwartzman, ML
AF Cao, Jian
   Thompson, Ellen
   Abraham, Nader G.
   Peterson, Stephen J.
   Zeldin, Darryl C.
   Schwartzman, Michal L.
TI Treatment With an EET Agonist in a Post Myocardial Infarction Model
   Increases Left Ventricular Ejection Fraction and Attenuates Cardiac
   Remodeling by Induction of HMOX1
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Myocardium; Cardiac hypertrophy; Inflammation; Angiogenesis; Infarction
C1 [Cao, Jian] Chinese Peoples Liberat Army Gen Hosp, Dept Geriatr Cardiol 1, Beijing, Peoples R China.
   [Thompson, Ellen; Abraham, Nader G.] Marshall Univ, Dept Med, Joan C Edwards Sch Med, Huntington, WV USA.
   [Peterson, Stephen J.] New York Methodist Weill Cornell Med Coll, Dept Med, Brooklyn, NY USA.
   [Zeldin, Darryl C.] NIEHS, LRB, Res Triangle Pk, NC 27709 USA.
   [Schwartzman, Michal L.] New York Med Coll, Dept Pharmacol, Valhalla, NY 10595 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 18792
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162907550
ER

PT J
AU Cheng, SS
   Claagett, B
   Correia, A
   Shah, A
   Gupta, D
   Skali, H
   Ni, HY
   Coresh, J
   Solomon, S
AF Cheng, Susan
   Claagett, Brian
   Correia, Andrew
   Shah, Amil
   Gupta, Deepak
   Skali, Hicham
   Ni, Hanyu
   Coresh, Josef
   Solomon, Scott
TI Time Trends in the Population Attributable Risk for Cardiovascular
   Disease: Atherosclerosis Risk in Communities Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Epidemiology; Risk factors; Cardiovascular disease
C1 [Cheng, Susan; Claagett, Brian; Shah, Amil; Gupta, Deepak; Skali, Hicham; Solomon, Scott] Brigham & Womens Hosp, Boston, MA 02115 USA.
   [Correia, Andrew] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
   [Ni, Hanyu] NHLBI, NIH, Boston, MA USA.
   [Coresh, Josef] Johns Hopkins Bloomberg Sch Publ Hlth, Cardiovasc Epidemiol & Comstock Cntr, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 18744
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162907528
ER

PT J
AU Cheng, S
   Larson, M
   McCabe, E
   Murabito, J
   Rhee, E
   Ho, J
   Jacques, P
   Ghorbani, A
   Magnusson, M
   Snuza, A
   Deik, A
   Pierce, K
   Bullock, K
   O'Donnell, C
   Melander, O
   Clish, C
   Vasan, R
   Gerszten, R
   Wang, T
AF Cheng, Susan
   Larson, Martin
   McCabe, Elizabeth
   Murabito, Joanne
   Rhee, Eugene
   Ho, Jennifer
   Jacques, Paul
   Ghorbani, Anahita
   Magnusson, Martin
   Snuza, Amanda
   Deik, Amy
   Pierce, Kerry
   Bullock, Kevin
   O'Donnell, Christonher
   Melander, Olle
   Clish, Clary
   Vasan, Ramachandran
   Gerszten, Robert
   Wang, Thomas
TI Metabolomic Correlates of Longevity in the Community
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Metabolomics; Aging; Epidemiology
C1 [Cheng, Susan] Brigham & Womens Hosp, Cambridge, MA USA.
   [Larson, Martin] Boston Univ, Dept Math & Stat, Framingham, MA USA.
   [McCabe, Elizabeth; Vasan, Ramachandran] Boston Univ, Boston, MA 02215 USA.
   [Murabito, Joanne; Ho, Jennifer] Boston Univ, Framingham, MA USA.
   [Rhee, Eugene; Ghorbani, Anahita; Gerszten, Robert] Massachusetts Gen Hosp, Boston, MA 02114 USA.
   [Jacques, Paul] Tufts Univ, Jean Mayer USDA HNRCA, Boston, MA 02111 USA.
   [Magnusson, Martin] Skane Univ Hosp, Dept Cardiol, Malmo, Sweden.
   [Snuza, Amanda; Deik, Amy; Pierce, Kerry; Bullock, Kevin; Clish, Clary] Broad Inst, Cambridge, MA USA.
   [O'Donnell, Christonher] NHLBI, Div Intramural Rsch, Framingham, MA USA.
   [Melander, Olle] Malmo Univ Hosp, Dept Endocrinol, Malmo, Sweden.
   [Wang, Thomas] Vanderbilt Univ, Nashville, MA USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 10472
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162901124
ER

PT J
AU Chun, EJ
   Onuma, OK
   Pencina, K
   Massaro, JM
   O'Donnell, CJ
   Hoffmann, U
AF Chun, Eun Ju
   Onuma, Oyere K.
   Pencina, Karol
   Massaro, Joseph M.
   O'Donnell, Christopher J.
   Hoffmann, Udo
TI Comparison of the Distribution and Predictive Value of Framingham Risk
   Factors and Coronary Artery Calcium for Major Coronary Events Between
   Asian (South Korean) and Framingham Cohorts
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Cardiovascular disease prevention; Cardiac CT; Risk factors
C1 [Chun, Eun Ju] Seoul Natl Univ, Bundang Hosp, Seoul, South Korea.
   [Onuma, Oyere K.; Hoffmann, Udo] Massachusetts Gen Hosp, Boston, MA 02114 USA.
   [Pencina, Karol] Boston Univ, Boston, MA 02215 USA.
   [Massaro, Joseph M.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
   [O'Donnell, Christopher J.] NHLBI, Framingham Heart Study, NIH, Framingham, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 18337
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162907325
ER

PT J
AU Cogle, CR
   Wise, E
   Meacham, AM
   Traverse, JH
   Henry, TD
   Perin, EC
   Willerson, JT
   Bolli, R
   Cooke, JP
   Anwaruddin, S
   Bhatnagar, A
   Cabreira-Hansen, M
   Grant, MB
   Lai, DJ
   Moye, LA
   Ebert, RF
   Olson, RE
   Resende, M
   Sayre, SL
   Schulman, IH
   Smith, D
   Zierold, C
   Pepine, CJ
   Taylor, DA
AF Cogle, Christopher R.
   Wise, Elizabeth
   Meacham, Amy M.
   Traverse, Jay H.
   Henry, Timothy D.
   Perin, Emerson C.
   Willerson, James T.
   Bolli, Roberto
   Cooke, John P.
   Anwaruddin, Saif
   Bhatnagar, Aruni
   Cabreira-Hansen, Maria
   Grant, Maria B.
   Lai, Dejian
   Moye, Lemuel A.
   Ebert, Ray F.
   Olson, Rachel E.
   Resende, Micheline
   Sayre, Shelly L.
   Schulman, Ivonne H.
   Smith, Deirdre
   Zierold, Claudia
   Pepine, Carl J.
   Taylor, Doris A.
CA CCTRN
TI Variable and Decreased Clonogenic Activity of Autologous Bone Marrow in
   Cell Therapy Patients With Ischemic Heart Disease, and CD34 as a
   Biomarker for Clinical Outcomes: Results From the Cardiovascular Cell
   Therapy Research Network (CCTRN)
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Stem/progenitor cells; Stem cell therapy; Endothelial progenitor cell;
   Regenerative medicine stem cells
C1 [Cogle, Christopher R.; Wise, Elizabeth; Meacham, Amy M.; Grant, Maria B.; Pepine, Carl J.] Univ Florida, Coll Med, Gainesville, FL USA.
   [Traverse, Jay H.; Henry, Timothy D.; Olson, Rachel E.] Minneapolis Heart Inst Fdn Abbott, Minneapolis, MN USA.
   [Perin, Emerson C.; Willerson, James T.; Cabreira-Hansen, Maria; Resende, Micheline; Smith, Deirdre; Taylor, Doris A.] St Lukes Episcopal Hosp, Texas Heart Inst, Houston, TX USA.
   [Bolli, Roberto; Bhatnagar, Aruni] Univ Louisville, Louisville, KY 40292 USA.
   [Cooke, John P.] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
   [Anwaruddin, Saif] Hosp Univ Penn, Philadelphia, PA 19104 USA.
   [Lai, Dejian] Univ Texas Houston, Sch Publ Hlth, Houston, TX USA.
   [Moye, Lemuel A.; Sayre, Shelly L.] Univ Texas Sch Publ Hlth, Houston, TX USA.
   [Ebert, Ray F.] NHLBI, Bethesda, MD 20892 USA.
   [Schulman, Ivonne H.] Univ Miami, Miami, FL USA.
   [Zierold, Claudia] Univ Minnesota, Sch Med, Minneapolis, MN 55455 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 17746
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162907051
ER

PT J
AU Costello, R
   Lentino, C
   Saldanha, L
   Engler, M
   Engler, M
   Srinivas, P
   Sempos, C
AF Costello, Rebecca
   Lentino, Cynthia
   Saldanha, Leila
   Engler, Mary
   Engler, Marguerite
   Srinivas, Pothur
   Sempos, Christopher
TI Reporting Quality of Studies Measuring Endothelial Dysfunction in Diet
   Intervention Studies
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Diet; Endothelial function; Interventional studies; Quality assessment
C1 [Costello, Rebecca; Lentino, Cynthia; Saldanha, Leila; Sempos, Christopher] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
   [Engler, Mary; Engler, Marguerite] NINR, NIH, Bethesda, MD 20892 USA.
   [Srinivas, Pothur] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 14875
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162904279
ER

PT J
AU Ebong, IA
   Watson, KE
   Goff, DC
   Bluemke, DA
   Srikanthan, P
   Horwich, T
   Bertoni, AG
AF Ebong, Imo A.
   Watson, Karol E.
   Goff, David C.
   Bluemke, David A.
   Srikanthan, Preethi
   Horwich, Tamara
   Bertoni, Alain G.
TI Age at Menopause and Incident Heart Failure: The Multi-Ethnic Study of
   Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Epidemiology; Heart failure; Risk factors
C1 [Ebong, Imo A.] Univ So Calif, Los Angeles, CA USA.
   [Watson, Karol E.; Srikanthan, Preethi; Horwich, Tamara] Univ Calif Los Angeles, Los Angeles, CA USA.
   [Goff, David C.] Colorado Sch Publ Hlth, Aurora, CO USA.
   [Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
   [Bertoni, Alain G.] Wake Forest Univ, Winston Salem, NC 27109 USA.
NR 0
TC 1
Z9 1
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 10384
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162901105
ER

PT J
AU Escolar, E
   Lamas, GA
   Mark, DB
   Ouyang, P
   Magaziner, A
   Boineau, R
   Miranda, R
   Goertz, C
   Rosenberg, Y
   Nahin, RL
   Nahas, R
   Lewis, EF
   Lindblad, L
   Lee, KL
AF Escolar, Esteban
   Lamas, Gervasio A.
   Mark, Daniel B.
   Ouyang, Pamela
   Magaziner, Allan
   Boineau, Robin
   Miranda, Ralph
   Goertz, Christine
   Rosenberg, Yves
   Nahin, Richard L.
   Nahas, Richard
   Lewis, Eldrin F.
   Lindblad, Lauren
   Lee, Kerry L.
TI Clinical Benefit of EDTA Chelation Therapy in Patients With Diabetes in
   the Trial to Assess Chelation Therapy (TACT)
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Myocardial infarction; Coronary artery disease; Clinical trials
C1 [Escolar, Esteban; Lamas, Gervasio A.] Mt Sinai Med Cntr, Div Cardiol, Miami Beach, FL USA.
   [Mark, Daniel B.; Lindblad, Lauren; Lee, Kerry L.] Duke Clin Rsch Inst, Durham, NC USA.
   [Ouyang, Pamela] Johns Hopkins Univ, Baltimore, MD USA.
   [Magaziner, Allan] Magaziner Cntr Wellness, Cherry Hill, NJ USA.
   [Boineau, Robin] NHLBI, HEART FAILURE & ARRHYTHMIAS BRANCH, Bethesda, MD USA.
   [Miranda, Ralph] Wholist Hlth Cntr, Greensburg, PA USA.
   [Goertz, Christine] Palmer Coll Chiropract, Davenport, IA USA.
   [Rosenberg, Yves] NHLBI, ATHEROTHROMBOSIS & CORONARY ARTERY DIS BRANCH, Bethesda, MD 20892 USA.
   [Nahin, Richard L.] Natl Cntr Complementary & Alternat Med, Bethesda, MD USA.
   [Nahas, Richard] Seekers Cntr Integrat Med, Ottawa, ON, Canada.
   [Lewis, Eldrin F.] Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 11546
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162901491
ER

PT J
AU Evans, KL
   Folt, DA
   Dawson, T
   He, WC
   Brewster, P
   Murphy, TP
   Cutlip, DF
   Dworkin, L
   Jamerson, K
   Henrich, W
   Reid, D
   Cooper, C
AF Evans, Kaleigh L.
   Folt, David A.
   Dawson, Taylor
   He, Wencan
   Brewster, Pamela
   Murphy, Timothy P.
   Cutlip, Donald F.
   Dworkin, Lance
   Jamerson, Kenneth
   Henrich, William
   Reid, Diane
   Cooper, ChristopherJ
TI Determinants of Angiotensin Converting Enzyme Inhibitor/Angiotensin
   Receptor Blocker Use in Patients With Atherosclerotic Renal Artery
   Stenosis and Effects on Blood Pressure
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Renal circulation; Hypertension; ACE inhibitor; Antihypertensive agents;
   Clinical trials
C1 [Evans, Kaleigh L.; Folt, David A.; Dawson, Taylor; He, Wencan; Brewster, Pamela; Cooper, ChristopherJ] Univ Toledo, Toledo, OH 43606 USA.
   [Murphy, Timothy P.; Dworkin, Lance] Brown Univ, Sch Med, Providence, RI 02912 USA.
   [Cutlip, Donald F.] Harvard Med Sch, Boston, MA USA.
   [Jamerson, Kenneth] Univ Michigan, Ann Arbor, MI 48109 USA.
   [Henrich, William] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
   [Reid, Diane] NHLBI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 11598
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162901514
ER

PT J
AU Faggioni, M
   Iyer, RV
   Baldo, M
   Shirali, A
   Johnson, C
   Van Winkle, M
   Franzini-Armstrong, C
   Huke, S
   Pfeifer, K
   Knollmann, BC
AF Faggioni, Michela
   Iyer, Ramesh V.
   Baldo, Marcelo
   Shirali, Aditya
   Johnson, Cameron
   Van Winkle, Matthew
   Franzini-Armstrong, Clara
   Huke, Sabine
   Pfeifer, Karl
   Knollmann, Bjorn C.
TI Myocardial Restoration of Casq2 Protein in Adult Casq2 Null Mice
   Reverses Myocyte Remodeling and Completely Prevents CPVT Phenotype
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Ventricular arrhythmia; Calcium; Transgenic models; Remodeling; Gene
   therapy
C1 [Faggioni, Michela; Baldo, Marcelo; Huke, Sabine; Knollmann, Bjorn C.] Vanderbilt Univ, Nashville, TN 37235 USA.
   [Iyer, Ramesh V.] Childrens Hosp Philadelphia, Sect Electrophysiol, Philadelphia, PA 19104 USA.
   [Shirali, Aditya; Johnson, Cameron; Van Winkle, Matthew; Pfeifer, Karl] NICHD, Sect Genom Imprinting, Bethesda, MD USA.
   [Franzini-Armstrong, Clara] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 15134
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162904411
ER

PT J
AU Folt, DA
   Evans, KL
   Brahmandam, S
   He, WC
   Brewster, P
   Murphy, TP
   Cutlip, DE
   Dworkin, L
   Jamerson, K
   Henrich, W
   Reid, D
   Cooper, CJ
AF Folt, David A.
   Evans, Kaleigh L.
   Brahmandam, Sravya
   He, Wencan
   Brewster, Pamela
   Murphy, Timothy P.
   Cutlip, Donald E.
   Dworkin, Lance
   Jamerson, Kenneth
   Henrich, William
   Reid, Diane
   Cooper, Christopher J.
TI Region and Physician Specialty Influence Medical Management of
   Atherosclerotic Renal Artery Stenosis
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Renal circulation; Antihypertensive agents; ACE inhibitor;
   Arteriosclerosis; Clinical trials
C1 [Folt, David A.; Evans, Kaleigh L.; Brahmandam, Sravya; He, Wencan; Brewster, Pamela; Cooper, Christopher J.] Univ Toledo, Coll Med & Life Sci, Toledo, OH 43606 USA.
   [Murphy, Timothy P.; Dworkin, Lance] Brown Univ, Sch Med, Providence, RI 02912 USA.
   [Cutlip, Donald E.] Harvard Univ, Sch Med, Boston, MA USA.
   [Jamerson, Kenneth] Univ Michigan, Ann Arbor, MI 48109 USA.
   [Henrich, William] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
   [Reid, Diane] NHLBI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 14746
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162904217
ER

PT J
AU Foppa, M
   Parmar, H
   Rayatzadeh, H
   Shaw, J
   Weingartner, S
   Gai, N
   Thomas, H
   Buxton, AE
   Warren, MEJ
   Manning, WJ
   Nezafat, R
AF Foppa, Murilo
   Parmar, Harsh
   Rayatzadeh, Hussein
   Shaw, Jaime
   Weingartner, Sebastian
   Gai, Neville
   Thomas, Hauser
   Buxton, Alfred E.
   Josephson, Mark E.
   Manning, Warren J.
   Nezafat, Reza
TI Paroxysmal Atrial Fibrillation is Associated With Diffuse Left
   Ventricular Fibrosis
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Cardiac MRI; Atrial fibrillation; Fibrosis; Cardiovascular imaging;
   Ablation, radiofrequency
C1 [Foppa, Murilo; Parmar, Harsh; Rayatzadeh, Hussein; Shaw, Jaime; Weingartner, Sebastian; Thomas, Hauser; Buxton, Alfred E.; Josephson, Mark E.; Manning, Warren J.; Nezafat, Reza] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
   [Gai, Neville] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 13427
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162903160
ER

PT J
AU Ghorbani, A
   Larson, MG
   Miller, KK
   Ho, JE
   Cheng, SS
   Rhee, EP
   Vasan, RS
   Gerszten, RE
   Wang, TJ
AF Ghorbani, Anahita
   Larson, Martin G.
   Miller, Karen K.
   Ho, Jennifer E.
   Cheng, Susan
   Rhee, Eugene P.
   Vasan, Ramachandran S.
   Gerszten, Robert E.
   Wang, Thomas J.
TI Sex-Related Differences in Plasma Metabolomic Profiles in Humans
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Metabolomics; Cardiovascular disease
C1 [Ghorbani, Anahita] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
   [Larson, Martin G.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
   [Larson, Martin G.; Ho, Jennifer E.; Cheng, Susan; Vasan, Ramachandran S.; Wang, Thomas J.] NHLBI, Framingham Heart Study, Boston, MA USA.
   [Miller, Karen K.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
   [Ho, Jennifer E.] Boston Med Cntr, Div Cardiol, Boston, MA USA.
   [Cheng, Susan] Brigham & Womens Hosp, Dept Med, Div Cardiol, Boston, MA USA.
   [Rhee, Eugene P.] Massachusetts Gen Hosp, Div Nephrol, Boston, MA 02114 USA.
   [Vasan, Ramachandran S.] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
   [Gerszten, Robert E.] Massachusetts Gen Hosp, Div Cardiol, Cardiovasc Rsch Cntr, Boston, MA 02114 USA.
   [Wang, Thomas J.] Vanderbilt Univ, Med Ctr, Vanderbilt Heart & Vasc Inst, Div Cardiovasc Med, Nashville, TN USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 16786
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162906154
ER

PT J
AU Gori, M
   Guota, DK
   Bello, N
   Cheng, S
   Claggett, B
   Shah, A
   Skali, H
   Folsom, AR
   Ballantyne, CM
   Astor, BC
   Klein, B
   Matsushita, K
   Aguilar, D
   Vardeny, O
   Ni, HY
   Selvin, E
   Solomon, SD
AF Gori, Mauro
   Guota, Deepak K.
   Bello, Natalie
   Cheng, Susan
   Claggett, Brian
   Shah, Amil
   Skali, Hicham
   Folsom, Aaron R.
   Ballantyne, Christie M.
   Astor, Brad C.
   Klein, Barbara
   Matsushita, Kunihiro
   Aguilar, David
   Vardeny, Orly
   Ni, Hanyu
   Selvin, Elizabeth
   Solomon, Scott D.
TI The Risk of Death in Relation to Traditional Markers of Target Organ
   Damage, Hs-troponin T, And NTproBNP, in Diabetics: The Atherosclerosis
   Risk in Communities (ARIC) Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Troponin; Risk factors; Cardiovascular disease
C1 [Gori, Mauro; Guota, Deepak K.; Bello, Natalie; Cheng, Susan; Claggett, Brian; Shah, Amil; Skali, Hicham; Solomon, Scott D.] Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA.
   [Folsom, Aaron R.] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
   [Ballantyne, Christie M.] Baylor Coll Med, Div Cardiovasc, Houston, TX 77030 USA.
   [Ballantyne, Christie M.] Methodist deBakey Heart & Vasc Cntr, Houston, TX USA.
   [Astor, Brad C.] Univ Wisconsin, Dept Med, Sch Med & Publ Hlth, Madison, WI USA.
   [Klein, Barbara] Univ Stn Clin, Dept Ophthalmol & Visual Sci, Madison, WI USA.
   [Matsushita, Kunihiro; Selvin, Elizabeth] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
   [Aguilar, David] Baylor Coll Med, Houston, TX 77030 USA.
   [Vardeny, Orly] Univ Wisconsin, Sch Pharm, Madison, WI 53706 USA.
   [Ni, Hanyu] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 17716
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162907035
ER

PT J
AU Greco, G
   Shi, W
   Michler, R
   Blackstone, E
   Kron, IL
   Moquete, E
   Woo, JY
   Moskowitz, AJ
   Thourani, V
   Gillinov, AM
   Gelijns, AC
   Argenziano, M
   Alexander, JH
   Perrault, LP
   Lee, A
   Burks, SG
   O'Gara, PT
   Bagiella, E
   Hohmann, SF
   Gardner, TJ
AF Greco, Giampaolo
   Shi, Wei
   Michler, Robert
   Blackstone, Eugene
   Kron, Irving L.
   Moquete, Ellen
   Woo, Joseph Y.
   Moskowitz, Alan J.
   Thourani, Vinod
   Gillinov, A. Marc
   Gelijns, Annetine C.
   Argenziano, Michael
   Alexander, John H.
   Perrault, Louis P.
   Lee, Albert
   Burks, Sandra G.
   O'Gara, Patrick T.
   Bagiella, Emilia
   Hohmann, Samuel F.
   Gardner, Timothy J.
TI The Economic Impact of Healthcare Associated Infections in Cardiac
   Surgery
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Cardiac surgery; Health policy; Health economics; Patient safety;
   Quality of medical care
C1 [Greco, Giampaolo; Shi, Wei; Moquete, Ellen; Moskowitz, Alan J.; Gelijns, Annetine C.; Bagiella, Emilia] Icahn Sch Med Mt Sinai, New York, NY USA.
   [Michler, Robert] Montefiore Einstein Heart Cntr, Bronx, NY USA.
   [Blackstone, Eugene] Cleveland Clin, Cleveland, OH 44106 USA.
   [Kron, Irving L.] Univ Virginia Hlth Syst, Charlottesville, VA USA.
   [Woo, Joseph Y.] Univ Penn, Div Cardiothorac Surg, Philadelphia, PA 19104 USA.
   [Thourani, Vinod] Emory Univ Hosp Midtown, Atlanta, GA USA.
   [Gillinov, A. Marc] Cleveland Clin, Dept Thorac & Cardiovasc Surg, Cleveland, OH 44106 USA.
   [Argenziano, Michael] Columbia Univ, Med Ctr, New York, NY USA.
   [Alexander, John H.] Duke Clin Rsch Inst, Duke Dept Med, Div Cardiol, Durham, NC USA.
   [Perrault, Louis P.] Montreal Heart Inst, Montreal, PQ H1T 1C8, Canada.
   [Lee, Albert] NHLBI, Adv Technol & Surg Branch, Bethesda, MD 20892 USA.
   [Burks, Sandra G.] Univ Virginia, Surg Therapeut Adv Cntr, Charlottesville, VA USA.
   [O'Gara, Patrick T.] Brigham & Womens Hosp, Boston, MA 02115 USA.
   [Hohmann, Samuel F.] Univ Hlth Consortium, Chicago, IL USA.
   [Gardner, Timothy J.] Christiana Care Hlth Syst, Cntr Heart & Vasc Hlth, Newark, DE USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 18267
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162907288
ER

PT J
AU Hoffmann, U
   Massaro, JM
   D'Agostino, R
   Kathiresan, S
   Fox, CS
   O'Donnell, CJ
AF Hoffmann, Udo
   Massaro, Joseph M.
   D'Agostino, Ralph
   Kathiresan, Sekar
   Fox, Caroline S.
   O'Donnell, Christopher J.
TI Cardiovascular Event Prediction and Risk Reclassification by Coronary,
   Aortic, and Valvular Calcification in the Framingham Heart Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Cardiovascular imaging; Epidemiology; Risk factors
C1 [Hoffmann, Udo; Kathiresan, Sekar] Massachusetts Gen Hosp, Boston, MA 02114 USA.
   [Massaro, Joseph M.; D'Agostino, Ralph] Boston Univ, Boston, MA 02215 USA.
   [Fox, Caroline S.; O'Donnell, Christopher J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 14097
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162903441
ER

PT J
AU Holmes, KW
   Silberbach, GM
   Liliana, P
   Maslen, CL
   Dietz, HC
   Ravekes, WJ
   LeMaire, SA
   Milewicz, DM
   Devereux, R
   Roman, MI
   Pyeritz, RE
   Shohet, R
   McDonnell, N
   Kroner, BY
   Kim, E
   Habashi, JP
   Tolunay, E
   Song, HK
AF Holmes, Kathrvn W.
   Silberbach, G. M.
   Liliana, Preiss
   Maslen, Cheryl L.
   Dietz, H. C.
   Ravekes, William J.
   LeMaire, Scott A.
   Milewicz, Dianna M.
   Devereux, Richard
   Roman, Mary I.
   Pyeritz, Reed E.
   Shohet, Ralph
   McDonnell, Nazli
   Kroner, Barbara Y.
   Kim, Eagle
   Habashi, Jennifer P.
   Tolunay, Eser
   Song, Howard K.
CA GenTAC Investigators
TI Bicuspid Aortic Valve and Marfan Syndrome: Two Strikes?
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
C1 [Holmes, Kathrvn W.; Silberbach, G. M.; Maslen, Cheryl L.; Song, Howard K.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
   [Liliana, Preiss] Rsch Triangle Int, Stat, Rockville, MD USA.
   [Dietz, H. C.; Ravekes, William J.; Habashi, Jennifer P.] Johns Hopkins Univ, Baltimore, MD USA.
   [LeMaire, Scott A.] Baylor Coll Med, Houston, TX USA.
   [Milewicz, Dianna M.] Univ Texas Huston, Houston, TX USA.
   [Devereux, Richard; Roman, Mary I.] Cornell Univ, New York, NY 10021 USA.
   [Pyeritz, Reed E.] Univ Penn, Philadelphia, PA 19104 USA.
   [Shohet, Ralph] Univ Hawaii, Queens Med Cntr, Honolulu, HI 96822 USA.
   [McDonnell, Nazli] Harbor Hosp, NIA, Baltimore, MD USA.
   [Kroner, Barbara Y.] RTI Int, Med, Rockville, MD USA.
   [Kim, Eagle] Univ Michigan, Ann Arbor, MI 48109 USA.
   [Tolunay, Eser] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 13178
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162903028
ER

PT J
AU Kassim, TA
   Ayers, C
   de Lemos, J
   Albert, M
   Powell-Wiley, TM
AF Kassim, Thaslim A.
   Ayers, Colby
   de Lemos, James
   Albert, Michelle
   Powell-Wiley, Tiffany M.
TI Neighborhood-Level Socioeconomic Deprivation Predicts Worsening Blood
   Pressure in a Multi-Ethnic Population: Longitudinal Data From the Dallas
   Heart Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Epidemiology; Hypertension
C1 [Kassim, Thaslim A.; Albert, Michelle] Howard Univ Hosp, Washington, DC USA.
   [Ayers, Colby; de Lemos, James] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
   [Powell-Wiley, Tiffany M.] NHLBI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 17283
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162906368
ER

PT J
AU Khan, H
   Kalogeropoulos, AP
   Georgiopoulou, VV
   Newman, AB
   Harris, TB
   Rodondi, N
   Bauer, DC
   Kritchevsky, SB
   Butler, J
AF Khan, Hassan
   Kalogeropoulos, Andreas P.
   Georgiopoulou, Vasiliki V.
   Newman, Anne B.
   Harris, Tamara B.
   Rodondi, Nicolas
   Bauer, Douglas C.
   Kritchevsky, Stephen B.
   Butler, Javed
TI Frailty With Risk of Incident Heart Failure in Older Adults
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Epidemiology; Elderly
C1 [Khan, Hassan] Univ Cambridge, Cambridge, England.
   [Kalogeropoulos, Andreas P.; Georgiopoulou, Vasiliki V.; Butler, Javed] Emory Univ, Atlanta, GA 30322 USA.
   [Newman, Anne B.] Emory Univ, Univ Pittsburgh, Pittsburgh, PA USA.
   [Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
   [Rodondi, Nicolas] Univ Bern, Inselspital, CH-3010 Bern, Switzerland.
   [Bauer, Douglas C.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
   [Kritchevsky, Stephen B.] Wake Forest Sch Med, Sect Gerontol & Geriatr Med, Winston Salem, NC USA.
RI Newman, Anne/C-6408-2013
OI Newman, Anne/0000-0002-0106-1150
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 13195
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162903037
ER

PT J
AU Kishi, S
   Magalhaes, TA
   George, RT
   Tanami, Y
   Dewey, M
   Laham, R
   Niinuma, H
   Schuijf, JD
   Vavere, AL
   Kitagawa, K
   Chen, MY
   Nomura, CH
   Rybicki, FJ
   Arbab-Zadeh, A
   Lima, JA
AF Kishi, Satoru
   Magalhaes, Tiago A.
   George, Richard T.
   Tanami, Yutaka
   Dewey, Marc
   Laham, RogerJ
   Niinuma, Hiroyuki
   Schuijf, Joanne D.
   Vavere, Andrea L.
   Kitagawa, Kakuya
   Chen, Marcus Y.
   Nomura, Cesar H.
   Rybicki, Frank J.
   Arbab-Zadeh, Armin
   Lima, Joao A.
TI The Relationship of Left Ventricular Mass With Coronary Artery Disease
   and Ischemic Heart Disease: The CORE320 Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Cardiac imaging; Computed tomography; Arterosclerosis; Ischemic heart
   disease
C1 [Kishi, Satoru; Magalhaes, Tiago A.; George, Richard T.; Vavere, Andrea L.; Arbab-Zadeh, Armin; Lima, Joao A.] Johns Hopkins Univ, Sch Med, Div Cardiol, Baltimore, MD USA.
   [Tanami, Yutaka] Keio Univ, Dept Radiol, Tokyo, Japan.
   [Dewey, Marc] Univ Berlin, Charite Med Sch, Div Cardiol, Berlin, Germany.
   [Laham, RogerJ] Beth Israel Deaconess Med Ctr, Div Cardiol, Boston, MA 02215 USA.
   [Niinuma, Hiroyuki] St Lukes Int Hosp, Div Cardiol, Tokyo, Japan.
   [Schuijf, Joanne D.] Leiden Univ, Med Ctr, Div Cardiol, Leiden, Netherlands.
   [Kitagawa, Kakuya] Mie Univ Hosp, Dept Radiol, Tsu, Mie, Japan.
   [Chen, Marcus Y.] NHLBI, Adv Cardiovasc Imaging Grp, NIH, Bethesda, MD 20892 USA.
   [Nomura, Cesar H.] Hosp Israelita Albert Einstein, Dept Radiol, Sco Paulo, Brazil.
   [Rybicki, Frank J.] Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 13081
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162902517
ER

PT J
AU Kizer, JR
   Bartz, T
   Mukamal, KJ
   Ix, JH
   Djousse, L
   Siscovick, DS
   Tracy, RP
   Newman, AB
   Gottdiener, JS
   Hirsch, CH
   Zieman, SJ
AF Kizer, Jorge R.
   Bartz, Traci
   Mukamal, Kenneth J.
   Ix, Joachim H.
   Djousse, Luc
   Siscovick, David S.
   Tracy, Russell P.
   Newman, Anne B.
   Gottdiener, John S.
   Hirsch, Calvin H.
   Zieman, Susan J.
TI Advanced Glycation Endproduct Carboxymethyl-Lysine (CML) and Incident
   Heart Failure in Older Persons
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Heart failure; Biomarkers; Aging; Epidemiology
C1 [Kizer, Jorge R.] Albert Einstein Coll Med, Bronx, NY 10467 USA.
   [Bartz, Traci; Siscovick, David S.] Univ Washington, Seattle, WA 98195 USA.
   [Mukamal, Kenneth J.] Beth Israel Deaconess Med Cntr, Brookline, MA USA.
   [Ix, Joachim H.] Univ Calif San Diego, La Jolla, CA 92093 USA.
   [Djousse, Luc] Brigham & Womens Hosp, Div Aging, Boston, MA 02115 USA.
   [Tracy, Russell P.] Univ Vermont, Colchester, VT USA.
   [Newman, Anne B.] Univ Pittsburgh, Pittsburgh, PA USA.
   [Gottdiener, John S.] Univ Maryland, Baltimore, MD 21201 USA.
   [Hirsch, Calvin H.] Univ Calif Davis, Sacramento, CA 95817 USA.
   [Zieman, Susan J.] NIA, Baltimore, MD 21224 USA.
RI Newman, Anne/C-6408-2013
OI Newman, Anne/0000-0002-0106-1150
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 13222
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162903053
ER

PT J
AU Kwan, AC
   May, H
   Cater, G
   Sibley, CT
   Rosen, B
   Lima, JA
   Lappe, D
   Muhlestein, JB
   Anderson, JL
   Bluemke, DA
AF Kwan, Alan C.
   May, Heidi
   Cater, George
   Sibley, Christopher T.
   Rosen, Boaz
   Lima, Joao A.
   Lappe, Donald
   Muhlestein, Joseph B.
   Anderson, Jeffrey L.
   Bluemke, David A.
TI Coronary Plaque Volume by Cardiac Computed Tomographic Angiography is
   Associated With Obesity in Diabetic Patients: The faCTor-64 Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Cardiovascular imaging; Coronary heart disease; Computed tomography;
   Plaque
C1 [Kwan, Alan C.; Cater, George; Sibley, Christopher T.; Rosen, Boaz; Bluemke, David A.] Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD USA.
   [May, Heidi; Lappe, Donald; Muhlestein, Joseph B.; Anderson, Jeffrey L.] Intermt Hlth Care, Intermt Heart Inst, Murray, UT USA.
   [Lima, Joao A.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 15070
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162904382
ER

PT J
AU LaBresh, KA
   Lazorick, S
   Furberg, R
   Ariza, A
   Whetstone, L
   Hobbs, C
   de Jesus, J
   Bender, R
   Salinas, I
   Binns, H
AF LaBresh, Kenneth A.
   Lazorick, Suzanne
   Furberg, Robert
   Ariza, Adolfo
   Whetstone, Lauren
   Hobbs, Connie
   de Jesus, Janet
   Bender, Randall
   Salinas, Ilse
   Binns, Helen
TI Improvement of Guideline Use in Young Hearts Strong Starts, a Cluster
   Randomized Trial of Cardiovascular Prevention in Pediatric Offices
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Cardiovascular disease prevention; Children; Guidelines
C1 [LaBresh, Kenneth A.] RTI Int, Waltham, MA USA.
   [Lazorick, Suzanne; Whetstone, Lauren] E Carolina Univ, Brody Sch Med, Greenville, NC USA.
   [Furberg, Robert] RTI Int, CAHIT, Rsch Traingle Pk, NC USA.
   [Ariza, Adolfo; Binns, Helen] Ann & Robert H Lurie Childrens Hosp, Pediat Practice Rsch Grp, Chicago, IL USA.
   [Hobbs, Connie] RTI Int, Hlth Commun, Rsch Traingle Pk, NC USA.
   [de Jesus, Janet] NHLBI, Div Applicat Rsch Discoveries, Bethesda, MD 20892 USA.
   [Bender, Randall] RTI Int, SSES, Rsch Traingle Pk, MA USA.
   [Salinas, Ilse] Ann & Robert H Lurie Childrens Hosp, Pediat Practice Reserch Grp, Chicago, IL USA.
RI LaBresh, Kenneth/A-6995-2017
OI LaBresh, Kenneth/0000-0001-9040-1956
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 13865
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162903333
ER

PT J
AU Lamas, GA
   Nahin, RL
   Lindblad, L
   Goertz, C
   Boineau, R
   Chappell, T
   Flaker, G
   Rozema, T
   Born, T
   Stylianou, M
   Lewis, EF
   Mark, DB
   Lee, KL
AF Lamas, Gervasio A.
   Nahin, Richard L.
   Lindblad, Lauren
   Goertz, Christine
   Boineau, Robin
   Chappell, Terry
   Flaker, Greg
   Rozema, Theodore
   Born, Tammy
   Stylianou, Mario
   Lewis, Eldrin F.
   Mark, Daniel B.
   Lee, Kerry L.
TI Clinical Benefit of EDTA-based Chelation Therapy and High-dose Oral
   Multivitamins and Multiminerals in TACT- An Expanded Comparison of 2
   Factorial Groups
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Myocardial infarction; Coronary artery disease; Clinical trials
C1 [Lamas, Gervasio A.] Mt Sinai Med Ctr, Div Cardiol, Miami Beach, FL 33140 USA.
   [Nahin, Richard L.] Natl Cntr Complementary & Alternat Med, Bethesda, MD USA.
   [Lindblad, Lauren; Mark, Daniel B.; Lee, Kerry L.] Duke Clin Rsch Inst, Durham, NC USA.
   [Goertz, Christine] Palmer Coll Chiropract W, Davenport, IA USA.
   [Boineau, Robin] NHLBI, Heart Failure & Arrhythmias Branch, Bethesda, MD 20892 USA.
   [Chappell, Terry] Celebrat Heath Assoc, Bluffton, OH USA.
   [Flaker, Greg] Univ Missouri Hlth Care, Columbia, MO USA.
   [Rozema, Theodore] Biogenesis Med Cntr, Landrum, SC USA.
   [Born, Tammy] Born Prevent Hlth Care Clin, Grand Rapids, MI USA.
   [Stylianou, Mario] NHLBI, Bethesda, MD 20892 USA.
   [Lewis, Eldrin F.] Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 11054
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162901308
ER

PT J
AU Lamprea-Montealegre, JA
   Astor, BC
   McClelland, R
   Grams, M
   Sibley, CT
   Ouyang, P
   de Boer, I
   Szklo, M
AF Lamprea-Montealegre, Julio A.
   Astor, Brad C.
   McClelland, Robyn
   Grams, Morgan
   Sibley, Cristopher T.
   Ouyang, Pamela
   de Boer, Ian
   Szklo, Moyses
TI LDL Phenotype-B is Strongly Associated With CHD Risk Among Individuals
   With CKD. The Multi-ethnic Study of Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Kidney; Lipids; Lipoproteins; Coronary heart disease
C1 [Lamprea-Montealegre, Julio A.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
   [Astor, Brad C.] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI USA.
   [McClelland, Robyn] Univ Washington, Seattle, WA 98195 USA.
   [Grams, Morgan] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
   [Sibley, Cristopher T.] NIH, Natl Institure Hlth, Bethesda, MD USA.
   [Ouyang, Pamela] Johns Hopkins Bayview Med Cntr, Baltimore, MD USA.
   [de Boer, Ian] Univ Washington, Baltimore, MD USA.
   [Szklo, Moyses] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 9258
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162900311
ER

PT J
AU Lee, H
   Abe, Y
   Lee, I
   Shrivastav, S
   Huttemann, M
   Hopfer, U
   Felder, RA
   Asico, LD
   Jose, PA
   Kopp, JB
AF Lee, Hewang
   Abe, Yoshifusa
   Lee, Icksoo
   Shrivastav, Shashi
   Huettemann, Maik
   Hopfer, Ulrich
   Felder, Robin A.
   Asico, Laureano D.
   Jose, Pedro A.
   Kopp, Jeffrey B.
TI Increased Renal Proximal Tubule Bioenergetic Activity Prior to the Onset
   Ofsustained Hypertension in Spontaneously Hypertensive Rats
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Mitochondria; Hypertension, renal; Renal function; Energy metabolism;
   Genetics
C1 [Lee, Hewang; Asico, Laureano D.; Jose, Pedro A.] Univ Maryland, Sch Med, Dept Med, Baltimore, MD 21201 USA.
   [Abe, Yoshifusa; Shrivastav, Shashi; Kopp, Jeffrey B.] NIDDKD, NIH, Kidney Dis Branch, Bethesda, MD USA.
   [Lee, Icksoo; Huettemann, Maik] Wayne State Univ, Sch Med, Genet & Cardiovasc Rsch Inst, Detroit, MI USA.
   [Hopfer, Ulrich] Case Western Reserve Univ, Sch Med, Dept Physiol & Biophys, Cleveland, OH 44106 USA.
   [Felder, Robin A.] Univ Virginia, Hlth Sci Ctr, Dept Pathol, Charlottesville, VA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 16455
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162906002
ER

PT J
AU Levy, D
   Yin, XY
   Lyas, A
   Ho, J
   Courchesne, PL
   Subramanian, S
   Hwang, SJ
   O'Donnell, CJ
   Ramachandran, VS
   Benjamin, EJ
   Fox, CS
   Massaro, JM
   Adourian, A
   D'Agostino, R
   Larson, MG
AF Levy, Daniel
   Yin, Xiaoyan
   Lyas, Asva
   Ho, Jennifer
   Courchesne, Paul L.
   Subramanian, Subha
   Hwang, Shi-Jen
   O'Donnell, Christopher J.
   Ramachandran, Vasan S.
   Benjamin, Emelia J.
   Fox, Caroline S.
   Massaro, Joseph M.
   Adourian, Aram
   D'Agostino, Ralph
   Larson, Martin G.
TI Protein Biomarkers of New-Onset Atherosclerotic Cardiovascular Disease
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Proteins; Risk factors; Epidemiology; Cardiovascular disease; Proteomics
C1 [Levy, Daniel; Courchesne, Paul L.; Subramanian, Subha; Hwang, Shi-Jen; O'Donnell, Christopher J.] NHLBI, Populat Sci Branch, Framingham Heart Study, Framingham, MA USA.
   [Yin, Xiaoyan; Lyas, Asva; Ho, Jennifer; D'Agostino, Ralph; Larson, Martin G.] Boston Univ, Boston, MA 02215 USA.
   [Ramachandran, Vasan S.; Benjamin, Emelia J.] Boston Univ, Sch Med, Boston, MA 02118 USA.
   [Fox, Caroline S.] Brigham & Womens Hosp, Populat Sci Branch, NHLBI, Framingham Heart Study, Framingham, MA USA.
   [Massaro, Joseph M.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
   [Adourian, Aram] BG Med, Computat Sci, Waltham, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 15535
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162905063
ER

PT J
AU Manavski, Y
   Carmona, G
   Bennewitz, K
   Tang, ZS
   Zhang, F
   Sakurai, A
   Gutkind, SJ
   Li, XR
   Kroll, J
   Dimmeler, S
   Chavakis, E
AF Manavski, Yosif
   Carmona, Guillaume
   Bennewitz, Katrin
   Tang, Zhongshu
   Zhang, Fan
   Sakurai, Atsuko
   Gutkind, Silvio J.
   Li, Xuri
   Kroll, Jens
   Dimmeler, Stefanie
   Chavakis, Emmanouil
TI Brag2, an Arf-GEF, Regulates Integrin-Dependent Endothelial Adhesion and
   is Involved in Developmental and Pathological Angiogenesis
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Angiogenesis; Endothelium; Vascular development; Endothelial
C1 [Manavski, Yosif; Dimmeler, Stefanie] Goethe Univ Frankfurt, Inst Cardiovasc Regenerat, D-60054 Frankfurt, Germany.
   [Carmona, Guillaume] MIT, David H Koch Inst Integrat Canc Rsch, Cambridge, MA 02139 USA.
   [Bennewitz, Katrin; Kroll, Jens] Heidelberg Univ, Med Fac Mannheim, Cntr Biomed & Med Technol Mannheim, Mannheim, Germany.
   [Tang, Zhongshu; Li, Xuri] Sun Yat Sen Univ, Zhongshan Ophthalm Cntr, Guangzhou 510275, Guangdong, Peoples R China.
   [Zhang, Fan] NEI, NIH, Bethesda, MD 20892 USA.
   [Sakurai, Atsuko; Gutkind, Silvio J.] Natl Inst Dent & Craniofacial Rsch, NIH, Bethesda, MD USA.
   [Chavakis, Emmanouil] Goethe Univ Frankfurt, Dept Internal Med 3, D-60054 Frankfurt, Germany.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 18516
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162907413
ER

PT J
AU McCrindle, BW
   Zak, V
   Breitbart, RE
   Mahony, L
   Shrader, P
   Lai, WW
   Burns, KM
   Colan, SD
   Williams, RV
   Goldberg, DJ
   Hill, KD
   Khaikin, S
   Atz, AM
AF McCrindle, Brian W.
   Zak, Victor
   Breitbart, Roger E.
   Mahony, Lynn
   Shrader, Peter
   Lai, Wyman W.
   Burns, Kristin M.
   Colan, Steven D.
   Williams, Richard V.
   Goldberg, David J.
   Hill, Kevin D.
   Khaikin, Svetlana
   Atz, Andrew M.
TI Patient, Medical and Laboratory Characteristics Associated With a
   Decline in Physical Functioning in Children and Adolescents After the
   Fontan Procedure
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Fontan physiology; Congenital heart disease; Congenital heart surgery;
   Quality of life
C1 [McCrindle, Brian W.; Khaikin, Svetlana] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
   [Zak, Victor; Shrader, Peter] New England Rsch Inst, Watertown, MA USA.
   [Breitbart, Roger E.; Colan, Steven D.] Boston Childrens Hosp, Boston, MA USA.
   [Mahony, Lynn] Univ Texas Southwestern Med Cntr, Dallas, TX USA.
   [Lai, Wyman W.] Columbia Univ, Med Cntr, New York, NY USA.
   [Burns, Kristin M.] NHLBI, NIH, Bethesda, MD 20892 USA.
   [Williams, Richard V.] Primary Childrens Med Cntr, Salt Lake City, UT USA.
   [Goldberg, David J.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
   [Hill, Kevin D.] Duke Univ, Med Cntr, Fayetteville, NC USA.
   [Atz, Andrew M.] MUSC, Childrens Hosp, Charleston, SC USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 10504
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162901127
ER

PT J
AU McDermott, M
   Criqui, M
   Domanchuk, K
   Ferrucci, L
   Guralnik, J
   Kibbe, M
   Liu, K
   Liao, YH
   Lloyd-Jones, D
   Spring, B
   Tian, L
   Zhao, LH
   Rejeski, WJ
AF McDermott, Mary
   Criqui, Michael
   Domanchuk, Kathryn
   Ferrucci, Luigi
   Guralnik, Jack
   Kibbe, Melina
   Liu, Kiang
   Liao, Yihua
   Lloyd-Jones, Donald
   Spring, Bonnie
   Tian, Lu
   Zhao, Lihui
   Rejeski, Walter J.
TI A Home-Based Exercise Intervention Significantly Improves Walking
   Performance in Peripheral Arterial Disease: One-Year Follow-Up From a
   Randomized Controlled Trial
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Peripheral arterial disease; Exercise tests; Interventional studies
C1 [McDermott, Mary; Domanchuk, Kathryn; Kibbe, Melina; Liu, Kiang; Liao, Yihua; Lloyd-Jones, Donald; Spring, Bonnie; Zhao, Lihui] Northwestern Univ, Chicago, IL 60611 USA.
   [Criqui, Michael] Univ Calif San Diego, La Jolla, CA 92093 USA.
   [Ferrucci, Luigi] NIA, NIH, Bethesda, MD 20892 USA.
   [Guralnik, Jack] Univ Maryland, Baltimore, MD 21201 USA.
   [Tian, Lu] Stanford Univ, Stanford, CA 94305 USA.
   [Rejeski, Walter J.] Wake Forest Univ, Winston Salem, NC 27109 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 14789
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162904244
ER

PT J
AU Miedema, MD
   Maziarz, M
   Biggs, ML
   Zieman, SJ
   Kizer, JR
   Ix, JH
   Mozaffarian, D
   Tracy, R
   Psaty, BM
   Siscovick, D
   Mukamal, KJ
   Djousse, L
AF Miedema, Michael D.
   Maziarz, Marlena
   Biggs, Mary Lou
   Zieman, Susan J.
   Kizer, Jorge R.
   Ix, Joachim H.
   Mozaffarian, Dariush
   Tracy, Russell
   Psaty, Bruce M.
   Siscovick, David
   Mukamal, Kenneth J.
   Djousse, Luc
TI Plasma Free Fatty Acids, Fatty Acid-Binding Protein 4, and Mortality in
   Older Adults in the Cardiovascular Health Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Biomarkers; Cardiovascular disease; Lipids
C1 [Miedema, Michael D.] Abbott NW Hosp, Minneapolis Heart Inst, Cardiovasc Dept, Minneapolis, MN 55407 USA.
   [Maziarz, Marlena; Biggs, Mary Lou] Univ Washington, Sch Publ Hlth & Community Med, Dept Biostat, Seattle, WA 98195 USA.
   [Zieman, Susan J.] NIA, NIH, Bethesda, MD 20892 USA.
   [Kizer, Jorge R.] Albert Einstein Coll Med, Dept Med & Epidemiol & Populat Hlth, New York, NY USA.
   [Ix, Joachim H.] Univ Calif San Diego, San Diego, CA 92103 USA.
   [Mozaffarian, Dariush] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
   [Tracy, Russell] Univ Vermont, Colchester Rsch Facil, Dept Pathol, Colchester, VT USA.
   [Psaty, Bruce M.; Siscovick, David] Univ Washington, Cardiovasc Hlth Rsch Unit, Seattle, WA 98195 USA.
   [Mukamal, Kenneth J.] Beth Israel Deaconess Med Cntr, Dept Med, Boston, MA USA.
   [Djousse, Luc] Brigham & Womens Hosp, Div Aging, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 18168
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162907247
ER

PT J
AU Miller, PS
   Moser, DK
   Pelter, MM
   Nesbitt, T
   Southard, J
   Robinson, S
   Cooper, LS
   Dracup, K
AF Miller, Pamela S.
   Moser, Debra K.
   Pelter, Michele M.
   Nesbitt, Thomas
   Southard, Jeffrey
   Robinson, Susan
   Cooper, Lawton S.
   Dracup, Kathleen
TI Does the Interaction of B-Type Natriuretic Peptide and Depressive
   Symptom Status Predict Cardiac Mortality and Re-Hospitalization in
   Rural-Dwelling Heart Failure Patients?
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Natriuretic peptide; Depression; Heart failure; Outcomes
C1 [Miller, Pamela S.; Robinson, Susan; Dracup, Kathleen] Univ Calif San Francisco, Sch Nursing, San Francisco, CA 94143 USA.
   [Moser, Debra K.] Univ Kentucky, Coll Nursing, Lexington, KY USA.
   [Pelter, Michele M.] Univ Nevada, Sch Nursing, Reno, NV 89557 USA.
   [Nesbitt, Thomas] Univ Calif Davis, Sch Med, Sacramento, CA 95817 USA.
   [Southard, Jeffrey] Univ Calif Davis, Sacramento, CA 95817 USA.
   [Cooper, Lawton S.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 18336
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162907324
ER

PT J
AU Mohandas, R
   Segal, MS
   Huo, TY
   Johnson, BD
   Handberg, EM
   Petersen, J
   Sopko, G
   Merz, CNB
   Pepine, CJ
AF Mohandas, Rajesh
   Segal, Mark S.
   Huo, Tianyao
   Johnson, B. Delia
   Handberg, Eileen M.
   Petersen, John
   Sopko, George
   Merz, C. Noel Bairey
   Pepine, Carl J.
TI Mild Renal Insufficiency is an Independent Predictor of Coronary
   Microvascular Dysfunction among Women With Symptoms/Signs of Ischemia: A
   report From the Women's Ischemia Syndrome Evaluation (WISE)
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Coronary microcirculation; Kidney
C1 [Mohandas, Rajesh; Segal, Mark S.] Univ Florida, Div Nephrol Hypertens & Transplantat, Gainesville, FL USA.
   [Huo, Tianyao; Handberg, Eileen M.; Petersen, John; Pepine, Carl J.] Univ Florida, Div Cardiol, Gainesville, FL USA.
   [Johnson, B. Delia] Univ Pittsburgh, Pittsburgh, PA USA.
   [Sopko, George] NHLBI, Div Heart & Vasc Dis, NIH, Bethesda, MD 20892 USA.
   [Merz, C. Noel Bairey] Cedars Sinai Med Cntr, Barbra Streis & Womens Heart Cntr, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 13274
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162903077
ER

PT J
AU Mohandas, R
   Segal, MS
   Srinivas, TR
   Johnson, BD
   Handberg, EM
   Petersen, JW
   Sopko, G
   Merz, CNB
   Pepine, CJ
AF Mohandas, Rajesh
   Segal, Mark S.
   Srinivas, Titte R.
   Johnson, B. Delia
   Handberg, Eileen M.
   Petersen, John W.
   Sopko, George
   Merz, C. Noel Bairey
   Pepine, Carl J.
TI Mild Renal Insufficiency Predicts Mortality and Adverse Events in Women
   With Cardiac Ischemia, Independent of the Underlying Obstructive
   Coronary Artery Disease
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Outcomes; Kidney; Coronary microcirculation
C1 [Mohandas, Rajesh; Segal, Mark S.] Univ Florida, Div Nephrol Hypertens & Transplantat, Gainesville, FL USA.
   [Srinivas, Titte R.] Med Univ S Carolina, Div Nephrol Hypertens & Transplantat, Charleston, SC 29425 USA.
   [Johnson, B. Delia] Univ Pittsburgh, Pittsburgh, PA USA.
   [Handberg, Eileen M.; Petersen, John W.; Pepine, Carl J.] Univ Florida, Div Cardiol, Gainesville, FL USA.
   [Sopko, George] NHLBI, Div Heart & Vasc Dis, NIH, Bethesda, MD 20892 USA.
   [Merz, C. Noel Bairey] Cedars Sinai Med Cntr, Barbra Streisand Womens Heart Cntr, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 13235
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162903058
ER

PT J
AU O'Connor, MY
   Ricks, M
   Courville, AB
   Thomas, F
   Yao, JH
   Katzmarzyk, PT
   Sumner, AE
AF O'Connor, Michelle Y.
   Ricks, Madia
   Courville, Amber B.
   Thomas, Francine
   Yao, Jianhua
   Katzmarzyk, Peter T.
   Sumner, Anne E.
TI Variation in the Waist Circumference of Risk in Black Populations: A
   Comparison of African Immigrants to African Americans
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Insulin resistance; Body mass index (BMI); Computed tomography; Risk
   factors; Adipose
C1 [O'Connor, Michelle Y.; Ricks, Madia; Sumner, Anne E.] NIDDK, NIH, Bethesda, MD 20892 USA.
   [Courville, Amber B.; Thomas, Francine; Yao, Jianhua] NIH, Clin Cntr, Bethesda, MD 20892 USA.
   [Katzmarzyk, Peter T.] Pennington Biomed Rsch Cntr, Phys Act & Obes Epidemiol Lab, Baton Rouge, LA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 13224
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162903055
ER

PT J
AU Oakley, RH
   Ren, RQ
   Cruz-Topete, D
   Willis, M
   Cidlowski, JA
AF Oakley, Robert H.
   Ren, Rongqin
   Cruz-Topete, Diana
   Willis, Monte
   Cidlowski, John A.
TI Essential Role for Cardiomyocyte Glucocorticoid Receptors for the
   Prevention of Heart Disease
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Cardiac hypertrophy; Heart failure; Gene expression
C1 [Oakley, Robert H.; Ren, Rongqin; Cruz-Topete, Diana; Cidlowski, John A.] NIEHS, Lab Signal Transduct, NIH, Rsch Triangle Pk, NC USA.
   [Willis, Monte] McAllister Heart Inst, Dept Pathol & Lab Med, Chapel Hill, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 13196
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162903038
ER

PT J
AU Onuma, OK
   Chun, EJ
   Pencina, K
   Massaro, JM
   O'Donnell, CJ
   Hoffmann, U
AF Onuma, Oyere K.
   Chun, Eun Ju
   Pencina, Karol
   Massaro, Joseph M.
   O'Donnell, Christopher J.
   Hoffmann, Udo
TI Performance of Framingham Risk Function With Coronary Artery Calcium in
   Predicting Major Coronary Events in an Asian Cohort
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Cardiovascular disease prevention; Cardiac CT; Risk factors
C1 [Onuma, Oyere K.; Hoffmann, Udo] Massachusetts Gen Hosp, Boston, MA 02114 USA.
   [Chun, Eun Ju] Seoul Natl Univ, Bundang Hosp, Seoul, South Korea.
   [Pencina, Karol] Boston Univ, Boston, MA 02215 USA.
   [Massaro, Joseph M.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
   [O'Donnell, Christopher J.] NHLBI, Framingham Heart Study, NIH, Framingham, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 18536
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162907424
ER

PT J
AU Panza, JA
   Velazquez, EI
   She, L
   Smith, PK
   Nicolau, JC
   Favaloro, RR
   Gradinac, S
   Chrzanowski, L
   Prabhakaran, D
   Howlett, JG
   Jasinski, M
   Hill, JA
   Desvigne-Nickens, P
   Jones, RH
   Lee, KL
   Rouleau, JL
AF Panza, Julio A.
   Velazquez, Eric I.
   She, Lilin
   Smith, Peter K.
   Nicolau, Jose C.
   Favaloro, Roberto R.
   Gradinac, Sinisa
   Chrzanowski, Lukasz
   Prabhakaran, Dorairai
   Howlett, Jonathan G.
   Jasinski, Marek
   Hill, James A.
   Desvigne-Nickens, Patrice
   Jones, Robert H.
   Lee, Kerry L.
   Rouleau, Jean L.
TI Impact of the Extent of Coronary and Myocardial Disease on the Treatment
   Effect of Surgical Revascularization in Patients With Ischemic Left
   Ventricular Dysfunction
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Ischemic heart disease; Outcomes; Cardiac surgery; Clinical trials;
   Myocardial revascularization
C1 [Panza, Julio A.] Washington Hosp Cntr, Div Cardiol, Washington, DC USA.
   [Velazquez, Eric I.] Duke Clin Rsch Inst, Div Cardiol, Durham, NC USA.
   [She, Lilin; Jones, Robert H.; Lee, Kerry L.] Duke Clin Rsch Inst, Durham, NC USA.
   [Smith, Peter K.] Duke Univ, Med Ctr, Durham, NC USA.
   [Nicolau, Jose C.] Inst Coracao, Div Cardiol, Sao Paulo, Brazil.
   [Favaloro, Roberto R.] Univ Hosp Favaloro Fdn, Div Cardiol, Buenos Aires, DF, Argentina.
   [Gradinac, Sinisa] Dedinje Cardiovasc Inst, Div Cardiol, Belgrade, Serbia.
   [Chrzanowski, Lukasz] Inst Kardiol AM, Div Cardiol, Lodtz, Poland.
   [Prabhakaran, Dorairai] Cntr Chron Dis Control, Div Cardiol, New Delhi, India.
   [Howlett, Jonathan G.] Foothills Med Cntr, Div Cardiol, Calgary, AB, Canada.
   [Jasinski, Marek] Med Univ Silesia, Div Cardiol, Katowice, Poland.
   [Hill, James A.] Univ Florida, Shands Hosp, Div Cardiol, Gainesville, FL USA.
   [Desvigne-Nickens, Patrice] NHLBI, Div Cardiol, NIH, Bethesda, MD 20892 USA.
   [Rouleau, Jean L.] Univ Montreal, Div Cardiol, Montreal, PQ, Canada.
RI Nicolau, Jose/E-1487-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 10721
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162901190
ER

PT J
AU Powell-Wiley, TM
   Hoehner, C
   Ayers, C
   Berrigan, D
   Agyemang, P
   Das, S
   Ballard-Barbash, R
   Leonard, T
AF Powell-Wiley, Tiffany M.
   Hoehner, Christine
   Ayers, Colby
   Berrigan, David
   Agyemang, Priscilla
   Das, Sandeep
   Ballard-Barbash, Rachel
   Leonard, Tammy
TI Moving to a Neighborhood of Higher Socioeconomic Deprivation Predicts
   Weight Gain in a Multi-Ethnic Population: Longitudinal Data From the
   Dallas Heart Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Obesity; Longitudinal studies; Disparities; Prevention
C1 [Powell-Wiley, Tiffany M.] NHLBI, NIH, Silver Spring, MD USA.
   [Hoehner, Christine] St Louis Univ, St Louis, MO 63103 USA.
   [Ayers, Colby] Univ Southwestern Med Cntr, Dallas, TX USA.
   [Berrigan, David; Ballard-Barbash, Rachel] NCI, NIH, Bethesda, MD 20892 USA.
   [Agyemang, Priscilla] NHLBI, NIH, Bethesda, MD 20892 USA.
   [Das, Sandeep] Univ Texas Southwestern Med Cntr, Dallas, TX USA.
   [Leonard, Tammy] Univ Texas Dallas, Richardson, TX 75083 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 14109
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162903448
ER

PT J
AU Probstfield, JL
   Boden, WE
   McBride, R
   Desvigne-Nickens, P
   Fleg, J
   Anderson, T
   Kashyap, M
AF Probstfield, Jeffrey L.
   Boden, William E.
   McBride, Ruth
   Desvigne-Nickens, Patrice
   Fleg, Jerome
   Anderson, Todd
   Kashyap, Moti
TI Comparison of Extended-Release Niacin versus Placebo in Statin-Treated
   Patients With Low Baseline Levels of HDL-C and Well-Controlled
   on-Treatment LDL-C: Extended One-Year Follow-Up Outcomes From AIM-HIGH
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Clinical trials; Lipids
C1 [Probstfield, Jeffrey L.] Univ Washington, Seattle, WA 98195 USA.
   [Boden, William E.] Samuel S Stratton VA Med Cntr, Albany, NY USA.
   [McBride, Ruth] Axio Rsch LLC, AIM HIGH Coordinating Cntr, Seattle, WA USA.
   [Desvigne-Nickens, Patrice] NHLBI, Cardiovasc Med Grp, NIH, Bethesda, MD 20892 USA.
   [Fleg, Jerome] NHLBI, NIH, Bethesda, MD 20892 USA.
   [Anderson, Todd] Foothills Med Cntr, Calgary, AB, Canada.
   [Kashyap, Moti] Long Beach VA Med Cntr, Long Beach, VA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 15068
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162904381
ER

PT J
AU Raiszadeh, F
   Bartz, T
   Zieman, SJ
   Mukamal, KJ
   Ix, JH
   Djousse, L
   Siscovick, D
   Tracy, RP
   Heckbert, SR
   Newman, AB
   Hussein, A
   Gottdiener, JS
   Kizer, JR
AF Raiszadeh, Farbod
   Bartz, Traci
   Zieman, Susan J.
   Mukamal, Kenneth J.
   Ix, Joachim H.
   Djousse, Luc
   Siscovick, David
   Tracy, Russell P.
   Heckbert, Susan R.
   Newman, Anne B.
   Hussein, Ayman
   Gottdiener, John S.
   Kizer, Jorge R.
TI Advanced Glycation Endproduct Carboxymethyl-Lysine (CML) and Risk of
   Atrial Fibrillation in Older Adults
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
C1 [Raiszadeh, Farbod; Kizer, Jorge R.] Montefiore Einstein Heart Cntr, Bronx, NY USA.
   [Bartz, Traci] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
   [Zieman, Susan J.] NIA, Div Geriatr & Clin Gerontol, Bethesda, MD 20892 USA.
   [Mukamal, Kenneth J.] Harvard Univ, Sch Med, Div Gen Med & Primary Care, Boston, MA USA.
   [Ix, Joachim H.] Univ Calif San Diego, Div Prevent Med, San Diego, CA 92103 USA.
   [Djousse, Luc] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
   [Siscovick, David; Heckbert, Susan R.] Univ Washington, Cardiovasc Hlth Rsch Unit, Seattle, WA 98195 USA.
   [Tracy, Russell P.] Univ Vermont, Dept Pathol, Colchester, VT USA.
   [Tracy, Russell P.] Univ Vermont, Dept Biochem, Colchester, VT USA.
   [Newman, Anne B.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
   [Hussein, Ayman] Univ Maryland, Med Cntr, Baltimore, MD 21201 USA.
   [Gottdiener, John S.] Univ Maryland Hosp, Baltimore, MD 21201 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 13849
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162903326
ER

PT J
AU Shamburek, RD
   Freeman, L
   Sampson, M
   Bakker-Arkema, R
   Krause, B
   Auerbach, B
   Homan, R
   Shamburek, A
   Schwartz, C
   Amar, M
   Remaley, A
AF Shamburek, Robert D.
   Freeman, Lita
   Sampson, Maureen
   Bakker-Arkema, Rebecca
   Krause, Brian
   Auerbach, Bruce
   Homan, Ryan
   Shamburek, Alexandra
   Schwartz, Charles
   Amar, Marcelo
   Remaley, Alan
TI Human Enzyme Replacement Therapy in a Patient With Familial Lecithin
   Cholesterol Acyltransferase Deficiency: Rapid Appearance of Normal
   Appearing HDL
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE HDL; HDL elevating therapies; Lipids; Lipoproteins; Metabolism
C1 [Shamburek, Robert D.; Freeman, Lita; Sampson, Maureen; Shamburek, Alexandra; Amar, Marcelo; Remaley, Alan] NHLBI, NIH, Bethesda, MD 20892 USA.
   [Bakker-Arkema, Rebecca; Krause, Brian; Auerbach, Bruce; Homan, Ryan] AlphaCore Pharma, Rsch, Ann Arbor, MI USA.
   [Schwartz, Charles] Virginia Commonwealth Univ, Richmond, VA USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 18673
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162907493
ER

PT J
AU Soetkamp, D
   Nguyen, TT
   Menazza, S
   Hirschhauser, C
   Boengler, K
   Aponte, A
   Gucek, M
   Murphy, E
   Schulz, R
AF Soetkamp, Daniel
   Nguyen, Tiffany T.
   Menazza, Sara
   Hirschhaeuser, Christine
   Boengler, Kerstin
   Aponte, Angel
   Gucek, Marjan
   Murphy, Elizabeth
   Schulz, Rainer
TI S-Nitrosylation of Mitochondrial Connexin 43: A possible Mechanism
   Mediating Ischemic Preconditioning in Rat Hearts
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Cardioprotection; Ischemia reperfusion; Mitochondria; Connexin; Nitric
   oxide
C1 [Soetkamp, Daniel; Hirschhaeuser, Christine; Boengler, Kerstin; Schulz, Rainer] Univ Giessen, Dept Med, D-35390 Giessen, Germany.
   [Nguyen, Tiffany T.; Menazza, Sara; Murphy, Elizabeth] NHLBI, NIH, Bethesda, MD 20892 USA.
   [Aponte, Angel; Gucek, Marjan] NHLBI, Prote Core Facil, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 13050
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162902497
ER

PT J
AU Tereshchenko, LG
   Rizzi, P
   Mewton, N
   Jardim, GV
   Murthy, S
   Strauss, D
   Liu, CY
   Marchlinski, F
   Spooner, P
   Berger, R
   Kellman, P
   Lima, J
AF Tereshchenko, Larisa G.
   Rizzi, Patricia
   Mewton, Nathan
   Jardim, Gustavo Volpe
   Murthy, Sindhoora
   Strauss, David
   Liu, Chia-Yiang
   Marchlinski, Francis
   Spooner, Peter
   Berger, Ronald
   Kellman, Peter
   Lima, Joao
TI Infiltrated Atrial Fat Characterizes Underlying Atrial Fibrillation
   Substrate in Patients at Risk
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Cardiac MRI; Atrial fibrillation
C1 [Tereshchenko, Larisa G.; Rizzi, Patricia; Mewton, Nathan; Jardim, Gustavo Volpe; Liu, Chia-Yiang; Spooner, Peter; Berger, Ronald; Lima, Joao] Johns Hopkins Univ Som, Baltimore, MD USA.
   [Murthy, Sindhoora] Johns Hopkins Univ, Baltimore, MD USA.
   [Strauss, David] US FDA, Silver Spring, MD USA.
   [Marchlinski, Francis] Hosp Univ Penn, Philadelphia, PA 19104 USA.
   [Kellman, Peter] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 12402
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162902224
ER

PT J
AU Valente, AJ
   Siva, SVPS
   Siddesha, JM
   Yoshida, T
   Siebenlist, UU
   Chandrasekar, B
AF Valente, Anthony J.
   Siva, Sakamuri S. V. P.
   Siddesha, Jalahalli M.
   Yoshida, Tadashi
   Siebenlist, Ulrich Ulrich
   Chandrasekar, Bysani
TI Silencing TRAF3IP2 by a Modified 27-mer siRNA Attenuates
   Pressure-Overload Induced Myocardial Hypertrophy and Fibrosis
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Hypertrophy; Fibrosis; Heart failure; Inflammation; Collagen
C1 [Valente, Anthony J.] Univ Texas HSC, San Antonio, TX USA.
   [Siva, Sakamuri S. V. P.; Siddesha, Jalahalli M.; Yoshida, Tadashi; Chandrasekar, Bysani] Tulane Univ, Sch Med, Inst Heart & Vasc, New Orleans, LA 70112 USA.
   [Siebenlist, Ulrich Ulrich] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 14663
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162904169
ER

PT J
AU Vargas, JD
   Manichaikul, A
   Rich, SS
   Rotter, JI
   Post, WS
   Pollack, JF
   Bluemke, DA
AF Vargas, Jose D.
   Manichaikul, Ani
   Rich, Stephen S.
   Rotter, Jerome I.
   Post, Wendy S.
   Pollack, Joseph F.
   Bluemke, David A.
TI Common Genetic Variants and Subclinical Atherosclerosis in the
   Multi-Ethnic Study of Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Subclinical atherosclerosis; Genetics; Genomics; Calcification
C1 [Vargas, Jose D.; Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
   [Manichaikul, Ani] Cntr Publ Hlth Genom, Dept Publ Hlth Sci, Div Biostat & Epidemiol, Charlottesville, VA USA.
   [Rich, Stephen S.] Cntr Publ Hlth Genom, Off Chair, Charlottesville, VA USA.
   [Rotter, Jerome I.] Med Genet Rsch Inst, Div Med Genet, Los Angeles, CA USA.
   [Post, Wendy S.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
   [Pollack, Joseph F.] Tufts Univ, Sch Med, Boston, MA 02111 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 18346
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162907331
ER

PT J
AU Vinogradova, TM
   Lakatta, EG
AF Vinogradova, Tatiana M.
   Lakatta, Edward G.
TI PKCd, but not PKCa, Regulates Spontaneous Firing of the Cardiac
   Pacemaker
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Sinoatrial node; Calcium; Protein kinase C; Cell signaling
C1 [Vinogradova, Tatiana M.; Lakatta, Edward G.] NIA, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 14120
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162903457
ER

PT J
AU Wang, SN
   Zhou, YF
   Andreyev, O
   Hoyt, R
   Hunt, T
   Horvath, KA
AF Wang, Suna
   Zhou, Yifu
   Andreyev, Oleg
   Hoyt, Robert
   Hunt, Timothy
   Horvath, Keith A.
TI Overexpression of FABP(3) Inhibits Human Bone Marrow Derived Mesenchymal
   Stem Cell Proliferation but Enhances Their Survival in Hypoxia
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Hypoxia; Gene expression; Stem cells; Ischemic heart disease
C1 [Wang, Suna] NHLBI, Cadiothorac Surg Rsch Program, NIH, Bethesda, MD 20892 USA.
   [Zhou, Yifu; Andreyev, Oleg; Hoyt, Robert; Hunt, Timothy; Horvath, Keith A.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 13
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162900014
ER

PT J
AU Weisfeldt, ML
   Brown, S
   Sanchez, B
   Aufderheide, T
   Christenson, J
   Daya, M
   Gaudio, M
   Kudenchuk, P
   Marquis, S
   Rea, T
   Sims, K
   Vaillancourt, C
   Wittwer, L
   Sopko, G
   Ornato, J
   Morrison, L
AF Weisfeldt, Myron L.
   Brown, Siobhan
   Sanchez, Brittany
   Aufderheide, Tom
   Christenson, Jim
   Daya, Mohamud
   Gaudio, Michelle
   Kudenchuk, Peter
   Marquis, Sean
   Rea, Thomas
   Sims, Katy
   Vaillancourt, Christian
   Wittwer, Lynn
   Sopko, George
   Ornato, Joseph
   Morrison, Laurie
CA ROC Investigators
TI Assessment of Arrest Procedures, Hospital Care and Functional Survival
   of Initial VT/VF Arrest Patients Shocked by a Bystander AED vs Patients
   Shocked by EMS
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Cardiopulmonary resuscitation
C1 [Weisfeldt, Myron L.] Johns Hopkins Sch Med, Baltimore, MD USA.
   [Brown, Siobhan; Sanchez, Brittany; Kudenchuk, Peter; Rea, Thomas; Sims, Katy] Univ Washington, Seattle, WA 98195 USA.
   [Aufderheide, Tom; Marquis, Sean] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
   [Christenson, Jim] Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
   [Daya, Mohamud; Wittwer, Lynn] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
   [Gaudio, Michelle; Morrison, Laurie] St Michaels Hosp, Toronto, ON M5B 1W8, Canada.
   [Vaillancourt, Christian] Ottawa Hosp Rsch Inst, Ottawa, ON, Canada.
   [Sopko, George] NHLBI, Bethesda, MD 20892 USA.
   [Ornato, Joseph] Virginia Commonwealth Univ Hlth Syst, Richmond, VA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 313
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162900254
ER

PT J
AU Wong, TC
   Piehler, KM
   Zareba, KM
   Lin, K
   Phrampus, A
   Patel, A
   Moon, JC
   Ugander, M
   Valeti, U
   Fu, B
   Chang, CC
   Mathier, M
   Kellman, P
   Butler, J
   Gheorghiade, M
   Schelbert, EB
AF Wong, Timothy C.
   Piehler, Kayla M.
   Zareba, Karolina M.
   Lin, Kathie
   Phrampus, Ashley
   Patel, Agam
   Moon, James C.
   Ugander, Martin
   Valeti, Uma
   Fu, Bo
   Chang, Chung-Chou
   Mathier, Michael
   Kellman, Peter
   Butler, Javed
   Gheorghiade, Mihai
   Schelbert, Erik B.
TI Myocardial Damage Detected by Late Gadolinium Enhancement Cardiovascular
   Magnetic Resonance is Associated With Incident Hospitalization for Heart
   Failure
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Cardiac MRI; Outcomes; Heart failure; Fibrosis
C1 [Wong, Timothy C.; Piehler, Kayla M.; Zareba, Karolina M.; Lin, Kathie; Phrampus, Ashley; Patel, Agam; Mathier, Michael; Schelbert, Erik B.] Univ Pittsburgh, Sch Med, Dept Med, Div Cardiol, Pittsburgh, PA 15213 USA.
   [Moon, James C.] UCL, Heart Hosp, Imaging Cntr, London, England.
   [Ugander, Martin] Karolinska Univ, Dept Clin Physiol, Stockholm, Sweden.
   [Valeti, Uma] Univ Minnesota, Div Cardiol, Minneapolis, MN USA.
   [Fu, Bo] Univ Pittsburgh, Pittsburgh, PA USA.
   [Chang, Chung-Chou] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA USA.
   [Kellman, Peter] NHLBI, Cardiac Energet Lab, Pittsburgh, PA USA.
   [Butler, Javed] Emory Univ, Sch Med, Div Cardiol, Dept Med, Atlanta, GA 30322 USA.
   [Gheorghiade, Mihai] Northwestern Univ, Dept Med, Div Cardiol, Feinberg Sch Med, Chicago, IL 60611 USA.
RI Zareba, Karolina/E-5049-2015; FU, BO/J-4063-2015
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 16511
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162906023
ER

PT J
AU Xie, A
   Liu, H
   Wang, QY
   Gu, LZ
   Liu, M
   Rutledge, C
   Li, J
   Vanden Hoek, TL
   Boheler, KR
   Dudley, SC
AF Xie, An
   Liu, Hong
   Wang, Qiongyin
   Gu, Lianzhi
   Liu, Man
   Rutledge, Cody
   Li, Jing
   Vanden Hoek, Terry L.
   Boheler, Kenneth R.
   Dudley, Samuel C.
TI Mitochondria Calcium Flux Plays an Important Role in Triggered Activity
   in Cardiomyocytes With Reduced Sarcoplasmic Reticulum Calcium Release
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Calcium; Mitochondria; Triggering mechanisms
C1 [Xie, An; Liu, Hong; Wang, Qiongyin; Gu, Lianzhi; Liu, Man; Rutledge, Cody; Li, Jing; Vanden Hoek, Terry L.; Dudley, Samuel C.] Univ Illinois, Chicago, IL USA.
   [Boheler, Kenneth R.] NIA, Mol Cardiol & Stem Cell Unit, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 15491
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162905032
ER

PT J
AU Yang, E
   Liu, ST
   Turkbey, E
   Ho, C
   Bluemke, DA
AF Yang, Eunice
   Liu, Songtao
   Turkbey, Evrim
   Ho, Carolyn
   Bluemke, David A.
TI Detection of Preclinical Hypertrophic Cardiomyopathy Mutations With
   Advanced Imaging: The Hypertrophic Cardiomyopathy Network (HCMNet) Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Cardiovascular imaging; Genetics; Hypertrophic cardiomyopathy; Diastolic
   function; Fibrosis
C1 [Yang, Eunice] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
   [Liu, Songtao; Turkbey, Evrim; Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
   [Ho, Carolyn] Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 12350
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162902203
ER

PT J
AU Yingchoncharoen, T
   Negishi, T
   Negishi, K
   Popovic, ZB
   Gai, N
   Tang, WH
   Flamm, SD
   Kwon, DH
AF Yingchoncharoen, Teerapat
   Negishi, Tomoko
   Negishi, Kazuaki
   Popovic, Zoran B.
   Gai, Neville
   Tang, W. H.
   Flamm, Scott D.
   Kwon, Deborah H.
TI Focal Fibrosis and Diffuse Fibrosis Are Predictors of Positive Left
   Ventricular Remodeling in Patients With Non-Ischemic Cardiomyopathy
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Ventricular remodeling; Cardiac MRI; Cardiomyopathy; Fibrosis; Follow-up
   studies
C1 [Yingchoncharoen, Teerapat; Negishi, Tomoko; Negishi, Kazuaki; Popovic, Zoran B.; Tang, W. H.; Flamm, Scott D.; Kwon, Deborah H.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
   [Gai, Neville] NIH, Clin Cntr, Bethesda, MD 20892 USA.
RI Negishi, Kazuaki/J-7242-2014
OI Negishi, Kazuaki/0000-0002-9086-2565
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 18189
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162907260
ER

PT J
AU Yousuf, O
   Beinart, R
   Khurram, IM
   Liu, ST
   Bluemke, DA
   DeWire, J
   Zimmerman, S
   Calkins, H
   Nazarian, S
AF Yousuf, Omair
   Beinart, Roy
   Khurram, Irfan M.
   Liu, Songtao
   Bluemke, David A.
   DeWire, Jane
   Zimmerman, Stefan
   Calkins, Hugh
   Nazarian, Saman
TI Cardiac Magnetic Resonance T1 Mapping Identifies Diffuse Ventricular
   Fibrosis in Patients With Atrial Fibrillation Undergoing First and
   Repeat Catheter Ablation
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Atrial fbrillation; Catheter abiaton; Magnetic resonance imaging
C1 [Yousuf, Omair; Beinart, Roy; Khurram, Irfan M.; DeWire, Jane; Zimmerman, Stefan; Calkins, Hugh; Nazarian, Saman] Johns Hopkins Univ, Baltimore, MD USA.
   [Liu, Songtao; Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 18458
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162907381
ER

PT J
AU Zhang, XL
   Wakabayashi, Y
   Hwang, SJ
   Yang, YQ
   Johnson, AD
   Zhu, J
   O'Donnell, CJ
AF Zhang, Xiaoling
   Wakabayashi, Yoshiyuki
   Hwang, Shih-Jen
   Yang, Yanqin
   Johnson, Andrew D.
   Zhu, Jun
   O'Donnell, Christopher J.
TI Characterizing the Human Coronary Aorta Vascular Endothelial Cell
   Transcriptome With RNA Sequencing
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions and Resuscitation Science Symposium of the
   American-Heart-Association
CY NOV 16-17, 2013
CL Dallas, TX
SP Amer Heart Assoc
DE Endothelial function; Genomics; Gene expression; Aorta; Cardiovascular
   disease
C1 [Zhang, Xiaoling; Hwang, Shih-Jen; Johnson, Andrew D.; O'Donnell, Christopher J.] NHLBIs Framingham Heart Study, Div Intramural Rsch, Framingham, MA USA.
   [Wakabayashi, Yoshiyuki; Yang, Yanqin; Zhu, Jun] NHLBI, DNA Sequencing & Genom Core, Bethesda, MD 20892 USA.
RI Johnson, Andrew/G-6520-2013
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 26
PY 2013
VL 128
IS 22
SU S
MA 17754
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AC0CR
UT WOS:000332162907055
ER

PT J
AU Miao, HX
   Chen, L
   Bennett, EE
   Adamo, NM
   Gomella, AA
   DeLuca, AM
   Patel, A
   Morgan, NY
   Wen, H
AF Miao, Houxun
   Chen, Lei
   Bennett, Eric E.
   Adamo, Nick M.
   Gomella, Andrew A.
   DeLuca, Alexa M.
   Patel, Ajay
   Morgan, Nicole Y.
   Wen, Han
TI Motionless phase stepping in X-ray phase contrast imaging with a compact
   source
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE radiography; CT; retrospective phase stepping; X-ray diffraction;
   tomosynthesis
ID FOURIER-TRANSFORM METHOD; GRATING INTERFEROMETER; SYNCHROTRON-RADIATION;
   TOMOGRAPHY
AB X-ray phase contrast imaging offers a way to visualize the internal structures of an object without the need to deposit significant radiation, and thereby alleviate the main concern in X-ray diagnostic imaging procedures today. Grating-based differential phase contrast imaging techniques are compatible with compact X-ray sources, which is a key requirement for the majority of clinical X-ray modalities. However, these methods are substantially limited by the need for mechanical phase stepping. We describe an electromagnetic phase-stepping method that eliminates mechanical motion, thus removing the constraints in speed, accuracy, and flexibility. The method is broadly applicable to both projection and tomography imaging modes. The transition from mechanical to electromagnetic scanning should greatly facilitate the translation of X-ray phase contrast techniques into mainstream applications.
C1 [Miao, Houxun; Bennett, Eric E.; Adamo, Nick M.; Gomella, Andrew A.; DeLuca, Alexa M.; Patel, Ajay; Wen, Han] NHLBI, Imaging Phys Lab, Biochem & Biophys Ctr, NIH, Bethesda, MD 20892 USA.
   [Chen, Lei] NIST, Ctr Nanoscale Sci & Technol, Gaithersburg, MD 20899 USA.
   [Morgan, Nicole Y.] Natl Inst Biomed Imaging & Bioengn, Microfabricat & Microfluid Unit, Biomed Engn & Phys Sci Shared Resource, NIH, Bethesda, MD 20892 USA.
RP Wen, H (reprint author), NHLBI, Imaging Phys Lab, Biochem & Biophys Ctr, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM han.wen@nih.gov
RI Miao, Houxun/N-8233-2013; Wen, Han/G-3081-2010
OI Wen, Han/0000-0001-6844-2997
FU National Institutes of Health; National Heart, Lung, and Blood
   Institute; National Institute of Biomedical Imaging and Bioengineering
FX We are grateful to the staff of the Nanofab Facility of National
   Institute of Standards and Technology for assistance with fabrication of
   the phase grating, and to Prof. Marco Stampanoni of Paul Scherrer
   Institute for helpful discussion on the fusion of phase and intensity
   images. This work was supported by the Intramural Research Program of
   the National Institutes of Health, including the National Heart, Lung,
   and Blood Institute and the National Institute of Biomedical Imaging and
   Bioengineering.
NR 38
TC 13
Z9 13
U1 0
U2 13
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 NOV 26
PY 2013
VL 110
IS 48
BP 19268
EP 19272
DI 10.1073/pnas.1311053110
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 257NB
UT WOS:000327390400043
PM 24218599
ER

PT J
AU Zhou, BR
   Feng, HQ
   Kato, H
   Dai, L
   Yang, YD
   Zhou, YQ
   Bai, YW
AF Zhou, Bing-Rui
   Feng, Hanqiao
   Kato, Hidenori
   Dai, Liang
   Yang, Yuedong
   Zhou, Yaoqi
   Bai, Yawen
TI Structural insights into the histone H1-nucleosome complex
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
ID CHROMATIN IN-VIVO; C-TERMINAL DOMAIN; LINKER-HISTONE; GLOBULAR DOMAIN;
   CRYSTAL-STRUCTURE; DNA INTERACTIONS; GENE-EXPRESSION; CORE PARTICLE;
   NUCLEOSOME; BINDING
AB Linker H1 histones facilitate formation of higher-order chromatin structures and play important roles in various cell functions. Despite several decades of effort, the structural basis of how H1 interacts with the nucleosome remains elusive. Here, we investigated Drosophila H1 in complex with the nucleosome, using solution nuclear magnetic resonance spectroscopy and other biophysical methods. We found that the globular domain of H1 bridges the nucleosome core and one 10-base pair linker DNA asymmetrically, with its alpha 3 helix facing the nucleosomal DNA near the dyad axis. Two short regions in the C-terminal tail of H1 and the C-terminal tail of one of the two H2A histones are also involved in the formation of the H1-nucleosome complex. Our results lead to a residue-specific structural model for the globular domain of the Drosophila H1 in complex with the nucleosome, which is different from all previous experiment-based models and has implications for chromatin dynamics in vivo.
C1 [Zhou, Bing-Rui; Feng, Hanqiao; Kato, Hidenori; Bai, Yawen] NCI, Lab Biochem & Mol Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Dai, Liang; Yang, Yuedong; Zhou, Yaoqi] Indiana Univ Purdue Univ, Sch Informat, Indianapolis, IN 46202 USA.
   [Dai, Liang; Yang, Yuedong; Zhou, Yaoqi] Indiana Univ Purdue Univ, Ctr Computat Biol & Bioinformat, Indiana Univ Sch Med, Indianapolis, IN 46202 USA.
RP Bai, YW (reprint author), NCI, Lab Biochem & Mol Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM yawen@helix.nih.gov
RI Dai, Liang/G-9680-2011; Zhou, Yaoqi/B-3284-2009; Yang, Yuedong
   /C-9394-2009
OI Dai, Liang/0000-0002-4672-6283; Zhou, Yaoqi/0000-0002-9958-5699; Yang,
   Yuedong /0000-0002-6782-2813
FU National Cancer Institute; National Institutes of Health (NIH); National
   Institute of General Medical Sciences of the NIH [R01GM085003]
FX We thank Dr. Jemima Barrowman for editing the manuscript. This work is
   supported by the intramural research program of National Cancer
   Institute and National Institutes of Health (NIH) (to Y.B.) and by the
   National Institute of General Medical Sciences of the NIH (R01GM085003,
   to Y.Z.).
NR 57
TC 52
Z9 56
U1 2
U2 20
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 NOV 26
PY 2013
VL 110
IS 48
BP 19390
EP 19395
DI 10.1073/pnas.1314905110
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 257NB
UT WOS:000327390400064
PM 24218562
ER

PT J
AU Kuschal, C
   DiGiovanna, JJ
   Khan, SG
   Gatti, RA
   Kraemer, KH
AF Kuschal, Christiane
   DiGiovanna, John. J.
   Khan, Sikandar G.
   Gatti, Richard A.
   Kraemer, Kenneth H.
TI Repair of UV photolesions in xeroderma pigmentosum group C cells induced
   by translational readthrough of premature termination codons
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE readthrough compounds; UV radiation
ID INDUCED DNA-DAMAGE; SINGLE-NUCLEOTIDE POLYMORPHISM; MESSENGER-RNA
   LEVELS; NONSENSE MUTATIONS; CYSTIC-FIBROSIS; READ-THROUGH; STOP CODON;
   ATM GENE; AMINOGLYCOSIDES; PROTEIN
AB About 12% of human genetic disorders involve premature termination codons (PTCs). Aminoglycoside antibiotics have been proposed for restoring full-length proteins by readthrough of PTC. To assess the efficiency of readthrough, we selected homozygous and compound heterozygous skin fibroblasts from xeroderma pigmentosum (XP) patients with different PTCs in the XPC DNA repair gene. XP patients have a nucleotide excision repair defect and a 10,000-fold increased risk of UV-induced skin cancer. In six of eight PTC-containing XP-C cells, treatment with Geneticin and gentamicin resulted in (i) stabilized XPC-mRNA, which would have been degraded by nonsense-mediated decay; (ii) increased expression of XPC protein that localized to UV-damaged sites; (iii) recruitment of XPB and XPD proteins to UV DNA damage sites; and (iv) increased repair of 6-4 photoproducts and cyclobutane pyrimidine dimers. Expression of PTC in a transfected vector revealed that readthrough depends on the PTC sequence and its location within the gene. This sensitive DNA repair assay system demonstrates the complexity of response to PTC readthrough inducers. The efficiency of aminoglycoside-mediated readthrough depends on the type and copy number of PTC, the downstream 4+ nucleotide, and the location within the exon. Treatment with small-molecule nonaminoglycoside compounds (PTC124, BZ16, or RTC14) resulted in similarly increased XPC mRNA expression and photoproduct removal with less toxicity than with the aminoglycosides. Characterizing PTC structure and parameters governing effective PTC readthrough may provide a unique prophylactic therapy for skin cancer prevention in XP-C patients.
C1 [Kuschal, Christiane; DiGiovanna, John. J.; Khan, Sikandar G.; Kraemer, Kenneth H.] NCI, Dermatol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Gatti, Richard A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA.
RP Kraemer, KH (reprint author), NCI, Dermatol Branch, Ctr Canc Res, Bldg 10, Bethesda, MD 20892 USA.
EM kraemerk@nih.gov
OI Kuschal, Christiane/0000-0001-6113-3585
FU Intramural Research Program of the Center for Cancer Research, National
   Cancer Institute, National Institutes of Health (NIH) [NS05528]
FX This research was supported by the Intramural Research Program of the
   Center for Cancer Research, National Cancer Institute, National
   Institutes of Health (NIH) (to C. K., J. J. D., S. G. K., and K. H. K.)
   and NIH R01 Grant NS05528 (to R. A. G.).
NR 44
TC 19
Z9 20
U1 0
U2 9
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 NOV 26
PY 2013
VL 110
IS 48
BP 19483
EP 19488
DI 10.1073/pnas.1312088110
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 257NB
UT WOS:000327390400080
PM 24218596
ER

PT J
AU Mitchell, RM
   Janssen, MJ
   Karavanova, I
   Vullhorst, D
   Furth, K
   Makusky, A
   Markey, SP
   Buonanno, A
AF Mitchell, Robert M.
   Janssen, Megan J.
   Karavanova, Irina
   Vullhorst, Detlef
   Furth, Katrina
   Makusky, Anthony
   Markey, Sanford P.
   Buonanno, Andres
TI ErbB4 reduces synaptic GABA(A) currents independent of its receptor
   tyrosine kinase activity
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE PKC; schizophrenia; hippocampus; parvalbumin; mIPSCs
ID HIPPOCAMPAL INTERNEURONS; ALPHA-1 SUBUNIT; INHIBITORY SYNAPSES;
   NERVOUS-SYSTEM; MICE LACKING; NEUREGULIN RECEPTOR; DYNAMIC MODULATION;
   PREFRONTAL CORTEX; MOUSE MODEL; SCHIZOPHRENIA
AB ErbB4 signaling in the central nervous system is implicated in neuropsychiatric disorders and epilepsy. In cortical tissue, ErbB4 associates with excitatory synapses located on inhibitory interneurons. However, biochemical and histological data described herein demonstrate that the vast majority of ErbB4 is extrasynaptic and detergent-soluble. To explore the function of this receptor population, we used unbiased proteomics, in combination with electrophysiological, biochemical, and cell biological techniques, to identify a clinically relevant ErbB4-interacting protein, the GABA(A) receptor alpha 1 subunit (GABAR alpha 1). We show that ErbB4 and GABAR alpha 1 are robustly coexpressed in hippocampal interneurons, and that ErbB4-null mice have diminished cortical GABAR alpha 1 expression. Moreover, we characterize a Neuregulin-mediated ErbB4 signaling modality, independent of receptor tyrosine kinase activity, that couples ErbB4 to decreased postsynaptic GABAR currents on inhibitory interneurons. Consistent with an evolving understanding of GABAR trafficking, this pathway requires both clathrin-mediated endocytosis and protein kinase C to reduce GABAR inhibitory currents, surface GABAR alpha 1 expression, and colocalization with the inhibitory postsynaptic protein gephyrin. Our results reveal a function of ErbB4, independent of its tyrosine kinase activity, that modulates postsynaptic inhibitory control of hippocampal interneurons and may provide a novel pharmacological target in the treatment of neuropsychiatric disorders and epilepsy.
C1 [Mitchell, Robert M.; Janssen, Megan J.; Karavanova, Irina; Vullhorst, Detlef; Furth, Katrina; Buonanno, Andres] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Mol Neurobiol, Bethesda, MD 20892 USA.
   [Furth, Katrina] Boston Univ, Grad Program Neurosci, Boston, MA 02215 USA.
   [Makusky, Anthony; Markey, Sanford P.] NIMH, Lab Neurotoxicol, Bethesda, MD 20892 USA.
RP Buonanno, A (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Mol Neurobiol, Bethesda, MD 20892 USA.
EM buonanno@mail.nih.gov
FU NICHD; NIMH Intramural Research Programs
FX We thank Dr. Carolyn Smith from the National Institute of Neurological
   Disorders and Stroke microscopy core facilities for expert assistance
   with confocal microscopy and Volocity software. We also thank Dr.
   Jean-Marc Fritschy for providing GABA<INF>A</INF> receptor alpha 1 and
   alpha 5 sub-unit-specific polyclonal antibodies. We are grateful to
   Daniel Abebe for expert assistance with rodent husbandry, Dr. Jody
   Martin for adeno-associated virus production, Dr. Swagata Roychowdhury
   for assistance with electrophysiological recordings, and Mr. Christopher
   R. Parrino for assistance with immunocytochemical experiments. This work
   was kindly supported by the NICHD and NIMH Intramural Research Programs.
NR 62
TC 7
Z9 7
U1 0
U2 10
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 NOV 26
PY 2013
VL 110
IS 48
BP 19603
EP 19608
DI 10.1073/pnas.1312791110
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 257NB
UT WOS:000327390400100
PM 24218551
ER

PT J
AU Jakobsen, MR
   Bak, RO
   Andersen, A
   Berg, RK
   Jensen, SB
   Jin, TC
   Laustsen, A
   Hansen, K
   Ostergaard, L
   Fitzgerald, KA
   Xiao, TS
   Mikkelsen, JG
   Mogensen, TH
   Paludan, SR
AF Jakobsen, Martin R.
   Bak, Rasmus O.
   Andersen, Annika
   Berg, Randi K.
   Jensen, Soren B.
   Jin, Tengchuan
   Laustsen, Anders
   Hansen, Kathrine
   Ostergaard, Lars
   Fitzgerald, Katherine A.
   Xiao, T. Sam
   Mikkelsen, Jacob G.
   Mogensen, Trine H.
   Paludan, Soren R.
TI IFI16 senses DNA forms of the lentiviral replication cycle and controls
   HIV-1 replication
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
ID DOUBLE-STRANDED-RNA; PLASMACYTOID DENDRITIC CELLS; INNATE IMMUNE
   RECOGNITION; IMMUNODEFICIENCY-VIRUS TYPE-1; GMP-AMP SYNTHASE; RIG-I
   HELICASE; CYTOSOLIC DNA; INTRACELLULAR DNA; HUMAN MACROPHAGES; ANTIVIRAL
   RESPONSES
AB Replication of lentiviruses generates different DNA forms, including RNA: DNA hybrids, ssDNA, and dsDNA. Nucleic acids stimulate innate immune responses, and pattern recognition receptors detecting dsDNA have been identified. However, sensors for ssDNA have not been reported, and the ability of RNA: DNA hybrids to stimulate innate immune responses is controversial. Using ssDNAs derived from HIV-1 proviral DNA, we report that this DNA form potently induces the expression of IFNs in primary human macrophages. This response was stimulated by stem regions in the DNA structure and was dependent on IFN-inducible protein 16 (IFI16), which bound immunostimulatory DNA directly and activated the stimulator of IFN genes -TANK-binding kinase 1 - IFN regulatory factors 3/7 (STING-TBK1-IRF3/7) pathway. Importantly, IFI16 colocalized and associated with lentiviral DNA in the cytoplasm in macrophages, and IFI16 knockdown in this cell type augmented lentiviral transduction and also HIV-1 replication. Thus, IFI16 is a sensor for DNA forms produced during the lentiviral replication cycle and regulates HIV-1 replication in macrophages.
C1 [Jakobsen, Martin R.; Bak, Rasmus O.; Andersen, Annika; Jensen, Soren B.; Laustsen, Anders; Hansen, Kathrine; Mikkelsen, Jacob G.; Mogensen, Trine H.; Paludan, Soren R.] Aarhus Univ, Dept Biomed, DK-8000 Aarhus C, Denmark.
   [Jakobsen, Martin R.; Berg, Randi K.; Laustsen, Anders; Hansen, Kathrine; Mikkelsen, Jacob G.; Mogensen, Trine H.; Paludan, Soren R.] Aarhus Univ, Aarhus Res Ctr Innate Immunol, DK-8000 Aarhus C, Denmark.
   [Berg, Randi K.; Ostergaard, Lars] Aarhus Univ, Dept Infect Dis, Hosp Skejby, Hosp Skejby, DK-8200 Aarhus, Denmark.
   [Jensen, Soren B.; Fitzgerald, Katherine A.] Univ Massachusetts, Div Infect Dis & Immunol, Dept Med, Sch Med, Worcester, MA 01655 USA.
   [Jin, Tengchuan; Xiao, T. Sam] NIAID, Lab Immunol, NIH, Bethesda, MD 20892 USA.
RP Jakobsen, MR (reprint author), Aarhus Univ, Dept Biomed, DK-8000 Aarhus C, Denmark.
EM mrj@immunology.au.dk; srp@microbiology.au.dk
RI Jin, Tengchuan/B-5883-2014; Xiao, Tsan/A-8590-2010; 
OI Jin, Tengchuan/0000-0002-1395-188X; Bak, Rasmus/0000-0002-7383-0297;
   Xiao, Tsan/0000-0001-9688-475X; Mikkelsen, Jacob
   Giehm/0000-0002-1322-3209
FU Danish Medical Research Council Research [09-072636, 11-114457,
   271-08-0864]; Sapere aude [10-081986]; Lundbeck Foundation [R83-A7598,
   R34-3855]; Kathrine og Vigo Skovgaards Fond; Novo Nordisk Foundation;
   Aase og Ejnar Danielsens Fond; Aarhus University Research Foundation;
   Division of Intramural Research, National Institute of Allergy and
   Infectious Diseases, National Institutes of Health
FX We thank Kirsten S. Petersen for technical support. This work was
   supported by Danish Medical Research Council Research Grants 09-072636
   (to S.R.P.), 11-114457 (to M.R.J.), and 271-08-0864 (to T.H.M.); by
   Sapere aude Grant 10-081986 (to M.R.J.); by Grants R83-A7598 and
   R34-3855 from the Lundbeck Foundation; and by the Kathrine og Vigo
   Skovgaards Fond, the Novo Nordisk Foundation, the Aase og Ejnar
   Danielsens Fond, and the Aarhus University Research Foundation. R.K.B.,
   R.O.B., and S.B.J. are recipients of PhD fellowships from the Faculty of
   Health Sciences, Aarhus University. T.S.X. is supported by the Division
   of Intramural Research, National Institute of Allergy and Infectious
   Diseases, National Institutes of Health.
NR 64
TC 98
Z9 98
U1 5
U2 13
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 NOV 26
PY 2013
VL 110
IS 48
BP E4571
EP E4580
DI 10.1073/pnas.1311669110
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 257NB
UT WOS:000327390400010
PM 24154727
ER

PT J
AU Krestinina, LY
   Davis, FG
   Schonfeld, S
   Preston, DL
   Degteva, M
   Epifanova, S
   Akleyev, AV
AF Krestinina, L. Y.
   Davis, F. G.
   Schonfeld, S.
   Preston, D. L.
   Degteva, M.
   Epifanova, S.
   Akleyev, A. V.
TI Leukaemia incidence in the Techa River Cohort: 1953-2007
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE leukaemia; ionising radiation; environmental exposure; cohort;
   strontium; haematological malignancies
ID MAYAK-PRODUCTION-ASSOCIATION; DOSE RECONSTRUCTION SYSTEM;
   RADIATION-EXPOSURE; CANCER-MORTALITY; RISK; POPULATION; WORKERS
AB Background: Little is known about leukaemia risk following chronic radiation exposures at low dose rates. The Techa River Cohort of individuals residing in riverside villages between 1950 and 1961 when releases from the Mayak plutonium production complex contaminated the river allows quantification of leukaemia risks associated with chronic low-dose-rate internal and external exposures.
   Methods: Excess relative risk models described the dose-response relationship between radiation dose on the basis of updated dose estimates and the incidence of haematological malignancies ascertained between 1953 and 2007 among 28 223 cohort members, adjusted for attained age, sex, and other factors.
   Results: Almost half of the 72 leukaemia cases (excluding chronic lymphocytic leukaemia (CLL)) were estimated to be associated with radiation exposure. These data are consistent with a linear dose response with no evidence of modification. The excess relative risk estimate was 0.22 per 100 mGy. There was no evidence of significant dose effect for CLL or other haematopoietic malignancies.
   Conclusion: These analyses demonstrate that radiation exposures, similar to those received by populations exposed as a consequence of nuclear accidents, are associated with long-term dose-related increases in leukaemia risks. Using updated dose estimates, the leukaemia risk per unit dose is about half of that based on previous dosimetry.
C1 [Krestinina, L. Y.; Degteva, M.; Epifanova, S.; Akleyev, A. V.] Urals Res Ctr Radiat Med, Epidemiol Lab, Chelyabinsk 454076, Russia.
   [Davis, F. G.] Univ Illinois, Sch Publ Hlth, Div Epidemiol Biostat, Chicago, IL 60612 USA.
   [Schonfeld, S.] Int Agcy Res Canc, Sect Environm & Radiat, F-69372 Lyon 08, France.
   [Schonfeld, S.] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Preston, D. L.] Hirosoft Int Co, Eureka, CA 95501 USA.
RP Davis, FG (reprint author), Univ Illinois, Sch Publ Hlth, Div Epidemiol Biostat, 1603 West Taylor St, Chicago, IL 60612 USA.
EM faith.davis@ualberta.ca
FU US Department of Energy, Office of Domestic and International Health
   Studies, Office of Health, Safety and Security; Russian Health Studies
   Program at the URCRM; UIC [DE-FC02-07HS0701]; National Cancer Institute,
   National Institutes of Health [HHSN261200900089C]; The Federal
   Department of the Russian Ministry of Health
FX The study is based on the work conducted by the URCRM researchers for
   over five decades involving collecting, storing, and processing
   information and clinical results in patients with haematological
   diseases. Our appreciation is extended to the following departments,
   directors, and their staff: the Regional Center of the National
   Radiation-Epidemiology Registry directed by NV Startsev, the
   Epidemiology Laboratory initially directed by MM Kossenko and currently
   directed by L Yu Krestinina, and the Biophysics Laboratory directed by
   MO Degteva, the Clinical inpatient department initially managed by Dr VI
   Kiryushkin, and later by Dr MM Kossenko. We are grateful for the close
   collaborations of the Oncology Dispensaries of Chelyabinsk and Kurgan
   Oblasts. We would like to express our gratitude to our late colleague
   and friend Elaine Ron (NCI) for the guidance and assistance she provided
   to us during the many years of our collaborative work. We are grateful
   to all colleagues who have contributed to the development and
   continuation of our international projects, including Mr Barrett Fountos
   (DOE) and Dr Martha Linet (NCI). We appreciate the thoughtful comments
   from the manuscript reviewers. This project is funded by the US
   Department of Energy, Office of Domestic and International Health
   Studies, Office of Health, Safety and Security, Russian Health Studies
   Program at the URCRM and UIC (DE-FC02-07HS0701) with scientific review
   by the Joint Coordinating Committee for Radiation Effects Research (a
   bilateral government committee representing agencies from the United
   States and the Russian Federation). This project incorporates data
   collected under the Intramural Research Program of the National Cancer
   Institute, National Institutes of Health (HHSN261200900089C). The
   Federal Department of the Russian Ministry of Health has provided
   support for all aspects of this study.
NR 35
TC 17
Z9 19
U1 2
U2 8
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 NOV 26
PY 2013
VL 109
IS 11
BP 2886
EP 2893
DI 10.1038/bjc.2013.614
PG 8
WC Oncology
SC Oncology
GA 262UG
UT WOS:000327762700018
PM 24129230
ER

PT J
AU Wang, JC
   Spiegel, N
   Bertelsen, S
   Le, N
   McKenna, N
   Budde, JP
   Harari, O
   Kapoor, M
   Brooks, A
   Hancock, D
   Tischfield, J
   Foroud, T
   Bierut, LJ
   Steinbach, JH
   Edenberg, HJ
   Traynor, BJ
   Goate, AM
AF Wang, Jen-Chyong
   Spiegel, Noah
   Bertelsen, Sarah
   Nhung Le
   McKenna, Nicholas
   Budde, John P.
   Harari, Oscar
   Kapoor, Manav
   Brooks, Andrew
   Hancock, Dana
   Tischfield, Jay
   Foroud, Tatiana
   Bierut, Laura J.
   Steinbach, Joe Henry
   Edenberg, Howard J.
   Traynor, Bryan J.
   Goate, Alison M.
TI Cis-Regulatory Variants Affect CHRNA5 mRNA Expression in Populations of
   African and European Ancestry
SO PLOS ONE
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; NICOTINE DEPENDENCE; LUNG-CANCER; SUBSTANCE
   DEPENDENCE; SUSCEPTIBILITY LOCUS; RECEPTOR GENES; RISK; TISSUE; SNPS;
   ADENOCARCINOMA
AB Variants within the gene cluster encoding alpha 3, alpha 5, and beta 4 nicotinic receptor subunits are major risk factors for substance dependence. The strongest impact on risk is associated with variation in the CHRNA5 gene, where at least two mechanisms are at work: amino acid variation and altered mRNA expression levels. The risk allele of the non-synonymous variant (rs16969968; D398N) primarily occurs on the haplotype containing the low mRNA expression allele. In populations of European ancestry, there are approximately 50 highly correlated variants in the CHRNA5-CHRNA3-CHRNB4 gene cluster and the adjacent PSMA4 gene region that are associated with CHRNA5 mRNA levels. It is not clear which of these variants contribute to the changes in CHRNA5 transcript level. Because populations of African ancestry have reduced linkage disequilibrium among variants spanning this gene cluster, eQTL mapping in subjects of African ancestry could potentially aid in defining the functional variants that affect CHRNA5 mRNA levels. We performed quantitative allele specific gene expression using frontal cortices derived from 49 subjects of African ancestry and 111 subjects of European ancestry. This method measures allele-specific transcript levels in the same individual, which eliminates other biological variation that occurs when comparing expression levels between different samples. This analysis confirmed that substance dependence associated variants have a direct cis-regulatory effect on CHRNA5 transcript levels in human frontal cortices of African and European ancestry and identified 10 highly correlated variants, located in a 9 kb region, that are potential functional variants modifying CHRNA5 mRNA expression levels.
C1 [Wang, Jen-Chyong; Spiegel, Noah; Bertelsen, Sarah; Nhung Le; McKenna, Nicholas; Budde, John P.; Harari, Oscar; Kapoor, Manav; Bierut, Laura J.; Goate, Alison M.] Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA.
   [Brooks, Andrew; Tischfield, Jay] Rutgers State Univ, Dept Genet, Piscataway, NJ USA.
   [Hancock, Dana] Res Triangle Inst, Dept Behav Hlth Epidemiol, Res Triangle Pk, NC 27709 USA.
   [Foroud, Tatiana; Edenberg, Howard J.] Indiana Univ Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA.
   [Steinbach, Joe Henry] Washington Univ, Sch Med, Dept Anesthesiol, St Louis, MO 63110 USA.
   [Edenberg, Howard J.] Indiana Univ Sch Med, Dept Biochem & Mol Biol, Indianapolis, IN 46202 USA.
   [Traynor, Bryan J.] NIA, Neuromuscular Dis Res Unit, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
   [Goate, Alison M.] Washington Univ, Sch Med, Dept Genet, St Louis, MO 63110 USA.
   [Goate, Alison M.] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA.
RP Goate, AM (reprint author), Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA.
EM goate@wustl.edu
RI Traynor, Bryan/G-5690-2010; 
OI Tischfield, Jay/0000-0003-3217-8287; Hancock, Dana/0000-0003-2240-3604;
   Edenberg, Howard/0000-0003-0344-9690
FU National Institute on Aging [P50 AG05681]; University of Sydney;
   National Health and Medical Research Council of Australia; Schizophrenia
   Research Institute; National Institute of Alcohol Abuse and Alcoholism;
   National Institute on Aging, National Institutes of Health;
   Collaborative Study on the Genetics of Alcoholism (COGA); National
   Institute on Alcohol Abuse and Alcoholism (NIH) [U10AA008401];
   Collaborative Study on the Genetics of Nicotine Dependence; NCI (NIH)
   [P01 CA89392]
FX ADRC is supported by grants from the National Institute on Aging P50
   AG05681. ABDP is supported by the University of Sydney, National Health
   and Medical Research Council of Australia, Schizophrenia Research
   Institute, and the National Institute of Alcohol Abuse and Alcoholism.
   NICHD is supported by the Intramural Research Program of the National
   Institute on Aging, National Institutes of Health. This study was
   supported in part by the Collaborative Study on the Genetics of
   Alcoholism (COGA) funded by the National Institute on Alcohol Abuse and
   Alcoholism (NIH Grant U10AA008401) and the Collaborative Study on the
   Genetics of Nicotine Dependence funded by NCI (NIH grant P01 CA89392).
   The funders had no role in study design, data collection and analysis,
   decision to publish, or preparation of the manuscript.
NR 37
TC 6
Z9 6
U1 1
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 26
PY 2013
VL 8
IS 11
AR e80204
DI 10.1371/journal.pone.0080204
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 259SK
UT WOS:000327546400017
ER

PT J
AU Wang, TG
   Choi, E
   Monaco, MCG
   Campanac, E
   Medynets, M
   Do, T
   Rao, P
   Johnson, KR
   Elkahloun, AG
   Von Geldern, G
   Johnson, T
   Subramaniam, S
   Hoffman, D
   Major, E
   Nath, A
AF Wang, Tongguang
   Choi, Elliot
   Monaco, Maria Chiara G.
   Campanac, Emilie
   Medynets, Marie
   Thao Do
   Rao, Prashant
   Johnson, Kory R.
   Elkahloun, Abdel G.
   Von Geldern, Gloria
   Johnson, Tory
   Subramaniam, Sriram
   Hoffman, Dax
   Major, Eugene
   Nath, Avindra
TI Derivation of Neural Stem Cells from Human Adult Peripheral CD34+Cells
   for an Autologous Model of Neuroinflammation
SO PLOS ONE
LA English
DT Article
ID HUMAN BONE-MARROW; MULTIPLE-SCLEROSIS; PRECURSOR CELLS; CORD BLOOD;
   IN-VITRO; DIRECT CONVERSION; ADIPOSE-TISSUE; SCHWANN-CELLS; IPS CELLS;
   T-CELLS
AB Proinflammatory factors from activated T cells inhibit neurogenesis in adult animal brain and cultured human fetal neural stem cells (NSC). However, the role of inhibition of neurogenesis in human neuroinflammatory diseases is still uncertain because of the difficulty in obtaining adult NSC from patients. Recent developments in cell reprogramming suggest that NSC may be derived directly from adult fibroblasts. We generated NSC from adult human peripheral CD34+ cells by transfecting the cells with Sendai virus constructs containing Sox2, Oct3/4, c-Myc and Klf4. The derived NSC could be differentiated to glial cells and action potential firing neurons. Co-culturing NSC with activated autologous T cells or treatment with recombinant granzyme B caused inhibition of neurogenesis as indicated by decreased NSC proliferation and neuronal differentiation. Thus, we have established a unique autologous in vitro model to study the pathophysiology of neuroinflammatory diseases that has potential for usage in personalized medicine.
C1 [Wang, Tongguang; Choi, Elliot; Medynets, Marie] NINDS, Translat Neurosci Ctr, NIH, Bethesda, MD 20892 USA.
   [Choi, Elliot; Von Geldern, Gloria; Johnson, Tory; Nath, Avindra] NINDS, Sect Infect Nervous Syst, NIH, Bethesda, MD 20892 USA.
   [Monaco, Maria Chiara G.; Major, Eugene] NINDS, Lab Mol Med & Neurosci, NIH, Bethesda, MD 20892 USA.
   [Campanac, Emilie; Hoffman, Dax] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Mol Neurophysiol & Biophys Unit, NIH, Bethesda, MD USA.
   [Thao Do; Rao, Prashant; Subramaniam, Sriram] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Johnson, Tory] NINDS, Bioinformat Sect, NIH, Bethesda, MD 20892 USA.
   [Elkahloun, Abdel G.] NHGRI, Canc Genet Branch, Bethesda, MD 20892 USA.
RP Wang, TG (reprint author), NINDS, Translat Neurosci Ctr, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM david.wang@nih.gov
RI Hoffman, Dax/E-5155-2011
OI Hoffman, Dax/0000-0001-6999-2157
FU NIH
FX This study was supported by intramural funds from NIH. The funders had
   no role in study design, data collection and analysis, decision to
   publish, or preparation of the manuscript.
NR 64
TC 10
Z9 10
U1 1
U2 11
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 26
PY 2013
VL 8
IS 11
AR e81720
DI 10.1371/journal.pone.0081720
PG 18
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 259SK
UT WOS:000327546400082
PM 24303066
ER

PT J
AU Schmidt, AM
   Zou, T
   Joshi, RP
   Leichner, TM
   Pimentel, MA
   Sommers, CL
   Kambayashi, T
AF Schmidt, Amanda M.
   Zou, Tao
   Joshi, Rohan P.
   Leichner, Theresa M.
   Pimentel, Matthew A.
   Sommers, Connie L.
   Kambayashi, Taku
TI Diacylglycerol Kinase zeta Limits the Generation of Natural Regulatory T
   Cells
SO SCIENCE SIGNALING
LA English
DT Article
ID ALPHA-CHAIN GENE; KAPPA-B FAMILY; C-REL; FOXP3 EXPRESSION; TRANSCRIPTION
   FACTOR; NEGATIVE SELECTION; IMMUNE TOLERANCE; SELF-TOLERANCE; IN-VIVO;
   RECEPTOR
AB Natural regulatory T (nT(reg)) cells are important for maintaining tolerance to self-and foreign antigens, and they are thought to develop from thymocytes that receive strong T cell receptor (TCR)-mediated signals in the thymus. TCR engagement leads to the activation of phospholipase C-gamma 1, which generates the lipid second messenger diacylglycerol (DAG) from phosphatidylinositol 4,5-bisphosphate. We used mice that lack the zeta isoform of DAG kinase (DGK zeta), which metabolizes DAG to terminate its signaling, to enhance TCR-mediated signaling and identify critical signaling events in nT(reg) cell development. Loss of DGK zeta resulted in increased numbers of thymic CD25(+)Foxp3(-)CD4(+)nT(reg) cell precursors and Foxp3(+)CD4(+)nT(reg) cells in a cell-autonomous manner. DGK zeta-deficient T cells exhibited increased nuclear translocation of the nuclear factor kappa B subunit c-Rel, as well as enhanced extracellular signal-regulated kinase (ERK) phosphorylation in response to TCR stimulation, suggesting that these downstream pathways may contribute to nT(reg) cell development. Indeed, reducing c-Rel abundance or blocking ERK phosphorylation abrogated the increased generation of nT(reg) cells by DGK zeta-deficient thymocytes. The extent of ERK phosphorylation correlated with TCR-mediated acquisition of Foxp3 in immature thymocytes in vitro. Furthermore, the development of nT(reg) cells was augmented in mice in which ERK activation was selectively enhanced in T cells. Together, these data suggest that DGK zeta regulates the development of nT(reg) cells by limiting the extent of activation of the ERK and c-Rel signaling pathways.
C1 [Schmidt, Amanda M.; Zou, Tao; Leichner, Theresa M.; Kambayashi, Taku] Univ Penn, Dept Pathol & Lab Med, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Joshi, Rohan P.; Pimentel, Matthew A.] Univ Penn, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA.
   [Sommers, Connie L.] NCI, Cellular & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Kambayashi, T (reprint author), Univ Penn, Dept Pathol & Lab Med, Perelman Sch Med, Philadelphia, PA 19104 USA.
EM taku.kambayashi@uphs.upenn.edu
FU National Blood Foundation; University of Pennsylvania; American Heart
   Association; NIH [R01HL111501, R01HL107589]; Center for Cancer
   Research/National Cancer Institute/NIH
FX This work was supported by grants from the National Blood Foundation,
   the University of Pennsylvania internal funds, the American Heart
   Association, the NIH (R01HL111501 and R01HL107589), and the Intramural
   Research Program of the Center for Cancer Research/National Cancer
   Institute/NIH.
NR 68
TC 9
Z9 10
U1 0
U2 2
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1945-0877
EI 1937-9145
J9 SCI SIGNAL
JI Sci. Signal.
PD NOV 26
PY 2013
VL 6
IS 303
AR ra101
DI 10.1126/scisignal.2004411
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 262JF
UT WOS:000327730000001
PM 24280042
ER

PT J
AU Hwang, WC
   Bakolitsa, C
   Punta, M
   Coggill, PC
   Bateman, A
   Axelrod, HL
   Rawlings, ND
   Sedova, M
   Peterson, SN
   Eberhardt, RY
   Aravind, L
   Pascual, J
   Godzik, A
AF Hwang, William C.
   Bakolitsa, Constantina
   Punta, Marco
   Coggill, Penelope C.
   Bateman, Alex
   Axelrod, Herbert L.
   Rawlings, Neil D.
   Sedova, Mayya
   Peterson, Scott N.
   Eberhardt, Ruth Y.
   Aravind, L.
   Pascual, Jaime
   Godzik, Adam
TI LUD, a new protein domain associated with lactate utilization
SO BMC BIOINFORMATICS
LA English
DT Article
DE LUD; DUF162; LutB; LutC; Domain of unknown function; Deinococcus
   radiodurans
ID GLUCOSAMINE-6-PHOSPHATE DEAMINASE; DEINOCOCCUS-RADIODURANS; FAMILIES
   DATABASE; SEQUENCE; CONSERVATION; MUTAGENESIS; GENOME; STATE; 3D
AB Background: A novel highly conserved protein domain, DUF162 [Pfam: PF02589], can be mapped to two proteins: LutB and LutC. Both proteins are encoded by a highly conserved LutABC operon, which has been implicated in lactate utilization in bacteria. Based on our analysis of its sequence, structure, and recent experimental evidence reported by other groups, we hereby redefine DUF162 as the LUD domain family.
   Results: JCSG solved the first crystal structure [PDB:2G40] from the LUD domain family: LutC protein, encoded by ORF DR_1909, of Deinococcus radiodurans. LutC shares features with domains in the functionally diverse ISOCOT superfamily. We have observed that the LUD domain has an increased abundance in the human gut microbiome.
   Conclusions: We propose a model for the substrate and cofactor binding and regulation in LUD domain. The significance of LUD-containing proteins in the human gut microbiome, and the implication of lactate metabolism in the radiation-resistance of Deinococcus radiodurans are discussed.
C1 [Hwang, William C.; Axelrod, Herbert L.; Sedova, Mayya; Godzik, Adam] Joint Ctr Struct Genom, La Jolla, CA 92037 USA.
   [Hwang, William C.; Bakolitsa, Constantina; Sedova, Mayya; Peterson, Scott N.; Godzik, Adam] Sanford Burnham Med Res Inst, La Jolla, CA 92037 USA.
   [Punta, Marco; Coggill, Penelope C.; Bateman, Alex; Rawlings, Neil D.; Eberhardt, Ruth Y.] Wellcome Trust Sanger Inst, Hinxton CB10 1SA, Cambs, England.
   [Bateman, Alex; Eberhardt, Ruth Y.] European Bioinformat Inst, European Mol Biol Lab, Hinxton CB10 1SD, Cambs, England.
   [Axelrod, Herbert L.] SLAC Natl Accelerator Lab, Stanford Synchrotron Radiat Lightsource, Menlo Pk, CA 94025 USA.
   [Aravind, L.] NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
   [Pascual, Jaime] Scripps Res Inst, Dept Mol & Expt Med, La Jolla, CA 92037 USA.
   [Godzik, Adam] Univ Calif San Diego, Ctr Res Biol Syst, La Jolla, CA 92093 USA.
   [Godzik, Adam] King Abdulaziz Univ, Ctr Excellence Genom Med Res, Jeddah 21589, Saudi Arabia.
RP Hwang, WC (reprint author), Joint Ctr Struct Genom, La Jolla, CA 92037 USA.
EM wchwang@sanfordburnham.org; adam@sanfordburnham.org
RI Godzik, Adam/A-7279-2009; Sedova, Mayya/L-5528-2016; Rawlings,
   Neil/M-5566-2013; 
OI Godzik, Adam/0000-0002-2425-852X; Sedova, Mayya/0000-0002-1121-2661;
   Rawlings, Neil/0000-0001-5557-7665; Bateman, Alex/0000-0002-6982-4660
FU Wellcome Trust [WT077044/Z/05/Z]; DOE Office of Biological and
   Environmental Research; National Institutes of Health, National
   Institute of General Medical Sciences [P41GM103393]; National Institutes
   of Health from the NIGMS Protein Structure Initiative [U54 GM094586]
FX Wellcome Trust (grant numbers WT077044/Z/05/Z); Funding for open access
   charge: Wellcome Trust (grant numbers WT077044/Z/05/Z); Portions of this
   research were carried out at the Stanford Synchrotron Radiation
   Lightsource, a Directorate of SLAC National Accelerator Laboratory and
   an Office of Science User Facility operated for the U. S. Department of
   Energy Office of Science by Stanford University. The SSRL Structural
   Molecular Biology Program is supported by the DOE Office of Biological
   and Environmental Research, and by the National Institutes of Health,
   National Institute of General Medical Sciences (including P41GM103393).
   The contents of this publication are solely the responsibility of the
   authors and do not necessarily represent the official views of NIGMS,
   NCRR or NIH. This work was supported in part by National Institutes of
   Health Grant U54 GM094586 from the NIGMS Protein Structure Initiative to
   the Joint Center for Structural Genomics.
NR 36
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PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2105
J9 BMC BIOINFORMATICS
JI BMC Bioinformatics
PD NOV 26
PY 2013
VL 14
AR 341
DI 10.1186/1471-2105-14-341
PG 9
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
   Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Mathematical & Computational Biology
GA 259ND
UT WOS:000327532700001
PM 24274019
ER

PT J
AU Jena, AB
   Sun, EC
   Prasad, V
AF Jena, Anupam B.
   Sun, Eric C.
   Prasad, Vinay
TI Firearm Legislation and Gun-Related Fatalities
SO JAMA INTERNAL MEDICINE
LA English
DT Letter
C1 [Jena, Anupam B.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
   [Sun, Eric C.] Stanford Univ Hosp, Dept Anesthesia, Stanford, CA 94305 USA.
   [Prasad, Vinay] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Jena, AB (reprint author), Harvard Univ, Sch Med, Dept Hlth Care Policy, 180 Longwood Ave, Boston, MA 02115 USA.
EM jena@hcp.med.harvard.edu
NR 2
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U1 1
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6106
EI 2168-6114
J9 JAMA INTERN MED
JI JAMA Intern. Med.
PD NOV 25
PY 2013
VL 173
IS 21
DI 10.1001/jamainternmed.2013.9958
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA AA2WG
UT WOS:000330954300017
ER

PT J
AU Reardon, BJ
   Hansen, JG
   Crystal, RG
   Houston, DK
   Kritchevsky, SB
   Harris, T
   Lohman, K
   Liu, YM
   O'Connor, GT
   Wilk, JB
   Mezey, J
   Gao, C
   Cassano, PA
AF Reardon, Brian J.
   Hansen, Joyanna G.
   Crystal, Ronald G.
   Houston, Denise K.
   Kritchevsky, Stephen B.
   Harris, Tamara
   Lohman, Kurt
   Liu, Yongmei
   O'Connor, George T.
   Wilk, Jemma B.
   Mezey, Jason
   Gao, Chuan
   Cassano, Patricia A.
TI Vitamin D-responsive SGPP2 variants associated with lung cell expression
   and lung function
SO BMC MEDICAL GENETICS
LA English
DT Article
DE Vitamin D; Airflow obstruction; FEV1; SGPP2; FEV1/FVC
ID OBSTRUCTIVE PULMONARY-DISEASE; GENOME-WIDE ASSOCIATION; GENE-EXPRESSION;
   D-RECEPTOR; COPD; HYPERRESPONSIVENESS; EXACERBATIONS; MECHANISMS;
   HEALTH; COHORT
AB Background: Vitamin D is associated with lung health in epidemiologic studies, but mechanisms mediating observed associations are poorly understood. This study explores mechanisms for an effect of vitamin D in lung through an in vivo gene expression study, an expression quantitative trait loci (eQTL) analysis in lung tissue, and a population-based cohort study of sequence variants.
   Methods: Microarray analysis investigated the association of gene expression in small airway epithelial cells with serum 25(OH) D in adult non-smokers. Sequence variants in candidate genes identified by the microarray were investigated in a lung tissue eQTL database, and also in relation to cross-sectional pulmonary function in the Health, Aging, and Body Composition (Health ABC) study, stratified by race, with replication in the Framingham Heart Study (FHS).
   Results: 13 candidate genes had significant differences in expression by serum 25(OH) D (nominal p < 0.05), and a genome-wide significant eQTL association was detected for SGPP2. In Health ABC, SGPP2 SNPs were associated with FEV1 in both European-and African-Americans, and the gene-level association was replicated in European-American FHS participants. SNPs in 5 additional candidate genes (DAPK1, FSTL1, KAL1, KCNS3, and RSAD2) were associated with FEV1 in Health ABC participants.
   Conclusions: SGPP2, a sphingosine-1-phosphate phosphatase, is a novel vitamin D-responsive gene associated with lung function. The identified associations will need to be followed up in further studies.
C1 [Reardon, Brian J.; Hansen, Joyanna G.; Cassano, Patricia A.] Cornell Univ, Div Nutr Sci, Ithaca, NY 14853 USA.
   [Crystal, Ronald G.] Weill Cornell Med Coll, Dept Med Genet, New York, NY USA.
   [Houston, Denise K.; Kritchevsky, Stephen B.] Wake Forest Sch Med, Sticht Ctr Aging, Winston Salem, NC 27157 USA.
   [Harris, Tamara] NIA, Intramural Res Program, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
   [Lohman, Kurt] Wake Forest Sch Med, Dept Biostat Sci, Div Publ Hlth Sci, Winston Salem, NC 27157 USA.
   [Liu, Yongmei] Wake Forest Sch Med, Dept Epidemiol & Prevent, Div Publ Hlth Sci, Winston Salem, NC 27157 USA.
   [O'Connor, George T.] Boston Univ, Sch Med, Dept Med, Sect Pulm Allergy & Crit Care Med, Boston, MA 02118 USA.
   [O'Connor, George T.; Wilk, Jemma B.] NHLBI, Framingham Heart Study, Framingham, MA USA.
   [Wilk, Jemma B.] Brigham & Womens Hosp, Dept Med, Div Aging, Boston, MA 02115 USA.
   [Wilk, Jemma B.] Harvard Univ, Sch Med, Boston, MA USA.
   [Mezey, Jason; Gao, Chuan] Cornell Univ, Ithaca, NY 14853 USA.
   [Mezey, Jason] Weill Cornell Med Coll, Dept Med Genet, New York, NY USA.
   [Cassano, Patricia A.] Weill Cornell Med Coll, Div Biostat & Epidemiol, Dept Publ Hlth, New York, NY USA.
RP Cassano, PA (reprint author), Cornell Univ, Div Nutr Sci, 209 Savage Hall, Ithaca, NY 14853 USA.
EM pac6@cornell.edu
FU National Institutes of Health, National Heart Lung and Blood Institute
   [R03 HL095414, P50 HL084936]; NRSA Institutional Research Training Grant
   [T32-DK-7158-36]; NIA [N01AG62101, N01AG62103, N01AG62106,
   R01-AG032098-01A1]; Ashken Foundation; National Institutes of Health
   [HHSN268200782096C]; Intramural Research Program of the NIH, National
   Institute on Aging; Framingham Heart Study of the NHLBI of the NIH;
   Boston University School of Medicine; NHLBI's Framingham Heart Study
   [N01-HC-25195]; Affymetrix, Inc [N02-HL-6-4278]; Robert Dawson Evans
   Endowment of the Department of Medicine at Boston University School of
   Medicine; Boston Medical Center;  [RC1-AG035835];  [R01-AG029364]
FX This research was supported by National Institutes of Health, National
   Heart Lung and Blood Institute R03 HL095414 (PAC) and P50 HL084936
   (RGC), by RC1-AG035835 (SK, PI; PAC, PI subcontract), and by NRSA
   Institutional Research Training Grant T32-DK-7158-36 (JGH). This
   research also was supported by R01-AG029364, by NIA contracts
   N01AG62101, N01AG62103, and N01AG62106, and by the Ashken Foundation
   (RGC). The genome-wide association study was funded by NIA grant
   R01-AG032098-01A1 to Wake Forest University Health Sciences and
   genotyping services were provided by the Center for Inherited Disease
   Research (CIDR). CIDR is fully funded through a federal contract from
   the National Institutes of Health to The Johns Hopkins University,
   contract number HHSN268200782096C. This research was supported in part
   by the Intramural Research Program of the NIH, National Institute on
   Aging. Research was conducted in part using data and resources from the
   Framingham Heart Study of the NHLBI of the NIH and Boston University
   School of Medicine. The analyses reflect intellectual input and resource
   development from the Framingham investigators participating in the SNP
   Health Association Resource (SHARe) project. This work was partially
   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). A portion of this research
   utilized the Linux Cluster for Genetic Analysis (LinGA-II) funded by the
   Robert Dawson Evans Endowment of the Department of Medicine at Boston
   University School of Medicine and Boston Medical Center.
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PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2350
J9 BMC MED GENET
JI BMC Med. Genet.
PD NOV 25
PY 2013
VL 14
AR 122
DI 10.1186/1471-2350-14-122
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 273AT
UT WOS:000328505700002
PM 24274704
ER

PT J
AU Adamson, SW
   Browning, RE
   Budachetri, K
   Ribeiro, JMC
   Karim, S
AF Adamson, Steven W.
   Browning, Rebecca E.
   Budachetri, Khemraj
   Ribeiro, Jose M. C.
   Karim, Shahid
TI Knockdown of Selenocysteine-Specific Elongation Factor in Amblyomma
   maculatum Alters the Pathogen Burden of Rickettsia parkeri with
   Epigenetic Control by the Sin3 Histone Deacetylase Corepressor Complex
SO PLOS ONE
LA English
DT Article
ID RETICULUM-ASSOCIATED DEGRADATION; METHIONINE SULFOXIDE REDUCTASE;
   PROSTATE-CANCER CELLS; GULF-COAST TICKS; SELENOPROTEIN SYNTHESIS;
   UNITED-STATES; BORRELIA-BURGDORFERI; ANAPLASMA-MARGINALE; ANTIOXIDANT
   SYSTEM; IXODES-SCAPULARIS
AB Selenocysteine is the 21st naturally-occurring amino acid. Selenoproteins have diverse functions and many remain uncharacterized, but they are typically associated with antioxidant activity. The incorporation of selenocysteine into the nascent polypeptide chain recodes the TGA stop codon and this process depends upon a number of essential factors including the selenocysteine elongation factor (SEF). The transcriptional expression of SEF did not change significantly in tick midguts throughout the blood meal, but decreased in salivary glands to 20% at the end of the fast feeding phase. Since selenoprotein translation requires this specialized elongation factor, we targeted this gene for knockdown by RNAi to gain a global view of the role selenoproteins play in tick physiology. We found no significant differences in tick engorgement and embryogenesis but detected no antioxidant capacity in tick saliva. The transcriptional profile of selenoproteins in R. parkeri-infected Amblyomma maculatum revealed declined activity of selenoprotein M and catalase and increased activity of selenoprotein O, selenoprotein S, and selenoprotein T. Furthermore, the pathogen burden was significantly altered in SEF-knockdowns. We then determined the global impact of SEF-knockdown by RNA-seq, and mapped huge shifts in secretory gene expression that could be the result of downregulation of the Sin3 histone deacetylase corepressor complex.
C1 [Adamson, Steven W.; Browning, Rebecca E.; Budachetri, Khemraj; Karim, Shahid] Univ So Mississippi, Dept Biol Sci, Hattiesburg, MS 39406 USA.
   [Ribeiro, Jose M. C.] NIAID, NIH, Vector Biol Sect, Lab Malaria & Vector Res, Bethesda, MD 20892 USA.
RP Karim, S (reprint author), Univ So Mississippi, Dept Biol Sci, Hattiesburg, MS 39406 USA.
EM shahid.karim@usm.edu
RI Ribeiro, Jose/J-7011-2015; Budachetri, Khemraj/B-8959-2017; 
OI Budachetri, Khemraj/0000-0003-1254-792X; Ribeiro,
   Jose/0000-0002-9107-0818
FU National Institute of Allergy and Infectious Diseases [AI099919]; United
   States Department of State [PGAP21049]; Intramural Research Program of
   the Division of Intramural Research, National Institute of Allergy and
   Infectious Diseases; National Institutes of Health National Institute of
   General Medical Sciences [P20RR016476]
FX Funding provided by National Institute of Allergy and Infectious
   Diseases award #AI099919, United States Department of State award
   #PGAP21049 (Pakistan-United States Science and Technology Cooperation
   Program) to SK. The Intramural Research Program of the Division of
   Intramural Research, National Institute of Allergy and Infectious
   Diseases, to JMCR and the National Institutes of Health National
   Institute of General Medical Sciences award #P20RR016476 to the MS-INBRE
   core facility. The funders had no role in study design, data collection
   and analysis, decision to publish, or preparation of the manuscript.
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U2 13
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 25
PY 2013
VL 8
IS 11
AR UNSP e82012
DI 10.1371/journal.pone.0082012
PG 19
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 259RH
UT WOS:000327543500125
PM 24282621
ER

PT J
AU Crous-Bou, M
   Rennert, G
   Cuadras, D
   Salazar, R
   Cordero, D
   Rennert, HS
   Lejbkowicz, F
   Kopelovich, L
   Lipkin, SM
   Gruber, SB
   Moreno, V
AF Crous-Bou, Marta
   Rennert, Gad
   Cuadras, Daniel
   Salazar, Ramon
   Cordero, David
   Rennert, Hedy Saltz
   Lejbkowicz, Flavio
   Kopelovich, Levy
   Lipkin, Steven Monroe
   Gruber, Stephen Bernard
   Moreno, Victor
TI Polymorphisms in Alcohol Metabolism Genes ADH1B and ALDH2, Alcohol
   Consumption and Colorectal Cancer
SO PLOS ONE
LA English
DT Article
ID DEHYDROGENASE POLYMORPHISMS; LIVER-DISEASE; RISK; ACETALDEHYDE;
   METAANALYSIS; SMOKING; ASSOCIATION; POPULATION; NUTRITION; STATINS
AB Background: Colorectal cancer (CRC) is a leading cause of cancer death worldwide. Epidemiological risk factors for CRC included alcohol intake, which is mainly metabolized to acetaldehyde by alcohol dehydrogenase and further oxidized to acetate by aldehyde dehydrogenase; consequently, the role of genes in the alcohol metabolism pathways is of particular interest. The aim of this study is to analyze the association between SNPs in ADH1B and ALDH2 genes and CRC risk, and also the main effect of alcohol consumption on CRC risk in the study population.
   Methodology/Principal Findings: SNPs from ADH1B and ALDH2 genes, included in alcohol metabolism pathway, were genotyped in 1694 CRC cases and 1851 matched controls from the Molecular Epidemiology of Colorectal Cancer study. Information on clinicopathological characteristics, lifestyle and dietary habits were also obtained. Logistic regression and association analysis were conducted. A positive association between alcohol consumption and CRC risk was observed in male participants from the Molecular Epidemiology of Colorectal Cancer study (MECC) study (OR = 1.47; 95% CI = 1.18-1.81). Moreover, the SNPs rs1229984 in ADH1B gene was found to be associated with CRC risk: under the recessive model, the OR was 1.75 for A/A genotype (95%CI = 1.21-2.52; p-value = 0.0025). A path analysis based on structural equation modeling showed a direct effect of ADH1B gene polymorphisms on colorectal carcinogenesis and also an indirect effect mediated through alcohol consumption.
   Conclusions/Significance: Genetic polymorphisms in the alcohol metabolism pathways have a potential role in colorectal carcinogenesis, probably due to the differences in the ethanol metabolism and acetaldehyde oxidation of these enzyme variants.
C1 [Crous-Bou, Marta; Cordero, David; Moreno, Victor] Catalan Inst Oncol, Canc Prevent & Control Program, Barcelona, Spain.
   [Crous-Bou, Marta; Cuadras, Daniel; Salazar, Ramon; Cordero, David; Moreno, Victor] Bellvitge Biomed Res Inst, Colorectal Canc Grp, Barcelona, Spain.
   [Crous-Bou, Marta; Cuadras, Daniel; Salazar, Ramon; Cordero, David; Moreno, Victor] Consorcio Invest Biomed Epidemiol & Salud Publ CI, Barcelona, Spain.
   [Rennert, Gad; Rennert, Hedy Saltz; Lejbkowicz, Flavio] Technion Israel Inst Technol, Dept Community Med & Epidemiol, Natl Canc Control Ctr, Clalit Hlth Serv, Haifa, Israel.
   [Rennert, Gad; Rennert, Hedy Saltz; Lejbkowicz, Flavio] Technion Israel Inst Technol, Med Carmel Med Ctr, B Rappaport Fac, Haifa, Israel.
   [Salazar, Ramon] Catalan Inst Oncol, Med Oncol Serv, Barcelona, Spain.
   [Kopelovich, Levy] NCI, Canc Prevent Div, Rockville, MD USA.
   [Lipkin, Steven Monroe] Weill Cornell Med Coll, Dept Med, New York, NY USA.
   [Gruber, Stephen Bernard] Univ Michigan Med Sch, Dept Internal Med Epidemiol & Human Genet, Ann Arbor, MI USA.
   [Gruber, Stephen Bernard] Univ So Calif, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
   [Moreno, Victor] Univ Barcelona, Fac Med, Dept Clin Sci, Barcelona 7, Spain.
RP Gruber, SB (reprint author), Univ Michigan Med Sch, Dept Internal Med Epidemiol & Human Genet, Ann Arbor, MI USA.
EM sgruber@usc.edu; v.moreno@iconcologia.net
OI Cuadras, Daniel/0000-0001-8780-1764; Moreno, Victor/0000-0002-2818-5487
FU National Cancer Institute [N01-CN43308, NCI R01-CA81488]; University of
   Michigan's Cancer Center Support Grant [5 P30 CA46592]; Catalan
   Institute of Oncology; Private Foundation of the Biomedical Research
   Institute of Bellvitge (IDIBELL); Instituto de Salud Carlos III
   [PI08-1635, PI08-1359, PS09-1037]; CIBERESP [CB06/02/2005]; Accion
   Transversal del Cancer; Catalan Government DURSI [2009SGR1489]; AECC
   (Spanish Association Against Cancer) Scientific Foundation; USC Norris
   Cancer Center Support Grant [NCI P30 CA014089]
FX This work was supported by a grant from the National Cancer Institute
   [N01-CN43308 (SML), NCI R01-CA81488 (SBG)], University of Michigan's
   Cancer Center Support Grant [5 P30 CA46592]. Also the Catalan Institute
   of Oncology and the Private Foundation of the Biomedical Research
   Institute of Bellvitge (IDIBELL), the Instituto de Salud Carlos III
   [grants PI08-1635, PI08-1359, PS09-1037], CIBERESP CB06/02/2005 and the
   "Accion Transversal del Cancer", the Catalan Government DURSI [grant
   2009SGR1489], and the AECC (Spanish Association Against Cancer)
   Scientific Foundation. USC Norris Cancer Center Support Grant [NCI P30
   CA014089 (SBG). No authors have financial conflict of interest with this
   manuscript. The funders had no role in study design, data collection and
   analysis, decision to publish, or preparation of the manuscript.
NR 45
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PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 25
PY 2013
VL 8
IS 11
AR e80158
DI 10.1371/journal.pone.0080158
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 259RH
UT WOS:000327543500021
PM 24282520
ER

PT J
AU Porat-Shliom, N
   Weigert, R
   Donaldson, JG
AF Porat-Shliom, Natalie
   Weigert, Roberto
   Donaldson, Julie G.
TI Endosomes Derived from Clathrin-Independent Endocytosis Serve as
   Precursors for Endothelial Lumen Formation
SO PLOS ONE
LA English
DT Article
ID MATRIX METALLOPROTEINASE INDUCER; HAMSTER OVARY CELLS;
   PHOSPHATIDYLINOSITOL 4,5-BISPHOSPHATE; MOLECULAR-MECHANISMS; RECYCLING
   PATHWAY; BIOLOGICAL TUBES; ZEBRAFISH EMBRYO; UNIQUE PLATFORM; ARF6
   RECRUITS; POLARITY
AB Clathrin-independent endocytosis (CIE) is a form of bulk plasma membrane (PM) endocytosis that allows cells to sample and evaluate PM composition. Once in endosomes, the internalized proteins and lipids can be recycled back to the PM or delivered to lysosomes for degradation. Endosomes arising from CIE contain lipid and signaling molecules suggesting that they might be involved in important biological processes. During vasculogenesis, new blood vessels are formed from precursor cells in a process involving internalization and accumulation of endocytic vesicles. Here, we found that CIE has a role in endothelial lumen formation. Specifically, we found that human vascular endothelial cells (HUVECs) utilize CIE for internalization of distinct cargo molecules and that in three-dimensional cultures CIE membranes are delivered to the newly formed lumen.
C1 [Porat-Shliom, Natalie; Donaldson, Julie G.] NHLBI, NIH, Cell Biol & Physiol Ctr, Bethesda, MD 20892 USA.
   [Porat-Shliom, Natalie; Weigert, Roberto] Natl Inst Dent & Craniofacial Res, NIH, Intracellular Membrane Trafficking Unit, Oral & Pharyngeal Canc Branch, Bethesda, MD USA.
RP Donaldson, JG (reprint author), NHLBI, NIH, Cell Biol & Physiol Ctr, Bldg 10, Bethesda, MD 20892 USA.
EM donaldsonj@helix.nih.gov
FU Intramural Research Program National Heart, Lung, and Blood Institute,
   National Institutes of Health [HL006060]
FX The research was supported by the Intramural Research Program (HL006060)
   of the National Heart, Lung, and Blood Institute, National Institutes of
   Health.
   http://www.nhlbi.nih.gov/research/intramural/researchers/pi/donaldson-ju
   lie/index.html. The funders had no role in study design, data collection
   and analysis, decision to publish, or preparation of the manuscript.
NR 51
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U2 4
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PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 25
PY 2013
VL 8
IS 11
AR e81987
DI 10.1371/journal.pone.0081987
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 259RH
UT WOS:000327543500124
PM 24282620
ER

PT J
AU Senese, VP
   De Falco, S
   Bornstein, MH
   Caria, A
   Buffolino, S
   Venuti, P
AF Senese, Vincenzo Paolo
   De Falco, Simona
   Bornstein, Marc H.
   Caria, Andrea
   Buffolino, Simona
   Venuti, Paola
TI Human Infant Faces Provoke Implicit Positive Affective Responses in
   Parents and Non-Parents Alike
SO PLOS ONE
LA English
DT Article
ID ASSOCIATION TEST; ANTISOCIAL-BEHAVIOR; SOCIAL COGNITION; YOUNG-CHILDREN;
   MOTHERS; BRAIN; SYSTEM; CRIES; RESPONSIVENESS; DETERMINANTS
AB Human infants' complete dependence on adult caregiving suggests that mechanisms associated with adult responsiveness to infant cues might be deeply embedded in the brain. Behavioural and neuroimaging research has produced converging evidence for adults' positive disposition to infant cues, but these studies have not investigated directly the valence of adults' reactions, how they are moderated by biological and social factors, and if they relate to child caregiving. This study examines implicit affective responses of 90 adults toward faces of human and non-human (cats and dogs) infants and adults. Implicit reactions were assessed with Single Category Implicit Association Tests, and reports of childrearing behaviours were assessed by the Parental Style Questionnaire. The results showed that human infant faces represent highly biologically relevant stimuli that capture attention and are implicitly associated with positive emotions. This reaction holds independent of gender and parenthood status and is associated with ideal parenting behaviors.
C1 [Senese, Vincenzo Paolo; Buffolino, Simona] Univ Naples 2, Dept Psychol, Psychometr Lab, Caserta, Italy.
   [De Falco, Simona; Venuti, Paola] Univ Trento, Dept Psychol & Cognit Sci, Trento, Italy.
   [Bornstein, Marc H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, US Dept HHS, Bethesda, MD USA.
   [Caria, Andrea] Univ Tubingen, Inst Med Psychol & Behav Neurobiol Eberhard Karls, Tubingen, Germany.
RP Senese, VP (reprint author), Univ Naples 2, Dept Psychol, Psychometr Lab, Caserta, Italy.
EM vincenzopaolo.senese@unina2.it
FU NIH, NICHD
FX This research was partially supported by the Intramural Research Program
   of the NIH, NICHD. The funders had no role in study design, data
   collection and analysis, decision to publish, or preparation of the
   manuscript. No additional external funding received for this study.
NR 77
TC 11
Z9 11
U1 2
U2 16
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 25
PY 2013
VL 8
IS 11
AR e80379
DI 10.1371/journal.pone.0080379
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 259RH
UT WOS:000327543500038
PM 24282537
ER

PT J
AU Zhang, XJ
   Lu, LH
   Wang, RR
   Wang, YP
   Luo, RH
   Lai, CC
   Yang, LM
   He, YP
   Zheng, YT
AF Zhang, Xing-Jie
   Lu, Li-He
   Wang, Rui-Rui
   Wang, Yue-Ping
   Luo, Rong-Hua
   Lai, Christopher Cong
   Yang, Liu-Meng
   He, Yan-Ping
   Zheng, Yong-Tang
TI DB-02, a C-6-Cyclohexylmethyl Substituted Pyrimidinone HIV-1 Reverse
   Transcriptase Inhibitor with Nanomolar Activity, Displays an Improved
   Sensitivity against K103N or Y181C Than S-DABOs
SO PLOS ONE
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; BENZYL-OXOPYRIMIDINE DERIVATIVES;
   STRUCTURE-BASED DESIGN; IN-VITRO SELECTION; DRUG-RESISTANCE;
   NONNUCLEOSIDE INHIBITORS; BIOLOGICAL EVALUATION; ANTI-HIV-1 ACTIVITY;
   WILD-TYPE; POTENT
AB 6-(cyclohexylmethyl)-5-ethyl-2-((2-oxo-2-phenylethyl)thio)pyrimidin-4(3H)-one (DB-02) is a member of the newly reported synthetic anti-HIV-1 compounds dihydro-aryl/alkylsulfanyl-cyclohexylmethyl-oxopyrimidines, S-DACOs. In vitro anti-HIV-1 activity and resistance profile studies have suggested that DB-02 has very low cytotoxicity (CC50>1mM) to cell lines and peripheral blood mononuclear cells (PBMCs). It displays potent anti-HIV-1 activity against laboratory adapted strains and primary isolated strains including different subtypes and tropism strains (EC(50)s range from 2.40 to 41.8 nM). Studies on site-directed mutagenesis, genotypic resistance profiles revealed that V106A was the major resistance contributor for the compound. Molecular docking analysis showed that DB-02 located in the hydrophobic pocket with interactions of Lys101, Val106, Leu234, His235. DB-02 also showed non-antagonistic effects to four approved antiretroviral drugs. All studies indicated that DB-02 would be a potential NNRTI with low cytotoxicity and improved activity.
C1 [Zhang, Xing-Jie; Wang, Rui-Rui; Luo, Rong-Hua; Yang, Liu-Meng; Zheng, Yong-Tang] Chinese Acad Sci, Key Lab Anim Models & Human Dis Mech, Kunming 650223, Yunnan, Peoples R China.
   [Zhang, Xing-Jie; Wang, Rui-Rui; Luo, Rong-Hua; Yang, Liu-Meng; Zheng, Yong-Tang] Chinese Acad Sci, Kunming Inst Zool, Kunming 650223, Yunnan, Peoples R China.
   [Zhang, Xing-Jie] Univ Chinese Acad Sci, Beijing, Peoples R China.
   [Lu, Li-He; Wang, Yue-Ping; He, Yan-Ping] Yunnan Univ, Sch Chem Sci & Technol, Key Lab Med Chem Nat Resource, Minist Educ, Kunming, Yunnan, Peoples R China.
   [Lai, Christopher Cong] NCI, Biol Chem Lab, Ctr Canc Res, NIH, Frederick, MD 21701 USA.
RP He, YP (reprint author), Yunnan Univ, Sch Chem Sci & Technol, Key Lab Med Chem Nat Resource, Minist Educ, Kunming, Yunnan, Peoples R China.
EM yphe@ynu.edu.cn; zhengyt@mail.kiz.ac.cn
FU 973 Program [2009CB522306]; Key Scientific and Technological Program of
   China Yunnan Province [2012ZX10001-006, 2012ZX10001-007,
   2012ZX09103-101-068, 2009BC018, 2010GA001, Y103951111]; National Science
   Foundation of China [21262044, 30560179, 30960459, 81001462, 81102483];
   Chinese Academy of Sciences [W8090303]
FX This work was supported in part by grants from the 973 Program
   (2009CB522306), the Key Scientific and Technological Program of China
   (2012ZX10001-006; 2012ZX10001-007, 2012ZX09103-101-068) and of Yunnan
   Province (2009BC018, 2010GA001, Y103951111), the National Science
   Foundation of China (21262044, 30560179, 30960459, 81001462, 81102483)
   and the Chinese Academy of Sciences (W8090303). The funders had no role
   in study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
NR 41
TC 8
Z9 8
U1 1
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 25
PY 2013
VL 8
IS 11
AR e81489
DI 10.1371/journal.pone.0081489
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 259RH
UT WOS:000327543500102
PM 24282600
ER

PT J
AU Bowne, SJ
   Sullivan, LS
   Avery, CE
   Sasser, EM
   Roorda, A
   Duncan, JL
   Wheaton, DH
   Birch, DG
   Branham, KE
   Heckenlively, JR
   Sieving, PA
   Daiger, SP
AF Bowne, Sara J.
   Sullivan, Lori S.
   Avery, Cheryl E.
   Sasser, Elizabeth M.
   Roorda, Austin
   Duncan, Jacque L.
   Wheaton, Dianna H.
   Birch, David G.
   Branham, Kari E.
   Heckenlively, John R.
   Sieving, Paul A.
   Daiger, Stephen P.
TI Mutations in the small nuclear riboprotein 200 kDa gene (SNRNP200) cause
   1.6% of autosomal dominant retinitis pigmentosa
SO MOLECULAR VISION
LA English
DT Article
ID DISEASE-CAUSING MUTATIONS; PROTEIN; PENETRANCE; FAMILIES; PRP8
AB Purpose: The purpose of this project was to determine the spectrum and frequency of mutations in the small nuclear riboprotein 200 kDa gene (SNRNP200) that cause autosomal dominant retinitis pigmentosa (adRP).
   Methods: A well-characterized adRP cohort of 251 families was tested for mutations in the exons and intron/exon junctions of SNRNP200 using fluorescent dideoxy sequencing. An additional 21 adRP families from the eyeGENE (R) Network were tested for possible mutations. Bioinformatic and segregation analysis was performed on novel variants.
   Results: SNRNP200 mutations were identified in seven of the families tested. Two previously reported mutations, p.Arg681Cys and p.Ser1087Leu, were found in two families each. One family had the previously reported p.Arg681His mutation. Two novel SNRNP200 variants, p.Pro682Ser and p.Ala542Val, were also identified in one family each. Bioinformatic and segregation analyses suggested that these novel variants are likely to be pathogenic. Clinical examination of patients with SNRNP200 mutations showed a wide range of clinical symptoms and severity, including one instance of non-penetrance.
   Conclusions: Mutations in SNRNP200 caused 1.6% of disease in our adRP cohort. Pathogenic mutations were found primarily in exons 16 and 25, but the novel p.Ala542Val mutation in exon 13 suggests that variation in other genetic regions is also responsible for causing dominant disease. SNRNP200 mutations were associated with a wide range of clinical symptoms similar to those of individuals with other splice-factor gene mutations.
C1 [Bowne, Sara J.; Sullivan, Lori S.; Avery, Cheryl E.; Sasser, Elizabeth M.; Daiger, Stephen P.] Univ Texas Hlth Sci Ctr Houston, Sch Publ Hlth, Ctr Human Genet, Houston, TX 77030 USA.
   [Roorda, Austin] Univ Calif Berkeley, Sch Optometry, Berkeley, CA 94720 USA.
   [Roorda, Austin] Univ Calif Berkeley, Vis Sci Grad Grp, Berkeley, CA 94720 USA.
   [Duncan, Jacque L.] Univ Calif San Francisco, Dept Ophthalmol, San Francisco, CA USA.
   [Wheaton, Dianna H.; Birch, David G.] Retina Fdn SW, Dallas, TX USA.
   [Branham, Kari E.; Heckenlively, John R.] Univ Michigan, Kellogg Eye Ctr, Ann Arbor, MI 48109 USA.
   [Sieving, Paul A.] NEI, Ophthalm Genet & Visual Funct Branch, NIH, Bethesda, MA USA.
RP Bowne, SJ (reprint author), Univ Texas Hlth Sci Ctr Houston, Sch Publ Hlth, Ctr Human Genet, 1200 Herman Pressler St, Houston, TX 77030 USA.
EM sara.j.bowne@uth.tmc.edu
OI Birch, David/0000-0002-6594-2897
FU National Ophthalmic Genotyping and Phenotyping Network or eyeGENE(R)
   [Protocol 06-EI-0236]; National Institutes of Health/National Eye
   Institute (NIH/NEI) [HHS-N-260-2007-00001-C]; NIH/NEI [R01EY007142];
   Foundation Fighting Blindness
FX This work was supported through the National Ophthalmic Genotyping and
   Phenotyping Network or eyeGENE (R) (Protocol 06-EI-0236), which is
   funded in part by the National Institutes of Health/National Eye
   Institute (NIH/NEI), under Contract No. HHS-N-260-2007-00001-C. Dr.
   Daiger is Director of a CLIA Certified Laboratory in the eyeGENE (R)
   Network. We thank the eyeGENE (R) Network participants and other
   research families for their valuable contributions to this research.
   Additional support was from NIH/NEI grant R01EY007142 (S.P.D.), Center
   and Module grants from the Foundation Fighting Blindness (D.G.B.,
   J.R.H., J.L.D., A.R., and S.P.D.), and grants from Research to Prevent
   Blindness (unrestricted grant and Physician-Scientist award, J.L.D.).
   Austin Roorda holds a patent on AOSLO technology through the University
   of Houston and the University of Rochester (US Patent # 7,118,216). The
   remaining authors have no commercial interests to disclose. Portions of
   this research were presented at the annual meeting of the Association
   for Research in Vision and Ophthalmology (ARVO), Invest. Ophthalmol.
   Vis. Sci. 2013, 54: E-Abstract 1329- A0023.
NR 26
TC 9
Z9 9
U1 1
U2 3
PU MOLECULAR VISION
PI ATLANTA
PA C/O JEFF BOATRIGHT, LAB B, 5500 EMORY EYE CENTER, 1327 CLIFTON RD, N E,
   ATLANTA, GA 30322 USA
SN 1090-0535
J9 MOL VIS
JI Mol. Vis.
PD NOV 24
PY 2013
VL 19
BP 2407
EP 2417
PG 11
WC Biochemistry & Molecular Biology; Ophthalmology
SC Biochemistry & Molecular Biology; Ophthalmology
GA 272OR
UT WOS:000328470600002
PM 24319334
ER

PT J
AU Stussman, BJ
   Bethell, CD
   Gray, C
   Nahin, RL
AF Stussman, Barbara J.
   Bethell, Christina D.
   Gray, Caroline
   Nahin, Richard L.
TI Development of the adult and child complementary medicine questionnaires
   fielded on the National Health Interview Survey
SO BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE
LA English
DT Article
DE Complementary therapies; Complementary medicine; Questionnaire
   development; Cognitive interviewing; National Health Interview Survey
   (NHIS)
ID UNITED-STATES ADULTS; ALTERNATIVE MEDICINE; SURVEY SF-36; THERAPIES;
   CARE; CAM; ASSOCIATION; INVOLVEMENT; PREVALENCE; HAPPINESS
AB The 2002, 2007, and 2012 complementary medicine questionnaires fielded on the National Health Interview Survey provide the most comprehensive data on complementary medicine available for the United States. They filled the void for large-scale, nationally representative, publicly available datasets on the out-of-pocket costs, prevalence, and reasons for use of complementary medicine in the U. S. Despite their wide use, this is the first article describing the multi-faceted and largely qualitative processes undertaken to develop the surveys. We hope this in-depth description enables policy makers and researchers to better judge the content validity and utility of the questionnaires and their resultant publications.
C1 [Stussman, Barbara J.; Nahin, Richard L.] NIH, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
   [Bethell, Christina D.] Oregon Hlth & Sci Univ, Sch Med, Child & Adolescent Hlth Measurement Initiat, Portland, OR 97201 USA.
   [Gray, Caroline] Hlth Policy Res Inst, Palo Alto Med Ctr, Palo Alto, CA USA.
RP Stussman, BJ (reprint author), NIH, Natl Ctr Complementary & Alternat Med, Bldg 10, Bethesda, MD 20892 USA.
EM stussmanbj@mail.nih.gov
OI Nahin, Richard/0000-0002-3682-4816
FU NIH/NCCAM [1 R21 AT004960]
FX BJS and RLN were employees of the federal government during the
   planning, analysis, and writing of this manuscript and performed their
   work as part of their official duties. No outside financial support was
   provided. CDB's work on this project was supported by NIH/NCCAM grant 1
   R21 AT004960. CG was employed by the federal government during the
   planning and analysis of this manuscript and received no financial
   support during the writing of the manuscript. The findings and
   conclusions of this report are those of the authors and collaborators
   and do not necessarily represent the views of the National Institutes of
   Health, National Center for Complementary and Alternative Medicine, the
   Oregon Health & Sciences University, School of Medicine, or the Palo
   Alto Medical Center, Health Policy Research Institute.
NR 65
TC 4
Z9 4
U1 5
U2 10
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1472-6882
J9 BMC COMPLEM ALTERN M
JI BMC Complement. Altern. Med.
PD NOV 23
PY 2013
VL 13
AR 328
DI 10.1186/1472-6882-13-328
PG 18
WC Integrative & Complementary Medicine
SC Integrative & Complementary Medicine
GA 271EM
UT WOS:000328374100002
PM 24267412
ER

PT J
AU Colbert, RA
   Ward, MM
AF Colbert, Robert A.
   Ward, Michael M.
TI 17 and 23: prime numbers for ankylosing spondylitis?
SO LANCET
LA English
DT Editorial Material
ID CELLS; SPONDYLOARTHRITIS; SECUKINUMAB; PSORIASIS; ANTIBODY
C1 [Colbert, Robert A.; Ward, Michael M.] NIAMSD, Intramural Res Program, Bethesda, MD 20892 USA.
RP Colbert, RA (reprint author), NIAMSD, Intramural Res Program, Bethesda, MD 20892 USA.
EM colbertr@mail.nih.gov
FU Intramural NIH HHS [ZIA AR041184-04]
NR 17
TC 1
Z9 1
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0140-6736
EI 1474-547X
J9 LANCET
JI Lancet
PD NOV 23
PY 2013
VL 382
IS 9906
BP 1682
EP 1683
DI 10.1016/S0140-6736(13)61913-3
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 259PX
UT WOS:000327539900006
PM 24035251
ER

PT J
AU Lin, YJ
   Chang, JS
   Liu, X
   Lin, TH
   Huang, SM
   Liao, CC
   Lin, CW
   Chien, WK
   Chen, JH
   Wu, JY
   Chen, CH
   Chang, LC
   Tsang, H
   Jeang, KT
   Chen, CY
   Tsai, FJ
AF Lin, Ying-Ju
   Chang, Jeng-Sheng
   Liu, Xiang
   Lin, Ting-Hsu
   Huang, Shao-Mei
   Liao, Chiu-Chu
   Lin, Cheng-Wen
   Chien, Wen-Kuei
   Chen, Jin-Hua
   Wu, Jer-Yuarn
   Chen, Chien-Hsiun
   Chang, Li-Ching
   Tsang, Hsinyi
   Jeang, Kuan-Teh
   Chen, Chia-Yen
   Tsai, Fuu-Jen
TI Sorting nexin 24 genetic variation associates with coronary artery
   aneurysm severity in Kawasaki disease patients
SO CELL AND BIOSCIENCE
LA English
DT Article
DE Kawasaki disease; Coronary artery aneurysm; Sorting nexin 24;
   Polymorphism
ID C-REACTIVE PROTEIN; P-SELECTIN; POLYMORPHISM; ABNORMALITIES;
   TRAFFICKING; EXPRESSION; VASCULITIS; INTERACTS; DATABASE; CELLS
AB Background: The sorting nexin (SNX) family is involved in endocytosis and protein trafficking and plays multiple roles in various diseases. The role of SNX proteins in Kawasaki disease (KD) is not known. We attempted to test whether genetic SNX variation associates with the risk of coronary artery aneurysm (CAA) formation in KD.
   Methods and results: Chi-square tests were used to identify SNX24 genetic variants associated with KD susceptibility and CAA formation in KD; models were adjusted for fever duration and time of first administration of intravenous immunoglobulin. We obtained clinical characteristics and genotypes from KD patients (76 with CAA and 186 without CAA) in a population-based retrospective KD cohort study (n = 262). Clinical and genetic factors were associated with CAA formation in KD. In addition, endothelial cell inflammation was evaluated. Significant correlation was observed between KD with CAA complications and the rs28891 single-nucleotide polymorphism in SNX24. Patients with CC + CT genotypes had lesser CAA complications. In lipopolysaccharide-treated human umbilical vein endothelial cells, siRNA knockdown of SNX24 significantly decreased gene expression of the proinflammatory cytokines IL-1 beta, IL-6, and IL-8.
   Conclusions: Polymorphisms in SNX24 may be used as genetic markers for the diagnosis and prognosis of CAA formation in KD.
C1 [Lin, Ying-Ju; Lin, Ting-Hsu; Huang, Shao-Mei; Liao, Chiu-Chu; Tsai, Fuu-Jen] China Med Univ Hosp, Dept Med Res, Taichung, Taiwan.
   [Lin, Ying-Ju; Wu, Jer-Yuarn; Chen, Chien-Hsiun; Tsai, Fuu-Jen] China Med Univ, Sch Chinese Med, Taichung, Taiwan.
   [Chang, Jeng-Sheng] China Med Univ Hosp, Dept Pediat, Taichung, Taiwan.
   [Liu, Xiang; Jeang, Kuan-Teh] NIAID, Mol Virol Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
   [Lin, Cheng-Wen] China Med Univ, Dept Med Lab Sci & Biotechnol, Taichung, Taiwan.
   [Chien, Wen-Kuei; Chen, Jin-Hua] China Med Univ, Biostat Ctr, Taichung, Taiwan.
   [Chien, Wen-Kuei; Chen, Jin-Hua] Taipei Med Univ, Biostat Ctr, Taipei, Taiwan.
   [Wu, Jer-Yuarn; Chen, Chien-Hsiun; Chang, Li-Ching] Acad Sinica, Inst Biomed Sci, Taipei, Taiwan.
   [Tsang, Hsinyi] NIAID, Immunogenet Mol Lab, NIH, Bethesda, MD 20892 USA.
   [Chen, Chia-Yen] NIAID, Viral Biochem Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
   [Tsai, Fuu-Jen] Asia Univ, Taichung, Taiwan.
RP Lin, YJ (reprint author), China Med Univ Hosp, Dept Med Res, Taichung, Taiwan.
EM yjlin.kath@gmail.com; d0704@mail.cmuh.org.tw
RI Liu, Xiang/F-5731-2014; Tsai, Fuu-Jen/J-4140-2015
FU CMU [CMU100-S-01]; CMUH [DMR-102-83]; Republic of China National Science
   Council [NSC101-2314- B-039-008-MY3]
FX Support for this research was provided by CMU (CMU100-S-01), CMUH
   (DMR-102-83), and the Republic of China National Science Council
   (NSC101-2314- B-039-008-MY3).
NR 44
TC 3
Z9 3
U1 1
U2 8
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 2045-3701
J9 CELL BIOSCI
JI Cell Biosci.
PD NOV 22
PY 2013
VL 3
AR 44
DI 10.1186/2045-3701-3-44
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 283HJ
UT WOS:000329236700001
PM 24268062
ER

PT J
AU Chattopadhyay, MK
   Tabor, H
AF Chattopadhyay, Manas K.
   Tabor, Herbert
TI Polyamines Are Critical for the Induction of the Glutamate
   Decarboxylase-dependent Acid Resistance System in Escherichia coli
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
DE Bacteria; Cyclic AMP (cAMP); Decarboxylase; Gene Expression; Glutamate;
   Microarray; Polyamines; Putrescine; Spermidine
ID SMALL-RNA; ENTERIC BACTERIA; GADE YHIE; GENES; RPOS; EXPRESSION; STRESS;
   PROTEIN; REGULATORS; ACTIVATOR
AB As part of our studies on the biological functions of polyamines, we have used a mutant of Escherichia coli that lacks all the genes for polyamine biosynthesis for a global transcriptional analysis on the effect of added polyamines. The most striking early response to the polyamine addition is the increased expression of the genes for the glutamate-dependent acid resistance system (GDAR) that is important for the survival of the bacteria when passing through the acid environment of the stomach. Not only were the two genes for glutamate decarboxylases (gadA and gadB) and the gene for glutamate--aminobutyrate antiporter (gadC) induced by the polyamine addition, but the various genes involved in the regulation of this system were also induced. We confirmed the importance of polyamines for the induction of the GDAR system by direct measurement of glutamate decarboxylase activity and acid survival. The effect of deletions of the regulatory genes on the GDAR system and the effects of overproduction of two of these genes were also studied. Strikingly, overproduction of the alternative sigma factor rpoS and of the regulatory gene gadE resulted in very high levels of glutamate decarboxylase and almost complete protection against acid stress even in the absence of any polyamines. Thus, these data show that a major function of polyamines in E. coli is protection against acid stress by increasing the synthesis of glutamate decarboxylase, presumably by increasing the levels of the rpoS and gadE regulators.
C1 [Chattopadhyay, Manas K.; Tabor, Herbert] NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
RP Chattopadhyay, MK (reprint author), NIDDK, NIH, 8 Ctr Dr,Bldg 8,Rm 219, Bethesda, MD 20892 USA.
EM manasc@intra.niddk.nih.gov
FU National Institutes of Health Intramural Research Program of the NIDDK
FX This work was supported, in whole or in part, by National Institutes of
   Health Intramural Research Program of the NIDDK.
NR 63
TC 10
Z9 11
U1 0
U2 10
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 22
PY 2013
VL 288
IS 47
BP 33559
EP 33570
DI 10.1074/jbc.M113.510552
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 255OR
UT WOS:000327250200006
PM 24097985
ER

PT J
AU Artamonov, MV
   Momotani, K
   Stevenson, A
   Trentham, DR
   Derewenda, U
   Derewenda, ZS
   Read, PW
   Gutkind, JS
   Somlyo, AV
AF Artamonov, Mykhaylo V.
   Momotani, Ko
   Stevenson, Andra
   Trentham, David R.
   Derewenda, Urszula
   Derewenda, Zygmunt S.
   Read, Paul W.
   Gutkind, J. Silvio
   Somlyo, Avril V.
TI Agonist-induced Ca2+ Sensitization in Smooth Muscle REDUNDANCY OF RHO
   GUANINE NUCLEOTIDE EXCHANGE FACTORS (RhoGEFs) AND RESPONSE KINETICS, A
   CAGED COMPOUND STUDY
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
DE Calcium; Guanine Nucleotide Exchange Factor (GEF); Rho; Signal
   Transduction; Smooth Muscle
ID HETEROTRIMERIC G-PROTEINS; LEUKEMIA-ASSOCIATED RHO; PDZ-RHOGEF; MYOSIN
   PHOSPHATASE; ANGIOTENSIN-II; ADENOSINE-TRIPHOSPHATE;
   SIGNAL-TRANSDUCTION; CRYSTAL-STRUCTURE; FLASH-PHOTOLYSIS; LIVING CELLS
AB Many agonists, acting through G-protein-coupled receptors and G subunits of the heterotrimeric G-proteins, induce contraction of smooth muscle through an increase of [Ca2+](i) as well as activation of the RhoA/RhoA-activated kinase pathway that amplifies the contractile force, a phenomenon known as Ca2+ sensitization. G(12/13) subunits are known to activate the regulator of G-protein signaling-like family of guanine nucleotide exchange factors (RhoGEFs), which includes PDZ-RhoGEF (PRG) and leukemia-associated RhoGEF (LARG). However, their contributions to Ca2+-sensitized force are not well understood. Using permeabilized blood vessels from PRG(-/-) mice and a new method to silence LARG in organ-cultured blood vessels, we show that both RhoGEFs are activated by the physiologically and pathophysiologically important thromboxane A(2) and endothelin-1 receptors. The co-activation is the result of direct and independent activation of both RhoGEFs as well as their co-recruitment due to heterodimerization. The isolated recombinant C-terminal domain of PRG, which is responsible for heterodimerization with LARG, strongly inhibited Ca2+-sensitized force. We used photolysis of caged phenylephrine, caged guanosine 5-O-(thiotriphosphate) (GTPS) in solution, and caged GTPS or caged GTP loaded on the RhoARhoGDI complex to show that the recruitment and activation of RhoGEFs is the cause of a significant time lag between the initial Ca2+ transient and phasic force components and the onset of Ca2+-sensitized force.
C1 [Artamonov, Mykhaylo V.; Momotani, Ko; Derewenda, Urszula; Derewenda, Zygmunt S.; Somlyo, Avril V.] Univ Virginia, Dept Mol Physiol & Biol Phys, Charlottesville, VA 22908 USA.
   [Artamonov, Mykhaylo V.; Momotani, Ko; Derewenda, Urszula; Derewenda, Zygmunt S.; Somlyo, Avril V.] Univ Virginia, Dept Radiat Oncol, Charlottesville, VA 22908 USA.
   [Stevenson, Andra] Merck Res Labs, Dept Cardiovasc Dis, Kenilworth, NJ 07033 USA.
   [Trentham, David R.] Kings Coll London, Sch Biomed Sci, Randall Div Cell & Mol Biophys, London SE1 1UK, England.
   [Gutkind, J. Silvio] NIDCR, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA.
RP Somlyo, AV (reprint author), Univ Virginia, Dept Mol Physiol & Biol Phys, POB 736, Charlottesville, VA 22903 USA.
EM avs5u@virginia.edu
FU National Institutes of Health [GM086457, R01DK088905]
FX This work was supported, in whole or in part, by National Institutes of
   Health Grants GM086457 and R01DK088905.
NR 49
TC 10
Z9 10
U1 0
U2 4
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 22
PY 2013
VL 288
IS 47
BP 34030
EP 34040
DI 10.1074/jbc.M113.514596
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 255OR
UT WOS:000327250200044
PM 24106280
ER

PT J
AU Luo, M
   Lu, XP
   Zhu, R
   Zhang, ZH
   Chow, CC
   Li, R
   Simons, SS
AF Luo, Min
   Lu, Xinping
   Zhu, Rong
   Zhang, Zhenhuan
   Chow, Carson C.
   Li, Rong
   Simons, S. Stoney, Jr.
TI A Conserved Protein Motif Is Required for Full Modulatory Activity of
   Negative Elongation Factor Subunits NELF-A and NELF-B in Modifying
   Glucocorticoid Receptor-regulated Gene Induction Properties
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
DE Gene Transcription; Glucocorticoid Receptor; Mathematical Modeling;
   Steroid Hormone; Transcription Factors; EC50; Gene Induction; NELF-A and
   NELF-B; Cofactor Action; Competitive Decelerator
ID RNA-POLYMERASE-II; BREAST-CANCER CELLS; CHROMATIN ACCESSIBILITY;
   MEDIATED REPRESSION; POL-II; TRANSCRIPTION; PROMOTER; EXPRESSION;
   BINDING; IDENTIFICATION
AB NELF-B is a BRCA1-interacting protein and subunit (with NELF-A, -C/D, and -E) of the human negative elongation factor (NELF) complex, which participates in RNA polymerase II pausing shortly after transcription initiation, especially for synchronized gene expression. We now report new activities of NELF-B and other NELF complex subunits, which are to attenuate glucocorticoid receptor (GR)-mediated gene induction, reduce the partial agonist activity of an antagonist, and increase the EC50 of an agonist during nonsynchronized expression of exogenous and endogenous reporters. Stable knockdown of endogenous NELF-B has the opposite effects on an exogenous gene. The GR ligand-binding domain suffices for these biological responses. ChIP assays reveal that NELF-B diminishes GR recruitment to promoter regions of two endogenous genes. Using a new competition assay, NELF-A and NELF-B are each shown to act independently as competitive decelerators at two steps after the site of GR action and before or at the site of reporter gene activity. A common motif in each NELF was identified that is required for full activity of both NELF-A and NELF-B. These studies allow us to position the actions of two new modulators of GR-regulated transactivation, NELF-A and NELF-B, relative to other factors in the overall gene induction sequence.
C1 [Luo, Min; Lu, Xinping; Zhu, Rong; Zhang, Zhenhuan; Simons, S. Stoney, Jr.] NIDDK, Steroid Hormones Sect, Lab Endocrinol & Receptor Biol, NIH, Bethesda, MD 20892 USA.
   [Chow, Carson C.] NIDDK, Lab Biol Modeling, NIH, Bethesda, MD 20892 USA.
   [Li, Rong] Univ Texas Hlth Sci Ctr San Antonio, Canc Therapy & Res Ctr, San Antonio, TX 78229 USA.
RP Simons, SS (reprint author), NIDDK, LERB, NIH, Bldg 10,8N-307B, Bethesda, MD 20892 USA.
EM stoneys@helix.nih.gov
FU National Institutes of Health, the NIDDK; Voelcker Scholar Award
FX This research was supported by the Intramural Research Program of the
   National Institutes of Health, the NIDDK, and a Voelcker Scholar Award
   (to R. L.).
NR 63
TC 5
Z9 5
U1 0
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 22
PY 2013
VL 288
IS 47
BP 34055
EP 34072
DI 10.1074/jbc.M113.512426
PG 18
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 255OR
UT WOS:000327250200049
PM 24097989
ER

PT J
AU Bosch, FX
   Broker, TR
   Forman, D
   Moscicki, AB
   Gillison, ML
   Doorbar, J
   Stern, PL
   Stanley, M
   Arbyn, M
   Poljak, M
   Cuzick, J
   Castle, PE
   Schiller, JT
   Markowitz, LE
   Fisher, WA
   Canfell, K
   Denny, LA
   Franco, EL
   Steben, M
   Kane, MA
   Schiffman, M
   Meijer, CJLM
   Sankaranarayanan, R
   Castellsague, X
   Kim, JJ
   Brotons, M
   Alemany, L
   Albero, G
   Diaz, M
   de Sanjose, S
AF Xavier Bosch, F.
   Broker, Thomas R.
   Forman, David
   Moscicki, Anna-Barbara
   Gillison, Maura L.
   Doorbar, John
   Stern, Peter L.
   Stanley, Margaret
   Arbyn, Marc
   Poljak, Mario
   Cuzick, Jack
   Castle, Philip E.
   Schiller, John T.
   Markowitz, Lauri E.
   Fisher, William A.
   Canfell, Karen
   Denny, Lynette A.
   Franco, Eduardo L.
   Steben, Marc
   Kane, Mark A.
   Schiffman, Mark
   Meijer, Chris J. L. M.
   Sankaranarayanan, Rengaswamy
   Castellsague, Xavier
   Kim, Jane J.
   Brotons, Maria
   Alemany, Laia
   Albero, Ginesa
   Diaz, Mireia
   de Sanjose, Silvia
CA ICO Monograph Comprehensive
TI Comprehensive Control of Human Papillomavirus Infections and Related
   Diseases
SO VACCINE
LA English
DT Review
DE HPV; Cervical cancer; Anal cancer; Penile cancer; Vaginal cancer; Vulvar
   cancer; Oropharyngeal cancer; Screening; HPV vaccination; HPV testing;
   Prevention
ID CERVICAL-CANCER; PREVENTION; COUNTRIES; VACCINES; WORLD
AB Infection with human papillomavirus (HPV) is recognized as one of the major causes of infection-related cancer worldwide, as well as the causal factor in other diseases. Strong evidence for a causal etiology with HPV has been stated by the International Agency for Research on Cancer for cancers of the cervix uteri, penis, vulva, vagina, anus and oropharynx (including base of the tongue and tonsils). Of the estimated 12.7 million new cancers occurring in 2008 worldwide, 4.8% were attributable to HPV infection, with substantially higher incidence and mortality rates seen in developing versus developed countries. In recent years, we have gained tremendous knowledge about HPVs and their interactions with host cells, tissues and the immune system; have validated and implemented strategies for safe and efficacious prophylactic vaccination against HPV infections; have developed increasingly sensitive and specific molecular diagnostic tools for HPV detection for use in cervical cancer screening; and have substantially increased global awareness of HPV and its many associated diseases in women, men, and children. While these achievements exemplify the success of biomedical research in generating important public health interventions, they also generate new and daunting challenges: costs of HPV prevention and medical care, the implementation of what is technically possible, socio-political resistance to prevention opportunities, and the very wide ranges of national economic capabilities and health care systems. Gains and challenges faced in the quest for comprehensive control of HPV infection and HPV-related cancers and other disease are summarized in this review. The information presented may be viewed in terms of a reframed paradigm of prevention of cervical cancer and other HPV-related diseases that will include strategic combinations of at least four major components: 1) routine introduction of HPV vaccines to women in all countries, 2) extension and simplification of existing screening programs using HPV-based technology, 3) extension of adapted screening programs to developing populations, and 4) consideration of the broader spectrum of cancers and other diseases preventable by HPV vaccination in women, as well as in men. Despite the huge advances already achieved, there must be ongoing efforts including international advocacy to achieve widespread optimally universal implementation of HPV prevention strategies in both developed and developing countries.
   This article summarizes information from the chapters presented in a special ICO Monograph 'Comprehensive Control of HPV Infections and Related Diseases' Vaccine Volume 30, Supplement 5, 2012. Additional details on each subtopic and full information regarding the supporting literature references may be found in the original chapters. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Xavier Bosch, F.; Castellsague, Xavier; Brotons, Maria; Alemany, Laia; Albero, Ginesa; Diaz, Mireia; de Sanjose, Silvia] IDIBELL, Catalan Inst Oncol ICO, Inst Catala Oncol, CERP, Lhospitalet De Llobregat, Barcelona, Spain.
   [Broker, Thomas R.] Univ Alabama Birmingham, Birmingham, AL USA.
   [Forman, David] Int Agcy Res Canc, Sect Canc Informat, F-69372 Lyon, France.
   [Moscicki, Anna-Barbara] Univ Calif San Francisco, Dept Pediat, Div Adolescent Med, San Francisco, CA USA.
   [Gillison, Maura L.] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
   [Doorbar, John] Natl Inst Med Res, Div Virol, London NW7 1AA, England.
   [Stern, Peter L.] Univ Manchester, Paterson Inst Canc Res, Manchester, Lancs, England.
   [Stanley, Margaret] Univ Cambridge, Dept Pathol, Cambridge CB2 1QP, England.
   [Arbyn, Marc] Sci Inst Publ Hlth, Canc Epidemiol Unit, Brussels, Belgium.
   [Arbyn, Marc] Univ Antwerp, Lab Cell Biol & Histol, B-2020 Antwerp, Belgium.
   [Poljak, Mario] Univ Ljubljana, Fac Med, Inst Microbiol & Immunol, Ljubljana, Slovenia.
   [Cuzick, Jack] Queen Mary Univ London, Wolfson Inst Prevent Med, London, England.
   [Castle, Philip E.] Global Canc Initiat, Chestertown, MD USA.
   [Schiller, John T.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Markowitz, Lauri E.] Ctr Dis Control & Prevent, Natl Ctr HIV Viral Hepatitis STD & TB Prevent, Atlanta, GA USA.
   [Fisher, William A.] Univ Western Ontario, Dept Psychol, Social Sci Ctr 7428, London, ON, Canada.
   [Fisher, William A.] Univ Western Ontario, Dept Obstet & Gynaecol, Social Sci Ctr 7428, London, ON, Canada.
   [Canfell, Karen] Univ NSW, Prince Wales Clin Sch, Lowy Canc Res Ctr, Kensington, NSW, Australia.
   [Canfell, Karen] NSW Canc Council, Canc Epidemiol Res Unit, Sydney, NSW, Australia.
   [Denny, Lynette A.] Univ Cape Town, Groote Schuur Hosp, Dept Obstet & Gynaecol, ZA-7925 Cape Town, South Africa.
   [Denny, Lynette A.] Univ Cape Town, Groote Schuur Hosp, Inst Infect Dis & Mol Med, ZA-7925 Cape Town, South Africa.
   [Franco, Eduardo L.] McGill Univ, Div Canc Epidemiol, Montreal, PQ, Canada.
   [Steben, Marc] Inst Natl Sante Publ Quebec, Montreal, PQ, Canada.
   [Kane, Mark A.] Consultant Immunizat Policy, Mercer Isl, WA USA.
   [Schiffman, Mark] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Meijer, Chris J. L. M.] Vrije Univ Amsterdam, Med Ctr, Dept Pathol, Amsterdam, Netherlands.
   [Sankaranarayanan, Rengaswamy] Int Agcy Res Canc, Screening Grp, F-69372 Lyon, France.
   [Castellsague, Xavier; Alemany, Laia; Albero, Ginesa; de Sanjose, Silvia] CIBERESP, Madrid, Spain.
   [Kim, Jane J.] Harvard Univ, Sch Publ Hlth, Ctr Hlth Decis Sci, Dept Hlth Policy & Management, Boston, MA 02115 USA.
RP Bosch, FX (reprint author), IDIBELL, Catalan Inst Oncol ICO, Inst Catala Oncol, CERP, Lhospitalet De Llobregat, Barcelona, Spain.
EM admincerp@iconcologia.net
RI de Sanjose Llongueras, Silvia/H-6339-2014; Albero, Ginesa/G-7248-2015;
   Bruni, Laia/N-5816-2014; BOSCH JOSE, FRANCESC XAVIER/J-6339-2012;
   Castellsague Pique, Xavier/N-5795-2014; Brotons, Maria/F-5383-2016; DIAZ
   SANCHIS, MIREIA/H-6335-2014; 
OI Qiao, You-Lin/0000-0001-6380-0871; Albero, Ginesa/0000-0002-9400-1914;
   Franco, Eduardo/0000-0002-4409-8084; BOSCH JOSE, FRANCESC
   XAVIER/0000-0002-7172-3412; Castellsague Pique,
   Xavier/0000-0002-0802-3595; Brotons, Maria/0000-0002-3057-0616; Bruni,
   Laia/0000-0003-3943-0326; Kjaer, Susanne/0000-0002-8347-1398
FU European Commission [HEALTH-F3-2010-242061, PREHDICT,
   HEALTH-F2-2011-282562, HPV AHEAD, 242061]; Instituto de Salud Carlos III
   (Spanish Government) [FIS PI08/1535, FIS PI10/02995, FIS PI11/02090, FIS
   PI11/02096, FIS PI11/02104, RCESP C03/09, RTICESP C03/10, RTIC
   RD06/0020/0095, RD12/0036/0056, CIBERESP]; Agencia de Gestio d'Ajuts
   Universitaris i de Recerca - Generalitat de Catalunya (Catalonian
   Government) [AGAUR 2005SGR00695, AGAUR 2009SGR126]; USPHS/NIH/National
   Cancer Institute (grant "Human Papillomavirus Gene Expression")
   [CA36200]; USPHS/NIH/National Cancer Institute (grant "Mechanisms of
   Human Papillomavirus DNA Replication") [CA83679]; US Public Health
   Service (National Cancer Institute, National Institutes of Health,
   Department of Health and Human Services) [R37 CA51323]; National
   Institute of AIDS and Infectious Disease [RC1 AI86051]; UK Medical
   Research Council [MC_U117584278]; Vrije Universiteit Amsterdam, the
   Netherlands [FP7-HEALTH-2011-282562]; Belgian Foundation Against Cancer
   (Brussels, Belgium); International Agency for Research on Cancer (Lyon,
   France); Cancer Research UK programme [A10404]; National Health and
   Medical Research Council, Australia [CDF APP1007994, 1007518];
   non-commercial government and academic consulting agreement in
   Australia; non-commercial government and academic consulting agreement
   in New Zealand; non-commercial government and academic consulting
   agreement in the UK; Cancer Council NSW, Australia; Bill and Melinda
   Gates Foundation, USA [35537]; U.S. National Cancer Institute [U54
   CA164336, R01 CA160744-01A1]; Bill and Melinda Gates Foundation [30505]
FX The work was partially supported by public grants from the European
   Commission (7th Framework Programme grants HEALTH-F3-2010-242061,
   PREHDICT and HEALTH-F2-2011-282562, HPV AHEAD), from the Instituto de
   Salud Carlos III (Spanish Government) (grants FIS PI08/1535, FIS
   PI10/02995, FIS PI11/02090, FIS PI11/02096, FIS PI11/02104, RCESP
   C03/09, RTICESP C03/10, RTIC RD06/0020/0095, RD12/0036/0056 and
   CIBERESP) and from the Agencia de Gestio d'Ajuts Universitaris i de
   Recerca - Generalitat de Catalunya (Catalonian Government) (grants AGAUR
   2005SGR00695 and AGAUR 2009SGR126), who had no role in data collection,
   analysis or interpretation of results. Thomas R. Broker receives
   research support from the USPHS/NIH/National Cancer Institute (grants
   "Human Papillomavirus Gene Expression" CA36200 and "Mechanisms of Human
   Papillomavirus DNA Replication" CA83679). Anna-Barbara Moscicki's work
   is supported by US Public Health Service grant R37 CA51323 (National
   Cancer Institute, National Institutes of Health, Department of Health
   and Human Services) and National Institute of AIDS and Infectious
   Disease RC1 AI86051. John Doorbar is funded by the UK Medical Research
   Council through program grant MC_U117584278 (Molecular Biology of Human
   Papillomavirus Infection). Marc Arbyn received financial support from:
   (1) the 7th Framework Programme of DG Research of the European
   Commission through the PREHDICT project (grant No. 242061, coordinated
   by the Vrije Universiteit Amsterdam, the Netherlands) and through the
   HPV AHEAD Network (FP7-HEALTH-2011-282562); (2) the Belgian Foundation
   Against Cancer (Brussels, Belgium); and (3) the International Agency for
   Research on Cancer (Lyon, France). Jack Cuzick was supported in part by
   Cancer Research UK programme grant A10404. Karen Canfell is supported by
   grants from the National Health and Medical Research Council, Australia
   (CDF APP1007994 and Project Grant #1007518), by non-commercial
   government and academic consulting agreements in Australia, New Zealand
   and the UK, and by Cancer Council NSW, Australia. Lynette A. Denny was
   partially supported by Bill and Melinda Gates Foundation, USA (35537).
   The work of Chris J.L.M. Meijer received support via the 7th Framework
   Programme of DG Research of the European commission through the PREHDICT
   project (grant 242061, coordinated via the Vrije Universiteit
   Amsterdam). Jane J. Kim is supported in part by grants from the U.S.
   National Cancer Institute (U54 CA164336, R01 CA160744-01A1) and the Bill
   and Melinda Gates Foundation (30505) for modeling of HPV and cervical
   cancer in developing countries.
NR 20
TC 89
Z9 90
U1 3
U2 28
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
EI 1873-2518
J9 VACCINE
JI Vaccine
PD NOV 22
PY 2013
VL 31
SU 8
BP 1
EP 31
DI 10.1016/j.vaccine.2013.07.026
PG 31
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 269IW
UT WOS:000328236000003
PM 24229716
ER

PT J
AU Goodall, S
   Gibson, AS
   Voller, B
   Lomarev, M
   Howatson, G
   Dang, N
   Hortobagyi, T
   Hallett, M
AF Goodall, Stuart
   Gibson, Alan St Clair
   Voller, Bernhard
   Lomarev, Mike
   Howatson, Glyn
   Nguyet Dang
   Hortobagyi, Tibor
   Hallett, Mark
TI Repetitive Transcranial Magnetic Stimulation Attenuates the Perception
   of Force Output Production in Non-Exercised Hand Muscles after
   Unilateral Exercise
SO PLOS ONE
LA English
DT Article
ID PRIMARY MOTOR CORTEX; THETA-BURST STIMULATION; CENTRAL-NERVOUS-SYSTEM;
   CROSS-LIMB TRANSFER; LOW-FREQUENCY; EVOKED-POTENTIALS; POSTEXERCISE
   DEPRESSION; PERFORMANCE GAINS; FATIGUE; MECHANISMS
AB We examined whether unilateral exercise creates perception bias in the non-exercised limb and ascertained whether rTMS applied to the primary motor cortex (M1) interferes with this perception. All participants completed 4 interventions: 1) 15-min learning period of intermittent isometric contractions at 35% MVC with the trained hand (EX), 2) 15-min learning period of intermittent isometric contractions at 35% MVC with the trained hand whilst receiving rTMS over the contralateral M1 (rTMS+EX); 3) 15-min of rTMS over the 'trained' M1 (rTMS) and 4) 15-min rest (Rest). Pre and post-interventions, the error of force output production, the perception of effort (RPE), motor evoked potentials (MEPs) and compound muscle action potentials (CMAPs) were measured in both hands. EX did not alter the error of force output production in the trained hand (Delta 3%; P>0.05); however, the error of force output production was reduced in the untrained hand (Delta 12%; P<0.05). rTMS+EX and rTMS alone did not show an attenuation in the error of force output production in either hand. EX increased RPE in the trained hand (9.1 +/- 0.5 vs. 11.3 +/- 0.7; P<0.01) but not the untrained hand (8.8 +/- 0.6 vs. 9.2 +/- 0.6; P>0.05). RPE was significantly higher after rTMS+EX in the trained hand (9.2 +/- 0.5 vs. 10.7 +/- 0.7; P<0.01) but ratings were unchanged in the untrained hand (8.5 +/- 0.6 vs. 9.2 +/- 0.5; P>0.05). The novel finding was that exercise alone reduced the error in force output production by over a third in the untrained hand. Further, when exercise was combined with rTMS the transfer of force perception was attenuated. These data suggest that the contralateral M1 of the trained hand might, in part, play an essential role for the transfer of force perception to the untrained hand.
C1 [Goodall, Stuart; Gibson, Alan St Clair; Howatson, Glyn] Northumbria Univ, Fac Hlth & Life Sci, Newcastle Upon Tyne NE1 8ST, Tyne & Wear, England.
   [Voller, Bernhard] Med Univ Vienna, Dept Neurol, Vienna, Austria.
   [Lomarev, Mike] Bekhterev Neuropsychol Inst, St Petersburg, Russia.
   [Howatson, Glyn] Northwest Univ, Sch Environm Sci & Dev, Water Res Grp, Potchefstroom, South Africa.
   [Nguyet Dang; Hallett, Mark] NINDS, Human Motor Control Sect, NIH, Bethesda, MD 20892 USA.
   [Hortobagyi, Tibor] Univ Groningen, Univ Med Ctr Groningen, NL-9713 AV Groningen, Netherlands.
RP Goodall, S (reprint author), Northumbria Univ, Fac Hlth & Life Sci, Newcastle Upon Tyne NE1 8ST, Tyne & Wear, England.
EM stuart.goodall@northumbria.ac.uk
OI Howatson, Glyn/0000-0001-8494-2043; Goodall, Stuart/0000-0001-9029-2171
FU National Institutes of Health; Northumbria University
FX This study was completed with funding from a National Institutes of
   Health Fogarty International Travelling Fellowship Award and the
   Strategic Investment Fund and Visiting Professors Fund at Northumbria
   University. The funders had no role in study design, data collection and
   analysis, decision to publish, or preparation of the manuscript.
NR 68
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Z9 4
U1 0
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 22
PY 2013
VL 8
IS 11
AR e80202
DI 10.1371/journal.pone.0080202
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 259QP
UT WOS:000327541700025
PM 24278259
ER

PT J
AU Lin, YJ
   Chang, JS
   Liu, X
   Hung, CH
   Lin, TH
   Huang, SM
   Jeang, KT
   Chen, CY
   Liao, CC
   Lin, CW
   Lai, CH
   Tien, N
   Lan, YC
   Ho, MW
   Chien, WK
   Chen, JH
   Huang, YC
   Tsang, H
   Wu, JY
   Chen, CH
   Chang, LC
   Tsai, FJ
AF Lin, Ying-Ju
   Chang, Jeng-Sheng
   Liu, Xiang
   Hung, Chien-Hui
   Lin, Ting-Hsu
   Huang, Shao-Mei
   Jeang, Kuan-Teh
   Chen, Chia-Yen
   Liao, Chiu-Chu
   Lin, Cheng-Wen
   Lai, Chih-Ho
   Tien, Ni
   Lan, Yu-Ching
   Ho, Mao-Wang
   Chien, Wen-Kuei
   Chen, Jin-Hua
   Huang, Yu-Chuen
   Tsang, Hsinyi
   Wu, Jer-Yuarn
   Chen, Chien-Hsiun
   Chang, Li-Ching
   Tsai, Fuu-Jen
TI Association between GRIN3A Gene Polymorphism in Kawasaki Disease and
   Coronary Artery Aneurysms in Taiwanese Children
SO PLOS ONE
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; TUMOR-NECROSIS-FACTOR; C-REACTIVE PROTEIN;
   ENDOTHELIAL-CELLS; NMDA RECEPTORS; SUSCEPTIBILITY; ACTIVATION; RISK;
   RNA; ABNORMALITIES
AB Kawasaki disease (KD) is pediatric systemic vasculitis with the classic complication of coronary artery aneurysm (CAA). It is the leading cause of acquired cardiovascular diseases in children. Some severe cases present with multi-organ involvement or neurological dysfunction. To identify the role of the glutamate receptor, ionotropic, N-methyl-D-aspartate 3A (GRIN3A) in KD, we investigated genetic variations in GRIN3A in a Taiwanese cohort of 262 KD patients (76 with and 186 without CAA complications). We used univariate and multivariate regression analyses to identify the associations between clinical characteristics and GRIN3A genetic variations in KD. According to univariate regression analysis, CAA formation in KD was significantly associated with fever duration (p < 0.0001), first Intravenous immunoglobulin (IVIG) used (days after day one of fever) (p < 0.0001), and the GRIN3A (rs7849782) genetic variant (p < 0.001). KD patients with GG+GC genotype showed a lower rate of developing CAA (GG+GC genotype: odds ratio = 0.26; 95% CI = 0.14-0.46). Significant associations were identified between KD with CAA complication and the GRIN3A (rs7849782) genetic variant by using multivariate regression analysis. Specifically, significant correlations were observed between KD with CAA complications and the presence of GG+GC genotypes for the GRIN3A rs7849782 single-nucleotide polymorphism (full model: odds ratio = 0.25; 95% CI = 0.14-0.46). Our results suggest that a polymorphism of the GRIN3A gene may play a role in KD pathogenesis.
C1 [Lin, Ying-Ju; Lin, Ting-Hsu; Huang, Shao-Mei; Liao, Chiu-Chu; Huang, Yu-Chuen; Tsai, Fuu-Jen] China Med Univ Hosp, Dept Med Res, Taichung, Taiwan.
   [Lin, Ying-Ju; Huang, Yu-Chuen; Wu, Jer-Yuarn; Chen, Chien-Hsiun; Tsai, Fuu-Jen] China Med Univ, Sch Chinese Med, Taichung, Taiwan.
   [Chang, Jeng-Sheng] China Med Univ Hosp, Dept Pediat, Taichung, Taiwan.
   [Liu, Xiang; Jeang, Kuan-Teh] NIAID, Mol Virol Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
   [Hung, Chien-Hui] Chang Gung Univ, Grad Inst Clin Med Sci, Chiayi, Taiwan.
   [Chen, Chia-Yen] NIAID, Viral Biochem Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
   [Lin, Cheng-Wen; Tien, Ni] China Med Univ, Dept Med Lab Sci & Biotechnol, Taichung, Taiwan.
   [Lai, Chih-Ho] China Med Univ, Sch Med, Dept Microbiol, Taichung, Taiwan.
   [Lan, Yu-Ching] China Med Univ, Dept Hlth Risk Management, Taichung, Taiwan.
   [Ho, Mao-Wang] China Med Univ Hosp, Infect Dis Sect, Dept Internal Med, Taichung, Taiwan.
   [Chien, Wen-Kuei; Chen, Jin-Hua] China Med Univ, Ctr Biostat, Taichung, Taiwan.
   [Chien, Wen-Kuei; Chen, Jin-Hua] Taipei Med Univ, Ctr Biostat, Taichung, Taiwan.
   [Tsang, Hsinyi] NIAID, Immunogenet Mol Lab, NIH, Bethesda, MD 20892 USA.
   [Wu, Jer-Yuarn; Chen, Chien-Hsiun; Chang, Li-Ching] Acad Sinica, Inst Biomed Sci, Taipei, Taiwan.
   [Tsai, Fuu-Jen] Asia Univ, Taichung, Taiwan.
RP Tsai, FJ (reprint author), China Med Univ Hosp, Dept Med Res, Taichung, Taiwan.
EM d0704@mail.cmuh.org.tw
RI Liu, Xiang/F-5731-2014; Tsai, Fuu-Jen/J-4140-2015; Lai,
   Chih-Ho/M-2433-2013; Lan, Yu-Ching/F-2449-2017
OI Lai, Chih-Ho/0000-0001-9229-818X; Lan, Yu-Ching/0000-0003-4781-6405
FU CMU [CMU100-S-01]; CMUH [DMR-102-034]; Republic of China National
   Science Council [NSC100-2320-B-039-012-MY3, NSC101-2314-B-039-008-MY3]
FX Support for this research was provided by CMU (CMU100-S-01), CMUH
   (DMR-102-034), and the Republic of China National Science Council
   (NSC100-2320-B-039-012-MY3; NSC101-2314-B-039-008-MY3). The funders had
   no role in study design, data collection and analysis, decision to
   publish, or preparation of the manuscript.
NR 56
TC 5
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U1 2
U2 12
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 22
PY 2013
VL 8
IS 11
AR UNSP e81384
DI 10.1371/journal.pone.0081384
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 259QP
UT WOS:000327541700061
PM 24278430
ER

PT J
AU Iida, N
   Dzutsev, A
   Stewart, CA
   Smith, L
   Bouladoux, N
   Weingarten, RA
   Molina, DA
   Salcedo, R
   Back, T
   Cramer, S
   Dai, RM
   Kiu, H
   Cardone, M
   Naik, S
   Patri, AK
   Wang, E
   Marincola, FM
   Frank, KM
   Belkaid, Y
   Trinchieri, G
   Goldszmid, RS
AF Iida, Noriho
   Dzutsev, Amiran
   Stewart, C. Andrew
   Smith, Loretta
   Bouladoux, Nicolas
   Weingarten, Rebecca A.
   Molina, Daniel A.
   Salcedo, Rosalba
   Back, Timothy
   Cramer, Sarah
   Dai, Ren-Ming
   Kiu, Hiu
   Cardone, Marco
   Naik, Shruti
   Patri, Anil K.
   Wang, Ena
   Marincola, Francesco M.
   Frank, Karen M.
   Belkaid, Yasmine
   Trinchieri, Giorgio
   Goldszmid, Romina S.
TI Commensal Bacteria Control Cancer Response to Therapy by Modulating the
   Tumor Microenvironment
SO SCIENCE
LA English
DT Article
ID OXIDATIVE STRESS; DENDRITIC CELLS; IMMUNE-SYSTEM; MICROBIOTA;
   INFLAMMATION; APOPTOSIS; ACTIVATION; CALIBRATE; SIGNALS; IMPACT
AB The gut microbiota influences both local and systemic inflammation. Inflammation contributes to development, progression, and treatment of cancer, but it remains unclear whether commensal bacteria affect inflammation in the sterile tumor microenvironment. Here, we show that disruption of the microbiota impairs the response of subcutaneous tumors to CpG-oligonucleotide immunotherapy and platinum chemotherapy. In antibiotics-treated or germ-free mice, tumor-infiltrating myeloid-derived cells responded poorly to therapy, resulting in lower cytokine production and tumor necrosis after CpG-oligonucleotide treatment and deficient production of reactive oxygen species and cytotoxicity after chemotherapy. Thus, optimal responses to cancer therapy require an intact commensal microbiota that mediates its effects by modulating myeloid-derived cell functions in the tumor microenvironment. These findings underscore the importance of the microbiota in the outcome of disease treatment.
C1 [Iida, Noriho; Dzutsev, Amiran; Stewart, C. Andrew; Smith, Loretta; Salcedo, Rosalba; Back, Timothy; Cramer, Sarah; Dai, Ren-Ming; Kiu, Hiu; Cardone, Marco; Trinchieri, Giorgio; Goldszmid, Romina S.] NCI, Canc & Inflammat Program, Frederick, MD 21702 USA.
   [Dzutsev, Amiran; Dai, Ren-Ming] Leidos Biomed Res Inc, Frederick Natl Lab, Frederick, MD 21702 USA.
   [Bouladoux, Nicolas; Naik, Shruti; Belkaid, Yasmine] NIAID, Mucosal Immunol Sect, Parasit Dis Lab, Bethesda, MD 20892 USA.
   [Weingarten, Rebecca A.; Frank, Karen M.] NIH, Microbiol Serv, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Molina, Daniel A.] Tech Resources Int Inc, Bethesda, MD 20817 USA.
   [Patri, Anil K.] Leidos Biomed Res Inc, Nanotechnol Characterizat Lab, Adv Technol Program, Frederick Natl Lab, Frederick, MD 21702 USA.
   [Wang, Ena; Marincola, Francesco M.] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Marincola, Francesco M.] Sidra Med & Res Ctr, Doha, Qatar.
RP Trinchieri, G (reprint author), NCI, Canc & Inflammat Program, Frederick, MD 21702 USA.
EM trinchig@mail.nih.gov; rgoldszmid@mail.nih.gov
RI Stewart, Charles/G-2470-2012; Nanotechnology Characterization Lab,
   NCL/K-8454-2012
FU NIH (NCI); NIH (Center for Cancer Research); NIH (NIAID); Japanese
   Society for Promotion of Science (JSPS) Research Fellowship for Japanese
   Biomedical and Behavioral Researchers at NIH
FX We greatly appreciate the support of D. Trageser-Cessler and A. Cesar in
   the NIAID germ-free facility; H. Zhou in the NIH Center for Human
   Immunology; T. Plona and K. Pike in the Laboratory of Molecular
   Technology, Leidos Biomedical Research, Inc.; and R. Winkler-Pickett, M.
   Karwan, and D. Zhao in the Cancer and Inflammation Program, CCR/NCI. We
   thank D. Klinman and A. Hurwitz for advice and R. Germain for critically
   reviewing the manuscript. The data presented in this manuscript are
   tabulated in the main paper and in the supplementary materials. This
   research was supported by the Intramural Research Program of the NIH
   (NCI, Center for Cancer Research, and NIAID) and the Japanese Society
   for Promotion of Science (JSPS) Research Fellowship for Japanese
   Biomedical and Behavioral Researchers at NIH. The 16S sequences were
   deposited in the Sequence Read Archive (SRA) under accession
   PRJNA221649. Array data were deposited at the Gene Expression Omnibus
   (GEO) with accession no. GSE51414.
NR 25
TC 216
Z9 225
U1 20
U2 131
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
EI 1095-9203
J9 SCIENCE
JI Science
PD NOV 22
PY 2013
VL 342
IS 6161
BP 967
EP 970
DI 10.1126/science.1240527
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255EZ
UT WOS:000327223500040
PM 24264989
ER

PT J
AU Koel, BF
   Burke, DF
   Bestebroer, TM
   van der Vliet, S
   Zondag, GCM
   Vervaet, G
   Skepner, E
   Lewis, NS
   Spronken, MIJ
   Russell, CA
   Eropkin, MY
   Hurt, AC
   Barr, IG
   de Jong, JC
   Rimmelzwaan, GF
   Osterhaus, ADME
   Fouchier, RAM
   Smith, DJ
AF Koel, Bjorn F.
   Burke, David F.
   Bestebroer, Theo M.
   van der Vliet, Stefan
   Zondag, Gerben C. M.
   Vervaet, Gaby
   Skepner, Eugene
   Lewis, Nicola S.
   Spronken, Monique I. J.
   Russell, Colin A.
   Eropkin, Mikhail Y.
   Hurt, Aeron C.
   Barr, Ian G.
   de Jong, Jan C.
   Rimmelzwaan, Guus F.
   Osterhaus, Albert D. M. E.
   Fouchier, Ron A. M.
   Smith, Derek J.
TI Substitutions Near the Receptor Binding Site Determine Major Antigenic
   Change During Influenza Virus Evolution
SO SCIENCE
LA English
DT Article
ID A VIRUSES; HEMAGGLUTININ; ANTIBODY; RECOGNITION
AB The molecular basis of antigenic drift was determined for the hemagglutinin (HA) of human influenza A/H3N2 virus. From 1968 to 2003, antigenic change was caused mainly by single amino acid substitutions, which occurred at only seven positions in HA immediately adjacent to the receptor binding site. Most of these substitutions were involved in antigenic change more than once. Equivalent positions were responsible for the recent antigenic changes of influenza B and A/H1N1 viruses. Substitution of a single amino acid at one of these positions substantially changed the virus-specific antibody response in infected ferrets. These findings have potentially far-reaching consequences for understanding the evolutionary mechanisms that govern influenza viruses.
C1 [Koel, Bjorn F.; Bestebroer, Theo M.; van der Vliet, Stefan; Vervaet, Gaby; Spronken, Monique I. J.; de Jong, Jan C.; Rimmelzwaan, Guus F.; Osterhaus, Albert D. M. E.; Fouchier, Ron A. M.; Smith, Derek J.] Erasmus MC, Dept Virosci, NL-3015 GE Rotterdam, Netherlands.
   [Burke, David F.; Skepner, Eugene; Lewis, Nicola S.; Smith, Derek J.] Univ Cambridge, Dept Zool, Ctr Pathogen Evolut, Cambridge CB2 3EJ, England.
   [Burke, David F.; Skepner, Eugene; Lewis, Nicola S.; Russell, Colin A.; Smith, Derek J.] Univ Cambridge, WHO Collaborating Ctr Modeling Evolut & Control E, Cambridge CB2 3EJ, England.
   [Zondag, Gerben C. M.] BaseClear BV, NL-2333 CC Leiden, Netherlands.
   [Zondag, Gerben C. M.] Leiden Univ, Luris, NL-2333 AA Leiden, Netherlands.
   [Russell, Colin A.] Univ Cambridge, Dept Vet Med, Cambridge CB3 0ES, England.
   [Eropkin, Mikhail Y.] All Union Influenza Res Inst, St Petersburg 197376, Russia.
   [Hurt, Aeron C.; Barr, Ian G.] VIDRL, WHO Collaborating Ctr Reference & Res Influenza, Melbourne, Vic 3051, Australia.
   [Smith, Derek J.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Fouchier, RAM (reprint author), Erasmus MC, Dept Virosci, NL-3015 GE Rotterdam, Netherlands.
EM r.fouchier@erasmusmc.nl; dsmith@zoo.cam.ac.uk
RI Fouchier, Ron/A-1911-2014; 
OI Fouchier, Ron/0000-0001-8095-2869; burke, david/0000-0001-8830-3951;
   Russell, Colin/0000-0002-2113-162X; Barr, Ian/0000-0002-7351-418X; Hurt,
   Aeron/0000-0003-1826-4314
FU NWO VICI grant; National Institute of Allergy and Infectious Diseases
   [HHSN266200700010C]; NIH [DP1-OD000490-01]; European Union [223498,
   278976]; Human Frontier Science Program [P0050/2008]; Australian
   Government Department of Health and Aging
FX We thank M. Aban, G. van Amerongen, C. Baas, R. van Beek, M. de Graaf,
   S. Herfst, S. James, M. Linster, K. Sutherland-Cash, and C. Whittleston
   for excellent technical assistance and discussions. D.F.B. and D.J.S.
   acknowledge the use of the CamGrid distributed computing resource.
   Supported by an NWO VICI grant, National Institute of Allergy and
   Infectious Diseases contract HHSN266200700010C, NIH Director's Pioneer
   Award DP1-OD000490-01, European Union FP7 program EMPERIE (223498),
   European Union FP7 program ANTIGONE (278976), and program grant
   P0050/2008 from the Human Frontier Science Program. The Melbourne WHO
   Collaborating Centre for Reference and Research on Influenza is
   supported by the Australian Government Department of Health and Aging.
   A.D.M.E.O. (on behalf of Viroclinics Biosciences B.V.) has advisory
   affiliations with GSK, Novartis, and Roche. A.D.M.E.O. and G.F.R. are
   consultants for Viroclinics Biosciences BV. A/H3N2 virus sequences were
   previously published by Smith et al. (16). The sequences of the
   influenza A/H1N1 and B viruses used in this study are available from the
   GISAID EpiFlu Database (www.gisaid.org) and are listed in table S6.
NR 21
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U1 7
U2 40
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
EI 1095-9203
J9 SCIENCE
JI Science
PD NOV 22
PY 2013
VL 342
IS 6161
BP 976
EP 979
DI 10.1126/science.1244730
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255EZ
UT WOS:000327223500042
PM 24264991
ER

PT J
AU Perry, AM
   Warnke, RA
   Hu, QL
   Gaulard, P
   Copie-Bergman, C
   Alkan, S
   Wang, HY
   Cheng, JX
   Bacon, CM
   Delabie, J
   Ranheim, E
   Kucuk, C
   Hu, XZ
   Weisenburger, DD
   Jaffe, ES
   Chan, WC
AF Perry, Anamarija M.
   Warnke, Roger A.
   Hu, Qinglong
   Gaulard, Philippe
   Copie-Bergman, Christiane
   Alkan, Serhan
   Wang, Huan-You
   Cheng, Jason X.
   Bacon, Chris M.
   Delabie, Jan
   Ranheim, Erik
   Kucuk, Can
   Hu, XiaoZhou
   Weisenburger, Dennis D.
   Jaffe, Elaine S.
   Chan, Wing C.
TI Indolent T-cell lymphoproliferative disease of the gastrointestinal
   tract
SO BLOOD
LA English
DT Article
ID CD8-POSITIVE LYMPHOID PROLIFERATION; MULTIPLE LYMPHOMATOUS POLYPOSIS;
   CLINICOPATHOLOGICAL FEATURES; STAT3 MUTATIONS; ENTEROPATHY; ENTITY;
   INFILTRATION; DISORDER; LEUKEMIA; EAR
AB Primary gastrointestinal (GI) T-cell lymphoma is an infrequent and aggressive disease. However, rare indolent clonal T-cell proliferations in the GI tract have been described. We report 10 cases of GI involvement by an indolent T-cell lymphoproliferative disease, including 6 men and 4 women with a median age of 48 years (range, 15-77 years). Presenting symptoms included abdominal pain, diarrhea, vomiting, food intolerance, and dyspepsia. The lesions involved oral cavity, esophagus, stomach, small intestine, and colon. The infiltrates were dense, but nondestructive, and composed of small, mature-appearing lymphoid cells. Eight cases were CD4(-)/CD8(+), 1 was CD4(+)/CD8(-), and another was CD4(-)/CD8(-). T-cell receptor-gamma chain gene rearrangement identified a clonal population in all 10 cases. There was no evidence of STAT3 SH2 domain mutation or activation. Six patients received chemotherapy because of an initial diagnosis of peripheral T-cell lymphoma, with little or no response, whereas the other 4 were followed without therapy. After a median follow-up of 38 months (range, 9-175 months), 9 patients were alive with persistent disease and 1 was free of disease. We propose the name "indolent T-LPD of the GI tract" for these lesions that can easily be mistaken for intestinal peripheral T-cell lymphoma, and lead to aggressive therapy.
C1 [Perry, Anamarija M.] Univ Manitoba, Dept Pathol, Winnipeg, MB R3T 2N2, Canada.
   [Warnke, Roger A.] Stanford Univ, Sch Med, Dept Pathol, Palo Alto, CA 94304 USA.
   [Hu, Qinglong] Carondelet St Joseph Hosp, Tucson Pathol Associates, Tucson, AZ USA.
   [Gaulard, Philippe; Copie-Bergman, Christiane] Hosp Henri Mondor, Dept Pathol, Creteil, France.
   [Alkan, Serhan] Cedars Sinai Med Ctr, Dept Pathol & Lab Med, Los Angeles, CA 90048 USA.
   [Wang, Huan-You] Univ Calif San Diego, Dept Pathol, San Diego, CA 92103 USA.
   [Cheng, Jason X.] Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA.
   [Bacon, Chris M.] Newcastle Univ, Northern Inst Canc Res, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
   [Delabie, Jan] Norwegian Radium Hosp, Dept Pathol, Oslo, Norway.
   [Ranheim, Erik] Univ Wisconsin, Dept Pathol & Lab Med, Madison, WI USA.
   [Kucuk, Can; Hu, XiaoZhou; Chan, Wing C.] Univ Nebraska Med Ctr, Dept Pathol & Microbiol, Omaha, NE USA.
   [Weisenburger, Dennis D.] City Hope Natl Med Ctr, Dept Pathol, Duarte, CA 91010 USA.
   [Jaffe, Elaine S.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
RP Chan, WC (reprint author), Univ Nebraska, Med Ctr, Dept Pathol & Microbiol, 983135 Nebraska Med Ctr, Omaha, NE 68198 USA.
EM ejaffe@mail.nih.gov; jchan@unmc.edu
RI Kucuk, Can/K-3913-2015; 
OI Kucuk, Can/0000-0001-5540-9012; Jaffe, Elaine/0000-0003-4632-0301;
   Delabie, Jan/0000-0001-5023-0689
NR 25
TC 25
Z9 28
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD NOV 21
PY 2013
VL 122
IS 22
BP 3599
EP 3606
DI 10.1182/blood-2013-07-512830
PG 8
WC Hematology
SC Hematology
GA 290BE
UT WOS:000329726200015
PM 24009234
ER

PT J
AU Pidala, J
   Wang, T
   Haagenson, M
   Spellman, SR
   Askar, M
   Battiwalla, M
   Baxter-Lowe, LA
   Bitan, M
   Fernandez-Vina, M
   Gandhi, M
   Jakubowski, AA
   Maiers, M
   Marino, SR
   Marsh, SGE
   Oudshoorn, M
   Palmer, J
   Prasad, VK
   Reddy, V
   Ringden, O
   Saber, W
   Santarone, S
   Schultz, KR
   Setterholm, M
   Trachtenberg, E
   Turner, EV
   Woolfrey, AE
   Lee, SJ
   Anasetti, C
AF Pidala, Joseph
   Wang, Tao
   Haagenson, Michael
   Spellman, Stephen R.
   Askar, Medhat
   Battiwalla, Minoo
   Baxter-Lowe, Lee Ann
   Bitan, Menachem
   Fernandez-Vina, Marcelo
   Gandhi, Manish
   Jakubowski, Ann A.
   Maiers, Martin
   Marino, Susana R.
   Marsh, Steven G. E.
   Oudshoorn, Machteld
   Palmer, Jeanne
   Prasad, Vinod K.
   Reddy, Vijay
   Ringden, Olle
   Saber, Wael
   Santarone, Stella
   Schultz, Kirk R.
   Setterholm, Michelle
   Trachtenberg, Elizabeth
   Turner, E. Victoria
   Woolfrey, Ann E.
   Lee, Stephanie J.
   Anasetti, Claudio
TI Amino acid substitution at peptide-binding pockets of HLA class I
   molecules increases risk of severe acute GVHD and mortality
SO BLOOD
LA English
DT Article
ID BONE-MARROW-TRANSPLANTATION; HEMATOPOIETIC-CELL TRANSPLANTATION;
   VERSUS-HOST-DISEASE; UNRELATED-DONOR; CHRONIC GRAFT; SIDE-CHAINS;
   RESOLUTION; RECOGNITION; MISMATCHES; SURVIVAL
AB HLA disparity has a negative impact on the outcomes of hematopoietic cell transplantation (HCT). We studied the independent impact of amino acid substitution (AAS) at peptide-binding positions 9, 99, 116, and 156, and killer immunoglobulin-like receptor binding position 77 of HLA-A, B, or C, on the risks for grade 3-4 acute graft-versus-host disease (GVHD), chronic GVHD, treatment-related mortality (TRM), relapse, and overall survival. In multivariate analysis, a mismatch at HLA-C position 116 was associated with increased risk for severe acute GVHD (hazard ratio [HR] = 1.45, 95% confidence interval [CI] = 1.15-1.82, P = .0016). Mismatch at HLA-C position 99 was associated with increased transplant-related mortality (HR = 1.37, 95% CI = 1.1-1.69, P = .0038). Mismatch at HLA-B position 9 was associated with increased chronic GVHD (HR = 2.28, 95% CI = 1.36-3.82, P = .0018). No AAS were significantly associated with outcome at HLA-A. Specific AAS pair combinations with a frequency > 30 were tested for association with HCT outcomes. Cysteine to tyrosine substitution at position 99 of HLA-C was associated with increased TRM (HR = 1.78, 95% = CI 1.27-2.51, P = .0009). These results demonstrate that donor-recipient mismatch for certain peptide-binding residues of the HLA class I molecule is associated with increased risk for acute and chronic GVHD and death.
C1 [Pidala, Joseph; Anasetti, Claudio] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
   [Wang, Tao; Saber, Wael] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
   [Haagenson, Michael; Spellman, Stephen R.] Ctr Int Blood & Marrow Transplant Res, Minneapolis, MN USA.
   [Askar, Medhat] Cleveland Clin, Transplantat Ctr, Cleveland, OH 44106 USA.
   [Battiwalla, Minoo] NHLBI, NIH, Bethesda, MD 20892 USA.
   [Baxter-Lowe, Lee Ann] Univ Calif San Francisco, Med Ctr, Immunogent & Transplantat Lab, San Francisco, CA USA.
   [Bitan, Menachem] Tel Aviv Univ, Tel Aviv Sourasky Med Ctr, Dept Pediat Hematol Oncol, IL-69978 Tel Aviv, Israel.
   [Fernandez-Vina, Marcelo] Stanford Univ Hosp & Clin, Pathol Blood Ctr, Stanford, CA USA.
   [Gandhi, Manish] Mayo Clin, Lab Med & Pathol, Rochester, MN USA.
   [Jakubowski, Ann A.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
   [Maiers, Martin; Setterholm, Michelle] Natl Marrow Donor Program, Minneapolis, MN USA.
   [Marino, Susana R.] Univ Chicago, Dept Pathol, Chicago, IL 60637 USA.
   [Marsh, Steven G. E.] UCL, London WC1E 6BT, England.
   [Oudshoorn, Machteld] Leiden Univ, Med Ctr, Europdonor Fdn, Leiden, Netherlands.
   [Palmer, Jeanne] Childrens Hosp Wisconsin, Div Hematol & Oncol, Milwaukee, WI 53201 USA.
   [Prasad, Vinod K.] Duke Univ, Med Ctr, Div Blood & Marrow Transplantat, Durham, NC USA.
   [Reddy, Vijay] Univ Florida, Gainesville, FL USA.
   [Ringden, Olle] Karolinska Univ Hosp, Dept Lab Med, Stockholm, Sweden.
   [Santarone, Stella] Osped Civile BMT Ctr, Dept Hematol, Pescara, Italy.
   [Schultz, Kirk R.] Univ British Columbia, British Columbias Childrens Hosp, Vancouver, BC, Canada.
   [Turner, E. Victoria] St Jude Childrens Res Hosp, HLA Lab, Memphis, TN 38105 USA.
   [Woolfrey, Ann E.; Lee, Stephanie J.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
RP Pidala, J (reprint author), H Lee Moffitt Canc Ctr & Res Inst, 12902 Magnolia Dr, Tampa, FL 33612 USA.
EM joseph.pidala@moffitt.org
OI Maiers, Martin/0000-0002-0198-2064
FU National Cancer Institute (NCI) [U24-CA076518]; National Heart, Lung,
   and Blood Institute (NHLBI); National Institute of Allergy and
   Infectious Diseases (NIAID); NHLBI [5U10HL069294]; NCI; Health Resources
   and Services Administration [HHSH250201200016C]; Office of Naval
   Research [N00014-12-1-0142, N00014-13-1-0039]; Office of Naval Research;
   Actinium Pharmaceuticals; Allos Therapeutics, Inc.; Amgen, Inc.; Ariad;
   Be the Match Foundation; Blue Cross and Blue Shield Association; Celgene
   Corporation; 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;
   Leukemia & Lymphoma Society; Medac GmbH; 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.; PerkinElmer, Inc.; Remedy
   Informatics; Sanofi US; Seattle Genetics; Sigma-tau Pharmaceuticals;
   Soligenix, Inc.; St. Baldrick's Foundation; StemCyte; 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; Wellpoint, 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 (NIAID); Grant/Cooperative
   Agreement 5U10HL069294 from NHLBI and NCI; contract HHSH250201200016C
   with Health Resources and Services Administration; 2 grants,
   N00014-12-1-0142 and N00014-13-1-0039, 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, 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.,
   PerkinElmer, 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, Health
   Resources and Services Administration, or any other agency of the U. S.
   Government.
NR 37
TC 35
Z9 35
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD NOV 21
PY 2013
VL 122
IS 22
BP 3651
EP 3658
DI 10.1182/blood-2013-05-501510
PG 8
WC Hematology
SC Hematology
GA 290BE
UT WOS:000329726200021
PM 23982174
ER

PT J
AU Kalnin, JR
   Berezhkovskii, AM
AF Kalnin, Juris R.
   Berezhkovskii, Alexander M.
TI Note: On the relation between Lifson-Jackson and Derrida formulas for
   effective diffusion coefficient
SO JOURNAL OF CHEMICAL PHYSICS
LA English
DT Letter
ID MOLECULAR MOTORS; KINETIC-MODELS; RANDOM-WALKS
C1 [Kalnin, Juris R.] Int Radio Astron Ctr VIRAC, Ventspils Engn Res Ctr, LV-3601 Ventspils, Latvia.
   [Berezhkovskii, Alexander M.] NIH, Math & Stat Comp Lab, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
RP Kalnin, JR (reprint author), Int Radio Astron Ctr VIRAC, Ventspils Engn Res Ctr, Inzenieru 101A, LV-3601 Ventspils, Latvia.
FU Intramural NIH HHS
NR 15
TC 2
Z9 2
U1 0
U2 7
PU AMER INST PHYSICS
PI MELVILLE
PA CIRCULATION & FULFILLMENT DIV, 2 HUNTINGTON QUADRANGLE, STE 1 N O 1,
   MELVILLE, NY 11747-4501 USA
SN 0021-9606
EI 1089-7690
J9 J CHEM PHYS
JI J. Chem. Phys.
PD NOV 21
PY 2013
VL 139
IS 19
AR 196101
DI 10.1063/1.4832035
PG 2
WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical
SC Chemistry; Physics
GA 262DS
UT WOS:000327714900048
PM 24320354
ER

PT J
AU Prustel, T
   Tachiya, M
AF Pruestel, Thorsten
   Tachiya, M.
TI Reversible diffusion-influenced reactions of an isolated pair on some
   two dimensional surfaces
SO JOURNAL OF CHEMICAL PHYSICS
LA English
DT Article
AB We investigate reversible diffusion-influenced reactions of an isolated pair in two dimensions. To this end, we employ convolution relations that permit deriving the survival probability of the reversible reaction directly in terms of the survival probability of the irreversible reaction. Furthermore, we make use of the mean reaction time approximation to write the irreversible survival probability in restricted spaces as a single exponential. In this way, we obtain exact and approximative expressions in the time domain for the reversible survival probability for three different two dimensional spatial domains: The infinite plane, the annular domain, and the surface of a sphere. Our obtained results should prove useful in the context of membrane-bound reversible diffusion-influenced reactions in cell biology. (C) 2013 AIP Publishing LLC.
C1 [Pruestel, Thorsten] NIAID, Lab Syst Biol, NIH, Bethesda, MD 20892 USA.
   [Tachiya, M.] Natl Inst Adv Ind Sci & Technol, Tsukuba, Ibaraki 3058565, Japan.
RP Prustel, T (reprint author), NIAID, Lab Syst Biol, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM prustelt@niaid.nih.gov; m.tachiya@aist.go.jp
FU National Institutes of Health (NIH), National Institute of Allergy and
   Infectious Diseases (NIAID); National Institute of Advanced Industrial
   Science and Technology (AIST)
FX This research was supported by the Intramural Research Program of the
   National Institutes of Health (NIH), National Institute of Allergy and
   Infectious Diseases (NIAID), and the National Institute of Advanced
   Industrial Science and Technology (AIST). T.P. would like to thank
   Martin Meier-Schellersheim for helpful comments.
NR 19
TC 3
Z9 3
U1 0
U2 9
PU AMER INST PHYSICS
PI MELVILLE
PA CIRCULATION & FULFILLMENT DIV, 2 HUNTINGTON QUADRANGLE, STE 1 N O 1,
   MELVILLE, NY 11747-4501 USA
SN 0021-9606
EI 1089-7690
J9 J CHEM PHYS
JI J. Chem. Phys.
PD NOV 21
PY 2013
VL 139
IS 19
AR 194103
DI 10.1063/1.4830218
PG 9
WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical
SC Chemistry; Physics
GA 262DS
UT WOS:000327714900006
PM 24320312
ER

PT J
AU Okamoto, M
   Hayase, S
   Miyakoshi, M
   Murata, T
   Kimura, S
AF Okamoto, Minoru
   Hayase, Suguru
   Miyakoshi, Masaaki
   Murata, Tsubasa
   Kimura, Shioko
TI Stem Cell Antigen 1-Positive Mesenchymal Cells Are the Origin of
   Follicular Cells during Thyroid Regeneration
SO PLOS ONE
LA English
DT Article
ID SIDE POPULATION CELLS; THYROTROPIN RECEPTOR GENE; ULTIMOBRANCHIAL BODY
   CYST; TRANSCRIPTION FACTOR-I; LABEL-RETAINING CELLS; TEMPLATE DNA
   STRANDS; PROGENITOR CELLS; C-CELLS; EXPRESSION; MOUSE
AB Many tissues are thought to contain adult stem/progenitor cells that are responsible for repair of the tissue where they reside upon damage and/or carcinogenesis, conditions when cellular homeostasis becomes uncontrolled. While the presence of stem/progenitor cells of the thyroid has been suggested, how these cells contribute to thyroid regeneration remains unclear. Here we show the origin of thyroid follicular cells and the process of their maturation to become follicular cells during regeneration. By using beta-galactosidase (beta-gal) reporter mice in conjunction with partial thyroidectomy as a model for thyroid regeneration, and bromodeoxyuridine (BrdU) long label-retaining cell analysis, we demonstrated that stem cell antigen 1 (Sca1) and BrdU-positive, but beta-gal and NKX2-1 negative cells were found in the non-follicular mesenchymal area 7 days after partial thyroidectomy. They temporarily co-expressed cytokeratin 14, and were observed in part of follicles by day 35 post-partial thyroidectomy. Sca1, BrdU, beta-gal, and NKX2-1-positive cells were found 120 days post-partial thyroidectomy. These results suggested that Sca1 and BrdU positive cells may participate in the formation of new thyroid follicles after partial thyroidectomy. The process of thyroid follicular cell regeneration was recapitulated in ex vivo thyroid slice collagen gel culture studies. These studies will facilitate research on thyroid stem/progenitor cells and their roles in thyroid diseases, particularly thyroid carcinomas.
C1 [Okamoto, Minoru; Hayase, Suguru; Miyakoshi, Masaaki; Murata, Tsubasa; Kimura, Shioko] NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
RP Kimura, S (reprint author), NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
EM kimuras@mail.nih.gov
FU National Cancer Institute, Center for Cancer Research, Intramural
   Research Program; Japanese Society for the Promotion of Science
FX This study was supported by the National Cancer Institute, Center for
   Cancer Research, Intramural Research Program. TM was supported by a
   fellowship from the Japanese Society for the Promotion of Science. The
   funders had no role in study design, data collection and analysis,
   decision to publish, or preparation of the manuscript.
NR 58
TC 5
Z9 5
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 21
PY 2013
VL 8
IS 11
AR e80801
DI 10.1371/journal.pone.0080801
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 259PW
UT WOS:000327539800083
PM 24278321
ER

PT J
AU Fernandez-Capetillo, O
   Nussenzweig, A
AF Fernandez-Capetillo, Oscar
   Nussenzweig, Andre
TI Naked Replication Forks Break apRPArt
SO CELL
LA English
DT Editorial Material
ID DNA; CHECKPOINT
AB Stalled replication forks occasionally collapse, leading to potentially catastrophic DNA double-strand breaks. Now, Toledo et al. (2013) reveal that fork breakage occurs when the pool of the single-strand DNA-binding protein RPA becomes exhausted. This study has important implications for the origin and treatment of cancers with high levels of replicative stress.
C1 [Fernandez-Capetillo, Oscar] Spanish Natl Canc Res Ctr CNIO, Genom Instabil Grp, Madrid 28029, Spain.
   [Nussenzweig, Andre] NCI, Lab Genome Integr, NIH, Bethesda, MD 20892 USA.
RP Fernandez-Capetillo, O (reprint author), Spanish Natl Canc Res Ctr CNIO, Genom Instabil Grp, Madrid 28029, Spain.
EM ofernandez@cnio.es; andre_nussenzweig@nih.gov
RI Fernandez-Capetillo, Oscar/H-3508-2015
OI Fernandez-Capetillo, Oscar/0000-0002-2690-6885
NR 8
TC 5
Z9 5
U1 0
U2 4
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
EI 1097-4172
J9 CELL
JI Cell
PD NOV 21
PY 2013
VL 155
IS 5
BP 979
EP 980
DI 10.1016/j.cell.2013.10.049
PG 2
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 259AU
UT WOS:000327500600002
PM 24267882
ER

PT J
AU Praetorius, C
   Grill, C
   Stacey, SN
   Metcalf, AM
   Gorkin, DU
   Robinson, KC
   Van Otterloo, E
   Kim, RSQ
   Bergsteinsdottir, K
   Ogmundsdottir, MH
   Magnusdottir, E
   Mishra, PJ
   Davis, SR
   Guo, T
   Zaidi, MR
   Helgason, AS
   Sigurdsson, MI
   Meltzer, PS
   Merlino, G
   Petit, V
   Larue, L
   Loftus, SK
   Adams, DR
   Sobhiafshar, U
   Emre, NCT
   Pavan, WJ
   Cornell, R
   Smith, AG
   McCallion, AS
   Fisher, DE
   Stefansson, K
   Sturm, RA
   Steingrimsson, E
AF Praetorius, Christian
   Grill, Christine
   Stacey, Simon N.
   Metcalf, Alexander M.
   Gorkin, David U.
   Robinson, Kathleen C.
   Van Otterloo, Eric
   Kim, Reuben S. Q.
   Bergsteinsdottir, Kristin
   Ogmundsdottir, Margret H.
   Magnusdottir, Erna
   Mishra, Pravin J.
   Davis, Sean R.
   Guo, Theresa
   Zaidi, M. Raza
   Helgason, Agnar S.
   Sigurdsson, Martin I.
   Meltzer, Paul S.
   Merlino, Glenn
   Petit, Valerie
   Larue, Lionel
   Loftus, Stacie K.
   Adams, David R.
   Sobhiafshar, Ulduz
   Emre, N. C. Tolga
   Pavan, William J.
   Cornell, Robert
   Smith, Aaron G.
   McCallion, Andrew S.
   Fisher, David E.
   Stefansson, Kari
   Sturm, Richard A.
   Steingrimsson, Eirikur
TI A Polymorphism in IRF4 Affects Human Pigmentation through a
   Tyrosinase-Dependent MITF/TFAP2A Pathway
SO CELL
LA English
DT Article
ID MICROPHTHALMIA TRANSCRIPTION FACTOR; CANCER SUSCEPTIBILITY;
   GENETIC-DETERMINANTS; COLORECTAL-CANCER; MULTIPLE-MYELOMA; EXPRESSION;
   VARIANTS; ENHANCER; MELANOCYTES; MELANOMA
AB Sequence polymorphisms linked to human diseases and phenotypes in genome-wide association studies often affect noncoding regions. A SNP within an intron of the gene encoding Interferon Regulatory Factor 4 (IRF4), a transcription factor with no known role in melanocyte biology, is strongly associated with sensitivity of skin to sun exposure, freckles, blue eyes, and brown hair color. Here, we demonstrate that this SNP lies within an enhancer of IRF4 transcription in melanocytes. The allele associated with this pigmentation phenotype impairs binding of the TFAP2A transcription factor that, together with the melanocyte master regulator MITF, regulates activity of the enhancer. Assays in zebrafish and mice reveal that IRF4 cooperates with MITF to activate expression of Tyrosinase (TYR), an essential enzyme in melanin synthesis. Our findings provide a clear example of a noncoding polymorphism that affects a phenotype by modulating a developmental gene regulatory network.
C1 [Praetorius, Christian; Grill, Christine; Bergsteinsdottir, Kristin; Ogmundsdottir, Margret H.; Magnusdottir, Erna; Sigurdsson, Martin I.; Steingrimsson, Eirikur] Univ Iceland, Fac Med, Dept Biochem & Mol Biol, Biomed Ctr, IS-101 Reykjavik, Iceland.
   [Stacey, Simon N.; Helgason, Agnar S.; Stefansson, Kari] Decode Genet, IS-101 Reykjavik, Iceland.
   [Metcalf, Alexander M.; Kim, Reuben S. Q.; Smith, Aaron G.; Sturm, Richard A.] Univ Queensland, Inst Mol Biosci, Brisbane, Qld 4072, Australia.
   [Gorkin, David U.; McCallion, Andrew S.] Johns Hopkins Univ, Sch Med, McKusick Nathans Inst Genet Med, Baltimore, MD 21205 USA.
   [Gorkin, David U.] Johns Hopkins Univ, Sch Med, Predoctoral Training Program Human Genet, Baltimore, MD 21205 USA.
   [Robinson, Kathleen C.; Fisher, David E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Dermatol, Boston, MA 02114 USA.
   [Van Otterloo, Eric; Cornell, Robert] Univ Iowa, Iowa City, IA 52242 USA.
   [Kim, Reuben S. Q.; Smith, Aaron G.] Univ Queensland, Sch Biomed Sci, Brisbane, Qld 4072, Australia.
   [Mishra, Pravin J.; Guo, Theresa; Zaidi, M. Raza; Merlino, Glenn] NCI, Lab Canc Biol & Genet, Bethesda, MD 20892 USA.
   [Davis, Sean R.; Meltzer, Paul S.] NCI, Genet Branch, Bethesda, MD 20892 USA.
   [Petit, Valerie; Larue, Lionel] Inst Curie, Ctr Rech, F-91405 Orsay, France.
   [Loftus, Stacie K.; Pavan, William J.] NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA.
   [Adams, David R.] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
   [Sobhiafshar, Ulduz; Emre, N. C. Tolga] Bogazici Univ, Dept Mol Biol & Genet, Lab Genome Regulat, TR-34342 Istanbul, Turkey.
RP Steingrimsson, E (reprint author), Univ Iceland, Fac Med, Dept Biochem & Mol Biol, Biomed Ctr, Vatnsmyrarvegur 16, IS-101 Reykjavik, Iceland.
EM eirikurs@hi.is
RI Sturm, Richard/C-9943-2009; Magnusdottir, Erna/H-5181-2013; Smith,
   Aaron/A-8329-2010; Helgason, Agnar/K-1522-2015; Larue,
   Lionel/I-6532-2016; Zaidi, M. Raza/H-1386-2016; Sigurdsson,
   Martin/I-9655-2016; 
OI Sturm, Richard/0000-0003-1301-0294; Magnusdottir,
   Erna/0000-0002-3369-4390; Zaidi, M. Raza/0000-0003-0480-3188;
   Sigurdsson, Martin/0000-0001-7054-0844; Praetorius,
   Christian/0000-0001-7514-5333
FU NIH [5R01 AR043369-16]; Melanoma Research Alliance; Dr. Miriam and
   Sheldon Adelson Medical Research Foundation; US-Israel Binational
   Science Foundation; Ligue Nationale Contre le Cancer; INCa; Icelandic
   Research Fund; Research Fund of the University of Iceland; Haskolasjodur
   Student Fund; Jules Verne Fund; National Institute of General Medical
   Sciences [GM071648]; National Institute of Neurological Disease and
   Stroke [NS062972]; National Human Genome Research Institute's Intramural
   Research Program; NSF Graduate Research Fellowship
FX We thank Thorunn Rafnar, Magnus Karl Magnusson, Unnur Thorsteinsdottir,
   Colin R. Goding, and Thorarinn Gudjonsson for critical comments on the
   manuscript. This work was supported by grants from NIH (5R01
   AR043369-16), Melanoma Research Alliance, Dr. Miriam and Sheldon Adelson
   Medical Research Foundation, US-Israel Binational Science Foundation (to
   D.E.F.), Ligue Nationale Contre le Cancer (Equipe labellisee) and INCa
   (to L.L.), the Icelandic Research Fund and the Research Fund of the
   University of Iceland (to E.S.), the Haskolasjodur Student Fund (to
   E.S., C.P., and C.G.), the Jules Verne Fund (to E.S. and L.L.), by the
   National Institute of General Medical Sciences (GM071648) and National
   Institute of Neurological Disease and Stroke (NS062972; to A.S.M.), the
   National Human Genome Research Institute's Intramural Research Program
   (to W.J.P. and S.L.), and an NSF Graduate Research Fellowship (to
   D.U.G.).
NR 51
TC 46
Z9 47
U1 7
U2 44
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
EI 1097-4172
J9 CELL
JI Cell
PD NOV 21
PY 2013
VL 155
IS 5
BP 1022
EP 1033
DI 10.1016/j.cell.2013.10.022
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 259AU
UT WOS:000327500600008
PM 24267888
ER

PT J
AU Lee, NN
   Chalamcharla, VR
   Reyes-Turcu, F
   Mehta, S
   Zofall, M
   Balachandran, V
   Dhakshnamoorthy, J
   Taneja, N
   Yamanaka, S
   Zhou, M
   Grewal, SIS
AF Lee, Nathan N.
   Chalamcharla, Venkata R.
   Reyes-Turcu, Francisca
   Mehta, Sameet
   Zofall, Martin
   Balachandran, Vanivilasini
   Dhakshnamoorthy, Jothy
   Taneja, Nitika
   Yamanaka, Soichiro
   Zhou, Ming
   Grewal, Shiv I. S.
TI Mtr4-like Protein Coordinates Nuclear RNA Processing for Heterochromatin
   Assembly and for Telomere Maintenance
SO CELL
LA English
DT Article
ID LONG NONCODING RNAS; YEAST SCHIZOSACCHAROMYCES-POMBE; DIRECTED DNA
   METHYLATION; MEIOTIC MESSENGER-RNAS; FISSION YEAST; POLY(A)-BINDING
   PROTEIN; SELECTIVE ELIMINATION; QUALITY-CONTROL; ANTISENSE RNA; S. POMBE
AB The regulation of protein-coding and noncoding RNAs is linked to nuclear processes, including chromatin modifications and gene silencing. However, the mechanisms that distinguish RNAs and mediate their functions are poorly understood. We describe a nuclear RNA-processing network in fission yeast with a core module comprising the Mtr4-like protein, Mtl1, and the zinc-finger protein, Red1. The Mtl1-Red1 core promotes degradation of mRNAs and noncoding RNAs and associates with different proteins to assemble heterochromatin via distinct mechanisms. Mtl1 also forms Red1-independent interactions with evolutionarily conserved proteins named Nrl1 and Ctr1, which associate with splicing factors. Whereas Nrl1 targets transcripts with cryptic introns to form heterochromatin at developmental genes and retrotransposons, Ctr1 functions in processing intron-containing telomerase RNA. Together with our discovery of widespread cryptic introns, including in noncoding RNAs, these findings reveal unique cellular strategies for recognizing regulatory RNAs and coordinating their functions in response to developmental and environmental cues.
C1 [Lee, Nathan N.; Chalamcharla, Venkata R.; Reyes-Turcu, Francisca; Mehta, Sameet; Zofall, Martin; Balachandran, Vanivilasini; Dhakshnamoorthy, Jothy; Taneja, Nitika; Yamanaka, Soichiro; Grewal, Shiv I. S.] NCI, Biochem & Mol Biol Lab, Bethesda, MD 20892 USA.
   [Lee, Nathan N.] NIH, Bethesda, MD 20892 USA.
   [Lee, Nathan N.] Johns Hopkins Univ, Grad Partnership Program, Bethesda, MD 20892 USA.
   [Zhou, Ming] Frederick Natl Lab Canc Res, Lab Prote & Analyt Technol, Frederick, MD 21702 USA.
RP Grewal, SIS (reprint author), NCI, Biochem & Mol Biol Lab, Bethesda, MD 20892 USA.
EM grewals@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health (NIH);
   National Cancer Institute and utilized the Helix Systems; Biowulf Linux
   cluster at the NIH
FX We thank P. FitzGerald for intron analysis, R. Allshire for the cwf10-1
   mutant, J. Barrowman for her valuable help in editing the manuscript,
   and M. Lichten for comments. This research was supported by the
   Intramural Research Program of the National Institutes of Health (NIH)
   and by the National Cancer Institute and utilized the Helix Systems and
   the Biowulf Linux cluster at the NIH.
NR 58
TC 39
Z9 39
U1 4
U2 21
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
EI 1097-4172
J9 CELL
JI Cell
PD NOV 21
PY 2013
VL 155
IS 5
BP 1061
EP 1074
DI 10.1016/j.cell.2013.10.027
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 259AU
UT WOS:000327500600011
PM 24210919
ER

PT J
AU Henriques, T
   Gilchrist, DA
   Nechaev, S
   Bern, M
   Muse, GW
   Burkholder, A
   Fargo, DC
   Adelman, K
AF Henriques, Telmo
   Gilchrist, Daniel A.
   Nechaev, Sergei
   Bern, Michael
   Muse, Ginger W.
   Burkholder, Adam
   Fargo, David C.
   Adelman, Karen
TI Stable Pausing by RNA Polymerase II Provides an Opportunity to Target
   and Integrate Regulatory Signals
SO MOLECULAR CELL
LA English
DT Article
ID P-TEFB; TRANSCRIPTIONAL ACTIVATION; HUMAN PROMOTERS; ELONGATION RATE;
   MESSENGER-RNA; NASCENT RNA; POL II; EXOSOME; GENES; TERMINATION
AB Metazoan gene expression is often regulated after the recruitment of RNA polymerase II (Pal II) to promoters, through the controlled release of promoter-proximally paused Pol II into productive RNA synthesis. Despite the prevalence of paused Pal II, very little is known about the dynamics of these early elongation complexes or the fate of the short transcription start site-associated (tss) RNAs they produce. Here, we demonstrate that paused elongation complexes can be remarkably stable, with half-lives exceeding 15 min at genes with inefficient pause release. Promoter-proximal termination by Pol II is infrequent, and released tssRNAs are targeted for rapid degradation. Further, we provide evidence that the predominant tssRNA species observed are nascent RNAs held within early elongation complexes. We propose that stable pausing of polymerase provides a temporal window of opportunity for recruitment of factors to modulate gene expression and that the nascent tssRNA represents an appealing target for these interactions.
C1 [Henriques, Telmo; Gilchrist, Daniel A.; Nechaev, Sergei; Bern, Michael; Muse, Ginger W.; Adelman, Karen] NIEHS, NIH, Lab Mol Carcinogenesis, Res Triangle Pk, NC 27709 USA.
   [Burkholder, Adam; Fargo, David C.] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
RP Adelman, K (reprint author), NIEHS, NIH, Lab Mol Carcinogenesis, POB 12233, Res Triangle Pk, NC 27709 USA.
EM adelmank@niehs.nih.gov
OI Gilchrist, Daniel/0000-0003-1668-2790
FU NIH [OD010949-10]; NIH, National Institute of Environmental Health
   Sciences [Z01 ES101987]
FX We would like to thank Erik Andrulis (Case Western Reserve) for the kind
   gift of the Rrp40 antibody, Michael Marr (Brandeis) for the TFIIA
   antibody, and the Drosophila Genomics Resource Center, supported by NIH
   grant OD010949-10 for S2 cells. This research was supported by the
   Intramural Research Program of the NIH, National Institute of
   Environmental Health Sciences, to K.A. (Z01 ES101987).
NR 44
TC 39
Z9 39
U1 4
U2 23
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
J9 MOL CELL
JI Mol. Cell
PD NOV 21
PY 2013
VL 52
IS 4
BP 517
EP 528
DI 10.1016/j.molcel.2013.10.001
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 257WM
UT WOS:000327418500007
PM 24184211
ER

PT J
AU Nakamura, Y
   Oscherwitz, J
   Cease, KB
   Chan, SM
   Munoz-Planillo, R
   Hasegawa, M
   Villaruz, AE
   Cheung, GYC
   McGavin, MJ
   Travers, JB
   Otto, M
   Inohara, N
   Nunez, G
AF Nakamura, Yuumi
   Oscherwitz, Jon
   Cease, Kemp B.
   Chan, Susana M.
   Munoz-Planillo, Raul
   Hasegawa, Mizuho
   Villaruz, Amer E.
   Cheung, Gordon Y. C.
   McGavin, Martin J.
   Travers, Jeffrey B.
   Otto, Michael
   Inohara, Naohiro
   Nunez, Gabriel
TI Staphylococcus delta-toxin induces allergic skin disease by activating
   mast cells
SO NATURE
LA English
DT Article
ID ATOPIC-DERMATITIS; IN-VIVO; AUREUS; VIRULENCE; IGE; MICE;
   IDENTIFICATION; DEFICIENT; RESPONSES; RELEASE
AB Atopic dermatitis is a chronic inflammatory skin disease that affects 15-30% of children and approximately 5% of adults in industrialized countries(1). Although the pathogenesis of atopic dermatitis is not fully understood, the disease is mediated by an abnormal immunoglobulin E immune response in the setting of skin barrier dysfunction(2). Mast cells contribute to immunoglobulin-E-mediated allergic disorders including atopic dermatitis(3). Upon activation, mast cells release their membrane-bound cytosolic granules leading to the release of several molecules that are important in the pathogenesis of atopic dermatitis and host defence(4). More than 90% of patients with atopic dermatitis are colonized with Staphylococcus aureus in the lesional skin whereas most healthy individuals do not harbour the pathogen(5). Several staphylococcal exotoxins can act as superantigens and/or antigens in models of atopic dermatitis(6). However, the role of these staphylococcal exotoxins in disease pathogenesis remains unclear. Here we report that culture supernatants of S. aureus contain potent mast-cell degranulation activity. Biochemical analysis identified delta-toxin as the mast cell degranulation-inducing factor produced by S. aureus. Mast cell degranulation induced by delta-toxin depended on phosphoinositide 3-kinase and calcium (Ca2+) influx; however, unlike that mediated by immunoglobulin-E crosslinking, it did not require the spleen tyrosine kinase. In addition, immunoglobulin-E enhanced delta-toxin-induced mast cell degranulation in the absence of antigen. Furthermore, S. aureus isolates recovered from patients with atopic dermatitis produced large amounts of delta-toxin. Skin colonization with S. aureus, but not a mutant deficient in delta-toxin, promoted immunoglobulin-E and interleukin-4 production, as well as inflammatory skin disease. Furthermore, enhancement of immunoglobulin E production and dermatitis by delta-toxin was abrogated in Kit(W-sh/W-sh) mast-cell-deficient mice and restored by mast cell reconstitution. These studies identify delta-toxin as a potent inducer of mast cell degranulation and suggest a mechanistic link between S. aureus colonization and allergic skin disease.
C1 [Nakamura, Yuumi; Chan, Susana M.; Munoz-Planillo, Raul; Hasegawa, Mizuho; Inohara, Naohiro; Nunez, Gabriel] Univ Michigan, Sch Med, Dept Pathol, Ann Arbor, MI 48109 USA.
   [Nakamura, Yuumi; Chan, Susana M.; Munoz-Planillo, Raul; Hasegawa, Mizuho; Inohara, Naohiro; Nunez, Gabriel] Univ Michigan, Sch Med, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
   [Oscherwitz, Jon; Cease, Kemp B.] Univ Michigan, Sch Med, Dept Internal Med, Div Hematol Oncol, Ann Arbor, MI 48109 USA.
   [Oscherwitz, Jon; Cease, Kemp B.] VA Ann Arbor Healthcare Syst, Ann Arbor, MI 48105 USA.
   [Villaruz, Amer E.; Cheung, Gordon Y. C.; Otto, Michael] NIAID, Lab Human Bacterial Pathogenesis, US Natl Inst Hlth, Bethesda, MD 20892 USA.
   [McGavin, Martin J.] Univ Western Ontario, Dept Microbiol & Immunol, London, ON N6A 5C1, Canada.
   [McGavin, Martin J.] Univ Western Ontario, Ctr Human Immunol, London, ON N6A 5C1, Canada.
   [Travers, Jeffrey B.] Indiana Univ Sch Med, Dept Dermatol, Indianapolis, IN 46202 USA.
RP Nunez, G (reprint author), Univ Michigan, Sch Med, Dept Pathol, Ann Arbor, MI 48109 USA.
EM gabriel.nunez@umich.edu
RI Nunez, Gabriel/A-7160-2014
FU Chiba University Global COE Program; Cell Science Research Foundation;
   Kanae Foundation for the Promotion of Medical Science; Department of
   Veterans Affairs [I01BX000429]; National Institute of Allergy and
   Infectious Diseases (NIAID), National Institutes of Health (NIH); NIH
   [R01AR059688, R01HL062996]; University of Michigan's Cancer Center
FX We thank S. Koonse for animal husbandry, J. Whitfield for enzyme-linked
   immunosorbent assays, S. Meshinchi for electron microscopy, V. Basrur
   for mass spectrometry, K. Kidwell for advice with statistical analysis,
   M. K. Oyoshi and R. S. Geha for experimental advice, V. Y. Tan for help
   with constructing the LAC P3-lux strain and A. Burberry for reviewing
   the manuscript. Y.N. was supported by fellowships from the Chiba
   University Global COE Program, the Cell Science Research Foundation and
   the Kanae Foundation for the Promotion of Medical Science. J.O. and
   K.B.C. were supported by Department of Veterans Affairs Merit Award
   I01BX000429. A.E.V., G.Y.C.C. and M.O. were supported by the Intramural
   Research Program of the National Institute of Allergy and Infectious
   Diseases (NIAID), National Institutes of Health (NIH). This work
   supported by NIH grants R01AR059688 to G.N. and R01HL062996 to J.B.T.
   and funds to the Michigan Comprehensive Cancer Center Immunology
   Monitoring Core from the University of Michigan's Cancer Center Support
   Grant.
NR 34
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PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
EI 1476-4687
J9 NATURE
JI Nature
PD NOV 21
PY 2013
VL 503
IS 7476
BP 397
EP +
DI 10.1038/nature12655
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 254KG
UT WOS:000327163200041
PM 24172897
ER

PT J
AU Powe, CE
   Evans, MK
   Wenger, J
   Zonderman, AB
   Berg, AH
   Nalls, M
   Tamez, H
   Zhang, DS
   Bhan, I
   Karumanchi, SA
   Powe, NR
   Thadhani, R
AF Powe, Camille E.
   Evans, Michele K.
   Wenger, Julia
   Zonderman, Alan B.
   Berg, Anders H.
   Nalls, Michael
   Tamez, Hector
   Zhang, Dongsheng
   Bhan, Ishir
   Karumanchi, S. Ananth
   Powe, Neil R.
   Thadhani, Ravi
TI Vitamin D-Binding Protein and Vitamin D Status of Black Americans and
   White Americans
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID BONE-MINERAL DENSITY; RANDOMIZED CONTROLLED-TRIAL; D DEFICIENCY;
   25-HYDROXYVITAMIN D; HIP-FRACTURES; SERUM 25-HYDROXYVITAMIN-D;
   PARATHYROID-HORMONE; AFRICAN-AMERICANS; D INSUFFICIENCY; OLDER-ADULTS
AB BackgroundLow levels of total 25-hydroxyvitamin D are common among black Americans. Vitamin D-binding protein has not been considered in the assessment of vitamin D deficiency.
   MethodsIn the Healthy Aging in Neighborhoods of Diversity across the Life Span cohort of blacks and whites (2085 participants), we measured levels of total 25-hydroxyvitamin D, vitamin D-binding protein, and parathyroid hormone as well as bone mineral density (BMD). We genotyped study participants for two common polymorphisms in the vitamin D-binding protein gene (rs7041 and rs4588). We estimated levels of bioavailable 25-hydroxyvitamin D in homozygous participants.
   ResultsMean (SE) levels of both total 25-hydroxyvitamin D and vitamin D-binding protein were lower in blacks than in whites (total 25-hydroxyvitamin D, 15.60.2 ng per milliliter vs. 25.80.4 ng per milliliter, P<0.001; vitamin D-binding protein, 1683 g per milliliter vs. 337 +/- 5 g per milliliter, P<0.001). Genetic polymorphisms independently appeared to explain 79.4% and 9.9% of the variation in levels of vitamin D-binding protein and total 25-hydroxyvitamin D, respectively. BMD was higher in blacks than in whites (1.05 +/- 0.01 g per square centimeter vs. 0.94 +/- 0.01 g per square centimeter, P<0.001). Levels of parathyroid hormone increased with decreasing levels of total or bioavailable 25-hydroxyvitamin D (P<0.001 for both relationships), yet within each quintile of parathyroid hormone concentration, blacks had significantly lower levels of total 25-hydroxyvitamin D than whites. Among homozygous participants, blacks and whites had similar levels of bioavailable 25-hydroxyvitamin D overall (2.9 +/- 0.1 ng per milliliter and 3.1 +/- 0.1 ng per milliliter, respectively; P=0.71) and within quintiles of parathyroid hormone concentration.
   Conclusions Community-dwelling black Americans, as compared with whites, had low levels of total 25-hydroxyvitamin D and vitamin D-binding protein, resulting in similar concentrations of estimated bioavailable 25-hydroxyvitamin D. Racial differences in the prevalence of common genetic polymorphisms provide a likely explanation for this observation.
C1 [Powe, Camille E.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
   [Wenger, Julia; Tamez, Hector; Bhan, Ishir; Thadhani, Ravi] Massachusetts Gen Hosp, Div Nephrol, Boston, MA 02114 USA.
   [Berg, Anders H.] Beth Israel Deaconess Med Ctr, Dept Pathol, Boston, MA 02215 USA.
   [Berg, Anders H.] Harvard Univ, Sch Med, Boston, MA USA.
   [Zhang, Dongsheng; Karumanchi, S. Ananth] Beth Israel Deaconess Med Ctr, Div Nephrol, Boston, MA 02215 USA.
   [Zhang, Dongsheng; Karumanchi, S. Ananth] Howard Hughes Med Inst, Boston, MA 02115 USA.
   [Evans, Michele K.; Zonderman, Alan B.] NIA, Lab Epidemiol & Populat Sci, NIH, Bethesda, MD 20892 USA.
   [Nalls, Michael] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
   [Powe, Neil R.] San Francisco Gen Hosp, Dept Med, San Francisco, CA 94110 USA.
   [Powe, Neil R.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP Evans, MK (reprint author), NIA, NIH, Biomed Res Ctr, 251 Bayview Blvd,Suite 100,Rm 4C-222, Baltimore, MD 21224 USA.
EM me42v@nih.gov; rthadhani@mgh.harvard.edu
OI Zonderman, Alan B/0000-0002-6523-4778
FU National Institute on Aging
FX Funded by the National Institute on Aging and others.
NR 41
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U1 2
U2 29
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 21
PY 2013
VL 369
IS 21
BP 1991
EP 2000
DI 10.1056/NEJMoa1306357
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 254KE
UT WOS:000327163000007
PM 24256378
ER

PT J
AU Xu, SLY
   Schwarz, JM
AF Xu, S. -L. -Y.
   Schwarz, J. M.
TI Contact processes in crowded environments
SO PHYSICAL REVIEW E
LA English
DT Article
ID ABSORBING PHASE-TRANSITIONS; GLASS-TRANSITION; CONSERVED FIELD;
   LATTICE-GAS; MODEL; COLLOIDS; SYSTEMS; STATE
AB Periodically sheared colloids at low densities demonstrate a dynamical phase transition from an inactive to active phase as the strain amplitude is increased. The inactive phase consists of no collisions (contacts) between particles in the steady state limit, while in the active phase collisions persist. To investigate this system at higher densities, we construct and study a conserved-particle-number contact process with three-body interactions, which are potentially more likely than two-body interactions at higher densities. For example, consider one active (diffusing) particle colliding with two inactive (nondiffusing) particles such that they become active and consider spontaneous inactivation. In mean field, this system exhibits a continuous dynamical phase transition. Simulations on square lattices also indicate a continuous transition with exponents similar to those measured for the conserved lattice gas (CLG) model. In contrast, the three-body interaction requiring two active particles to activate one inactive particle exhibits a discontinuous transition. Finally, inspired by kinetically constrained models of the glass transition, we investigate the "caging effect" at even higher particle densities to look for a second dynamical phase transition back to an inactive phase. Square lattice simulations suggest a continuous transition with a new set of exponents differing from both the CLG model and what is known as directed percolation, indicating a potentially new universality class for a contact process with a conserved particle number.
C1 [Xu, S. -L. -Y.] NIH, Bethesda, MD 20892 USA.
   [Schwarz, J. M.] Syracuse Univ, Dept Phys, Syracuse, NY 13244 USA.
RP Xu, SLY (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
FU  [NSF-DMR-CAREER-0645373]
FX J.M.S. kindly acknowledges discussions early on in the project with
   Bismayan Chakrabarti on conserved particle versions of k-core
   percolation and funding support from NSF-DMR-CAREER-0645373. The authors
   also thank a referee for making us aware of Refs. [16,17].
NR 38
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U1 1
U2 5
PU AMER PHYSICAL SOC
PI COLLEGE PK
PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA
SN 1539-3755
EI 1550-2376
J9 PHYS REV E
JI Phys. Rev. E
PD NOV 21
PY 2013
VL 88
IS 5
AR 052130
DI 10.1103/PhysRevE.88.052130
PG 10
WC Physics, Fluids & Plasmas; Physics, Mathematical
SC Physics
GA 255LU
UT WOS:000327241500001
PM 24329237
ER

PT J
AU Yeung, CL
   Ngo, VN
   Grohar, PJ
   Arnaldez, FI
   Asante, A
   Wan, X
   Khan, J
   Hewitt, SM
   Khanna, C
   Staudt, LM
   Helman, LJ
AF Yeung, C. L.
   Ngo, V. N.
   Grohar, P. J.
   Arnaldez, F. I.
   Asante, A.
   Wan, X.
   Khan, J.
   Hewitt, S. M.
   Khanna, C.
   Staudt, L. M.
   Helman, L. J.
TI Loss-of-function screen in rhabdomyosarcoma identifies CRKL-YES as a
   critical signal for tumor growth
SO ONCOGENE
LA English
DT Article
DE rhabdomyosarcoma; CRKL; SRC; YES; dasatinib
ID CHRONIC MYELOGENOUS LEUKEMIA; ALVEOLAR RHABDOMYOSARCOMA; CHROMOSOMAL
   LOCALIZATION; CELLS; CANCER; GENE; PATHWAY; PROTEIN; FUSION; FAMILY
AB To identify novel signaling pathways necessary for rhabdomyosarcoma (RMS) survival, we performed a loss-of-function screen using an inducible small hairpin RNA (shRNA) library in an alveolar and an embryonal RMS cell line. This screen identified CRKL expression as necessary for growth of alveolar RMS and embryonal RMS both in vitro and in vivo. We also found that CRKL was uniformly highly expressed in both RMS cell lines and tumor tissue. As CRKL is a member of the CRK adapter protein family that contains an SH2 and two SH3 domains and is involved in signal transduction from multiple tyrosine kinase receptors, we evaluated CRKL interaction with multiple tyrosine kinase receptor signaling pathways in RMS cells. While we saw no interaction of CRKL with IGFIR, MET or PI3KAKT/mTOR pathways, we determined that CRKL signaling was associated with SRC family kinase (SFK) signaling, specifically with YES kinase. Inhibition of SFK signaling with dasatinib or another SFK inhibitor, sarcatinib, suppressed RMS cell growth in vitro and in vivo. These data identify CRKL as a novel critical component of RMS growth. This study also demonstrates the use of functional screening to identify a potentially novel therapeutic target and treatment approach for these highly aggressive pediatric cancers.
C1 [Yeung, C. L.; Grohar, P. J.; Arnaldez, F. I.; Asante, A.; Wan, X.; Khan, J.; Khanna, C.; Helman, L. J.] NCI, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Ngo, V. N.] City Hope Natl Med Ctr, Beckman Res Inst, Div Hematopoiet Stem Cell & Leukemia Res, Duarte, CA 91010 USA.
   [Hewitt, S. M.] NCI, Ctr Canc Res, Pathol Lab, Bethesda, MD 20892 USA.
   [Staudt, L. M.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Helman, LJ (reprint author), NCI, Pediat Oncol Branch, Ctr Canc Res, Bldg 31,Room 3A11, Bethesda, MD 20892 USA.
EM helmanl@nih.gov
RI Khan, Javed/P-9157-2014; 
OI Khan, Javed/0000-0002-5858-0488; Hewitt, Stephen/0000-0001-8283-1788
FU National Cancer Institute
FX This work was supported through funding to the Intramural Research
   Program of the National Cancer Institute. We would also like to thank
   the many patients and their families who continue to contribute to and
   inform our research. We thank Dr Su Young Kim experiments, Elena
   Kuznetsova, Dr Arnulfo Mendoza, and Dr Melinda G Hollings-head for
   advice and help with xenograft experiment. We also thank the Children's
   Oncology Group Soft-Tissue Sarcoma Committee for providing the tissue
   microarrays for analysis of CRKL expression. We thank Joan Massague for
   the sharing the Addgene plasmid 26 980.
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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 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD NOV 21
PY 2013
VL 32
IS 47
BP 5429
EP 5438
DI 10.1038/onc.2012.590
PG 10
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
GA 254PM
UT WOS:000327177600006
PM 23318429
ER

PT J
AU Cho, A
   Haruyama, N
   Hall, B
   Danton, MJS
   Zhang, L
   Arany, P
   Mooney, DJ
   Harichane, Y
   Goldberg, M
   Gibson, CW
   Kulkarni, AB
AF Cho, Andrew
   Haruyama, Naoto
   Hall, Bradford
   Danton, Mary Jo S.
   Zhang, Lu
   Arany, Praveen
   Mooney, David J.
   Harichane, Yassine
   Goldberg, Michel
   Gibson, Carolyn W.
   Kulkarni, Ashok B.
TI TGF-beta Regulates Enamel Mineralization and Maturation through KLK4
   Expression
SO PLOS ONE
LA English
DT Article
ID AMELOGENESIS IMPERFECTA PHENOTYPE; MATRIX-METALLOPROTEINASE 20; MICE
   DISPLAY; NULL MICE; AMELOBLASTS; APOPTOSIS; DEFECTS; TOOTH; GENE;
   DIFFERENTIATION
AB Transforming growth factor-beta (TGF-beta) signaling plays an important role in regulating crucial biological processes such as cell proliferation, differentiation, apoptosis, and extracellular matrix remodeling. Many of these processes are also an integral part of amelogenesis. In order to delineate a precise role of TGF-beta signaling during amelogenesis, we developed a transgenic mouse line that harbors bovine amelogenin promoter-driven Cre recombinase, and bred this line with TGF-beta receptor II floxed mice to generate ameloblast-specific TGF-beta receptor II conditional knockout (cKO) mice. Histological analysis of the teeth at postnatal day 7 (P7) showed altered enamel matrix composition in the cKO mice as compared to the floxed mice that had enamel similar to the wild-type mice. The mu CT and SEM analyses revealed decreased mineral content in the cKO enamel concomitant with increased attrition and thinner enamel crystallites. Although the mRNA levels remained unaltered, immunostaining revealed increased amelogenin, ameloblastin, and enamelin localization in the cKO enamel at the maturation stage. Interestingly, KLK4 mRNA levels were significantly reduced in the cKO teeth along with a slight increase in MMP-20 levels, suggesting that normal enamel maturation is regulated by TGF-beta signaling through the expression of KLK4. Thus, our study indicates that TGF-beta signaling plays an important role in ameloblast functions and enamel maturation.
C1 [Cho, Andrew; Kulkarni, Ashok B.] Natl Inst Dent & Craniofacial Res, Gene Transfer Core, NIH, Bethesda, MD USA.
   [Cho, Andrew; Haruyama, Naoto; Hall, Bradford; Danton, Mary Jo S.; Zhang, Lu; Kulkarni, Ashok B.] Natl Inst Dent & Craniofacial Res, Funct Genom Sect, Lab Cell & Dev Biol, NIH, Bethesda, MD USA.
   [Haruyama, Naoto] Tokyo Med & Dent Univ, Global Ctr Excellence GCOE Program, Int Res Ctr Mol Sci Tooth & Bone Dis, Tokyo, Japan.
   [Arany, Praveen; Mooney, David J.] Harvard Univ, Cambridge, MA 02138 USA.
   [Harichane, Yassine; Goldberg, Michel] Univ Paris 05, Paris, France.
   [Gibson, Carolyn W.] Univ Penn, Philadelphia, PA 19104 USA.
RP Kulkarni, AB (reprint author), Natl Inst Dent & Craniofacial Res, Gene Transfer Core, NIH, Bethesda, MD USA.
EM ak40m@nih.gov
RI Haruyama, Naoto/D-1993-2011
OI Haruyama, Naoto/0000-0001-6225-5816
FU Division of Intramural Research, NIDCR, NIH; System Consortium on Organ
   Design and Engineering [R01DE019023-01]; JSPS KAKENHI [22792040]
FX This work was supported by the Division of Intramural Research, NIDCR,
   NIH (ABK), System Consortium on Organ Design and Engineering (DJM,
   R01DE019023-01), and JSPS KAKENHI (#22792040 to NH). The funders had no
   role in study, data collection and analysis, decision to publish, or
   preparation of the abstract.
NR 35
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U1 0
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 20
PY 2013
VL 8
IS 11
AR e82267
DI 10.1371/journal.pone.0082267
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 256LY
UT WOS:000327313100168
PM 24278477
ER

PT J
AU Hu, YZ
   Chen, X
   Gu, H
   Yang, YH
AF Hu, Yuzheng
   Chen, Xi
   Gu, Hong
   Yang, Yihong
TI Resting-State Glutamate and GABA Concentrations Predict Task-Induced
   Deactivation in the Default Mode Network
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID MAGNETIC-RESONANCE SPECTROSCOPY; ANTERIOR CINGULATE CORTEX; PREMENSTRUAL
   DYSPHORIC DISORDER; J-COUPLED METABOLITES; IN-VIVO; HUMAN BRAIN;
   FUNCTIONAL MRI; WORKING-MEMORY; RAT-BRAIN; BLOOD OXYGENATION
AB Deactivation of the human brain's default mode network (DMN) is regarded as suppression of endogenous activity to support exogenous task-related processes. This phenomenon has important functional relevance and insufficient DMN deactivation has been implicated in several neuropsychiatric disorders. However, the neurochemical mechanism of the DMN's deactivation remains largely unknown. In the present study, we test the hypothesis that the major excitatory and inhibitory neurotransmitters, glutamate and GABA, respectively, are associated with DMN deactivation. We used magnetic resonance spectroscopy to measure neurotransmitter concentrations in the posterior cingulate cortex/precuneus (PCC/PCu), a key component of the DMN, and functional magnetic resonance imaging to evaluate DMN deactivation induced by an n-back working memory task. Our results demonstrate significant associations of glutamate and GABA with DMN deactivation. Specifically, high regional GABA concentration in the PCC/PCu area is associated with enhanced deactivation induced by the task in the same region, whereas high glutamate concentration is associated with reduced deactivation. Furthermore, the association between GABA and DMN deactivation increases with the cognitive loads. These neurochemical characteristics of DMN deactivation may provide novel insights toward better understanding of the DMN's functions under normal physiological conditions and dysfunctions in neuropsychiatric disorders.
C1 [Hu, Yuzheng; Chen, Xi; Gu, Hong; Yang, Yihong] NIDA, Neuroimaging Res Branch, NIH, Baltimore, MD 21224 USA.
RP Yang, YH (reprint author), NIDA, Neuroimaging Res Branch, NIH, Baltimore, MD 21224 USA.
EM yihongyang@mail.nih.gov
RI Chen, Xi/E-7514-2011
FU National Institute on Drug Abuse, National Institutes of Health
FX This work was supported by the Intramural Research Program of the
   National Institute on Drug Abuse, National Institutes of Health. We
   thank Siemens Medical Solutions USA for providing an MEGA-PRESS sequence
   and Dr. Vani Pariyadath for help in manuscript preparation.
NR 62
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U2 13
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 20
PY 2013
VL 33
IS 47
BP 18566
EP 18573
DI 10.1523/JNEUROSCI.1973-13.2013
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 258HC
UT WOS:000327449000020
PM 24259578
ER

PT J
AU Karp, DD
   Lee, SJ
   Keller, SM
   Wright, GS
   Aisner, S
   Belinsky, SA
   Johnson, DH
   Johnston, MR
   Goodman, G
   Clamon, G
   Okawara, G
   Marks, R
   Frechette, E
   McCaskill-Stevens, W
   Lippman, SM
   Ruckdeschel, J
   Khuri, FR
AF Karp, Daniel D.
   Lee, Sandra J.
   Keller, Steven M.
   Wright, Gail Shaw
   Aisner, Seena
   Belinsky, Steven Alan
   Johnson, David H.
   Johnston, Michael R.
   Goodman, Gary
   Clamon, Gerald
   Okawara, Gordon
   Marks, Randolph
   Frechette, Eric
   McCaskill-Stevens, Worta
   Lippman, Scott M.
   Ruckdeschel, John
   Khuri, Fadlo R.
TI Randomized, Double-Blind, Placebo-Controlled, Phase III Chemoprevention
   Trial of Selenium Supplementation in Patients With Resected Stage I
   Non-Small-Cell Lung Cancer: ECOG 5597
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID 2ND PRIMARY TUMORS; BRONCHIAL SQUAMOUS METAPLASIA; FORMER SMOKERS;
   BETA-CAROTENE; VITAMIN-A; CARDIOVASCULAR-DISEASE; NECK-CANCER;
   PREVENTION; ISOTRETINOIN; RISK
AB Purpose Selenium has been reported to have chemopreventive benefits in lung cancer. We conducted a double-blind, placebo-controlled trial to evaluate the incidence of second primary tumors (SPTs) in patients with resected non-small-cell lung cancer (NSCLC) receiving selenium supplementation.
   Patients and Methods Patients with completely resected stage I NSCLC were randomly assigned to take selenized yeast 200 g versus placebo daily for 48 months. Participation was 6 to 36 months postoperatively and required a negative mediastinal node biopsy, no excessive vitamin intake, normal liver function, negative chest x-ray, and no other evidence of recurrence.
   Results The first interim analysis in October 2009, with 46% of the projected end points accumulated, showed a trend in favor of the placebo group with a low likelihood that the trial would become positive; thus, the study was stopped. One thousand seven hundred seventy-two participants were enrolled, with 1,561 patients randomly assigned. Analysis was updated in June 2011 with the maturation of 54% of the planned end points. Two hundred fifty-two SPTs (from 224 patients) developed, of which 98 (from 97 patients) were lung cancer (38.9%). Lung and overall SPT incidence were 1.62 and 3.54 per 100 person-years, respectively, for selenium versus 1.30 and 3.39 per 100 person-years, respectively, for placebo (P = .294). Five-year disease-free survival was 74.4% for selenium recipients versus 79.6% for placebo recipients. Grade 1 to 2 toxicity occurred in 31% of selenium recipients and 26% of placebo recipients, and grade 3 toxicity occurred in less than 2% of selenium recipients versus 3% of placebo recipients. Compliance was excellent. No increase in diabetes mellitus or skin cancer was detected.
   Conclusion Selenium was safe but conferred no benefit over placebo in the prevention of SPT in patients with resected NSCLC.
C1 [Karp, Daniel D.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
   [Johnson, David H.] Univ Texas Southwestern, Dallas, TX USA.
   [Lee, Sandra J.] Dana Farber Canc Inst, Boston, MA 02115 USA.
   [Keller, Steven M.] Montefiore Med Ctr, Bronx, NY 10467 USA.
   [Wright, Gail Shaw] Florida Canc Specialists, New Port Richey, FL USA.
   [Aisner, Seena] Univ Med & Dent New Jersey, New Jersey Med Sch, Canc Inst New Jersey, Newark, NJ 07103 USA.
   [Belinsky, Steven Alan] Lovelace Resp Res Inst, Albuquerque, NM USA.
   [Goodman, Gary] Swedish Med Ctr, Inst Canc, Seattle, WA USA.
   [Goodman, Gary] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
   [Clamon, Gerald] Univ Iowa, Iowa City, IA USA.
   [Marks, Randolph] Mayo Clin, Rochester, MN USA.
   [McCaskill-Stevens, Worta] NCI, Rockville, MD USA.
   [Lippman, Scott M.] Univ Calif San Diego, Ctr Canc, San Diego, CA 92103 USA.
   [Ruckdeschel, John] Intermt Healthcare, Salt Lake City, UT USA.
   [Khuri, Fadlo R.] Emory Univ, Atlanta, GA 30322 USA.
   [Johnston, Michael R.] Dalhousie Univ, Halifax, NS, Canada.
   [Johnston, Michael R.] Natl Canc Inst Canada, Clin Trials Grp, Kingston, ON, Canada.
   [Okawara, Gordon] McMaster Univ, Hamilton, ON, Canada.
   [Frechette, Eric] Hop Laval, Quebec City, PQ, Canada.
RP Khuri, FR (reprint author), Emory Univ, Winship Canc Inst, 1365 C Clifton Rd NE, Atlanta, GA 30322 USA.
EM fkhuri@emory.edu
FU Public Health Service [CA037403, CA14958, CA80775, CA73590, CA107868,
   CA49957, CA31946, CA33601, CA32102, CA20319, CA25224, CA21661, CA37422];
   National Cancer Institute, National Institutes of Health; Department of
   Health and Human Services
FX Supported in part by Public Health Service Grants No. CA037403, CA14958,
   CA80775, CA73590, CA107868, CA49957, CA31946, CA33601, CA32102, CA20319,
   CA25224, CA21661, and CA37422 and grants from the National Cancer
   Institute, National Institutes of Health, and Department of Health and
   Human Services.
NR 35
TC 21
Z9 21
U1 0
U2 8
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 NOV 20
PY 2013
VL 31
IS 33
BP 4179
EP +
DI 10.1200/JCO.2013.49.2173
PG 12
WC Oncology
SC Oncology
GA 253LM
UT WOS:000327088000004
PM 24002495
ER

PT J
AU Lad, N
   Sharma, R
   Marquez, VE
   Mascarenhas, M
AF Lad, Nitin
   Sharma, Rajiv
   Marquez, Victor E.
   Mascarenhas, Malcolm
TI A new synthesis of sultams from amino alcohols
SO TETRAHEDRON LETTERS
LA English
DT Article
DE Cyclization; Sultams; Aminoalcohols
ID SULTONES
AB The base-mediated cyclization of N,O-dimesylate derivatives of cyclic and acyclic amino alcohols provides a simple access to five- and six-member sultams: isothiazolidine-1,1-dioxides and thiazinane-1,1-dioxides respectively. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Lad, Nitin; Sharma, Rajiv; Mascarenhas, Malcolm] Piramal Enterprises Ltd, Dept Med Chem, Bombay 400063, Maharashtra, India.
   [Marquez, Victor E.] NCI, Lab Med Chem, DBS, NIH,FCRDC, Frederick, MD 21702 USA.
RP Mascarenhas, M (reprint author), Piramal Enterprises Ltd, Dept Med Chem, 1 Nirlon Complex, Bombay 400063, Maharashtra, India.
EM malcolm.mascarenhas@piramal.com
NR 19
TC 1
Z9 1
U1 0
U2 6
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0040-4039
J9 TETRAHEDRON LETT
JI Tetrahedron Lett.
PD NOV 20
PY 2013
VL 54
IS 47
BP 6307
EP 6309
DI 10.1016/j.tetlet.2013.09.021
PG 3
WC Chemistry, Organic
SC Chemistry
GA 245AD
UT WOS:000326430400005
ER

PT J
AU Ferrada, M
   O'Grady, NP
AF Ferrada, Marcela
   O'Grady, Naomi P.
TI A microbial preparation did not reduce diarrhea in older inpatients
   receiving antibiotics
SO ANNALS OF INTERNAL MEDICINE
LA English
DT Editorial Material
ID DIFFICILE-ASSOCIATED DIARRHEA; PREVENTION; PROBIOTICS
C1 [Ferrada, Marcela; O'Grady, Naomi P.] NIH, Bethesda, MD 20892 USA.
RP Ferrada, M (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
NR 2
TC 1
Z9 1
U1 2
U2 2
PU AMER COLL PHYSICIANS
PI PHILADELPHIA
PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA
SN 0003-4819
EI 1539-3704
J9 ANN INTERN MED
JI Ann. Intern. Med.
PD NOV 19
PY 2013
VL 159
IS 10
AR JC9
DI 10.7326/0003-4819-159-10-201311190-02009
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 276FB
UT WOS:000328732700008
PM 24247699
ER

PT J
AU Dombi, E
   Ardern-Holmes, SL
   Babovic-Vuksanovic, D
   Barker, FG
   Connor, S
   Evans, DG
   Fisher, MJ
   Goutagny, S
   Harris, GJ
   Jaramillo, D
   Karajannis, MA
   Korf, BR
   Mautner, V
   Plotkin, SR
   Poussaint, TY
   Robertson, K
   Shih, CS
   Widemann, BC
AF Dombi, Eva
   Ardern-Holmes, Simone L.
   Babovic-Vuksanovic, Dusica
   Barker, Fred G.
   Connor, Steve
   Evans, D. Gareth
   Fisher, Michael J.
   Goutagny, Stephane
   Harris, Gordon J.
   Jaramillo, Diego
   Karajannis, Matthias A.
   Korf, Bruce R.
   Mautner, Victor
   Plotkin, Scott R.
   Poussaint, Tina Y.
   Robertson, Kent
   Shih, Chie-Schin
   Widemann, Brigitte C.
CA REiNS Int Collaboration
TI Recommendations for imaging tumor response in neurofibromatosis clinical
   trials
SO NEUROLOGY
LA English
DT Article
ID PHASE-I TRIAL; VESTIBULAR SCHWANNOMA GROWTH; PLEXIFORM NEUROFIBROMAS;
   NATURAL-HISTORY; GRADE GLIOMAS; SOLID TUMORS; TYPE-2; CHILDREN;
   CRITERIA; NEUROONCOLOGY
AB Objective: Neurofibromatosis (NF)-related benign tumors such as plexiform neurofibromas (PN) and vestibular schwannomas (VS) can cause substantial morbidity. Clinical trials directed at these tumors have become available. Due to differences in disease manifestations and the natural history of NF-related tumors, response criteria used for solid cancers (1-dimensional/RECIST [Response Evaluation Criteria in Solid Tumors] and bidimensional/World Health Organization) have limited applicability. No standardized response criteria for benign NF tumors exist. The goal of the Tumor Measurement Working Group of the REiNS (Response Evaluation in Neurofibromatosis and Schwannomatosis) committee is to propose consensus guidelines for the evaluation of imaging response in clinical trials for NF tumors.
   Methods: Currently used imaging endpoints, designs of NF clinical trials, and knowledge of the natural history of NF-related tumors, in particular PN and VS, were reviewed. Consensus recommendations for response evaluation for future studies were developed based on this review and the expertise of group members.
   Results: MRI with volumetric analysis is recommended to sensitively and reproducibly evaluate changes in tumor size in clinical trials. Volumetric analysis requires adherence to specific imaging recommendations. A 20% volume change was chosen to indicate a decrease or increase in tumor size. Use of these criteria in future trials will enable meaningful comparison of results across studies.
   Conclusions: The proposed imaging response evaluation guidelines, along with validated clinical outcome measures, will maximize the ability to identify potentially active agents for patients with NF and benign tumors.
C1 [Dombi, Eva; Widemann, Brigitte C.] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
   [Ardern-Holmes, Simone L.] Childrens Hosp Westmead, Dept Neurol, Sydney, NSW, Australia.
   [Babovic-Vuksanovic, Dusica] Mayo Clin, Dept Med Genet, Rochester, MN USA.
   [Barker, Fred G.] Massachusetts Gen Hosp, Neurosurg Serv, Boston, MA 02114 USA.
   [Harris, Gordon J.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
   [Plotkin, Scott R.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
   [Plotkin, Scott R.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
   [Connor, Steve] Kings Coll Hosp London, Dept Neuroradiol, London, England.
   [Evans, D. Gareth] St Marys Hosp, Dept Med Genet, MAHSC, Manchester M13 0JH, Lancs, England.
   [Fisher, Michael J.] Childrens Hosp Philadelphia, Div Oncol, Philadelphia, PA 19104 USA.
   [Jaramillo, Diego] Childrens Hosp Philadelphia, Dept Radiol, Philadelphia, PA 19104 USA.
   [Fisher, Michael J.] Univ Penn, Dept Pediat, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Goutagny, Stephane] Hop Beaujon, Dept Neurosurg, Clichy, France.
   [Karajannis, Matthias A.] NYU Langone Med Ctr, Div Pediat Hematol Oncol, New York, NY USA.
   [Karajannis, Matthias A.] NYU Langone Med Ctr, NYU Canc Inst, New York, NY USA.
   [Korf, Bruce R.] Univ Alabama Birmingham, Dept Genet, Birmingham, AL USA.
   [Mautner, Victor] Univ Med Ctr Hamburg Eppendorf, Dept Neurol, Hamburg, Germany.
   [Poussaint, Tina Y.] Boston Childrens Hosp, Dept Radiol, Boston, MA USA.
   [Robertson, Kent; Shih, Chie-Schin] James Whitcomb Riley Hosp Children, Dept Pediat, Indianapolis, IN 46202 USA.
RP Dombi, E (reprint author), NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
EM dombie@mail.nih.gov
FU Intramural Research Program of the NIH, National Cancer Institute,
   Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
   NIH, National Cancer Institute, Center for Cancer Research.
NR 35
TC 20
Z9 20
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
EI 1526-632X
J9 NEUROLOGY
JI Neurology
PD NOV 19
PY 2013
VL 81
IS 21
SU 1
BP S33
EP S40
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 304GH
UT WOS:000330734600005
PM 24249804
ER

PT J
AU Fisher, MJ
   Avery, RA
   Allen, JC
   Ardern-Holmes, SL
   Bilaniuk, LT
   Ferner, RE
   Gutmann, DH
   Listernick, R
   Martin, S
   Ullrich, NJ
   Liu, GT
AF Fisher, Michael J.
   Avery, Robert A.
   Allen, Jeffrey C.
   Ardern-Holmes, Simone L.
   Bilaniuk, Larissa T.
   Ferner, Rosalie E.
   Gutmann, David H.
   Listernick, Robert
   Martin, Staci
   Ullrich, Nicole J.
   Liu, Grant T.
CA REiNS Int Collaboration
TI Functional outcome measures for NF1-associated optic pathway glioma
   clinical trials
SO NEUROLOGY
LA English
DT Article
ID VISUAL-EVOKED POTENTIALS; QUALITY-OF-LIFE; LOW-GRADE GLIOMAS;
   NEUROFIBROMATOSIS TYPE-I; FIBER LAYER THICKNESS; MULTIPLE-SCLEROSIS;
   YOUNG-CHILDREN; FUNCTION QUESTIONNAIRE; COHERENCE TOMOGRAPHY; LETTER
   ACUITY
AB Objective: The goal of the Response Evaluation in Neurofibromatosis and Schwannomatosis Visual Outcomes Committee is to define the best functional outcome measures for future neurofibromatosis type 1 (NF1)-associated optic pathway glioma (OPG) clinical trials.
   Methods: The committee considered the components of vision, other ophthalmologic parameters affected by OPG, potential biomarkers of visual function, and quality of life measures to arrive at consensus-based, evidence-driven recommendations for objective and measurable functional endpoints for OPG trials.
   Results: Visual acuity (VA) assessments using consistent quantitative testing methods are recommended as the main functional outcome measure for NF1-OPG clinical trials. Teller acuity cards are recommended for use as the primary VA endpoint, and HOTV as a secondary endpoint once subjects are old enough to complete it. The optic disc should be assessed for pallor, as this appears to be a contributory variable that may affect the interpretation of VA change over time. Given the importance of capturing patient-reported outcomes in clinical trials, evaluating visual quality of life using the Children's Visual Function Questionnaire as a secondary endpoint is also proposed.
   Conclusions: The use of these key functional endpoints will be essential for evaluating the efficacy of future OPG clinical trials.
C1 [Fisher, Michael J.] Childrens Hosp Philadelphia, Div Oncol, Philadelphia, PA 19104 USA.
   [Bilaniuk, Larissa T.] Childrens Hosp Philadelphia, Neuroradiol Sect, Dept Radiol, Philadelphia, PA 19104 USA.
   [Liu, Grant T.] Childrens Hosp Philadelphia, Neuroophthalmol Serv, Philadelphia, PA 19104 USA.
   [Fisher, Michael J.] Univ Penn, Dept Pediat, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Liu, Grant T.] Univ Penn, Dept Neurol, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Liu, Grant T.] Univ Penn, Dept Ophthalmol, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Avery, Robert A.] Childrens Natl Med Ctr, Dept Neurol, Gilbert Family Neurofibromatosis Inst, Washington, DC 20010 USA.
   [Avery, Robert A.] Childrens Natl Med Ctr, Dept Ophthalmol, Gilbert Family Neurofibromatosis Inst, Washington, DC 20010 USA.
   [Avery, Robert A.] Childrens Natl Med Ctr, Dept Pediat, Gilbert Family Neurofibromatosis Inst, Washington, DC 20010 USA.
   [Allen, Jeffrey C.] NYU Langone Med Ctr, NYU Canc Inst, Dept Pediat, New York, NY USA.
   [Allen, Jeffrey C.] NYU Langone Med Ctr, NYU Canc Inst, Dept Neurol, New York, NY USA.
   [Ardern-Holmes, Simone L.] Univ Sydney, Childrens Hosp, Westmead Clin Sch, Sydney, NSW 2006, Australia.
   [Ardern-Holmes, Simone L.] Childrens Hosp Westmead, Dept Neurol, Sydney, NSW, Australia.
   [Bilaniuk, Larissa T.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
   [Ferner, Rosalie E.] Guys & St Thomas NHS Fdn Trust, Dept Neurol, London, England.
   Kings Coll London, Inst Psychiat, London WC2R 2LS, England.
   [Gutmann, David H.] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA.
   [Listernick, Robert] Northwestern Univ, Dept Pediat, Feinberg Sch Med, Evanston, IL 60208 USA.
   [Listernick, Robert] Ann & Robert H Lurie Childrens Hosp Chicago, Chicago, IL USA.
   [Martin, Staci] NCI, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA.
   [Ullrich, Nicole J.] Harvard Univ, Sch Med, Dept Neurol, Boston Childrens Hosp, Boston, MA 02115 USA.
RP Fisher, MJ (reprint author), Childrens Hosp Philadelphia, Div Oncol, Philadelphia, PA 19104 USA.
EM fisherm@email.chop.edu
FU Children's Tumor Foundation; Department of Defense [W81XWH-12-1-0155,
   W81XWH-05-1-0615, W81XWH-08-1-0051]; Thrasher Research Fund; Sarcoma
   Alliance for Research through Collaboration; Pediatric Low Grade
   Astrocytoma Foundation; Bayer; Children's Discovery Institute; NIH
   [NR009651-01, UL1RR031988/UL1TR000075, NS065547, NS072916, NCT00879034];
   Gilbert Family Neurofibromatosis Institute; Novartis Pharmaceuticals
   Australia; Children's Tumor Foundation of Australia; NICHD
   [UO1HD068541-01]; European Neurofibromatosis Association; UCSD; Johns
   Hopkins University; Memorial Sloan-Kettering Cancer Center; Cleveland
   Clinic Foundation; University of Minnesota; Biomarin; MD Anderson Cancer
   Center; University of Toronto; Dana Farber Cancer Institute; University
   of Chicago; National Brain Tumor Society; James S. McDonnell Foundation;
   Department of Defense; National Cancer Institute [CA136573, CA141549,
   CA160882]; Children's Discovery Institute [MC-II-2012-212]; National
   Cancer Foundation Children's Oncology Group; University of Alabama at
   Birmingham Research Foundation
FX M. Fisher received reimbursement from the Children's Tumor Foundation to
   attend their annual Neurofibromatosis Conference, is funded by the
   Department of Defense (W81XWH-12-1-0155, W81XWH-05-1-0615), Thrasher
   Research Fund, the Children's Tumor Foundation, and Sarcoma Alliance for
   Research through Collaboration, and received research support from the
   Pediatric Low Grade Astrocytoma Foundation, Bayer, Children's Discovery
   Institute, NIH (NR009651-01), and the Department of Defense
   (W81XWH-08-1-0051). R. Avery is funded by NIH grants K23-EY022673 and
   UL1RR031988/UL1TR000075, and received research support from the Gilbert
   Family Neurofibromatosis Institute. J.Allen reports no disclosures. S.
   Ardern-Holmes served on a scientific advisory board for Novartis
   Pharmaceuticals Australia, received funding for a trip from Novartis
   Pharmaceuticals Australia, and receives research support from The
   Children's Tumor Foundation of Australia. L. Bilaniuk receives research
   support from the NICHD #UO1HD068541-01. R. Ferner received funding for
   travel from the Children's Tumor Foundation and the European
   Neurofibromatosis Association. She receives royalties from Springer for
   the book Neurofibromatoses in Clinical Practice. D. Gutmann serves on
   the scientific advisory board of the Brain Tumor Funder's Collaborative
   and the editorial board of Experimental Neurology. He holds the patent
   on the neurofibromatosis gene U. S. Patent No. 5,859,195), for which he
   receives royalties annually, and a patent for Neurofibromin Pathway
   Modulators (U. S. Patent No. 8,101,606). He has received honoraria for
   invited lectureships at UCSD, Johns Hopkins University, Memorial
   Sloan-Kettering Cancer Center, Cleveland Clinic Foundation, University
   of Minnesota, Biomarin, MD Anderson Cancer Center, University of
   Toronto, Dana Farber Cancer Institute, and the University of Chicago. He
   receives research support from the National Brain Tumor Society, James
   S. McDonnell Foundation, Department of Defense, National Cancer
   Institute (grants CA136573, CA141549, and CA160882), Children's
   Discovery Institute (grant MC-II-2012-212), and the NIH (grants NS065547
   and NS072916). R. Listernick serves as an editorial board member of
   Pediatric Annals. He received honoraria for oral presentations from
   Children's Hospital of Colorado and American Academy of Pediatrics. S.
   Martin received funding for a trip from the Children's Tumor Foundation.
   N. Ullrich receives funding from the Department of Defense
   (W81XWH-05-1-0615), the NIH (NCT00879034), the National Cancer
   Foundation Children's Oncology Group, and the Children's Tumor
   Foundation. She holds patents for a method of diagnosing and treating
   gliomas (US 5905027, 6028174, 6319891, 6429187, and 6870029), for which
   she receives royalty payments from the University of Alabama at
   Birmingham Research Foundation. She also receives royalties from
   UpTo-Date for the publication of "The " choking game" and other
   strangulation activities in children and adolescents." She has received
   travel expenses and/or honoraria for lectures or educational activities
   not funded by industry, and has served as an expert witness for
   O'Connor, O'Connor, Bresee & First and Bays, Lung, Rose & Holma. G. Liu
   has consulted for Ipsen and received book royalties from Elsevier. Go to
   Neurology. org for full disclosures.
NR 63
TC 24
Z9 24
U1 1
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
EI 1526-632X
J9 NEUROLOGY
JI Neurology
PD NOV 19
PY 2013
VL 81
IS 21
SU 1
BP S15
EP S24
PG 10
WC Clinical Neurology
SC Neurosciences & Neurology
GA 304GH
UT WOS:000330734600003
PM 24249802
ER

PT J
AU Plotkin, SR
   Blakeley, JO
   Dombi, E
   Fisher, MJ
   Hanemann, CO
   Walsh, KS
   Wolters, PL
   Widemann, BC
AF Plotkin, Scott R.
   Blakeley, Jaishri O.
   Dombi, Eva
   Fisher, Michael J.
   Hanemann, C. Oliver
   Walsh, Karin S.
   Wolters, Pamela L.
   Widemann, Brigitte C.
TI Achieving consensus for clinical trials The REiNS International
   Collaboration
SO NEUROLOGY
LA English
DT Article
ID PHASE-I TRIAL; NEUROFIBROMATOSIS TYPE-I; PLEXIFORM NEUROFIBROMAS; SOLID
   TUMORS; CHILDREN; TYPE-1; PIRFENIDONE; THERAPY
AB The neurofibromatoses (NF)-including neurofibromatosis 1 (NF1), neurofibromatosis 2 (NF2), and schwannomatosis-are related tumor-suppressor syndromes characterized by a predisposition to multiple tumor types and other disease manifestations, which often result in functional disability, reduced quality of life, pain, and, in some cases, malignancy. With increasing knowledge of the biology and pathogenesis of NF, clinical trials with targeted agents directed at NF tumors have become available. Most clinical trials for patients with NF have used designs and endpoints similar to oncology trials. However, differences in the disease manifestations and natural history of NF (compared to cancers) require the development of new designs and endpoints to perform meaningful NF clinical trials. The Response Evaluation in Neurofibromatosis and Schwannomatosis (REiNS) International Collaboration was established in 2011 at the Children's Tumor Foundation meeting to achieve consensus within the NF community about the design of future clinical trials, with a specific emphasis on endpoints. The REiNS Collaboration includes 7 working groups that focus on imaging of tumor response; functional, visual, patient-reported, and neurocognitive outcomes; whole-body MRI; and disease biomarkers. This supplement includes the first series of recommendations by the REiNS Collaboration. The hope is that these recommendations will be used by members of the group and by researchers outside of the REiNS International Collaboration to standardize the measurement of outcomes and thus improve clinical trials for patients with NF. Ultimately, we plan to engage industry partners and national regulatory agencies in this process to facilitate the approval of drugs for patients with NF.
C1 [Plotkin, Scott R.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
   [Plotkin, Scott R.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
   [Blakeley, Jaishri O.] Johns Hopkins, Dept Neurol Neurosurg & Oncol, Baltimore, MD USA.
   [Dombi, Eva; Wolters, Pamela L.; Widemann, Brigitte C.] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
   [Fisher, Michael J.] Childrens Hosp Penn, Dept Pediat, Div Oncol, Philadelphia, PA USA.
   [Hanemann, C. Oliver] Univ Plymouth, Peninsula Sch Med, Plymouth PL4 8AA, Devon, England.
   [Hanemann, C. Oliver] Univ Plymouth, Peninsula Sch Dent, Plymouth PL4 8AA, Devon, England.
   [Walsh, Karin S.] Childrens Natl Med Ctr, Jennifer & Daniel Gilbert Neurofibromatosis Inst, Washington, DC 20010 USA.
RP Plotkin, SR (reprint author), Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
EM splotkin@partners.org
FU Children's Tumor Foundation
FX Supported by the Children's Tumor Foundation.
NR 22
TC 10
Z9 10
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
EI 1526-632X
J9 NEUROLOGY
JI Neurology
PD NOV 19
PY 2013
VL 81
IS 21
SU 1
BP S1
EP S5
PG 5
WC Clinical Neurology
SC Neurosciences & Neurology
GA 304GH
UT WOS:000330734600001
PM 24249801
ER

PT J
AU Widemann, BC
   Blakeley, JO
   Dombi, E
   Fisher, MJ
   Hanemann, CO
   Walsh, KS
   Wolters, PL
   Plotkin, SR
AF Widemann, Brigitte C.
   Blakeley, Jaishri O.
   Dombi, Eva
   Fisher, Michael J.
   Hanemann, Clemens O.
   Walsh, Karin S.
   Wolters, Pamela L.
   Plotkin, Scott R.
TI Conclusions and future directions for the REiNS International
   Collaboration
SO NEUROLOGY
LA English
DT Article
ID PLEXIFORM NEUROFIBROMAS; RESPONSE ASSESSMENT; GRADE GLIOMAS; WORKING
   GROUP; NEUROONCOLOGY; SCHWANNOMATOSIS; INHIBITOR; DEFICITS; CHILDREN;
   TRIALS
AB The Response Evaluation in Neurofibromatosis and Schwannomatosis (REiNS) International Collaboration was established with the goal to develop consensus recommendations for the use of endpoints in neurofibromatosis (NF) clinical trials. This supplement includes the first series of REiNS recommendations for the use of patient-reported, functional, and visual outcomes, and for the evaluation of imaging response in NF clinical trials. Recommendations for neurocognitive outcome measures, the use of whole-body MRI in NF, the evaluation of potential biomarkers of disease, and the comprehensive evaluation of functional and patient-reported outcomes in NF are in development. The REiNS recommendations are made based on current knowledge. Experience with the use of the recommended endpoints in clinical trials, development of new tools and technologies, new knowledge of the natural history of NF, and advances in the methods used to analyze endpoints will likely lead to modifications of the currently proposed guidelines, which will be shared with the NF research community through the REiNS Web site www.reinscollaboration.org. Due to the clinical complexity of NF, there is a need to seek expertise from multiple medical disciplines, regulatory agencies, and industry to develop trial endpoints and designs, which will lead to the identification and approval of effective treatments for NF tumor and nontumor manifestations. The REiNS Collaboration welcomes anyone interested in providing his or her expertise toward this effort.
C1 [Widemann, Brigitte C.; Dombi, Eva; Wolters, Pamela L.] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
   [Blakeley, Jaishri O.] Johns Hopkins, Dept Neurol Neurosurg & Oncol, Baltimore, MD USA.
   [Fisher, Michael J.] Childrens Hosp Penn, Dept Pediat, Div Oncol, Philadelphia, PA USA.
   [Hanemann, Clemens O.] Univ Plymouth, Peninsula Sch Med, Plymouth PL4 8AA, Devon, England.
   [Hanemann, Clemens O.] Univ Plymouth, Peninsula Sch Dent, Plymouth PL4 8AA, Devon, England.
   [Walsh, Karin S.] Childrens Natl Med Ctr, Jennifer & Daniel Gilbert Neurofibromatosis Inst, Washington, DC 20010 USA.
   [Plotkin, Scott R.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
   [Plotkin, Scott R.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
RP Widemann, BC (reprint author), NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
EM widemanb@mail.nih.gov
FU Children's Tumor Foundation; intramural research program of the Center
   for Cancer Research, NCI
FX Supported by the Children's Tumor Foundation and the intramural research
   program of the Center for Cancer Research, NCI.
NR 15
TC 6
Z9 6
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
EI 1526-632X
J9 NEUROLOGY
JI Neurology
PD NOV 19
PY 2013
VL 81
IS 21
SU 1
BP S41
EP S44
PG 4
WC Clinical Neurology
SC Neurosciences & Neurology
GA 304GH
UT WOS:000330734600006
PM 24249805
ER

PT J
AU Wolters, PL
   Martin, S
   Merker, VL
   Gardner, KL
   Hingtgen, CM
   Tonsgard, JH
   Schorry, EK
   Baldwin, A
AF Wolters, Pamela L.
   Martin, Staci
   Merker, Vanessa L.
   Gardner, Kathy L.
   Hingtgen, Cynthia M.
   Tonsgard, James H.
   Schorry, Elizabeth K.
   Baldwin, Andrea
CA REiNS Int Collaboration
TI Patient-reported outcomes in neurofibromatosis and schwannomatosis
   clinical trials
SO NEUROLOGY
LA English
DT Article
ID QUALITY-OF-LIFE; PAIN INTENSITY; RATING-SCALES; PLEXIFORM NEUROFIBROMAS;
   SELF-REPORT; CHILDREN; CANCER; RECOMMENDATIONS; SURGERY
AB Objectives: Neurofibromatosis (NF) is a genetic disease with multiple clinical manifestations that can significantly impact quality of life (QOL). Clinical trials should include patient-reported outcomes (PROs) as endpoints to assess treatment effects on various aspects of QOL, but there is no consensus on the selection and use of such measures in NF. This article describes the PRO Working Group of the Response Evaluation in Neurofibromatosis and Schwannomatosis (REiNS) Collaboration, its main goals, methods for identifying appropriate PRO measures for NF clinical trials, and recommendations for assessing pain intensity.
   Methods: The REiNS PRO group selected core endpoint domains important to assess in NF. The members developed criteria to rate PRO measures, including patient characteristics, psychometric properties, and feasibility, and utilized a systematic process to evaluate PROs for NF clinical trials. Within the subdomain of pain intensity, the group reviewed the Numerical Rating Scale-11 (NRS-11), the Visual Analogue Scale, and the Faces Pain Scale-Revised using this process.
   Results: Based on the review criteria, each of these pain intensity scales is brief, reliable, valid, and widely used. However, the NRS-11 was given the highest rating for use in NF clinical trials due to recommendations from pain experts and other consensus groups, its extensive use in research, strong psychometric data including sensitivity to change, and excellent feasibility in ages >= 8 years.
   Conclusions: The systematic review criteria and process are effective for identifying appropriate PRO measures and provide information utilized by the REiNS Collaboration to achieve consensus regarding PROs in NF clinical trials.
C1 [Wolters, Pamela L.; Martin, Staci; Baldwin, Andrea] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
   [Merker, Vanessa L.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
   [Merker, Vanessa L.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
   [Gardner, Kathy L.] Vet Adm Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
   [Gardner, Kathy L.] Univ Pittsburgh, Pittsburgh, PA 15260 USA.
   [Hingtgen, Cynthia M.] Michigan State Univ, Dept Clin Neurosci, Spectrum Hlth Med Grp, E Lansing, MI 48824 USA.
   Michigan State Univ, Coll Human Med, E Lansing, MI 48824 USA.
   [Tonsgard, James H.] Univ Chicago, Pritzker Sch Med, Chicago, IL 60637 USA.
   [Schorry, Elizabeth K.] Cincinnati Childrens Hosp, Div Human Genet, Cincinnati, OH USA.
RP Wolters, PL (reprint author), NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
EM woltersp@mail.nih.gov
FU Intramural Research Program of the NIH, National Cancer Institute
FX This research is supported by the Intramural Research Program of the
   NIH, National Cancer Institute.
NR 38
TC 12
Z9 12
U1 2
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
EI 1526-632X
J9 NEUROLOGY
JI Neurology
PD NOV 19
PY 2013
VL 81
IS 21
SU 1
BP S6
EP S14
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA 304GH
UT WOS:000330734600002
PM 24249806
ER

PT J
AU Kovalchik, SA
   De Matteis, S
   Landi, MT
   Caporaso, NE
   Varadhan, R
   Consonni, D
   Bergen, AW
   Katki, HA
   Wacholder, S
AF Kovalchik, Stephanie A.
   De Matteis, Sara
   Landi, Maria Teresa
   Caporaso, Neil E.
   Varadhan, Ravi
   Consonni, Dario
   Bergen, Andrew W.
   Katki, Hormuzd A.
   Wacholder, Sholom
TI A regression model for risk difference estimation in population-based
   case-control studies clarifies gender differences in lung cancer risk of
   smokers and never smokers
SO BMC MEDICAL RESEARCH METHODOLOGY
LA English
DT Article
DE Additive risk; Absolute risk; Case-control study; EAGLE; Lung cancer;
   Risk assessment; Sex factors; Smoking
ID BINOMIAL REGRESSION; WOMEN; SMOKING; RATIOS; MEN; METAANALYSIS;
   SELECTION; ETIOLOGY; RATES
AB Background: Additive risk models are necessary for understanding the joint effects of exposures on individual and population disease risk. Yet technical challenges have limited the consideration of additive risk models in case-control studies.
   Methods: Using a flexible risk regression model that allows additive and multiplicative components to estimate absolute risks and risk differences, we report a new analysis of data from the population-based case-control Environment And Genetics in Lung cancer Etiology study, conducted in Northern Italy between 2002-2005. The analysis provides estimates of the gender-specific absolute risk (cumulative risk) for non-smoking-and smoking-associated lung cancer, adjusted for demographic, occupational, and smoking history variables.
   Results: In the multiple-variable lexpit regression, the adjusted 3-year absolute risk of lung cancer in never smokers was 4.6 per 100,000 persons higher in women than men. However, the absolute increase in 3-year risk of lung cancer for every 10 additional pack-years smoked was less for women than men, 13.6 versus 52.9 per 100,000 persons.
   Conclusions: In a Northern Italian population, the absolute risk of lung cancer among never smokers is higher in women than men but among smokers is lower in women than men. Lexpit regression is a novel approach to additive-multiplicative risk modeling that can contribute to clearer interpretation of population-based case-control studies.
C1 [Kovalchik, Stephanie A.] RAND Corp, Econ Sociol & Stat Dept, Santa Monica, CA USA.
   [De Matteis, Sara; Consonni, Dario] Fdn IRCCS Ca Granda Osped Maggiore Policlin, Dept Prevent Med, Epidemiol Unit, Milan, Italy.
   [Landi, Maria Teresa; Caporaso, Neil E.; Katki, Hormuzd A.; Wacholder, Sholom] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Varadhan, Ravi] Johns Hopkins Univ, Sch Med, Dept Med, Div Geriatr Med & Gerontol, Baltimore, MD 21205 USA.
   [Bergen, Andrew W.] SRI Int, Ctr Hlth Sci, Mol Genet Program, Menlo Pk, CA 94025 USA.
RP Kovalchik, SA (reprint author), RAND Corp, Econ Sociol & Stat Dept, Santa Monica, CA USA.
EM skovalch@rand.org
RI Katki, Hormuzd/B-4003-2015; Consonni, Dario/K-7943-2016; 
OI Consonni, Dario/0000-0002-8935-3843; Bergen, Andrew/0000-0002-1237-7644
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. Dr. Varadhan is a Brookdale Leadership
   in Aging Fellow at the Johns Hopkins University School of Medicine.
NR 36
TC 6
Z9 6
U1 1
U2 11
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2288
J9 BMC MED RES METHODOL
JI BMC Med. Res. Methodol.
PD NOV 19
PY 2013
VL 13
AR 143
DI 10.1186/1471-2288-13-143
PG 8
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 282ZW
UT WOS:000329214900002
PM 24252624
ER

PT J
AU Cho, H
   Klabunde, CN
   Yabroff, KR
   Wang, ZQ
   Meekins, A
   Lansdorp-Vogelaar, I
   Mariotto, AB
AF Cho, Hyunsoon
   Klabunde, Carrie N.
   Yabroff, K. Robin
   Wang, Zhuoqiao
   Meekins, Angela
   Lansdorp-Vogelaar, Iris
   Mariotto, Angela B.
TI Comorbidity-Adjusted Life Expectancy: A New Tool to Inform
   Recommendations for Optimal Screening Strategies
SO ANNALS OF INTERNAL MEDICINE
LA English
DT Article
ID CANCER-PATIENTS; CLAIMS DATA; ELDERLY POPULATION; COLORECTAL-CANCER;
   DECISION-MAKING; MEDICARE CLAIMS; CERVICAL-CANCER; TIME-SCALE;
   STATEMENT; SURVIVAL
AB Background: Many guidelines recommend considering health status and life expectancy when making cancer screening decisions for elderly persons.
   Objective: To estimate life expectancy for elderly persons without a history of cancer, taking into account comorbid conditions.
   Design: Population-based cohort study.
   Setting: A 5% sample of Medicare beneficiaries in selected geographic areas, including their claims and vital status information.
   Participants: Medicare beneficiaries aged 66 years or older between 1992 and 2005 without a history of cancer (n = 407 749).
   Measurements: Medicare claims were used to identify comorbid conditions included in the Charlson index. Survival probabilities were estimated by comorbidity group (no, low/medium, and high) and for the 3 most prevalent conditions (diabetes, chronic obstructive pulmonary disease, and congestive heart failure) by using the Cox proportional hazards model. Comorbidity-adjusted life expectancy was calculated based on comparisons of survival models with U. S. life tables. Survival probabilities from the U. S. life tables providing the most similar survival experience to the cohort of interest were used.
   Results: Persons with higher levels of comorbidity had shorter life expectancies, whereas those with no comorbid conditions, including very elderly persons, had favorable life expectancies relative to an average person of the same chronological age. The estimated life expectancy at age 75 years was approximately 3 years longer for persons with no comorbid conditions and approximately 3 years shorter for those with high comorbidity relative to the average U. S. population.
   Limitations: The cohort was limited to Medicare fee-for-service beneficiaries aged 66 years or older living in selected geographic areas. Data from the Surveillance, Epidemiology, and End Results cancer registry and Medicare claims lack information on functional status and severity of comorbidity, which might influence life expectancy in elderly persons.
   Conclusion: Life expectancy varies considerably by comorbidity status in elderly persons. Comorbidity-adjusted life expectancy may help physicians tailor recommendations for stopping or continuing cancer screening for individual patients.
C1 NCI, Bethesda, MD 20892 USA.
   Informat Serv Management, Calverton, MD USA.
   Erasmus MC, Rotterdam, Netherlands.
RP Cho, H (reprint author), NCI, Data Modeling Branch, Surveillance Res Program, Div Canc Control & Populat Sci, 9609 Med Ctr Dr, Bethesda, MD 20892 USA.
EM hyunsoon.cho@nih.gov
OI Yabroff, K. Robin/0000-0003-0644-5572
FU National Cancer Institute at the National Institutes of Health; Centers
   for Disease Control [U01-CA-152959 and U01 CA152926]
FX This study received no external funding. Dr. Lansdorp-ogelaar was
   supported by the National Cancer Institute at the National Institutes of
   Health and the Centers for Disease Control (grants U01-CA-152959 and U01
   CA152926.
NR 39
TC 45
Z9 45
U1 0
U2 13
PU AMER COLL PHYSICIANS
PI PHILADELPHIA
PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA
SN 0003-4819
EI 1539-3704
J9 ANN INTERN MED
JI Ann. Intern. Med.
PD NOV 19
PY 2013
VL 159
IS 10
BP 667
EP +
DI 10.7326/0003-4819-159-10-201311190-00005
PG 14
WC Medicine, General & Internal
SC General & Internal Medicine
GA 276FB
UT WOS:000328732700015
PM 24247672
ER

PT J
AU Lei, HY
   Li, TW
   Hung, GC
   Li, BJ
   Tsai, S
   Lo, SC
AF Lei, Haiyan
   Li, Tianwei
   Hung, Guo-Chiuan
   Li, Bingjie
   Tsai, Shien
   Lo, Shyh-Ching
TI Identification and characterization of EBV genomes in spontaneously
   immortalized human peripheral blood B lymphocytes by NGS technology
SO BMC GENOMICS
LA English
DT Article
DE Epstein Barr Virus; Mycoplasma; Next-generation sequencing; Human
   immortalized B lymphocytes
ID EPSTEIN-BARR-VIRUS; NASOPHARYNGEAL CARCINOMA; GASTRIC-CARCINOMA; VIRAL
   GENOMES; DNA-SEQUENCE; CELLS; LYMPHOMA; BIOPSIES
AB Background: We conducted genomic sequencing to identify Epstein Barr Virus (EBV) genomes in 2 human peripheral blood B lymphocytes that underwent spontaneous immortalization promoted by mycoplasma infections in culture, using the high-throughput sequencing (HTS) Illumina MiSeq platform. The purpose of this study was to examine if rapid detection and characterization of a viral agent could be effectively achieved by HTS using a platform that has become readily available in general biology laboratories.
   Results: Raw read sequences, averaging 175 bps in length, were mapped with DNA databases of human, bacteria, fungi and virus genomes using the CLC Genomics Workbench bioinformatics tool. Overall 37,757 out of 49,520,834 total reads in one lymphocyte line (# K4413-Mi) and 28,178 out of 45,335,960 reads in the other lymphocyte line (# K4123-Mi) were identified as EBV sequences. The two EBV genomes with estimated 35.22-fold and 31.06-fold sequence coverage respectively, designated K4413-Mi EBV and K4123-Mi EBV (GenBank accession number KC440852 and KC440851 respectively), are characteristic of type-1 EBV.
   Conclusions: Sequence comparison and phylogenetic analysis among K4413-Mi EBV, K4123-Mi EBV and the EBV genomes previously reported to GenBank as well as the NA12878 EBV genome assembled from database of the 1000 Genome Project showed that these 2 EBVs are most closely related to B95-8, an EBV previously isolated from a patient with infectious mononucleosis and WT-EBV. They are less similar to EBVs associated with nasopharyngeal carcinoma (NPC) from Hong Kong and China as well as the Akata strain of a case of Burkitt's lymphoma from Japan. They are most different from type 2 EBV found in Western African Burkitt's lymphoma.
C1 [Lei, Haiyan; Li, Tianwei; Hung, Guo-Chiuan; Li, Bingjie; Tsai, Shien; Lo, Shyh-Ching] Food & Drug Adm, Ctr Biol Evaluat & Res, Div Cellular & Gene Therapies, Tissue Microbiol Lab,Off Cellular Tissue & Gene T, Bethesda, MD 20892 USA.
RP Lo, SC (reprint author), Food & Drug Adm, Ctr Biol Evaluat & Res, Div Cellular & Gene Therapies, Tissue Microbiol Lab,Off Cellular Tissue & Gene T, NIH Bldg 29B,Rm 1NN06,29 Lincoln Dr, Bethesda, MD 20892 USA.
EM ShyhChing.Lo@fda.hhs.gov
FU FDA Modernizing Science research grant; U.S. Department of Energy; U.S.
   Food and Drug Administration
FX The study was supported in part by FDA Modernizing Science research
   grant and supported in part by an appointment to the Research
   Participation Program at the CBER of FDA administered by the Oak Ridge
   Institute for Science and Education through an interagency agreement
   between the U.S. Department of Energy and the U.S. Food and Drug
   Administration.
NR 22
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U1 1
U2 11
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PD NOV 19
PY 2013
VL 14
AR 804
DI 10.1186/1471-2164-14-804
PG 9
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 274YM
UT WOS:000328642100005
PM 24252203
ER

PT J
AU Kravitz, AV
   Bonci, A
AF Kravitz, Alexxai V.
   Bonci, Antonello
TI Optogenetics, physiology, and emotions
SO FRONTIERS IN BEHAVIORAL NEUROSCIENCE
LA English
DT Editorial Material
DE optogenetics; emotions; anxiety; depression; reward; physiological;
   synchrony
ID IN-VIVO; NUCLEUS-ACCUMBENS; STRIATAL NEURONS; COCAINE; STIMULATION;
   CORTEX; INHIBITION; AMYGDALA; SEEKING; REWARD
C1 [Kravitz, Alexxai V.] NIDDK, Diabet Endocrinol & Obes Branch, Bethesda, MD 20892 USA.
   [Bonci, Antonello] NIDA, Baltimore, MD USA.
RP Kravitz, AV (reprint author), NIDDK, Diabet Endocrinol & Obes Branch, Bethesda, MD 20892 USA.
EM lex.kravitz@nih.gov
NR 44
TC 6
Z9 6
U1 0
U2 14
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5153
J9 FRONT BEHAV NEUROSCI
JI Front. Behav. Neurosci.
PD NOV 19
PY 2013
VL 7
AR 169
DI 10.3389/fnbeh.2013.00169
PG 4
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 263BS
UT WOS:000327782200001
PM 24312032
ER

PT J
AU Yang, M
   Loureiro, D
   Kalikhman, D
   Crawley, JN
AF Yang, Mu
   Loureiro, Darren
   Kalikhman, David
   Crawley, Jacqueline N.
TI Male mice emit distinct ultrasonic vocalizations when the female leaves
   the social interaction arena
SO FRONTIERS IN BEHAVIORAL NEUROSCIENCE
LA English
DT Article
DE ultrasonic vocalizations; USV; mouse models of autism; mouse model of
   communication; social interaction; social behaviors
ID PLUS TF/J MICE; MOUSE MODEL; MUS-MUSCULUS; VOCAL COMMUNICATION; UNUSUAL
   REPERTOIRE; MUTANT MICE; AUTISM; BEHAVIOR; EXPERIENCE; COURTSHIP
AB Adult male mice emit large number of complex ultrasonic vocalizations (USVs) when interacting with adult females. Call numbers and call categories differ greatly among inbred mouse strains. Little is known about USV emissions when the social partner departs. To investigate whether call repertoires and call rates are different when the male is interacting with a female and after the removal of the female, we designed a novel male-female social interaction test in which vocalizations were recorded across three phases. During phase 1, the male subject freely interacts with an unfamiliar estrus female mouse in a clean cage for 5 min. During phase 2, the female is removed while the male remains in the cage for 3 min. During phase 3, the same female is returned to the cage to rejoin the male subject mouse for 3 min. C57BL/6J (B6), FVB.129P2-Pde6b(+) Tyr(c-ch)/Ant (FVB), and BTBR T+ tf/J (BTBR) male subject mice were tested in this paradigm. All three strains emitted USVs during their initial interaction with the female partner. When the female was reintroduced in phase 3, numbers of USVs were similar to the initial introductory phase 1. Strain comparisons indicated fewer calls in pairs of BTBR males and stimulus females than in pairs of B6 males and stimulus females and pairs of FVB males and stimulus females. In the absence of the female, all FVB males vocalized, while only one third of B6 males and one third of BTBR males vocalized. In all three strains, changes in call category repertoires were detected after the female was removed. Call categories reverted to the phase 1 pattern when the female was returned in phase 3. Present findings indicate that males of commonly used inbred strains emit USVs when a partner female leaves the testing arena, suggesting that removing a salient social stimulus may be a unique approach to elicit USVs from mice. Our three-phase paradigm may also be useful for studying attention to social cues, and qualitative differences in vocalizations when a social partner is present vs. suddenly absent.
C1 [Yang, Mu; Crawley, Jacqueline N.] Univ Calif Davis, Dept Psychiat & Behav Sci, Sch Med, Sacramento, CA 95817 USA.
   [Yang, Mu; Loureiro, Darren; Kalikhman, David; Crawley, Jacqueline N.] NIMH, Lab Behav Neurosci, Bethesda, MD 20892 USA.
RP Yang, M (reprint author), Univ Calif Davis, Dept Psychiat & Behav Sci, Sch Med, Room 1001,Res 2 Bldg 96,4625 2nd Ave, Sacramento, CA 95817 USA.
EM mu.yang@ucdmc.ucdavis.edu
FU National Institute of Mental Health Intramural Research Program; MIND
   Institute
FX This work was supported by the National Institute of Mental Health
   Intramural Research Program. The experiments were conducted at National
   Institutes of Health. A significant portion of data analysis was done in
   our current laboratory at University of California, Davis, with support
   from the MIND Institute.
NR 59
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U1 2
U2 10
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5153
J9 FRONT BEHAV NEUROSCI
JI Front. Behav. Neurosci.
PD NOV 19
PY 2013
VL 7
AR 159
DI 10.3389/fnbeh.2013.00159
PG 13
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 263AC
UT WOS:000327778000001
PM 24312027
ER

PT J
AU Sawetzki, T
   Eggleton, CD
   Desai, SA
   Marr, DWM
AF Sawetzki, Tobias
   Eggleton, Charles D.
   Desai, Sanjay A.
   Marr, David W. M.
TI Viscoelasticity as a Biomarker for High-Throughput Flow Cytometry
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID RED-BLOOD-CELLS; ATOMIC-FORCE MICROSCOPY; DIODE-LASER BARS;
   MECHANICAL-PROPERTIES; PLASMODIUM-FALCIPARUM; OPTICAL DEFORMABILITY;
   MICROFLUIDIC SYSTEMS; SINGLE CELLS; LIVING CELLS; CANCER
AB The mechanical properties of living cells are a label-free biophysical marker of cell viability and health; however, their use has been greatly limited by low measurement throughput. Although examining individual cells at high rates is now commonplace with fluorescence activated cell sorters, development of comparable techniques that nondestructively probe cell mechanics remains challenging. A fundamental hurdle is the signal response time. Where light scattering and fluorescence signatures are virtually instantaneous, the cell stress relaxation, typically occurring on the order of seconds, limits the potential speed of elastic property measurement. To overcome this intrinsic barrier to rapid analysis, we show here that cell viscoelastic properties measured at frequencies far higher than those associated with cell relaxation can be used as a means of identifying significant differences in cell phenotype. In these studies, we explore changes in erythrocyte mechanical properties caused by infection with Plasmodium falciparum and find that the elastic response alone fails to detect malaria at high frequencies. At time-scales associated with rapid assays, however, we observe that the inelastic response shows significant changes and can be used as a reliable indicator of infection, establishing the dynamic viscoelasticity as a basis for nondestructive mechanical analogs of current high-throughput cell classification methods.
C1 [Sawetzki, Tobias; Marr, David W. M.] Colorado Sch Mines, Dept Chem & Biol Engn, Golden, CO 80401 USA.
   [Eggleton, Charles D.] Univ Maryland Baltimore Cty, Dept Mech Engn, Baltimore, MD 21228 USA.
   [Desai, Sanjay A.] NIAID, Lab Malaria & Vector Res, Rockville, MD USA.
RP Marr, DWM (reprint author), Colorado Sch Mines, Dept Chem & Biol Engn, Golden, CO 80401 USA.
EM dmarr@mines.edu
FU National Science Foundation [DBI-0852868]; National Institutes of Health
   [1R01 AI079347]; Intramural Research Program of the National Institutes
   of Health, National Institute of Allergy and Infectious Diseases
FX We acknowledge support from the National Science Foundation grant No.
   DBI-0852868, the National Institutes of Health under grant No. 1R01
   AI079347, and the Intramural Research Program of the National Institutes
   of Health, National Institute of Allergy and Infectious Diseases.
NR 47
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U1 1
U2 29
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 NOV 19
PY 2013
VL 105
IS 10
BP 2281
EP 2288
DI 10.1016/j.bpj.2013.10.003
PG 8
WC Biophysics
SC Biophysics
GA 256BQ
UT WOS:000327285100009
PM 24268140
ER

PT J
AU Eberhardt, RY
   Chang, YY
   Bateman, A
   Murzin, AG
   Axelrod, HL
   Hwang, WC
   Aravind, L
AF Eberhardt, Ruth Y.
   Chang, Yuanyuan
   Bateman, Alex
   Murzin, Alexey G.
   Axelrod, Herbert L.
   Hwang, William C.
   Aravind, L.
TI Filling out the structural map of the NTF2-like superfamily
SO BMC BIOINFORMATICS
LA English
DT Article
DE NTF2-like superfamily; Protein function prediction; Protein structure;
   Ligand-binding; JCSG; 3D structure; Protein family
ID IV SECRETION SYSTEM; CRYSTAL-STRUCTURE; PROTEIN MODELS; SEQUENCE;
   DATABASE; GENOMICS; VIRB8; CRYSTALLOGRAPHY; IDENTIFICATION; INFORMATION
AB Background: The NTF2-like superfamily is a versatile group of protein domains sharing a common fold. The sequences of these domains are very diverse and they share no common sequence motif. These domains serve a range of different functions within the proteins in which they are found, including both catalytic and non-catalytic versions. Clues to the function of protein domains belonging to such a diverse superfamily can be gleaned from analysis of the proteins and organisms in which they are found.
   Results: Here we describe three protein domains of unknown function found mainly in bacteria: DUF3828, DUF3887 and DUF4878. Structures of representatives of each of these domains: BT_3511 from Bacteroides thetaiotaomicron (strain VPI-5482) [PDB:3KZT], Cj0202c from Campylobacter jejuni subsp. jejuni serotype O:2 (strain NCTC 11168) [PDB: 3K7C], rumgna_01855) and RUMGNA_01855 from Ruminococcus gnavus (strain ATCC 29149) [PDB:4HYZ] have been solved by X-ray crystallography. All three domains are similar in structure and all belong to the NTF2-like superfamily. Although the function of these domains remains unknown at present, our analysis enables us to present a hypothesis concerning their role.
   Conclusions: Our analysis of these three protein domains suggests a potential non-catalytic ligand-binding role. This may regulate the activities of domains with which they are combined in the same polypeptide or via operonic linkages, such as signaling domains (e.g. serine/threonine protein kinase), peptidoglycan-processing hydrolases (e.g. NlpC/P60 peptidases) or nucleic acid binding domains (e.g. Zn-ribbons).
C1 [Eberhardt, Ruth Y.] Wellcome Trust Sanger Inst, Hinxton CB10 1SA, Cambs, England.
   [Eberhardt, Ruth Y.; Bateman, Alex] European Bioinformat Inst, European Mol Biol Lab, Hinxton CB10 1SD, Cambs, England.
   [Chang, Yuanyuan; Hwang, William C.] Sanford Burnham Med Res Inst, La Jolla, CA 92037 USA.
   [Murzin, Alexey G.] MRC Lab Mol Biol, Cambridge CB2 0QH, England.
   [Axelrod, Herbert L.] SLAC Natl Accelerator Lab, Stanford Synchrotron Radiat Lightsource, Menlo Pk, CA USA.
   [Aravind, L.] NIH, Natl Ctr Biotechnol Informat, NLM, Bethesda, MD 20814 USA.
RP Eberhardt, RY (reprint author), Wellcome Trust Sanger Inst, Wellcome Trust Genome Campus, Hinxton CB10 1SA, Cambs, England.
EM re3@sanger.ac.uk
OI Bateman, Alex/0000-0002-6982-4660
FU Wellcome Trust [WT077044/7/05/7]; Howard Hughes Medical Institute;
   National Library of Medicine, USA; NIH [R01GM101457]; UK Medical
   Research Council [MC_U105192716]; National Institutes of Health [U54
   GM094586]; National Science Foundation [IIS-0646708, IIS-1153617]; DOE
   Office of Biological and Environmental Research, and by the National
   Institutes of Health, National Institute of General Medical Sciences
   [P41GM103393]
FX Wellcome Trust (grant numbers WT077044/7/05/7); Howard Hughes Medical
   Institute; Work by LA is supported by the intramural funds of the
   National Library of Medicine, USA.; NIH (R01GM101457); Work by AGM was
   supported by the UK Medical Research Council [MC_U105192716]; This work
   was supported in part by National Institutes of Health Grant U54
   GM094586 from the NIGMS Protein Structure Initiative to the Joint Center
   for Structural Genomics. The DUF annotation jamboree was supported by
   National Science Foundation (IIS-0646708 and IIS-1153617); Portions of
   this research were carried out at the Stanford Synchrotron Radiation
   Lightsource, a Directorate of SI AC National Accelerator Laboratory and
   an Office of Science User Facility operated for the U. S. Department of
   Energy Office of Science by Stanford University. The SSRL Structural
   Molecular Biology Program is supported by the DOE Office of Biological
   and Environmental Research, and by the National Institutes of Health,
   National Institute of General Medical Sciences (including P41GM103393).
   The contents of this publication are solely the responsibility of the
   authors and do not necessarily represent the official views of NIGMS,
   NCRR or NIH.
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PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2105
J9 BMC BIOINFORMATICS
JI BMC Bioinformatics
PD NOV 19
PY 2013
VL 14
AR 327
DI 10.1186/1471-2105-14-327
PG 11
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
   Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Mathematical & Computational Biology
GA 259MQ
UT WOS:000327531400002
PM 24246060
ER

PT J
AU Alsarraj, J
   Faraji, F
   Geiger, TR
   Mattaini, KR
   Williams, M
   Wu, J
   Ha, NH
   Merlino, T
   Walker, RC
   Bosley, AD
   Xiao, Z
   Andresson, T
   Esposito, D
   Smithers, N
   Lugo, D
   Prinjha, R
   Day, A
   Crawford, NPS
   Ozato, K
   Gardner, K
   Hunter, KW
AF Alsarraj, Jude
   Faraji, Farhoud
   Geiger, Thomas R.
   Mattaini, Katherine R.
   Williams, Mia
   Wu, Josephine
   Ha, Ngoc-Han
   Merlino, Tyler
   Walker, Renard C.
   Bosley, Allen D.
   Xiao, Zhen
   Andresson, Thorkell
   Esposito, Dominic
   Smithers, Nicholas
   Lugo, Dave
   Prinjha, Rab
   Day, Anup
   Crawford, Nigel P. S.
   Ozato, Keiko
   Gardner, Kevin
   Hunter, Kent W.
TI BRD4 Short Isoform Interacts with RRP1B, SIPA1 and Components of the
   LINC Complex at the Inner Face of the Nuclear Membrane
SO PLOS ONE
LA English
DT Article
ID BROMODOMAIN PROTEIN BRD4; BREAST-CANCER SURVIVAL; NUT MIDLINE CARCINOMA;
   P-TEFB; C-MYC; FLUORESCENCE COMPLEMENTATION; MITOTIC CHROMOSOMES; BET
   BROMODOMAINS; HISTONE TAILS; CHROMATIN
AB Recent studies suggest that BET inhibitors are effective anti-cancer therapeutics. Here we show that BET inhibitors are effective against murine primary mammary tumors, but not pulmonary metastases. BRD4, a target of BET inhibitors, encodes two isoforms with opposite effects on tumor progression. To gain insights into why BET inhibition was ineffective against metastases the pro-metastatic short isoform of BRD4 was characterized using mass spectrometry and cellular fractionation. Our data show that the pro-metastatic short isoform interacts with the LINC complex and the metastasis-associated proteins RRP1B and SIPA1 at the inner face of the nuclear membrane. Furthermore, histone binding arrays revealed that the short isoform has a broader acetylated histone binding pattern relative to the long isoform. These differential biochemical and nuclear localization properties revealed in our study provide novel insights into the opposing roles of BRD4 isoforms in metastatic breast cancer progression.
C1 [Alsarraj, Jude; Faraji, Farhoud; Geiger, Thomas R.; Mattaini, Katherine R.; Williams, Mia; Wu, Josephine; Ha, Ngoc-Han; Merlino, Tyler; Walker, Renard C.; Hunter, Kent W.] NCI, Ctr Canc Res, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
   [Faraji, Farhoud] St Louis Univ, Sch Med, Dept Biochem & Mol Biol, St Louis, MO 63104 USA.
   [Bosley, Allen D.; Xiao, Zhen; Andresson, Thorkell; Esposito, Dominic] Frederick Natl Lab Canc Res, Lab Prote & Analyt Technol, Frederick, MD USA.
   [Smithers, Nicholas; Lugo, Dave; Prinjha, Rab] GlaxoSmithKline, Immuno Inflammat Therapeut Area, Epinova DPU & Quantitat Pharmacol, Stevenage, Herts, England.
   [Day, Anup; Ozato, Keiko] Natl Inst Child Hlth & Human Dev, Lab Mol Growth Regulat, NIH, Bethesda, MD USA.
   [Crawford, Nigel P. S.] NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA.
   [Gardner, Kevin] NCI, Ctr Canc Res, Genet Branch, NIH, Bethesda, MD 20892 USA.
RP Hunter, KW (reprint author), Univ Washington, Sch Med, Dept Med, Div Cardiol, Seattle, WA 98195 USA.
EM hunter@mail.nih.gov
OI Faraji, Farhoud/0000-0001-5078-813X
FU Intramural Research Program of the NIH, National Cancer Institute,
   Center for Cancer Research;  [ZIA BC 011255]
FX Intramural project number/grant number ZIA BC 011255. This research was
   supported by the Intramural Research Program of the NIH, National Cancer
   Institute, Center for Cancer Research. The funders had no role in study
   design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
NR 58
TC 11
Z9 11
U1 3
U2 12
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 19
PY 2013
VL 8
IS 11
AR UNSP e80746
DI 10.1371/journal.pone.0080746
PG 17
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 256LO
UT WOS:000327311900093
PM 24260471
ER

PT J
AU Barbieri, E
   De Preter, K
   Capasso, M
   Johansson, P
   Man, TK
   Chen, ZW
   Stowers, P
   Tonini, GP
   Speleman, F
   Shohet, JM
AF Barbieri, Eveline
   De Preter, Katleen
   Capasso, Mario
   Johansson, Peter
   Man, Tsz-Kwong
   Chen, Zaowen
   Stowers, Paris
   Tonini, Gian Paolo
   Speleman, Frank
   Shohet, Jason M.
TI A p53 Drug Response Signature Identifies Prognostic Genes in High-Risk
   Neuroblastoma
SO PLOS ONE
LA English
DT Article
ID CHROMATIN ASSEMBLY FACTOR-1; RIBONUCLEOTIDE REDUCTASE INHIBITORS; MDM2
   ANTAGONIST NUTLIN-3; QUANTITATIVE PCR DATA; WILD-TYPE P53; IN-VIVO;
   TRANSCRIPTIONAL REPRESSION; P53/MDM2/P14(ARF) PATHWAY;
   FUNCTIONAL-ANALYSIS; TARGET GENES
AB Chemotherapy induces apoptosis and tumor regression primarily through activation of p53-mediated transcription. Neuroblastoma is a p53 wild type malignancy at diagnosis and repression of p53 signaling plays an important role in its pathogenesis. Recently developed small molecule inhibitors of the MDM2-p53 interaction are able to overcome this repression and potently activate p53 dependent apoptosis in malignancies with intact p53 downstream signaling. We used the small molecule MDM2 inhibitor, Nutlin-3a, to determine the p53 drug response signature in neuroblastoma cells. In addition to p53 mediated apoptotic signatures, GSEA and pathway analysis identified a set of p53-repressed genes that were reciprocally over-expressed in neuroblastoma patients with the worst overall outcome in multiple clinical cohorts. Multifactorial regression analysis identified a subset of four genes (CHAF1A, RRM2, MCM3, and MCM6) whose expression together strongly predicted overall and event-free survival (p < 0.0001). The expression of these four genes was then validated by quantitative PCR in a large independent clinical cohort. Our findings further support the concept that oncogene-driven transcriptional networks opposing p53 activation are essential for the aggressive behavior and poor response to therapy of high-risk neuroblastoma.
C1 [Barbieri, Eveline; Man, Tsz-Kwong; Chen, Zaowen; Stowers, Paris; Shohet, Jason M.] Baylor Coll Med, Texas Childrens Canc Ctr, Houston, TX 77030 USA.
   [Barbieri, Eveline; Man, Tsz-Kwong; Chen, Zaowen; Stowers, Paris; Shohet, Jason M.] Baylor Coll Med, Dept Pediat, Ctr Cell & Gene Therapy, Houston, TX 77030 USA.
   [De Preter, Katleen] Univ Ghent, Ctr Med Genet, B-9000 Ghent, Belgium.
   [Capasso, Mario] Univ Naples Federico II, Dept Biochem & Med Biotechnol, CEINGE Biotecnol Avanzate, Naples, Italy.
   [Johansson, Peter] NCI, Oncogen Sect, Pediat Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
   [Tonini, Gian Paolo] Univ Padua, Pediat Res Inst, Padua, Italy.
RP Shohet, JM (reprint author), Baylor Coll Med, Texas Childrens Canc Ctr, Houston, TX 77030 USA.
EM jmshohet@txch.org
RI De Preter, Katleen/I-7135-2013; Johansson, Peter/K-1053-2014; Capasso,
   Mario/D-1617-2014; 
OI De Preter, Katleen/0000-0002-7726-5096; Johansson,
   Peter/0000-0001-7015-5452; Capasso, Mario/0000-0003-3306-1259
FU Ale's Lemonade Stand Foundation; Children's Cancer Research Foundation;
   American Cancer Society; Flemish Fund for Scientific Research;
   Associazione Italiana per la Lotta al Neuroblastoma; MIUR - FIRB Ricerca
   in Futuro
FX This work was supported by Ale's Lemonade Stand Foundation (EB, JMS),
   the Children's Cancer Research Foundation (EB) and a Research Scholar
   Grant from the American Cancer Society (JMS). KDP is supported by the
   Flemish Fund for Scientific Research. MC is supported by Associazione
   Italiana per la Lotta al Neuroblastoma and MIUR - FIRB Ricerca in
   Futuro. The funders had no role in study design, data collection and
   analysis, decision to publish, or preparation of the manuscript.
NR 58
TC 13
Z9 16
U1 1
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 19
PY 2013
VL 8
IS 11
AR e79843
DI 10.1371/journal.pone.0079843
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 256LO
UT WOS:000327311900048
PM 24348903
ER

PT J
AU Englund, JA
   Karron, RA
   Cunningham, CK
   LaRussa, P
   Melvin, A
   Yogev, R
   Handelsman, E
   Siberry, GK
   Thumar, B
   Schappell, E
   Bull, CV
   Chu, HY
   Schaap-Nutt, A
   Buchholz, U
   Collins, PL
   Schmidt, AC
AF Englund, Janet A.
   Karron, Ruth A.
   Cunningham, Coleen K.
   LaRussa, Philip
   Melvin, Ann
   Yogev, Ram
   Handelsman, Ed
   Siberry, George K.
   Thumar, Bhavanji
   Schappell, Elizabeth
   Bull, Catherine V.
   Chu, Helen Y.
   Schaap-Nutt, Anne
   Buchholz, Ursula
   Collins, Peter L.
   Schmidt, Alexander C.
CA Int Maternal Pediat Adolescent
TI Safety and infectivity of two doses of live-attenuated recombinant
   cold-passaged human parainfluenza type 3 virus vaccine rHPIV3cp45 in
   HPIV3-seronegative young children
SO VACCINE
LA English
DT Article
DE Parainfluenza; Live-attenuated vaccine; Recombinant virus vaccine;
   Pediatric vaccine
ID RESPIRATORY SYNCYTIAL VIRUS; TRANSPLANT RECIPIENTS; WEANLING HAMSTERS;
   HEALTHY INFANTS; PROGRESS; IMMUNOGENICITY; MUTANTS; AGE
AB Background: Human parainfluenza virus type 3 (HPIV3) is a common cause of upper and lower respiratory tract illness in infants and young children. Live-attenuated cold-adapted HPIV3 vaccines have been evaluated in infants but a suitable interval for administration of a second dose of vaccine has not been defined.
   Methods: HPIV3-seronegative children between the ages of 6 and 36 months were randomized 2:1 in a blinded study to receive two doses of 10(5) TCID50 (50% tissue culture infectious dose) of live-attenuated, recombinant cold-passaged human PIV3 vaccine (rHPIV3cp45) or placebo 6 months apart. Serum antibody levels were assessed prior to and approximately 4-6 weeks after each dose. Vaccine virus infectivity, defined as detection of vaccine-HPIV3 in nasal wash and/or a >= 4-fold rise in serum antibody titer, and reactogenicity were assessed on days 3, 7, and 14 following immunization.
   Results: Forty HPIV3-seronegative children (median age 13 months; range 6-35 months) were enrolled; 27 (68%) received vaccine and 13 (32%) received placebo. Infectivity was detected in 25 (96%) of 26 evaluable vaccinees following doses 1 and 9 of 26 subject (35%) following dose 2. Among those who shed virus, the median duration of viral shedding was 12 days (range 6-15 days) after dose 1 and 6 days (range 3-8 days) after dose 2, with a mean peak log(10) viral titer of 3.4 PFU/mL (SD: 1.0) after dose 1 compared to 1.5 PFU/mL (SD: 0.92) after dose 2. Overall, reactogenicity was mild, with no difference in rates of fever and upper respiratory infection symptoms between vaccine and placebo groups.
   Conclusion: rHPIV3cp45 was immunogenic and well-tolerated in seronegative young children. A second dose administered 6 months after the initial dose was restricted in those previously infected with vaccine virus; however, the second dose boosted antibody responses and induced antibody responses in two previously uninfected children. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Englund, Janet A.; Melvin, Ann; Bull, Catherine V.; Chu, Helen Y.] Univ Washington, Seattle Childrens Hosp, Seattle, WA 98105 USA.
   [Karron, Ruth A.; Thumar, Bhavanji; Schappell, Elizabeth] Johns Hopkins Univ, Ctr Immunizat Res, Bloomberg Sch Publ Hlth, Baltimore, MD 21295 USA.
   [Cunningham, Coleen K.] Duke Univ, Med Ctr, Durham, NC USA.
   [LaRussa, Philip] Columbia Univ, Dept Pediat, New York, NY 10027 USA.
   [Yogev, Ram] Northwestern Univ, Lurie Childrens Hosp Chicago, Feinberg Sch Med, Chicago, IL 60611 USA.
   [Handelsman, Ed] NIAID, Div Aids, Bethesda, MD 20892 USA.
   [Siberry, George K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Maternal & Pediat Infect Dis Branch, Bethesda, MD USA.
   [Schaap-Nutt, Anne; Buchholz, Ursula; Collins, Peter L.; Schmidt, Alexander C.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Englund, JA (reprint author), Seattle Childrens Hosp, 4800 Sand Point Way NE,MA 7-234, Seattle, WA 98105 USA.
EM janet.englund@seattlechildrens.org
OI Frenkel, Lisa M/0000-0001-9566-8959; Chu, Helen/0000-0001-8502-9600;
   Schappell, Elizaeth/0000-0003-2142-5318
FU Intramural Research program of the National Institutes of Allergy and
   Infectious Diseases (NIAID), National Institutes of Health (NIH); NIAID
   [HSN272200900010C]; Johns Hopkins Bloomberg School of Public Health
   [HSN272200900010C]; National Center for Research Resources; National
   Center for Advancing Translational Sciences, National Institutes of
   Health [UL1RR025014]; National Institute of Allergy and Infectious
   Diseases (NIAID) [U01 AI068632]; Eunice Kennedy Shriver National
   Institute of Child Health and Human Development (NICHD); National
   Institute of Mental Health (NIMH) [AI068632]; Statistical and Data
   Analysis Center at Harvard School of Public Health, under the National
   Institute of Allergy and Infectious Diseases [1 U01 AI068616]; IMPAACT
   Group; NICHD [N01-DK-9-001/HHSN267200800001C]
FX This study was funded by the Intramural Research program of the National
   Institutes of Allergy and Infectious Diseases (NIAID), National
   Institutes of Health (NIH). Clinical trials were conducted as part of
   contracts between NIAID and the Johns Hopkins Bloomberg School of Public
   Health (HSN272200900010C). In Seattle, this project was supported by the
   National Center for Research Resources and the National Center for
   Advancing Translational Sciences, National Institutes of Health, through
   Grant UL1RR025014. Overall support for the International Maternal
   Pediatric Adolescent AIDS Clinical Trials Group (IMPAACT) was provided
   by the National Institute of Allergy and Infectious Diseases (NIAID)
   [U01 AI068632], the Eunice Kennedy Shriver National Institute of Child
   Health and Human Development (NICHD), and the National Institute of
   Mental Health (NIMH) [AI068632]. This work was supported by the
   Statistical and Data Analysis Center at Harvard School of Public Health,
   under the National Institute of Allergy and Infectious Diseases
   cooperative agreement #1 U01 AI068616 with the IMPAACT Group. Support of
   the sites was provided by the National Institute of Allergy and
   Infectious Diseases (NIAID) and the NICHD International and Domestic
   Pediatric and Maternal HIV Clinical Trials Network funded by NICHD
   (contract number N01-DK-9-001/HHSN267200800001C). Conflict of interest:
   No conflicts of interests or financial disclosures are reported by any
   authors. A. Schmidt is currently an employee of GlaxoSmithKline.
NR 27
TC 11
Z9 11
U1 0
U2 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
EI 1873-2518
J9 VACCINE
JI Vaccine
PD NOV 19
PY 2013
VL 31
IS 48
BP 5706
EP 5712
DI 10.1016/j.vaccine.2013.09.046
PG 7
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 260FL
UT WOS:000327580300013
PM 24103895
ER

PT J
AU Durbin, AP
   Wright, PF
   Cox, A
   Kagucia, W
   Elwood, D
   Henderson, S
   Wanionek, K
   Speicher, J
   Whitehead, SS
   Pletnev, AG
AF Durbin, Anna P.
   Wright, Peter F.
   Cox, Amber
   Kagucia, Wangeci
   Elwood, Daniel
   Henderson, Susan
   Wanionek, Kimberli
   Speicher, Jim
   Whitehead, Stephen S.
   Pletnev, Alexander G.
TI The live attenuated chimeric vaccine rWN/DEN4 Delta 30 is well-tolerated
   and immunogenic in healthy flavivirus-naive adult volunteers
SO VACCINE
LA English
DT Article
DE West Nile virus (WNV); Live attenuated WNV vaccine; Clinical trial
ID WEST-NILE-VIRUS; RHESUS-MONKEYS; 3'-UNTRANSLATED REGION; PROTECTIVE
   EFFICACY; UNITED-STATES; CANDIDATE; TYPE-4; ENCEPHALITIS; SAFE;
   INFECTION
AB WNV has become the leading vector-borne cause of meningoencephalitis in the United States. Although the majority of WNV infections result in asymptomatic illness, approximately 20% of infections result in West Nile fever and 1% in West Nile neuroinvasive disease (WNND), which causes encephalitis, meningitis, or flaccid paralysis. The elderly are at particular risk for WNND, with more than half the cases occurring in persons older than sixty years of age. There is no licensed treatment for WNND, nor is there any licensed vaccine for humans for the prevention of WNV infection. The Laboratory of Infectious Diseases at the National Institutes of Health has developed a recombinant live attenuated WNV vaccine based on chimerization of the wild-type WNV NY99 genome with that of the live attenuated DENV-4 candidate vaccine rDEN4 Delta 30. The genes encoding the prM and envelope proteins of DENV-4 were replaced with those of WNV NY99 and the resultant virus was designated rWN/DEN4 Delta 30. The vaccine was evaluated in healthy flavivirus-naive adult volunteers age 18-50 years in two separate studies, both of which are reported here. The first study evaluated 10(3) or 10(4) PFU of the vaccine given as a single dose; the second study evaluated 105 PFU of the vaccine given as two doses 6 months apart. The vaccine was well-tolerated and immunogenic at all three doses, inducing seroconversion to WNV NY99 in 74% (10(3) PFU), 75% (10(4) PFU), and 55% (10(5) PFU) of subjects after a single dose. A second 10(5) PFU dose of rWN/DEN4 Delta 30 given 6 months after the first dose increased the seroconversion rate 89%. Based on the encouraging results from these studies, further evaluation of the candidate vaccine in adults older than 50 years of age is planned. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Durbin, Anna P.; Cox, Amber; Kagucia, Wangeci; Elwood, Daniel; Wanionek, Kimberli] Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Immunizat Res, Dept Int Hlth, Baltimore, MD 21205 USA.
   [Wright, Peter F.; Henderson, Susan] Vanderbilt Univ, Dept Pediat, Nashville, TN USA.
   [Speicher, Jim; Whitehead, Stephen S.; Pletnev, Alexander G.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Durbin, AP (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, 624N Broadway,Room 217, Baltimore, MD 21205 USA.
EM adurbin@jhsph.edu
FU National Institute of Allergy and Infectious Diseases Intramural
   Research Program, National Institutes of Health [NO1-AI-15444]
FX These studies were supported by the National Institute of Allergy and
   Infectious Diseases Intramural Research Program, National Institutes of
   Health (No. NO1-AI-15444), through a contract with the Johns Hopkins
   Bloomberg School of Public Health and a subcontract with Vanderbilt
   University Medical Center.
NR 32
TC 17
Z9 17
U1 0
U2 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
EI 1873-2518
J9 VACCINE
JI Vaccine
PD NOV 19
PY 2013
VL 31
IS 48
BP 5772
EP 5777
DI 10.1016/j.vaccine.2013.07.064
PG 6
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 260FL
UT WOS:000327580300022
PM 23968769
ER

PT J
AU Robles, AI
   Harris, CC
AF Robles, Ana I.
   Harris, Curtis C.
TI A primate-specific microRNA enters the lung cancer landscape
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Editorial Material
ID C-ELEGANS; CELL; EXPRESSION; LIN-14
C1 [Robles, Ana I.; Harris, Curtis C.] NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Harris, CC (reprint author), NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bldg 37, Bethesda, MD 20892 USA.
EM curtis_harris@nih.gov
FU Intramural NIH HHS
NR 20
TC 1
Z9 1
U1 1
U2 4
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 NOV 19
PY 2013
VL 110
IS 47
BP 18748
EP 18749
DI 10.1073/pnas.1318740110
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 253PD
UT WOS:000327100600027
PM 24191054
ER

PT J
AU Liu, J
   Cinar, R
   Xiong, KM
   Godlewski, G
   Jourdan, T
   Lin, YH
   Ntambi, JM
   Kunos, G
AF Liu, Jie
   Cinar, Resat
   Xiong, Keming
   Godlewski, Grzegorz
   Jourdan, Tony
   Lin, Yuhong
   Ntambi, James M.
   Kunos, George
TI Monounsaturated fatty acids generated via stearoyl CoA desaturase-1 are
   endogenous inhibitors of fatty acid amide hydrolase
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
ID HEPATIC CB1 RECEPTORS; INSULIN-RESISTANCE; MONOGLYCERIDE LIPASE;
   ANANDAMIDE SYNTHESIS; GLUCOSE-TOLERANCE; LEPTIN RESISTANCE;
   RISK-FACTORS; MICE; LIVER; DIET
AB High-fat diet (HFD)-induced obesity and insulin resistance are associated with increased activity of the endocannabinoid/CB1 receptor (CB1R) system that promotes the hepatic expression of lipogenic genes, including stearoyl-CoA desaturase-1 (SCD1). Mice deficient in CB1R or SCD1 remain lean and insulin-sensitive on an HFD, suggesting a functional link between the two systems. The HFD-induced increase in the hepatic levels of the endocannabinoid anandamide [i.e., arachidonoylethanolamide (AEA)] has been attributed to reduced activity of the AEA-degrading enzyme fatty acid amide hydrolase (FAAH). Here we show that HFD-induced increased hepatic AEA levels and decreased FAAH activity are absent in SCD1(-/-)mice, and the monounsaturated fatty acid (MUFA) products of SCD1, palmitoleic and oleic acid, inhibit FAAH activity in vitro at low micromolar concentrations. HFD markedly increases hepatic SCD1 activity in WT mice as well as in CB1R-/- mice with transgenic reexpression of CB1R in hepatocytes, but not in global CB1R-/- mice. Treatment of HFD-fed mice with the SCD1 inhibitor A939572 prevents the diet-induced reduction of hepatic FAAH activity, normalizes hepatic AEA levels, and improves insulin sensitivity. SCD1(-/-) mice on an HFD remain insulin-sensitive, but develop glucose intolerance and insulin resistance in response to chronic treatment with the FAAH inhibitor URB597. An HFD rich in MUFA or feeding mice pure oleic acid fail to inhibit hepatic FAAH activity. We conclude that MUFAs generated via SCD1 activity, but not diet-derived MUFAs, function as endogenous FAAH inhibitors mediating the HFD-induced increase in hepatic AEA, which then activates hepatic CB1R to induce insulin resistance.
C1 [Liu, Jie; Cinar, Resat; Xiong, Keming; Godlewski, Grzegorz; Jourdan, Tony; Kunos, George] NIAAA, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA.
   [Lin, Yuhong] NIAAA, Lab Membrane Biochem & Biophys, NIH, Bethesda, MD 20892 USA.
   [Ntambi, James M.] Univ Wisconsin, Dept Biochem, Madison, WI 53706 USA.
   [Ntambi, James M.] Univ Wisconsin, Dept Nutr Sci, Madison, WI 53706 USA.
RP Liu, J (reprint author), NIAAA, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA.
EM jiel@mail.nih.gov; george.kunos@nih.gov
OI CINAR, RESAT/0000-0002-8597-7253
NR 50
TC 13
Z9 15
U1 1
U2 8
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 NOV 19
PY 2013
VL 110
IS 47
BP 18832
EP 18837
DI 10.1073/pnas.1309469110
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 253PD
UT WOS:000327100600041
PM 24191036
ER

PT J
AU Mashimo, M
   Kato, J
   Moss, J
AF Mashimo, Masato
   Kato, Jiro
   Moss, Joel
TI ADP-ribosyl-acceptor hydrolase 3 regulates poly (ADP-ribose) degradation
   and cell death during oxidative stress
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE posttranslational modification; cytotoxicity
ID APOPTOSIS-INDUCING FACTOR; HUMAN POLY(ADP-RIBOSE) GLYCOHYDROLASE;
   DNA-DAMAGE; PARG ACTIVITY; ISOFORMS; POLYMERASE; DEPLETION; MICE;
   CHROMATINOLYSIS; CYTOTOXICITY
AB Poly (ADP ribose) (PAR) formation catalyzed by PAR polymerase 1 in response to genotoxic stress mediates cell death due to necrosis and apoptosis. PAR glycohydrolase (PARG) has been thought to be the only enzyme responsible for hydrolysis of PAR in vivo. However, we show an alternative PAR-degradation pathway, resulting from action of ADP ribosyl-acceptor hydrolase (ARH) 3. PARG and ARH3, acting in tandem, regulate nuclear and cytoplasmic PAR degradation following hydrogen peroxide (H2O2) exposure. PAR is responsible for induction of parthanatos, a mechanism for caspase-independent cell death, triggered by apoptosis-inducing factor (AIF) release from mitochondria and its translocation to the nucleus, where it initiates DNA cleavage. PARG, by generating protein-free PAR from poly-ADP ribosylated protein, makes PAR translocation possible. A protective effect of ARH3 results from its lowering of PAR levels in the nucleus and the cytoplasm, thereby preventing release of AIF from mitochondria and its accumulation in the nucleus. Thus, PARG release of PAR attached to nuclear proteins, followed by ARH3 cleavage of PAR, is essential in regulating PAR-dependent AIF release from mitochondria and parthanatos.
C1 [Mashimo, Masato; Kato, Jiro; Moss, Joel] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
RP Moss, J (reprint author), NHLBI, Cardiovasc & Pulm Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM mossj@nhlbi.nih.gov
FU Intramural Research Program, National Institutes of Health, National
   Heart, Lung, and Blood Institute
FX This study was supported by the Intramural Research Program, National
   Institutes of Health, National Heart, Lung, and Blood Institute.
NR 43
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U2 8
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 NOV 19
PY 2013
VL 110
IS 47
BP 18964
EP 18969
DI 10.1073/pnas.1312783110
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 253PD
UT WOS:000327100600063
PM 24191052
ER

PT J
AU Batchelor, TT
   Gerstner, ER
   Emblem, KE
   Duda, DG
   Kalpathy-Cramer, J
   Snuderl, M
   Ancukiewicz, M
   Polaskova, P
   Pinho, MC
   Jennings, D
   Plotkin, SR
   Chi, AS
   Eichler, AF
   Dietrich, J
   Hochberg, FH
   Lu-Emerson, C
   Iafrate, AJ
   Ivy, SP
   Rosen, BR
   Loeffler, JS
   Wen, PY
   Sorensen, AG
   Jain, RK
AF Batchelor, Tracy T.
   Gerstner, Elizabeth R.
   Emblem, Kyrre E.
   Duda, Dan G.
   Kalpathy-Cramer, Jayashree
   Snuderl, Matija
   Ancukiewicz, Marek
   Polaskova, Pavlina
   Pinho, Marco C.
   Jennings, Dominique
   Plotkin, Scott R.
   Chi, Andrew S.
   Eichler, April F.
   Dietrich, Jorg
   Hochberg, Fred H.
   Lu-Emerson, Christine
   Iafrate, A. John
   Ivy, S. Percy
   Rosen, Bruce R.
   Loeffler, Jay S.
   Wen, Patrick Y.
   Sorensen, A. Greg
   Jain, Rakesh K.
TI Improved tumor oxygenation and survival in glioblastoma patients who
   show increased blood perfusion after cediranib and chemoradiation
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE brain tumor; personalized treatment
ID TYROSINE KINASE INHIBITOR; GROWTH-FACTOR RECEPTOR; ANTIANGIOGENIC
   THERAPY; VASCULAR NORMALIZATION; RECURRENT GLIOBLASTOMA; RECTAL-CANCER;
   PHASE-II; TEMOZOLOMIDE; BEVACIZUMAB; RADIATION
AB Antiangiogenic therapy has shown clear activity and improved survival benefit for certain tumor types. However, an incomplete understanding of the mechanisms of action of antiangiogenic agents has hindered optimization and broader application of this new therapeutic modality. In particular, the impact of antiangiogenic therapy on tumor blood flow and oxygenation status (i.e., the role of vessel pruning versus normalization) remains controversial. This controversy has become critical as multiple phase III trials of antiVEGF agents combined with cytotoxics failed to show overall survival benefit in newly diagnosed glioblastoma (nGBM) patients and several other cancers. Here, we shed light on mechanisms of nGBM response to cediranib, a pan-VEGF receptor tyrosine kinase inhibitor, using MRI techniques and blood biomarkers in prospective phase II clinical trials of cediranib with chemoradiation vs. chemoradiation alone in nGBM patients. We demonstrate that improved perfusion occurs only in a subset of patients in cediranib-containing regimens, and is associated with improved overall survival in these nGBM patients. Moreover, an increase in perfusion is associated with improved tumor oxygenation status as well as with pharmacodynamic biomarkers, such as changes in plasma placenta growth factor and sVEGFR2. Finally, treatment resistance was associated with elevated plasma IL-8 and sVEGFR1 posttherapy. In conclusion, tumor perfusion changes after antiangiogenic therapy may distinguish responders vs. nonresponders early in the course of this expensive and potentially toxic formof therapy, and these results may provide newinsight into the selection of glioblastoma patients most likely to benefit from anti-VEGF treatments.
C1 [Batchelor, Tracy T.; Gerstner, Elizabeth R.; Plotkin, Scott R.; Chi, Andrew S.; Eichler, April F.; Dietrich, Jorg; Hochberg, Fred H.; Lu-Emerson, Christine] Massachusetts Gen Hosp, Dept Neurol, Ctr Canc, Boston, MA 02114 USA.
   [Batchelor, Tracy T.; Duda, Dan G.; Ancukiewicz, Marek; Loeffler, Jay S.; Jain, Rakesh K.] Massachusetts Gen Hosp, Dept Radiat Oncol, Ctr Canc, Boston, MA 02114 USA.
   [Emblem, Kyrre E.; Kalpathy-Cramer, Jayashree; Polaskova, Pavlina; Pinho, Marco C.; Jennings, Dominique; Rosen, Bruce R.; Sorensen, A. Greg] Massachusetts Gen Hosp, Dept Radiol, Ctr Canc, Boston, MA 02114 USA.
   [Snuderl, Matija; Iafrate, A. John] Massachusetts Gen Hosp, Dept Pathol, Ctr Canc, Boston, MA 02114 USA.
   [Wen, Patrick Y.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
   [Emblem, Kyrre E.; Kalpathy-Cramer, Jayashree; Polaskova, Pavlina; Pinho, Marco C.; Jennings, Dominique; Rosen, Bruce R.; Sorensen, A. Greg] Harvard Mit Div Hlth Sci & Technol, Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
   [Ivy, S. Percy] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
   [Wen, Patrick Y.] Dana Farber Canc Inst, Dept Med Oncol, Ctr Neurooncol, Boston, MA 02114 USA.
RP Batchelor, TT (reprint author), Massachusetts Gen Hosp, Dept Neurol, Ctr Canc, Boston, MA 02114 USA.
EM tbatchelor@partners.org; jain@steele.mgh.harvard.edu
RI Emblem, Kyrre/H-6691-2012; 
OI Emblem, Kyrre/0000-0002-6580-9519; Pinho, Marco/0000-0002-4645-1638;
   Kalpathy-Cramer, Jayashree/0000-0001-8906-9618; Snuderl,
   Matija/0000-0003-0752-0917
FU National Institutes of Health [R01CA129371, K24CA125440A, P01CA080124,
   R01CA163815, N01CM-2008-00060C, 5R01NS060918, 1U01CA154601,
   R01CA159258]; Proton Beam/Federal Share Program; National Foundation for
   Cancer Research; Merck; Norwegian Research Council Grant [191088/V50];
   South-Eastern Norway Regional Health Authority Grant [2013069]; Harvard
   Clinical and Translational Science Center (National Center for Research
   Resources and the National Center for Advancing Translational Sciences,
   National Institutes of Health Award) [8UL1TR000170-05]; Harvard
   University
FX We thank A. Khachatryan, C. Koppel, O. Pulluqi, and C. Smith for
   outstanding technical support for biomarker studies. This work was
   funded by National Institutes of Health Grants R01CA129371 and
   K24CA125440A (to T.T.B.), P01CA080124 and R01CA163815 (to R.K.J.),
   N01CM-2008-00060C and 5R01NS060918 (to A.G.S.), 1U01CA154601 (to
   B.R.R.), and R01CA159258 (to D.G.D.); the Proton Beam/Federal Share
   Program (R.K.J and D.G.D.); the National Foundation for Cancer Research
   (R.K.J.); Merck (A.G.S. and E.R.G.); Norwegian Research Council Grant
   191088/V50 and South-Eastern Norway Regional Health Authority Grant
   2013069 (to K.E.E.); and the Harvard Clinical and Translational Science
   Center (National Center for Research Resources and the National Center
   for Advancing Translational Sciences, National Institutes of Health
   Award 8UL1TR000170-05 and financial contributions from Harvard
   University and its affiliated academic health care centers).
NR 44
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U1 6
U2 19
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 NOV 19
PY 2013
VL 110
IS 47
BP 19059
EP 19064
DI 10.1073/pnas.1318022110
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 253PD
UT WOS:000327100600079
PM 24190997
ER

PT J
AU Kim, JH
   O'Brien, KM
   Sharma, R
   Boshoff, HIM
   Rehren, G
   Chakraborty, S
   Wallach, JB
   Monteleone, M
   Wilson, DJ
   Aldrich, CC
   Barry, CE
   Rhee, KY
   Ehrt, S
   Schnappinger, D
AF Kim, Jee-Hyun
   O'Brien, Kathryn M.
   Sharma, Ritu
   Boshoff, Helena I. M.
   Rehren, German
   Chakraborty, Sumit
   Wallach, Joshua B.
   Monteleone, Mercedes
   Wilson, Daniel J.
   Aldrich, Courtney C.
   Barry, Clifton E., III
   Rhee, Kyu Y.
   Ehrt, Sabine
   Schnappinger, Dirk
TI A genetic strategy to identify targets for the development of drugs that
   prevent bacterial persistence
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
ID ACID MONONUCLEOTIDE ADENYLYLTRANSFERASE; MYCOBACTERIUM-TUBERCULOSIS;
   TUBERCLE-BACILLI; DISCOVERY; NAD; IDENTIFICATION; REPRESSORS; GROWTH;
   CELLS
AB Antibacterial drug development suffers from a paucity of targets whose inhibition kills replicating and nonreplicating bacteria. The latter include phenotypically dormant cells, known as persisters, which are tolerant to many antibiotics and often contribute to failure in the treatment of chronic infections. This is nowhere more apparent than in tuberculosis caused by Mycobacterium tuberculosis, a pathogen that tolerates many antibiotics once it ceases to replicate. We developed a strategy to identify proteins that Mycobacterium tuberculosis requires to both grow and persist and whose inhibition has the potential to prevent drug tolerance and persister formation. This strategy is based on a tunable dual-control genetic switch that provides a regulatory range spanning three orders of magnitude, quickly depletes proteins in both replicating and nonreplicating mycobacteria, and exhibits increased robustness to phenotypic reversion. Using this switch, we demonstrated that depletion of the nicotinamide adenine dinucleotide synthetase (NadE) rapidly killed Mycobacterium tuberculosis under conditions of standard growth and nonreplicative persistence induced by oxygen and nutrient limitation as well as during the acute and chronic phases of infection in mice. These findings establish the dual-control switch as a robust tool with which to probe the essentiality of Mycobacterium tuberculosis proteins under different conditions, including those that induce antibiotic tolerance, and NadE as a target with the potential to shorten current tuberculosis chemotherapies.
C1 [Kim, Jee-Hyun; O'Brien, Kathryn M.; Sharma, Ritu; Rehren, German; Wallach, Joshua B.; Monteleone, Mercedes; Ehrt, Sabine; Schnappinger, Dirk] Weill Cornell Med Coll, Dept Microbiol & Immunol, New York, NY 10065 USA.
   [Boshoff, Helena I. M.; Barry, Clifton E., III] NIAID, TB Res Sect, NIH, Bethesda, MD 20892 USA.
   [Chakraborty, Sumit; Rhee, Kyu Y.] Weill Cornell Med Coll, Dept Med, New York, NY 10065 USA.
   [Wilson, Daniel J.; Aldrich, Courtney C.] Univ Minnesota, Ctr Drug Design, Minneapolis, MN 55455 USA.
RP Schnappinger, D (reprint author), Weill Cornell Med Coll, Dept Microbiol & Immunol, New York, NY 10065 USA.
EM dis2003@med.cornell.edu
RI Barry, III, Clifton/H-3839-2012; Sharma, Ritu/N-9487-2015; Monteleone,
   Maria/J-1813-2014
OI Sharma, Ritu/0000-0002-9972-883X; Monteleone, Maria/0000-0003-0777-3965
FU Bill and Melinda Gates Foundation; Wellcome Trust through the Grand
   Challenges in Global Health Initiative; National Institutes of Health
   (NIH) [AI089911]; Intramural Research Program of the National Institute
   of Allergy and Infectious Diseases, NIH;  [42848];  [OPP1024065]; 
   [OPP10204050]
FX We thank C. Nathan for PrcB-specific antiserum. This work was supported
   by Grants 42848 and OPP1024065 (to D.S.) and OPP10204050 (to K.Y.R.);
   the Bill and Melinda Gates Foundation and the Wellcome Trust through the
   Grand Challenges in Global Health Initiative (to D.S., S.E., C.C.A., and
   C.E.B.); the National Institutes of Health (NIH) Grant AI089911 (to D.
   S.); and the Intramural Research Program of the National Institute of
   Allergy and Infectious Diseases, NIH (to C.E.B.).
NR 43
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U1 4
U2 20
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 NOV 19
PY 2013
VL 110
IS 47
BP 19095
EP 19100
DI 10.1073/pnas.1315860110
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 253PD
UT WOS:000327100600085
PM 24191058
ER

PT J
AU Durkee, CA
   Sarlls, JE
   Hommer, DW
   Momenan, R
AF Durkee, Caitlin A.
   Sarlls, Joelle E.
   Hommer, Daniel W.
   Momenan, Reza
TI White Matter Microstructure Alterations: A Study of Alcoholics with and
   without Post-Traumatic Stress Disorder
SO PLOS ONE
LA English
DT Article
ID SUBSTANCE-DEPENDENT PATIENTS; ANTERIOR CINGULATE; ABSTINENT ALCOHOLICS;
   HIPPOCAMPAL VOLUME; MAMMILLARY BODIES; PREFRONTAL CORTEX; TRAUMA
   SURVIVORS; CORPUS-CALLOSUM; FUNCTIONAL MRI; BRAIN VOLUMES
AB Many brain imaging studies have demonstrated reductions in gray and white matter volumes in alcoholism, with fewer investigators using diffusion tensor imaging (DTI) to examine the integrity of white matter pathways. Among various medical conditions, alcoholism and post-traumatic stress disorder (PTSD) are two comorbid diseases that have similar degenerative effects on the white matter integrity. Therefore, understanding and differentiating these effects would be very important in characterizing alcoholism and PTSD. Alcoholics are known to have neurocognitive deficits in decision-making, particularly in decisions related to emotionally-motivated behavior, while individuals with PTSD have deficits in emotional regulation and enhanced fear response. It is widely believed that these types of abnormalities in both alcoholism and PTSD are related to fronto-limbic dysfunction. In addition, previous studies have shown cortico-limbic fiber degradation through fiber tracking in alcoholism. DTI was used to measure white matter fractional anisotropy (FA), which provides information about tissue microstructure, possibly indicating white matter integrity. We quantitatively investigated the microstructure of white matter through whole brain DTI analysis in healthy volunteers (HV) and alcohol dependent subjects without PTSD (ALC) and with PTSD (ALC+PTSD). These data show significant differences in FA between alcoholics and non-alcoholic HVs, with no significant differences in FA between ALC and ALC+PTSD in any white matter structure. We performed a post-hoc region of interest analysis that allowed us to incorporate multiple covariates into the analysis and found similar results. HV had higher FA in several areas implicated in the reward circuit, emotion, and executive functioning, suggesting that there may be microstructural abnormalities in white matter pathways that contribute to neurocognitive and executive functioning deficits observed in alcoholics. Furthermore, our data do not reveal any differences between ALC and ALC+PTSD, suggesting that the effect of alcohol on white matter microstructure may be more significant than any effect caused by PTSD.
C1 [Durkee, Caitlin A.; Hommer, Daniel W.; Momenan, Reza] NIAAA, Sect Brain Electrophysiol & Imaging, Lab Clin & Translat Studies, NIH, Bethesda, MD 20892 USA.
   [Sarlls, Joelle E.] NINDS, NIH MRI Res Facil, NIH, Bethesda, MD 20892 USA.
RP Momenan, R (reprint author), NIAAA, Sect Brain Electrophysiol & Imaging, Lab Clin & Translat Studies, NIH, Bethesda, MD 20892 USA.
EM rezam@mail.nih.gov
NR 74
TC 6
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U1 2
U2 16
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 18
PY 2013
VL 8
IS 11
AR UNSP e80952
DI 10.1371/journal.pone.0080952
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 256KH
UT WOS:000327308500184
PM 24260518
ER

PT J
AU Livigni, A
   Peradziryi, H
   Sharov, AA
   Chia, G
   Hammachi, F
   Migueles, RP
   Sukparangsi, W
   Pernagallo, S
   Bradley, M
   Nichols, J
   Ko, MSH
   Brickman, JM
AF Livigni, Alessandra
   Peradziryi, Hanna
   Sharov, Alexei A.
   Chia, Gloryn
   Hammachi, Fella
   Migueles, Rosa Porter
   Sukparangsi, Woranop
   Pernagallo, Salvatore
   Bradley, Mark
   Nichols, Jennifer
   Ko, Minoru S. H.
   Brickman, Joshua M.
TI A Conserved Oct4/POUV-Dependent Network Links Adhesion and Migration to
   Progenitor Maintenance
SO CURRENT BIOLOGY
LA English
DT Article
ID EMBRYONIC STEM-CELLS; TRANSCRIPTIONAL REGULATORY CIRCUITRY; E-CADHERIN;
   XENOPUS-EMBRYOS; BETA-CATENIN; OCT4; PLURIPOTENCY; EXPRESSION; PROTEIN;
   DIFFERENTIATION
AB Background: The class V POU domain transcription factor Oct4 (Pou5f1) is a pivotal regulator of embryonic stem cell (ESC) self-renewal and reprogramming of somatic cells to induced pluripotent stem (iPS) cells. Oct4 is also an important evolutionarily conserved regulator of progenitor cell differentiation during embryonic development.
   Results: Here we examine the function of Oct4 homologs in Xenopus embryos and compare this to the role of Oct4 in maintaining mammalian embryo-derived stem cells. Based on a combination of expression profiling of Oct4/POUV-depleted Xenopus embryos and in silico analysis of existing mammalian Oct4 target data sets, we defined a set of evolutionary-conserved Oct4/POUV targets. Most of these targets were regulators of cell adhesion. This is consistent with Oct4/POUV phenotypes observed in the adherens junctions in Xenopus ectoderm, mouse embryonic, and epiblast stem cells. A number of these targets could rescue both Oct4/POUV phenotypes in cellular adhesion and multipotent progenitor cell maintenance, whereas expression of cadherins on their own could only transiently support adhesion and block differentiation in both ESC and Xenopus embryos.
   Conclusions: Currently, the list of Oct4 transcriptional targets contains thousands of genes. Using evolutionary conservation, we identified a core set of functionally relevant factors that linked the maintenance of adhesion to Oct4/POUV. We found that the regulation of adhesion by the Oct4/POUV network occurred at both transcriptional and posttranslational levels and was required for pluripotency.
C1 [Livigni, Alessandra; Hammachi, Fella; Migueles, Rosa Porter; Brickman, Joshua M.] Univ Edinburgh, Sch Biol Sci, Inst Stem Cell Res, MRC,Ctr Regenerat Med, Edinburgh EH16 4UU, Midlothian, Scotland.
   [Peradziryi, Hanna; Sukparangsi, Woranop; Brickman, Joshua M.] Univ Copenhagen, Danish Stem Cell Ctr DanStem, DK-2200 Copenhagen, Denmark.
   [Sharov, Alexei A.; Ko, Minoru S. H.] NIA, Genet Lab, NIH, Biomed Res Ctr, Baltimore, MD 21224 USA.
   [Chia, Gloryn; Nichols, Jennifer] Univ Cambridge, Wellcome Trust Ctr Stem Cell Res, Cambridge CB2 1QR, England.
   [Pernagallo, Salvatore; Bradley, Mark] Univ Edinburgh, Sch Chem, Edinburgh EH9 3JJ, Midlothian, Scotland.
   [Ko, Minoru S. H.] Keio Univ, Dept Syst Med, Shinjuku Ku, Tokyo 160, Japan.
RP Brickman, JM (reprint author), Univ Edinburgh, Sch Biol Sci, Inst Stem Cell Res, MRC,Ctr Regenerat Med, 5 Little France Dr, Edinburgh EH16 4UU, Midlothian, Scotland.
EM joshua.brickman@sund.ku.dk
OI Ko, Minoru/0000-0002-3530-3015; Brickman, Joshua/0000-0003-1580-7491
FU Medical Research Council (MRC) [G0701428]; Novo Nordisk Foundation; NIH;
   National Institute on Aging [Z01AG AG000656, Z01AG000662]; MRC Senior
   Non-Clinical Fellowship
FX We thank Dawood Dudekula, Joe Mee, Lucy Jones, Yong Qian, Valeria Berno,
   Ron Wilkie, Marylin Thomson, Helen Henderson, Laure Plantard, and Gelo
   dela Cruz for technical assistance. We are grateful to H. Sive, M.
   Taira, H. Niwa, P. McCrea, I. Chambers, S. Lowell, H. Lickert, P .Tesar,
   and J. Chenoweth for plasmids and data sets. We thank Anne
   Grapin-Botton, Sally Lowell, and Adam Laing for critical reading of this
   manuscript. This work was supported by the Medical Research Council
   (MRC) (G0701428) and the Novo Nordisk Foundation (to J.M.B.) and by the
   Intramural Research Program of the NIH and the National Institute on
   Aging (Z01AG AG000656 and Z01AG000662) (to M.S.H.K.). J.M.B. was
   supported by an MRC Senior Non-Clinical Fellowship.
NR 53
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U1 0
U2 6
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0960-9822
EI 1879-0445
J9 CURR BIOL
JI Curr. Biol.
PD NOV 18
PY 2013
VL 23
IS 22
BP 2233
EP 2244
DI 10.1016/j.cub.2013.09.048
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 257VX
UT WOS:000327417000021
PM 24210613
ER

PT J
AU Klebba, JE
   Buster, DW
   Nguyen, AL
   Swatkoski, S
   Gucek, M
   Rusan, NM
   Rogers, GC
AF Klebba, Joseph E.
   Buster, Daniel W.
   Nguyen, Annie L.
   Swatkoski, Stephen
   Gucek, Marjan
   Rusan, Nasser M.
   Rogers, Gregory C.
TI Polo-like Kinase 4 Autodestructs by Generating Its Slimb-Binding
   Phosphodegron
SO CURRENT BIOLOGY
LA English
DT Article
ID CENTRIOLE DUPLICATION; BETA-TRCP; PLK4; CENTROSOME; PROTEIN; SCAFFOLD;
   REVEALS; NUMBER; DOMAIN
AB Polo-like kinase 4 (Plk4) is a conserved master regulator of centriole assembly [1]. Previously, we found that Drosophila Plk4 protein levels are actively suppressed during interphase [2]. Degradation of interphase Plk4 prevents centriole overduplication and is mediated by the ubiquitin-ligase complex SCFSlimb/beta TrCP [3, 4]. Since Plk4 stability depends on its activity [5, 6], we studied the consequences of inactivating Plk4 or perturbing its phosphorylation state within its Slimb-recognition motif (SRM). Mass spectrometry of in-vitro-phosphorylated Plk4 and Plk4 purified from cells reveals that it is directly responsible for extensively autophosphorylating and generating its Slimb-binding phosphodegron. Phosphorylatable residues within this regulatory region were systematically mutated to determine their impact on Plk4 protein levels and centriole duplication when expressed in S2 cells. Notably, autophosphorylation of a single residue (Ser293) within the SRM is critical for Slimb binding and ubiquitination. Our data also demonstrate that autophosphorylation of numerous residues flanking S293 collectively contribute to establishing a high-affinity binding site for SCFSlimb. Taken together, our findings suggest that Plk4 directly generates its own phosphodegron and can do so without the assistance of an additional kinase(s).
C1 [Klebba, Joseph E.; Buster, Daniel W.; Nguyen, Annie L.; Rogers, Gregory C.] Univ Arizona, Ctr Canc, Dept Cellular & Mol Med, Tucson, AZ 85724 USA.
   [Rusan, Nasser M.] NHLBI, Natl Inst Hlth, Bethesda, MD 20892 USA.
   [Swatkoski, Stephen; Gucek, Marjan] NHLBI, Natl Inst Hlth, Prote Core, Bethesda, MD 20892 USA.
RP Rogers, GC (reprint author), Univ Arizona, Ctr Canc, Dept Cellular & Mol Med, Tucson, AZ 85724 USA.
EM gcrogers@email.arizona.edu
RI Rusan, Nasser/P-3511-2016
FU NCI [P30 CA23074]; GI SPORE [NCI/NIH P50 CA95060]; National Science
   Foundation [1158151]; Arizona Biomedical Research Commission [1210];
   TRIF Imaging Fellowship Program; Division of Intramural Research at the
   NIH/NHLBI [1ZIAHL006104]
FX We thank P. Krieg for comments on the manuscript as well as M.
   Bettencourt-Dias and her lab for sharing results prior to publication.
   G.C.R. is grateful for support from the NCI P30 CA23074 and GI SPORE
   (NCI/NIH P50 CA95060), the National Science Foundation (1158151), and
   the Arizona Biomedical Research Commission (1210), as well as support
   from the TRIF Imaging Fellowship Program to J.E.K. S.S., M.G., and
   N.M.R. are supported by the Division of Intramural Research at the
   NIH/NHLBI (1ZIAHL006104).
NR 27
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U1 0
U2 7
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0960-9822
EI 1879-0445
J9 CURR BIOL
JI Curr. Biol.
PD NOV 18
PY 2013
VL 23
IS 22
BP 2255
EP 2261
DI 10.1016/j.cub.2013.09.019
PG 7
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 257VX
UT WOS:000327417000023
PM 24184097
ER

PT J
AU Deenick, EK
   Avery, DT
   Chan, A
   Berglund, LJ
   Ives, ML
   Moens, L
   Stoddard, JL
   Bustamante, J
   Boisson-Dupuis, S
   Tsumura, M
   Kobayashi, M
   Arkwright, PD
   Averbuch, D
   Engelhard, D
   Roesler, J
   Peake, J
   Wong, M
   Adelstein, S
   Choo, S
   Smart, JM
   French, MA
   Fulcher, DA
   Cook, MC
   Picard, C
   Durandy, A
   Klein, C
   Holland, SM
   Uzel, G
   Casanova, JL
   Ma, CS
   Tangye, SG
AF Deenick, Elissa K.
   Avery, Danielle T.
   Chan, Anna
   Berglund, Lucinda J.
   Ives, Megan L.
   Moens, Leen
   Stoddard, Jennifer L.
   Bustamante, Jacinta
   Boisson-Dupuis, Stephanie
   Tsumura, Miyuki
   Kobayashi, Masao
   Arkwright, Peter D.
   Averbuch, Diana
   Engelhard, Dan
   Roesler, Joachim
   Peake, Jane
   Wong, Melanie
   Adelstein, Stephen
   Choo, Sharon
   Smart, Joanne M.
   French, Martyn A.
   Fulcher, David A.
   Cook, Matthew C.
   Picard, Capucine
   Durandy, Anne
   Klein, Christoph
   Holland, Steven M.
   Uzel, Gulbu
   Casanova, Jean-Laurent
   Ma, Cindy S.
   Tangye, Stuart G.
TI Naive and memory human B cells have distinct requirements for STAT3
   activation to differentiate into antibody-secreting plasma cells
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID HYPER-IGE SYNDROME; LINKED LYMPHOPROLIFERATIVE DISEASE; CLASS-SWITCH
   RECOMBINATION; COMMON GAMMA-CHAIN; T-CELLS; IMMUNE-RESPONSES; IL-21
   RECEPTOR; UP-REGULATION; INTRINSIC DIFFERENCES; SIGNAL TRANSDUCER
AB Long-lived antibody memory is mediated by the combined effects of long-lived plasma cells (PCs) and memory B cells generated in response to T cell-dependent antigens (Ags). IL-10 and IL-21 can activate multiple signaling pathways, including STAT1, STAT3, and STAT5; ERK; PI3K/Akt, and potently promote human B cell differentiation. We previously showed that loss-of-function mutations in STAT3, but not STAT1, abrogate IL-10- and IL-21-mediated differentiation of human naive B cells into plasmablasts. We report here that, in contrast to naive B cells, STAT3-deficient memory B cells responded to these STAT3-activating cytokines, differentiating into plasmablasts and secreting high levels of IgM, IgG, and IgA, as well as Ag-specific IgG. This was associated with the induction of the molecular machinery necessary for PC formation. Mutations in IL21R, however, abolished IL-21-induced responses of both naive and memory human B cells and compromised memory B cell formation in vivo. These findings reveal a key role for IL-21R/STAT3 signaling in regulating human B cell function. Furthermore, our results indicate that the threshold of STAT3 activation required for differentiation is lower in memory compared with naive B cells, thereby identifying an intrinsic difference in the mechanism underlying differentiation of naive versus memory B cells.
C1 [Deenick, Elissa K.; Avery, Danielle T.; Chan, Anna; Berglund, Lucinda J.; Ives, Megan L.; Moens, Leen; Ma, Cindy S.; Tangye, Stuart G.] St Vincents Hosp, Garvan Inst Med Res, Immunol Res Program, Immunol & Immunodeficiency Grp, Darlinghurst, NSW 2010, Australia.
   [Deenick, Elissa K.; Berglund, Lucinda J.; Ives, Megan L.; Ma, Cindy S.; Tangye, Stuart G.] Univ New S Wales, St Vincents Clin Sch, Sydney, NSW 2052, Australia.
   [Berglund, Lucinda J.; Fulcher, David A.] Westmead Hosp, Inst Clin Pathol & Med Res, Dept Immunol, Westmead, NSW 2145, Australia.
   [Stoddard, Jennifer L.] NIAID, Ctr Clin, NIH, Bethesda, MD 20892 USA.
   [Holland, Steven M.; Uzel, Gulbu] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
   [Bustamante, Jacinta; Boisson-Dupuis, Stephanie; Picard, Capucine; Casanova, Jean-Laurent] Univ Paris 05, Necker Med Sch, INSERM, Lab Human Genet Infect Dis,Necker Branch,U980, F-75993 Paris, France.
   [Bustamante, Jacinta; Picard, Capucine; Durandy, Anne] Hop Necker Enfants Malad, AP HP, Study Ctr Primary Immunodeficiencies, F-75015 Paris, France.
   [Bustamante, Jacinta; Picard, Capucine; Durandy, Anne; Casanova, Jean-Laurent] Univ Paris 05, Inst Imagine, F-75015 Paris, France.
   [Boisson-Dupuis, Stephanie; Casanova, Jean-Laurent] Rockefeller Univ, Rockefeller Branch, St Giles Lab Human Genet Infect Dis, New York, NY 10065 USA.
   [Tsumura, Miyuki; Kobayashi, Masao] Hiroshima Univ, Grad Sch Biomed & Hlth Sci, Dept Pediat, Hiroshima 7390511, Japan.
   [Arkwright, Peter D.] Univ Manchester, Royal Manchester Childrens Hosp, Manchester M13 9WL, Lancs, England.
   [Averbuch, Diana; Engelhard, Dan] Hadassah Hebrew Univ, Med Ctr, Dept Pediat & Pediat Infect Dis, IL-91120 Jerusalem, Israel.
   [Roesler, Joachim] Univ Clin Carl Gustav Carus, Dept Pediat, D-01307 Dresden, Germany.
   [Peake, Jane] Royal Childrens Hosp Brisbane, Dept Paediat & Child Hlth, Brisbane, Qld 4029, Australia.
   [Wong, Melanie] Childrens Hosp Westmead, Dept Allergy & Immunol, Westmead, NSW 2145, Australia.
   [Adelstein, Stephen] Royal Prince Alfred Hosp, Dept Clin Immunol, Sydney, NSW 2050, Australia.
   [Choo, Sharon; Smart, Joanne M.] Royal Childrens Hosp Melbourne, Dept Allergy & Immunol, Parkville, Vic 3052, Australia.
   [French, Martyn A.] Royal Perth Hosp, Dept Clin Immunol, Perth, WA 6000, Australia.
   [French, Martyn A.] Univ Western Australia, Sch Pathol & Lab Med, Crawley, WA 6009, Australia.
   [Cook, Matthew C.] Australian Natl Univ, Sch Med, Canberra, ACT 0200, Australia.
   [Cook, Matthew C.] Australian Natl Univ, John Curtin Sch Med Res, Canberra, ACT 0200, Australia.
   [Cook, Matthew C.] Canberra Hosp, Dept Immunol, Canberra, ACT 2601, Australia.
   [Durandy, Anne] Hop Necker Enfants Malad, INSERM, U768, F-75743 Paris, France.
   [Klein, Christoph] Univ Munich, Dr Von Haunerschen Kinderspital, Dept Pediat, D-80337 Munich, Germany.
RP Tangye, SG (reprint author), St Vincents Hosp, Garvan Inst Med Res, Immunol Res Program, Immunol & Immunodeficiency Grp, Darlinghurst, NSW 2010, Australia.
EM s.tangye@garvan.org.au
RI Tangye, Stuart/H-4023-2014; Peake, Jane/B-4488-2011; Adelstein,
   Stephen/I-7936-2016; 
OI Adelstein, Stephen/0000-0001-7221-6298; Deenick,
   Elissa/0000-0002-9271-0004; Picard, Capucine/0000-0001-8788-5056;
   Arkwright, Peter/0000-0002-7411-5375
FU National Health and Medical Research Council (NHMRC) of Australia;
   Rockefeller University Center for 541 Clinical and Translational science
   [5UL1RR024143]; NHMRC of Australia; Research Foundation-Flanders (FWO),
   Belgium
FX This work was funded by project and program grants from the National
   Health and Medical Research Council (NHMRC) of Australia (to E.K.
   Deenick, C.S. Ma, D.A. Fulcher, M.C. Cook, and S.G. Tangye) and the
   Rockefeller University Center for 541 Clinical and Translational science
   (5UL1RR024143 to J.L. Casanova). C.S. Ma is a recipient of a Career
   Development Fellowship, L.J. Berglund is a recipient of a Medical
   Postgraduate Scholarship, and S.G. Tangye is a recipient of a Principal
   Research Fellowship from the NHMRC of Australia. L. Moens is the
   recipient of a Postdoctoral Fellowship from the Research
   Foundation-Flanders (FWO), Belgium.
NR 69
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U1 2
U2 14
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0022-1007
EI 1540-9538
J9 J EXP MED
JI J. Exp. Med.
PD NOV 18
PY 2013
VL 210
IS 12
BP 2739
EP 2753
DI 10.1084/jem.20130323
PG 15
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 258GF
UT WOS:000327446600018
PM 24218138
ER

PT J
AU Truex, K
   Webster, LA
   Duan, LM
   Sham, LJ
   Steel, DG
AF Truex, Katherine
   Webster, L. A.
   Duan, L. -M.
   Sham, L. J.
   Steel, D. G.
TI Coherent control with optical pulses for deterministic spin-photon
   entanglement
SO PHYSICAL REVIEW B
LA English
DT Article
ID SINGLE QUANTUM-DOT; STATE; SPECTROSCOPY
AB We present a procedure for the optical coherent control of quantum bits within a quantum dot spin-exciton system, as a preliminary step to implementing a proposal by Yao, Liu, and Sham [Phys. Rev. Lett. 95, 030504 (2005)] for deterministic spin-photon entanglement. The experiment proposed here utilizes a series of picosecond optical pulses from a single laser to coherently control a single self-assembled quantum dot in a magnetic field, creating the precursor state in 25 ps with a predicted fidelity of 0.991. If allowed to decay in an appropriate cavity, the ideal precursor superposition state would create maximum spin-photon entanglement. Numerical simulations using values typical of InAs quantum dots give a predicted entropy of entanglement of 0.929, largely limited by radiative decay and electron spin flips.
C1 [Truex, Katherine; Webster, L. A.; Duan, L. -M.; Steel, D. G.] Univ Michigan, HM Randall Lab Phys, Ann Arbor, MI 48109 USA.
   [Sham, L. J.] Univ Calif San Diego, Dept Phys, La Jolla, CA 92093 USA.
RP Truex, K (reprint author), NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
EM dst@umich.edu
OI Sham, Lu/0000-0001-5718-2077
FU NSF; ARO; DARPA; AFOSR
FX This work was supported by NSF, ARO, DARPA, and AFOSR.
NR 61
TC 3
Z9 3
U1 0
U2 20
PU AMER PHYSICAL SOC
PI COLLEGE PK
PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA
SN 1098-0121
EI 1550-235X
J9 PHYS REV B
JI Phys. Rev. B
PD NOV 18
PY 2013
VL 88
IS 19
AR 195306
DI 10.1103/PhysRevB.88.195306
PG 10
WC Physics, Condensed Matter
SC Physics
GA 254IN
UT WOS:000327158600005
ER

PT J
AU Rider, CV
   Carlin, DJ
   DeVito, MJ
   Thompson, CL
   Walker, NJ
AF Rider, Cynthia V.
   Carlin, Danielle J.
   DeVito, Micheal J.
   Thompson, Claudia L.
   Walker, Nigel J.
TI Mixtures research at NIEHS: An evolving program
SO TOXICOLOGY
LA English
DT Article
DE Combined exposures; Cumulative; Multi-pollutant; Co-exposure; Stressors
ID CUMULATIVE RISK-ASSESSMENT; B6C3F1 MICE; CHEMICALS; PRODUCTS; QUALITY
AB The National Institute of Environmental Health Sciences (NIEHS) has a rich history in evaluating the toxicity of mixtures. The types of mixtures assessed by the Division of the National Toxicology Program (DNTP) and the extramural community (through the Division of Extramural Research and Training, DERT) have included a broad range of chemicals and toxicants, with each study having a unique set of questions and design considerations. Some examples of the types of mixtures studied include: groundwater contaminants, pesticides/fertilizers, dioxin-like chemicals (assessing the toxic equivalency approach), drug combinations, air pollution, metals, polycyclic aromatic hydrocarbons, technical mixtures (e.g., pentachlorophenol, flame retardants), and mixed entities (e.g., herbals, asbestos). These endeavors have provided excellent data on the toxicity of specific mixtures and have been informative to the human health risk assessment process in general (e.g., providing data on low dose exposures to environmental chemicals). However, the mixtures research effort at NIEHS, to date, has been driven by test article nominations to the DNTP or by investigator-initiated research through DERT. Recently, the NIEHS has embarked upon an effort to coordinate mixtures research across both intramural and extramural divisions in order to maximize mixtures research results. A path forward for NIEHS mixtures research will be based on feedback from a Request for Information (RFI) designed to gather up-to-date views on the knowledge gaps and roadblocks to evaluating mixtures and performing cumulative risk assessment, and a workshop organized to bring together mixtures experts from risk assessment, exposure science, biology, epidemiology, and statistics. The future of mixtures research at NIEHS will include projects from nominations to DNTP, studies by extramural investigators, and collaborations across government agencies that address high-priority questions in the field of mixtures research. Published by Elsevier Ireland Ltd.
C1 [Rider, Cynthia V.; DeVito, Micheal J.; Walker, Nigel J.] NIEHS, Div Natl Toxicol Program, NIH, Res Triangle Pk, NC 27709 USA.
   [Carlin, Danielle J.; Thompson, Claudia L.] NIEHS, Div Extramural Res & Training, NIH, Res Triangle Pk, NC 27709 USA.
RP Walker, NJ (reprint author), NIEHS, NIH, 111 Alexander Dr,POB 12233,MD K2-02, Res Triangle Pk, NC 27709 USA.
EM ridercv@niehs.nih.gov; carlindj@niehs.nih.gov; devitom@niehs.nih.gov;
   thomps14@niehs.nih.gov; walker3@niehs.nih.gov
RI Walker, Nigel/D-6583-2012
OI Walker, Nigel/0000-0002-9111-6855
FU NIEHS; NIH
FX The authors would like to thank Dr. Chad Blystone and Dr. Heather Henry
   for critical review of the manuscript. This research was supported by
   NIEHS and by the Intramural Research program of the NIH. This article is
   the work product of a group of employees of the NIEHS, National
   Institutes of Health (NIH), however, the statements contained herein do
   not necessarily represent the statements, opinions or conclusions of the
   NIEHS, NIH or the United States Government. The content of this
   publication does not necessarily reflect the views or the 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 25
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U1 3
U2 31
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0300-483X
J9 TOXICOLOGY
JI Toxicology
PD NOV 16
PY 2013
VL 313
IS 2-3
SI SI
BP 94
EP 102
DI 10.1016/j.tox.2012.10.017
PG 9
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 280AQ
UT WOS:000329001400004
PM 23146757
ER

PT J
AU Rostved, AA
   Sassi, M
   Kurtzhals, JAL
   Sorensen, SS
   Rasmussen, A
   Ross, C
   Gogineni, E
   Huber, C
   Kutty, G
   Kovacs, JA
   Helweg-Larsen, J
AF Rostved, Andreas A.
   Sassi, Monica
   Kurtzhals, Jorgen A. L.
   Sorensen, Soren Schwartz
   Rasmussen, Allan
   Ross, Christian
   Gogineni, Emile
   Huber, Charles
   Kutty, Geetha
   Kovacs, Joseph A.
   Helweg-Larsen, Jannik
TI Outbreak of Pneumocystis Pneumonia in Renal and Liver Transplant
   Patients Caused by Genotypically Distinct Strains of Pneumocystis
   jirovecii
SO TRANSPLANTATION
LA English
DT Article
DE Pneumocystis jirovecii; Pneumocystis pneumonia; Liver transplant; Renal
   transplant; Outbreak
ID MOLECULAR EVIDENCE; CARINII-PNEUMONIA; INTERHUMAN TRANSMISSION;
   RISK-FACTORS; RECIPIENTS; CLUSTER; IMMUNOSUPPRESSION; PROPHYLAXIS;
   COMORBIDITY; INFECTION
AB Background. An outbreak of 29 cases of Pneumocystis jirovecii pneumonia (PCP) occurred among renal and liver transplant recipients (RTR and LTR) in the largest Danish transplantation centre between 2007 and 2010, when routine PCP prophylaxis was not used.
   Methods. P. jirovecii isolates from 22 transplant cases, 2 colonized RTRs, and 19 Pneumocystis control samples were genotyped by restriction fragment length polymorphism and multilocus sequence typing analysis. Contact tracing was used to investigate transmission. Potential risk factors were compared between PCP cases and matched non-PCP transplant patients.
   Results. Three unique Pneumocystis genotypes were shared among 19 of the RTRs, LTRs, and a colonized RTR in three distinct clusters, two of which overlapped temporally. In contrast, Pneumocystis control samples harbored a wide range of genotypes. Evidence of possible nosocomial transmission was observed. Among several potential risk factors, only cytomegalovirus viremia was consistently associated with PCP (P=0.03; P=0.009). Mycophenolate mofetil was associated with PCP risk only in the RTR population (P=0.04).
   Conclusion. We identified three large groups infected with unique strains of Pneumocystis and provide evidence of an outbreak profile and nosocomial transmission. LTRs may be infected in PCP outbreaks simultaneously with RTRs and by the same strains, most likely by interhuman transmission. Patients are at risk several years after transplantation, but the risk is highest during the first 6 months after transplantation. Because patients at risk cannot be identified clinically and outbreaks cannot be predicted, 6 months of PCP chemoprophylaxis should be considered for all RTRs and LTRs.
C1 [Rostved, Andreas A.; Helweg-Larsen, Jannik] Copenhagen Univ Hosp, Rigshosp, Dept Infect Dis, DK-2100 Copenhagen, Denmark.
   [Sassi, Monica; Gogineni, Emile; Kutty, Geetha; Kovacs, Joseph A.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Kurtzhals, Jorgen A. L.] Copenhagen Univ Hosp, Rigshosp, Ctr Med Parasitol, Dept Clin Microbiol, DK-2100 Copenhagen, Denmark.
   [Kurtzhals, Jorgen A. L.] Univ Copenhagen, Dept Int Hlth Immunol & Microbiol, Copenhagen, Denmark.
   [Sorensen, Soren Schwartz] Copenhagen Univ Hosp, Rigshosp, Dept Nephrol, DK-2100 Copenhagen, Denmark.
   [Rostved, Andreas A.; Rasmussen, Allan; Ross, Christian] Copenhagen Univ Hosp, Rigshosp, Dept Surg Gastroenterol, DK-2100 Copenhagen, Denmark.
   [Huber, Charles] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Helweg-Larsen, J (reprint author), Copenhagen Univ Hosp, Rigshosp, Dept Infect Dis, Blegdamsvej 9, DK-2100 Copenhagen, Denmark.
EM jhelweg@dadlnet.dk
OI Kurtzhals, Jorgen/0000-0003-2760-8713; Rasmussen,
   Allan/0000-0002-9550-4767
FU Danish Kidney Association's Research Foundation; Helen and Ejnar Bjornow
   Foundation; Intramural Research Program of the National Institutes of
   Health Clinical Center
FX This work was supported by two independent grants from the Danish Kidney
   Association's Research Foundation and The Helen and Ejnar Bjornow
   Foundation (A.A.R.). This research was supported in part by the
   Intramural Research Program of the National Institutes of Health
   Clinical Center.
NR 37
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Z9 13
U1 2
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0041-1337
EI 1534-6080
J9 TRANSPLANTATION
JI Transplantation
PD NOV 15
PY 2013
VL 96
IS 9
BP 834
EP 842
DI 10.1097/TP.0b013e3182a1618c
PG 9
WC Immunology; Surgery; Transplantation
SC Immunology; Surgery; Transplantation
GA 299HE
UT WOS:000330386000011
PM 23903011
ER

PT J
AU Bhaskaran, K
   Ebonyi, AO
   Walther, B
   Walther, M
AF Bhaskaran, Krishnan
   Ebonyi, Augustine O.
   Walther, Brigitte
   Walther, Michael
TI Predictors of hyperlactataemia among children presenting with malaria in
   a low transmission area in The Gambia
SO MALARIA JOURNAL
LA English
DT Article
DE Hyperlactataemia; Lactate; Malaria; Children
ID SEVERE FALCIPARUM-MALARIA; AFRICAN CHILDREN; ACIDOSIS; INTENSITY;
   FEATURES; CARE; AGE
AB Background: Hyperlactataemia and metabolic acidosis are important risk factors for malaria death, but measuring lactate at the point of care is not financially viable in many resource-poor settings. This study aimed to identify combinations of routinely available parameters that could identify children at high risk of hyperlactataemia.
   Methods: Using data from a study of Gambian children aged six months to 16 years with severe or uncomplicated malaria, logistic regression modelling with a forward stepwise model selection process was used to develop a predictive model for hyperlactataemia from routinely available demographic, clinical and laboratory parameters. Potential predictors of hyperlactataemia considered for the modelling process were patient characteristics (age, sex, prior use of anti-malarials, and weight percentile for age), respiratory symptoms (deep breathing, irregular respiration, use of accessory muscles of respiration, lung crepitations, grunting respiration, cough, and age-specific respiratory rate), other clinical parameters recorded at presentation (duration of symptoms, Blantyre coma score, number of convulsions prior to admission, axillary temperature, dehydration, severe prostration, splenomegaly) and laboratory measures from blood tests (percentage parasitaemia, white cell count, lymphocyte count, neutrophil count, monocyte count, platelet count, haemoglobin level, blood glucose level).
   Results: 495 children were included, and 68 (14%) had laboratory-confirmed hyperlactataemia (lactate > 7 mmol/L). Four features were independently associated with increased hyperlactataemia risk in a multivariable age- and sex-adjusted model: lower Blantyre score (odds ratio (OR) compared to score 5 = 2.68 (95% CI, 1.03-6.96) for score 3-4 and 6.18 (95% CI, 2.24-17.07) for score 0-2, p = 0.001), higher percentage parasitaemia (OR = 1.07 (1.03-1.11) per 0031% increase, p < 0.001), high respiratory rate for age (OR = 3.09 (1.50-6.38) per unit increase, p = 0.002), and deep breathing (OR = 2.81 (1.20-6.60), p = 0.02). Cross-validated predictions from the final model achieved area under the receiver operating characteristic curve of 0.83.
   Conclusions: This study identified predictors of hyperlactataemia requiring only simple bedside clinical examination and blood film examination that can be carried out in resource-limited settings to quickly identify children at risk of dangerously raised lactate. A simple spreadsheet tool implementing the final model is supplied as supplementary material.
C1 [Bhaskaran, Krishnan] London Sch Hyg & Trop Med, Dept Noncommunicable Dis Epidemiol, London WC1, England.
   [Ebonyi, Augustine O.; Walther, Brigitte; Walther, Michael] MRC Labs UK, Gambia Unit, Fajara, Gambia.
   [Walther, Michael] NIAID, NIH, Div Intramural Res, Lab Malaria Immunol & Vaccinol, Rockville, MD USA.
RP Bhaskaran, K (reprint author), London Sch Hyg & Trop Med, Dept Noncommunicable Dis Epidemiol, London WC1, England.
EM krishnan.bhaskaran@lshtm.ac.uk
FU Medical Research Council Laboratories (UK); National Institute for
   Health Research postdoctoral fellowship
FX The original study on which this analysis is based was funded by Medical
   Research Council Laboratories (UK), The Gambia. KB is funded by a
   National Institute for Health Research postdoctoral fellowship. The MRC
   and National Institute for Health Research had no role in the design,
   analysis, writing up, or decision to publish.
NR 27
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U1 0
U2 0
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 NOV 15
PY 2013
VL 12
AR 423
DI 10.1186/1475-2875-12-423
PG 11
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 281MI
UT WOS:000329105300006
PM 24237749
ER

PT J
AU Liu, WY
   Jeganathan, G
   Amiri, S
   Morgan, KM
   Ryan, BM
   Pine, SR
AF Liu, Wenyu
   Jeganathan, Gajan
   Amiri, Sohrab
   Morgan, Katherine M.
   Ryan, Brid M.
   Pine, Sharon R.
TI Asymmetric segregation of template DNA strands in basal-like human
   breast cancer cell lines
SO MOLECULAR CANCER
LA English
DT Article
DE Non-random chromosome segregation; Asymmetric cell division; Immortal
   DNA strand hypothesis; Breast cancer; Cancer stem cells
ID LABEL-RETAINING CELLS; MESENCHYMAL STEM-CELLS; SISTER CHROMATIDS;
   CHROMOSOME SEGREGATION; IDENTIFICATION; DIVISION; CARCINOMA; MITOSIS;
   COSEGREGATION; EXPRESSION
AB Background and methods: Stem or progenitor cells from healthy tissues have the capacity to co-segregate their template DNA strands during mitosis. Here, we set out to test whether breast cancer cell lines also possess the ability to asymmetrically segregate their template DNA strands via non-random chromosome co-segregation, and whether this ability correlates with certain properties attributed to breast cancer stem cells (CSCs). We quantified the frequency of asymmetric segregation of template DNA strands in 12 human breast cancer cell lines, and correlated the frequency to molecular subtype, CD44(+)/CD24(-/lo) phenotype, and invasion/migration ability. We tested if co-culture with human mesenchymal stem cells, which are known to increase self-renewal, can alter the frequency of asymmetric segregation of template DNA in breast cancer.
   Results: We found a positive correlation between asymmetric segregation of template DNA and the breast cancer basal-like and claudin-low subtypes. There was an inverse correlation between asymmetric segregation of template DNA and Her2 expression. Breast cancer samples with evidence of asymmetric segregation of template DNA had significantly increased invasion and borderline significantly increased migration abilities. Samples with high CD44(+)/CD24(-/lo) surface expression were more likely to harbor a consistent population of cells that asymmetrically segregated its template DNA; however, symmetric self-renewal was enriched in the CD44(+)/CD24(-/lo) population. Co-culturing breast cancer cells with human mesenchymal stem cells expanded the breast CSC pool and decreased the frequency of asymmetric segregation of template DNA.
   Conclusions: Breast cancer cells within the basal-like subtype can asymmetrically segregate their template DNA strands through non-random chromosome segregation. The frequency of asymmetric segregation of template DNA can be modulated by external factors that influence expansion or self-renewal of CSC populations. Future studies to uncover the underlying mechanisms driving asymmetric segregation of template DNA and dictating cell fate at the time of cell division may explain how CSCs are maintained in tumors.
C1 [Liu, Wenyu; Jeganathan, Gajan; Amiri, Sohrab; Morgan, Katherine M.; Pine, Sharon R.] Rutgers State Univ, Rutgers Canc Inst New Jersey, New Brunswick, NJ 08903 USA.
   [Ryan, Brid M.] NCI, Human Carcinogenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Morgan, Katherine M.] Rutgers State Univ, Robert Wood Johnson Med Sch, New Brunswick, NJ 08903 USA.
RP Pine, SR (reprint author), Rutgers State Univ, Rutgers Canc Inst New Jersey, 195 Little Albany St, New Brunswick, NJ 08903 USA.
EM pinesr@cinj.rutgers.edu
RI Liu, Wenyu/C-2781-2014; 
OI Liu, Wenyu/0000-0002-0244-3038; Ryan, Brid/0000-0003-0038-131X
FU National Institutes of Health (NCI) [K22 CA140719]; Rutgers Cancer
   Institute of New Jersey
FX SRP was supported by a grant from the National Institutes of Health
   (NCI, K22 CA140719) and the Rutgers Cancer Institute of New Jersey. We
   thank Arthur Roberts for cell sorting services, from the Flow Cytometry
   and Cell Sorting Shared Resource, Cancer Institute of New Jersey
   (P30CA072720). We thank Dr. Joseph Bertino, M.D., for helpful comments
   and suggestions.
NR 52
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U1 0
U2 6
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD NOV 15
PY 2013
VL 12
AR 139
DI 10.1186/1476-4598-12-139
PG 10
WC Biochemistry & Molecular Biology; Oncology
SC Biochemistry & Molecular Biology; Oncology
GA 281UK
UT WOS:000329126300002
PM 24238140
ER

PT J
AU Zhang, HT
   Curreli, F
   Waheed, AA
   Mercredi, PY
   Mehta, M
   Bhargava, P
   Scacalossi, D
   Tong, XH
   Lee, S
   Cooper, A
   Summers, MF
   Freed, EO
   Debnath, AK
AF Zhang, Hongtao
   Curreli, Francesca
   Waheed, Abdul A.
   Mercredi, Peter Y.
   Mehta, Mansi
   Bhargava, Pallavi
   Scacalossi, Daniel
   Tong, Xiaohe
   Lee, Shawn
   Cooper, Alan
   Summers, Michael F.
   Freed, Eric O.
   Debnath, Asim K.
TI Dual-acting stapled peptides target both HIV-1 entry and assembly
SO RETROVIROLOGY
LA English
DT Article
DE HIV-1; Capsid; Virus assembly; Virus entry; Stapled peptides; NMR; SPR;
   ITC; Drug-resistance
ID HUMAN-IMMUNODEFICIENCY-VIRUS; ENVELOPE GLYCOPROTEIN GP120;
   DRUG-RESISTANT HIV-1; N-TERMINAL DOMAIN; CAPSID PROTEIN; IN-VITRO; V3
   LOOP; CCR5 CORECEPTOR; SULFATED POLYSACCHARIDES; DIMERIZATION DOMAIN
AB Background: Previously, we reported the conversion of the 12-mer linear and cell-impermeable peptide CAI to a cell-penetrating peptide NYAD-1 by using an i, i + 4 hydrocarbon stapling technique and confirmed its binding to the C-terminal domain (CTD) of the HIV-1 capsid (CA) protein with an improved affinity (Kd similar to 1 mu M) compared to CAI (Kd similar to 15 mu M). NYAD-1 disrupts the formation of both immature-and mature-like virus particles in in vitro and cell-based assembly assays. In addition, it displays potent anti-HIV-1 activity in cell culture against a range of laboratory-adapted and primary HIV-1 isolates.
   Results: In this report, we expanded the study to i, i + 7 hydrocarbon-stapled peptides to delineate their mechanism of action and antiviral activity. We identified three potent inhibitors, NYAD-36, -66 and -67, which showed strong binding to CA in NMR and isothermal titration calorimetry (ITC) studies and disrupted the formation of mature-like particles. They showed typical a-helical structures and penetrated cells; however, the cell penetration was not as efficient as observed with the i, i + 4 peptides. Unlike NYAD-1, the i, i + 7 peptides did not have any effect on virus release; however, they impaired Gag precursor processing. HIV-1 particles produced in the presence of these peptides displayed impaired infectivity. Consistent with an effect on virus entry, selection for viral resistance led to the emergence of two mutations in the gp120 subunit of the viral envelope (Env) glycoprotein, V120Q and A327P, located in the conserved region 1 (C1) and the base of the V3 loop, respectively.
   Conclusion: The i, i + 7 stapled peptides derived from CAI unexpectedly target both CA and the V3 loop of gp120. This dual-targeted activity is dependent on their ability to penetrate cells as well as their net charge. This mechanistic revelation will be useful in further modifying these peptides as potent anti-HIV-1 agents.
C1 [Zhang, Hongtao; Curreli, Francesca; Scacalossi, Daniel; Debnath, Asim K.] New York Blood Ctr, Lindsley F Kimball Res Inst, Lab Mol Modeling, New York, NY 10065 USA.
   [Waheed, Abdul A.; Freed, Eric O.] NCI, Virus Cell Interact Sect, HIV Drug Resistance Program, Frederick, MD 21702 USA.
   [Mercredi, Peter Y.; Mehta, Mansi; Bhargava, Pallavi] Univ Maryland, Howard Hughes Med Inst, Baltimore, MD 21250 USA.
   [Mercredi, Peter Y.; Mehta, Mansi; Bhargava, Pallavi] Univ Maryland, Dept Chem & Biochem, Baltimore, MD 21250 USA.
   [Tong, Xiaohe; Lee, Shawn] CPC Sci Inc, Sunnyvale, CA 94089 USA.
   [Cooper, Alan] Univ Glasgow, Sch Chem, Glasgow G12 8QQ, Lanark, Scotland.
RP Debnath, AK (reprint author), New York Blood Ctr, Lindsley F Kimball Res Inst, Lab Mol Modeling, 310 E 67th St, New York, NY 10065 USA.
EM adebnath@nybloodcenter.org
RI Cooper, Alan/F-7813-2011
OI Cooper, Alan/0000-0001-6709-7343
FU NIH [RO1 AI081604, R01 AI30917]; intramural fund from the New York Blood
   Center; NIH IMSD grant for maximizing doctoral student diversity [R25
   MBRS-IMSD GM55036]; Intramural Research Program of the Center for Cancer
   Research, National Cancer Institute, NIH
FX This study was supported by NIH Grant RO1 AI081604 (AKD) and the
   intramural fund from the New York Blood Center (AKD). NMR and turbidity
   studies were supported by NIH Grant R01 AI30917 (MFS). PYM was supported
   by NIH IMSD grant R25 MBRS-IMSD GM55036 for maximizing doctoral student
   diversity. This work was supported in part by the Intramural Research
   Program of the Center for Cancer Research, National Cancer Institute,
   NIH (EF). We thank Lyudmil Angelov (confocal microscopy) and Yelena
   Oksov (electron microscopy) for their technical help. We thank K. Waki
   for constructing the pCMVdeltaR8.2/PR-clone and. J. Burns for providing
   the VSV-G expression vector. HIV-Ig was obtained from the NIH AIDS
   Research and Reference Reagent Program.
NR 77
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U1 6
U2 21
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PD NOV 15
PY 2013
VL 10
AR 136
DI 10.1186/1742-4690-10-136
PG 20
WC Virology
SC Virology
GA 280QQ
UT WOS:000329046300001
PM 24237936
ER

PT J
AU Xu, J
   Xu, ZF
   Zhou, JY
   Zhuang, ZP
   Wang, EH
   Boerner, J
   Wu, GS
AF Xu, Jing
   Xu, Zhengfan
   Zhou, Jun-Ying
   Zhuang, Zhengping
   Wang, Enhua
   Boerner, Julie
   Wu, Gen Sheng
TI Regulation of the Src-PP2A Interaction in Tumor Necrosis Factor
   (TNF)-related Apoptosis-inducing Ligand (TRAIL)-induced Apoptosis
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
DE Cell Death; Phosphorylation; PP2A; Src; Trail
ID TRAIL-INDUCED APOPTOSIS; PROTEIN PHOSPHATASE 2A; DEATH RECEPTOR GENE;
   BREAST-CANCER; LIPID RAFTS; CELL-DEATH; PHASE-I; SRC; FAMILY; MECHANISM
AB Background: The mechanisms of TRAIL resistance in cancer cells are not fully understood. Results: TRAIL activates Src, which in turn phosphorylates caspase-8. Src inhibition increases TRAIL-induced apoptosis. TRAIL also relieves PP2A-mediated Src inhibition, leading to Src activation. Conclusion: The interaction between Src and PP2A plays an important role in TRAIL resistance. Significance: Inhibition of Src survival signaling may enhance TRAIL-induced apoptosis in cancer cells.
   TNF-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis in transformed and tumor cells but not in normal cells, making it a promising agent for cancer therapy. However, many cancer cells are resistant to TRAIL, and the underlying mechanisms are not fully understood. Here, we show that the regulation of the PP2A and Src interaction plays a critical role in TRAIL resistance. Specifically, we show that TRAIL treatment activates the tyrosine kinase Src, which subsequently phosphorylates caspase-8 at tyrosine 380, leading to the inhibition of caspase-8 activation. We also show that upon TRAIL treatment, Src, caspase-8, and PP2A/C (a catalytic subunit of the PP2A phosphatase) are redistributed into lipid rafts, a microdomain of the plasma membrane enriched with cholesterol, where PP2A dephosphorylates Src at tyrosine 418 and in turn inhibits caspase-8 phosphorylation. Furthermore, we find that TRAIL treatment causes PP2A/C degradation. These data suggest that the balance between Src-mediated caspase-8 phosphorylation and the inactivation of Src-mediated caspase-8 phosphorylation by PP2A determines the outcome of TRAIL treatment in breast cancer cells. Therefore, this work identifies a novel mechanism by which the interaction between PP2A and Src in the context of caspase-8 activation modulates TRAIL sensitivity in cancer cells.
C1 [Xu, Jing; Xu, Zhengfan; Zhou, Jun-Ying; Boerner, Julie; Wu, Gen Sheng] Wayne State Univ, Sch Med, Depts Oncol, Karmanos Canc Inst, Detroit, MI 48201 USA.
   [Xu, Jing; Xu, Zhengfan; Zhou, Jun-Ying; Boerner, Julie; Wu, Gen Sheng] Wayne State Univ, Sch Med, Dept Pathol, Karmanos Canc Inst, Detroit, MI 48201 USA.
   [Xu, Zhengfan; Wang, Enhua] China Med Univ, Dept Pathol, Affiliated Hosp 1, Shenyang 110001, Peoples R China.
   [Xu, Zhengfan; Wang, Enhua] China Med Univ, Coll Basic Med Sci, Shenyang 110001, Peoples R China.
   [Zhuang, Zhengping] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
RP Wu, GS (reprint author), Wayne State Univ, Sch Med, Depts Oncol, Karmanos Canc Inst, Detroit, MI 48201 USA.
EM wug@karmanos.org
FU Karmanos Cancer Institute Strategic Research Initiative grant; National
   Institutes of Health [P30 CA22453]
FX This work was supported by a Karmanos Cancer Institute Strategic
   Research Initiative grant supported in part by National Institutes of
   Health Grant P30 CA22453.
NR 39
TC 8
Z9 8
U1 0
U2 7
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 15
PY 2013
VL 288
IS 46
BP 33263
EP 33271
DI 10.1074/jbc.M113.508093
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 277TH
UT WOS:000328841700040
PM 24100030
ER

PT J
AU Billington, N
   Wang, AB
   Mao, J
   Adelstein, RS
   Sellers, JR
AF Billington, Neil
   Wang, Aibing
   Mao, Jian
   Adelstein, Robert S.
   Sellers, James R.
TI Characterization of Three Full-length Human Nonmuscle Myosin II Paralogs
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
DE Actin; ATPases; Cytoskeleton; Electron Microscopy (EM); Molecular
   Motors; Myosin
ID SMOOTH-MUSCLE MYOSIN; LIGHT-CHAIN PHOSPHORYLATION; HUMAN PLATELET
   MYOSIN; VERTEBRATE NONMUSCLE; THICK FILAMENTS; CELL-ADHESION;
   COILED-COILS; HEAD-HEAD; ACTIN; MEROMYOSIN
AB Nonmuscle myosin IIs (NM IIs) are a group of molecular motors involved in a wide variety of cellular processes including cytokinesis, migration, and control of cell morphology. There are three paralogs of the NM II heavy chain in humans (IIA, IIB, and IIC), each encoded by a separate gene. These paralogs are expressed at different levels according to cell type and have different roles and intracellular distributions in vivo. Most previous studies on NM II used tissue-purified protein or expressed fragments of the molecule, which presents potential drawbacks for characterizing individual paralogs of the intact protein in vitro. To circumvent current limitations and approach their native properties, we have successfully expressed and purified the three full-length human NM II proteins with their light chains, using the baculovirus/Sf9 system. The enzymatic and structural properties of the three paralogs were characterized. Although each NM II is capable of forming bipolar filaments, those formed by IIC tend to contain fewer constituent molecules than those of IIA and IIB. All paralogs adopt the compact conformation in the presence of ATP. Phosphorylation of the regulatory light chain leads to assembly into filaments, which bind to actin in the presence of ATP. The nature of interactions with actin filaments is shown with different paralogs exhibiting different actin binding behaviors under equivalent conditions. The data show that although NM IIA and IIB form filaments with similar properties, NM IIC forms filaments that are less well suited to roles such as tension maintenance within the cell.
C1 [Billington, Neil; Sellers, James R.] NHLBI, Lab Mol Physiol, NIH, Bethesda, MD 20892 USA.
   [Wang, Aibing; Mao, Jian; Adelstein, Robert S.] NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA.
RP Adelstein, RS (reprint author), NHLBI, Mol Cardiol Lab, NIH, 10 Ctr Dr,10-6C103B, Bethesda, MD 20892 USA.
EM Adelster@nhlbi.nih.gov; sellersj@nhlbi.nih.gov
OI Adelstein, Robert/0000-0002-8683-2144
FU Electron Microscopy Core Facility of the NHLBI
FX We thank the Electron Microscopy Core Facility of the NHLBI for support,
   advice, and use of facilities. We also thank Mary Anne Conti for
   critical reading of the manuscript.
NR 79
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Z9 36
U1 0
U2 10
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 15
PY 2013
VL 288
IS 46
BP 33398
EP 33410
DI 10.1074/jbc.M113.499848
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 277TH
UT WOS:000328841700053
PM 24072716
ER

PT J
AU Bizzarro, B
   Barros, MS
   Maciel, C
   Gueroni, DI
   Lino, CN
   Campopiano, J
   Kotsyfakis, M
   Amarante-Mendes, GP
   Calvo, E
   Capurro, ML
   Sa-Nunes, A
AF Bizzarro, Bruna
   Barros, Michele S.
   Maciel, Ceres
   Gueroni, Daniele I.
   Lino, Ciro N.
   Campopiano, Julia
   Kotsyfakis, Michalis
   Amarante-Mendes, Gustavo P.
   Calvo, Eric
   Capurro, Margareth L.
   Sa-Nunes, Anderson
TI Effects of Aedes aegypti salivary components on dendritic cell and
   lymphocyte biology
SO PARASITES & VECTORS
LA English
DT Article
DE Dendritic cells; T cells; Aedes aegypti; Saliva; Apoptosis
ID IXODES-SCAPULARIS SALIVA; HOST IMMUNE-RESPONSE; T-CELLS; DIFFERENTIAL
   MODULATION; VIRUS-INFECTION; GLAND EXTRACT; MOSQUITO; MEMORY;
   INFLAMMATION; COAGULATION
AB Background: Saliva is a key element of interaction between hematophagous mosquitoes and their vertebrate hosts. In addition to allowing a successful blood meal by neutralizing or delaying hemostatic responses, the salivary cocktail is also able to modulate the effector mechanisms of host immune responses facilitating, in turn, the transmission of several types of microorganisms. Understanding how the mosquito uses its salivary components to circumvent host immunity might help to clarify the mechanisms of transmission of such pathogens and disease establishment.
   Methods: Flow cytometry was used to evaluate if increasing concentrations of A. aegypti salivary gland extract (SGE) affects bone marrow-derived DC differentiation and maturation. Lymphocyte proliferation in the presence of SGE was estimated by a colorimetric assay. Western blot and Annexin V staining assays were used to assess apoptosis in these cells. Naive and memory cells from mosquito-bite exposed mice or OVA-immunized mice and their respective controls were analyzed by flow cytometry.
   Results: Concentration-response curves were employed to evaluate A. aegypti SGE effects on DC and lymphocyte biology. DCs differentiation from bone marrow precursors, their maturation and function were not directly affected by A. aegypti SGE (concentrations ranging from 2.5 to 40 mu g/mL). On the other hand, lymphocytes were very sensitive to the salivary components and died in the presence of A. aegypti SGE, even at concentrations as low as 0.1 mu g/mL. In addition, A. aegypti SGE was shown to induce apoptosis in all lymphocyte populations evaluated (CD4(+) and CD8(+) T cells, and B cells) through a mechanism involving caspase-3 and caspase-8, but not Bim. By using different approaches to generate memory cells, we were able to verify that these cells are resistant to SGE effects.
   Conclusion: Our results show that lymphocytes, and not DCs, are the primary target of A. aegypti salivary components. In the presence of A. aegypti SGE, naive lymphocyte populations die by apoptosis in a caspase-3- and caspase-8-dependent pathway, while memory cells are selectively more resistant to its effects. The present work contributes to elucidate the activities of A. aegypti salivary molecules on the antigen presenting cell-lymphocyte axis and in the biology of these cells.
C1 [Bizzarro, Bruna; Barros, Michele S.; Maciel, Ceres; Gueroni, Daniele I.; Lino, Ciro N.; Sa-Nunes, Anderson] Univ Sao Paulo, Inst Ciencias Biomed, Dept Imunol, Lab Imunol Expt, BR-05508900 Sao Paulo, Brazil.
   [Campopiano, Julia; Amarante-Mendes, Gustavo P.] Univ Sao Paulo, Inst Ciencias Biomed, Dept Imunol, Lab Biol Celular & Mol, BR-05508900 Sao Paulo, Brazil.
   [Kotsyfakis, Michalis] Acad Sci Czech Republic, Inst Parasitol, Ctr Biol, Lab Genom & Prote Dis Vectors, CR-37005 Ceske Budejovice, Czech Republic.
   [Amarante-Mendes, Gustavo P.] Inst Nacl Ciencia & Tecnol, Inst Invest Imunol, Sao Paulo, Brazil.
   [Calvo, Eric] NIAID, Sect Vector Biol, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
   [Capurro, Margareth L.] Univ Sao Paulo, Inst Ciencias Biomed, Dept Parasitol, Lab Mosquitos Geneticamente Modificados, BR-05508900 Sao Paulo, Brazil.
   [Capurro, Margareth L.; Sa-Nunes, Anderson] Conselho Nacl Desenvolvimento Cient & Tecnol INCT, Inst Nacl Ciencia & Tecnol Entomol Mol, Rio De Janeiro, Brazil.
RP Sa-Nunes, A (reprint author), Univ Sao Paulo, Inst Ciencias Biomed, Dept Imunol, Lab Imunol Expt, BR-05508900 Sao Paulo, Brazil.
EM sanunes@usp.br
RI Capurro, Margareth/F-8679-2012; Kotsyfakis, Michail/G-9525-2014;
   Campopiano, Julia/O-9979-2015; Sa-Nunes, Anderson/D-8667-2012; Bizzarro,
   Bruna/K-4778-2016; Amarante Mendes, Gustavo/C-8187-2012
OI Calvo, Eric/0000-0001-7880-2730; Capurro, Margareth/0000-0002-7480-2116;
   Kotsyfakis, Michail/0000-0002-7526-1876; Sa-Nunes,
   Anderson/0000-0002-1859-4973; Bizzarro, Bruna/0000-0001-6315-0549;
   Amarante Mendes, Gustavo/0000-0002-7851-6205
FU FAPESP [2009/12247-5, 2010/18216-1, 2011/06626-3, 2011/15569-3,
   2009/09892-6, 2009/53637-0]; CNPq [134660/2010-2, 302194/2009-6];
   Casadinho/PROCAD (MCTI/CNPq/MEC/CAPES) [552258/2011-3]; Brazilian
   Malaria Network (MCT/CNPq/MS/SCTIE/DECIT/PRONEX) [555648/2009-5];
   Arthropod Vectors (NAP-MOBIARVE, University of Sao Paulo)
FX The authors would like to thank Dr. Momtchilo Russo and Dr. Sonia Jancar
   (Department of Immunology, ICB/USP, Brazil) for providing some reagents
   and equipments used in this work; Dr. Philippe Bouillet (Walter and
   Elisa Hall Institute of Medical Research, Australia) for providing the
   BIM<SUP>-/-</SUP> mice; and Dr. Jose M. Ribeiro (Laboratory of Malaria
   and Vector Research, NIAID/NIH, USA) for encouragement and support. The
   authors also thank Van M. Pham (Laboratory of Malaria and Vector
   Research, NIAID/NIH, USA) and Sandra Alexandre (Department of
   Immunology, ICB/USP) for their technical assistance. The following
   authors were recipients of fellowships: B. B. (FAPESP 2009/12247-5); M.
   S.B. (CNPq 134660/2010-2); C.M. (FAPESP 2010/18216-1); D.I.G. (FAPESP
   2011/06626-3); C.N.L. (FAPESP 2011/15569-3). This work was supported by
   grants from FAPESP (2009/09892-6 and 2009/53637-0), CNPq
   (302194/2009-6), Casadinho/PROCAD (MCTI/CNPq/MEC/CAPES 552258/2011-3),
   Brazilian Malaria Network (MCT/CNPq/MS/SCTIE/DECIT/PRONEX
   555648/2009-5), and Research Network on Bioactive Molecules from
   Arthropod Vectors (NAP-MOBIARVE, University of Sao Paulo). We dedicated
   this paper to the memory of Alexandre A. Peixoto.
NR 49
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Z9 10
U1 2
U2 11
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1756-3305
J9 PARASITE VECTOR
JI Parasites Vectors
PD NOV 15
PY 2013
VL 6
AR 329
DI 10.1186/1756-3305-6-329
PG 13
WC Parasitology
SC Parasitology
GA 277QH
UT WOS:000328833800001
PM 24238038
ER

PT J
AU Kim, H
   Gao, W
   Ho, M
AF Kim, Heungnam
   Gao, Wei
   Ho, Mitchell
TI Novel Immunocytokine IL12-SS1 (Fv) Inhibits Mesothelioma Tumor Growth in
   Nude Mice
SO PLOS ONE
LA English
DT Article
ID HUMAN MONOCLONAL-ANTIBODY; POTENT ANTITUMOR-ACTIVITY;
   NECROSIS-FACTOR-ALPHA; SOFT-TISSUE SARCOMAS; PHASE-I TRIAL;
   HIGH-AFFINITY; RECOMBINANT IMMUNOTOXIN; MALIGNANT MESOTHELIOMA;
   CANCER-IMMUNOTHERAPY; INTERFERON-GAMMA
AB Mesothelin is a glycosylphosphatidylinositol-anchored glycoprotein that is highly expressed on the cell surface of malignant mesothelioma. Monoclonal antibodies against mesothelin are being evaluated for the treatment of mesothelioma. Immunocytokines represent a novel class of armed antibodies. To provide an alternative approach to current mesothelin-targeted antibody therapies, we have developed a novel immunocytokine based on interleukin-12 (IL12) and the SS1 Fv specific for mesothelin. IL12 possesses potent anti-tumor activity in a wide variety of solid tumors. The newly-developed recombinant immunocytokine, IL12-SS1 (Fv), was produced in insect cells using a baculovirus-insect cell expression system. The SS1 single-chain Fv was fused to the C terminus of the p35 subunit of IL12 through a short linker (GSADGG). The single-chain IL12-SS1 (Fv) immunocytokine bound native mesothelin proteins on malignant mesothelioma (NCI-H226) and ovarian (OVCAR-3) cells as well as recombinant mesothelin on A431/H9 cells. The immunocytokine retained sufficient bioactivity of IL12 and significantly inhibited human malignant mesothelioma (NCI-H226) grown in the peritoneal cavity of nude mice and showed comparable anti-tumor activity to that of the SS1P immunotoxin. IL12-SS1 (Fv) is the first reported immunocytokine to mesothelin-positive tumors and may be an attractive addition to mesothelin-targeted cancer therapies.
C1 [Kim, Heungnam; Gao, Wei; Ho, Mitchell] NCI, Antibody Therapy Sect, Mol Biol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Ho, M (reprint author), NCI, Antibody Therapy Sect, Mol Biol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
EM homi@mail.nih.gov
RI Ho, Mitchell/F-5059-2015
FU National Institutes of Health, National Cancer Institute; Center for
   Cancer Research; Mesothelioma Applied Research Foundation
FX This research was supported by the Intramural Research Program of the
   National Institutes of Health, National Cancer Institute, and Center for
   Cancer Research. This work was also possible because of a Mesothelioma
   Applied Research Foundation Craig Kozicki Memorial Grant to MH. The
   funders had no role in study design, data collection and analysis,
   decision to publish, or preparation of the manuscript.
NR 45
TC 8
Z9 8
U1 2
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 15
PY 2013
VL 8
IS 11
AR UNSP e81919
DI 10.1371/journal.pone.0081919
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255RX
UT WOS:000327258600119
PM 24260587
ER

PT J
AU Kretschmer, F
   Kretschmer, V
   Kunze, VP
   Kretzberg, J
AF Kretschmer, Friedrich
   Kretschmer, Viola
   Kunze, Vincent P.
   Kretzberg, Jutta
TI OMR-Arena: Automated Measurement and Stimulation System to Determine
   Mouse Visual Thresholds Based on Optomotor Responses
SO PLOS ONE
LA English
DT Article
ID EYE-MOVEMENTS; SPATIAL VISION; MICE; ACUITY; SENSITIVITY; ZEBRAFISH;
   RATS; PLASTICITY; BEHAVIORS; GOLDFISH
AB Measurement of the optomotor response is a common way to determine thresholds of the visual system in animals. Particularly in mice, it is frequently used to characterize the visual performance of different genetically modified strains or to test the effect of various drugs on visual performance. Several methods have been developed to facilitate the presentation of stimuli using computer screens or projectors. Common methods are either based on the measurement of eye movement during optokinetic reflex behavior or rely on the measurement of head and/or body-movements during optomotor responses. Eye-movements can easily and objectively be quantified, but their measurement requires invasive fixation of the animals. Head movements can be observed in freely moving animals, but until now depended on the judgment of a human observer who reported the counted tracking movements of the animal during an experiment. In this study we present a novel measurement and stimulation system based on open source building plans and software. This system presents appropriate 3600 stimuli while simultaneously video-tracking the animal's head-movements without fixation. The on-line determined head gaze is used to adjust the stimulus to the head position, as well as to automatically calculate visual acuity. Exemplary, we show that automatically measured visual response curves of mice match the results obtained by a human observer very well. The spatial acuity thresholds yielded by the automatic analysis are also consistent with the human observer approach and with published results. Hence, OMR-arena provides an affordable, convenient and objective way to measure mouse visual performance.
C1 [Kretschmer, Friedrich] NEI, Retinal Circuit Dev & Genet Unit, Neurobiol Neurodegenerat & Repair Lab, NIH, Bethesda, MD 20892 USA.
   [Kretschmer, Viola; Kunze, Vincent P.; Kretzberg, Jutta] Carl von Ossietzky Univ Oldenburg, D-26111 Oldenburg, Germany.
   [Kretzberg, Jutta] Carl von Ossietzky Univ Oldenburg, Res Ctr Neurosensory Sci, D-26111 Oldenburg, Germany.
RP Kretschmer, F (reprint author), NEI, Retinal Circuit Dev & Genet Unit, Neurobiol Neurodegenerat & Repair Lab, NIH, Bethesda, MD 20892 USA.
EM friedrich.kretschmer@nih.gov
FU German research foundation [DFG FOR 701]
FX The work was supported by German research foundation, DFG FOR 701. The
   funders had no role in study design, data collection and analysis,
   decision to publish, or preparation of the manuscript.
NR 45
TC 5
Z9 5
U1 1
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 15
PY 2013
VL 8
IS 11
AR e78058
DI 10.1371/journal.pone.0078058
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255RX
UT WOS:000327258600005
PM 24260105
ER

PT J
AU Tarca, AL
   Bhatti, G
   Romero, R
AF Tarca, Adi L.
   Bhatti, Gaurav
   Romero, Roberto
TI A Comparison of Gene Set Analysis Methods in Terms of Sensitivity,
   Prioritization and Specificity
SO PLOS ONE
LA English
DT Article
ID PATHWAY LEVEL ANALYSIS; EXPRESSION; BIOLOGY; ASSOCIATION; MICROARRAY;
   ENRICHMENT; LISTS
AB Identification of functional sets of genes associated with conditions of interest from omics data was first reported in 1999, and since, a plethora of enrichment methods were published for systematic analysis of gene sets collections including Gene Ontology and biological pathways. Despite their widespread usage in reducing the complexity of omics experiment results, their performance is poorly understood. Leveraging the existence of disease specific gene sets in KEGG and Metacore (R) databases, we compared the performance of sixteen methods under relaxed assumptions while using 42 real datasets (over 1,400 samples). Most of the methods ranked high the gene sets designed for specific diseases whenever samples from affected individuals were compared against controls via microarrays. The top methods for gene set prioritization were different from the top ones in terms of sensitivity, and four of the sixteen methods had large false positives rates assessed by permuting the phenotype of the samples. The best overall methods among those that generated reasonably low false positive rates, when permuting phenotypes, were PLAGE, GLOBALTEST, and PADOG. The best method in the category that generated higher than expected false positives was MRGSE.
C1 [Tarca, Adi L.] Wayne State Univ, Dept Comp Sci, Detroit, MI 48202 USA.
   [Tarca, Adi L.; Bhatti, Gaurav; Romero, Roberto] NICHHD, Perinatol Res Branch, NIH, Rockville, 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.
RP Tarca, AL (reprint author), Wayne State Univ, Dept Comp Sci, Detroit, MI 48202 USA.
EM atarca@med.wayne.edu
FU Intramural Research Program of the Eunice Kennedy Shriver National
   Institute of Child Health and Human Development, National Institutes of
   Health, U.S. Department of Health and Human Services
FX The funders had no role in study design, data collection and analysis,
   decision to publish, or preparation of the manuscript. AT, GB, and RR
   were supported, in part, by the Intramural Research Program of the
   Eunice Kennedy Shriver National Institute of Child Health and Human
   Development, National Institutes of Health, U.S. Department of Health
   and Human Services.
NR 33
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U1 1
U2 14
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 15
PY 2013
VL 8
IS 11
AR e79217
DI 10.1371/journal.pone.0079217
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255RX
UT WOS:000327258600022
PM 24260172
ER

PT J
AU Wohl, DA
   Kendall, MA
   Feinberg, J
   Alston-Smith, B
   Owens, S
   Chafey, S
   Marco, M
   Maxwell, S
   Benson, C
   Keiser, P
   van der Horst, C
   Jacobson, MA
AF Wohl, David A.
   Kendall, Michelle A.
   Feinberg, Judith
   Alston-Smith, Beverly
   Owens, Susan
   Chafey, Suzette
   Marco, Michael
   Maxwell, Sharon
   Benson, Constance
   Keiser, Philip
   van der Horst, Charles
   Jacobson, Mark A.
CA A5030 Study Team
TI The Clinical Impact of Continuing to Prescribe Antiretroviral Therapy in
   Patients with Advanced AIDS Who Manifest No Virologic or Immunologic
   Benefit
SO PLOS ONE
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; AVIUM COMPLEX INFECTION; C-REACTIVE
   PROTEIN; HIV-INFECTION; CARDIOVASCULAR-DISEASE; RISK; MORTALITY;
   SURVIVAL; INDIVIDUALS; PROPHYLAXIS
AB Introduction: Despite the efficacy and tolerability of modern antiretroviral therapy (ART), many patients with advanced AIDS prescribed these regimens do not achieve viral suppression or immune reconstitution as a result of poor adherence, drug resistance, or both. The clinical outcomes of continued ART prescription for such patients have not been well characterized.
   Methods: We examined the causes and predictors of all-cause mortality, AIDS-defining conditions, and serious non-AIDSdefining events among a cohort of participants in a clinical trial of pre-emptive therapy for CMV disease. We focused on participants who, despite ART had failed to achieve virologic suppression and substantive immune reconstitution.
   Results: 233 ART-receiving participants entered with a median baseline CD4+ T cell count of 30/mm(3) and plasma HIV RNA of 5 log10 copies/mL. During a median 96 weeks of follow-up, 24.0% died (a mortality rate of 10.7/100 patient-years); 27.5% reported a new AIDS-defining condition, and 22.3% a new serious non-AIDS event. Of the deaths, 42.8% were due to an AIDS-defining condition, 44.6% were due to a non-AIDS-defining condition, and 12.5% were of unknown etiology. Decreased risk of mortality was associated with baseline CD4+ T cell count >= 25/mm(3) and lower baseline HIV RNA.
   Conclusions: Among patients with advanced AIDS prescribed modern ART who achieve neither virologic suppression nor immune reconstitution, crude mortality percentages appear to be lower than reported in cohorts of patients studied a decade earlier. Also, in contrast to the era before modern ART became available, nearly half of the deaths in our modern-era study were caused by serious non-AIDS-defining events. Even among the most advanced AIDS patients who were not obtaining apparent immunologic and virologic benefit from ART, continued prescription of these medications appears to alter the natural history of AIDS-improving survival and shifting the causes of death from AIDS-to non-AIDS-defining conditions.
C1 [Wohl, David A.; van der Horst, Charles] Univ N Carolina, Chapel Hill, NC 27515 USA.
   [Kendall, Michelle A.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
   [Feinberg, Judith] Univ Cincinnati, Cincinnati, OH USA.
   [Alston-Smith, Beverly] NIH, Div Aids, Bethesda, MD 20892 USA.
   [Owens, Susan] Frontier Sci & Technol Fdn, Amherst, NY USA.
   [Chafey, Suzette] Univ Calif Los Angeles, Los Angeles, CA USA.
   [Marco, Michael] Columbia Univ, New York, NY USA.
   [Maxwell, Sharon] Univ Washington, Seattle, WA 98195 USA.
   [Benson, Constance] Univ Calif San Diego, San Diego, CA 92103 USA.
   [Keiser, Philip] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
   [Jacobson, Mark A.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP Wohl, DA (reprint author), Univ N Carolina, Chapel Hill, NC 27515 USA.
EM wohl@med.unc.edu; kendall@sdac.harvard.edu; Judith.Feinberg@uc.edu;
   balston@niaid.nih.gov; owens.susan@fstrf.org; schafey@mednet.ucla.edu;
   mjacobson@php.ucsf.edu
RI Kendall, Michelle/B-7665-2016
OI Kendall, Michelle/0000-0001-9160-4544
FU AIDS Clinical Trials Group; National Institute of Allergy and Infectious
   Diseases [AI68636, AI68634, AI69432, AI46376, AI69450, AI 69513-01,
   AI69423-01, AI69439, AI32783-13, AI069556, AI27660, AI069502-01,
   AI069434, AI27664, AI46370, AI69532-01, AI69411, AI69494-01]; University
   of North Carolina CFAR [AI50410]; University of Pennsylvania CFAR
   [5-P30-AI045008- 07]; NIAID [AI69474, AI069501, AI34853, AI27659,
   AI27661, AI69495, AI69471, AI46381, AI32782, AI69470-01, AI27673,
   A19418, AI69477-01, RR00051, RR00046, M01-RR00096]
FX This study was supported in part by the AIDS Clinical Trials Group
   funded by the National Institute of Allergy and Infectious Diseases
   (AI68636 for ACTG and AI68634 for SDAC), AI69432 to the UC San Diego
   Medical Center (C. Benson, S. Spector), AI46376 to the UT Southwestern
   Medical Center (P. Keiser), AI69450 to the University of Colorado Health
   Sciences Center (G. Ray), AI 69513-01 to the University of Cincinnati,
   AI69423-01 to the University of North Carolina (D. A. Wohl), AI69439 to
   Vanderbilt University, AI32783-13 to the University of Pennsylvania,
   AI069556 toStanford University, AI27660 to the UCLA Medical Center (S.
   Chafey), AI069502-01 to San Francisco General Hospital (M. A. Jacobson),
   AI069434 and AI27664 to the University ofWashington, Seattle, AI46370 to
   Beth Israel Medical Center (C. Crumpacker), AI69532-01 to NYU/NYC HHC at
   Bellevue, AI69411 the University of Rochester, AI69494-01 to the
   University of Pittsburgh, AI69474 to Ohio State University, AI069501 to
   Case Western Reserve University, AI34853 to University of Hawaii at
   Manoa, AI27659 to Harvard University/Massachusetts General Hospital,
   AI27661 to University of Minnesota, AI69495 to Washington University,
   St. Louis (S. Maxwell), AI69471 to Northwestern University (N. Lurain),
   AI46381 to Miriam Hospital, AI32782 to University of Texas, Galveston,
   AI69470-01 to Columbia University/Weil Medical College of Cornell,
   AI27673 to University of Southern California, A19418 to Emory
   University, and AI69477-01 to the University of Miami. This research was
   supported in part by the General Clinical Research Center Units funded
   by the National Center for Research Resources, RR00051 to the University
   of Colorado Health Sciences Center (G. Ray), RR00046 to the University
   of North Carolina (D. A. Wohl), and M01-RR00096 to NYU/ NYC HHC at
   Bellevue. Additional support was provided by the University of North
   Carolina CFAR GrantAI50410 and University of Pennsylvania CFAR Grant
   5-P30-AI045008- 07. ParticipatingA5030 sites: J. Hoffman, S. Cahill (UC
   San Diego Medical Center); T. Petersen, P. Keiser (UT Southwestern
   Medical Center); B. Putnam, R. Levinson (University of Colorado Health
   Sciences Center); J. Feinberg, J. Baer (University of Cincinnati); C.
   Zelasky, S. Pedersen (University of North Carolina); J. Nicotera, V.
   Bailey (Vanderbilt University); C. Nichols, J. Quinn (University of
   Pennsylvania, Philadelphia); J. Norris, S. Valle (Stanford University);
   A. Moe, A. Johiro (UCLA Medical Center); M. Jacobson, J. Volinski (San
   Francisco General Hospital); S. Storey, J. Schouten, (University of
   Washington); D. Mildvan, M. Revuelta (Beth Israel Medical Center); R.
   Hutt, M. Vasquez (NYU/NYC HHC at Bellevue); C Greisberger, R Reichman,
   (Rochester University); S. Riddler, B. Rutecki (University of
   Pittsburgh); S. L. Koletar, D. Gochnour(Ohio State University); R. A.
   Salata, P. Walton (Case Western Reserve University); University of
   Hawaii at Manoa, Leahi; Harvard; Massachusetts General Hospital;
   University of Minnesota; M. Rodriguez, L. Kessels (Washington
   University); K. Coleman, A. Lyons (Northwestern University); K. T.
   Tashima, H. Sousa (Miriam Hospital); W. A. O'Brien, C. Mogridge
   (University of Texas, Galveston); J. Noel Connor, M. Crawford (Columbia
   Collaborative HIV/AIDS Clinical Trials Unit); University of Southern
   California; Methodist Hospital of Indiana; M. Palmore, E. R. Patrick
   (Emory University); and H. H. Bolivar, M. A. Fischl (University of
   Miami). The funders had no role in study design, data collection and
   analysis, decision to publish, or preparation of the manuscript.
NR 20
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PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 15
PY 2013
VL 8
IS 11
AR e78676
DI 10.1371/journal.pone.0078676
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255RX
UT WOS:000327258600007
PM 24260125
ER

PT J
AU Yan, S
   Hou, GJ
   Sehwieters, CD
   Ahmed, S
   Williams, JC
   Polenova, T
AF Yan, Si
   Hou, Guangjin
   Sehwieters, Charles D.
   Ahmed, Shubhir
   Williams, John C.
   Polenova, Tatyana
TI Three-Dimensional Structure of CAP-Gly Domain of Mammalian Dynactin
   Determined by Magic Angle Spinning NMR Spectroscopy: Conformational
   Plasticity and Interactions with End-Binding Protein EB1
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Article
DE magic angle spinning; dynactin; CAP-Gly; p150(Glued) domain; end-binding
   protein EB1
ID SOLID-STATE NMR; ESCHERICHIA-COLI THIOREDOXIN; MOLECULAR-STRUCTURE
   DETERMINATION; SECONDARY STRUCTURE-ANALYSIS; MICROTUBULE PLUS ENDS;
   MOTOR-NEURON DISEASE; RESONANCE ASSIGNMENTS; CHEMICAL-SHIFT; TORSION
   ANGLES; XPLOR-NIH
AB Microtubules and their associated proteins play important roles in vesicle and organelle transport, cell motility and cell division. Perturbation of these processes by mutation typically gives rise to severe pathological conditions. In our efforts to obtain atomic information on microtubule-associated protein/microtubule interactions with the goal to understand mechanisms that might potentially assist in the development of treatments for these diseases, we have determined the three-dimensional structure of CAP-Gly (cytoskeleton-associated protein, glycine-rich) domain of mammalian dynactin by magic angle spinning NMR spectroscopy. We observe two conformations in the 132 strand encompassing residues T43-V44-A45, residues that are adjacent to the disease-associated mutation, G59S. Upon binding of CAP-Gly to microtubule plus-end tracking protein EB1, the CAP-Gly shifts to a single conformer. We find extensive chemical shift perturbations in several stretches of residues of CAP-Gly upon binding to EB1, from which we define accurately the CAP-Gly/EB1 binding interface. We also observe that the loop regions may exhibit unique flexibility, especially in the GKNDG motif, which participates in the microtubule binding. This study in conjunction with our previous reports suggests that conformational plasticity is an intrinsic property of CAP-Gly likely due to its unusually high loop content and may be required for its biological functions. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Yan, Si; Hou, Guangjin; Polenova, Tatyana] Univ Delaware, Dept Chem & Biochem, Newark, DE 19716 USA.
   [Sehwieters, Charles D.] NIH, Imaging Sci Lab, Ctr Informat Technol, Bethesda, MD 20892 USA.
   [Ahmed, Shubhir; Williams, John C.] City Hope Natl Med Ctr, Beckman Res Inst, Dept Mol Med, Duarte, CA 91010 USA.
RP Polenova, T (reprint author), Univ Delaware, Dept Chem & Biochem, Newark, DE 19716 USA.
EM tpolenov@udel.edu
OI Ahmed, Shubbir/0000-0003-1655-6735
FU NIH (National Institute of General Medical Sciences) [R01GM085396,
   8P30GM103519-03]; NIH (National Center for Research Resources)
   [5P30RR031160-03]; NIH Intramural Research Program of the Center for
   Information Technology; National Science Foundation [CHE0959496]
FX This work was supported by NIH (grants R01GM085396 and 8P30GM103519-03
   from National Institute of General Medical Sciences and grant
   5P30RR031160-03 from National Center for Research Resources). C.D.S. was
   supported by the NIH Intramural Research Program of the Center for
   Information Technology. We acknowledge the support of the National
   Science Foundation (grant CHE0959496) for the acquisition of the 850-MHz
   NMR spectrometer at the University of Delaware.
NR 56
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U1 1
U2 16
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0022-2836
EI 1089-8638
J9 J MOL BIOL
JI J. Mol. Biol.
PD NOV 15
PY 2013
VL 425
IS 22
BP 4249
EP 4266
DI 10.1016/j.jmb.2013.04.027
PG 18
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 267LY
UT WOS:000328100500019
PM 23648839
ER

PT J
AU Lots, IS
   Robinson, SE
   Abeles, M
AF Lots, I. Shapira
   Robinson, S. E.
   Abeles, M.
TI Extracting cortical current dipoles from MEG recordings
SO JOURNAL OF NEUROSCIENCE METHODS
LA English
DT Article
DE MEG; Cortex; Synthetic-aperture-magnetometry; Current-dipoles;
   Evoked-response
ID BEAMFORMERS; EEG
AB A novel way of using synthetic aperture magnetometry to extract local current dipoles is proposed. This method is used to extract the current-dipoles at multiple points in the cortex. It is shown that in this way the correlation between cortical points is lower and falls faster with distance when compared to the original MEG and other methods. Evoked auditory responses are well localized. They show higher signal to noise ratio and are more reproducible then the MEG evoked fields. (C) 2013 Elsevier B.V. All rights reserved.
C1 [Lots, I. Shapira; Abeles, M.] Bar Ilan Univ, Gonda Multidisciplinary Brain Res Ctr, IL-52900 Ramat Gan, Israel.
   [Robinson, S. E.] NIMH, MEG Core Grp, NIH, Bethesda, MD 20892 USA.
   [Abeles, M.] Hebrew Univ Jerusalem, Jerusalem, Israel.
RP Abeles, M (reprint author), Bar Ilan Univ, Gonda Multidisciplinary Brain Res Ctr, IL-52900 Ramat Gan, Israel.
EM Moshe.Abeles@biu.ac.il
FU I-CORE Program of the Planning and Budgeting Committee; Israel Science
   Foundation [51/11]
FX This research was supported in part by the I-CORE Program of the
   Planning and Budgeting Committee and The Israel Science Foundation
   (grant No. 51/11). We thank Dr. Yuval Harpaz for his help in the MEG
   recordings.
NR 11
TC 2
Z9 2
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0270
EI 1872-678X
J9 J NEUROSCI METH
JI J. Neurosci. Methods
PD NOV 15
PY 2013
VL 220
IS 2
SI SI
BP 190
EP 196
DI 10.1016/j.jneumeth.2013.04.024
PG 7
WC Biochemical Research Methods; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 265AJ
UT WOS:000327921800009
ER

PT J
AU Pongpiachan, S
   Tipmanee, D
   Deelaman, W
   Muprasit, J
   Feldens, P
   Schwarzer, K
AF Pongpiachan, S.
   Tipmanee, D.
   Deelaman, W.
   Muprasit, J.
   Feldens, P.
   Schwarzer, K.
TI Risk assessment of the presence of polycyclic aromatic hydrocarbons
   (PAHs) in coastal areas of Thailand affected by the 2004 tsunami
SO MARINE POLLUTION BULLETIN
LA English
DT Article
DE Tsunami; Polycyclic aromatic hydrocarbons (PAHs); Risk assessment; Total
   toxic benzo[a]pyrene equivalent; Soil cleanup target level (SCTL)
ID TRAP MASS-SPECTROMETRY; GAS-CHROMATOGRAPHY; VERTICAL-DISTRIBUTION;
   SEDIMENTS; SOILS; SEA; CONTAMINATION; IMPACTS; BANGKOK; ZONE
AB The total concentrations of twelve, likely carcinogenic, polycyclic aromatic hydrocarbons (PAHs) (i.e., phenanthrene (Phe), anthracene (An), fluoranthene (Fluo), pyrene (Pyr), benz[a]anthracene (B[a]A), chrysene (Chry), benzo[b]fluoranthene (B[b]F), benzo[k]fluoranthene (B[k]F), benzo[a]pyrene (B[a]P), indeno[1,2,3-cd]pyrene (Ind), dibenz[a,h]anthracene (D[a,h]A), and benzolg,h,i]perylene (B[g,h]P) in backwash deposits of the 2004 Khao Lak tsunami were carefully investigated and compared with the concentrations of world marine sediments (WMS). In general, El2PAHs in this study (i.e., 69.43 70.67 ng g(-1)) were considerably lower than those values observed in marine sediments from Boston (54,253 ng g(-1)), coastal sediments from Barcelona Harbour (15,069 ng g-1), and riverine sediment from Guangzhou Channel (12,525 ng g(-1)), but were greater than values from coastal sediments in Rosas Bay (12 ng g(-1)), Santa Ponsa Bay (26 ng g-1) and Le Planier (34 ng g-1). The total toxic benzo[a]pyrene equivalent (TEe") values calculated for Khao Lak coastal sediments (KCS), Khao Lak terrestrial soils (KTS), and Songkhla Lake sediments (SLS) were 10.3 12.2 ng g-1, 16.0 47.7 ng g-1, and 5.67 5.39 ng g-1, respectively. Concentrations of PAHs at all study sites resulted in risk levels that fell into the "acceptable" range of the US EPA model and were much lower than those of other WMS. The cancer risk levels of PAH content in KCS ranged from 7.44 x 10(-8) to 2.90 x 10(-7), with an average of 1.64 x 10(-7) 8.01 x 10(-8); this value is 119 times lower than that of WMS. In addition, soil cleanup target levels (SCTLs) for both non-carcinogens (i.e., Phe, An, Fluo and Pyr) and carcinogens (i.e., B[a]A, Chry, B[b]F, B[k1F, B[a]P, Ind, D[a,h]A and B[g,h,i1P) in the KTS samples were estimated for all target groups, with an average value of 115,902 197,229 ng g-1. Crown Copyright @ 2013 Published by Elsevier Ltd. All rights reserved.
C1 [Pongpiachan, S.] NIDA, NIDA Ctr Res & Dev Disaster Prevent & Management, Sch Social & Environm Dev, Bangkok 10240, Thailand.
   [Tipmanee, D.] Chulalongkorn Univ, Int Postgrad Program Environm Management, Grad Sch, Bangkok, Thailand.
   [Deelaman, W.; Muprasit, J.] Prince Songkla Univ, Fac Environm Management, Hat Yai 90112, Songkla, Thailand.
   [Feldens, P.; Schwarzer, K.] Univ Kiel, Inst Geosci Sedimentol Coastal & Continental Shel, D-24118 Kiel, Germany.
RP Pongpiachan, S (reprint author), NIDA, NIDA Ctr Res & Dev Disaster Prevent & Management, Sch Social & Environm Dev, 118 Moo3,Sereethai Rd, Bangkok 10240, Thailand.
EM pongpiajun@gmail.com
FU National Research Council of Thailand (NRCT)
FX This work was performed with the approval of the National Institute of
   Development Administration (NIDA) and financial support from the
   National Research Council of Thailand (NRCT). The author acknowledges
   Assist. Prof. Dr. Charnwit Kositanont, Ms. Teeta Intasaen and Assist.
   Prof. Dr. Penjai Sompongchaiyakul from Chulalongkorn University for
   their contributions to field sampling and laboratory work.
NR 67
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U1 2
U2 29
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0025-326X
EI 1879-3363
J9 MAR POLLUT BULL
JI Mar. Pollut. Bull.
PD NOV 15
PY 2013
VL 76
IS 1-2
BP 370
EP 378
DI 10.1016/j.marpolbul.2013.07.052
PG 9
WC Environmental Sciences; Marine & Freshwater Biology
SC Environmental Sciences & Ecology; Marine & Freshwater Biology
GA 266EI
UT WOS:000328005800057
PM 23993069
ER

PT J
AU Li, HQ
   Zhong, YW
   Wang, ZF
   Gao, J
   Xu, J
   Chu, WY
   Zhang, JS
   Fang, SY
   Du, SJ
AF Li, Huiqing
   Zhong, Yongwang
   Wang, Zengfeng
   Gao, Jie
   Xu, Jin
   Chu, Wuying
   Zhang, Jianshe
   Fang, Shenyun
   Du, Shao Jun
TI Smyd1b is required for skeletal and cardiac muscle function in zebrafish
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID PROTEIN-QUALITY CONTROL; MYOSIN HEAVY-CHAIN; CAENORHABDITIS-ELEGANS;
   LYSINE-METHYLATION; HISTONE METHYLTRANSFERASE; MYOFIBRIL ORGANIZATION;
   TRANSCRIPTION FACTOR; UNC-45 CHAPERONE; MOUSE CD8B; IN-VIVO
AB Smyd1b is a member of the Smyd family that is specifically expressed in skeletal and cardiac muscles. Smyd1b plays a key role in thick filament assembly during myofibrillogenesis in skeletal muscles of zebrafish embryos. To better characterize Smyd1b function and its mechanism of action in myofibrillogenesis, we analyzed the effects of smyd1b knockdown on myofibrillogenesis in skeletal and cardiac muscles of zebrafish embryos. The results show that knockdown of smyd1b causes significant disruption of myofibril organization in both skeletal and cardiac muscles of zebrafish embryos. Microarray and quantitative reverse transcription-PCR analyses show that knockdown of smyd1b up-regulates heat shock protein 90 (hsp90) and unc45b gene expression. Biochemical analysis reveals that Smyd1b can be coimmunoprecipitated with heat shock protein 90 alpha-1 and Unc45b, two myosin chaperones expressed in muscle cells. Consistent with its potential function in myosin folding and assembly, knockdown of smyd1b significantly reduces myosin protein accumulation without affecting mRNA expression. This likely results from increased myosin degradation involving unc45b overexpression. Together these data support the idea that Smyd1b may work together with myosin chaperones to control myosin folding, degradation, and assembly into sarcomeres during myofibrillogenesis.
C1 [Li, Huiqing; Gao, Jie; Xu, Jin; Du, Shao Jun] Univ Maryland, Sch Med, Dept Biochem & Mol Biol, Baltimore, MD 21202 USA.
   [Zhong, Yongwang; Fang, Shenyun] Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA.
   [Wang, Zengfeng] NCI, Pathol Lab, Bethesda, MD 20892 USA.
   [Chu, Wuying; Zhang, Jianshe] Changsha Univ, Dept Bioengn & Environm Sci, Changsha 410003, Hunan, Peoples R China.
RP Du, SJ (reprint author), Univ Maryland, Sch Med, Dept Biochem & Mol Biol, Baltimore, MD 21202 USA.
EM sdu@som.umaryland.edu
RI Zhong, Yongwang/A-2527-2012; Fang, Shengyun/H-3802-2011; 
OI du, Jim/0000-0001-9227-4153
FU United States-Israel Binational Agricultural Research and Development
   Fund [IS-8713-08]; Maryland Stem Cell Research Fund; Natural Science
   Foundation of China [31230076]
FX This research was supported by research grants from the United
   States-Israel Binational Agricultural Research and Development Fund
   (IS-8713-08), the Maryland Stem Cell Research Fund, and a key research
   project grant from the Natural Science Foundation of China (31230076).
   We thank Vivien Xie and Nick Du for proofreading the manuscript.
NR 56
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U1 0
U2 16
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 NOV 15
PY 2013
VL 24
IS 22
BP 3511
EP 3521
DI 10.1091/mbc.E13-06-0352
PG 11
WC Cell Biology
SC Cell Biology
GA 267UU
UT WOS:000328124600003
PM 24068325
ER

PT J
AU Vanzolini, KL
   Jiang, ZJ
   Zhang, XQ
   Vieira, LCC
   Correa, AG
   Cardoso, CL
   Cass, QB
   Moaddel, R
AF Vanzolini, Kenia Lourenco
   Jiang, Zhengjin
   Zhang, Xiaoqi
   Curcino Vieira, Lucas Campos
   Correa, Arlene Goncalvez
   Cardoso, Carmen Lucia
   Cass, Quezia Bezerra
   Moaddel, Ruin
TI Acetylcholinesterase immobilized capillary reactors coupled to protein
   coated magnetic beads: A new tool for plant extract ligand screening
SO TALANTA
LA English
DT Article
DE Binding affinities; Acetylcholinesterase inhibitor; Non-linear
   chromatography
ID TANDEM MASS-SPECTROMETRY; STATIONARY-PHASE; NONCOMPETITIVE INHIBITORS;
   NATURAL-PRODUCTS; ENZYME REACTOR; IDENTIFICATION; ALKALOIDS
AB The use of immobilized capillary enzyme reactors (ICERs) and enzymes coated to magnetic beads ((NT or CT)-MB) for ligand screening has been adopted as a new technique of high throughput screening (HTS). In this work the selected target was the enzyme acetylcholinesterase (AChE), which acts on the central nervous system and is a validated target for the treatment of Alzheimer's disease, as well as for new insecticides. A new approach for the screening of plant extracts was developed based on the ligand fishing experiments and zonal chromatography. For that, the magnetic beads were used for the ligand fishing experiments and capillary bioreactors for the activity assays. The latter was employed also under non-linear conditions to determine the affinity constants of known ligands, for the first time, as well as for the active fished ligand. Published by Elsevier B.V.
C1 [Vanzolini, Kenia Lourenco; Curcino Vieira, Lucas Campos; Correa, Arlene Goncalvez; Cass, Quezia Bezerra] Univ Fed Sao Carlos, Dept Quim, BR-13565905 Sao Carlos, SP, Brazil.
   [Vanzolini, Kenia Lourenco; Moaddel, Ruin] NIA, Biomed Res Ctr, NIH, Baltimore, MD 21224 USA.
   [Jiang, Zhengjin; Zhang, Xiaoqi; Moaddel, Ruin] Jinan Univ, Dept Pharm, Guangzhou 510632, Guangdong, Peoples R China.
   [Jiang, Zhengjin; Zhang, Xiaoqi; Moaddel, Ruin] Jinan Univ, Guangdong Prov Key Lab Pharmacodynam Constituents, Guangzhou 510632, Guangdong, Peoples R China.
   [Cardoso, Carmen Lucia] Univ Sao Paulo, Fac Filosofia Ciencias & Letras Ribeirao Preto, Dept Quim, BR-14040901 Sao Paulo, SP, Brazil.
RP Moaddel, R (reprint author), NIA, Bioanalyt & Drug Discovery Unit, Lab Clin Invest, NIH, Suite 100,8C232 Biomed Res Ctr,251 Bayview Blvd, Baltimore, MD 21224 USA.
EM moaddelru@grc.nia.nih.gov
RI Cass, Quezia/B-8188-2012; Correa, Arlene/C-1926-2012; CEPID-FAPESP,
   CIBFar/J-2382-2015; Vanzolini, Kenia/B-1370-2013; Cardoso, Carmen
   Lucia/C-4422-2012
OI Cass, Quezia/0000-0002-6550-1194; Correa, Arlene/0000-0003-4247-2228;
   CEPID-FAPESP, CIBFar/0000-0003-2719-0302; Cardoso, Carmen
   Lucia/0000-0001-6239-6651
FU Intramural Research Program of the National Institute of Aging NIH;
   Brazilian Agency for support and Evaluation of Graduate Education
   (CAPES)
FX This research was supported by the Intramural Research Program of the
   National Institute of Aging NIH, by the Brazilian Agency for support and
   Evaluation of Graduate Education (CAPES). The authors also thank the
   National Institute of Science and Technology (INCT), Controle
   Biorracional de Insetos Praga (CBIP), and National Council for
   Scientific and Technological Development (CNPq).
NR 25
TC 15
Z9 15
U1 5
U2 51
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0039-9140
EI 1873-3573
J9 TALANTA
JI Talanta
PD NOV 15
PY 2013
VL 116
BP 647
EP 652
DI 10.1016/j.talanta.2013.07.046
PG 6
WC Chemistry, Analytical
SC Chemistry
GA 268MW
UT WOS:000328176000094
ER

PT J
AU Kobayashi, SD
   Olsen, RJ
   LaCasse, RA
   Safronetz, D
   Ashraf, M
   Porter, AR
   Braughton, KR
   Feldmann, F
   Clifton, DR
   Kash, JC
   Bailey, JR
   Gardner, DJ
   Otto, M
   Brining, DL
   Kreiswirth, BN
   Taubenberger, JK
   Parnell, MJ
   Feldmann, H
   Musser, JM
   DeLeo, FR
AF Kobayashi, Scott D.
   Olsen, Randall J.
   LaCasse, Rachel A.
   Safronetz, David
   Ashraf, Madiha
   Porter, Adeline R.
   Braughton, Kevin R.
   Feldmann, Friederike
   Clifton, Dawn R.
   Kash, John C.
   Bailey, John R.
   Gardner, Donald J.
   Otto, Michael
   Brining, Douglas L.
   Kreiswirth, Barry N.
   Taubenberger, Jeffrey K.
   Parnell, Michael J.
   Feldmann, Heinz
   Musser, James M.
   DeLeo, Frank R.
TI Seasonal H3N2 influenza A virus fails to enhance Staphylococcus aureus
   co-infection in a non-human primate respiratory tract infection model
SO VIRULENCE
LA English
DT Article
DE Staphylococcus aureus; influenza a virus; coinfection; USA300; MRSA;
   pneumonia
ID PANTON-VALENTINE LEUKOCIDIN; COMMUNITY-ACQUIRED PNEUMONIA;
   UNITED-STATES; PANDEMIC INFLUENZA; BACTERIAL COINFECTION; EPIDEMIC;
   PREVALENCE; GENE; MICE; PATHOGENS
AB Staphylococcus aureus community-acquired pneumonia is often associated with influenza or an influenza-like syndrome. Morbidity and mortality due to methicillin-resistant S. aureus (MRSA) or influenza and pneumonia, which includes bacterial co-infection, are among the top causes of death by infectious diseases in the United States. We developed a non-lethal IAV (H3N2)/S. aureus co-infection model in cynomolgus macaques (Macaca fascicularis) to test the hypothesis that seasonal influenza A virus (IAV) infection predisposes non-human primates to severe S. aureus pneumonia. Infection and disease progression were monitored by clinical assessment of animal health; analysis of blood chemistry, nasal swabs, and X-rays; and gross pathology and histopathology of lungs from infected animals. Seasonal IAV infection in healthy cynomolgus macaques caused mild pneumonia, but unexpectedly, did not predispose these animals to subsequent severe infection with the community-associated MRSA clone USA300. We conclude that in our co-infection model, seasonal IAV infection alone is not sufficient to promote severe S. aureus pneumonia in otherwise healthy non-human primates. The implication of these findings is that comorbidity factors in addition to IAV infection are required to predispose individuals to secondary S. aureus pneumonia.
C1 [Kobayashi, Scott D.; Porter, Adeline R.; Braughton, Kevin R.; Otto, Michael; DeLeo, Frank R.] NIAID, Lab Human Bacterial Pathogenesis, Rocky Mt Labs, NIH, Hamilton, MT USA.
   [Olsen, Randall J.; Ashraf, Madiha; Musser, James M.] Methodist Hosp, Ctr Mol & Translat Human Infect Dis Res, Res Inst, Houston, TX 77030 USA.
   [Olsen, Randall J.; Musser, James M.] Methodist Hosp, Dept Pathol & Genom Med, Houston, TX 77030 USA.
   [LaCasse, Rachel A.; Bailey, John R.; Gardner, Donald J.; Brining, Douglas L.; Parnell, Michael J.] NIAID, Vet Branch, Rocky Mt Labs, NIH, Hamilton, MT USA.
   [Safronetz, David; Clifton, Dawn R.; Feldmann, Heinz] NIAID, Virol Lab, Rocky Mt Labs, NIH, Hamilton, MT USA.
   [Ashraf, Madiha] Methodist Hosp, Dept Med, Houston, TX 77030 USA.
   [Feldmann, Friederike] NIAID, Off Operat Management, Rocky Mt Labs, NIH, Hamilton, MT USA.
   [Kash, John C.; Taubenberger, Jeffrey K.] NIAID, Infect Dis Lab, NIH, Hamilton, MT USA.
   [Kreiswirth, Barry N.] Univ Med & Dent New Jersey, Publ Hlth Res Inst, Newark, NJ 07103 USA.
RP DeLeo, FR (reprint author), NIAID, Lab Human Bacterial Pathogenesis, Rocky Mt Labs, NIH, Hamilton, MT USA.
EM fdeleo@niaid.nih.gov
OI DeLeo, Frank/0000-0003-3150-2516; Otto, Michael/0000-0002-2222-4115
FU Intramural Research Program of the National Institute of Allergy and
   Infectious Diseases, National Institutes of Health
FX We thank Anita Mora (NIAID) for performing photography and preparation
   of images for publication, and the staff of the Rocky Mountain
   Veterinary Branch (NIAID) for assistance with basic animal care and
   procedures. This article was supported by the Intramural Research
   Program of the National Institute of Allergy and Infectious Diseases,
   National Institutes of Health.
NR 50
TC 4
Z9 4
U1 0
U2 6
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 2150-5594
EI 2150-5608
J9 VIRULENCE
JI Virulence
PD NOV 15
PY 2013
VL 4
IS 8
BP 707
EP 715
DI 10.4161/viru.26572
PG 9
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 257XK
UT WOS:000327420900009
PM 24104465
ER

PT J
AU Buice, MA
   Chow, CC
AF Buice, Michael A.
   Chow, Carson C.
TI Generalized activity equations for spiking neural network dynamics
SO FRONTIERS IN COMPUTATIONAL NEUROSCIENCE
LA English
DT Article
DE mean field theory; theta model; fokker-planck; correlations; finite size
   networks; wilson-cowan model; population rate; fluctuations
ID MEAN-FIELD ANALYSIS; LARGE-SCALE MODEL; COUPLED OSCILLATORS;
   ASYNCHRONOUS STATES; POPULATION; SYNCHRONY; SYSTEMS; INPUTS
AB Much progress has been made in uncovering the computational capabilities of spiking neural networks. However, spiking neurons will always be more expensive to simulate compared to rate neurons beacause of the inherent disparity in time scales-the spike duration time is much shorter than the inter-spike time, which is much shorter than any learning time scale. In numerical analysis, this is a classic stiff problem. Spiking neurons are also much more difficult to study analytically. One possible approach to making spiking networks more tractable is to augment mean field activity models with some information about spiking correlations. For example, such a generalized activity model could carry information about spiking rates and correlations between spikes self-consistently. Here, we will show how this can be accomplished by constructing a complete formal probabilistic description of the network and then expanding around a small parameter such as the inverse of the number of neurons in the network. The mean field theory of the system gives a rate-like description. The first order terms in the perturbation expansion keep track of covariances.
C1 [Buice, Michael A.] Allen Inst Brain Sci, Modeling Anal & Theory Team, Seattle, WA USA.
   [Chow, Carson C.] NIDDK, Lab Biol Modeling, NIH, Bethesda, MD 20814 USA.
RP Chow, CC (reprint author), NIDDK, Lab Biol Modeling, NIH, Bldg 12A Room 4007,12 South Dr, Bethesda, MD 20814 USA.
EM carsonc@mail.nih.gov
FU Intramural Research Program of the NIH, NIDDK
FX This work was supported by the Intramural Research Program of the NIH,
   NIDDK.
NR 35
TC 4
Z9 4
U1 1
U2 5
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5188
J9 FRONT COMPUT NEUROSC
JI Front. Comput. Neurosci.
PD NOV 15
PY 2013
VL 7
AR UNSP 162
DI 10.3389/fncom.2013.00162
PG 10
WC Mathematical & Computational Biology; Neurosciences
SC Mathematical & Computational Biology; Neurosciences & Neurology
GA 263OR
UT WOS:000327818400001
PM 24298252
ER

PT J
AU Kendzia, B
   Behrens, T
   Jockel, KH
   Siemiatycki, J
   Kromhout, H
   Vermeulen, R
   Peters, S
   Van Gelder, R
   Olsson, A
   Bruske, I
   Wichmann, HE
   Stucker, I
   Guida, F
   Tardon, A
   Merletti, F
   Mirabelli, D
   Richiardi, L
   Pohlabeln, H
   Ahrens, W
   Landi, MT
   Caporaso, N
   Consonni, D
   Zaridze, D
   Szeszenia-Dabrowska, N
   Lissowska, J
   Gustavsson, P
   Marcus, M
   Fabianova, E
   't Mannetje, A
   Pearce, N
   Tse, LA
   Yu, ITS
   Rudnai, P
   Bencko, V
   Janout, V
   Mates, D
   Foretova, L
   Forastiere, F
   McLaughlin, J
   Demers, P
   Bueno-de-Mesquita, B
   Boffetta, P
   Schuz, J
   Straif, K
   Pesch, B
   Bruning, T
AF Kendzia, Benjamin
   Behrens, Thomas
   Joeckel, Karl-Heinz
   Siemiatycki, Jack
   Kromhout, Hans
   Vermeulen, Roel
   Peters, Susan
   Van Gelder, Rainer
   Olsson, Ann
   Brueske, Irene
   Wichmann, H. -Erich
   Stuecker, Isabelle
   Guida, Florence
   Tardon, Adonina
   Merletti, Franco
   Mirabelli, Dario
   Richiardi, Lorenzo
   Pohlabeln, Hermann
   Ahrens, Wolfgang
   Landi, Maria Teresa
   Caporaso, Neil
   Consonni, Dario
   Zaridze, David
   Szeszenia-Dabrowska, Neonila
   Lissowska, Jolanta
   Gustavsson, Per
   Marcus, Michael
   Fabianova, Eleonora
   't Mannetje, Andrea
   Pearce, Neil
   Tse, Lap Ah
   Yu, Ignatius Tak-sun
   Rudnai, Peter
   Bencko, Vladimir
   Janout, Vladimir
   Mates, Dana
   Foretova, Lenka
   Forastiere, Francesco
   McLaughlin, John
   Demers, Paul
   Bueno-de-Mesquita, Bas
   Boffetta, Paolo
   Schuez, Joachim
   Straif, Kurt
   Pesch, Beate
   Bruening, Thomas
TI Welding and Lung Cancer in a Pooled Analysis of Case-Control Studies
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE case-control studies; lung cancer; occupational exposure; welding
ID DNA-REPAIR GENES; CASE-REFERENT; RISK-FACTORS; POPULATION; EXPOSURE;
   OCCUPATION; MEN; POLYMORPHISMS; MESOTHELIOMA; GERMANY
AB Several epidemiologic studies have indicated an increased risk of lung cancer among welders. We used the SYNERGY project database to assess welding as a risk factor for developing lung cancer. The database includes data on 15,483 male lung cancer cases and 18,388 male controls from 16 studies in Europe, Canada, China, and New Zealand conducted between 1985 and 2010. Odds ratios and 95 confidence intervals between regular or occasional welding and lung cancer were estimated, with adjustment for smoking, age, study center, and employment in other occupations associated with lung cancer risk. Overall, 568 cases and 427 controls had ever worked as welders and had an odds ratio of developing lung cancer of 1.44 (95 confidence interval: 1.25, 1.67) with the odds ratio increasing for longer duration of welding. In never and light smokers, the odds ratio was 1.96 (95 confidence interval: 1.37, 2.79). The odds ratios were somewhat higher for squamous and small cell lung cancers than for adenocarcinoma. Another 1,994 cases and 1,930 controls had ever worked in occupations with occasional welding. Work in any of these occupations was associated with some elevation of risk, though not as much as observed in regular welders. Our findings lend further support to the hypothesis that welding is associated with an increased risk of lung cancer.
C1 [Kendzia, Benjamin; Behrens, Thomas; Pearce, Neil; Bruening, Thomas] Ruhr Univ Bochum IPA, Inst Prevent & Occupat Med, German Social Accid Insurance Inst, D-44789 Bochum, Germany.
   [Joeckel, Karl-Heinz] Univ Hosp Essen, Inst Med Informat Biometry & Epidemiol, Essen, Germany.
   [Siemiatycki, Jack] Univ Montreal Hosp Res Ctr, Montreal, PQ, Canada.
   [Siemiatycki, Jack] Sch Publ Hlth, Montreal, PQ, Canada.
   [Kromhout, Hans; Vermeulen, Roel; Peters, Susan] Univ Utrecht, Environm Epidemiol Div, Inst Risk Assessment Sci, Utrecht, Netherlands.
   [Peters, Susan] Univ Western Australia, Western Australian Inst Med Res, Perth, WA 6009, Australia.
   [Van Gelder, Rainer] German Social Accid Insurance, Inst Occupat Safety & Hlth, St Augustin, Germany.
   [Olsson, Ann; Schuez, Joachim; Straif, Kurt] Int Agcy Res Canc, F-69372 Lyon, France.
   [Olsson, Ann; Gustavsson, Per] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden.
   [Brueske, Irene; Wichmann, H. -Erich] Helmholtz Ctr Munich, Inst Epidemiol 1, Neuherberg, Germany.
   [Stuecker, Isabelle; Guida, Florence] INSERM, Ctr Res Epidemiol & Populat Hlth, Environm Epidemiol Canc Team, Villejuif, France.
   [Tardon, Adonina] Univ Oviedo, Mol Epidemiol Canc Unit, Univ Inst Oncol, Oviedo, Spain.
   [Merletti, Franco; Mirabelli, Dario; Richiardi, Lorenzo] CPO Piemonte, Canc Epidemiol Unit, Turin, Italy.
   [Merletti, Franco; Mirabelli, Dario; Richiardi, Lorenzo] Univ Turin, Turin, Italy.
   [Pohlabeln, Hermann; Ahrens, Wolfgang] Leibniz Inst Prevent Res & Epidemiol, Bremen, Germany.
   [Ahrens, Wolfgang] Univ Bremen, Inst Stat, D-28359 Bremen, Germany.
   [Landi, Maria Teresa; Caporaso, Neil] NCI, Bethesda, MD 20892 USA.
   [Consonni, Dario] Osped Maggiore Policlin, Epidemiol Unit, Fdn Ist Ricovero & Cura Carattere Sci CaGranda, Milan, Italy.
   [Zaridze, David] Russian Acad Med Sci, Canc Res Ctr, Inst Carcinogenesis, Moscow, Russia.
   [Szeszenia-Dabrowska, Neonila] Nofer Inst Occupat Med, Lodz, Poland.
   [Lissowska, Jolanta] M Sklodowska Curie Canc Ctr & Inst Oncol, Warsaw, Poland.
   [Marcus, Michael] Univ Liverpool, Roy Castle Lung Canc Res Programme, Canc Res Ctr, Liverpool L69 3BX, Merseyside, England.
   [Fabianova, Eleonora] Reg Author Publ Hlth, Banska Bystric, Slovakia.
   ['t Mannetje, Andrea; Pearce, Neil] Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand.
   [Tse, Lap Ah; Yu, Ignatius Tak-sun] Chinese Univ Hong Kong, Sch Publ Hlth & Primary Care, Hong Kong, Hong Kong, Peoples R China.
   [Rudnai, Peter] Natl Inst Environm Hlth, Budapest, Hungary.
   [Bencko, Vladimir] Charles Univ Prague, Inst Hyg & Epidemiol, Prague, Czech Republic.
   [Janout, Vladimir] Palacky Univ, CR-77147 Olomouc, Czech Republic.
   [Mates, Dana] Natl Inst Publ Hlth, Bucharest, Romania.
   [Foretova, Lenka] Masaryk Mem Canc Inst, Brno, Czech Republic.
   [Forastiere, Francesco] Asl Roma E, Dept Epidemiol, Rome, Italy.
   [McLaughlin, John; Demers, Paul] Occupat Canc Res Ctr, Toronto, ON, Canada.
   [Bueno-de-Mesquita, Bas] Natl Inst Publ Hlth & Environm Protect, NL-3720 BA Bilthoven, Netherlands.
   [Boffetta, Paolo] Mt Sinai Sch Med, Tisch Canc Inst, New York, NY USA.
   [Boffetta, Paolo] Int Prevent Res Inst, Lyon, France.
RP Pesch, B (reprint author), Ruhr Univ Bochum IPA, Inst Prevent & Occupat Med, German Social Accid Insurance Inst, Burkle de la Camp Pl 1, D-44789 Bochum, Germany.
EM pesch@ipa-dguv.de
RI Bruske, Irene/N-3125-2013; Yu, Ignatius Tak Sun/A-9936-2008; Janout,
   Vladimir/M-5133-2014; Szeszenia-Dabrowska, Neonila/F-7190-2010; Bruning,
   Thomas/G-8120-2015; Forastiere, Francesco/J-9067-2016; Consonni,
   Dario/K-7943-2016; Vermeulen, Roel/F-8037-2011; 
OI richiardi, lorenzo/0000-0003-0316-9402; Ahrens,
   Wolfgang/0000-0003-3777-570X; Bruning, Thomas/0000-0001-9560-5464;
   Forastiere, Francesco/0000-0002-9162-5684; Consonni,
   Dario/0000-0002-8935-3843; Vermeulen, Roel/0000-0003-4082-8163; Peters,
   Susan/0000-0001-5662-1971; Pearce, Neil/0000-0002-9938-7852; mates,
   dana/0000-0002-6219-9807
FU German Social Accident Insurance [FP 271]; Canadian Institutes for
   Health Research; Guzzo-SRC Chair in Environment and Cancer; National
   Cancer Institute of Canada; Canadian Cancer Society; Workplace Safety
   and Insurance Board; Cancer Care Ontario; French Agency of Health
   Security; Fondation de France; French National Research Agency; National
   Institute of Cancer; Foundation for Medical Research; French Institute
   for Public Health Surveillance; Health Ministry; Organization for the
   Research on Cancer; French Ministry of Work, Solidarity, and Public
   Function; Federal Ministry of Education, Science, Research, and
   Technology [01 HK 173/0]; Federal Ministry of Science [01 HK 546/8];
   Ministry of Labour and Social Affairs [IIIb7-27/13]; Associazione
   Italiana per la Ricerca sul Cancro
FX This work was supported by the German Social Accident Insurance (grant
   FP 271). The Montreal case-control study of environmental causes of lung
   cancer was supported by the Canadian Institutes for Health Research and
   Guzzo-SRC Chair in Environment and Cancer. The Toronto lung cancer
   case-control study was funded by the National Cancer Institute of Canada
   with funds provided by the Canadian Cancer Society, and the occupational
   analysis was conducted by the Occupational Cancer Research Centre, which
   was supported by the Workplace Safety and Insurance Board, the Canadian
   Cancer Society, and Cancer Care Ontario. The Investigations Cancers
   Respiratoires et Environnement Study was supported by the French Agency
   of Health Security; the Fondation de France; the French National
   Research Agency; the National Institute of Cancer; the Foundation for
   Medical Research; the French Institute for Public Health Surveillance;
   the Health Ministry; the Organization for the Research on Cancer; and
   the French Ministry of Work, Solidarity, and Public Function. The Lung
   Cancer in France Study was supported by the Fondation de France. The
   lung cancer study in Paris was funded by Organization for the Research
   on Cancer. The Arbeit und Technik Study in Germany was funded by the
   Federal Ministry of Education, Science, Research, and Technology (grant
   01 HK 173/0). The Humanisierung des Arbeitslebens Study was funded by
   the Federal Ministry of Science (grant 01 HK 546/8) and the Ministry of
   Labour and Social Affairs (grant IIIb7-27/13). The INCO Copernicus Study
   was supported by a grant from the European Commission's INCO-COPERNICUS
   program (contract IC15-CT96-0313). The INCO-Poland study was supported
   by the Polish State Committee for Scientific Research (grant
   SPUB-M-COPERNICUS/P-05/DZ-30/99/2000). In Liverpool, the work was funded
   by the Roy Castle Foundation as part of the Liverpool Lung Project. The
   Environment and Genetics in Lung Cancer Etiology Study was funded by the
   Intramural Research Program of the National Institutes of Health,
   National Cancer Institute, Division of Cancer Epidemiology and Genetics,
   Bethesda, Maryland (grants U01DA020830 and RC2DA028793); the
   Environmental Epidemiology Program of the Lombardy region of Italy; and
   the Istituto Nazionale per l'Assicurazione Contro gli Infortuni sul
   Lavoro, Rome, Italy. The case-control study of lung cancer in Turin,
   Italy, and the Veneto region of Italy was supported by the Italian
   Association for Cancer Research, Piedmont region, Compagnia di San
   Paolo, Italy. The Rome lung cancer case-control study was conducted with
   partial support from the European Union Nuclear Fission Safety Program
   (grant F14P-CT96-0055) and from the administrative region of Lazio. The
   Monitoring van Risicofactoren en Gezondheid in Nederland study was
   supported by the Dutch Ministry of Health, Welfare, and Sports, National
   Institute of Public Health and the Environment, and the Europe Against
   Cancer Program. The Cancer de Pulmon en Asturias Study was supported by
   the Instituto Universitario de Oncologia, Universidad de Oviedo,
   Asturias, the Fondo de Investigacion Sanitaria, and the Ciber de
   Epidemiologia y Salud Publica, Spain. The Lung Cancer in Stockholm Study
   was supported by the Swedish Council for Work Life Research and the
   Swedish Environmental Protection Agency. The Male Lung Cancer,
   Occupational Exposures, and Smoking Study in Hong Kong was supported by
   a grant from the Research Grants Council of the Hong Kong Special
   Administrative Region, Hong Kong, China (project CUHK4460/03M).; The
   Occupational Cancer in New Zealand Study was funded by the Health
   Research Council of New Zealand, the New Zealand Department of Labour,
   Lottery Health Research, and the Cancer Society of New Zealand.
NR 40
TC 11
Z9 12
U1 3
U2 25
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 NOV 15
PY 2013
VL 178
IS 10
BP 1513
EP 1525
DI 10.1093/aje/kwt201
PG 13
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 257PG
UT WOS:000327396800001
PM 24052544
ER

PT J
AU Lobbestael, E
   Zhao, J
   Rudenko, LN
   Beylina, A
   Gao, FY
   Wetter, J
   Beullens, M
   Bollen, M
   Cookson, MR
   Baekelandt, V
   Nichols, RJ
   Taymans, JM
AF Lobbestael, Evy
   Zhao, Jing
   Rudenko, Lakov N.
   Beylina, Aleksandra
   Gao, Fangye
   Wetter, Justin
   Beullens, Monique
   Bollen, Mathieu
   Cookson, Mark R.
   Baekelandt, Veerle
   Nichols, R. Jeremy
   Taymans, Jean-Marc
TI Identification of protein phosphatase 1 as a regulator of the LRRK2
   phosphorylation cycle
SO BIOCHEMICAL JOURNAL
LA English
DT Article
DE leucine-rich repeat kinase 2 (LRRK2); protein phosphatase 1 (PP1);
   Parkinson's disease; phosphorylation; phosphatase inhibition; skein-like
   structure
ID DISEASE-ASSOCIATED MUTATIONS; PARKINSONS-DISEASE; KINASE-ACTIVITY;
   GTP-BINDING; SERINE/THREONINE PHOSPHATASES; CYTOPLASMIC LOCALIZATION;
   ASSOCIATION; INHIBITION; VARIANTS; GENETICS
AB A cluster of phosphorylation sites in LRRK2 (leucine-rich repeat kinase 2), including Ser(910), Ser(935), Ser(955) and Ser(973), is important for PD (Parkinson's disease) pathogenesis as several PD-linked LRRK2 mutants are dephosphorylated at these sites. LRRK2 is also dephosphorylated in cells after pharmacological inhibition of its kinase activity, which is currently proposed as a strategy for disease-modifying PD therapy. Despite this importance of LRRK2 dephosphorylation in mutant LRRK2 pathological mechanism(s) and in LRRK2's response to inhibition, the mechanism by which this occurs is unknown. Therefore we aimed to identify the phosphatase for LRRK2. Using a panel of recombinant phosphatases, we found that PP1 (protein phosphatase 1) efficiently dephosphorylates LRRK2 in vitro. PP1 activity on LRRK2 dephosphorylation was confirmed in cells using PP1 inhibition to reverse LRRK2 dephosphorylation induced by the potent LRRK2 kinase inhibitor LRRK2-IN1 as well as in R1441G mutant LRRK2. We also found that PP1 and LRRK2 can form a complex in cells. Furthermore, we observed that PP1 inhibition modulates LRRK2's cellular phenotype by reducing skein-like LRRK2-positive structures associated with dephosphorylation. In conclusion, the present study reveals PP1 as the physiological LRRK2 phosphatase, responsible for LRRK2 dephosphorylation observed in PD mutant LRRK2 and after LRRK2 kinase inhibition.
C1 [Lobbestael, Evy; Gao, Fangye; Baekelandt, Veerle; Taymans, Jean-Marc] Katholieke Univ Leuven, Lab Neurobiol & Gene Therapy, Dept Neurosci, B-3000 Louvain, Belgium.
   [Zhao, Jing; Nichols, R. Jeremy] Parkinsons Inst, Sunnyvale, CA 94085 USA.
   [Rudenko, Lakov N.; Beylina, Aleksandra; Cookson, Mark R.] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
   [Wetter, Justin] Life Technol Corp, Primary & Stem Cell Syst, Madison, WI 53719 USA.
   [Beullens, Monique; Bollen, Mathieu] Katholieke Univ Leuven, Lab Biosignaling & Therapeut, Dept Cellular & Mol Med, B-3000 Louvain, Belgium.
RP Nichols, RJ (reprint author), Parkinsons Inst, 675 Almanor Ave, Sunnyvale, CA 94085 USA.
EM jnichols@parkinsonsinstitute.org; jean-marc.taymans@med.kuleuven.be
RI Zhao, Jing/C-7359-2016; 
OI Zhao, Jing/0000-0002-8575-8181; Taymans, Jean-Marc/0000-0001-5503-5524
FU Michael J. Fox Foundation; FWO (Research Foundation -
   Flanders)-Vlaanderen FWO project [G.0666.09]; IWT (Agency for Innovation
   by Science and Technology) [SBO/80020]; KU Leuven [OT/08/052A,
   IOF-KP/07/001]; Intramural Research Program of the National Institutes
   of Health, National Institute on Aging; benevolence of the Brin/Wojcicki
   foundation
FX This study was supported by the Michael J. Fox Foundation (to J.-M.T.,
   V.B. and R.J.N.). We thank the FWO (Research Foundation -
   Flanders)-Vlaanderen FWO project [number G.0666.09 (to VB.)] and
   fellowships to E.L. and J.M.T., the IWT (Agency for Innovation by
   Science and Technology) SBO/80020 project Neuro-TARGET to VB, and the KU
   Leuven [grant numbers OT/08/052A and IOF-KP/07/001 (to VB.)] for their
   support. This research was also supported in part by the Intramural
   Research Program of the National Institutes of Health, National
   Institute on Aging (to M.R.C.). This research was also supported in part
   by the benevolence of the Brin/Wojcicki foundation (to R.J.N.) and the
   Fund Druwe-Eerdekens managed by the King Baudouin Foundation (to J.-M
   T.).
NR 47
TC 25
Z9 25
U1 0
U2 6
PU PORTLAND PRESS LTD
PI LONDON
PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND
SN 0264-6021
J9 BIOCHEM J
JI Biochem. J.
PD NOV 15
PY 2013
VL 456
BP 119
EP 128
DI 10.1042/BJ20121772
PN 1
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 260BZ
UT WOS:000327571300012
PM 23937259
ER

PT J
AU Zhang, B
   Davidson, MM
   Zhou, HN
   Wang, CX
   Walker, WF
   Hei, TK
AF Zhang, Bo
   Davidson, Mercy M.
   Zhou, Hongning
   Wang, Chunxin
   Walker, Winsome F.
   Hei, Tom K.
TI Cytoplasmic Irradiation Results in Mitochondrial Dysfunction and
   DRP1-Dependent Mitochondrial Fission
SO CANCER RESEARCH
LA English
DT Article
ID DYNAMIN-RELATED PROTEIN-1; GENOMIC INSTABILITY; IONIZING-RADIATION;
   ALZHEIMERS-DISEASE; FUSION PROTEINS; DNA-DAMAGE; CELLS; DRP1;
   BIOGENESIS; METABOLISM
AB Direct DNA damage is often considered the primary cause of cancer in patients exposed to ionizing radiation or environmental carcinogens. Although mitochondria are known to play an important role in radiation-induced cellular response, the mechanisms by which cytoplasmic stimuli modulate mitochondrial dynamics and functions are largely unknown. In the present study, we examined changes in mitochondrial dynamics and functions triggered by a particle damage to the mitochondria in human small airway epithelial cells, using a precision microbeam irradiator with a beam width of 1 mm. Targeted cytoplasmic irradiation using this device resulted in mitochondrial fragmentation and a reduction of cytochrome c oxidase and succinate dehydrogenase activity, when compared with nonirradiated controls, suggesting a reduction in respiratory chain function. In addition, mitochondrial fragmentation or fission was associated with increased expression of the dynamin-like protein DRP1, which promotes mitochondrial fission. DRP1 inhibition by the drug mdivi-1 prevented radiation-induced mitochondrial fission, but respiratory chain function in mitochondria inhibited by radiation persisted for 12 hours. Irradiated cells also showed an increase in mitochondria-derived superoxide that could be quenched by dimethyl sulfoxide. Taken together, our results provide a mechanistic explanation for the extranuclear, nontargeted effects of ionizing radiation. (C) 2013 AACR.
C1 [Zhang, Bo; Zhou, Hongning; Hei, Tom K.] Columbia Univ, Coll Phys & Surg, Ctr Radiol Res, New York, NY 10032 USA.
   [Davidson, Mercy M.; Walker, Winsome F.] Columbia Univ, Dept Radiat Oncol, New York, NY 10032 USA.
   [Wang, Chunxin] NINDS, Biochem Sect, NIH, Bethesda, MD 20892 USA.
RP Hei, TK (reprint author), Columbia Univ, Coll Phys & Surg, Ctr Radiol Res, 630 West 168th St,VC 11-205-218, New York, NY 10032 USA.
EM tkh1@columbia.edu
RI Wang, Chunxin/B-9312-2016
OI Wang, Chunxin/0000-0001-6015-6806
FU NIH [5P01-CA49062-20, 5P01-CA49062-22, R01-ES 12888-06, 5R01-ES
   12888-07, EB-002033]; National Institute of Neurological Diseases and
   Stroke, NIH
FX This research was supported by the NIH grants 5P01-CA49062-20,
   5P01-CA49062-22, R01-ES 12888-06, and 5R01-ES 12888-07. The Radiological
   Research Accelerator Facilities is an NIH sponsored Resource Center
   through grant EB-002033 (National Institute of Biomedical Imaging and
   Bioengineering). C. Wang is supported in part by the Intramural Research
   Program of the National Institute of Neurological Diseases and Stroke,
   NIH.
NR 46
TC 19
Z9 21
U1 1
U2 12
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD NOV 15
PY 2013
VL 73
IS 22
BP 6700
EP 6710
DI 10.1158/0008-5472.CAN-13-1411
PG 11
WC Oncology
SC Oncology
GA 256NY
UT WOS:000327321700016
PM 24080278
ER

PT J
AU Liu, FF
   Okunieff, P
   Bernhard, EJ
   Stone, HB
   Yoo, S
   Coleman, CN
   Vikram, B
   Brown, M
   Buatti, J
   Guha, C
AF Liu, Fei-Fei
   Okunieff, Paul
   Bernhard, Eric J.
   Stone, Helen B.
   Yoo, Stephen
   Coleman, C. Norman
   Vikram, Bhadrasain
   Brown, Martin
   Buatti, John
   Guha, Chandan
CA Workshop Participants
TI Lessons Learned from Radiation Oncology Clinical Trials
SO CLINICAL CANCER RESEARCH
LA English
DT Review
ID GROWTH-FACTOR RECEPTOR; PHASE-III TRIAL; SQUAMOUS-CELL CARCINOMA;
   LOCALLY ADVANCED HEAD; LUNG-CANCER; NECK-CANCER; QUALITY-ASSURANCE;
   ANDROGEN SUPPRESSION; PROSTATE-CANCER; STK33 KINASE
AB A workshop entitled "Lessons Learned from Radiation Oncology Trials" was held on December 7-8, 2011, in Bethesda, MD, to present and discuss some of the recently conducted radiation oncology clinical trials with a focus on those that failed to refute the null hypothesis. The objectives of this workshop were to summarize and examine the questions that these trials provoked, to assess the quality and limitations of the preclinical data that supported the hypotheses underlying these trials, and to consider possible solutions to these challenges for the design of future clinical trials. Several themes emerged from the discussions: (i) opportunities to learn from null-hypothesis trials through tissue and imaging studies; (ii) value of preclinical data supporting the design of combinatorial therapies; (iii) significance of validated biomarkers; (iv) necessity of quality assurance in radiotherapy delivery; (v) conduct of sufficiently powered studies to address the central hypotheses; and (vi) importance of publishing results of the trials regardless of the outcome. The fact that well-designed hypothesis-driven clinical trials produce null or negative results is expected given the limitations of trial design and complexities of cancer biology. It is important to understand the reasons underlying such null results, however, to effectively merge the technologic innovations with the rapidly evolving biology for maximal patient benefit through the design of future clinical trials. (C) 2013 AACR.
C1 [Liu, Fei-Fei] Princess Margaret Canc Ctr, Dept Radiat Oncol, Toronto, ON M5G 2M9, Canada.
   [Okunieff, Paul] Univ Florida, Shands Canc Ctr, Dept Radiat Oncol, Gainesville, FL USA.
   [Bernhard, Eric J.; Stone, Helen B.; Coleman, C. Norman] NCI, Radiat Res Program, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
   [Yoo, Stephen] NCI, Mol Radiat Therapeut Branch, Div Canc Treatment & Diag, Rockville, MD 20852 USA.
   [Vikram, Bhadrasain] NCI, Clin Radiat Oncol Branch, Rockville, MD 20852 USA.
   [Brown, Martin] Stanford Univ, Dept Radiat Oncol, Palo Alto, CA 94304 USA.
   [Buatti, John] Univ Iowa Hosp & Clin, Dept Radiat Oncol, Iowa City, IA 52242 USA.
   [Guha, Chandan] Albert Einstein Coll Med, Dept Radiat Oncol, Bronx, NY 10467 USA.
   [Guha, Chandan] Montefiore Med Ctr, Bronx, NY 10467 USA.
RP Liu, FF (reprint author), Princess Margaret Canc Ctr, Dept Radiat Oncol, 610 Univ Ave, Toronto, ON M5G 2M9, Canada.
EM Fei-Fei.Liu@rmp.uhn.on.ca; vikramb@mail.nih.gov; cguha@montefiore.org
OI Spence, Tara/0000-0001-7098-4103
FU NCI
FX This work has been supported by funds from the NCI.
NR 80
TC 10
Z9 10
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 NOV 15
PY 2013
VL 19
IS 22
BP 6089
EP 6100
DI 10.1158/1078-0432.CCR-13-1116
PG 12
WC Oncology
SC Oncology
GA 256NU
UT WOS:000327320900006
PM 24043463
ER

PT J
AU Ardiani, A
   Farsaci, B
   Rogers, CJ
   Protter, A
   Guo, ZM
   King, TH
   Apelian, D
   Hodge, JW
AF Ardiani, Andressa
   Farsaci, Benedetto
   Rogers, Connie J.
   Protter, Andy
   Guo, Zhimin
   King, Thomas H.
   Apelian, David
   Hodge, James W.
TI Combination Therapy with a Second-Generation Androgen Receptor
   Antagonist and a Metastasis Vaccine Improves Survival in a Spontaneous
   Prostate Cancer Model
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID REARRANGEMENT EXCISION CIRCLES; RAT VENTRAL PROSTATE; T-CELLS; ANTITUMOR
   RESPONSES; TRANSGENIC MOUSE; TWIST EXPRESSION; IMMUNE-RESPONSE;
   DENDRITIC CELLS; ANTIGEN CASCADE; CASTRATION
AB Purpose: Enzalutamide, a second-generation androgen antagonist, was approved by the U. S. Food and Drug Administration (FDA) for castration-resistant prostate cancer (CRPC) treatment. Immunotherapy has been shown to be a promising strategy for prostate cancer. This study was performed to provide data to support the combination of enzalutamide and immunotherapy for CRPC treatment.
   Experimental Design: Male C57BL/6 or TRAMP (transgenic adenocarcinoma of the mouse prostate) prostate cancer model mice were exposed to enzalutamide and/or a therapeutic vaccine targeting Twist, an antigen involved in epithelial-to-mesenchymal transition and metastasis. The physiologic and immunologic effects of enzalutamide were characterized. The generation of Twist-specific immunity by Twist-vaccine was assessed. Finally, the combination of enzalutamide and Twist-vaccine to improve TRAMP mice overall survival was evaluated.
   Results: Enzalutamide mediated immunogenic modulation in TRAMP-C2 cells. In vivo, enzalutamide mediated reduced genitourinary tissue weight, enlargement of the thymus, and increased levels of T-cell excision circles. Because no changes were seen in T-cell function, as determined by CD4(+)T-cell proliferation and regulatory T cell (Treg) functional assays, enzalutamide was determined to be immune inert. Enzalutamide did not diminish the ability of Twist-vaccine to generate Twist-specific immunity. Twist was confirmed as a valid tumor antigen in TRAMP mice by immunohistochemistry. The combination of enzalutamide and Twist-vaccine resulted in significantly increased overall survival of TRAMP mice compared with other treatment groups (27.5 vs. 10.3 weeks). Notably, the effectiveness of the combination therapy increased with disease stage, i.e., the greatest survival benefit was seen in mice with advanced-stage prostate tumors.
   Conclusions: These data support the combination of enzalutamide and immunotherapy as a promising treatment strategy for CRPC. (C) 2013 AACR.
C1 [Ardiani, Andressa; Farsaci, Benedetto; Rogers, Connie J.; Hodge, James W.] NCI, Lab Tumor Immunol & Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Protter, Andy] Medivation Inc, San Francisco, CA USA.
   [Guo, Zhimin; King, Thomas H.; Apelian, David] GlobeImmune Inc, Louisville, CO USA.
RP Hodge, JW (reprint author), NCI, NIH, 9000 Rockville Pike,10 Ctr Dr,Room 8B13,MSC 1750, Bethesda, MD 20892 USA.
EM jh241d@nih.gov
RI Farsaci, Benedetto/L-9837-2014; Hodge, James/D-5518-2015
OI Farsaci, Benedetto/0000-0001-8275-2561; Hodge, James/0000-0001-5282-3154
FU Intramural Research Program of the Center for Cancer Research, National
   Cancer Institute, NIH; GlobeImmune, Inc.; National Cancer Institute
FX This research was supported by the Intramural Research Program of the
   Center for Cancer Research, National Cancer Institute, NIH, and a
   Cooperative Research and Development Agreement between GlobeImmune,
   Inc., and the National Cancer Institute.
NR 45
TC 23
Z9 23
U1 0
U2 9
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 NOV 15
PY 2013
VL 19
IS 22
BP 6205
EP 6218
DI 10.1158/1078-0432.CCR-13-1026
PG 14
WC Oncology
SC Oncology
GA 256NU
UT WOS:000327320900016
PM 24048332
ER

PT J
AU Gajjar, A
   Stewart, CF
   Ellison, DW
   Kaste, S
   Kun, LE
   Packer, RJ
   Goldman, S
   Chintagumpala, M
   Wallace, D
   Takebe, N
   Boyett, JM
   Gilbertson, RJ
   Curran, T
AF Gajjar, Amar
   Stewart, Clinton F.
   Ellison, David W.
   Kaste, Sue
   Kun, Larry E.
   Packer, Roger J.
   Goldman, Stewart
   Chintagumpala, Murali
   Wallace, Dana
   Takebe, Naoko
   Boyett, James M.
   Gilbertson, Richard J.
   Curran, Tom
TI Phase I Study of Vismodegib in Children with Recurrent or Refractory
   Medulloblastoma: A Pediatric Brain Tumor Consortium Study
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID HEDGEHOG PATHWAY INHIBITOR; MOLECULE KINASE INHIBITORS; BASAL-CELL
   CARCINOMA; TARGETING CANCER; GDC-0449; MICE; CHILDHOOD; MUTATIONS;
   SUBGROUPS
AB Purpose: To investigate the safety, dose-limiting toxicities, and pharmacokinetics of the smoothened inhibitor vismodegib in children with refractory or relapsed medulloblastoma.
   Experimental design: Initially, vismodegib was administered daily at 85 mg/m(2) and escalated to 170 mg/m(2). The study was then revised to investigate a flat-dosing schedule of 150 mg for patients with small body surface area (BSA, 0.67-1.32 m(2)) or 300 mg for those who were larger (BSA, 1.33-2.20 m(2)). Pharmacokinetics were performed during the first course of therapy, and the right knees of all patients were imaged to monitor bone toxicity. Immunohistochemical analysis was done to identify patients with Sonic Hedgehog (SHH)-subtype medulloblastoma.
   Results: Thirteen eligible patients were enrolled in the initial study: 6 received 85 mg/m(2) vismodegib, and 7 received 170 mg/m(2). Twenty eligible patients were enrolled in the flat-dosing part of the study: 10 at each dosage level. Three dose-limiting toxicities were observed, but no drug-related bone toxicity was documented. The median (range) vismodegib penetration in the cerebrospinal fluid (CSF) was 0.53 (0.26-0.78), when expressed as a ratio of the concentration of vismodegib in the CSF to that of the unbound drug in plasma. Antitumor activity was seen in 1 of 3 patients with SHH-subtype disease whose tumors were evaluable, and in none of the patients in the other subgroups.
   Conclusions: Vismodegib was well tolerated in children with recurrent or refractory medulloblastoma; only two dose-limiting toxicities were observed with flat dosing. The recommended phase II study dose is 150 or 300 mg, depending on the patient's BSA. (C) 2013 AACR.
C1 [Gajjar, Amar; Kaste, Sue; Gilbertson, Richard J.] St Jude Childrens Res Hosp, Dept Oncol, Memphis, TN 38105 USA.
   [Stewart, Clinton F.] St Jude Childrens Res Hosp, Dept Pharmaceut Sci, Memphis, TN 38105 USA.
   [Ellison, David W.] St Jude Childrens Res Hosp, Dept Pathol, Memphis, TN 38105 USA.
   [Kaste, Sue; Kun, Larry E.] St Jude Childrens Res Hosp, Dept Radiol Sci, Memphis, TN 38105 USA.
   [Wallace, Dana; Boyett, James M.] St Jude Childrens Res Hosp, Dept Biostat, Memphis, TN 38105 USA.
   [Gilbertson, Richard J.] St Jude Childrens Res Hosp, Dept Dev Neurobiol, Memphis, TN 38105 USA.
   [Packer, Roger J.] Childrens Natl Med Ctr, Ctr Neurosci Res, Washington, DC 20010 USA.
   [Goldman, Stewart] Ann & Robert H Lurie Childrens Hosp Chicago, Div Hematol Oncol, Chicago, IL USA.
   [Chintagumpala, Murali] Texas Childrens Hosp, Dept Pediat, Houston, TX 77030 USA.
   [Takebe, Naoko] NCI, Invest Drug Branch, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
   [Curran, Tom] Childrens Hosp Philadelphia, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
RP Gajjar, A (reprint author), St Jude Childrens Res Hosp, Dept Oncol, MS 260,262 Danny Thomas Pl, Memphis, TN 38105 USA.
EM amar.gajjar@stjude.org
RI Curran, Tom/D-7515-2011; 
OI Curran, Tom/0000-0003-1444-7551
FU National Institutes of Health [U01 CA81457, P01 CA 096832]; Cancer
   Center CORE [CA 21765]; Noyes Brain Tumor Foundation; Musicians Against
   Childhood Cancer (MACC); America Lebanese Syrian Associated Charities
   (ALSAC)
FX This work was supported, in part, by the National Institutes of Health
   (grant no. U01 CA81457 to the Pediatric Brain Tumor Consortium; grant
   no. P01 CA 096832 to T. Curran and R. Gilbertson), the Cancer Center
   CORE (grant no. CA 21765), the Noyes Brain Tumor Foundation, Musicians
   Against Childhood Cancer (MACC), and the America Lebanese Syrian
   Associated Charities (ALSAC).
NR 36
TC 56
Z9 58
U1 1
U2 10
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 NOV 15
PY 2013
VL 19
IS 22
BP 6305
EP 6312
DI 10.1158/1078-0432.CCR-13-1425
PG 8
WC Oncology
SC Oncology
GA 256NU
UT WOS:000327320900025
PM 24077351
ER

PT J
AU Burotto, M
   Stetler-Stevenson, M
   Arons, E
   Zhou, H
   Wilson, W
   Kreitman, RJ
AF Burotto, Mauricio
   Stetler-Stevenson, Maryalice
   Arons, Evgeny
   Zhou, Hong
   Wilson, Wyndham
   Kreitman, Robert J.
TI Bendamustine and Rituximab in Relapsed and Refractory Hairy Cell
   Leukemia
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID MINIMAL RESIDUAL DISEASE; CHRONIC LYMPHOCYTIC-LEUKEMIA; MULTICENTER
   PHASE-II; NON-HODGKIN-LYMPHOMA; PREVIOUSLY UNTREATED PATIENTS;
   POLYMERASE-CHAIN-REACTION; TERM-FOLLOW-UP; MULTIPLE-MYELOMA; CYTOTOXIC
   DRUGS; PLUS RITUXIMAB
AB Purpose: To determine tolerability and for the first time explore efficacy of bendamustine-rituximab (BR) in multiply relapsed/refractory hairy cell leukemia (HCL), using two different dose levels of bendamustine.
   Experimental Design: Patients with HCL with >= 2 prior therapies requiring treatment received rituximab 375 mg/m(2) days 1 and 15 plus bendamustine 70 (n = 6) or 90 (n = 6) mg/m(2), days 1 and 2, for six cycles at 4-week intervals.
   Results: At 70 and 90 mg/m(2)/dose of bendamustine, overall response rate was 100%, with three (50%) and four (67%) complete remissions (CR) in each respective group. Minimal residual disease (MRD) was absent in 67% and 100% of CRs, respectively. All six without MRD remain in CR at 30 to 35 (median, 31) months of follow-up. Soluble CD22 and CD25 levels decreased with all responses, with median values decreasing from 17.7 and 42 ng/mL at baseline to undetectable and 2 ng/mL after CR, respectively (P < 0.001). Of 12 patients receiving 72 cycles of BR, the most common toxicities were hematologic, including thrombocytopenia (83%), lymphopenia (75%), leukopenia (58%), and neutropenia (42%). Grade III and IV hematologic toxicity included lymphopenia and thrombocytopenia (each 75%), leukopenia (58%), and neutropenia (25%). No significant dose-related differences were detected in response or toxicity.
   Conclusion: BR has significant activity in HCL. Bendamustine at either 70 or 90 mg/m(2)/dose was highly effective in multiply relapsed/refractory HCL and could be considered for achieving durable CRs without MRD in patients after failure of standard therapies. As it was not dose-limiting, 90 mg/m(2)/dose was chosen for future testing. (C)2013 AACR.
C1 [Burotto, Mauricio; Arons, Evgeny; Zhou, Hong; Kreitman, Robert J.] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
   [Stetler-Stevenson, Maryalice] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
   [Wilson, Wyndham] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
RP Kreitman, RJ (reprint author), NIH, 37-5124B,37 Convent Dr,MSC 4255, Bethesda, MD 20892 USA.
EM kreitmar@mail.nih.gov
FU NCI, NIH; Hairy Cell Leukemia Research Foundation
FX This work was supported by the intramural research program, NCI, NIH,
   and also in part by the Hairy Cell Leukemia Research Foundation.
NR 47
TC 15
Z9 15
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 15
PY 2013
VL 19
IS 22
BP 6313
EP 6321
DI 10.1158/1078-0432.CCR-13-1848
PG 9
WC Oncology
SC Oncology
GA 256NU
UT WOS:000327320900026
PM 24097860
ER

PT J
AU Asante, D
   MacCarthy-Morrogh, L
   Townley, AK
   Weiss, MA
   Katayama, K
   Palmer, KJ
   Suzuki, H
   Westlake, CJ
   Stephens, DJ
AF Asante, David
   MacCarthy-Morrogh, Lucy
   Townley, Anna K.
   Weiss, Matthew A.
   Katayama, Kentaro
   Palmer, Krysten J.
   Suzuki, Hiroetsu
   Westlake, Chris J.
   Stephens, David J.
TI A role for the Golgi matrix protein giantin in ciliogenesis through
   control of the localization of dynein-2
SO JOURNAL OF CELL SCIENCE
LA English
DT Article
DE Golgi; Cilia; Dynein
ID LIGHT INTERMEDIATE CHAIN; RETROGRADE INTRAFLAGELLAR TRANSPORT;
   OSTEOCHONDRODYSPLASIA RAT OCD/OCD; CONGENITAL OSTEOCHONDRODYSPLASIA;
   CYTOPLASMIC DYNEIN; EPIPHYSEAL CARTILAGE; MAMMALIAN-CELLS; CILIUM
   LENGTH; IN-VIVO; OCD OCD
AB The correct formation of primary cilia is central to the development and function of nearly all cells and tissues. Cilia grow from the mother centriole by extension of a microtubule core, the axoneme, which is then surrounded with a specialized ciliary membrane that is continuous with the plasma membrane. Intraflagellar transport moves particles along the length of the axoneme to direct assembly of the cilium and is also required for proper cilia function. The microtubule motor, cytoplasmic dynein-2 mediates retrograde transport along the axoneme from the tip to the base; dynein-2 is also required for some aspects of cilia formation. In most cells, the Golgi lies adjacent to the centrioles and key components of the cilia machinery localize to this organelle. Golgi-localized proteins have also been implicated in ciliogenesis and in intraflagellar transport. Here, we show that the transmembrane Golgi matrix protein giantin (GOLGB1) is required for ciliogenesis. We show that giantin is not required for the Rab11-Rabin8-Rab8 pathway that has been implicated in the early stages of ciliary membrane formation. Instead we find that suppression of giantin results in mis-localization of WDR34, the intermediate chain of dynein-2. Highly effective depletion of giantin or WDR34 leads to an inability of cells to form primary cilia. Partial depletion of giantin or of WDR34 leads to an increase in cilia length consistent with the concept that giantin acts through dynein-2. Our data implicate giantin in ciliogenesis through control of dynein-2 localization.
C1 [Asante, David; MacCarthy-Morrogh, Lucy; Townley, Anna K.; Palmer, Krysten J.; Stephens, David J.] Univ Bristol, Sch Biochem, Cell Biol Labs, Bristol BS8 1TD, Avon, England.
   [Weiss, Matthew A.; Westlake, Chris J.] NCI, Lab Cell & Dev Signaling, Frederick, MD 21072 USA.
   [Katayama, Kentaro; Suzuki, Hiroetsu] Nippon Vet & Life Sci Univ, Vet Physiol Lab, Musashino, Tokyo 1808602, Japan.
RP Stephens, DJ (reprint author), Univ Bristol, Sch Biochem, Cell Biol Labs, Med Sci Bldg, Bristol BS8 1TD, Avon, England.
EM david.stephens@bristol.ac.uk
FU UK Medical Research Council [G0801848, J000604/1]; U.S. National
   Institutes of Health
FX This work was funded by the UK Medical Research Council [grant numbers
   G0801848 and J000604/1] and a doctoral training studentship (to D.J.S.).
   M. A. W. and C.J.W. are funded by the U.S. National Institutes of
   Health. Deposited in PMC for release after 6 months.
NR 50
TC 10
Z9 10
U1 1
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 NOV 15
PY 2013
VL 126
IS 22
BP 5189
EP +
DI 10.1242/jcs.131664
PG 13
WC Cell Biology
SC Cell Biology
GA 257BK
UT WOS:000327357700011
PM 24046448
ER

PT J
AU Wilder, EL
   Tabak, LA
   Pettigrew, RI
   Collins, FS
AF Wilder, Elizabeth L.
   Tabak, Lawrence A.
   Pettigrew, Roderic I.
   Collins, Francis S.
TI Biomedical Research: Strength from Diversity
SO SCIENCE
LA English
DT Letter
C1 [Wilder, Elizabeth L.; Tabak, Lawrence A.; Pettigrew, Roderic I.; Collins, Francis S.] NIH, Bethesda, MD 20892 USA.
RP Collins, FS (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
EM collinsf@mail.nih.gov
FU Intramural NIH HHS [Z99 EB999999]
NR 3
TC 3
Z9 3
U1 0
U2 8
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
EI 1095-9203
J9 SCIENCE
JI Science
PD NOV 15
PY 2013
VL 342
IS 6160
BP 798
EP 798
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 251IY
UT WOS:000326923000009
PM 24233704
ER

PT J
AU Sato, S
   Shirakawa, H
   Tomita, S
   Tohkin, M
   Gonzalez, FJ
   Komai, M
AF Sato, Shoko
   Shirakawa, Hitoshi
   Tomita, Shuhei
   Tohkin, Masahiro
   Gonzalez, Frank J.
   Komai, Michio
TI The aryl hydrocarbon receptor and glucocorticoid receptor interact to
   activate human metallothionein 2A
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE 3-Methylcholanthrene; Aryl hydrocarbon receptor; Dexamethasone;
   Glucocorticoid receptor; Metallothionein; Transcription
ID NF-KAPPA-B; GENE-EXPRESSION; MESSENGER-RNA; MOUSE-LIVER;
   2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN TCDD; DIOXIN RECEPTOR; AH RECEPTOR;
   TRANSCRIPTION; INDUCTION; PROMOTER
AB Although the aryl hydrocarbon receptor (AHR) and glucocorticoid receptor (GR) play essential roles in mammalian development, stress responses, and other physiological events, crosstalk between these receptors has been the subject of much debate. Metallothioneins are classic glucocorticoid-inducible genes that were reported to increase upon treatment with AHR agonists in rodent tissues and cultured human cells. In this study, the mechanism of human metallothionein 2A (MT2A) gene transcription activation by AHR was investigated. Cotreatment with 3-methylcholanthrene and dexamethasone, agonists of AHR and GR respectively, synergistically increased MT2A mRNA levels in HepG2 cells. MT2A induction was suppressed by RNA interference against AHR or GR. Coimmunoprecipitation experiments revealed a physical interaction between AHR and GR proteins. Moreover, chromatin immunoprecipitation assays indicated that AHR was recruited to the glucocorticoid response element in the MT2A promoter. Thus, we provide a novel mechanism whereby AHR modulates expression of human MT2A via the glucocorticoid response element and protein-protein interactions with GR. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Sato, Shoko; Shirakawa, Hitoshi; Komai, Michio] Tohoku Univ, Grad Sch Agr Sci, Lab Nutr, Sendai, Miyagi 9818555, Japan.
   [Tomita, Shuhei] Dept Pathophysiol & Therapeut Sci, Div Mol Pharmacol, Yonago, Tottori 6838503, Japan.
   [Tohkin, Masahiro] Nagoya City Univ, Grad Sch Pharmaceut Sci, Dept Med Safety Sci, Nagoya, Aichi 2678603, Japan.
   [Gonzalez, Frank J.] NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Shirakawa, H (reprint author), 1-1 Tsutsumidori Amamiyamachi,Aoba Ku, Sendai, Miyagi 9818555, Japan.
EM satosho@rs.tus.ac.jp; shirakah@m.tohoku.ac.jp;
   tomita@med.tottori-u.ac.jp; tohkin@phar.nagoya-cu.ac.jp;
   gonzalef@mail.nih.gov; mkomai@m.tohoku.ac.jp
RI Shirakawa, Hitoshi/D-1406-2009
FU Japan Food Industry Center
FX This work was partially supported by a grant from the Japan Food
   Industry Center. The authors gratefully acknowledge the technical
   assistance of Misato Maeda and Yoshie Higuchi in Tohoku University.
NR 41
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U2 5
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 NOV 15
PY 2013
VL 273
IS 1
BP 90
EP 99
DI 10.1016/j.taap.2013.08.017
PG 10
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 256DN
UT WOS:000327290000011
PM 23994556
ER

PT J
AU Kumar, S
   Wuerffel, R
   Achour, I
   Lajoie, B
   Sen, R
   Dekker, J
   Feeney, AJ
   Kenter, AL
AF Kumar, Satyendra
   Wuerffel, Robert
   Achour, Ikbel
   Lajoie, Bryan
   Sen, Ranjan
   Dekker, Job
   Feeney, Ann J.
   Kenter, Amy L.
TI Flexible ordering of antibody class switch and V(D)J joining during
   B-cell ontogeny
SO GENES & DEVELOPMENT
LA English
DT Article
DE B-cell development; Ag gene rearrangement; gene expression
ID CYTIDINE DEAMINASE EXPRESSION; SOMATIC HYPERMUTATION; CHROMOSOMAL
   TRANSLOCATIONS; AID EXPRESSION; S-MU; RECOMBINATION; MICE; ELEMENTS;
   CENTERS; ABSENCE
AB V(D)J joining is mediated by RAG recombinase during early B-lymphocyte development in the bone marrow (BM). Activation-induced deaminase initiates isotype switching in mature B cells of secondary lymphoid structures. Previous studies questioned the strict ontological partitioning of these processes. We show that pro-B cells undergo robust switching to a subset of immunoglobulin H (IgH) isotypes. Chromatin studies reveal that in pro-B cells, the spatial organization of the Igh locus may restrict switching to this subset of isotypes. We demonstrate that in the BM, V(D)J joining and switching are interchangeably inducible, providing an explanation for the hyper-IgE phenotype of Omenn syndrome.
C1 [Kumar, Satyendra; Wuerffel, Robert; Achour, Ikbel; Kenter, Amy L.] Univ Illinois, Coll Med, Dept Microbiol & Immunol, Chicago, IL 60612 USA.
   [Lajoie, Bryan; Dekker, Job] Univ Massachusetts, Sch Med, Dept Biochem & Mol Biol, Programs Syst Biol, Worcester, MA 01605 USA.
   [Sen, Ranjan] NIA, Gene Regulat Sect, Lab Cellular & Mol Biol, NIH, Baltimore, MD 21224 USA.
   [Feeney, Ann J.] Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
RP Kenter, AL (reprint author), Univ Illinois, Coll Med, Dept Microbiol & Immunol, Chicago, IL 60612 USA.
EM star1@uic.edu
FU National Institutes of Health [AI052400, AI082918, HG003143, HG00459];
   W.M. Keck Foundation; Intramural Research Program of the National
   Institute on Aging (Baltimore, MD)
FX We thank A. Baumgart (The Scripps Research Institute), K. G. Becker, and
   W. H. Wood (Research Resources Branch, National Institute on
   Aging/National Institutes of Health) for technical help, and Dr. B.
   Sleckman (Washington University) for Abelson transformed cell lines.
   This work was supported by the National Institutes of Health (AI052400
   to A.L.K., AI082918 to A.J.F., and HG003143 and HG00459 to J.D), the
   W.M. Keck Foundation (to J.D), and the Intramural Research Program of
   the National Institute on Aging (Baltimore, MD) (to R.S.).
NR 32
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U1 2
U2 10
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 0890-9369
EI 1549-5477
J9 GENE DEV
JI Genes Dev.
PD NOV 15
PY 2013
VL 27
IS 22
BP 2439
EP 2444
DI 10.1101/gad.227165.113
PG 6
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA 256NW
UT WOS:000327321300005
PM 24240234
ER

PT J
AU Sofer, T
   Schifano, ED
   Hoppin, JA
   Hou, LF
   Baccarelli, AA
AF Sofer, Tamar
   Schifano, Elizabeth D.
   Hoppin, Jane A.
   Hou, Lifang
   Baccarelli, Andrea A.
TI A-clustering: a novel method for the detection of co-regulated
   methylation regions, and regions associated with exposure
SO BIOINFORMATICS
LA English
DT Article
ID FALSE DISCOVERY RATE; CPG ISLANDS; MICROARRAY; EXPRESSION; MODELS;
   GENOME; SITES
AB Motivation: DNA methylation is a heritable modifiable chemical process that affects gene transcription and is associated with other molecular markers (e. g. gene expression) and biomarkers (e. g. cancer or other diseases). Current technology measures methylation in hundred of thousands, or millions of CpG sites throughout the genome. It is evident that neighboring CpG sites are often highly correlated with each other, and current literature suggests that clusters of adjacent CpG sites are co-regulated.
   Results: We develop the Adjacent Site Clustering (A-clustering) algorithm to detect sets of neighboring CpG sites that are correlated with each other. To detect methylation regions associated with exposure, we propose an analysis pipeline for high-dimensional methylation data in which CpG sites within regions identified by A-clustering are modeled as multivariate responses to environmental exposure using a generalized estimating equation approach that assumes exposure equally affects all sites in the cluster. We develop a correlation preserving simulation scheme, and study the proposed methodology via simulations. We study the clusters detected by the algorithm on high dimensional dataset of peripheral blood methylation of pesticide applicators.
C1 [Sofer, Tamar] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
   [Schifano, Elizabeth D.] Univ Connecticut, Dept Stat, Storrs, CT 06269 USA.
   [Hoppin, Jane A.] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
   [Hou, Lifang] Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
   [Baccarelli, Andrea A.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02215 USA.
   [Baccarelli, Andrea A.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02215 USA.
RP Sofer, T (reprint author), Harvard Univ, Sch Publ Hlth, Dept Biostat, 677 Huntington Ave,SPH2,4th Floor, Boston, MA 02115 USA.
EM tsofer@hsph.harvard.edu
OI Baccarelli, Andrea/0000-0002-3436-0640; Sofer, Tamar/0000-0001-8520-8860
FU NIH [1RC1ES018461-01]; National Institutes of Health, National Institute
   of Environmental Health Sciences [Z01 ES049030]; National Cancer
   Institute [Z01 CP044008]; National Institute of Environmental Health
   Sciences [R01-ES013067, R01-ES020268]
FX This work was supported by NIH award 1RC1ES018461-01, by the Intramural
   Research Program of the National Institutes of Health, National
   Institute of Environmental Health Sciences (Z01 ES049030) and National
   Cancer Institute (Z01 CP044008) and grants number R01-ES013067 and
   R01-ES020268 from the National Institute of Environmental Health
   Sciences.
NR 22
TC 27
Z9 27
U1 1
U2 6
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1367-4803
EI 1460-2059
J9 BIOINFORMATICS
JI Bioinformatics
PD NOV 15
PY 2013
VL 29
IS 22
BP 2884
EP 2891
DI 10.1093/bioinformatics/btt498
PG 8
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
   Computer Science, Interdisciplinary Applications; Mathematical &
   Computational Biology; Statistics & Probability
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Computer Science; Mathematical & Computational Biology; Mathematics
GA 247TG
UT WOS:000326643600010
PM 23990415
ER

PT J
AU Tarca, AL
   Lauria, M
   Unger, M
   Bilal, E
   Boue, S
   Dey, KK
   Hoeng, J
   Koeppl, H
   Martin, F
   Meyer, P
   Nandy, P
   Norel, R
   Peitsch, M
   Rice, JJ
   Romero, R
   Stolovitzky, G
   Talikka, M
   Xiang, Y
   Zechner, C
AF Tarca, Adi L.
   Lauria, Mario
   Unger, Michael
   Bilal, Erhan
   Boue, Stephanie
   Dey, Kushal Kumar
   Hoeng, Julia
   Koeppl, Heinz
   Martin, Florian
   Meyer, Pablo
   Nandy, Preetam
   Norel, Raquel
   Peitsch, Manuel
   Rice, Jeremy J.
   Romero, Roberto
   Stolovitzky, Gustavo
   Talikka, Marja
   Xiang, Yang
   Zechner, Christoph
CA IMPROVER DSC Collaborators
TI Strengths and limitations of microarray-based phenotype prediction:
   lessons learned from the IMPROVER Diagnostic Signature Challenge
SO BIOINFORMATICS
LA English
DT Article
ID ALLOMAP GENE-EXPRESSION; BREAST-CANCER; MODELS; CLASSIFICATION;
   VERIFICATION; THERAPY
AB Motivation: After more than a decade since microarrays were used to predict phenotype of biological samples, real-life applications for disease screening and identification of patients who would best benefit from treatment are still emerging. The interest of the scientific community in identifying best approaches to develop such prediction models was reaffirmed in a competition style international collaboration called IMPROVER Diagnostic Signature Challenge whose results we describe herein.
   Results: Fifty-four teams used public data to develop prediction models in four disease areas including multiple sclerosis, lung cancer, psoriasis and chronic obstructive pulmonary disease, and made predictions on blinded new data that we generated. Teams were scored using three metrics that captured various aspects of the quality of predictions, and best performers were awarded. This article presents the challenge results and introduces to the community the approaches of the best overall three performers, as well as an R package that implements the approach of the best overall team. The analyses of model performance data submitted in the challenge as well as additional simulations that we have performed revealed that (i) the quality of predictions depends more on the disease endpoint than on the particular approaches used in the challenge; (ii) the most important modeling factor (e. g. data preprocessing, feature selection and classifier type) is problem dependent; and (iii) for optimal results datasets and methods have to be carefully matched. Biomedical factors such as the disease severity and confidence in diagnostic were found to be associated with the misclassification rates across the different teams.
C1 [Tarca, Adi L.] Wayne State Univ, Dept Comp Sci, Detroit, MI 48201 USA.
   [Tarca, Adi L.; Romero, Roberto] NICHD, Perinatol Res Branch, NIH, Detroit, MI 48201 USA.
   [Lauria, Mario] Microsoft Res Univ Trento Ctr Computat & Syst Bio, I-38068 Rovereto, Italy.
   [Unger, Michael; Dey, Kushal Kumar; Koeppl, Heinz; Nandy, Preetam; Zechner, Christoph] ETH, CH-8092 Zurich, Switzerland.
   [Bilal, Erhan; Meyer, Pablo; Norel, Raquel; Rice, Jeremy J.; Stolovitzky, Gustavo] IBM Corp, Thomas J Watson Res Ctr, Yorktown Hts, NY 10598 USA.
   [Boue, Stephanie; Hoeng, Julia; Martin, Florian; Peitsch, Manuel; Talikka, Marja; Xiang, Yang] Philip Morris Int, Res & Dev, CH-2000 Neuchatel, Switzerland.
RP Stolovitzky, G (reprint author), IBM Corp, Thomas J Watson Res Ctr, Yorktown Hts, NY 10598 USA.
EM gustavo@us.ibm.com
RI Haibe-Kains, Benjamin/D-3702-2011; Di Camillo, Barbara/L-3202-2013; 
OI Haibe-Kains, Benjamin/0000-0002-7684-0079; Di Camillo,
   Barbara/0000-0001-8415-4688; Boue, Stephanie/0000-0003-0680-4168; Aloy,
   Patrick/0000-0002-3557-0236; Norel, Raquel/0000-0001-7737-4172; Lauria,
   Mario/0000-0001-5983-7292; Peddinti, Gopal/0000-0002-8767-968X
FU Eunice Kennedy Shriver National Institute of Child Health and Human
   Development, National Institutes of Health, U.S. Department of Health
   and Human Services [N01-HD-2-3342]; Philip Morris International; Swiss
   National Science Foundation [PP00P2_128503]; SystemsX.ch, the Swiss
   Initiative for Systems Biology
FX Intramural Research Program of the Eunice Kennedy Shriver National
   Institute of Child Health and Human Development, National Institutes of
   Health, U.S. Department of Health and Human Services (N01-HD-2-3342) (A.
   T. and R. R., in part). DSC best overall performer grant from Philip
   Morris International (to A. T.). Swiss National Science Foundation
   (PP00P2_128503) and from SystemsX.ch, the Swiss Initiative for Systems
   Biology (to M. U., P.N., C.Z. and H.K.).
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PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1367-4803
EI 1460-2059
J9 BIOINFORMATICS
JI Bioinformatics
PD NOV 15
PY 2013
VL 29
IS 22
BP 2892
EP 2899
DI 10.1093/bioinformatics/btt492
PG 8
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
   Computer Science, Interdisciplinary Applications; Mathematical &
   Computational Biology; Statistics & Probability
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Computer Science; Mathematical & Computational Biology; Mathematics
GA 247TG
UT WOS:000326643600011
PM 23966112
ER

PT J
AU Lim, SC
   Friemel, M
   Marum, JE
   Tucker, EJ
   Bruno, DL
   Riley, LG
   Christodoulou, J
   Kirk, EP
   Boneh, A
   DeGennaro, CM
   Springer, M
   Mootha, VK
   Rouault, TA
   Leimkuhler, S
   Thorburn, DR
   Compton, AG
AF Lim, Sze Chern
   Friemel, Martin
   Marum, Justine E.
   Tucker, Elena J.
   Bruno, Damien L.
   Riley, Lisa G.
   Christodoulou, John
   Kirk, Edwin P.
   Boneh, Avihu
   DeGennaro, Christine M.
   Springer, Michael
   Mootha, Vamsi K.
   Rouault, Tracey A.
   Leimkuehler, Silke
   Thorburn, David R.
   Compton, Alison G.
TI Mutations in LYRM4, encoding ironsulfur cluster biogenesis factor ISD11,
   cause deficiency of multiple respiratory chain complexes
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID IRON-SULFUR CLUSTER; CYTOSOLIC FE/S PROTEINS; MITOCHONDRIAL DISEASE;
   SCAFFOLD PROTEIN; CYSTEINE DESULFURASE; ESCHERICHIA-COLI;
   LACTIC-ACIDOSIS; CAUSES MYOPATHY; I DEFICIENCY; 1ST YEAR
AB Ironsulfur clusters (ISCs) are important prosthetic groups that define the functions of many proteins. Proteins with ISCs (called ironsulfur or FeS proteins) are present in mitochondria, the cytosol, the endoplasmic reticulum and the nucleus. They participate in various biological pathways including oxidative phosphorylation (OXPHOS), the citric acid cycle, iron homeostasis, heme biosynthesis and DNA repair. Here, we report a homozygous mutation in LYRM4 in two patients with combined OXPHOS deficiency. LYRM4 encodes the ISD11 protein, which forms a complex with, and stabilizes, the sulfur donor NFS1. The homozygous mutation (c.203GT, p.R68L) was identified via massively parallel sequencing of 1000 mitochondrial genes (MitoExome sequencing) in a patient with deficiency of complexes I, II and III in muscle and liver. These three complexes contain ISCs. Sanger sequencing identified the same mutation in his similarly affected cousin, who had a more severe phenotype and died while a neonate. Complex IV was also deficient in her skeletal muscle. Several other FeS proteins were also affected in both patients, including the aconitases and ferrochelatase. Mutant ISD11 only partially complemented for an ISD11 deletion in yeast. Our in vitro studies showed that the l-cysteine desulfurase activity of NFS1 was barely present when co-expressed with mutant ISD11. Our findings are consistent with a defect in the early step of ISC assembly affecting a broad variety of FeS proteins. The differences in biochemical and clinical features between the two patients may relate to limited availability of cysteine in the newborn period and suggest a potential approach to therapy.
C1 [Lim, Sze Chern; Marum, Justine E.; Tucker, Elena J.; Bruno, Damien L.; Boneh, Avihu; Thorburn, David R.; Compton, Alison G.] Royal Childrens Hosp, Murdoch Childrens Res Inst, Parkville, Vic 3052, Australia.
   [Lim, Sze Chern; Marum, Justine E.; Tucker, Elena J.; Boneh, Avihu; Thorburn, David R.; Compton, Alison G.] Univ Melbourne, Dept Paediat, Parkville, Vic 3052, Australia.
   [Friemel, Martin; Leimkuehler, Silke] Univ Potsdam, Dept Mol Enzymol, Inst Biochem & Biol, D-14476 Potsdam, Germany.
   [Bruno, Damien L.; Boneh, Avihu; Thorburn, David R.] Royal Childrens Hosp, Victorian Clin Genet Serv, Parkville, Vic 3052, Australia.
   [Riley, Lisa G.; Christodoulou, John] Childrens Hosp, Genet Metab Disorders Res Unit, Westmead, NSW 2145, Australia.
   [Christodoulou, John] Univ Sydney, Discipline Paediat & Child Hlth, Sydney, NSW 2006, Australia.
   [Christodoulou, John] Univ Sydney, Discipline Genet Med, Sydney, NSW 2006, Australia.
   [Kirk, Edwin P.] Sydney Childrens Hosp, Dept Med Genet, Randwick, NSW 2031, Australia.
   [DeGennaro, Christine M.; Springer, Michael; Mootha, Vamsi K.] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA.
   [Mootha, Vamsi K.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
   [Mootha, Vamsi K.] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
   [Mootha, Vamsi K.] Broad Inst Harvard & Massachusetts Inst Technol, Cambridge, MA 02141 USA.
   [Rouault, Tracey A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Mol Med, NIH, Bethesda, MD 20892 USA.
RP Compton, AG (reprint author), Royal Childrens Hosp, Murdoch Childrens Res Inst, Flemington Rd, Parkville, Vic 3052, Australia.
EM alison.compton@mcri.edu.au
RI Bruno, Damien/C-3665-2013; Christodoulou, John/E-5866-2015; Lim, Sze
   Chern/I-6763-2013; 
OI Lim, Sze Chern/0000-0003-0312-9937; Kirk, Edwin/0000-0002-4662-0024;
   thorburn, david/0000-0002-7725-9470; Compton,
   Alison/0000-0002-2725-7055; Christodoulou, John/0000-0002-8431-0641
FU NHLBI Lung GO Sequencing Project [HL-102923]; NHLBI WHI Sequencing
   Project [HL-102924]; NHLBI Broad GO Sequencing Project [HL-102925];
   NHLBI Seattle GO Sequencing Project [HL-102926]; NHLBI Heart GO
   Sequencing Project [HL-103010]; NHLBI Melbourne Research Scholarship;
   NHLBI Australian National Health and Medical Research Council; NHLBI
   Victorian Government; NHLBI Eunice Kennedy Shriver National Institute of
   Child Health and Human Development; NHLBI Deutsche
   Forschungsgemeinschaft
FX The authors thank the NHLBI GO Exome Sequencing Project and its ongoing
   studies which produced and provided exome variant calls for comparison:
   the Lung GO Sequencing Project (HL-102923), the WHI Sequencing Project
   (HL-102924), the Broad GO Sequencing Project (HL-102925), the Seattle GO
   Sequencing Project (HL-102926) and the Heart GO Sequencing Project
   (HL-103010). This work was supported by a Melbourne Research Scholarship
   (to S. C. L.), grants and a Principal Research Fellowship from the
   Australian National Health and Medical Research Council (to D. R. T.),
   the Victorian Government's Operational Infrastructure Support Program
   (to D. R. T.) and support from the intramural program of the Eunice
   Kennedy Shriver National Institute of Child Health and Human Development
   (to T. A. R.), and the Deutsche Forschungsgemeinschaft (to S.L.).
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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 NOV 15
PY 2013
VL 22
IS 22
BP 4460
EP 4473
DI 10.1093/hmg/ddt295
PG 14
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 248EA
UT WOS:000326675300002
PM 23814038
ER

PT J
AU Yu, CR
   Kim, SH
   Mahdi, RM
   Egwuagu, CE
AF Yu, Cheng-Rong
   Kim, Sung-Hye
   Mahdi, Rashid M.
   Egwuagu, Charles E.
TI SOCS3 Deletion in T Lymphocytes Suppresses Development of Chronic Ocular
   Inflammation via Upregulation of CTLA-4 and Expansion of Regulatory T
   Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID CYTOKINE SIGNALING 3; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; RETINAL
   CELLS; GROWTH-FACTOR; HELPER-CELLS; TC17 CELLS; UVEITIS; PROTEINS;
   INTERLEUKIN-27; ACTIVATION
AB Suppressors of cytokine signaling (SOCS) proteins are negative-feedback regulators of the JAK/STAT pathway, and SOCS3 contributes to host immunity by regulating the intensity and duration of cytokine signals and inflammatory responses. Mice with Socs3 deletion in myeloid cells exhibit enhanced STAT3 signaling, expansion of Th1 and Th17 cells, and develop severe experimental autoimmune encephalomyelitis. Interestingly, development of the unique IL-17/IFN-gamma double-producing (Th17/IFN-gamma and Tc17/IFN-gamma) subsets that exhibit strong cytotoxic activities and are associated with pathogenesis of several autoimmune diseases has recently been shown to depend on epigenetic suppression of SOCS3 expression, further suggesting involvement of SOCS3 in autoimmunity and tumor immunity. In this study, we generated mice with Socs3 deletion in the CD4 T cell compartment (CD4-SOCS3 knockout [KO]) to determine in vivo effects of the loss of Socs3 in the T cell-mediated autoimmune disease, experimental autoimmune uveitis (EAU). In contrast to the exacerbation of experimental autoimmune encephalomyelitis in myeloid-specific SOCS3-deleted mice, CD4-SOCS3KO mice were protected from acute and chronic uveitis. Protection from EAU correlated with enhanced expression of CTLA-4 and expansion of IL-10-producing regulatory T cells with augmented suppressive activities. We further show that SOCS3 interacts with CTLA-4 and negatively regulates CTLA-4 levels in T cells, providing a mechanistic explanation for the expansion of regulatory T cells in CD4-SOCS3 during EAU. Contrary to in vitro epigenetic studies, Th17/IFN-gamma and Tc17/IFN-gamma populations were markedly reduced in CD4-SOCS3KO, suggesting that SOCS3 promotes expansion of the Th17/IFN-gamma subset associated with development of severe uveitis. Thus, SOCS3 is a potential therapeutic target in uveitis and other autoinflammatory diseases.
C1 [Yu, Cheng-Rong; Kim, Sung-Hye; Mahdi, Rashid M.; Egwuagu, Charles E.] NEI, Mol Immunol Sect, NIH, Bethesda, MD 20892 USA.
RP Egwuagu, CE (reprint author), NEI, Mol Immunol Sect, NIH, Bldg 10,Room 10N116,10 Ctr Dr, Bethesda, MD 20892 USA.
EM egwuaguc@nei.nih.gov
FU Intramural NIH HHS [ZIA EY000280-22, Z99 EY999999, ZIA EY000280-21, ZIA
   EY000315-21, ZIA EY000315-22, ZIA EY000372-11, ZIA EY000372-12, ZIA
   EY000372-13]
NR 48
TC 3
Z9 4
U1 0
U2 8
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 NOV 15
PY 2013
VL 191
IS 10
BP 5036
EP 5043
DI 10.4049/jimmunol.1301132
PG 8
WC Immunology
SC Immunology
GA 247AK
UT WOS:000326584600018
PM 24101549
ER

PT J
AU Quinn, KM
   Yamamoto, A
   Costa, A
   Darrah, PA
   Lindsay, RWB
   Hegde, ST
   Johnson, TR
   Flynn, BJ
   Lore, K
   Seder, RA
AF Quinn, Kylie M.
   Yamamoto, Ayako
   Costa, Andreia
   Darrah, Patricia A.
   Lindsay, Ross W. B.
   Hegde, Sonia T.
   Johnson, Teresa R.
   Flynn, Barbara J.
   Lore, Karin
   Seder, Robert A.
TI Coadministration of Polyinosinic: Polycytidylic Acid and
   Immunostimulatory Complexes Modifies Antigen Processing in Dendritic
   Cell Subsets and Enhances HIV Gag-Specific T Cell Immunity
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID DOUBLE-STRANDED-RNA; DIFFERENTIATION-ASSOCIATED GENE-5; TOLL-LIKE
   RECEPTOR-3; CROSS-PRESENTATION; IN-VIVO; NONHUMAN-PRIMATES; ISCOMATRIX
   ADJUVANT; THERAPEUTIC VACCINES; PROTECTIVE CAPACITY; LEISHMANIA-MAJOR
AB Currently approved adjuvants induce protective Ab responses but are more limited for generating cellular immunity. In this study, we assessed the effect of combining two adjuvants with distinct mechanisms of action on their ability to prime T cells: the TLR3 ligand, polyinosinic: polycytidylic acid (poly I:C), and immunostimulatory complexes (ISCOMs). Each adjuvant was administered alone or together with HIV Gag protein (Gag), and the magnitude, quality, and phenotype of Gag-specific T cell responses were assessed. For CD8 T cells, all adjuvants induced a comparable response magnitude, but combining poly I: C with ISCOMs induced a high frequency of CD127(+), IL-2-producing cells with decreased expression of Tbet compared with either adjuvant alone. For CD4 T cells, combining poly I: C and ISCOMs increased the frequency of multifunctional cells, producing IFN-gamma, IL-2, and TNF, and the total magnitude of the response compared with either adjuvant alone. CD8 or CD4 T cell responses induced by both adjuvants mediated protection against Gag-expressing Listeria monocytogenes or vaccinia viral infections. Poly I: C and ISCOMs can alter Ag uptake and/or processing, and we therefore used fluorescently labeled HIV Gag and DQ-OVA to assess these mechanisms, respectively, in multiple dendritic cell subsets. Poly I: C promoted uptake and retention of Ag, whereas ISCOMs enhanced Ag degradation. Combining poly I: C and ISCOMs caused substantial death of dendritic cells but persistence of degraded Ag. These data illustrate how combining adjuvants, such as poly I: C and ISCOMs, that modulate Ag processing and have potent innate activity, can enhance the magnitude, quality, and phenotype of T cell immunity.
C1 [Quinn, Kylie M.; Yamamoto, Ayako; Costa, Andreia; Darrah, Patricia A.; Lindsay, Ross W. B.; Hegde, Sonia T.; Johnson, Teresa R.; Flynn, Barbara J.; Lore, Karin; Seder, Robert A.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
   [Lore, Karin] Karolinska Inst, Dept Med, Ctr Infect Med, SE-17177 Stockholm, Sweden.
RP Seder, RA (reprint author), NIAID, Cellular Immunol Sect, Vaccine Res Ctr, NIH, 40 Convent Dr MSC 3025,Bldg 40,Room 3512, Bethesda, MD 20892 USA.
EM rseder@mail.nih.gov
OI Hegde, Sonia/0000-0001-6426-0096
FU Foundation for the National Institutes of Health; Collaboration for AIDS
   Vaccine Discovery Award from the Bill and Melinda Gates Foundation
   [OPP1039775]
FX This work was supported in part by a grant from the Foundation for the
   National Institutes of Health with support from Collaboration for AIDS
   Vaccine Discovery Award OPP1039775 from the Bill and Melinda Gates
   Foundation.
NR 74
TC 8
Z9 8
U1 0
U2 8
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 NOV 15
PY 2013
VL 191
IS 10
BP 5085
EP 5096
DI 10.4049/jimmunol.1301730
PG 12
WC Immunology
SC Immunology
GA 247AK
UT WOS:000326584600023
PM 24089189
ER

PT J
AU Chen, SM
   Li, YL
   Depontieu, FR
   McMiller, TL
   English, AM
   Shabanowitz, J
   Kos, F
   Sidney, J
   Sette, A
   Rosenberg, SA
   Hunt, DF
   Mariuzza, RA
   Topalian, SL
AF Chen, Shuming
   Li, Yili
   Depontieu, Florence R.
   McMiller, Tracee L.
   English, A. Michelle
   Shabanowitz, Jeffrey
   Kos, Ferdynand
   Sidney, John
   Sette, Alessandro
   Rosenberg, Steven A.
   Hunt, Donald F.
   Mariuzza, Roy A.
   Topalian, Suzanne L.
TI Structure-Based Design of Altered MHC Class II-Restricted Peptide
   Ligands with Heterogeneous Immunogenicity
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID T-CELL-RECEPTOR; MELANOMA ANTIGEN GP100; HISTOCOMPATIBILITY
   COMPLEX-BINDING; COLONY-STIMULATING FACTOR; MASS-SPECTROMETRY; HLA-DR4
   DRA-ASTERISK-0101; METASTATIC MELANOMA; MULTIPLE EPITOPES;
   CROSS-REACTIVITY; TUMOR-ANTIGEN
AB Insights gained from characterizing MHC-peptide-TCR interactions have held the promise that directed structural modifications can have predictable functional consequences. The ability to manipulate T cell reactivity synthetically or through genetic engineering might thus be translated into new therapies for common diseases such as cancer and autoimmune disorders. In the current study, we determined the crystal structure of HLA-DR4 in complex with the nonmutated dominant gp100 epitope gp100(44-59), associated with many melanomas. Altered peptide ligands (APLs) were designed to enhance MHC binding and hence T cell recognition of gp100 in HLA-DR4(+) melanoma patients. Increased MHC binding of several APLs was observed, validating this approach biochemically. Nevertheless, heterogeneous preferences of CD4(+) T cells from several HLA-DR4(+) melanoma patients for different gp100 APLs suggested highly variable TCR usage, even among six patients who had been vaccinated against the wild-type gp100 peptide. This heterogeneity prevented the selection of an APL candidate for developing an improved generic gp100 vaccine in melanoma. Our results are consistent with the idea that even conservative changes in MHC anchor residues may result in subtle, yet crucial, effects on peptide contacts with the TCR or on peptide dynamics, such that alterations intended to enhance immunogenicity may be unpredictable or counterproductive. They also underscore a critical knowledge gap that needs to be filled before structural and in vitro observations can be used reliably to devise new immunotherapies for cancer and other disorders.
C1 [Chen, Shuming; Depontieu, Florence R.; McMiller, Tracee L.; Topalian, Suzanne L.] Johns Hopkins Univ, Sch Med, Dept Surg, Baltimore, MD 21287 USA.
   [Chen, Shuming; Depontieu, Florence R.; McMiller, Tracee L.; Kos, Ferdynand; Topalian, Suzanne L.] Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21287 USA.
   [Li, Yili; Mariuzza, Roy A.] Univ Maryland, Inst Biosci & Biotechnol Res, WM Keck Lab Struct Biol, Rockville, MD 20852 USA.
   [English, A. Michelle; Shabanowitz, Jeffrey; Hunt, Donald F.] Univ Virginia, Dept Biochem, Charlottesville, VA 22908 USA.
   [Kos, Ferdynand] Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21287 USA.
   [Sidney, John; Sette, Alessandro] La Jolla Inst Allergy & Immunol, La Jolla, CA 92037 USA.
   [Rosenberg, Steven A.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
RP Topalian, SL (reprint author), Johns Hopkins Univ, Sch Med, Dept Surg, 1550 Orleans St,Canc Res Bldg 2,Room 508, Baltimore, MD 21287 USA.
EM rmariuzz@umd.edu; stopali1@jhmi.edu
RI RENART-DEPONTIEU, Florence/H-2461-2014
OI RENART-DEPONTIEU, Florence/0000-0003-0277-0116
FU National Institutes of Health (NIH)-National Institute of Allergy and
   Infectious Diseases Grant [AI073654]; NIH-National Institute of Allergy
   and Infectious Diseases [HHSN272200900044C]; NIH Grant [AI033993]
FX This work was supported by National Institutes of Health (NIH)-National
   Institute of Allergy and Infectious Diseases Grant AI073654 (to R.A.M.
   and S.L.T.), NIH-National Institute of Allergy and Infectious Diseases
   Contract HHSN272200900044C (to A.S.), and NIH Grant AI033993 (to
   D.F.H.).
NR 62
TC 6
Z9 7
U1 2
U2 13
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD NOV 15
PY 2013
VL 191
IS 10
BP 5097
EP 5106
DI 10.4049/jimmunol.1300467
PG 10
WC Immunology
SC Immunology
GA 247AK
UT WOS:000326584600024
PM 24108701
ER

PT J
AU Niciu, MJ
   Luckenbaugh, DA
   Ionescu, DF
   Mathews, DC
   Richards, EM
   Zarate, CA
AF Niciu, Mark J.
   Luckenbaugh, David A.
   Ionescu, Dawn F.
   Mathews, Daniel C.
   Richards, Erica M.
   Zarate, Carlos A., Jr.
TI Subanesthetic Dose Ketamine Does Not Induce an Affective Switch in Three
   Independent Samples of Treatment-Resistant Major Depression
SO BIOLOGICAL PSYCHIATRY
LA English
DT Letter
ID D-ASPARTATE ANTAGONIST; ADD-ON TRIAL; BIPOLAR DEPRESSION; DISORDER;
   MANIA; SYMPTOMS; INFUSION
C1 [Niciu, Mark J.; Luckenbaugh, David A.; Ionescu, Dawn F.; Mathews, Daniel C.; Richards, Erica M.; Zarate, Carlos A., Jr.] NIMH, NIH, Expt Therapeut & Pathophysiol Branch, Intramural Res Program, Bethesda, MD 20892 USA.
   [Zarate, Carlos A., Jr.] George Washington Univ, Washington, DC USA.
RP Zarate, CA (reprint author), NIMH, NIH, Expt Therapeut & Pathophysiol Branch, Intramural Res Program, Bethesda, MD 20892 USA.
EM zaratec@mail.nih.gov
RI Niciu, Mark/J-1766-2014; Ionescu, Dawn/K-5675-2015
OI Niciu, Mark/0000-0002-5612-3021; 
FU Intramural NIH HHS [Z99 MH999999]
NR 12
TC 14
Z9 14
U1 1
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD NOV 15
PY 2013
VL 74
IS 10
BP E23
EP E24
DI 10.1016/j.biopsych.2013.01.038
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 238TM
UT WOS:000325972700003
PM 23726512
ER

PT J
AU Pinsky, PF
   Church, TR
   Izmirlian, G
   Kramer, BS
AF Pinsky, Paul F.
   Church, Timothy R.
   Izmirlian, Grant
   Kramer, Barnett S.
TI The National Lung Screening Trial: Results Stratified by Demographics,
   Smoking History, and Lung Cancer Histology
SO CANCER
LA English
DT Article
DE computed tomography; screening; lung cancer; histology; sex
ID CT SCREEN
AB BACKGROUNDThe National Lung Screening Trial (NLST), which compared lung cancer screening with low-dose computed tomography (LDCT) versus chest radiography (CXR), demonstrated a statistically significant mortality benefit of LDCT screening. In the current study, the authors performed a post hoc analysis to examine whether the benefit was affected by various baseline factors, including age, sex, and smoking status, and whether it differed by tumor histology.
   METHODSLung cancer death rates were computed as events over person-years of observation; the mortality risk ratio (RR) was defined as the lung cancer death rate in the LDCT versus CXR trial arms. Poisson regression was used to test for interactions of sex, age (<65 years vs 65 years), and smoking status (current vs former) with trial arm. Mortality RRs were also computed for specific lung cancer histologies.
   RESULTSThe overall mortality RR was 0.92 in men and 0.73 in women, with a P value for interaction of .08. RRs were similar for individuals aged <65 years versus those aged 65 years (0.82 vs 0.87), and for current versus former smokers (0.81 vs 0.91). By tumor histology, mortality RRs were 0.75 for adenocarcinoma, 0.71 for all non-small cell lung cancers except squamous, 1.23 for squamous cell carcinoma, and 0.90 for small cell carcinoma. RRs were similar for men and women for nonsquamous non-small cell lung cancers (0.71 and 0.70, respectively); women were found to have lower RRs for small cell and squamous cell carcinoma.
   CONCLUSIONSA benefit of LDCT did not appear to vary substantially by age or smoking status; there was weak evidence of a differential benefit by sex. A differential benefit across lung cancer histologies may exist. Cancer 2013;119:3976-3983. Published 2013. This article is a U.S. Government work and is in the public domain in the USA.
C1 [Pinsky, Paul F.; Izmirlian, Grant; Kramer, Barnett S.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
   [Church, Timothy R.] Univ Minnesota, Sch Publ Hlth, Div Environm Hlth Serv, Minneapolis, MN USA.
RP Pinsky, PF (reprint author), NCI, Canc Prevent Div, 9609 Med Ctr Dr,Rm 5E212, Bethesda, MD 20892 USA.
EM pp4f@nih.gov
OI Church, Timothy R./0000-0003-3292-5035
FU National Institutes of Health [U01-CA-80098, U01-CA-79778, N01-CN-25511,
   N01-CN-20012, N01-CN-20013, N01-CN-20014, N01-CN-20015, N01-CN-20016,
   N01-CN-20018, N01-CN-25522, N01-CN-25524, N01-CN-75022, N01-CN-25476,
   N02-CN-63300]
FX This research was funded by the following National Institutes of Health
   grants and contracts: U01-CA-80098, U01-CA-79778, N01-CN-25511,
   N01-CN-20012, N01-CN-20013, N01-CN-20014, N01-CN-20015, N01-CN-20016,
   N01-CN-20018, N01-CN-25522, N01-CN-25524, N01-CN-75022, N01-CN-25476,
   and N02-CN-63300.
NR 12
TC 15
Z9 15
U1 2
U2 19
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 NOV 15
PY 2013
VL 119
IS 22
BP 3976
EP 3983
DI 10.1002/cncr.28326
PG 8
WC Oncology
SC Oncology
GA 244VO
UT WOS:000326418500015
ER

PT J
AU Kuhs, KAL
   Gonzalez, P
   Struijk, L
   Castro, F
   Hildesheim, A
   van Doorn, LJ
   Rodriguez, AC
   Schiffman, M
   Quint, W
   Lowy, DR
   Porras, C
   DelVecchio, C
   Katki, HA
   Jimenez, S
   Safaeian, M
   Schiller, J
   Solomon, D
   Wacholder, S
   Herrero, R
   Kreimer, AR
AF Kuhs, Krystle A. Lang
   Gonzalez, Paula
   Struijk, Linda
   Castro, Felipe
   Hildesheim, Allan
   van Doorn, Leen-Jan
   Cecilia Rodriguez, Ana
   Schiffman, Mark
   Quint, Wim
   Lowy, Douglas R.
   Porras, Carolina
   DelVecchio, Corey
   Katki, Hormuzd A.
   Jimenez, Silvia
   Safaeian, Mahboobeh
   Schiller, John
   Solomon, Diane
   Wacholder, Sholom
   Herrero, Rolando
   Kreimer, Aimee R.
CA Costa Rica Vaccine Trial Grp
TI Prevalence of and Risk Factors for Oral Human Papillomavirus Among Young
   Women in Costa Rica
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
DE human papillomavirus vaccine; HPV; oropharynx cancer; Costa Rica;
   Guanacaste; oral HPV DNA
ID SQUAMOUS-CELL CARCINOMAS; NECK-CANCER INCIDENCE; HPV INFECTION;
   HEALTHY-INDIVIDUALS; BROAD-SPECTRUM; UNITED-STATES; GENOMIC DNA; HEAD;
   MUCOSA; TRENDS
AB Background. Little is known about the epidemiology of oral human papillomavirus (HPV) in Latin America.
   Methods. Women (N = 5838) aged 22-29 in the control and vaccine arms of an HPV-16/18 vaccine trial in Costa Rica had oral, cervical, and anal specimens collected. Samples were tested for alpha mucosal HPV types (SPF10/LiPA(25) version 1); a subset of oral samples (n = 500) was tested for cutaneous HPV types in the genera alpha, beta, gamma, mu, and nu.
   Results. In the control arm (n = 2926), 1.9% of women had an oral alpha mucosal HPV detected, 1.3% had carcinogenic HPV, and 0.4% had HPV-16; similar patterns for non-16/18 HPV types were observed in the vaccine arm. Independent risk factors for any oral alpha mucosal HPV among women in the control arm included marital status (adjusted odds ratio [AOR], 3.2; 95% confidence interval [CI], 1.8-5.7 for single compared to married/living as married), number of sexual partners (AOR, 2.4; 95% CI, 1.0-6.1 for >= 4 partners compared to 0-1 partners), chronic sinusitis (AOR, 3.1; 95% CI, 1.5-6.7), and cervical HPV infection (AOR, 2.6; 95% CI, 1.4-4.6). Detection of beta HPV was common (18.6%) and not associated with sexual activity.
   Conclusions. Unlike cutaneous HPV types, alpha mucosal HPV types were uncommon in the oral region and were predominately associated with sexual behavior.
   Clinical Trials Registration. NCT00128661.
C1 [Kuhs, Krystle A. Lang; Castro, Felipe; Hildesheim, Allan; Schiffman, Mark; Lowy, Douglas R.; Katki, Hormuzd A.; Safaeian, Mahboobeh; Schiller, John; Solomon, Diane; Wacholder, Sholom; Kreimer, Aimee R.] NCI, NIH, Bethesda, MD 20892 USA.
   [Gonzalez, Paula; Cecilia Rodriguez, Ana; Jimenez, Silvia] Fdn INCIENSA, Proyecto Epidemiol Guanacaste, San Jose, Costa Rica.
   [Gonzalez, Paula; Herrero, Rolando] Int Agcy Res Canc, Prevent & Implementat Grp, F-69372 Lyon, France.
   [Struijk, Linda; van Doorn, Leen-Jan; Quint, Wim; Porras, Carolina] DDL Diagnost Lab, Rijswijk, Netherlands.
   [DelVecchio, Corey] Informat Management Serv Inc, Silver Spring, MD USA.
RP Kuhs, KAL (reprint author), NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,RM 6-E210, Bethesda, MD 20892 USA.
EM krystle.kuhs@nih.gov
RI Kreimer, Aimee/H-1687-2015; Castro, Felipe/N-4241-2013; Katki,
   Hormuzd/B-4003-2015; Hildesheim, Allan/B-9760-2015
OI Hildesheim, Allan/0000-0003-0257-2363
FU NCI [N01-CP-11005]; National Institutes of Health Office of Research on
   Women's Health
FX This work was supported by the NCI (contract N01-CP-11005), with funding
   support from the National Institutes of Health Office of Research on
   Women's Health. Vaccine was provided for our trial by GlaxoSmithKline
   Biologicals (GSK), under a Clinical Trials Agreement with the NCI.
   Cervarix is a registered trademark of the GlaxoSmithKline Biologicals
   group of companies. GSK also provided support for aspects of the trial
   associated with regulatory submission needs of the company under Food
   and Drug Administration BB-IND 7920.
NR 39
TC 14
Z9 14
U1 1
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
EI 1537-6613
J9 J INFECT DIS
JI J. Infect. Dis.
PD NOV 15
PY 2013
VL 208
IS 10
BP 1643
EP 1652
DI 10.1093/infdis/jit369
PG 10
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 244HI
UT WOS:000326378000015
ER

PT J
AU Talaat, KR
   Karron, RA
   Thumar, B
   McMahon, BA
   Schmidt, AC
   Collins, PL
   Buchholz, UJ
AF Talaat, Kawsar R.
   Karron, Ruth A.
   Thumar, Bhagvanji
   McMahon, Bridget A.
   Schmidt, Alexander C.
   Collins, Peter L.
   Buchholz, Ursula J.
TI Experimental Infection of Adults With Recombinant Wild-Type Human
   Metapneumovirus
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
DE human metapneumovirus; HMPV; challenge
ID RESPIRATORY SYNCYTIAL VIRUS; PHASE-I TRIAL; HEALTHY-ADULTS; VACCINE
   CANDIDATE; YOUNG-CHILDREN; TRACT DISEASE; LIVE; INFLUENZA; INFANTS;
   SEROPREVALENCE
AB Background. Human metapneumovirus (HMPV) causes lower respiratory tract infections in young children. rHMPV-SHs is a recombinant HMPV (rHMPV) based on a biologically derived wild-type HMPV strain. We characterized its infectivity and immunogenicity in healthy adults to determine whether it would be suitable for use as the parent virus for the development of live attenuated rHMPV vaccines.
   Methods. Twenty-one healthy adults were inoculated intranasally with 10(6) plaque-forming units of rHMPV-SHs. Respiratory symptoms and shedding of challenge virus were assessed. Neutralizing antibody responses, serum immunoglobulin G and A, and nasal wash specimen immunoglobulin A antibody responses to the HMPV F protein were also measured. Induction of nasal cytokines was assessed with electrochemiluminescence assays.
   Results. Nine subjects (43%) were infected with challenge virus as determined by virus detection and/or >= 4-fold rise in serum antibody titers. Peak viral shedding occurred on days 7-9 after infection. Four weeks after inoculation, 35% of subjects had any antibody response. Six of 9 infected subjects had respiratory symptoms, and 3 had headache after inoculation. Cytokine patterns differed considerably between subjects with similar illness severity and viral shedding.
   Conclusions. The rHMPV-SHs virus is infectious and is a suitable parent virus for development of live-attenuated HMPV vaccine candidates.
   Clinical Trials Registration. NCT01109329.
C1 [Talaat, Kawsar R.; Karron, Ruth A.; Thumar, Bhagvanji; McMahon, Bridget A.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Int Hlth, Ctr Immunizat Res, Baltimore, MD USA.
   [Schmidt, Alexander C.; Collins, Peter L.; Buchholz, Ursula J.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Talaat, KR (reprint author), JHSPH, Ctr Immunizat Res, 624 N Broadway,Room 249, Baltimore, MD 21205 USA.
EM ktalaat@jhsph.edu
FU NIAID, (National Institutes of Health) [N01-AI-15444]; NIAID, the
   National Institutes of Health; MedImmune
FX This research was supported in part by the Intramural Research Program
   of the NIAID, (National Institutes of Health contract N01-AI-15444) and
   a Collaborative Research and Development Agreement between NIAID, the
   National Institutes of Health, and MedImmune.
NR 42
TC 10
Z9 11
U1 0
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
EI 1537-6613
J9 J INFECT DIS
JI J. Infect. Dis.
PD NOV 15
PY 2013
VL 208
IS 10
BP 1669
EP 1678
DI 10.1093/infdis/jit356
PG 10
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 244HI
UT WOS:000326378000018
PM 23908489
ER

PT J
AU Hicks, R
   Giacino, J
   Harrison-Felix, C
   Manley, G
   Valadka, A
   Wilde, EA
AF Hicks, Ramona
   Giacino, Joseph
   Harrison-Felix, Cynthia
   Manley, Geoffrey
   Valadka, Alex
   Wilde, Elisabeth A.
TI Progress in Developing Common Data Elements for Traumatic Brain Injury
   Research: Version Two - The End of the Beginning
SO JOURNAL OF NEUROTRAUMA
LA English
DT Article
DE acute; chronic; collaboration; concussion; data standardization;
   epidemiology; rehabilitation
ID WORKING GROUP; PEDIATRIC CONSIDERATIONS; PSYCHOLOGICAL HEALTH;
   CLINICAL-ASSESSMENT; OUTCOME MEASURES; RECOMMENDATIONS; DEMOGRAPHICS;
   BIOSPECIMENS; SCORE
AB To accelerate data sharing and research on traumatic brain injury (TBI), several federal agencies have been collaborating to support the development and implementation of common data elements (CDEs). The first recommendations for CDEs were made in 2010, and were well suited for hospital-based studies of acute TBI in adults. To broaden the utility of the TBI CDEs, experts were asked to update the recommendations to make them relevant to all ages, levels of injury severity, and phases of recovery. The second version of the TBI CDEs (v.2) was organized around four major study types: 1) epidemiological research; 2) studies on acute, hospitalized patients; 3) studies of the rehabilitation for moderate/severe TBI; and 4) mild TBI/concussion research. Given the heterogeneity of TBI, only a small set of core CDEs were found to be relevant across all study types. However, within groups, a much larger set of highly relevant CDEs were identified, and these were called basic CDEs. In addition, an expanded number of supplemental CDEs were specified and recommended for use depending upon the study goals. Version 2 provides a rich data dictionary for TBI research with about 900 CDEs. Many of the CDEs overlap across the study types, which will facilitate comparisons and meta-analysis across studies. Further modifications of the CDEs should be based on evaluation of their usefulness following implementation across a range of studies.
C1 [Hicks, Ramona] NINDS, Bethesda, MD 20892 USA.
   [Giacino, Joseph] Harvard Univ, Sch Med, Spaulding Rehabil Hosp, Dept Phys Med & Rehabil, Boston, MA USA.
   [Harrison-Felix, Cynthia] Craig Hosp, Dept Phys Med & Rehabil, Englewood, CO USA.
   [Harrison-Felix, Cynthia] Univ Colorado, Dept Phys Med & Rehabil, Denver, CO 80202 USA.
   [Manley, Geoffrey] Univ Calif San Francisco, Dept Neurol Surg, San Francisco, CA USA.
   [Valadka, Alex] Seton Brain & Spine Inst, Austin, TX USA.
   [Wilde, Elisabeth A.] Baylor Coll Med, Dept Phys Med & Rehabil, Houston, TX 77030 USA.
   [Wilde, Elisabeth A.] Baylor Coll Med, Dept Neurol, Houston, TX 77030 USA.
   [Wilde, Elisabeth A.] Baylor Coll Med, Dept Radiol, Houston, TX 77030 USA.
   [Wilde, Elisabeth A.] Michael E DeBakey VA Med Ctr, Houston, TX USA.
RP Hicks, R (reprint author), NINDS, NIH, 6001 Execut Blvd,Room 2206, Bethesda, MD 20892 USA.
EM hicksra@mail.nih.gov
NR 26
TC 22
Z9 22
U1 1
U2 5
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0897-7151
EI 1557-9042
J9 J NEUROTRAUM
JI J. Neurotrauma
PD NOV 15
PY 2013
VL 30
IS 22
BP 1852
EP 1861
DI 10.1089/neu.2013.2938
PG 10
WC Critical Care Medicine; Clinical Neurology; Neurosciences
SC General & Internal Medicine; Neurosciences & Neurology
GA 243PH
UT WOS:000326328400003
PM 23725058
ER

PT J
AU Sibley, CT
   Vavere, AL
   Gottlieb, I
   Cox, C
   Matheson, M
   Spooner, A
   Godoy, G
   Fernandes, V
   Wasserman, BA
   Bluemke, DA
   Lima, JAC
AF Sibley, Christopher T.
   Vavere, Andrea L.
   Gottlieb, Ilan
   Cox, Christopher
   Matheson, Matthew
   Spooner, Amy
   Godoy, Gustavo
   Fernandes, Veronica
   Wasserman, Bruce A.
   Bluemke, David A.
   Lima, Joao A. C.
TI MRI-measured regression of carotid atherosclerosis induced by statins
   with and without niacin in a randomised controlled trial: the NIA plaque
   study
SO HEART
LA English
DT Article
ID INTIMA-MEDIA THICKNESS; EXTENDED-RELEASE NIACIN; HIGH ATHEROTHROMBOSIS
   INTERVENTION; HDL/HIGH TRIGLYCERIDES IMPACT; PLACEBO-CONTROLLED TRIAL;
   HEALTH OUTCOMES TRIAL; HDL CHOLESTEROL; CARDIOVASCULAR EVENTS; METABOLIC
   SYNDROME; BLOOD CHOLESTEROL
AB Objective To evaluate the benefit of niacin in addition to statin therapy on plaque regression among older individuals with established atherosclerosis.
   Design Randomised, controlled, double-blind clinical trial.
   Setting University outpatient center.
   Patients 145 patients older than 65 years, half of them older than 75years of age, with established atherosclerosis were enrolled.
   Interventions Participants received either extended release niacin (1500mg daily) or placebo in addition to statin therapy to reach their National Cholesterol Education Program-defined low density lipoprotein (LDL) cholesterol target.
   Main Outcome Measures The primary endpoint was reduction in the wall volume of the internal carotid artery (ICA) measured by MRI.
   Results After 18months, high density lipoprotein cholesterol was higher with statins plus niacin compared with statins alone (1.60.4 vs 1.4 +/- 0.4mmol/L p<0.001). Both groups had significant decreases in the main outcome measure of ICA wall volume, which regressed at 0.5%/month (SEM 0.2, p=0.004) in the statins plus placebo group and at 0.7%/month in the statins plus niacin group (SEM 0.2, p<0.001). There was no difference in the rate of regression between groups (p=0.49).
   Conclusions Treatment with statin therapy to presently recommended LDL levels, with or without niacin, resulted in significant atherosclerosis reduction.
C1 [Sibley, Christopher T.; Bluemke, David A.] NIH, Dept Radiol & Imaging Sci, Ctr Clin, Bethesda, MD 20892 USA.
   [Sibley, Christopher T.; Vavere, Andrea L.; Gottlieb, Ilan; Spooner, Amy; Godoy, Gustavo; Fernandes, Veronica; Lima, Joao A. C.] Johns Hopkins Sch Med, Dept Med, Baltimore, MD USA.
   [Cox, Christopher; Matheson, Matthew] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
   [Wasserman, Bruce A.; Bluemke, David A.; Lima, Joao A. C.] Johns Hopkins Sch Med, Dept Radiol, Baltimore, MD USA.
RP Lima, JAC (reprint author), Johns Hopkins Univ Hosp, Dept Med, Div Cardiol, 600 N Wolfe St, Baltimore, MD 21287 USA.
EM jlima@jhmi.edu
OI Bluemke, David/0000-0002-8323-8086
FU National Institute on Aging [AG-021570]; intramural research program of
   the NIH Clinical Center;  [T32-HL-007227-35]
FX This work was supported by grant AG-021570 from the National Institute
   on Aging. Kos Pharmaceuticals, later acquired by Abbott Pharmaceuticals
   provided study drug at no cost and funding to complete data analysis. Dr
   Sibley was supported by grant T32-HL-007227-35 and by the intramural
   research program of the NIH Clinical Center. Funding sources had no role
   in study design and conduct; data collection, interpretation or
   analysis; or in manuscript preparation or approval.
NR 30
TC 14
Z9 15
U1 0
U2 7
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1355-6037
EI 1468-201X
J9 HEART
JI Heart
PD NOV 15
PY 2013
VL 99
IS 22
BP 1675
EP 1680
DI 10.1136/heartjnl-2013-303926
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 240MQ
UT WOS:000326101300010
PM 23872591
ER

PT J
AU Kaess, BM
   Gona, P
   Larson, MG
   Cheng, S
   Aragam, J
   Kenchaiah, S
   Benjamin, EJ
   Vasan, RS
AF Kaess, Bernhard M.
   Gona, Philimon
   Larson, Martin G.
   Cheng, Susan
   Aragam, Jayashree
   Kenchaiah, Satish
   Benjamin, Emelia J.
   Vasan, Ramachandran S.
TI Secular trends in echocardiographic left ventricular mass in the
   community: the Framingham Heart Study
SO HEART
LA English
DT Article
ID GENDER-DIFFERENCES; RISK-FACTORS; HYPERTROPHY; HYPERTENSION; FAILURE;
   LIFE; INDIVIDUALS; PREVALENCE; REGRESSION; REDUCTION
AB Objective To investigate secular trends in echocardiographically determined left ventricular mass (LVM).
   Design, setting and participants Longitudinal community-based cohort study in Framingham, Massachussetts. LVM was calculated from routine echocardiography in 4320 participants (52% women) of the Framingham offspring cohort at examination cycles 4 (1987-1991), 5 (1991-1995), 6 (1995-1998) and 8 (2005-2008), totalling 13971 person-observations.
   Main outcome measures Sex-specific trends in mean LVM (and its components, LV diastolic diameter (LVDD) and LV wall thickness (LVWT)), and LVM indexed to body surface area (BSA).
   Results In men, age-adjusted LVM modestly increased from examination 4 to 8 (192g to 198g, p-trend=0.0005), whereas, in women it decreased from 147g at examination 4 to 140g at examination 8 (p-trend<0.0001). The trend for increasing LVM in men tracked with an increasing LVDD (p-trend=0.0002), whereas the decline in LVM in women was accompanied by a decrease in LVWT (p-trend<0.0001). Indexing LVM to BSA abolished the increasing trend in men (p-trend=0.49), whereas, the decreasing trend in women was maintained.
   Conclusions In our longitudinal analysis of a large community-based sample spanning two decades, we observed sex-related differences in trends in LVM, with a modest increase of LVM in men (likely attributable to increasing body size), but a decrease in women. Additional studies are warranted to elucidate the basis for these sex-related differences.
C1 [Kaess, Bernhard M.; Gona, Philimon; Larson, Martin G.; Benjamin, Emelia J.; Vasan, Ramachandran S.] NHLBI, Framingham, MA USA.
   [Kaess, Bernhard M.; Gona, Philimon; Larson, Martin G.; Benjamin, Emelia J.; Vasan, Ramachandran S.] Boston Univ, Framingham Heart Study, Framingham, MA USA.
   [Kaess, Bernhard M.] Tech Univ Munich, Deutsch Herzzentrum, D-80290 Munich, Germany.
   [Kaess, Bernhard M.] Univ Klinikum Regensburg, Klin & Poliklin Innere Med 2, Regensburg, Germany.
   [Gona, Philimon] Univ Massachusetts, Med Ctr, Dept Quantitat Hlth Sci, Worcester, MA USA.
   [Larson, Martin G.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
   [Cheng, Susan] Harvard Univ, Brigham & Womens Hosp, Div Cardiovasc Med, Sch,Boston, Boston, MA 02115 USA.
   [Aragam, Jayashree] Vet Adm Hosp, West Roxbury, MA USA.
   [Aragam, Jayashree; Vasan, Ramachandran S.] Harvard Univ, Sch Med, Boston, MA USA.
   [Kenchaiah, Satish; Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Med, Sect Prevent Med, Boston, MA 02118 USA.
   [Kenchaiah, Satish; Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Med, Sect Cardiol, Boston, MA 02118 USA.
   [Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Framingham, MA USA.
RP Vasan, RS (reprint author), Framingham Heart Dis Epidemiol Study, 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA.
EM vasan@bu.edu
RI Kenchaiah, Satish/A-1519-2016; 
OI Ramachandran, Vasan/0000-0001-7357-5970; Benjamin,
   Emelia/0000-0003-4076-2336
FU National Heart, Lung and Blood Institute's Framingham Heart Study
   [N01-HC-25195, R01HL080124, K99-HL-107642]; Ellison Foundation
FX This work was supported by the National Heart, Lung and Blood
   Institute's Framingham Heart Study (Contract No. N01-HC-25195),
   R01HL080124 (RSV), and K99-HL-107642 (SC). Dr Cheng was also supported
   by a grant from the Ellison Foundation.
NR 30
TC 5
Z9 5
U1 0
U2 4
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1355-6037
EI 1468-201X
J9 HEART
JI Heart
PD NOV 15
PY 2013
VL 99
IS 22
BP 1693
EP 1698
DI 10.1136/heartjnl-2013-304600
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 240MQ
UT WOS:000326101300013
PM 24041649
ER

PT J
AU Tager, AM
   Pensiero, M
   Allen, TM
AF Tager, Andrew M.
   Pensiero, Michael
   Allen, Todd M.
TI Recent Advances in Humanized Mice: Accelerating the Development of an
   HIV Vaccine
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
DE HIV; humanized mice; vaccine; CD8+T cells; CTL; antibodies
ID SEVERE COMBINED IMMUNODEFICIENCY; HUMAN IMMUNE-SYSTEM; T-CELL RESPONSES;
   SCID-HU MOUSE; RHESUS-MONKEYS; INFECTION; MODEL; ACQUISITION; TRIAL;
   TRANSPLANTATION
AB Recent advances in the development of humanized mice hold great promise to advance our understanding of protective immunity to human immunodeficiency virus (HIV) infection and to aid in the design of an effective HIV vaccine. This supplement of the Journal of Infectious Diseases summarizes work in the humanized mouse model presented at an HIV Humanized Mouse workshop in Boston, Massachusetts, in November 2012, including recent advances in the development of humanized mice, the trafficking of human immune cells following mucosal HIV transmission, the role of immune activation and Toll-like receptor agonists in the control of HIV, the induction and efficacy of HIV-specific cellular and humoral immune responses, and the preclinical modeling of novel anti-HIV therapeutics. Many gaps remain in our understanding of how to design an effective HIV vaccine and novel therapeutics to eliminate the viral reservoir. Promising early results from studies in humanized mice suggest great potential and enthusiasm for this model to accelerate these critical areas of HIV research.
C1 [Tager, Andrew M.] Harvard Univ, Sch Med, Massachusetts Gen Hosp,Div Rheumatol Allergy & Im, Ctr Immunol & Inflammatory Dis, Cambridge, MA 02138 USA.
   [Tager, Andrew M.; Allen, Todd M.] MIT, Ragon Inst MGH, Cambridge, MA 02139 USA.
   [Tager, Andrew M.; Allen, Todd M.] Harvard Univ, Boston, MA 02115 USA.
   [Pensiero, Michael] NIAID, Vaccine Translat Res Branch, NIH, Bethesda, MD 20892 USA.
RP Allen, TM (reprint author), MIT, Ragon Inst MGH, 400 Technol Sq, Cambridge, MA 02139 USA.
EM tallen2@partners.org
RI Allen, Todd/F-5473-2011
FU National Institute of Allergy and Infectious Diseases [R01-AI090698,
   HIVRAD P01-AI104715]; Harvard University Center for AIDS Research
   [P30-AI060354]; Harvard University Center for AIDS Research; National
   Institute of Allergy and Infectious Diseases, National Institutes of
   Health; Ragon Institute of MGH, MIT, and Harvard
FX This work was supported by the National Institute of Allergy and
   Infectious Diseases (grants R01-AI090698 and HIVRAD P01-AI104715 to T.
   M. A.) and the Harvard University Center for AIDS Research (grant
   P30-AI060354). Attendance at the Humanized Mouse Meeting was funded by
   the Harvard University Center for AIDS Research; the National Institute
   of Allergy and Infectious Diseases, National Institutes of Health; and
   the Ragon Institute of MGH, MIT, and Harvard.
NR 41
TC 10
Z9 10
U1 1
U2 12
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
EI 1537-6613
J9 J INFECT DIS
JI J. Infect. Dis.
PD NOV 15
PY 2013
VL 208
SU 2
BP S121
EP S124
DI 10.1093/infdis/jit451
PG 4
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 244HM
UT WOS:000326378500001
PM 24151317
ER

PT J
AU Smalt, CJ
   Gonzalez-Castillo, J
   Talavage, TM
   Pisoni, DB
   Svirsky, MA
AF Smalt, Christopher J.
   Gonzalez-Castillo, Javier
   Talavage, Thomas M.
   Pisoni, David B.
   Svirsky, Mario A.
TI Neural correlates of adaptation in freely-moving normal hearing subjects
   under cochlear implant acoustic simulations
SO NEUROIMAGE
LA English
DT Article
ID POSTERIOR CINGULATE CORTEX; NOISE-VOCODED WORDS; INDIVIDUAL-DIFFERENCES;
   SPEECH RECOGNITION; FRONTAL-CORTEX; LANGUAGE AREAS; HUMAN BRAIN;
   ACTIVATION; COMPREHENSION; FMRI
AB Neurobiological correlates of adaptation to spectrally degraded speech were investigated with fMRI before and after exposure to a portable real-time speech processor that implements an acoustic simulation model of a cochlear implant (CI). The speech processor, in conjunction with isolating insert earphones and a microphone to capture environment sounds, was worn by participants over a two week chronic exposure period. fMRI and behavioral speech comprehension testing were conducted before and after this two week period. After using the simulator each day for 2 h, participants significantly improved in word and sentence recognition scores. fMRI shows that these improvements came accompanied by changes in patterns of neuronal activation. In particular, we found additional recruitment of visual, motor, and working memory areas after the perceptual training period. These findings suggest that the human brain is able to adapt in a short period of time to a degraded auditory signal under a natural learning environment, and gives insight on how a CI might interact with the central nervous system. This paradigm can be furthered to investigate neural correlates of new rehabilitation, training, and signal processing strategies non-invasively in normal hearing listeners to improve CI patient outcomes. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Smalt, Christopher J.; Talavage, Thomas M.] Purdue Univ, Sch Elect & Comp Engn, W Lafayette, IN 47907 USA.
   [Gonzalez-Castillo, Javier] NIMH, Sect Funct Imaging Methods, Lab Brain & Cognit, Bethesda, MD 20892 USA.
   [Pisoni, David B.] Indiana Univ, Dept Psychol & Brain Sci, Bloomington, IN USA.
   [Svirsky, Mario A.] NYU, Dept Otolaryngol, Sch Med, New York, NY 10016 USA.
RP Smalt, CJ (reprint author), Purdue Univ, Sch Elect & Comp Engn, W Lafayette, IN 47907 USA.
EM smaltcj@gmail.com
RI Svirsky, Mario/A-4160-2008; 
OI Svirsky, Mario/0000-0002-9238-0682; Gonzalez-Castillo,
   Javier/0000-0002-6520-5125
FU NIH [R01 DC 000111-35, R01 DC03937]; NIDCD [T32 DC00030]
FX This work was partially supported by funding from by NIH R01 DC
   000111-35 (D.B.P.), NIH R01 DC03937 (M.A.S), and NIDCD T32 DC00030
   (C.J.S).
NR 53
TC 4
Z9 4
U1 1
U2 30
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD NOV 15
PY 2013
VL 82
BP 500
EP 509
DI 10.1016/j.neuroimage.2013.06.001
PG 10
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
   Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 220FQ
UT WOS:000324568400047
PM 23751864
ER

PT J
AU Guttmacher, AE
   Hirschfeld, S
   Collins, FS
AF Guttmacher, Alan E.
   Hirschfeld, Steven
   Collins, Francis S.
TI The National Children's Study-A Proposed Plan
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
C1 [Guttmacher, Alan E.; Hirschfeld, Steven] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA.
   [Collins, Francis S.] NIH, Off Director, Bethesda, MD 20892 USA.
RP Guttmacher, AE (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA.
RI Hirschfeld, Steven/E-2987-2016
OI Hirschfeld, Steven/0000-0003-0627-7249
NR 1
TC 14
Z9 14
U1 0
U2 2
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 14
PY 2013
VL 369
IS 20
BP 1873
EP 1875
DI 10.1056/NEJMp1311150
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 300MP
UT WOS:000330468300003
PM 24224620
ER

PT J
AU Dunleavy, K
   Pittaluga, S
   Shovlin, M
   Steinberg, SM
   Cole, D
   Grant, C
   Widemann, B
   Staudt, LM
   Jaffe, ES
   Little, RF
   Wilson, WH
AF Dunleavy, Kieron
   Pittaluga, Stefania
   Shovlin, Margaret
   Steinberg, Seth M.
   Cole, Diane
   Grant, Cliona
   Widemann, Brigitte
   Staudt, Louis M.
   Jaffe, Elaine S.
   Little, Richard F.
   Wilson, Wyndham H.
TI Low-Intensity Therapy in Adults with Burkitt's Lymphoma
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID DOSE-ADJUSTED EPOCH; B-CELL LYMPHOMA; NON-HODGKINS-LYMPHOMA; EVENT-FREE
   SURVIVAL; CHEMOTHERAPY REGIMEN; CODOX-M/IVAC; ANTIRETROVIRAL THERAPY;
   CHILDREN; RITUXIMAB; DOXORUBICIN
AB BACKGROUND
   Burkitt's lymphoma is an aggressive B-cell lymphoma that occurs in children and adults and is largely curable with the use of intensive and toxic chemotherapy. Current treatments are less effective and have more severe side effects in adults and patients with immunodeficiency than in children.
   METHODS
   We studied low-intensity treatment consisting of infused etoposide, doxorubicin, and cyclophosphamide with vincristine, prednisone, and rituximab (EPOCH-R) in patients with untreated Burkitt's lymphoma. Two EPOCH-R regimens were tested: a standard dose-adjusted combination in human immunodeficiency virus (HIV)-negative patients (DA-EPOCH-R group) and a lower-dose short-course combination with a double dose of rituximab in HIV-positive patients (SC-EPOCH-RR group).
   RESULTS
   A total of 30 consecutive patients were treated; 19 patients were in the DA-EPOCH-R group, and 11 in the SC-EPOCH-RR group. The overall median age of the patients was 33 years, and 40% were 40 years of age or older; 73% of the patients had intermediate-risk disease, and 10% had high-risk disease. The principal toxic events, fever and neutropenia, were observed during 22% of the DA-EPOCH-R treatment cycles and 10% of the SC-EPOCH-RR treatment cycles. The tumor lysis syndrome developed in 1 patient; no treatment-related deaths occurred. The median cumulative doses of doxorubicin-etoposide and cyclophosphamide administered in the SC-EPOCH-RR group were 47% and 57% lower, respectively, than those administered in the DA-EPOCH-R group. With median follow-up times of 86 months in the DA-EPOCH-R group and 73 months in the SC-EPOCH-RR group, the rates of freedom from progression of disease and overall survival were, respectively, 95% and 100% with DA-EPOCH-R and 100% and 90% with SC-EPOCH-RR. None of the patients died from Burkitt's lymphoma.
   CONCLUSIONS
   In this uncontrolled prospective study, low-intensity EPOCH-R-based treatment was highly effective in adults with sporadic or immunodeficiency-associated Burkitt's lymphoma.
C1 [Dunleavy, Kieron; Pittaluga, Stefania; Shovlin, Margaret; Steinberg, Seth M.; Cole, Diane; Grant, Cliona; Widemann, Brigitte; Staudt, Louis M.; Jaffe, Elaine S.; Little, Richard F.; Wilson, Wyndham H.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Wilson, WH (reprint author), NCI, Lymphoid Malignancy Branch, Bldg 10,Rm 4N-115,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM wilsonw@mail.nih.gov
OI Jaffe, Elaine/0000-0003-4632-0301
FU National Cancer Institute
FX Funded by the National Cancer Institute; ClinicalTrials.gov numbers,
   NCT00001337 and NCT00006436.
NR 41
TC 70
Z9 71
U1 0
U2 5
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 14
PY 2013
VL 369
IS 20
BP 1915
EP 1925
DI 10.1056/NEJMoa1308392
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 300MP
UT WOS:000330468300009
PM 24224624
ER

PT J
AU Gordon, D
   Taddei-Peters, W
   Mascette, A
   Antman, M
   Kaufmann, PG
   Lauer, MS
AF Gordon, David
   Taddei-Peters, Wendy
   Mascette, Alice
   Antman, Melissa
   Kaufmann, Peter G.
   Lauer, Michael S.
TI Publication of Trials Funded by the National Heart, Lung, and Blood
   Institute
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID BIAS
AB Background
   Rapid publication of clinical trials is essential in order for the findings to yield maximal benefits for public health and scientific progress. Factors affecting the speed of publication of the main results of government-funded trials have not been well characterized.
   Methods
   We analyzed 244 extramural randomized clinical trials of cardiovascular interventions that were supported by the National Heart, Lung, and Blood Institute (NHLBI). We selected trials for which data collection had been completed between January 1, 2000, and December 31, 2011. Our primary outcome measure was the time between completion of the trial and publication of the main results in a peer-reviewed journal.
   Results
   As of March 31, 2012, the main results of 156 trials (64%) had been published (Kaplan-Meier median time to publication, 25 months, with 57% published within 30 months). Trials that focused on clinical events were published more rapidly than those that focused on surrogate measures (median, 9 months vs. 31 months; P<0.001). The only independent predictors of more rapid publication were a focus on clinical events rather than surrogate end points (adjusted publication rate ratio, 2.11; 95% confidence interval, 1.26 to 3.53; P = 0.004) and higher costs of conducting the trial, up to a threshold of approximately $5 million (P<0.001). The 37 trials that focused on clinical events and cost at least $5 million accounted for 67% of the funds spent on clinical trials but received 82% of the citations. After adjustment of the analysis for a focus on clinical events and for cost, trial results that were classified as positive were published more quickly than those classified as negative.
   Conclusions
   Results of less than two thirds of NHLBI-funded randomized clinical trials of cardiovascular interventions were published within 30 months after completion of the trial. Trials that focused on clinical events were published more quickly than those that focused on surrogate end points.
C1 [Gordon, David; Taddei-Peters, Wendy; Mascette, Alice] NHLBI, Off Special Projects, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
   [Antman, Melissa] NHLBI, Off Sci & Technol, Bethesda, MD 20892 USA.
   [Kaufmann, Peter G.] NHLBI, Clin Applicat & Prevent Branch, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
   [Lauer, Michael S.] NHLBI, Off Director, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
RP Lauer, MS (reprint author), 6701 Rockledge Dr,Rm 8128, Bethesda, MD 20892 USA.
EM lauerm@nhlbi.nih.gov
FU National Heart, Lung, and Blood Institute
FX Funded by the National Heart, Lung, and Blood Institute.
NR 12
TC 45
Z9 45
U1 0
U2 1
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 14
PY 2013
VL 369
IS 20
BP 1926
EP 1934
DI 10.1056/NEJMsa1300237
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 300MP
UT WOS:000330468300010
PM 24224625
ER

PT J
AU Xue, H
   Kellman, P
   LaRocca, G
   Arai, AE
   Hansen, MS
AF Xue, Hui
   Kellman, Peter
   LaRocca, Gina
   Arai, Andrew E.
   Hansen, Michael S.
TI High spatial and temporal resolution retrospective cine cardiovascular
   magnetic resonance from shortened free breathing real-time acquisitions
SO JOURNAL OF CARDIOVASCULAR MAGNETIC RESONANCE
LA English
DT Article
DE Retrospective reconstruction; Myocardial function; Motion correction;
   Real-time imaging; Cardiac MRI
ID K-T FOCUSS; MOTION CORRECTION; DYNAMIC MRI; RECONSTRUCTION; IMAGES;
   SENSE; HOLD
AB Background: Cine cardiovascular magnetic resonance (CMR) is challenging in patients who cannot perform repeated breath holds. Real-time, free-breathing acquisition is an alternative, but image quality is typically inferior. There is a clinical need for techniques that achieve similar image quality to the segmented cine using a free breathing acquisition. Previously, high quality retrospectively gated cine images have been reconstructed from real-time acquisitions using parallel imaging and motion correction. These methods had limited clinical applicability due to lengthy acquisitions and volumetric measurements obtained with such methods have not previously been evaluated systematically.
   Methods: This study introduces a new retrospective reconstruction scheme for real-time cine imaging which aims to shorten the required acquisition. A real-time acquisition of 16-20s per acquired slice was inputted into a retrospective cine reconstruction algorithm, which employed non-rigid registration to remove respiratory motion and SPIRiT non-linear reconstruction with temporal regularization to fill in missing data. The algorithm was used to reconstruct cine loops with high spatial (1.3-1.8 x 1.8-2.1 mm(2)) and temporal resolution (retrospectively gated, 30 cardiac phases, temporal resolution 34.3 +/- 9.1 ms). Validation was performed in 15 healthy volunteers using two different acquisition resolutions (256 x 144/192 x 128 matrix sizes). For each subject, 9 to 12 short axis and 3 long axis slices were imaged with both segmented and real-time acquisitions. The retrospectively reconstructed real-time cine images were compared to a traditional segmented breath-held acquisition in terms of image quality scores. Image quality scoring was performed by two experts using a scale between 1 and 5 (poor to good). For every subject, LAX and three SAX slices were selected and reviewed in the random order. The reviewers were blinded to the reconstruction approach and acquisition protocols and scores were given to segmented and retrospective cine series. Volumetric measurements of cardiac function were also compared by manually tracing the myocardium for segmented and retrospective cines.
   Results: Mean image quality scores were similar for short axis and long axis views for both tested resolutions. Short axis scores were 4.52/4.31 (high/low matrix sizes) for breath-hold vs. 4.54/4.56 for real-time (paired t-test, P = 0.756/0.011). Long axis scores were 4.09/4.37 vs. 3.99/4.29 (P = 0.475/0.463). Mean ejection fraction was 60.8/61.4 for breath-held acquisitions vs. 60.3/60.3 for real-time acquisitions (P = 0.439/0.093). No significant differences were seen in end-diastolic volume (P = 0.460/0.268) but there was a trend towards a small overestimation of end-systolic volume of 2.0/2.5 ml, which did not reach statistical significance (P = 0.052/0.083).
   Conclusions: Real-time free breathing CMR can be used to obtain high quality retrospectively gated cine images in 16-20s per slice. Volumetric measurements and image quality scores were similar in images from breath-held segmented and free breathing, real-time acquisitions. Further speedup of image reconstruction is still needed.
C1 [Xue, Hui; Kellman, Peter; LaRocca, Gina; Arai, Andrew E.; Hansen, Michael S.] NHLBI, NIH, Bethesda, MD 20814 USA.
RP Xue, H (reprint author), NHLBI, NIH, 10 Ctr Dr, Bethesda, MD 20814 USA.
EM hui.xue@nih.gov
RI Hansen, Michael/J-5391-2015
OI Hansen, Michael/0000-0002-8087-8731
NR 23
TC 16
Z9 16
U1 0
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1097-6647
EI 1532-429X
J9 J CARDIOVASC MAGN R
JI J. Cardiov. Magn. Reson.
PD NOV 14
PY 2013
VL 15
AR 102
DI 10.1186/1532-429X-15-102
PG 15
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
   Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
   Medical Imaging
GA 287UO
UT WOS:000329567900001
PM 24228930
ER

PT J
AU Kostelecky, B
   Trimble, EL
   Bhatia, K
AF Kostelecky, Brenda
   Trimble, Edward L.
   Bhatia, Kishor
TI Learning lessons from cancer centers in low- and middle-income countries
SO INFECTIOUS AGENTS AND CANCER
LA English
DT Editorial Material
ID WESTERN KENYA
AB Infectious Agents and Cancer is introducing a new section on Cancer Centers in Low-and Middle-Income Countries intended to provide the oncology community with detailed information about lessons learned in cancer control in resource-limited settings. The growing burden of cancer and the high rates of infection-related cancers in Low- and Middle-Income Countries (LMICs) argue for exploring the successes and challenges of cancer centers in low-resource settings. Detailed analyses are needed on how successful cancer centers have developed and managed such key components as strategic partnerships, trained cancer professionals, sustainable funding, appropriate technology, and research capacity. Many examples exist wherein local cancer centers have made significant progress and as such, the series will provide a platform to showcase detailed features of cancer institutes in LMICs and provide valuable information for those seeking to replicate successful models and to help invigorate efforts to build cancer capacity.
C1 [Kostelecky, Brenda; Trimble, Edward L.] NCI, Ctr Global Hlth, NIH, Rockville, MD 20850 USA.
   [Bhatia, Kishor] NCI, Off HIV & AIDS Malignancy, NIH, Rockville, MD 20850 USA.
RP Bhatia, K (reprint author), NCI, Off HIV & AIDS Malignancy, NIH, 9609 Med Ctr Dr, Rockville, MD 20850 USA.
EM bhatiak@mail.nih.gov
NR 13
TC 4
Z9 4
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1750-9378
J9 INFECT AGENTS CANCER
JI Infect. Agents Cancer
PD NOV 14
PY 2013
VL 8
AR 44
DI 10.1186/1750-9378-8-44
PG 3
WC Oncology; Immunology
SC Oncology; Immunology
GA 281HM
UT WOS:000329090800001
PM 24228782
ER

PT J
AU Rokic, MB
   Stojilkovic, SS
AF Rokic, Milos B.
   Stojilkovic, Stanko S.
TI Two open states of P2X receptor channels
SO FRONTIERS IN CELLULAR NEUROSCIENCE
LA English
DT Article
DE ATP; purinergic receptor channels; gating; pore opening; pore dilation;
   NMDG; YO-PRO-1
ID EXTRACELLULAR ATP; PORE FORMATION; PERMEABILITY DYNAMICS;
   FUNCTIONAL-PROPERTIES; GATING PROPERTIES; CYTOSOLIC DOMAIN;
   PLASMA-MEMBRANE; ION CHANNELS; MAST-CELLS; PANNEXIN 1
AB The occupancy of the orthosteric ligand binding sites of P2X receptor (P2XR) channels causes the rapid opening of a small cation-permeable pore, followed by a gradual dilation that renders the pore permeable to large organic cations. Electrophysiologically, this phenomenon was shown using whole-cell current recording on P2X2R-, P2X2/X5R-, P2X4R- and P2X7R-expressing cells that were bathed in N-methyl-D-glucamine (NMDG(+))-containing buffers in the presence and/or absence of small monovalent and divalent cations. The pore dilation of P2X4R and P2X7R caused a secondary current growth, whereas that of P2X2R showed a sustained kinetic coupling of dilation and desensitization, leading to receptor channel closure. The pore size of the P2X7R open and dilated states was estimated to be approximately 0.85 nm and greater than 1 nm, respectively. The P2XR pore dilation was also observed in intact cells by measurement of fluorescent dye uptake/release, application of polyethylene glycols of different sizes, and atomic force microscopy. However, pore dilation was not observed at the single channel level. Structural data describing the dilated state are not available, and the relevance of orthosteric and allosteric ligand interactions to pore dilation was not studied.
C1 [Rokic, Milos B.; Stojilkovic, Stanko S.] Eunice Kennedy Shiver Natl Inst Child Hlth & Huma, Sect Cellular Signaling, Program Dev Neurosci, NIH, Bethesda, MD 20892 USA.
RP Stojilkovic, SS (reprint author), Eunice Kennedy Shiver Natl Inst Child Hlth & Huma, Sect Cellular Signaling, Program Dev Neurosci, NIH, Bldg 49,Room 6A36, Bethesda, MD 20892 USA.
EM stojilks@mail.nih.gov
RI ROKIC, MILOS/O-7204-2014
OI ROKIC, MILOS/0000-0002-9148-2716
FU Intramural Research Program of the National Institute of Child Health
   and Human Development
FX This work was supported by the Intramural Research Program of the
   National Institute of Child Health and Human Development.
NR 74
TC 16
Z9 16
U1 1
U2 8
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5102
J9 FRONT CELL NEUROSCI
JI Front. Cell. Neurosci.
PD NOV 14
PY 2013
VL 7
AR 215
DI 10.3389/fncel.2013.00215
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 264AV
UT WOS:000327850200001
PM 24312007
ER

PT J
AU Morgan, RA
AF Morgan, Richard A.
TI Risky business: target choice in adoptive cell therapy
SO BLOOD
LA English
DT Editorial Material
ID T-CELLS; ANTIGEN
C1 Natl Inst Hlth, Bethesda, MD USA.
RP Morgan, RA (reprint author), Natl Inst Hlth, Bethesda, MD USA.
NR 8
TC 2
Z9 2
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD NOV 14
PY 2013
VL 122
IS 20
BP 3392
EP 3394
DI 10.1182/blood-2013-09-527622
PG 5
WC Hematology
SC Hematology
GA 261LM
UT WOS:000327666500002
PM 24235126
ER

PT J
AU Morton, LM
   Freedman, DM
AF Morton, Lindsay M.
   Freedman, D. Michal
TI Shedding light on UVR and Hodgkin lymphoma
SO BLOOD
LA English
DT Editorial Material
ID ULTRAVIOLET-RADIATION; 25-HYDROXYVITAMIN D; RISK; EXPOSURE
C1 [Morton, Lindsay M.; Freedman, D. Michal] Natl Inst Hlth, Bethesda, MD USA.
RP Morton, LM (reprint author), Natl Inst Hlth, Bethesda, MD USA.
RI Morton, Lindsay/B-5234-2015
OI Morton, Lindsay/0000-0001-9767-2310
NR 10
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD NOV 14
PY 2013
VL 122
IS 20
BP 3395
EP 3397
DI 10.1182/blood-2013-09-527648
PG 7
WC Hematology
SC Hematology
GA 261LM
UT WOS:000327666500004
PM 24235128
ER

PT J
AU Pepe, A
   Pamment, M
   Kim, YS
   Lee, S
   Lee, MJ
   Beebe, K
   Filikov, A
   Neckers, L
   Trepel, JB
   Malhotra, SV
AF Pepe, Antonella
   Pamment, Michael
   Kim, Yeong Sang
   Lee, Sunmin
   Lee, Mm-Jung
   Beebe, Kristin
   Filikov, Anton
   Neckers, Len
   Trepel, Jane B.
   Malhotra, Sanjay V.
TI Synthesis and Structure-Activity Relationship Studies of Novel
   Dihydropyridones as Androgen Receptor Modulators
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID LIGAND-BINDING DOMAIN; RESISTANT PROSTATE-CANCER; ENANTIOPURE
   2,3-DIHYDRO-4-PYRIDONES; ASYMMETRIC-SYNTHESIS; UNTREATED PATIENTS;
   NUCLEAR RECEPTORS; BICALUTAMIDE; ANTIANDROGEN; SUPERFAMILY; MONOTHERAPY
AB A library of 3-hydroxy-2,3-dihydropyridones was synthesized, and their activities as antiandrogens were tested in the human prostate cancer cell line LNCaP. Structure-activity relationship (SAR) studies resulted in the identification of a potent compound whose activity is comparable to that of MDV3100. Homology modeling and molecular mechanics were used to build a structural model of the androgen receptor ligand binding domain and to investigate the structural basis of the antagonism. The model is qualitatively consistent with the observed SAR. Moreover, the enrichment plot shows that screening with the model performs significantly better than random screening. Therefore, the model probably represents a realistic conformation of the antagonist form and can be utilized for structure-based design of novel antiandrogens.
C1 [Pepe, Antonella; Pamment, Michael; Filikov, Anton; Malhotra, Sanjay V.] SAIC Frederick Inc, Frederick Natl Lab Canc Res, Lab Synthet Chem, Frederick, MD 21702 USA.
   [Kim, Yeong Sang; Lee, Sunmin; Lee, Mm-Jung; Trepel, Jane B.] NCI, Dev Therapeut Branch, NIH, Bethesda, MD 20892 USA.
   [Beebe, Kristin; Neckers, Len] NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Malhotra, SV (reprint author), SAIC Frederick Inc, Frederick Natl Lab Canc Res, Lab Synthet Chem, Frederick, MD 21702 USA.
EM malhotrasa@mail.nih.gov
FU National Cancer Institute (NCI) Developmental Therapeutics Program; NCI;
   National Institutes of Health; SAIC-Frederick [HSN261200800001E]
FX A.P., A.F., M.P., and S.V.M. thank the National Cancer Institute (NCI)
   Developmental Therapeutics Program. This project was funded in whole or
   in part with federal funds from the NCI, National Institutes of Health,
   to the Intramural Research Program (Y.S.K, S.L., M.-J.L., and J.T.) and
   to SAIC-Frederick under Contract HSN261200800001E.
NR 39
TC 7
Z9 7
U1 0
U2 14
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
EI 1520-4804
J9 J MED CHEM
JI J. Med. Chem.
PD NOV 14
PY 2013
VL 56
IS 21
BP 8280
EP 8297
DI 10.1021/jm301714s
PG 18
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 253TB
UT WOS:000327111100005
PM 24044500
ER

PT J
AU Costi, R
   Metifiot, M
   Esposito, F
   Crucitti, GC
   Pescatori, L
   Messore, A
   Scipione, L
   Tortorella, S
   Zinzula, L
   Novellino, E
   Pommier, Y
   Tramontano, E
   Marchand, C
   Di Santo, R
AF Costi, Roberta
   Metifiot, Mathieu
   Esposito, Francesca
   Crucitti, Giuliana Cuzzucoli
   Pescatori, Luca
   Messore, Antonella
   Scipione, Luigi
   Tortorella, Silvano
   Zinzula, Luca
   Novellino, Ettore
   Pommier, Yves
   Tramontano, Enzo
   Marchand, Christophe
   Di Santo, Roberto
TI 6-(1-Benzyl-1H-pyrrol-2-yl)-2,4-dioxo-5-hexenoic Acids as Dual
   Inhibitors of Recombinant HIV-1 Integrase and Ribonuclease H,
   Synthesized by a Parallel Synthesis Approach
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; CELL-BASED ASSAYS; RNASE-H;
   REVERSE-TRANSCRIPTASE; DIKETO ACID; TYPE-1 INTEGRASE; BIOLOGICAL
   EVALUATION; STRAND TRANSFER; INFECTED-CELLS; DERIVATIVES
AB The increasing efficiency of HAART has helped to transform HIV/AIDS into a chronic disease. Still, resistance and drug drug interactions warrant the development of new anti-HIV agents. We previously discovered hit 6, active against HIV-1 replication and targeting RNase H in vitro. Because of its diketo-acid moiety, we speculated that this chemotype could serve to develop dual inhibitors of both RNase H and integrase. Here, we describe a new series of 1-benzyl-pyrrolyl diketohexenoic derivatives, 7a-y and 8a-y, synthesized following a parallel solution-phase approach. Those 50 analogues have been tested on recombinant enzymes (RNase H and integrase) and in cell-based assays. Approximately half (22) exibited inhibition of HIV replication. Compounds 7b, 7u, and 8g were the most active against the RNase H activity of reverse-transcriptase, with IC50 values of 3, 3, and 2.5 mu M, respectively. Compound 8g was also the most potent integrase inhibitor with an IC50 value of 26 nM.
C1 [Costi, Roberta; Crucitti, Giuliana Cuzzucoli; Pescatori, Luca; Messore, Antonella; Scipione, Luigi; Tortorella, Silvano; Di Santo, Roberto] Univ Roma La Sapienza, Dipartimento Chim & Tecnol Farmaco, Ist Pasteur, Fdn Cenci Bolognetti, I-00185 Rome, Italy.
   [Metifiot, Mathieu; Pommier, Yves; Marchand, Christophe] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Esposito, Francesca; Zinzula, Luca; Tramontano, Enzo] Univ Cagliari, Dept Life & Environm Sci, I-09124 Cagliari, Italy.
   [Novellino, Ettore] Univ Naples Federico II, Dipartimento Farm, I-80131 Naples, Italy.
RP Costi, R (reprint author), Univ Roma La Sapienza, Dipartimento Chim & Tecnol Farmaco, Ist Pasteur, Fdn Cenci Bolognetti, Ple Aldo Moro 5, I-00185 Rome, Italy.
EM roberta.costi@uniroma1.it; marchand@nih.gov
RI Pescatori, Luca/H-5917-2016; Tramontano, Enzo/B-4919-2012; Esposito,
   Francesca/I-8879-2012; 
OI Pescatori, Luca/0000-0003-4734-7856; Tramontano,
   Enzo/0000-0002-4849-0980; Esposito, Francesca/0000-0001-9725-7977;
   COSTI, Roberta/0000-0002-1314-9029; TORTORELLA,
   Silvano/0000-0002-3279-9182; scipione, luigi/0000-0002-2006-7005; Di
   Santo, Roberto/0000-0002-4279-7666
FU Italian MIUR; Italian Ministry of Health; CHAARM; RAS; PO Sardinia FSE
   [CRP2_683]; LR [7/2007, CRP2_682]; National Institutes of Health
   Intramural Program, Center for Cancer Research, National Cancer
   Institute; National Institutes of Health grants from the AIDS Intramural
   Targeted Program (IATAP)
FX We thank Italian MIUR for financial support PRIN 2010, the Italian
   Ministry of Health for financial support AIDS 2009-2010 and Fondazione
   Banco di Sardegna. R.D.S. and R.C. thanks CHAARM project for partial
   support. Francesca Esposito and Luca Zinzula were supported by RAS
   fellowships, cofinanced with funds of PO Sardinia FSE 2007-2013 and of
   LR 7/2007, projects CRP2_683 and CRP2_682, respectively. Our studies
   were also supported by the National Institutes of Health Intramural
   Program, Center for Cancer Research, National Cancer Institute and by
   National Institutes of Health grants from the AIDS Intramural Targeted
   Program (IATAP). The following reagent was obtained through the NIH AIDS
   Reagent Program, Division of AIDS, NIAID, NIH: HeLa-CD4-LTR-beta-gal
   from Dr. Michael Emerman.<SUP>32</SUP>
NR 33
TC 18
Z9 18
U1 0
U2 12
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
EI 1520-4804
J9 J MED CHEM
JI J. Med. Chem.
PD NOV 14
PY 2013
VL 56
IS 21
BP 8588
EP 8598
DI 10.1021/jm401040b
PG 11
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 253TB
UT WOS:000327111100029
PM 24124919
ER

PT J
AU Carroll, FI
   Gichinga, MG
   Williams, JD
   Vardy, E
   Roth, BL
   Mascarella, SW
   Thomas, JB
   Navarro, HA
AF Carroll, F. Ivy
   Gichinga, Moses G.
   Williams, John D.
   Vardy, Eyal
   Roth, Bryan L.
   Mascarella, S. Wayne
   Thomas, James B.
   Navarro, Hernan A.
TI 4 beta-Methyl-5-(3-hydroxyphenyl)morphan Opioid Agonist and Partial
   Agonist Derived from a 4 beta-Methyl-5-(3-hydroxyphenyl)morphan Pure
   Antagonist
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID RECEPTOR ANTAGONIST; DELTA-RECEPTOR; HIGHLY POTENT; KAPPA; DISCOVERY;
   RATS; ALVIMOPAN; FEAR
AB In previous studies we reported that addition of 7 alpha-acylamino groups to N-phenylpropyl-4 beta-methyl-5-(3-hydroxyphenyl)morphan (4) led to compounds that were pure opioid receptor antagonists. In contrast to these findings we report in this study that addition of a 7 alpha-amino (5a), 7 alpha-alkylamino (5b-e), or 7 alpha-dialkylamino (5f-h) group to 4 leads to opioid receptor ligands with varying degrees of agonist/antagonist activity. The 7 alpha-amino and 7 alpha-methylamino analogues were full agonists at the mu and delta receptors and antagonists at the kappa receptor. The 7 alpha-cyclopropylmethylamino analogue 5h was a full agonist at the mu receptor with weaker agonist activity at the delta and kappa receptors. Whereas the addition of a 7 alpha-acylamino group to the pure nonselective opioid receptor antagonist N-phenylpropyl-4 beta-methyl-5-(3-hydroxyphenyl)morphan (4) led to kappa selective pure opioid receptor antagonist, the addition of a 7 alpha-amino, 7 alpha-alkylamino, or 7 alpha-dialkylamino group to 4 leads to opioid ligands that are largely mu or delta agonist with mixed agonist/antagonist properties.
C1 [Carroll, F. Ivy; Gichinga, Moses G.; Williams, John D.; Mascarella, S. Wayne; Thomas, James B.; Navarro, Hernan A.] Res Triangle Inst, Ctr Organ & Med Chem, Res Triangle Pk, NC 27709 USA.
   [Vardy, Eyal; Roth, Bryan L.] Univ N Carolina, Dept Pharmacol, Natl Inst Mental Hlth Psychoact Drug Screening Pr, Chapel Hill Med Sch, Chapel Hill, NC 27599 USA.
   [Vardy, Eyal; Roth, Bryan L.] Univ N Carolina, Div Chem Biol & Med Chem, Chapel Hill Med Sch, Chapel Hill, NC 27599 USA.
RP Carroll, FI (reprint author), Res Triangle Inst, Ctr Organ & Med Chem, POB 12194, Res Triangle Pk, NC 27709 USA.
EM fic@rti.org
RI Roth, Bryan/F-3928-2010; 
OI Mascarella, Wayne/0000-0003-0092-8178
FU National Institute on Drug Abuse [DA09045]
FX This research was supported by the National Institute on Drug Abuse
   (Grant DA09045).
NR 27
TC 3
Z9 3
U1 2
U2 8
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
EI 1520-4804
J9 J MED CHEM
JI J. Med. Chem.
PD NOV 14
PY 2013
VL 56
IS 21
BP 8826
EP 8833
DI 10.1021/jm401250s
PG 8
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 253TB
UT WOS:000327111100047
PM 24144404
ER

PT J
AU Liu, F
   Barsyte-Lovejoy, D
   Li, FL
   Xiong, Y
   Korboukh, V
   Huang, XP
   Allali-Hassani, A
   Janzen, WP
   Roth, BL
   Frye, SV
   Arrowsmith, CH
   Brown, PJ
   Vedadi, M
   Jin, J
AF Liu, Feng
   Barsyte-Lovejoy, Dalia
   Li, Fengling
   Xiong, Yan
   Korboukh, Victoria
   Huang, Xi-Ping
   Allali-Hassani, Abdellah
   Janzen, William P.
   Roth, Bryan L.
   Frye, Stephen V.
   Arrowsmith, Cheryl H.
   Brown, Peter J.
   Vedadi, Masoud
   Jin, Jian
TI Discovery of an in Vivo Chemical Probe of the Lysine Methyltransferases
   G9a and GLP
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID SUBTELOMERIC DELETION SYNDROME; SMALL-MOLECULE INHIBITOR; PLURIPOTENT
   STEM-CELLS; HISTONE METHYLTRANSFERASE; SELECTIVE INHIBITORS; DNA
   METHYLATION; STRUCTURAL BASIS; DRUG DISCOVERY; CANCER-CELLS; EZH2
AB Among epigenetic "writers", "readers", and "erasers", the lysine methyltransferases G9a and GLP, which catalyze mono- and dimethylation of histone H3 lysine 9 (H3K9me2) and nonhistone proteins, have been implicated in a variety of human diseases. A "toolkit" of well-characterized chemical probes will allow biological and disease hypotheses concerning these proteins to be tested in cell-based and animal models with high confidence. We previously discovered potent and selective G9a/GLP inhibitors including the cellular chemical probe UNC0638, which displays an excellent separation of functional potency and cell toxicity. However, this inhibitor is not suitable for animal studies due to its poor pharmacokinetic (PK) properties. Here, we report the discovery of the first G9a and GLP in vivo chemical probe UNC0642, which not only maintains high in vitro and cellular potency, low cell toxicity, and excellent selectivity, but also displays improved in vivo PK properties, making it suitable for animal studies.
C1 [Liu, Feng; Xiong, Yan; Korboukh, Victoria; Janzen, William P.; Frye, Stephen V.; Jin, Jian] Univ N Carolina, UNC Eshelman Sch Pharm, Div Chem Biol & Med Chem, Ctr Integrat Chem Biol & Drug Discovery, Chapel Hill, NC 27599 USA.
   [Huang, Xi-Ping; Roth, Bryan L.] Univ N Carolina, NIMH, Psychoact Drug Screening Program, Chapel Hill, NC 27599 USA.
   [Jin, Jian] Univ N Carolina, Sch Med, Dept Pharmacol, Chapel Hill, NC 27599 USA.
   [Jin, Jian] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
   [Barsyte-Lovejoy, Dalia; Li, Fengling; Allali-Hassani, Abdellah; Arrowsmith, Cheryl H.; Brown, Peter J.; Vedadi, Masoud] Univ Toronto, Struct Genom Consortium, Toronto, ON M5G 1L7, Canada.
RP Jin, J (reprint author), Univ N Carolina, UNC Eshelman Sch Pharm, Div Chem Biol & Med Chem, Ctr Integrat Chem Biol & Drug Discovery, Chapel Hill, NC 27599 USA.
EM jianjin@unc.edu
RI Roth, Bryan/F-3928-2010
FU National Institute of General Medical Sciences of the National
   Institutes of Health [R01GM103893]; University Cancer Research Fund;
   University of North Carolina at Chapel Hill; V Foundation for Cancer
   Research; Structural Genomics Consortium, a registered charity
   [1097737]; Canada Foundation for Innovation; Eli Lilly Canada;
   GlaxoSmithKline; Ontario Ministry of Economic Development and
   Innovation; Novartis Research Foundation; Pfizer; AbbVie; Takeda;
   Janssen; Boehringer Ingelheim; Wellcome Trust
FX The research described here was supported by grant R01GM103893 from the
   National Institute of General Medical Sciences of the National
   Institutes of Health, the University Cancer Research Fund and Carolina
   Partnership from University of North Carolina at Chapel Hill, the V
   Foundation for Cancer Research, and the Structural Genomics Consortium,
   a registered charity (number 1097737) that receives funds from the
   Canada Foundation for Innovation, Eli Lilly Canada, GlaxoSmithKline, the
   Ontario Ministry of Economic Development and Innovation, the Novartis
   Research Foundation, Pfizer, AbbVie, Takeda, Janssen, Boehringer
   Ingelheim and the Wellcome Trust.
NR 60
TC 52
Z9 53
U1 0
U2 30
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
EI 1520-4804
J9 J MED CHEM
JI J. Med. Chem.
PD NOV 14
PY 2013
VL 56
IS 21
BP 8931
EP 8942
DI 10.1021/jm401480r
PG 12
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 253TB
UT WOS:000327111100056
PM 24102134
ER

PT J
AU Volkow, ND
   Swanson, JM
AF Volkow, Nora D.
   Swanson, James M.
TI Adult Attention Deficit-Hyperactivity Disorder
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID DEFICIT/HYPERACTIVITY DISORDER; PRESCRIPTION STIMULANTS; FOLLOW-UP;
   ADHD; METAANALYSIS; MEDICATIONS; NEUROSCIENCE; ASSOCIATION; COMORBIDITY;
   ATOMOXETINE
AB Short-term trials involving adults with ADHD have shown significant improvements in symptoms with stimulants and atomoxetine; however, data on long-term benefits and risks of these medications, particularly among older persons, have been insufficient. ForewordThis Journal feature begins with a case vignette highlighting a common clinical problem. Evidence supporting various strategies is then presented, followed by a review of formal guidelines, when they exist. The article ends with the authors' clinical recommendations.StageA 31-year-old middle-school teacher sought medical help because she was having trouble keeping up with her job assignments and responsibilities. Her primary symptoms were an inability to stay focused and being easily distracted. She reported daydreaming with multiple thoughts at the same time, an inability to complete tasks on time, frequently forgetting to do things at work, and being unable to remain still during solitary activities (e.g., watching a movie and reading a book). Her friends described her as excessively talkative, disorganized, impatient, and careless. From childhood, her teachers noted that she was inattentive and messy and often did ...
   Attention Deficit-Hyperactivity Disorder in Adults
   The recognition that attention deficit-hyperactivity disorder (ADHD) persists after adolescence has led to an increase in its diagnosis and treatment in adults. Randomized trials show clinically significant improvements in ADHD symptoms and in daily functioning with the use of approved medications (stimulants and atomoxetine) for ADHD in adults. Clinical trials of medications for ADHD have been largely short-term and have predominantly involved young and middle-aged adults. Data are lacking on long-term benefits and risks and on risks among elderly patients. The absolute risk of serious cardiovascular adverse events associated with ADHD medications appears to be very low. However, the observed increases in pulse rate and blood pressure with stimulant use underscore the need for caution in prescribing these agents for patients with cardiovascular disease. The risk of addiction to stimulant medications prescribed for the treatment of ADHD in adults is low, but the clinician should be aware of their potential for abuse and dependence.
C1 [Volkow, Nora D.] NIDA, Rockville, MD 20892 USA.
   [Swanson, James M.] Univ Calif Irvine, Sch Med, Irvine, CA 92717 USA.
RP Volkow, ND (reprint author), NIDA, 6001 Executive Blvd,Rm 5274,MSC 9581, Rockville, MD 20892 USA.
EM nvolkow@nida.nih.gov
FU Noven Pharmaceuticals; Johnson Johnson; Janssen
FX Dr. Swanson reports receiving consulting fees to his institution from
   Noven Pharmaceuticals, lecture fees from Johnson & Johnson and Janssen,
   travel support from Shire, and payment for providing testimony as an
   expert witness for Janssen-Ortho on the pharmacokinetic and
   pharmacodynamic properties of methylphenidate, and filing a lawsuit to
   be named as an inventor on filed patents 6,930,129; 8,163,798; and
   6,919,373 regarding a method for treating attention
   deficit-hyperactivity disorder. No other potential conflict of interest
   relevant to this article was reported.
NR 51
TC 38
Z9 39
U1 5
U2 39
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 14
PY 2013
VL 369
IS 20
BP 1935
EP 1944
DI 10.1056/NEJMcp1212625
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 251AN
UT WOS:000326899000002
PM 24224626
ER

PT J
AU Beck-Johnson, LM
   Nelson, WA
   Paaijmans, KP
   Read, AF
   Thomas, MB
   Bjornstad, ON
AF Beck-Johnson, Lindsay M.
   Nelson, William A.
   Paaijmans, Krijn P.
   Read, Andrew F.
   Thomas, Matthew B.
   Bjornstad, Ottar N.
TI The Effect of Temperature on Anopheles Mosquito Population Dynamics and
   the Potential for Malaria Transmission
SO PLOS ONE
LA English
DT Article
ID EAST-AFRICAN HIGHLANDS; GAMBIAE GILES COMPLEX; PLASMODIUM-FALCIPARUM;
   CLIMATE-CHANGE; STRUCTURED POPULATIONS; GENERATION SEPARATION; DEPENDENT
   DEVELOPMENT; IMMATURE STAGES; AQUATIC STAGES; BODY-SIZE
AB The parasites that cause malaria depend on Anopheles mosquitoes for transmission; because of this, mosquito population dynamics are a key determinant of malaria risk. Development and survival rates of both the Anopheles mosquitoes and the Plasmodium parasites that cause malaria depend on temperature, making this a potential driver of mosquito population dynamics and malaria transmission. We developed a temperature-dependent, stage-structured delayed differential equation model to better understand how climate determines risk. Including the full mosquito life cycle in the model reveals that the mosquito population abundance is more sensitive to temperature than previously thought because it is strongly influenced by the dynamics of the juvenile mosquito stages whose vital rates are also temperature-dependent. Additionally, the model predicts a peak in abundance of mosquitoes old enough to vector malaria at more accurate temperatures than previous models. Our results point to the importance of incorporating detailed vector biology into models for predicting the risk for vector borne diseases.
C1 [Beck-Johnson, Lindsay M.; Paaijmans, Krijn P.; Read, Andrew F.; Thomas, Matthew B.; Bjornstad, Ottar N.] Penn State Univ, Ctr Infect Dis Dynam, University Pk, PA 16802 USA.
   [Beck-Johnson, Lindsay M.; Read, Andrew F.; Bjornstad, Ottar N.] Penn State Univ, Dept Biol, University Pk, PA 16802 USA.
   [Nelson, William A.] Queens Univ, Dept Biol, Kingston, ON K7L 3N6, Canada.
   [Paaijmans, Krijn P.; Read, Andrew F.; Thomas, Matthew B.; Bjornstad, Ottar N.] Penn State Univ, Dept Entomol, University Pk, PA 16802 USA.
   [Read, Andrew F.; Bjornstad, Ottar N.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Beck-Johnson, LM (reprint author), Penn State Univ, Ctr Infect Dis Dynam, University Pk, PA 16802 USA.
EM lmb404@psu.edu
FU United States Department of Agriculture National Research Initiative
   [2006-35302-17149]; National Science Foundation-EID program grant
   [EF-0914384]
FX This research was supported by United States Department of Agriculture
   National Research Initiative 2006-35302-17149 to ONB, www.usda.gov, and
   by National Science Foundation-EID program grant EF-0914384 to MBT and
   AFR, www.nsf.gov. The funders had no role in study design, data
   collection and analysis, decision to publish or preparation of the
   manuscript.
NR 60
TC 32
Z9 33
U1 4
U2 66
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 14
PY 2013
VL 8
IS 11
AR e79276
DI 10.1371/journal.pone.0079276
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 254DJ
UT WOS:000327143800053
PM 24244467
ER

PT J
AU Yamamizu, K
   Furuta, S
   Hamada, Y
   Yamashita, A
   Kuzumaki, N
   Narita, M
   Doi, K
   Katayama, S
   Nagase, H
   Yamashita, JK
   Narita, M
AF Yamamizu, Kohei
   Furuta, Sadayoshi
   Hamada, Yusuke
   Yamashita, Akira
   Kuzumaki, Naoko
   Narita, Michiko
   Doi, Kento
   Katayama, Shiori
   Nagase, Hiroshi
   Yamashita, Jun K.
   Narita, Minoru
TI kappa Opioids inhibit tumor angiogenesis by suppressing VEGF signaling
SO SCIENTIFIC REPORTS
LA English
DT Article
ID ANTI-VEGF; MORPHINE; GROWTH; TUMORIGENESIS; CANCER; SYSTEM; SWITCH;
   CELLS
AB Opioids are effective analgesics for the management of moderate to severe cancer pain. Here we show that kappa opioid receptor (KOR) agonists act as anti-angiogenic factors in tumors. Treatment with KOR agonists, U50,488H and TRK820, significantly inhibited human umbilical vein endothelial cell (HUVEC) migration and tube formation by suppressing VEGFR2 expression. In contrast, treatment with a m opioid receptor agonist, DAMGO, or a delta opioid receptor agonist, SNC80, did not prevent angiogenesis in HUVECs. Lewis lung carcinoma (LLC) or B16 melanoma grafted in KOR knockout mice showed increased proliferation and remarkably enhanced tumor angiogenesis compared with those in wild type mice. On the other hand, repeated intraperitoneal injection of TRK820 (0.1-10 mu g/kg, b.i.d.) significantly inhibited tumor growth by suppressing tumor angiogenesis. These findings indicate that KOR agonists play an important role in tumor angiogenesis and this knowledge could lead to a novel strategy for cancer therapy.
C1 [Yamamizu, Kohei; Doi, Kento; Katayama, Shiori; Yamashita, Jun K.] Kyoto Univ, Stem Cell Res Ctr, Inst Frontier Med Sci, Lab Stem Cell Differentiat, Kyoto, Japan.
   [Yamamizu, Kohei; Doi, Kento; Katayama, Shiori; Yamashita, Jun K.] Kyoto Univ, Ctr iPS Cell Res & Applicat CiRA, Dept Cell Growth & Differentiat, Kyoto, Japan.
   [Yamamizu, Kohei] NIA, Genet Lab, NIH, Baltimore, MD 21224 USA.
   [Furuta, Sadayoshi; Hamada, Yusuke; Yamashita, Akira; Narita, Michiko; Narita, Minoru] Hoshi Univ, Sch Pharm & Pharmaceut Sci, Dept Pharmacol, Tokyo 142, Japan.
   [Kuzumaki, Naoko] Keio Univ, Sch Med, Dept Physiol, Tokyo 160, Japan.
   [Nagase, Hiroshi] Univ Tsukuba, Int Inst Integrat Sleep Med IIIS, Dept Med Chem, Tsukuba, Ibaraki, Japan.
RP Yamamizu, K (reprint author), Kyoto Univ, Stem Cell Res Ctr, Inst Frontier Med Sci, Lab Stem Cell Differentiat, Kyoto, Japan.
EM kohei.yamamizu@nih.gov; narita@hoshi.ac.jp
FU National Cancer Center Research and Development; NIH, National Institute
   on Aging; Kanae Foundation, Japan; Uehara Memorial Foundation, Japan;
   Naito Foundation, Japan; Japan Society for Promotion of Science (JSPS)
FX We thank Dr. Masabumi Shibuya and Dr. Masashi Muramatsu (Tokyo Medical
   and Dental University, Tokyo, Japan) for kindly giving LLC and B16
   cells. This study was supported by grants from the National Cancer
   Center Research and Development, and the Intramural Research Program of
   the NIH, National Institute on Aging. K.Y. was supported by the
   postdoctoral fellowships from the Kanae Foundation, Japan, Uehara
   Memorial Foundation, Japan, Naito Foundation, Japan, and the Japan
   Society for Promotion of Science (JSPS).
NR 23
TC 9
Z9 9
U1 0
U2 10
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 NOV 14
PY 2013
VL 3
AR 3213
DI 10.1038/srep03213
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 252PV
UT WOS:000327020700003
PM 24225480
ER

PT J
AU Shingai, M
   Nishimura, Y
   Klein, F
   Mouquet, H
   Donau, OK
   Plishka, R
   Buckler-White, A
   Seaman, M
   Piatak, M
   Lifson, JD
   Dimitrov, DS
   Nussenzweig, MC
   Martin, MA
AF Shingai, Masashi
   Nishimura, Yoshiaki
   Klein, Florian
   Mouquet, Hugo
   Donau, Olivia K.
   Plishka, Ronald
   Buckler-White, Alicia
   Seaman, Michael
   Piatak, Michael, Jr.
   Lifson, Jeffrey D.
   Dimitrov, Dimiter S.
   Nussenzweig, Michel C.
   Martin, Malcolm A.
TI Antibody-mediated immunotherapy of macaques chronically infected with
   SHIV suppresses viraemia
SO NATURE
LA English
DT Article
ID SIMIAN/HUMAN IMMUNODEFICIENCY VIRUS; NEUTRALIZATION IN-VITRO; PASSIVE
   TRANSFER; RHESUS MACAQUES; POTENT NEUTRALIZATION; ENVELOPE GLYCOPROTEIN;
   HIV-ANTIBODIES; BROAD; VACCINE; PROTECTION
AB Neutralizing antibodies can confer immunity to primate lentiviruses by blocking infection in macaque models of AIDS(1-4). However, earlier studies of anti-human immunodeficiency virus type 1 (HIV-1) neutralizing antibodies administered to infected individuals or humanized mice reported poor control of virus replication and the rapid emergence of resistant variants(5-7). A new generation of anti-HIV-1 monoclonal antibodies, possessing extraordinary potency and breadth of neutralizing activity, has recently been isolated from infected individuals(8). These neutralizing antibodies target different regions of the HIV-1 envelope glycoprotein including the CD4-binding site, glycans located in the V1/V2, V3 and V4 regions, and the membrane proximal external region of gp41 (refs 9-14). Here we have examined two of the new antibodies, directed to the CD4-binding site and the V3 region (3BNC117 and 10-1074, respectively), for their ability to block infection and suppress viraemia in macaques infected with the R5 tropic simian-human immunodeficiency virus (SHIV)-AD8, which emulates many of the pathogenic and immunogenic properties of HIV-1 during infections of rhesus macaques(15,16). Either antibody alone can potently block virus acquisition. When administered individually to recently infected macaques, the 10-1074 antibody caused a rapid decline in virus load to undetectable levels for 4-7 days, followed by virus rebound during which neutralization-resistant variants became detectable. When administered together, a single treatment rapidly suppressed plasma viraemia for 3-5 weeks in some long-term chronically SHIV-infected animals with low CD41 T-cell levels. A second cycle of anti-HIV-1 monoclonal antibody therapy, administered to two previously treated animals, successfully controlled virus rebound. These results indicate that immunotherapy or a combination of immunotherapy plus conventional antiretroviral drugs might be useful as a treatment for chronically HIV-1-infected individuals experiencing immune dysfunction.
C1 [Shingai, Masashi; Nishimura, Yoshiaki; Donau, Olivia K.; Plishka, Ronald; Buckler-White, Alicia; Martin, Malcolm A.] NIAID, Lab Mol Microbiol, NIH, Bethesda, MD 20892 USA.
   [Klein, Florian; Nussenzweig, Michel C.] Rockefeller Univ, Lab Mol Immunol, New York, NY 10065 USA.
   [Mouquet, Hugo] Inst Pasteur, Dept Immunol, Lab Humoral Response Pathogens, F-75015 Paris, France.
   [Seaman, Michael] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Ctr Virol & Vaccine Res, Boston, MA 02115 USA.
   [Piatak, Michael, Jr.; Lifson, Jeffrey D.] SAIC Frederick Inc, AIDS & Canc Virus Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
   [Dimitrov, Dimiter S.; Nussenzweig, Michel C.] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Nussenzweig, Michel C.] Rockefeller Univ, Howard Hughes Med Inst, New York, NY 10065 USA.
RP Nussenzweig, MC (reprint author), Rockefeller Univ, Lab Mol Immunol, New York, NY 10065 USA.
EM nussen@mail.rockefeller.edu; malm@nih.gov
RI Mouquet, Hugo/M-2750-2014
FU Intramural Research Program of the National Institute of Allergy and
   Infectious Diseases, National Institutes of Health (NIH); National
   Cancer Institute, NIH [HHSN261200800001E]
FX We thank K. Tomioka and R. Kruthers for determining plasma viral RNA
   loads and B. Skopets, W. Magnanelli and R. Petros for diligently
   assisting in the maintenance of animals and assisting with procedures.
   We also thank D. R. Burton, The Scripps Institute, for providing
   anti-dengue virus neutralizing monoclonal antibody (DEN-3). This work
   was supported by the Intramural Research Program of the National
   Institute of Allergy and Infectious Diseases, National Institutes of
   Health (NIH) and, in part, with federal funds from the National Cancer
   Institute, NIH, under contract HHSN261200800001E.
NR 30
TC 173
Z9 176
U1 2
U2 31
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
EI 1476-4687
J9 NATURE
JI Nature
PD NOV 14
PY 2013
VL 503
IS 7475
BP 277
EP +
DI 10.1038/nature12746
PG 15
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 250YX
UT WOS:000326894200054
PM 24172896
ER

PT J
AU Cunnington, AJ
   Walther, M
   Riley, EM
AF Cunnington, Aubrey J.
   Walther, Michael
   Riley, Eleanor M.
TI Piecing Together the Puzzle of Severe Malaria
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Article
ID PLASMODIUM-FALCIPARUM MALARIA; BRAIN ENDOTHELIAL-CELLS; PARASITE
   SEQUESTRATION; CEREBRAL MALARIA; CHILDREN; GENES; DYSFUNCTION;
   MECHANISMS; BINDING; SUBSET
AB Severe malaria manifests as several overlapping syndromes with high mortality. Interaction of parasites with endothelial protein C receptors and high parasite biomass have recently been identifed as key determinants of severe disease. However, gaps in our understanding of severe malaria might hinder translation of these fndings into new therapies.
C1 [Cunnington, Aubrey J.] Univ London Imperial Coll Sci Technol & Med, Paediat Sect, London W2 1PG, England.
   [Walther, Michael] NIAID, NIH, Div Intramural Res, Immune Regulat Sect,Lab Malaria Immunol & Vaccino, Rockville, MD 20852 USA.
   [Riley, Eleanor M.] London Sch Hyg & Trop Med, Dept Immunol & Infect, London WC1E 7HT, England.
RP Cunnington, AJ (reprint author), Univ London Imperial Coll Sci Technol & Med, Paediat Sect, Norfolk Pl, London W2 1PG, England.
EM a.cunnington@imperial.ac.uk
OI Cunnington, Aubrey/0000-0002-1305-3529
FU Medical Research Council [G0701427]
NR 28
TC 6
Z9 6
U1 0
U2 2
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1946-6234
EI 1946-6242
J9 SCI TRANSL MED
JI Sci. Transl. Med.
PD NOV 13
PY 2013
VL 5
IS 211
AR 211ps18
DI 10.1126/scitranslmed.3007432
PG 5
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 252NN
UT WOS:000327012900002
PM 24225942
ER

PT J
AU Ashizawa, T
   Figueroa, KP
   Perlman, SL
   Gomez, CM
   Wilmot, GR
   Schmahmann, JD
   Ying, SH
   Zesiewicz, TA
   Paulson, HL
   Shakkottai, VG
   Bushara, KO
   Kuo, SH
   Geschwind, MD
   Xia, GB
   Mazzoni, P
   Krischer, JP
   Cuthbertson, D
   Holbert, AR
   Ferguson, JH
   Pulst, SM
   Subramony, SH
AF Ashizawa, Tetsuo
   Figueroa, Karla P.
   Perlman, Susan L.
   Gomez, Christopher M.
   Wilmot, George R.
   Schmahmann, Jeremy D.
   Ying, Sarah H.
   Zesiewicz, Theresa A.
   Paulson, Henry L.
   Shakkottai, Vikram G.
   Bushara, Khalaf O.
   Kuo, Sheng-Han
   Geschwind, Michael D.
   Xia, Guangbin
   Mazzoni, Pietro
   Krischer, Jeffrey P.
   Cuthbertson, David
   Holbert, Amy Roberts
   Ferguson, John H.
   Pulst, Stefan M.
   Subramony, S. H.
TI Clinical characteristics of patients with spinocerebellar ataxias 1, 2,
   3 and 6 in the US; a prospective observational study
SO ORPHANET JOURNAL OF RARE DISEASES
LA English
DT Article
DE Spinocerebellar ataxia; Natural history; SARA; Progression rate
ID DOMINANT CEREBELLAR ATAXIAS; NATURAL-HISTORY; SCALE
AB Background: All spinocerebellar ataxias (SCAs) are rare diseases. SCA1, 2, 3 and 6 are the four most common SCAs, all caused by expanded polyglutamine-coding CAG repeats. Their pathomechanisms are becoming increasingly clear and well-designed clinical trials will be needed.
   Methods: To characterize the clinical manifestations of spinocerebellar ataxia (SCA) 1, 2, 3 and 6 and their natural histories in the United States (US), we conducted a prospective multicenter study utilized a protocol identical to the European consortium study, using the Scale for the Assessment and Rating of Ataxia (SARA) score as the primary outcome, with follow-ups every 6 months up to 2 years.
   Results: We enrolled 345 patients (60 SCA1, 75 SCA2, 138 SCA3 and 72 SCA6) at 12 US centers. SCA6 patients had a significantly later onset, and SCA2 patients showed greater upper-body ataxia than patients with the remaining SCAs. The annual increase of SARA score was greater in SCA1 patients (mean +/- SE: 1.61 +/- 0.41) than in SCA2 (0.71 +/- 0.31), SCA3 (0.65 +/- 0.24) and SCA6 (0.87 +/- 0.28) patients (p = 0.049). The functional stage also worsened faster in SCA1 than in SCA2, 3 and 6 (p = 0.002).
   Conclusions: The proportions of different SCA patients in US differ from those in the European consortium study, but as in the European patients, SCA1 progress faster than those with SCA2, 3 and 6. Later onset in SCA6 and greater upper body ataxia in SCA2 were noted. We conclude that progression rates of these SCAs were comparable between US and Europe cohorts, suggesting the feasibility of international collaborative clinical studies.
C1 [Ashizawa, Tetsuo; Xia, Guangbin; Subramony, S. H.] Univ Florida, Dept Neurol, Gainesville, FL 32611 USA.
   [Ashizawa, Tetsuo; Xia, Guangbin; Subramony, S. H.] Univ Florida, McKnight Brain Inst, Gainesville, FL 32611 USA.
   [Figueroa, Karla P.; Pulst, Stefan M.] Univ Utah, Dept Neurol, Salt Lake City, UT USA.
   [Perlman, Susan L.] Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90024 USA.
   [Gomez, Christopher M.] Univ Chicago, Dept Neurol, Chicago, IL 60637 USA.
   [Wilmot, George R.] Emory Univ, Dept Neurol, Atlanta, GA 30322 USA.
   [Schmahmann, Jeremy D.] Harvard Univ, Sch Med, Dept Neurol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
   [Ying, Sarah H.] Johns Hopkins Univ, Sch Med, Dept Radiol, Baltimore, MD 21205 USA.
   [Ying, Sarah H.] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
   [Ying, Sarah H.] Johns Hopkins Univ, Sch Med, Dept Ophthalmol, Baltimore, MD 21205 USA.
   [Zesiewicz, Theresa A.] Univ S Florida, Dept Neurol, Tampa, FL 33620 USA.
   [Paulson, Henry L.; Shakkottai, Vikram G.] Univ Michigan, Dept Neurol, Ann Arbor, MI USA.
   [Bushara, Khalaf O.] Univ Minnesota, Dept Neurol, Minneapolis, MN 55455 USA.
   [Kuo, Sheng-Han; Mazzoni, Pietro] Columbia Univ, Dept Neurol, New York, NY USA.
   [Geschwind, Michael D.] UCSF, Dept Neurol, San Francisco, CA USA.
   [Krischer, Jeffrey P.; Cuthbertson, David; Holbert, Amy Roberts] Univ S Florida, Data Management Coordinating Ctr, Tampa, FL USA.
   [Ferguson, John H.] NIH, ORDR NCATS, Bethesda, MD 20892 USA.
RP Ashizawa, T (reprint author), Univ Florida, Dept Neurol, 1149 S Newell Dr,L3-100, Gainesville, FL 32611 USA.
EM ashizawa@ufl.edu
FU NIH [NS068897]
FX This study was supported by NIH grant NS068897 to TA. We thank local
   support groups and the National Ataxia Foundation Chapters. We also
   thank following clinical research coordinators: Bettye Robinson and
   Rebecca McMurray (Emory University), Elizabeth Sullivan (University of
   Michigan), J McMore (Massachusetts General Hospital), Brian Jung (Johns
   Hopkins University), Vicky Staszak (University of Chicago), Sharone
   Trifkin, Tarshia Nulliah and Maria Casado (UCLA), Gigi Satris (UCSF),
   Diane Hutter (University of Minnesota), Jessica Shaw and Kelly Sullivan
   (University of South Florida), and Rebecca Beaulier and Phuong Deleyroll
   (University of Florida).
NR 18
TC 16
Z9 18
U1 2
U2 7
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1750-1172
J9 ORPHANET J RARE DIS
JI Orphanet J. Rare Dis.
PD NOV 13
PY 2013
VL 8
AR 177
DI 10.1186/1750-1172-8-177
PG 8
WC Genetics & Heredity; Medicine, Research & Experimental
SC Genetics & Heredity; Research & Experimental Medicine
GA 286KE
UT WOS:000329466700002
PM 24225362
ER

PT J
AU Luu, N
   Wen, L
   Fu, LZ
   Fujimoto, K
   Shi, YB
   Sun, GH
AF Luu, Nga
   Wen, Luan
   Fu, Liezhen
   Fujimoto, Kenta
   Shi, Yun-Bo
   Sun, Guihong
TI Differential regulation of two histidine ammonia-lyase genes during
   Xenopus development implicates distinct functions during thyroid
   hormone-induced formation of adult stem cells
SO CELL AND BIOSCIENCE
LA English
DT Article
DE Thyroid hormone; Metamorphosis; Xenopus; Thyroid hormone receptor; Stem
   cells; Intestine; Histidase
ID TYPE-1 MATRIX-METALLOPROTEINASE; INTESTINAL CONNECTIVE-TISSUE; AMPHIBIAN
   METAMORPHOSIS; POSTEMBRYONIC DEVELOPMENT; ANURAN METAMORPHOSIS;
   MOLECULAR-CLONING; GELATINASE-A; TR-ALPHA; LAEVIS; RECEPTOR
AB Background: Organ-specific, adult stem cells are essential for organ-homeostasis and tissue repair and regeneration. The formation of such stem cells during vertebrate development remains to be investigated. Frog metamorphosis offers an excellent opportunity to study the formation of adult stem cells as this process involves essentially the transformations of all larval tissues/organs into the adult form. Of particular interest is the remodeling of the intestine. Early studies in Xenopus laevis have shown that this process involves complete degeneration of the larval epithelium and de novo formation of adult stem cells through dedifferentiation of some larval epithelial cells. A major advantage of this metamorphosis model is its total dependence on thyroid hormone (T3). In an effort to identify genes that are important for stem cell development, we have previously carried out tissue-specific microarray analysis of intestinal gene expression during Xenopus laevis metamorphosis.
   Results: We report the detailed characterization of one of the genes thus identified, the histidine ammonia-lyase (HAL) gene, which encodes an enzyme known as histidase or histidinase. We show that there are two duplicated HAL genes, HAL1 and HAL2, in both Xenopus laevis and Xenopus tropicalis, a highly related but diploid species. Interestingly, only HAL2 is highly upregulated by T3 and appears to be specifically expressed in the adult intestinal progenitor/stem cells while HAL1 is not expressed in the intestine during metamorphosis. Furthermore, when analyzed in whole animals, HAL1 appears to be expressed only during embryogenesis but not metamorphosis while the opposite appears to be true for HAL2.
   Conclusions: Our results suggest that the duplicated HAL genes have distinct functions with HAL2 likely involved in the formation and/or proliferation of the adult stem cells during metamorphosis.
C1 [Sun, Guihong] Wuhan Univ, Sch Basic Med Sci, Wuhan 430072, Peoples R China.
   [Luu, Nga; Wen, Luan; Fu, Liezhen; Fujimoto, Kenta; Shi, Yun-Bo] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Mol Morphogenesis, PCRM, NIH, Bethesda, MD 20892 USA.
RP Shi, YB (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Mol Morphogenesis, PCRM, NIH, 18 Lib Dr, Bethesda, MD 20892 USA.
EM Shi@helix.nih.gov; ghsunlab@whu.edu.cn
FU NICHD, NIH; National Natural Science Foundation of China [30870113]
FX This work was supported in part by the intramural Research Program of
   NICHD, NIH and in part by the National Natural Science Foundation of
   China (No. 30870113).
NR 58
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Z9 4
U1 0
U2 6
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 2045-3701
J9 CELL BIOSCI
JI Cell Biosci.
PD NOV 13
PY 2013
VL 3
AR 43
DI 10.1186/2045-3701-3-43
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 283HI
UT WOS:000329236600001
PM 24499573
ER

PT J
AU Flegg, JA
   Guerin, PJ
   Nosten, F
   Ashley, EA
   Phyo, AP
   Dondorp, AM
   Fairhurst, RM
   Socheat, D
   Borrmann, S
   Bjorkman, A
   Martensson, A
   Mayxay, M
   Newton, PN
   Bethell, D
   Se, Y
   Noedl, H
   Diakite, M
   Djimde, AA
   Hien, TT
   White, NJ
   Stepniewska, K
AF Flegg, Jennifer A.
   Guerin, Philippe J.
   Nosten, Francois
   Ashley, Elizabeth A.
   Phyo, Aung Pyae
   Dondorp, Arjen M.
   Fairhurst, Rick M.
   Socheat, Duong
   Borrmann, Steffen
   Bjorkman, Anders
   Martensson, Andreas
   Mayxay, Mayfong
   Newton, Paul N.
   Bethell, Delia
   Se, Youry
   Noedl, Harald
   Diakite, Mahamadou
   Djimde, Abdoulaye A.
   Hien, Tran T.
   White, Nicholas J.
   Stepniewska, Kasia
TI Optimal sampling designs for estimation of Plasmodium falciparum
   clearance rates in patients treated with artemisinin derivatives
SO MALARIA JOURNAL
LA English
DT Article
DE Plasmodium falciparum; Malaria; Artemisinin resistance; Parasite
   clearance; Simulation
ID PARASITE CLEARANCE; WESTERN CAMBODIA; IN-VIVO; MALARIA; RESISTANCE;
   SUSCEPTIBILITY; ARTESUNATE
AB Background: The emergence of Plasmodium falciparum resistance to artemisinins in Southeast Asia threatens the control of malaria worldwide. The pharmacodynamic hallmark of artemisinin derivatives is rapid parasite clearance (a short parasite half-life), therefore, the in vivo phenotype of slow clearance defines the reduced susceptibility to the drug. Measurement of parasite counts every six hours during the first three days after treatment have been recommended to measure the parasite clearance half-life, but it remains unclear whether simpler sampling intervals and frequencies might also be sufficient to reliably estimate this parameter.
   Methods: A total of 2,746 parasite density-time profiles were selected from 13 clinical trials in Thailand, Cambodia, Mali, Vietnam, and Kenya. In these studies, parasite densities were measured every six hours until negative after treatment with an artemisinin derivative (alone or in combination with a partner drug). The WWARN Parasite Clearance Estimator (PCE) tool was used to estimate "reference" half-lives from these six-hourly measurements. The effect of four alternative sampling schedules on half-life estimation was investigated, and compared to the reference half-life (time zero, 6, 12, 24 (A1); zero, 6, 18, 24 (A2); zero, 12, 18, 24 (A3) or zero, 12, 24 (A4) hours and then every 12 hours). Statistical bootstrap methods were used to estimate the sampling distribution of half-lives for parasite populations with different geometric mean half-lives. A simulation study was performed to investigate a suite of 16 potential alternative schedules and half-life estimates generated by each of the schedules were compared to the "true" half-life. The candidate schedules in the simulation study included (among others) six-hourly sampling, schedule A1, schedule A4, and a convenience sampling schedule at six, seven, 24, 25, 48 and 49 hours.
   Results: The median (range) parasite half-life for all clinical studies combined was 3.1 (0.7-12.9) hours. Schedule A1 consistently performed the best, and schedule A4 the worst, both for the individual patient estimates and for the populations generated with the bootstrapping algorithm. In both cases, the differences between the reference and alternative schedules decreased as half-life increased. In the simulation study, 24-hourly sampling performed the worst, and six-hourly sampling the best. The simulation study confirmed that more dense parasite sampling schedules are required to accurately estimate half-life for profiles with short half-life (<= three hours) and/or low initial parasite density (<= 10,000 per mu L). Among schedules in the simulation study with six or fewer measurements in the first 48 hours, a schedule with measurements at times (time windows) of 0 (0-2), 6 (4-8), 12 (10-14), 24 (22-26), 36 (34-36) and 48 (46-50) hours, or at times 6, 7 (two samples in time window 5-8), 24, 25 (two samples during time 23-26), and 48, 49 (two samples during time 47-50) hours, until negative most accurately estimated the "true" half-life. For a given schedule, continuing sampling after two days had little effect on the estimation of half-life, provided that adequate sampling was performed in the first two days and the half-life was less than three hours. If the measured parasitaemia at two days exceeded 1,000 per mu L, continued sampling for at least once a day was needed for accurate half-life estimates.
   Conclusions: This study has revealed important insights on sampling schedules for accurate and reliable estimation of Plasmodium falciparum half-life following treatment with an artemisinin derivative (alone or in combination with a partner drug). Accurate measurement of short half-lives (rapid clearance) requires more dense sampling schedules (with more than twice daily sampling). A more intensive sampling schedule is, therefore, recommended in locations where P. falciparum susceptibility to artemisinins is not known and the necessary resources are available. Counting parasite density at six hours is important, and less frequent sampling is satisfactory for estimating long parasite half-lives in areas where artemisinin resistance is present.
C1 [Flegg, Jennifer A.; Guerin, Philippe J.; Stepniewska, Kasia] Univ Oxford, WorldWide Antimalarial Resistance Network WWARN, Oxford, England.
   [Flegg, Jennifer A.; Guerin, Philippe J.; Nosten, Francois; Ashley, Elizabeth A.; Dondorp, Arjen M.; Newton, Paul N.; Hien, Tran T.; White, Nicholas J.; Stepniewska, Kasia] Univ Oxford, Nuffield Dept Med, Ctr Trop Med, Oxford, England.
   [Nosten, Francois; Ashley, Elizabeth A.; Phyo, Aung Pyae; Dondorp, Arjen M.; White, Nicholas J.] Mahidol Univ, Fac Trop Med, Mahidol Oxford Trop Med Res Unit, Bangkok, Thailand.
   [Nosten, Francois; Phyo, Aung Pyae] Mahidol Univ, Fac Trop Med, Shoklo Malaria Res Unit, Mahidol Oxford Trop Med Res Unit, Mae Sot, Thailand.
   [Fairhurst, Rick M.] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
   [Socheat, Duong] Ctr Parasitol Entomol & Malaria Control, Phnom Penh, Cambodia.
   [Borrmann, Steffen] Kenya Govt Med Res Ctr, Wellcome Trust Res Programme, Kilifi, Kenya.
   [Bjorkman, Anders; Martensson, Andreas] Karolinska Inst, Dept Med Solna, Infect Dis Unit, Stockholm, Sweden.
   [Martensson, Andreas] Karolinska Inst, Dept Publ Hlth Sci, Stockholm, Sweden.
   [Mayxay, Mayfong; Newton, Paul N.] Mahosot Hosp, Lao Oxford Mahosot Hosp Wellcome Trust Res Unit L, Microbiol Lab, Viangchan, Laos.
   [Bethell, Delia] AFRIMS, Dept Immunol & Med, Bangkok, Thailand.
   [Se, Youry] AFRIMS, Phnom Penh, Cambodia.
   [Noedl, Harald] Med Univ Vienna, Inst Specif Prophylaxis & Trop Med, Vienna, Austria.
   [Diakite, Mahamadou; Djimde, Abdoulaye A.] Univ Bamako, Malaria Res & Training Ctr, Bamako, Mali.
   [Hien, Tran T.] OUCRU, Ho Chi Minh City, Vietnam.
RP Flegg, JA (reprint author), Univ Oxford, WorldWide Antimalarial Resistance Network WWARN, Oxford, England.
EM jennifer.flegg@wwarn.org
OI Flegg, Jennifer/0000-0002-8809-726X; Borrmann,
   Steffen/0000-0001-9189-4393; Nosten, Francois/0000-0002-7951-0745;
   Guerin, Philippe/0000-0002-6008-2963; Pyae Phyo,
   Aung/0000-0002-0383-9624
FU Bill and Melinda Gates Foundation; NIAID, NIH
FX This study was supported by the Bill and Melinda Gates Foundation and in
   part by the Intramural Research Program of the NIAID, NIH. Francois
   Nosten, Elizabeth Ashley, Aung Pyae Phyo, Arjen M, Mayfong Mayxay, Paul
   N Newton, Tran Tinh Hien, and Nicholas J White are all supported by the
   Wellcome Trust. All clinical studies were approved by the respective
   ethics committees or institutional review boards of each collaborative
   entity and host country of conduct. All subjects provided informed
   consent before study participation, and parents or legal guardians
   provided informed consent on behalf of their children.
NR 27
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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 NOV 13
PY 2013
VL 12
AR 411
DI 10.1186/1475-2875-12-411
PG 14
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 281ME
UT WOS:000329104900002
PM 24225303
ER

PT J
AU Becker, S
   Ceko, M
   Louis-Foster, M
   Elfassy, NM
   Leyton, M
   Shir, Y
   Schweinhardt, P
AF Becker, Susanne
   Ceko, Marta
   Louis-Foster, Mytsumi
   Elfassy, Nathaniel M.
   Leyton, Marco
   Shir, Yoram
   Schweinhardt, Petra
TI Dopamine and Pain Sensitivity: Neither Sulpiride nor Acute Phenylalanine
   and Tyrosine Depletion Have Effects on Thermal Pain Sensations in
   Healthy Volunteers
SO PLOS ONE
LA English
DT Article
ID POSITRON-EMISSION-TOMOGRAPHY; NUCLEUS-ACCUMBENS; PARKINSONS-DISEASE;
   CATECHOLAMINE SYNTHESIS; FIBROMYALGIA PATIENTS; TEMPORAL SUMMATION;
   DOUBLE-BLIND; AMINO-ACIDS; EFFECT SIZE; ANTINOCICEPTIVE ACTIONS
AB Based on animal studies and some indirect clinical evidence, dopamine has been suggested to have anti-nociceptive effects. Here, we investigated directly the effects of increased and decreased availability of extracellular dopamine on pain perception in healthy volunteers. In Study 1, participants ingested, in separate sessions, a placebo and a low dose of the centrally acting D2-receptor antagonist sulpiride, intended to increase synaptic dopamine via predominant pre-synaptic blockade. No effects were seen on thermal pain thresholds, tolerance, or temporal summation. Study 2 used the acute phenylalanine and tyrosine depletion (APTD) method to transiently decrease dopamine availability. In one session participants ingested a mixture that depletes the dopamine amino acid precursors, phenylalanine and tyrosine. In the other session they ingested a nutritionally balanced control mixture. APTD led to a small mood-lowering response following aversive thermal stimulation, but had no effects on the perception of cold, warm, or pain stimuli. In both studies the experimental manipulation of dopaminergic neurotransmission was successful as indicated by manipulation checks. The results contradict proposals that dopamine has direct anti-nociceptive effects in acute experimental pain. Based on dopamine's well-known role in reward processing, we hypothesize that also in the context of pain, dopamine acts on stimulus salience and might play a role in the initiation of avoidance behavior rather than having direct antinociceptive effects in acute experimental pain.
C1 [Becker, Susanne; Louis-Foster, Mytsumi; Elfassy, Nathaniel M.; Schweinhardt, Petra] McGill Univ, Alan Edwards Ctr Res Pain, Montreal, PQ, Canada.
   [Becker, Susanne; Louis-Foster, Mytsumi; Elfassy, Nathaniel M.; Schweinhardt, Petra] McGill Univ, Fac Dent, Montreal, PQ, Canada.
   [Becker, Susanne] Heidelberg Univ, Med Fac Mannheim, Cent Inst Mental Hlth, Dept Cognit & Clin Neurosci, Mannheim, Germany.
   [Ceko, Marta] NIH, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
   [Leyton, Marco; Schweinhardt, Petra] McGill Univ, Fac Med, Dept Neurol & Neurosurg, Montreal, PQ, Canada.
   [Leyton, Marco] McGill Univ, Dept Psychiat, Montreal, PQ, Canada.
   [Leyton, Marco] Concordia Univ, Ctr Studies Behav Neurobiol, Montreal, PQ H3G 1M8, Canada.
   [Shir, Yoram] McGill Univ, Ctr Hlth, Montreal Gen Hosp, Alan Edwards Pain Management Unit, Montreal, PQ, Canada.
RP Becker, S (reprint author), McGill Univ, Alan Edwards Ctr Res Pain, Montreal, PQ, Canada.
EM susanne.becker@zi-mannheim.de
OI CEKO, MARTA/0000-0001-8679-8145
FU International Association for the Study of Pain (IASP); German Research
   Foundation [BE4309/2-1]; Canadian Institutes for Health Research
   [MOP-102636]
FX This work was supported by the International Association for the Study
   of Pain (IASP) (no grant number) http://www.iasp-pain.org; The German
   Research Foundation, BE4309/2-1, http://www.dfg.de/en/; Canadian
   Institutes for Health Research, MOP-102636, http://www.cihr-irsc.gc.ca/;
   The funders had no role in study design, data collection and analysis,
   decision to publish, or preparation of the manuscript.
NR 93
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U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 13
PY 2013
VL 8
IS 11
AR e80766
DI 10.1371/journal.pone.0080766
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255QK
UT WOS:000327254700202
PM 24236199
ER

PT J
AU Chau, JY
   Grunseit, AC
   Chey, T
   Stamatakis, E
   Brown, WJ
   Matthews, CE
   Bauman, AE
   van der Ploeg, HP
AF Chau, Josephine Y.
   Grunseit, Anne C.
   Chey, Tien
   Stamatakis, Emmanuel
   Brown, Wendy J.
   Matthews, Charles E.
   Bauman, Adrian E.
   van der Ploeg, Hidde P.
TI Daily Sitting Time and All-Cause Mortality: A Meta-Analysis
SO PLOS ONE
LA English
DT Article
ID DOSE-RESPONSE DATA; PHYSICAL-ACTIVITY; SEDENTARY BEHAVIORS;
   CARDIOVASCULAR-DISEASE; PROSPECTIVE COHORT; HEALTH OUTCOMES; US ADULTS;
   EPIDEMIOLOGY; QUALITY; SPENT
AB Objective: To quantify the association between daily total sitting and all-cause mortality risk and to examine dose-response relationships with and without adjustment for moderate-to-vigorous physical activity.
   Methods: Studies published from 1989 to January 2013 were identified via searches of multiple databases, reference lists of systematic reviews on sitting and health, and from authors' personal literature databases. We included prospective cohort studies that had total daily sitting time as a quantitative exposure variable, all-cause mortality as the outcome and reported estimates of relative risk, or odds ratios or hazard ratios with 95% confidence intervals. Two authors independently extracted the data and summary estimates of associations were computed using random effects models.
   Results: Six studies were included, involving data from 595,086 adults and 29,162 deaths over 3,565,569 person-years of follow-up. Study participants were mainly female, middle-aged or older adults from high-income countries; mean study quality score was 12/15 points. Associations between daily total sitting time and all-cause mortality were not linear. With physical activity adjustment, the spline model of best fit had dose-response HRs of 1.00 (95% CI:0.98-1.03), 1.02 (95% CI: 0.99-1.05) and 1.05 (95% CI:1.02-1.08) for every 1-hour increase in sitting time in intervals between 0-3, >3-7 and >7 h/day total sitting, respectively. This model estimated a 34% higher mortality risk for adults sitting 10 h/day, after taking physical activity into account. The overall weighted population attributable fraction for all-cause mortality for total daily sitting time was 5.9%, after adjusting for physical activity.
   Conclusions: Higher amounts of daily total sitting time are associated with greater risk of all-cause mortality and moderate-to-vigorous physical activity appears to attenuate the hazardous association. These findings provide a starting point for identifying a threshold on which to base clinical and public health recommendations for overall sitting time, in addition to physical activity guidelines.
C1 [Chau, Josephine Y.; Grunseit, Anne C.; Chey, Tien; Stamatakis, Emmanuel; Bauman, Adrian E.; van der Ploeg, Hidde P.] Univ Sydney, Sch Publ Hlth, Prevent Res Collaborat, Sydney, NSW 2006, Australia.
   [Stamatakis, Emmanuel] UCL, Dept Epidemiol & Publ Hlth, Div Populat Hlth, PARG, London, England.
   [Brown, Wendy J.] Univ Queensland, Sch Human Movement Studies, Ctr Res Exercise Phys Act & Hlth, Brisbane, Qld, Australia.
   [Matthews, Charles E.] Natl Canc Inst, Div Canc Epidemiol & Genet, Nutr Epidemiol Branch, Bethesda, MD USA.
   [van der Ploeg, Hidde P.] Vrije Univ Amsterdam, Med Ctr, EMGO Inst Hlth & Care Res, Dept Publ & Occupat Hlth, Amsterdam, Netherlands.
RP Chau, JY (reprint author), Univ Sydney, Sch Publ Hlth, Prevent Res Collaborat, Sydney, NSW 2006, Australia.
EM josephine.chau@sydney.edu.au
RI Brown, Wendy/G-2201-2010; matthews, Charles/E-8073-2015; 
OI Brown, Wendy/0000-0001-9093-4509; matthews, Charles/0000-0001-8037-3103;
   van der Ploeg, Hidde/0000-0002-3719-5249
FU Australian National Health and Medical Research Council [569940];
   National Institute for Health Research (UK) through a Career Development
   Fellowship
FX This research is supported by funding from Australian National Health
   and Medical Research Council Program Grant (No. 569940; to WJB and AEB).
   ES is funded by the National Institute for Health Research (UK) through
   a Career Development Fellowship. The funders had no role in study
   design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
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U2 29
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 13
PY 2013
VL 8
IS 11
AR UNSP e80000
DI 10.1371/journal.pone.0080000
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255QK
UT WOS:000327254700169
PM 24236168
ER

PT J
AU Gadalla, SM
   Pfeiffer, RM
   Kristinsson, SY
   Bjorkholm, M
   Hilbert, JE
   Moxley, RT
   Landgren, O
   Greene, MH
AF Gadalla, Shahinaz M.
   Pfeiffer, Ruth M.
   Kristinsson, Sigurdur Y.
   Bjorkholm, Magnus
   Hilbert, James E.
   Moxley, Richard T., III
   Landgren, Ola
   Greene, Mark H.
TI Quantifying Cancer Absolute Risk and Cancer Mortality in the Presence of
   Competing Events after a Myotonic Dystrophy Diagnosis
SO PLOS ONE
LA English
DT Article
ID MUSCULAR-DYSTROPHY; CTG REPEAT; SURVIVAL; GENE; EXPANSION; TYPE-1; DEATH
AB Recent studies show that patients with myotonic dystrophy (DM) have an increased risk of specific malignancies, but estimates of absolute cancer risk accounting for competing events are lacking. Using the Swedish Patient Registry, we identified 1,081 patients with an inpatient and/or outpatient diagnosis of DM between 1987 and 2007. Date and cause of death and date of cancer diagnosis were extracted from the Swedish Cause of Death and Cancer Registries. We calculated non-parametric estimates of absolute cancer risk and cancer mortality accounting for the high non-cancer competing mortality associated with DM. Absolute cancer risk after DM diagnosis was 1.6% (95% CI=0.4-4%), 5% (95% CI=3-9%) and 9% (95% CI=6-13%) at ages 40, 50 and 60 years, respectively. Females had a higher absolute risk of all cancers combined than males: 9% (95% CI=4-14), and 13% (95% CI=9-20) vs. 2% (95% CI=0.7-6) and 4% (95% CI=2-8) by ages 50 and 60 years, respectively) and developed cancer at younger ages (median age =51 years, range=22-74 vs. 57, range=43-84, respectively, p=0.02). Cancer deaths accounted for 10% of all deaths, with an absolute cancer mortality risk of 2% (95% CI=1-4.5%), 4% (95% CI=2-6%), and 6% (95% CI=4-9%) by ages 50, 60, and 70 years, respectively. No gender difference in cancer-specific mortality was observed (p=0.6). In conclusion, cancer significantly contributes to morbidity and mortality in DM patients, even after accounting for high competing DM mortality from non-neoplastic causes. It is important to apply population-appropriate, validated cancer screening strategies in DM patients.
C1 [Gadalla, Shahinaz M.; Greene, Mark H.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Pfeiffer, Ruth M.] NCI, Biostat Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Kristinsson, Sigurdur Y.; Bjorkholm, Magnus] Karolinska Univ Hosp Solna, Div Hematol, Dept Med, Stockholm, Sweden.
   [Kristinsson, Sigurdur Y.; Bjorkholm, Magnus] Karolinska Inst, Stockholm, Sweden.
   [Kristinsson, Sigurdur Y.] Univ Iceland, Fac Med, Reykjavik, Iceland.
   [Kristinsson, Sigurdur Y.] Landspitali Natl Univ Hosp, Dept Hematol, Reykjavik, Iceland.
   [Hilbert, James E.; Moxley, Richard T., III] Univ Rochester, Med Ctr, Dept Neurol, Neuromuscular Dis Ctr, Rochester, NY 14642 USA.
   [Landgren, Ola] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
RP Greene, MH (reprint author), NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
EM greenem@mail.nih.gov
RI Kristinsson, Sigurdur /M-2910-2015
OI Kristinsson, Sigurdur /0000-0002-4964-7476
FU Swedish Cancer Society; Stockholm County Council; Karolinska Institutet
   Foundations; Intramural Research Program of the National Cancer
   Institute, USA [N02CP31003-3]; University of Rochester's Senator Paul D.
   Wellstone Muscular Dystrophy Cooperative Research Center
   [NIH/U54/NS048843]
FX This work was supported by the Swedish Cancer Society, Stockholm County
   Council, the Karolinska Institutet Foundations, the Intramural Research
   Program of the National Cancer Institute, USA (contract N02CP31003-3),
   and the University of Rochester's Senator Paul D. Wellstone Muscular
   Dystrophy Cooperative Research Center (NIH/U54/NS048843). The funders
   had no role in study design, data collection and analysis, decision to
   publish, or preparation of the manuscript.
NR 26
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U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 13
PY 2013
VL 8
IS 11
AR e79851
DI 10.1371/journal.pone.0079851
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255QK
UT WOS:000327254700164
PM 24236163
ER

PT J
AU Laeyendecker, O
   Kulich, M
   Donnell, D
   Komarek, A
   Omelka, M
   Mullis, CE
   Szekeres, G
   Piwowar-Manning, E
   Fiamma, A
   Gray, RH
   Lutalo, T
   Morrison, CS
   Salata, RA
   Chipato, T
   Celum, C
   Kahle, EM
   Taha, TE
   Kumwenda, NI
   Karim, QA
   Naranbhai, V
   Lingappa, JR
   Sweat, MD
   Coates, T
   Eshleman, SH
AF Laeyendecker, Oliver
   Kulich, Michal
   Donnell, Deborah
   Komarek, Arnost
   Omelka, Marek
   Mullis, Caroline E.
   Szekeres, Greg
   Piwowar-Manning, Estelle
   Fiamma, Agnes
   Gray, Ronald H.
   Lutalo, Tom
   Morrison, Charles S.
   Salata, Robert A.
   Chipato, Tsungai
   Celum, Connie
   Kahle, Erin M.
   Taha, Taha E.
   Kumwenda, Newton I.
   Karim, Quarraisha Abdool
   Naranbhai, Vivek
   Lingappa, Jairam R.
   Sweat, Michael D.
   Coates, Thomas
   Eshleman, Susan H.
TI Development of Methods for Cross-Sectional HIV Incidence Estimation in a
   Large, Community Randomized Trial
SO PLOS ONE
LA English
DT Article
ID BED-ENZYME IMMUNOASSAY; PROJECT ACCEPT; RAKAI DISTRICT; UNITED-STATES;
   PREVENTION; TRANSMISSION; UGANDA; SPECIFICITY; CHALLENGES; ACYCLOVIR
AB Background: Accurate methods of HIV incidence determination are critically needed to monitor the epidemic and determine the population level impact of prevention trials. One such trial, Project Accept, a Phase III, community-randomized trial, evaluated the impact of enhanced, community-based voluntary counseling and testing on population-level HIV incidence. The primary endpoint of the trial was based on a single, cross-sectional, post-intervention HIV incidence assessment.
   Methods and Findings: Test performance of HIV incidence determination was evaluated for 403 multi-assay algorithms [MAAs] that included the BED capture immunoassay [BED-CEIA] alone, an avidity assay alone, and combinations of these assays at different cutoff values with and without CD4 and viral load testing on samples from seven African cohorts (5,325 samples from 3,436 individuals with known duration of HIV infection [1 month to >10 years]). The mean window period (average time individuals appear positive for a given algorithm) and performance in estimating an incidence estimate (in terms of bias and variance) of these MAAs were evaluated in three simulated epidemic scenarios (stable, emerging and waning). The power of different test methods to detect a 35% reduction in incidence in the matched communities of Project Accept was also assessed. A MAA was identified that included BED-CEIA, the avidity assay, CD4 cell count, and viral load that had a window period of 259 days, accurately estimated HIV incidence in all three epidemic settings and provided sufficient power to detect an intervention effect in Project Accept.
   Conclusions: In a Southern African setting, HIV incidence estimates and intervention effects can be accurately estimated from cross-sectional surveys using a MAA. The improved accuracy in cross-sectional incidence testing that a MAA provides is a powerful tool for HIV surveillance and program evaluation.
C1 [Laeyendecker, Oliver] NIAID, NIH, Bethesda, MD 20892 USA.
   [Laeyendecker, Oliver; Mullis, Caroline E.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
   [Kulich, Michal; Komarek, Arnost; Omelka, Marek] Charles Univ Prague, Fac Math & Phys, Dept Probabil & Stat, Prague, Czech Republic.
   [Donnell, Deborah] Fred Hutchinson Canc Res Ctr, Stat Ctr HIV AIDS Res & Prevent, Seattle, WA 98104 USA.
   [Szekeres, Greg; Fiamma, Agnes; Coates, Thomas] Univ Calif Los Angeles, UCLA Program Global Hlth, Los Angeles, CA USA.
   [Piwowar-Manning, Estelle; Eshleman, Susan H.] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
   [Gray, Ronald H.; Taha, Taha E.; Kumwenda, Newton I.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
   [Gray, Ronald H.; Lutalo, Tom] Rakai Hlth Sci Program, Entebbe, Uganda.
   [Morrison, Charles S.] Family Hlth Int, Clin Sci, Durham, NC USA.
   [Salata, Robert A.] Case Western Reserve Univ, Div Infect Dis & HIV Med, Cleveland, OH 44106 USA.
   [Salata, Robert A.] Univ Hosp Cleveland, Case Med Ctr, Cleveland, OH 44106 USA.
   [Chipato, Tsungai] Univ Zimbabwe, Harare, Zimbabwe.
   [Celum, Connie] Univ Washington, Dept Global Hlth Med & Epidemiol, Seattle, WA 98195 USA.
   [Kahle, Erin M.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
   [Karim, Quarraisha Abdool] Columbia Univ, Dept Epidemiol, Mailman Sch Publ Hlth, New York, NY USA.
   [Naranbhai, Vivek] Univ KwaZulu Natal, Nelson R Mandela Sch Med, Doris Duke Med Res Inst, Ctr AIDS Programme Res South Africa CAPRISA, Congella, South Africa.
   [Lingappa, Jairam R.] Univ Washington, Dept Global Hlth, Seattle, WA 98195 USA.
   [Lingappa, Jairam R.] Univ Washington, Dept Med & Pediat, Seattle, WA 98195 USA.
   [Sweat, Michael D.] Med Univ S Carolina, Dept Psychiat & Behav Sci, Charleston, SC 29425 USA.
RP Laeyendecker, O (reprint author), NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM olaeyen1@jhmi.edu
RI Komarek, Arnost/A-5534-2012; Kulich, Michal/B-1483-2013; Omelka,
   Marek/I-2447-2014; 
OI Komarek, Arnost/0000-0001-8778-3762; Kulich, Michal/0000-0002-2812-8968;
   Omelka, Marek/0000-0002-0396-9373; Laeyendecker,
   Oliver/0000-0002-6429-4760; Donnell, Deborah/0000-0002-0587-7480;
   Naranbhai, Vivek/0000-0003-4281-8882
FU U.S. National Institute of Mental Health [U01MH066687, U01MH066688,
   U01MH066701, U01MH066702]; HPTN Network Laboratory
   [U01AI068613/UM1AI068613]; SCHARP [U01AI068617/UM1AI068617]; HIV
   Prevention Trials Network of the Division of AIDS of the U.S. National
   Institute of Allergy and Infectious Diseases [U01AI068619/UM1AI068619];
   Office of AIDS Research of the U.S. National Institutes of Health;
   Division of Intramural Research, NIAID, NIH [R01-AI095068]; PEPI [U50
   PS022061-05, U50/CC0222061]; U.S. Centers for Disease Control and
   Prevention; Eunice Kennedy Shriver National Institute of Child Health
   and Human Development, NIH; Bill and Melinda Gates Foundation [26469];
   US National Institutes of Health [P30 A127757, P01 057005, K08
   AI0744248]; NIAID [R01 A134826, K22 AI092150-01, R01 A134265]; NICHD
   [RO1 HD 050180]; World Bank STI Project, Uganda; Henry M. Jackson
   Foundation; Fogarty Foundation [5D43TW00010]
FX Primary sources of support: This research was sponsored by the U.S.
   National Institute of Mental Health as a cooperative agreement, through
   contracts U01MH066687 Johns Hopkins University - David Celentano, PI);
   U01MH066688 Medical University of South Carolina - Michael Sweat, PI);
   U01MH066701 University of California, Los Angeles - Thomas J. Coates,
   PI); and U01MH066702 University of California, San Francisco - Stephen
   F. Morin, PI). In addition, this work was supported as HPTN Protocol 043
   through contracts U01AI068613/UM1AI068613 HPTN Network Laboratory -
   Susan Eshleman, PI); U01AI068617/UM1AI068617 SCHARP - Deborah Donnell,
   PI); and U01AI068619/UM1AI068619 HIV Prevention Trials Network - Sten
   Vermund/Wafaa El-Sadr, PIs) of the Division of AIDS of the U.S. National
   Institute of Allergy and Infectious Diseases; and by the Office of AIDS
   Research of the U. S. National Institutes of Health. Views expressed are
   those of the authors, and not necessarily those of sponsoring agencies.
   Additional support was provided by the Division of Intramural Research,
   NIAID, NIH and from R01-AI095068 Susan Eshleman/Ron Brookmeyer, PIs).
   Support for studies that provided samples and data for this work: 1)
   PEPI- Malawi Study: Cooperative Agreement U50 PS022061-05; Award #
   U50/CC0222061) from the U.S. Centers for Disease Control and Prevention
   and the Eunice Kennedy Shriver National Institute of Child Health and
   Human Development, NIH. 2) Partners in Prevention HSV/HIV Transmission
   Study funded by the Bill and Melinda Gates Foundation grant 26469) with
   support from the US National Institutes of Health P30 A127757 to the
   University of Washington Center for AIDS Research, P01 057005, and K08
   AI0744248). 3) Rakai Health Sciences Program was funded by NIAID grants
   R01 A134826, K22 AI092150-01, and R01 A134265); NICHD grant RO1 HD
   050180); the World Bank STI Project, Uganda; the Henry M. Jackson
   Foundation; the Fogarty Foundation grant 5D43TW00010).
NR 36
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PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 13
PY 2013
VL 8
IS 11
AR e78818
DI 10.1371/journal.pone.0078818
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255QK
UT WOS:000327254700051
PM 24236054
ER

PT J
AU Spong, CY
AF Spong, Catherine Y.
TI New Definition of Term Pregnancy Reply
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Letter
ID LATE-PRETERM; RISK
C1 [Spong, Catherine Y.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Spong, CY (reprint author), NICHHD, 6100 Execut Blvd,Room 4B03,MSC 7510, Bethesda, MD 20892 USA.
EM spongc@mail.nih.gov
NR 6
TC 2
Z9 2
U1 0
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 13
PY 2013
VL 310
IS 18
BP 1986
EP 1987
DI 10.1001/jama.2013.277999
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 250EJ
UT WOS:000326832900028
PM 24219959
ER

PT J
AU Beason-Held, LL
   Goh, JO
   An, Y
   Kraut, MA
   O'Brien, RJ
   Ferrucci, L
   Resnick, SM
AF Beason-Held, Lori L.
   Goh, Joshua O.
   An, Yang
   Kraut, Michael A.
   O'Brien, Richard J.
   Ferrucci, Luigi
   Resnick, Susan M.
TI Changes in Brain Function Occur Years before the Onset of Cognitive
   Impairment
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID VISUAL WORKING-MEMORY; DEFAULT-MODE NETWORK; CEREBRAL-BLOOD-FLOW;
   ALZHEIMERS-DISEASE; AMYLOID DEPOSITION; AGE; CORTEX; MRI; TASK;
   DEACTIVATION
AB To develop targeted intervention strategies for the treatment of Alzheimer's disease, we first need to identify early markers of brain changes that occur before the onset of cognitive impairment. Here, we examine changes in resting-state brain function in humans from the Baltimore Longitudinal Study of Aging. We compared longitudinal changes in regional cerebral blood flow (rCBF), assessed by O-15-water PET, over a mean 7 year period between participants who eventually developed cognitive impairment (n = 22) and those who remained cognitively normal (n = 99). Annual PET assessments began an average of 11 years before the onset of cognitive impairment in the subsequently impaired group, so all participants were cognitively normal during the scanning interval. A voxel-based mixed model analysis was used to compare groups with and without subsequent impairment. Participants with subsequent impairment showed significantly greater longitudinal rCBF increases in orbito-frontal, medial frontal, and anterior cingulate regions, and greater longitudinal decreases in parietal, temporal, and thalamic regions compared with those who maintained cognitive health. These changes were linear in nature and were not influenced by longitudinal changes in regional tissue volume. Although all participants were cognitively normal during the scanning interval, most of the accelerated rCBF changes seen in the subsequently impaired group occurred within regions thought to be critical for the maintenance of cognitive function. These changes also occurred within regions that show early accumulation of pathology in Alzheimer's disease, suggesting that there may be a connection between early pathologic change and early changes in brain function.
C1 [Beason-Held, Lori L.; Goh, Joshua O.; An, Yang; Ferrucci, Luigi; Resnick, Susan M.] NIA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
   [Goh, Joshua O.] Natl Taiwan Univ, Coll Med, Grad Inst Brain & Mind Sci, Taipei 100, Taiwan.
   [Kraut, Michael A.] Johns Hopkins Univ Hosp, Dept Radiol, Baltimore, MD 21287 USA.
   [O'Brien, Richard J.] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21224 USA.
RP Beason-Held, LL (reprint author), NIA, LBN, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM heldlo@mail.nih.gov
RI GOH, JOSHUA/C-8063-2016
OI GOH, JOSHUA/0000-0001-7808-5452
FU Intramural Research Program of the National Institutes of Health,
   National Institute on Aging, and Research and Development
   [N01-AG-3-2124]
FX This work was supported in part by the Intramural Research Program of
   the National Institutes of Health, National Institute on Aging, and
   Research and Development Contract N01-AG-3-2124. We thank the BLSA
   participants and staff for their dedication to these studies and the
   staff of the Johns Hopkins PET facility for their assistance.
NR 49
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U2 8
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 13
PY 2013
VL 33
IS 46
BP 18008
EP 18014
DI 10.1523/JNEUROSCI.1402-13.2013
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 252PU
UT WOS:000327020600005
PM 24227712
ER

PT J
AU Luccardini, C
   Hennekinne, L
   Viou, L
   Yanagida, M
   Murakami, F
   Kessaris, N
   Ma, XF
   Adelstein, RS
   Mege, RM
   Metin, C
AF Luccardini, Camilla
   Hennekinne, Laetitia
   Viou, Lucie
   Yanagida, Mitsutoshi
   Murakami, Fujio
   Kessaris, Nicoletta
   Ma, Xufei
   Adelstein, Robert S.
   Mege, Rene-Marc
   Metin, Christine
TI N-Cadherin Sustains Motility and Polarity of Future Cortical
   Interneurons during Tangential Migration
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID GROWTH CONE MIGRATION; CELL-CYCLE EXIT; NEURONAL MIGRATION; ADHESION
   MOLECULES; NEURAL PRECURSORS; MOUSE EMBRYOS; BRAIN; MORPHOGENESIS;
   EXPRESSION; FOREBRAIN
AB In the developing brain, cortical GABAergic interneurons migrate long distances from the medial ganglionic eminence (MGE) in which they are generated, to the cortex in which they settle. MGE cells express the cell adhesion molecule N-cadherin, a homophilic cell-cell adhesion molecule that regulates numerous steps of brain development, from neuroepithelium morphogenesis to synapse formation. N-cadherin is also expressed in embryonic territories crossed by MGE cells during their migration. In this study, we demonstrate that N-cadherin is a key player in the long-distance migration of future cortical interneurons. Using N-cadherin-coated substrate, we show that N-cadherin-dependent adhesion promotes the migration of mouse MGE cells in vitro. Conversely, mouse MGE cells electroporated with a construct interfering with cadherin function show reduced cell motility, leading process instability, and impaired polarization associated with abnormal myosin IIB dynamics. In vivo, the capability of electroporated MGE cells to invade the developing cortical plate is altered. Using genetic ablation of N-cadherin in mouse embryos, we show that N-cadherin-depleted MGEs are severely disorganized. MGE cells hardly exit the disorganized proliferative area. N-cadherin ablation at the postmitotic stage, which does not affect MGE morphogenesis, alters MGE cell motility and directionality. The tangential migration to the cortex of N-cadherin ablated MGE cells is delayed, and their radial migration within the cortical plate is perturbed. Altogether, these results identify N-cadherin as a pivotal adhesion substrate that activates cell motility in future cortical interneurons and maintains cell polarity over their long-distance migration to the developing cortex.
C1 [Luccardini, Camilla; Hennekinne, Laetitia; Viou, Lucie; Mege, Rene-Marc; Metin, Christine] INSERM, Inst Fer Moulin, Unite Mixte Rech 839, F-75005 Paris, France.
   [Luccardini, Camilla; Hennekinne, Laetitia; Viou, Lucie; Mege, Rene-Marc; Metin, Christine] Univ Paris 06, F-75005 Paris, France.
   [Yanagida, Mitsutoshi; Murakami, Fujio] Osaka Univ, Grad Sch Frontier Biosci, Suita, Osaka 5650871, Japan.
   [Kessaris, Nicoletta] UCL, Wolfson Inst Biomed Res, London WC1E 6BT, England.
   [Kessaris, Nicoletta] UCL, Dept Cell & Dev Biol, London WC1E 6BT, England.
   [Adelstein, Robert S.] Natl Heart Lung & Blood Inst, NIH, Mol Cardiol Lab, Bethesda, MD 20892 USA.
RP Metin, C (reprint author), Inst Natl Sante & Rech Med, Inst Fer Moulin, Unite 839, 17 Rue Fer Moulin, F-750045 Paris, France.
EM christine.metin@inserm.fr
RI Metin, Christine/E-4995-2017; 
OI Mege, Rene-Marc/0000-0001-8128-5543; Adelstein,
   Robert/0000-0002-8683-2144
FU Institut National de la Sante et de la Recherche Medicale (INSERM);
   Agence Nationale pour la Recherche (ANR); Japan Society for the
   Promotion of Science (JSPS); Fondation J. Lejeune; Fondation pour la
   Recherche sur le Cerveau; Association pour la Recherche sur le Cancer;
   l'Association Francaise Contre les Myopathies; Neuropole Ile de France;
   ANR; Ministere de la Recherche et Technologie; INSERM-JSPS
FX This work was supported by Institut National de la Sante et de la
   Recherche Medicale (INSERM), Agence Nationale pour la Recherche (ANR
   Grant MRGENE), Japan Society for the Promotion of Science (JSPS),
   Fondation J. Lejeune and Fondation pour la Recherche sur le Cerveau,
   Association pour la Recherche sur le Cancer, and l'Association Francaise
   Contre les Myopathies. C.L. was supported by a grant from Neuropole Ile
   de France and by the Grant MRGENE from ANR, L.V. by a Ministere de la
   Recherche et Technologie fellowship, and L.V. and M.Y. by an INSERM-JSPS
   travel grant. We thank V. Castellani, F. Francis, and P. Gaspar for
   reading and comments on this manuscript, K. Aubrey for English revision,
   F. Matsuzaki and M. Bornens for reagents, and Institut du Fer a Moulin
   Imaging Facility and Animal Facility.
NR 52
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U1 0
U2 4
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 13
PY 2013
VL 33
IS 46
BP 18149
EP 18160
DI 10.1523/JNEUROSCI.0593-13.2013
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 252PU
UT WOS:000327020600017
PM 24227724
ER

PT J
AU Joiner, WM
   Cavanaugh, J
   Wurtz, RH
AF Joiner, Wilsaan M.
   Cavanaugh, James
   Wurtz, Robert H.
TI Compression and Suppression of Shifting Receptive Field Activity in
   Frontal Eye Field Neurons
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID VISUAL-PERCEPTION; MOVEMENTS; SACCADES; MECHANISMS; STABILITY;
   DIRECTION; SIGNALS; CORTEX; MONKEY; SPACE
AB Before each saccade, neurons in frontal eye field anticipate the impending eye movement by showing sensitivity to stimuli appearing where the neuron's receptive field will be at the end of the saccade, referred to as the future field (FF) of the neuron. We explored the time course of this anticipatory activity in monkeys by briefly flashing stimuli in the FF at different times before saccades. Different neurons showed substantial variation in FF time course, but two salient observations emerged. First, when we compared the time span of stimulus probes before the saccade to the time span of FF activity, we found a striking temporal compression of FF activity, similar to compression seen for perisaccadic stimuli in human psychophysics. Second, neurons with distinct FF activity also showed suppression at the time of the saccade. The increase in FF activity and the decrease with suppression were temporally independent, making the patterns of activity difficult to separate. We resolved this by constructing a simple model with values for the start, peak, and duration of FF activity and suppression for each neuron. The model revealed the different time courses of FF sensitivity and suppression, suggesting that information about the impending saccade triggering suppression reaches the frontal eye field through a different pathway, or a different mechanism, than that triggering FF activity. Recognition of the variations in the time course of anticipatory FF activity provides critical information on its function and its relation to human visual perception at the time of the saccade.
C1 [Joiner, Wilsaan M.; Cavanaugh, James; Wurtz, Robert H.] NEI, NIH, Sensorimotor Res Lab, Bethesda, MD 20892 USA.
   [Joiner, Wilsaan M.] George Mason Univ, Dept Bioengn, Fairfax, VA 22030 USA.
RP Joiner, WM (reprint author), George Mason Univ, Dept Bioengn, Nguyen Engn Bldg,1G5,4400 Univ Dr,Room 3800, Fairfax, VA 22030 USA.
EM wjoiner2@gmu.edu
FU National Eye Institute Intramural Research Program at the National
   Institutes of Health
FX Supported by the National Eye Institute Intramural Research Program at
   the National Institutes of Health. We are grateful to Altah Nichols and
   Tom Ruffner for machine shop support.
NR 23
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U1 0
U2 3
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 13
PY 2013
VL 33
IS 46
BP 18259
EP 18269
DI 10.1523/JNEUROSCI.2964-13.2013
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 252PU
UT WOS:000327020600028
PM 24227735
ER

PT J
AU Hong, S
   Hikosaka, O
AF Hong, Simon
   Hikosaka, Okihide
TI Diverse sources of reward value signals in the basal ganglia nuclei
   transmitted to the lateral habenula in the monkey
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE orthodromic stimulation; patchy activation; striosome; patch; matrix;
   striatum; dopamine; motivation
ID VENTRAL STRIATOPALLIDOTHALAMIC PROJECTION; ROSTROMEDIAL TEGMENTAL
   NUCLEUS; CODES HEDONIC REWARD; TASTE TURNS GOOD; SUBSTANTIA-NIGRA;
   DOPAMINE NEURONS; GLOBUS-PALLIDUS; PRIMATE STRIATUM; CAUDATE-NUCLEUS;
   MACAQUE MONKEY
AB The lateral habenula (LHb) plays an important role in motivational decision making. Neurons in the primate LHb signal negative 'reward prediction errors' and inhibit midbrain dopamine (DA) neurons. These negative reward prediction error signals in the LHb are, at least partly, provided by a distinct group of neurons in the border region of the globus pallidus internal segment (GPb). However, it is still unclear whether other basal ganglia nuclei provide the LHb with reward signals, either through the GPb or through different circuits. As a first step to answer this question, we electrically stimulated various parts of the basal ganglia and monitored the neural activity in the LHb in the awake monkey. First, we found that low intensity stimulations in the GPb and the internal segment of the globus pallidus (GPi) evoked a short latency (5 ms) excitatory response in LHb neurons. Second, LHb neurons were inhibited by stimulations in the ventral pallidum (VP). These results suggest that reward-related signals are transmitted to the LHb mainly through excitatory connections from the GPb and inhibitory connections from the VP. Finally, excitations or inhibitions are induced in LHb neurons from diverse but patchy regions in the striatum. These effects have considerably longer latencies, suggesting that they may be mediated by the GPb or the VP. The patchy nature of the stimulation effect raises the possibility that the striosomes are the source of reward-related signals transmitted to the LHb.
C1 [Hong, Simon] MIT, Dept Brain & Cognit Sci, McGovern Inst Brain Res, Cambridge, MA 02139 USA.
   [Hong, Simon; Hikosaka, Okihide] NEI, Sensorimotor Res Lab, NIH, Bethesda, MD 20892 USA.
RP Hong, S (reprint author), MIT, Dept Brain & Cognit Sci, McGovern Inst Brain Res, 49 Convent Dr, Cambridge, MA 02139 USA.
EM simon_h@mit.edu
NR 56
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U1 0
U2 7
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD NOV 13
PY 2013
VL 7
AR 778
DI 10.3389/fnhum.2013.00778
PG 7
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 250SV
UT WOS:000326875600001
PM 24294200
ER

PT J
AU Brichacek, B
   Lagenaur, LA
   Lee, PP
   Venzon, D
   Hamer, DH
AF Brichacek, Beda
   Lagenaur, Laurel A.
   Lee, Peter P.
   Venzon, David
   Hamer, Dean H.
TI In Vivo Evaluation of Safety and Toxicity of a Lactobacillus jensenii
   Producing Modified Cyanovirin-N in a Rhesus Macaque Vaginal Challenge
   Model
SO PLOS ONE
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; SEXUALLY-TRANSMITTED-DISEASES;
   GENITAL-TRACT INFLAMMATION; BACTERIAL VAGINOSIS; RECEPTOR ANTAGONIST;
   MICROBICIDE SAFETY; HIV TRANSMISSION; MACACA-MULATTA; COITAL-ACT;
   ACQUISITION
AB Sexual transmission of human immunodeficiency virus type 1 (HIV-1) across the cervicovaginal mucosa in women is influenced by many factors including the microbiota and the presence of underlying inflammation. It is important that potential HIV preventative agents do not alter the mucosal environment in a way that enhances HIV acquisition. We examined the impact of a "live'' microbicide on the vaginal mucosal environment in a rhesus macaque repeated vaginal simian-HIV (SHIVSF162P3) challenge model. The microbicide contained a human vaginal Lactobacillus jensenii expressing the HIV-1 entry inhibitor, modified Cyanovirin-N (mCV-N), and henceforth called LB-mCV-N. Macaques were colonized vaginally each week with LB-mCV-N and sampled six days after colonization for culturable bacteria, pH and cervical-vaginal cytokines during the duration of the six-week study. We show that macaques that retained the engineered LB-mCV-N strain in their vaginal microbiota, during SHIV challenge, had lower pH, when colonization levels were higher, and had no evidence of inflammatory cytokines. Indeed, Interleukin-13, a mediator of inflammation, was detected less often in LB-mCV-N colonized macaques than in controls and we found higher levels of Interleukin 1 receptor antagonist (IL-1RA) in LB-mCV-N colonized macaques during the SHIV challenge period. We noted an inverse correlation between levels of mucosal IL-1RA and peak plasma viral load, thus higher IL-1RA correlated with lower viral load in LB-mCV-N treated macaques. These data support the use of LB-mCV-N as a safe "live'' microbicide and suggest that lactobacilli themselves may positively impact the mucosal environment.
C1 [Brichacek, Beda; Lagenaur, Laurel A.; Hamer, Dean H.] NCI, Vaccine Branch, NIH, Bethesda, MD 20892 USA.
   [Lagenaur, Laurel A.; Lee, Peter P.] Osel Inc, Mountain View, CA USA.
   [Venzon, David] NCI, Biostat & Data Management Sect, NIH, Rockville, MD USA.
RP Lagenaur, LA (reprint author), Osel Inc, Mountain View, CA USA.
EM llagenaur@mail.nih.gov
FU NIH's Intramural AIDS Targeted Antiviral Program (IATAP); NIH
   [5R33AI071978-05, 3R33AI071978-04S1]
FX NIH's Intramural AIDS Targeted Antiviral Program (IATAP) provided
   funding for the challenge study. This work was also supported by NIH
   grants 5R33AI071978-05 and 3R33AI071978-04S1. Funders had no role in
   study design, data collection, analysis, decision to publish or
   preparation of this manuscript.
NR 46
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U2 10
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 12
PY 2013
VL 8
IS 11
AR e78817
DI 10.1371/journal.pone.0078817
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255PK
UT WOS:000327252100054
PM 24265721
ER

PT J
AU Rah, JC
   Bas, E
   Colonell, J
   Mishchenko, Y
   Karsh, B
   Fetter, RD
   Myers, EW
   Chklovskii, DB
   Svoboda, K
   Harris, TD
   Isaac, JTR
AF Rah, Jong-Cheol
   Bas, Erhan
   Colonell, Jennifer
   Mishchenko, Yuriy
   Karsh, Bill
   Fetter, Richard D.
   Myers, Eugene W.
   Chklovskii, Dmitri B.
   Svoboda, Karel
   Harris, Timothy D.
   Isaac, John T. R.
TI Thalamocortical input onto layer 5 pyramidal neurons measured using
   quantitative large-scale array tomography
SO FRONTIERS IN NEURAL CIRCUITS
LA English
DT Article
DE array tomography; electron microscopy; thalamocortical synapse;
   dendritic integration; synapse distribution; barrel cortex; neural
   circuits
ID SPINY STELLATE NEURONS; RAT VIBRISSAL CORTEX; CAT VISUAL-CORTEX;
   SOMATOSENSORY CORTEX; SYNAPTIC INPUTS; 3-DIMENSIONAL STRUCTURE; BASAL
   DENDRITES; SILENT SYNAPSES; IN-VIVO; CELLS
AB The subcellular locations of synapses on pyramidal neurons strongly influences dendritic integration and synaptic plasticity. Despite this, there is little quantitative data on spatial distributions of specific types of synaptic input. Here we use array tomography (AT), a high-resolution optical microscopy method, to examine thalamocortical (TC) input onto layer 5 pyramidal neurons. We first verified the ability of AT to identify synapses using parallel electron microscopic analysis of TC synapses in layer 4. We then use large-scale array tomography (LSAT) to measure TC synapse distribution on L5 pyramidal neurons in a 1.00 x 0.83 x 0.21 mm(3) volume of mouse somatosensory cortex. We found that TC synapses primarily target basal dendrites in layer 5, but also make a considerable input to proximal apical dendrites in L4, consistent with previous work. Our analysis further suggests that TC inputs are biased toward certain branches and, within branches, synapses show significant clustering with an excess of TC synapse nearest neighbors within 5-15 mu m compared to a random distribution. Thus, we show that AT is a sensitive and quantitative method to map specific types of synaptic input on the dendrites of entire neurons. We anticipate that this technique will be of wide utility for mapping functionally-relevant anatomical connectivity in neural circuits.
C1 [Rah, Jong-Cheol; Bas, Erhan; Colonell, Jennifer; Karsh, Bill; Fetter, Richard D.; Myers, Eugene W.; Chklovskii, Dmitri B.; Svoboda, Karel; Harris, Timothy D.] Howard Hughes Med Inst, Ashburn, VA 20147 USA.
   [Rah, Jong-Cheol; Isaac, John T. R.] NINDS, Dev Synapt Plast Sect, NIH, Bethesda, MD 20892 USA.
   [Mishchenko, Yuriy] Toros Univ, Dept Engn, Mersin, Turkey.
RP Rah, JC (reprint author), Howard Hughes Med Inst, Janelia Farm Res Campus,19700 Helix Dr, Ashburn, VA 20147 USA.
EM rahj@janelia.hhmi.org
FU JFRC Visiting Scientist program; NINDS intramural research program
FX The authors thank Dr. Thomas Reese for helpful discussion, Drs. Wei-Ping
   Li, Paul Gallant, Mehdi Bolorizadeh, Eric Trautman, Fernando Amat, and
   Albert Cardona for technical support, NCI editors for review of the
   initial manuscript. The work was supported by JFRC Visiting Scientist
   program (Jong-Cheol Rah) and the NINDS intramural research program
   (Jong-Cheol Rah, John T. R. Isaac).
NR 77
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Z9 17
U1 3
U2 15
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5110
J9 FRONT NEURAL CIRCUIT
JI Front. Neural Circuits
PD NOV 12
PY 2013
VL 7
AR UNSP 177
DI 10.3389/fncir.2013.00177
PG 16
WC Neurosciences
SC Neurosciences & Neurology
GA 270AX
UT WOS:000328289100001
PM 24273494
ER

PT J
AU Bonhoeffer, J
   Imoukhuede, EB
   Aldrovandi, G
   Bachtiar, NS
   Chan, ES
   Chang, S
   Chen, RT
   Fernandopulleh, R
   Goldenthal, KL
   Heffelfinger, JD
   Hossain, S
   Jevaji, I
   Khamesipour, A
   Kochhar, S
   Makhene, M
   Malkin, E
   Nalin, D
   Prevots, R
   Ramasamy, R
   Sellers, S
   Vekemans, J
   Walker, KB
   Wilson, P
   Wong, V
   Zaman, K
   Heininger, U
AF Bonhoeffer, Jan
   Imoukhuede, Egeruan B.
   Aldrovandi, Grace
   Bachtiar, Novilia S.
   Chan, Eng-Soon
   Chang, Soju
   Chen, Robert T.
   Fernandopulleh, Rohini
   Goldenthal, Karen L.
   Heffelfinger, James D.
   Hossain, Shah
   Jevaji, Indira
   Khamesipour, Ali
   Kochhar, Sonali
   Makhene, Mamodikoe
   Malkin, Elissa
   Nalin, David
   Prevots, Rebecca
   Ramasamy, Ranjan
   Sellers, Sarah
   Vekemans, Johan
   Walker, Kenneth B.
   Wilson, Pam
   Wong, Virginia
   Zaman, Khalequz
   Heininger, Ulrich
CA Brighton Collaboration Clinical
TI Template protocol for clinical trials investigating vaccines Focus on
   safety elements
SO VACCINE
LA English
DT Article
DE Vaccine; Immunization; Safety; Protocol; Clinical trial
ID EVENT FOLLOWING IMMUNIZATION; CASE-DEFINITION; DATA-COLLECTION;
   INJECTION SITE; GUIDELINES; EXPOSURE; VIRUS; CHILDREN; INFANTS
AB This document is intended as a guide to the protocol development for trials of prophylactic vaccines. The template may serve phases I-IV clinical trials protocol development to include safety relevant information as required by the regulatory authorities and as deemed useful by the investigators. This document may also be helpful for future site strengthening efforts. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Bonhoeffer, Jan; Heininger, Ulrich] Univ Basel, Univ Childrens Hosp UKBB, CH-4056 Basel, Switzerland.
   [Imoukhuede, Egeruan B.] European Vaccine Initiat, Heidelberg, Germany.
   [Aldrovandi, Grace] Childrens Hosp Los Angeles, Saban Res Inst, Los Angeles, CA USA.
   [Chang, Soju; Jevaji, Indira; Makhene, Mamodikoe] NIH, Bethesda, MD USA.
   [Chen, Robert T.; Heffelfinger, James D.] Ctr Dis Control & Prevent, Atlanta, GA 30329 USA.
   [Fernandopulleh, Rohini] Univ Colombo, Colombo, Sri Lanka.
   [Khamesipour, Ali] Univ Tehran Med Sci, Tehran, Iran.
   [Ramasamy, Ranjan] Univ Brunei Darussalam, Inst Hlth Sci, Darussalam, Brunei.
   [Wilson, Pam] Harvard Clin Res Inst, Boston, MA USA.
   [Wong, Virginia] Univ Hong Kong, Dept Paediat & Adolescent Med, Hong Kong, Hong Kong, Peoples R China.
RP Bonhoeffer, J (reprint author), Univ Basel, Univ Childrens Hosp UKBB, Spitalstr 33, CH-4056 Basel, Switzerland.
EM contact@brightoncollaboration.org
RI Bonhoeffer, Jan/E-5903-2014; Chiappini, Elena/D-1118-2012; 
OI Chiappini, Elena/0000-0002-1476-4752; McConkey,
   Samuel/0000-0001-9085-7793; Imoukhuede, Egeruan
   Babatunde/0000-0001-6679-0904; Ramasamy, Ranjan/0000-0003-0246-7053
FU European Commission [223532]
FX The INYVAX project is funded by the European Commission under the
   Framework programme 7, project number 223532. This document does not
   necessarily reflect the opinion of the European Commission. Conflict of
   interest statement: None of the authors has claimed conflict of
   interest.
NR 31
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U1 0
U2 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
EI 1873-2518
J9 VACCINE
JI Vaccine
PD NOV 12
PY 2013
VL 31
IS 47
BP 5602
EP 5620
DI 10.1016/j.vaccine.2013.02.041
PG 19
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 257WZ
UT WOS:000327419800016
PM 23499603
ER

PT J
AU Portal, D
   Zhou, HF
   Zhao, B
   Kharchenko, PV
   Lowry, E
   Wong, L
   Quackenbush, J
   Holloway, D
   Jiang, SZ
   Lu, Y
   Kieff, E
AF Portal, Daniel
   Zhou, Hufeng
   Zhao, Bo
   Kharchenko, Peter V.
   Lowry, Elizabeth
   Wong, Limsoon
   Quackenbush, John
   Holloway, Dustin
   Jiang, Sizun
   Lu, Yong
   Kieff, Elliott
TI Epstein-Barr virus nuclear antigen leader protein localizes to promoters
   and enhancers with cell transcription factors and EBNA2
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE genome-wide ChIP-seq analysis; gene expression
ID NUCLEAR-PROTEIN-2 ACIDIC DOMAIN; SIGNAL-BINDING-PROTEIN; HUMAN
   B-LYMPHOCYTES; GENE-EXPRESSION; CYCLIN D2; DNA-DAMAGE; CTCF; LP;
   TRANSFORMATION; COHESIN
AB Epstein-Barr virus (EBV) nuclear antigens EBNALP (LP) and EBNA2 (E2) are coexpressed in EBV-infected B lymphocytes and are critical for lymphoblastoid cell line outgrowth. LP removes NCOR and RBPJ repressive complexes from promoters, enhancers, and matrix-associated deacetylase bodies, whereas E2 activates transcription from distal enhancers. LP ChIP-seq analyses identified 19,224 LP sites of which similar to 50% were +/- 2 kb of a transcriptional start site. LP sites were enriched for B-cell transcription factors (TFs), YY1, SP1, PAX5, BATF, IRF4, ETS1, RAD21, PU.1, CTCF, RBPJ, ZNF143, SMC3, NF kappa B, TBLR, and EBF. E2 sites were also highly enriched for LP-associated cell TFs and were more highly occupied by RBPJ and EBF. LP sites were highly marked by H3K4me3, H3K27ac, H2Az, H3K9ac, RNAPII, and P300, indicative of activated transcription. LP sites were 29% colocalized with E2 (LP/E2). LP/E2 sites were more similar to LP than to E2 sites in associated cell TFs, RNAPII, P300, and histone H3K4me3, H3K9ac, H3K27ac, and H2Az occupancy, and were more highly transcribed than LP or E2 sites. Gene affected by CTCF and LP cooccupancy were more highly expressed than genes affected by CTCF alone. LP was at myc enhancers and promoters and of MYC regulated ccnd2, 23 med complex components, and MYC regulated cell survival genes, igf2r and bcl2. These data implicate LP and associated TFs and DNA looping factors CTCF, RAD21, SMC3, and YY1/INO80 chromatin-remodeling complexes in repressor depletion and gene activation necessary for lymphoblastoid cell line growth and survival.
C1 [Portal, Daniel; Zhou, Hufeng; Zhao, Bo; Lowry, Elizabeth; Jiang, Sizun; Kieff, Elliott] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
   [Portal, Daniel; Zhou, Hufeng; Zhao, Bo; Lowry, Elizabeth; Jiang, Sizun; Kieff, Elliott] Harvard Univ, Dept Microbiol & Immunobiol, Boston, MA 02115 USA.
   [Zhou, Hufeng; Wong, Limsoon] Natl Univ Singapore, Sch Comp, Singapore 117417, Singapore.
   [Kharchenko, Peter V.; Jiang, Sizun] Harvard Univ, Sch Med, Ctr Biomed Informat, Boston, MA 02115 USA.
   [Quackenbush, John; Holloway, Dustin] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
   [Lu, Yong] NIAID, Lab Syst Biol, NIH, Bethesda, MD 20892 USA.
RP Kieff, E (reprint author), Brigham & Womens Hosp, Dept Med, 75 Francis St, Boston, MA 02115 USA.
EM ekieff@rics.bwh.harvard.edu
RI Wong, Limsoon/E-5033-2010; Zhou, Hufeng/M-1307-2014
OI Wong, Limsoon/0000-0003-1241-5441; Zhou, Hufeng/0000-0001-9382-5674
FU National Cancer Institute of the National Institutes of Health of the US
   Public Health Service [R01CA131354, R01CA170023, R01CA047006]
FX This research was supported by Grants R01CA131354, R01CA170023, and
   R01CA047006 from the National Cancer Institute of the National
   Institutes of Health of the US Public Health Service.
NR 59
TC 23
Z9 24
U1 0
U2 12
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 NOV 12
PY 2013
VL 110
IS 46
BP 18537
EP 18542
DI 10.1073/pnas.1317608110
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 250DQ
UT WOS:000326830900057
PM 24167291
ER

PT J
AU Ahluwalia, D
   Schaaper, RM
AF Ahluwalia, Deepti
   Schaaper, Roel M.
TI Hypermutability and error catastrophe due to defects in ribonucleotide
   reductase
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
ID DNA MISMATCH REPAIR; MEDIATED CELL-DEATH; COLI MUTATOR MUTD5;
   ESCHERICHIA-COLI; SUBSTRATE-SPECIFICITY; REPLICATION FIDELITY; PROTEIN
   R1; MUTAGENESIS; MUTATIONS; GENE
AB The enzyme ribonucleotide reductase (RNR) plays a critical role in the production of deoxynucleoside-5'-triphosphates (dNTPs), the building blocks for DNA synthesis and replication. The levels of the cellular dNTPs are tightly controlled, in large part through allosteric control of RNR. One important reason for controlling the dNTPs relates to their ability to affect the fidelity of DNA replication and, hence, the cellular mutation rate. We have previously isolated a set of mutants of Escherichia coli RNR that are characterized by altered dNTP pools and increased mutation rates (mutator mutants). Here, we show that one particular set of RNR mutants, carrying alterations at the enzyme's allosteric specificity site, is characterized by relatively modest dNTP pool deviations but exceptionally strong mutator phenotypes, when measured in a mutational forward assay (>1,000-fold increases). We provide evidence indicating that this high mutability is due to a saturation of the DNA mismatch repair system, leading to hypermutability and error catastrophe. The results indicate that, surprisingly, even modest deviations of the cellular dNTP pools, particularly when the pool deviations promote particular types of replication errors, can have dramatic consequences for mutation rates.
C1 [Ahluwalia, Deepti; Schaaper, Roel M.] NIEHS, Mol Genet Lab, Res Triangle Pk, NC 27709 USA.
RP Schaaper, RM (reprint author), NIEHS, Mol Genet Lab, Res Triangle Pk, NC 27709 USA.
EM schaaper@niehs.nih.gov
FU NIEHS [Z01 ES065086]
FX We thank Drs. Thomas Kunkel and Jessica Williams [National Institute of
   Environmental Health Sciences (NIEHS)] for their helpful comments on the
   manuscript for this paper and Dr. Rachelle Bienstock (NIEHS) for
   preparing Fig. 1. The NIEHS DNA Sequencing Core is acknowledged for the
   sequencing of the E. coli rpoB mutants. This work was supported by
   Project Z01 ES065086 of the Intramural Research Program, NIEHS.
NR 52
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Z9 13
U1 1
U2 15
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 NOV 12
PY 2013
VL 110
IS 46
BP 18596
EP 18601
DI 10.1073/pnas.1310849110
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 250DQ
UT WOS:000326830900067
PM 24167285
ER

PT J
AU Kortum, RL
   Balagopalan, L
   Alexander, CP
   Garcia, J
   Pinski, JM
   Merrill, RK
   Nguyen, PH
   Li, WM
   Agarwal, I
   Akpan, IO
   Sommers, CL
   Samelson, LE
AF Kortum, Robert L.
   Balagopalan, Lakshmi
   Alexander, Clayton P.
   Garcia, Julie
   Pinski, John M.
   Merrill, Robert K.
   Nguyen, Phan H.
   Li, Wenmei
   Agarwal, Isha
   Akpan, Itoro O.
   Sommers, Connie L.
   Samelson, Lawrence E.
TI The Ability of Sos1 to Oligomerize the Adaptor Protein LAT Is Separable
   from Its Guanine Nucleotide Exchange Activity in Vivo
SO SCIENCE SIGNALING
LA English
DT Article
ID T-CELL DEVELOPMENT; ANTIGEN RECEPTOR; THYMOCYTE DIFFERENTIATION;
   SIGNALING COMPLEXES; IMMATURE THYMOCYTES; RAS ACTIVATION; GRB2; BINDING;
   SURFACE; MICE
AB The activation of the small guanosine triphosphatase Ras by the guanine nucleotide exchange factor (GEF) Sos1 (Son of Sevenless 1) is a central feature of many receptor-stimulated signaling pathways. In developing T cells (thymocytes), Sos1-dependent activation of extracellular signal-regulated kinase (ERK) is required to stimulate cellular proliferation and differentiation. We showed that in addition to its GEF activity, Sos1 acted as a scaffold to nucleate oligomerization of the T cell adaptor protein LAT (linker for activation of T cells) in vivo. The scaffold function of Sos1 depended on its ability to bind to the adaptor protein Grb2. Furthermore, the GEF activity of Sos1 and the Sos1-dependent oligomerization of LAT were separable functions in vivo. Whereas the GEF activity of Sos1 was required for optimal ERK phosphorylation in response to T cell receptor (TCR) stimulation, the Sos1-dependent oligomerization of LAT was required for maximal TCR-dependent phosphorylation and activation of phospholipase C-gamma 1 and Ca2+ signaling. Finally, both of these Sos1 functions were required for early thymocyte proliferation. Whereas transgenic restoration of either the GEF activity or the LAT oligomerization functions of Sos1 alone failed to rescue thymocyte development in Sos1-deficient mice, simultaneous reconstitution of these two signals in the same cell restored normal T cell development. This ability of Sos1 to act both as a RasGEF and as a scaffold to nucleate Grb2-dependent adaptor oligomerization may also occur in other Grb2-dependent pathways, such as those activated by growth factor receptors.
C1 [Kortum, Robert L.; Balagopalan, Lakshmi; Alexander, Clayton P.; Garcia, Julie; Pinski, John M.; Merrill, Robert K.; Nguyen, Phan H.; Li, Wenmei; Agarwal, Isha; Akpan, Itoro O.; Sommers, Connie L.; Samelson, Lawrence E.] NCI, Lab Cellular & Mol Biol, NIH, Bethesda, MD 20892 USA.
RP Samelson, LE (reprint author), NCI, Lab Cellular & Mol Biol, NIH, Bethesda, MD 20892 USA.
EM samelsonl@helix.nih.gov
FU Intramural Research Program of the Center for Cancer Research, NCI, NIH;
   Pharmacology Research and Training (PRAT) Fellowship, National Institute
   of General Medical Sciences, NIH
FX This research was supported by the Intramural Research Program of the
   Center for Cancer Research, NCI, NIH. R. L. K. received additional
   support from a Pharmacology Research and Training (PRAT) Fellowship,
   National Institute of General Medical Sciences, NIH.
NR 46
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Z9 13
U1 0
U2 9
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1945-0877
EI 1937-9145
J9 SCI SIGNAL
JI Sci. Signal.
PD NOV 12
PY 2013
VL 6
IS 301
AR ra99
DI 10.1126/scisignal.2004494
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 253EV
UT WOS:000327066400002
PM 24222714
ER

PT J
AU Cao, HB
   Duan, JB
   Lin, DD
   Calhoun, V
   Wang, YP
AF Cao, Hongbao
   Duan, Junbo
   Lin, Dongdong
   Calhoun, Vince
   Wang, Yu-Ping
TI Integrating fMRI and SNP data for biomarker identification for
   schizophrenia with a sparse representation based variable selection
   method
SO BMC MEDICAL GENOMICS
LA English
DT Article
ID BRAIN-FUNCTION; PARALLEL ICA; RECOVERY; GENE; APPROXIMATION; NOISE
AB Background: In recent years, both single-nucleotide polymorphism (SNP) array and functional magnetic resonance imaging (fMRI) have been widely used for the study of schizophrenia (SCZ). In addition, a few studies have been reported integrating both SNPs data and fMRI data for comprehensive analysis.
   Methods: In this study, a novel sparse representation based variable selection (SRVS) method has been proposed and tested on a simulation data set to demonstrate its multi-resolution properties. Then the SRVS method was applied to an integrative analysis of two different SCZ data sets, a Single-nucleotide polymorphism (SNP) data set and a functional resonance imaging (fMRI) data set, including 92 cases and 116 controls. Biomarkers for the disease were identified and validated with a multivariate classification approach followed by a leave one out (LOO) cross-validation. Then we compared the results with that of a previously reported sparse representation based feature selection method.
   Results: Results showed that biomarkers from our proposed SRVS method gave significantly higher classification accuracy in discriminating SCZ patients from healthy controls than that of the previous reported sparse representation method. Furthermore, using biomarkers from both data sets led to better classification accuracy than using single type of biomarkers, which suggests the advantage of integrative analysis of different types of data.
   Conclusions: The proposed SRVS algorithm is effective in identifying significant biomarkers for complicated disease as SCZ. Integrating different types of data (e.g. SNP and fMRI data) may identify complementary biomarkers benefitting the diagnosis accuracy of the disease.
C1 [Cao, Hongbao] NIMH, Unit Stat Genom, NIH, Bethesda, MD 20892 USA.
   [Duan, Junbo; Lin, Dongdong; Wang, Yu-Ping] Tulane Univ, Dept Biomed Engn, New Orleans, LA 70118 USA.
   [Duan, Junbo; Wang, Yu-Ping] Tulane Univ, Dept Biostat & Bioinformat, New Orleans, LA 70118 USA.
   [Calhoun, Vince] Mind Res Network, Albuquerque, NM USA.
   [Calhoun, Vince] Univ New Mexico, Dept Elect & Comp Engn, Albuquerque, NM 87131 USA.
RP Wang, YP (reprint author), Tulane Univ, Dept Biomed Engn, New Orleans, LA 70118 USA.
EM wyp@tulane.edu
RI Cao, Hongbao/G-8253-2014; Lin, Dongdong/A-8337-2017
OI Cao, Hongbao/0000-0001-9190-0511; 
FU NIH; NSF
FX This work is partially supported by the NIH and NSF.
NR 35
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U1 2
U2 10
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1755-8794
J9 BMC MED GENOMICS
JI BMC Med. Genomics
PD NOV 11
PY 2013
VL 6
SU 3
AR S2
DI 10.1186/1755-8794-6-S3-S2
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 286CJ
UT WOS:000329441800002
PM 24565219
ER

PT J
AU Guo, XL
   Mattera, R
   Ren, XF
   Chen, Y
   Retamal, C
   Gonzalez, A
   Bonifacino, JS
AF Guo, Xiaoli
   Mattera, Rafael
   Ren, Xuefeng
   Chen, Yu
   Retamal, Claudio
   Gonzalez, Alfonso
   Bonifacino, Juan S.
TI The Adaptor Protein-1 mu 1B Subunit Expands the Repertoire of
   Basolateral Sorting Signal Recognition in Epithelial Cells
SO DEVELOPMENTAL CELL
LA English
DT Article
ID ADP-RIBOSYLATION FACTOR; CANINE KIDNEY-CELLS; MDCK CELLS; CYTOPLASMIC
   DOMAIN; GOLGI MEMBRANES; COATED VESICLES; LDL RECEPTOR; RECYCLING
   ENDOSOMES; POLARIZED EPITHELIA; GAMMA-ADAPTIN
AB An outstanding question in protein sorting is why polarized epithelial cells express two isoforms of the mu 1 subunit of the AP-1 clathrin adaptor complex: the ubiquitous mu 1A and the epithelial-specific mu 1B. Previous studies led to the notion that mu 1A and mu 1B mediate basolateral sorting predominantly from the trans-Golgi network (TGN) and recycling endosomes, respectively. Using improved analytical tools, however, we find that mu 1A and mu 1B largely colocalize with each other. They also colocalize to similar extents with TGN and recycling endosome markers, as well as with basolateral cargoes transiting biosynthetic and endocytic-recycling routes. Instead, the two isoforms differ in their signal-recognition specificity. In particular, mu 1B preferentially binds a subset of signals from cargoes that are sorted basolaterally in a mu 1B-dependent manner. We conclude that expression of distinct mu 1 isoforms in epithelial cells expands the repertoire of signals recognized by AP-1 for sorting of a broader range of cargoes to the basolateral surface.
C1 [Guo, Xiaoli; Mattera, Rafael; Ren, Xuefeng; Chen, Yu; Bonifacino, Juan S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, NIH, Bethesda, MD 20892 USA.
   [Retamal, Claudio; Gonzalez, Alfonso] Pontificia Univ Catolica Chile, Fac Ciencias Biol, Ctr Envejecimiento & Regenerac, Fac Med,Dept Inmunol Clin & Reumatol, Santiago 6510260, Chile.
RP Bonifacino, JS (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, NIH, Bethesda, MD 20892 USA.
EM bonifacinoj@helix.nih.gov
RI Guo, Xiaoli/O-3906-2014
FU Intramural Program of the Eunice Kennedy Shriver National Institute of
   Child Health and Human Development; Basal Financial Program of CONICYT
   [PFB12/2007]
FX We thank X. Zhu and N. Tsai for technical assistance; M. Jarnik for
   electron microscopy analysis; and G. Bu, K. Matter, and J. Donaldson for
   gifts of reagents. This work was funded by the Intramural Program of the
   Eunice Kennedy Shriver National Institute of Child Health and Human
   Development and the Basal Financial Program, grant PFB12/2007, of
   CONICYT (C.R. and A.G.).
NR 57
TC 25
Z9 26
U1 1
U2 3
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1534-5807
EI 1878-1551
J9 DEV CELL
JI Dev. Cell
PD NOV 11
PY 2013
VL 27
IS 3
BP 353
EP 366
DI 10.1016/j.devcel.2013.10.006
PG 14
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA 257VZ
UT WOS:000327417200012
PM 24229647
ER

PT J
AU Ghazarian, AA
   Murphy, MA
   Khan, MR
   Saksvig, BI
   Altekruse, SF
AF Ghazarian, Armen A.
   Murphy, Megan A.
   Khan, Maria R.
   Saksvig, Brit I.
   Altekruse, Sean F.
TI Area-Level Attributes and Esophageal Adenocarcinoma in Surveillance,
   Epidemiology and End Results Registries
SO PLOS ONE
LA English
DT Article
ID BREAST-CANCER; STAGE; SURVIVAL; RISK; DIAGNOSIS; PATTERNS
AB Purpose: To examine the associations between area-level socioeconomic attributes and stage of esophageal adenocarcinoma diagnoses in 16 SEER cancer registries during 2000-2007.
   Methods: Odds ratios (OR) and 95% confidence intervals (CI) were calculated using multivariable logistic regression models to assess the relationship between distant-stage esophageal adenocarcinoma and individual, census tract, and county-level attributes.
   Results: Among cases with data on birthplace, no significant association was seen between reported birth within versus outside the United States and distant-stage cancer (adjusted OR=1.02, 95% CI: 0.85-1.22). Living in an area with a higher percentage of residents born outside the United States than the national average was associated with distant-stage esophageal adenocarcinoma; census tract level: >11.8%, (OR=1.10, 95% CI: 1.01-1.19), county level: >11.8%, (OR=1.14, 95% CI: 1.05-1.24). No association was observed between median household income and distant-stage cancer at either census tract or county levels.
   Conclusion: The finding of greater odds of distant-stage esophageal adenocarcinoma among cases residing in SEER areas with higher proportion of non-U.S. Natives suggests local areas where esophageal cancer control efforts might be focused. Missing data at the individual level was a limitation of the present study. Furthermore, inconsistent associations with foreign birth at individual-versus area-levels cautions against using area-level attributes as proxies for case attributes.
C1 [Ghazarian, Armen A.; Murphy, Megan A.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Khan, Maria R.; Saksvig, Brit I.] Univ Maryland, Sch Publ Hlth, Dept Epidemiol & Biostat, College Pk, MD 20742 USA.
   [Altekruse, Sean F.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Ghazarian, AA (reprint author), NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
EM armen.ghazarian@nih.gov
FU National Cancer Institute
FX The funding source for this manuscript is through the National Cancer
   Institute contracts to SEER registries The funders had no role in study
   design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
NR 19
TC 0
Z9 0
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 11
PY 2013
VL 8
IS 11
AR e81613
DI 10.1371/journal.pone.0081613
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255EG
UT WOS:000327221600221
PM 24244745
ER

PT J
AU Horwitz, B
   Hwang, C
   Alstott, J
AF Horwitz, Barry
   Hwang, Chuhern
   Alstott, Jeff
TI Interpreting the effects of altered brain anatomical connectivity on
   fMRI functional connectivity: a role for computational neural modeling
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE neural modeling; fMRI; functional connectivity; brain disorders; huma
   nbrain
ID HUMAN CEREBRAL-CORTEX; ALZHEIMERS-DISEASE; WORKING-MEMORY; NEURONAL
   DYNAMICS; NETWORK ANALYSIS; VISUAL PATHWAYS; STATE; SCHIZOPHRENIA;
   SYSTEMS; AUTISM
AB Recently, there have been a large number of studies using resting state fMRI to characterize abnormal brain connectivity in patients with a variety of neurological, psychiatric, and developmental disorders. However, interpreting what the differences in resting state fMRI functional connectivity (rsfMRI-FC) actually reflect in terms of the underlying neural pathology has proved to be elusive because of the complexity of brain anatomical connectivity. The same is the case for task-based fMRI studies. In the last few years, several groups have used large-scale neural modeling to help provide some insight into the relationship between brain anatomical connectivity and the corresponding patterns of fMRI-FC. In this paper we review several efforts at using large-scale neural modeling to investigate the relationship between structural connectivity and functional/effective connectivity to determine how alterations in structural connectivity are manifested in altered patterns of functional/effective connectivity. Because the alterations made in the anatomical connectivity between specific brain regions in the model are known in detail, one can use the results of these simulations to determine the corresponding alterations in rsfMRI-FC. Many of these simulation studies found that structural connectivity changes do not necessarily result in matching changes in functional/effective connectivity in the areas of structural modification. Often, it was observed that increases in functional/effective connectivity in the altered brain did not necessarily correspond to increases in the strength of the anatomical connection weights. Note that increases in rsfMRI-FC in patients have been interpreted in some cases as resulting from neural plasticity. These results suggest that this interpretation can be mistaken. The relevance of these simulation findings to the use of functional/effective fMRI connectivity as biomarkers for brain disorders is also discussed
C1 [Horwitz, Barry; Hwang, Chuhern] Natl Inst Deafness & Other Commun Disorders, Brain Imaging & Modeling Sect, NIH, Bethesda, MD 20892 USA.
   [Hwang, Chuhern] Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD USA.
   [Hwang, Chuhern] Univ Virginia, Dept Biomed Engn, Charlottesville, VA USA.
   [Alstott, Jeff] NIMH, Sect Crit Brain Dynam, NIH, Bethesda, MD 20892 USA.
   [Alstott, Jeff] Univ Cambridge, Brain Mapping Unit, Behav & Clin Neurosci Inst, Cambridge CB2 1TN, England.
RP Horwitz, B (reprint author), Natl Inst Deafness & Other Commun Disorders, Brain Imaging & Modeling Sect, NIH, 10 Ctr Dr,Room 5D39,MSC 1402, Bethesda, MD 20892 USA.
EM horwitzb@nidcd.nih.gov
FU ntramural Research Programs of the National Institute on Deafness; Other
   Communication Disorders, the National Institute of Mental Health;
   National Institute of Biomedical Imaging and Bioengineering; National
   Institutes of Health
FX This work was supported by the Intramural Research Programs of the
   National Institute on Deafness and Other Communication Disorders, the
   National Institute of Mental Health, and the National Institute of
   Biomedical Imaging and Bioengineering, all part of the National
   Institutes of Health. The simulations performed for this paper utilized
   the high-performance computational capabilities of the Biowulf Linux
   cluster at the National Institutes of Health, Bethesda, MD. The authors
   wish to thank the two reviewers for a number of useful comments and
   suggestions
NR 81
TC 5
Z9 6
U1 2
U2 20
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD NOV 11
PY 2013
VL 7
AR 649
DI 10.3389/fnhum.2013.00649
PG 11
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 248TU
UT WOS:000326727600001
PM 24273500
ER

PT J
AU Hou, HL
   Sun, L
   Siddoway, BA
   Petralia, RS
   Yang, HT
   Gu, H
   Nairn, AC
   Xia, HH
AF Hou, Hailong
   Sun, Lu
   Siddoway, Benjamin A.
   Petralia, Ronald S.
   Yang, Hongtian
   Gu, Hua
   Nairn, Angus C.
   Xia, Houhui
TI Synaptic NMDA receptor stimulation activates PP1 by inhibiting its
   phosphorylation by Cdk5
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID LONG-TERM DEPRESSION; PROTEIN PHOSPHATASE-ACTIVITY; DEPENDENT KINASE-5
   CDK5; POSTSYNAPTIC DENSITY; GENE-EXPRESSION; HIPPOCAMPAL-NEURONS;
   CATALYTIC SUBUNIT; CELL-CYCLE; IN-VIVO; PLASTICITY
AB The serine/threonine protein phosphatase protein phosphatase 1 (PP1) is known to play an important role in learning and memory by mediating local and downstream aspects of synaptic signaling, but how PP1 activity is controlled in different forms of synaptic plasticity remains unknown. We find that synaptic N-methyl-D-aspartate (NMDA) receptor stimulation in neurons leads to activation of PP1 through a mechanism involving inhibitory phosphorylation at Thr320 by Cdk5. Synaptic stimulation led to proteasome-dependent degradation of the Cdk5 regulator p35, inactivation of Cdk5, and increased auto-dephosphorylation of Thr320 of PP1. We also found that neither inhibitor-1 nor calcineurin were involved in the control of PP1 activity in response to synaptic NMDA receptor stimulation. Rather, the PP1 regulatory protein, inhibitor-2, formed a complex with PP1 that was controlled by synaptic stimulation. Finally, we found that inhibitor-2 was critical for the induction of long-term depression in primary neurons. Our work fills a major gap regarding the regulation of PP1 in synaptic plasticity.
C1 [Hou, Hailong; Sun, Lu; Siddoway, Benjamin A.; Yang, Hongtian; Gu, Hua; Xia, Houhui] LSU Hlth Sci Ctr, Ctr Neurosci, New Orleans, LA 70112 USA.
   [Petralia, Ronald S.] NIDCD, NIH, Bethesda, MD 20892 USA.
   [Nairn, Angus C.] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT 06511 USA.
RP Xia, HH (reprint author), LSU Hlth Sci Ctr, Ctr Neurosci, New Orleans, LA 70112 USA.
EM hxia@lsuhsc.edu
OI Nairn, Angus/0000-0002-7075-0195
FU NIH [DA10044, R01NS060879]; NSF [IOS-0824393]; NARSAD [2006YI]; LSU
   Research Enhancement Fund; NIDCD Intramural Research Program
FX This work is supported by the NIH (DA10044 to A.C. Nairn; and
   R01NS060879), NSF (IOS-0824393), NARSAD (2006YI), LSU Research
   Enhancement Fund (to H. Xia), and the NIDCD Intramural Research Program
   (to R.S. Petralia).
NR 60
TC 15
Z9 15
U1 0
U2 2
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0021-9525
EI 1540-8140
J9 J CELL BIOL
JI J. Cell Biol.
PD NOV 11
PY 2013
VL 203
IS 3
BP 521
EP 535
DI 10.1083/jcb.201303035
PG 15
WC Cell Biology
SC Cell Biology
GA 251FD
UT WOS:000326912300015
PM 24189275
ER

PT J
AU Vitolins, MZ
   Griffin, L
   Tomlinson, WV
   Vuky, J
   Adams, PT
   Moose, D
   Frizzell, B
   Lesser, GJ
   Naughton, M
   Radford, JE
   Shaw, EG
AF Vitolins, Mara Z.
   Griffin, Leah
   Tomlinson, W. Vic
   Vuky, Jacqueline
   Adams, Paul T.
   Moose, Dawn
   Frizzell, Bart
   Lesser, Glenn J.
   Naughton, Michelle
   Radford, James E., Jr.
   Shaw, Edward G.
TI Randomized Trial to Assess the Impact of Venlafaxine and Soy Protein on
   Hot Flashes and Quality of Life in Men With Prostate Cancer
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID BREAST-CANCER; FUNCTIONAL ASSESSMENT; POSTMENOPAUSAL WOMEN; THERAPY;
   FLUSHES; SUPPLEMENTATION; PHYTOESTROGENS
AB Purpose
   Hot flashes occur in approximately 80% of androgen-deprived men. Few intervention studies have been conducted to relieve hot flashes in men.
   Patients and Methods
   Eligible androgen-deprived men were randomly assigned to one of four daily regimens (2 x 2 factorial design) for 12 weeks: milk protein powder and placebo pill, venlafaxine and milk protein powder, soy protein powder and placebo pill, or venlafaxine and soy protein powder. The primary end point was hot flash symptom severity score (HFSSS), defined as number of hot flashes times severity. The secondary end point was quality of life (QoL), assessed by using the Functional Assessment of Cancer Therapy-Prostate.
   Results
   In all, 120 men age 46 to 91 years participated. Most were white (78%) and overweight or obese (83%). Toxicity was minimal. Neither venlafaxine nor soy protein alone or in combination had a significant effect on HFSSS. Soy protein, but not venlafaxine, improved measures of QoL.
   Conclusion
   In androgen-deprived men, neither venlafaxine nor soy proved effective in reducing hot flashes. Interventions that appear effective for decreasing hot flashes in women may not always turn out to be effective in men. (C) 2013 by American Society of Clinical Oncology
C1 [Vitolins, Mara Z.; Griffin, Leah; Frizzell, Bart; Lesser, Glenn J.; Naughton, Michelle; Shaw, Edward G.] Wake Forest Sch Med, Winston Salem, NC 27157 USA.
   [Moose, Dawn] Novant Hlth, Winston Salem, NC USA.
   [Radford, James E., Jr.] Hendersonville Hematol Oncol, Hendersonville, NC USA.
   [Tomlinson, W. Vic] AnMed Hlth, Anderson, SC USA.
   [Vuky, Jacqueline] Virginia Mason Med Ctr, Seattle, WA 98101 USA.
   [Adams, Paul T.] Genesys Reg Med Ctr, Natl Surg Adjuvant Breast & Bowel Project, Flint, MI USA.
RP Vitolins, MZ (reprint author), Wake Forest Sch Med, Div Publ Hlth Sci, Dept Epidemiol & Prevent, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM mvitolin@wakehealth.edu
FU National Cancer Institute/Division of Cancer Prevention [U10 CA 081851];
   National Center for Complementary and Alternative Medicine (NCCAM) [U10
   CA 081851-06S2]; Physicians Pharmaceuticals; NCCAM [U10 CA081851-06S2]
FX Supported by Grant No. U10 CA 081851 from the National Cancer
   Institute/Division of Cancer Prevention, Grant No. U10 CA 081851-06S2
   from the National Center for Complementary and Alternative Medicine
   (NCCAM), and Physicians Pharmaceuticals. Funding for the purchase of the
   EffexorXR tablets and placebo pills was obtained through Grant No. U10
   CA081851-06S2 from NCCAM. The soy and milk protein powders were provided
   free of charge by Physicians Pharmaceuticals.
NR 22
TC 12
Z9 12
U1 0
U2 6
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 NOV 10
PY 2013
VL 31
IS 32
BP 4092
EP +
DI 10.1200/JCO.2012.48.1432
PG 8
WC Oncology
SC Oncology
GA 301LG
UT WOS:000330533200011
PM 24081940
ER

PT J
AU Baker, SG
AF Baker, Stuart G.
TI Causal inference, probability theory, and graphical insights
SO STATISTICS IN MEDICINE
LA English
DT Article
DE BK-Plot; causal graph; confounder; instrumental variable; observational
   study; Simpson's paradox
ID UNDERSTANDING BIAS AMPLIFICATION; SIMPSONS PARADOX; STRATIFICATION
AB Causal inference from observational studies is a fundamental topic in biostatistics. The causal graph literature typically views probability theory as insufficient to express causal concepts in observational studies. In contrast, the view here is that probability theory is a desirable and sufficient basis for many topics in causal inference for the following two reasons. First, probability theory is generally more flexible than causal graphs: Besides explaining such causal graph topics as M-bias (adjusting for a collider) and bias amplification and attenuation (when adjusting for instrumental variable), probability theory is also the foundation of the paired availability design for historical controls, which does not fit into a causal graph framework. Second, probability theory is the basis for insightful graphical displays including the BK-Plot for understanding Simpson's paradox with a binary confounder, the BK2-Plot for understanding bias amplification and attenuation in the presence of an unobserved binary confounder, and the PAD-Plot for understanding the principal stratification component of the paired availability design. Published 2013. This article is a US Government work and is in the public domain in the USA.
C1 NCI, Biometry Res Grp, Bethesda, MD 20892 USA.
RP Baker, SG (reprint author), NCI, Biometry Res Grp, Bethesda, MD 20892 USA.
EM sb16i@nih.gov
FU National Institutes of Health
FX This work was supported by the National Institutes of Health. The author
   thanks Jessica Myers, the reviewers, and the associate editor for
   helpful comments.
NR 37
TC 8
Z9 8
U1 0
U2 15
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
EI 1097-0258
J9 STAT MED
JI Stat. Med.
PD NOV 10
PY 2013
VL 32
IS 25
BP 4319
EP 4330
DI 10.1002/sim.5828
PG 12
WC Mathematical & Computational Biology; Public, Environmental &
   Occupational Health; Medical Informatics; Medicine, Research &
   Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
   Occupational Health; Medical Informatics; Research & Experimental
   Medicine; Mathematics
GA 230PH
UT WOS:000325353700001
PM 23661231
ER

PT J
AU Baker, SG
AF Baker, Stuart G.
TI Additional thoughts on causal inference, probability theory, and
   graphical insights
SO STATISTICS IN MEDICINE
LA English
DT Editorial Material
ID CANCER
C1 NCI, Biometry Res Grp, Bethesda, MD 20892 USA.
RP Baker, SG (reprint author), NCI, Biometry Res Grp, Bethesda, MD 20892 USA.
EM sb16i@nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 25
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
EI 1097-0258
J9 STAT MED
JI Stat. Med.
PD NOV 10
PY 2013
VL 32
IS 25
BP 4334
EP 4337
DI 10.1002/sim.5917
PG 4
WC Mathematical & Computational Biology; Public, Environmental &
   Occupational Health; Medical Informatics; Medicine, Research &
   Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
   Occupational Health; Medical Informatics; Research & Experimental
   Medicine; Mathematics
GA 230PH
UT WOS:000325353700003
PM 25564688
ER

PT J
AU Rodrigo, L
   Blanco, I
   Bobes, J
   de Serres, FJ
AF Rodrigo, Luis
   Blanco, Ignacio
   Bobes, Julio
   de Serres, Frederick J.
TI Clinical impact of a gluten-free diet on health-related quality of life
   in seven fibromyalgia syndrome patients with associated celiac disease
SO BMC GASTROENTEROLOGY
LA English
DT Article
DE Gluten-free diet; Celiac disease; Fibromyalgia syndrome; Irritable bowel
   syndrome; Health-related quality of life
ID IRRITABLE-BOWEL-SYNDROME; VISUAL ANALOG SCALES; SPANISH VERSION;
   PREVALENCE; CRITERIA; PAIN; CLASSIFICATION; QUESTIONNAIRE; MULTICENTER;
   SYMPTOMS
AB Background: Celiac disease (CD) is an autoimmune disorder, characterized by the presence of gastrointestinal and multisystem symptoms, which occasionally mimic those of Irritable Bowel Syndrome (IBS) and Fibromyalgia Syndrome (FMS). To assess the effectiveness of a Gluten-Free Diet (GFD) in seven adult female screening-detected CD subjects, categorized as severe IBS and FMS patients.
   Methods: All subjects showed villous atrophy in duodenal biopsies, were HLA-DQ2/DQ8-positive, and fulfilled the Rome III and ACR 1990 criteria respectively for IBS and FMS classification. GFD effectiveness was assessed at baseline and after 1 year, examining the score changes in the Tender Points (TPs) test, Fibromyalgia Impact Questionnaire (FIQ), Health Assessment Questionnaire (HAQ), Short Form Health Survey (SF-36), Visual Analogue Scales (VAS) for gastrointestinal complaints, pain and tiredness, drug prescriptions and tissue-Trans-Glutaminase (tTG) serum levels.
   Results: At baseline, all patients had poor Quality of Life and VAS scores, a high number of TPs and drug prescriptions, and increased tTG levels. After 1 year of GFD, all outcome measures significantly improved, with a decrease of 51-60% in TPs, FIQ, HAQ, and VAS scales, and in the number of prescribed drugs, accompanied by an increase of 48-60% in SF-36 Physical and Mental Component Summary scores, and a decrease of tTG to normal values.
   Conclusion: Results of this pilot study show that the adherence to a GFD by CD-related IBS/FMS patients can simultaneously improve CD and IBS/FMS symptoms, and indicate the merit of further research on a larger cohort.
C1 [Rodrigo, Luis] HUCA, Oviedo 33006, Principality Of, Spain.
   [Blanco, Ignacio] FICYT, Biomed Res Off Principal Asturias, Oviedo 33009, Principality Of, Spain.
   [Bobes, Julio] Univ Oviedo, Dept Med, Psychiat Area, E-33006 Oviedo, Principality Of, Spain.
   [de Serres, Frederick J.] NIEHS, Res Triangle Pk, NC 27709 USA.
RP Rodrigo, L (reprint author), HUCA, Celestino Villamil S-N, Oviedo 33006, Principality Of, Spain.
EM lrodrigosaez@gmail.com
NR 37
TC 7
Z9 8
U1 0
U2 8
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-230X
J9 BMC GASTROENTEROL
JI BMC Gastroenterol.
PD NOV 9
PY 2013
VL 13
AR 157
DI 10.1186/1471-230X-13-157
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 272QS
UT WOS:000328475900002
PM 24209578
ER

PT J
AU Sturgill, D
   Malone, JH
   Sun, X
   Smith, HE
   Rabinow, L
   Samson, ML
   Oliver, B
AF Sturgill, David
   Malone, John H.
   Sun, Xia
   Smith, Harold E.
   Rabinow, Leonard
   Samson, Marie-Laure
   Oliver, Brian
TI Design of RNA splicing analysis null models for post hoc filtering of
   Drosophila head RNA-Seq data with the splicing analysis kit (Spanki)
SO BMC BIOINFORMATICS
LA English
DT Article
ID ENDOPLASMIC-RETICULUM; GENE-EXPRESSION; HUMAN GENOME; MELANOGASTER;
   ALIGNMENT; DIFFERENTIATION; QUANTIFICATION; TRANSCRIPTOMES; JUNCTIONS;
   SIMULATOR
AB Background: The production of multiple transcript isoforms from one gene is a major source of transcriptome complexity. RNA-Seq experiments, in which transcripts are converted to cDNA and sequenced, allow the resolution and quantification of alternative transcript isoforms. However, methods to analyze splicing are underdeveloped and errors resulting in incorrect splicing calls occur in every experiment.
   Results: We used RNA-Seq data to develop sequencing and aligner error models. By applying these error models to known input from simulations, we found that errors result from false alignment to minor splice motifs and antisense stands, shifted junction positions, paralog joining, and repeat induced gaps. By using a series of quantitative and qualitative filters, we eliminated diagnosed errors in the simulation, and applied this to RNA-Seq data from Drosophila melanogaster heads. We used high-confidence junction detections to specifically interrogate local splicing differences between transcripts. This method out-performed commonly used RNA-seq methods to identify known alternative splicing events in the Drosophila sex determination pathway. We describe a flexible software package to perform these tasks called Splicing Analysis Kit (Spanki), available at http://www.cbcb umd.edu/software/spanki.
   Conclusions: Splice-junction centric analysis of RNA-Seq data provides advantages in specificity for detection of alternative splicing. Our software provides tools to better understand error profiles in RNA-Seq data and improve inference from this new technology. The splice-junction centric approach that this software enables will provide more accurate estimates of differentially regulated splicing than current tools.
C1 [Sturgill, David; Smith, Harold E.; Oliver, Brian] NIDDK, NIH, Bethesda, MD 20892 USA.
   [Sturgill, David; Oliver, Brian] Univ Maryland, Program Computat Biol Bioinformat & Genom, College Pk, MD 20742 USA.
   [Malone, John H.] Univ Connecticut, Dept Mol & Cell Biol, Storrs, CT 06269 USA.
   [Sun, Xia; Rabinow, Leonard; Samson, Marie-Laure] Univ Paris 11, Ctr Neurosci Paris Sud, CNRS UMR 8195, F-91405 Orsay, France.
RP Sturgill, D (reprint author), NIDDK, NIH, 50 South Dr, Bethesda, MD 20892 USA.
EM dave.sturgill@gmail.com
FU Intramural Research Programs of the National Institutes of Health (NIH);
   National Institute of Diabetes and Digestive and Kidney Diseases
   (NIDDK); pre-doctoral Intramural Research Training Award fellowship
   through the NIH; China Scholarship Council; Universite Paris Sud, the
   CNRS and IFCPAR award [4903A]
FX We thank Michael Sammeth for sharing source code and Trudy Mackay for
   isogenic flies. Ryan Dale provided technical advice. We also thank Steve
   Mount, fellow members of our labs, and the modENCODE Drosophila
   transcription group (Sue Celniker, Roger Hoskins, Steven Brenner,
   Brenton Graveley, Peter Cherbas, and Thomas Gingeras), for stimulating
   discussion, advice, feedback, and encouragement. This study utilized the
   highperformance 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 Programs of the National Institutes of Health (NIH), National
   Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). DS was
   supported by a pre-doctoral Intramural Research Training Award
   fellowship through the NIH Graduate Partnerships Program. XS was
   supported by a graduate fellowship from the China Scholarship Council.
   Work in the laboratory of LR and MLS is supported by the Universite
   Paris Sud, the CNRS and IFCPAR award number 4903A to LR.
NR 55
TC 14
Z9 14
U1 0
U2 11
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2105
J9 BMC BIOINFORMATICS
JI BMC Bioinformatics
PD NOV 9
PY 2013
VL 14
AR 320
DI 10.1186/1471-2105-14-320
PG 18
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
   Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Mathematical & Computational Biology
GA 259LY
UT WOS:000327529600001
PM 24209455
ER

PT J
AU Cotton, MF
   Violari, A
   Otwombe, K
   Panchia, R
   Dobbels, E
   Rabie, H
   Josipovic, D
   Liberty, A
   Lazarus, E
   Innes, S
   van Rensburg, AJ
   Pelser, W
   Truter, H
   Madhi, SA
   Handelsman, E
   Jean-Philippe, P
   McIntyre, JA
   Gibb, DM
   Babiker, AG
AF Cotton, Mark F.
   Violari, Avy
   Otwombe, Kennedy
   Panchia, Ravindre
   Dobbels, Els
   Rabie, Helena
   Josipovic, Deirdre
   Liberty, Afaaf
   Lazarus, Erica
   Innes, Steve
   van Rensburg, Anita Janse
   Pelser, Wilma
   Truter, Handre
   Madhi, Shabir A.
   Handelsman, Edward
   Jean-Philippe, Patrick
   McIntyre, James A.
   Gibb, Diana M.
   Babiker, Abdel G.
CA CHER Study Team
TI Early time-limited antiretroviral therapy versus deferred therapy in
   South African infants infected with HIV: results from the children with
   HIV early antiretroviral (CHER) randomised trial
SO LANCET
LA English
DT Article
ID NEURODEVELOPMENTAL OUTCOMES; MORTALITY; AGE; NEVIRAPINE
AB Background Interim results from the children with HIV early antiretroviral (CHER) trial showed that early antiretroviral therapy (ART) was life-saving for infants infected with HIV. In view of the few treatment options and the potential toxicity associated with lifelong ART, in the CHER trial we compared early time-limited ART with deferred ART.
   Methods CHER was an open-label randomised controlled trial of HIV-infected asymptomatic infants younger than 12 weeks in two South African trial sites with a percentage of CD4-positive T lymphocytes (CD4%) of 25% or higher. 377 infants were randomly allocated to one of three groups: deferred ART (ART-Def), immediate ART for 40 weeks (ART-40W), or immediate ART for 96 weeks (ART-96W), with subsequent treatment interruption. The randomisation schedule was stratifi ed by clinical site with permuted blocks of random sizes to balance the numbers of infants allocated to each group. Criteria for ART initiation in the ART-Def group and re-initiation after interruption in the other groups were CD4% less than 25% in infancy; otherwise, the criteria were CD4% less than 20% or Centers for Disease Control and Prevention severe stage B or stage C disease. Combination therapy of lopinavir-ritonavir, zidovudine, and lamivudine was the fi rst-line treatment regimen at ART initiation and re-initiation. The primary endpoint was time to failure of fi rst-line ART (immunological, clinical, or virological) or death. Comparisons were done by intention-to-treat analysis, with use of time-to-event methods. This trial is registered with ClinicalTrials. gov, number NCT00102960.
   Findings 377 infants were enrolled, with a median age of 7 4 weeks, CD4% of 35%, and HIV RNA log 5 7 copies per mL. Median follow-up was 4 8 years; 34 infants (9%) were lost to follow-up. Median time to ART initiation in the ART-Def group was 20 weeks (IQR 16-25). Time to restarting of ART after interruption was 33 weeks (26-45) in ART40W and 70 weeks (35-109) in ART-96W; at the end of the trial, 19% of patients in ART-40W and 32% of patients in ART-96W remained off ART. Proportions of follow-up time spent on ART were 81% in the ART-Def group, 70% in the ART-40W group, and 69% in the ART-96W group. 48 (38%) of 125 children in the ART-Def group, 32 (25%) of 126 in the ART-40W group, and 26 (21%) of 126 in the ART-96W group reached the primary endpoint. The hazard ratio, relative to ART-Def, was 0 59 (95% CI 0 38-0 93, p= 0 02) for ART-40W and 0 47 (0 27-0 76, p= 0 002) for ART-96W. Three children in ART-Def, three in ART-40W, and one in ART-96W switched to second-line ART.
   Interpretation Early time-limited ART had better clinical and immunological outcomes than deferred ART, with no evidence of excess disease progression during subsequent treatment interruption and less overall ART exposure than deferred ART. Longer time on primary ART permits longer subsequent interruption, with marginally better outcomes.
C1 [Cotton, Mark F.; Dobbels, Els; Rabie, Helena; Innes, Steve; van Rensburg, Anita Janse] Univ Stellenbosch, Fac Med & Hlth Sci, Childrens Infect Dis Clin Res Unit, ZA-7505 Tygerberg, South Africa.
   [Violari, Avy; Otwombe, Kennedy; Panchia, Ravindre; Josipovic, Deirdre; Liberty, Afaaf; Lazarus, Erica; Pelser, Wilma; Truter, Handre] Univ Witwatersrand, Perinatal HIV Res Unit, Johannesburg, South Africa.
   [Madhi, Shabir A.] Univ Witwatersrand, Med Res Council Resp & Meningeal Pathogens Res Un, Johannesburg, South Africa.
   [Madhi, Shabir A.] Univ Witwatersrand, Natl Res Fdn Vaccine Preventable Dis, Dept Sci & Technol, Johannesburg, South Africa.
   [Handelsman, Edward] NIAID, Div Aids, US Natl Inst Hlth, Bethesda, MD 20892 USA.
   [Jean-Philippe, Patrick] HJF DAIDS, Bethesda, MD USA.
   [McIntyre, James A.] Univ Cape Town, Anova Hlth Inst, ZA-7925 Cape Town, South Africa.
   [McIntyre, James A.] Univ Cape Town, Sch Publ Hlth & Family Med, ZA-7925 Cape Town, South Africa.
   [Gibb, Diana M.; Babiker, Abdel G.] Med Res Council Clin Trials Unit, London, England.
RP Cotton, MF (reprint author), Univ Stellenbosch, Fac Med & Hlth Sci, Childrens Infect Dis Clin Res Unit, ZA-7505 Tygerberg, South Africa.
EM mcot@sun.ac.za
OI Innes, Steve/0000-0003-3969-8680
FU US National Institutes of Health
FX Funding US National Institutes of Health.
NR 32
TC 51
Z9 53
U1 0
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0140-6736
EI 1474-547X
J9 LANCET
JI Lancet
PD NOV 9
PY 2013
VL 382
IS 9904
BP 1555
EP 1563
DI 10.1016/S0140-6736(13)61409-9
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 247NE
UT WOS:000326623900027
PM 24209829
ER

PT J
AU Xiong, YQ
   Lee, HJ
   Mariko, B
   Lu, YC
   Dannenberg, AJ
   Haka, AS
   Maxfield, FR
   Camerer, E
   Proia, RL
   Hla, T
AF Xiong, Yuquan
   Lee, Hyeuk Jong
   Mariko, Boubacar
   Lu, Yi-Chien
   Dannenberg, Andrew J.
   Haka, Abigail S.
   Maxfield, Frederick R.
   Camerer, Eric
   Proia, Richard L.
   Hla, Timothy
TI Sphingosine Kinases Are Not Required for Inflammatory Responses in
   Macrophages
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
DE Autophagy; Ceramide; Inflammation; Lysosomes; Macrophages; Sphingolipid;
   Sphingosine 1-Phosphate
ID ISOLATED RAT HEPATOCYTES; ENDOTHELIAL-CELLS;
   FUNCTIONAL-CHARACTERIZATION; SPHINGOLIPID METABOLISM; LYMPHOCYTE EGRESS;
   MOLECULAR-CLONING; KNOCKOUT MICE; SPHINGOSINE-1-PHOSPHATE; AUTOPHAGY;
   1-PHOSPHATE
AB Sphingosine kinases (Sphks), which catalyze the formation of sphingosine 1-phosphate (S1P) from sphingosine, have been implicated as essential intracellular messengers in inflammatory responses. Specifically, intracellular Sphk1-derived S1P was reported to be required for NFB induction during inflammatory cytokine action. To examine the role of intracellular S1P in the inflammatory response of innate immune cells, we derived murine macrophages that lack both Sphk1 and Sphk2 (M phi Sphk dKO). Compared with WT counterparts, M phi Sphk dKO cells showed marked suppression of intracellular S1P levels whereas sphingosine and ceramide levels were strongly up-regulated. Cellular proliferation and apoptosis were similar in M phi Sphk dKO cells compared with WT counterparts. Treatment of WT and M phi Sphk dKO with inflammatory mediators TNF or Escherichia coli LPS resulted in similar NFB activation and cytokine expression. Furthermore, LPS-induced inflammatory responses, mortality, and thioglycolate-induced macrophage recruitment to the peritoneum were indistinguishable between M phi Sphk dKO and littermate control mice. Interestingly, autophagic markers were constitutively induced in bone marrow-derived macrophages from Sphk dKO mice. Treatment with exogenous sphingosine further enhanced intracellular sphingolipid levels and autophagosomes. Inhibition of autophagy resulted in caspase-dependent cell death. Together, these data suggest that attenuation of Sphk activity, particularly Sphk2, leads to increased intracellular sphingolipids and autophagy in macrophages.
C1 [Xiong, Yuquan; Lee, Hyeuk Jong; Lu, Yi-Chien; Hla, Timothy] Cornell Univ, Weill Cornell Med Coll, Dept Pathol & Lab Med, Ctr Vasc Biol, New York, NY 10065 USA.
   [Lee, Hyeuk Jong; Dannenberg, Andrew J.] Cornell Univ, Weill Cornell Med Coll, Dept Med, New York, NY 10065 USA.
   [Haka, Abigail S.; Maxfield, Frederick R.] Cornell Univ, Weill Cornell Med Coll, Dept Biochem, New York, NY 10065 USA.
   [Mariko, Boubacar] Paris Cardiovasc Res Ctr, INSERM, U970, F-75015 Paris, France.
   [Mariko, Boubacar; Camerer, Eric] Univ Paris 05, F-75015 Paris, France.
   [Proia, Richard L.] NIDDK, NIH, Bethesda, MD 20892 USA.
RP Hla, T (reprint author), Cornell Univ, Weill Cornell Med Coll, Dept Pathol & Lab Med, Ctr Vasc Biol, 1300 York Ave, New York, NY 10065 USA.
EM tih2002@med.cornell.edu
RI Hla, Timothy/G-5873-2012; 
OI Hla, Timothy/0000-0001-8355-4065; Maxfield,
   Frederick/0000-0003-4396-8866
FU National Institutes of Health [HL67330, HL70694, HL89934]; INSERM
   Avenir; Marie Curie Actions; French National Research Agency; Fondation
   de France; Lipidomics Shared Resource, Hollings Cancer Center, Medical
   University of South Carolina [P30 CA138313]; Lipidomics Core in the
   South Carolina Lipidomics and Pathobiology COBRE [P20 RR017677]; NIDDK,
   National Institutes of Health
FX This work was supported, in whole or in part, by National Institutes of
   Health Grants HL67330, HL70694, and HL89934 (to T. H). This work was
   also supported by INSERM Avenir, Marie Curie Actions, the French
   National Research Agency, Fondation de France, and the Ile-de-France
   Region (to E.C.). Sphingolipid measurements were supported by the
   Lipidomics Shared Resource, Hollings Cancer Center, Medical University
   of South Carolina Grant P30 CA138313 and the Lipidomics Core in the
   South Carolina Lipidomics and Pathobiology COBRE Grant P20 RR017677.;
   Supported by the intramural funds of the NIDDK, National Institutes of
   Health.
NR 58
TC 18
Z9 18
U1 1
U2 6
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 8
PY 2013
VL 288
IS 45
BP 32563
EP 32573
DI 10.1074/jbc.M113.483750
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 275MQ
UT WOS:000328681700039
PM 24081141
ER

PT J
AU Kapoor, K
   Bhatnagar, J
   Chufan, EE
   Ambudkar, SV
AF Kapoor, Khyati
   Bhatnagar, Jaya
   Chufan, Eduardo E.
   Ambudkar, Suresh V.
TI Mutations in Intracellular Loops 1 and 3 Lead to Misfolding of Human
   P-glycoprotein (ABCB1) That Can Be Rescued by Cyclosporine A, Which
   Reduces Its Association with Chaperone Hsp70
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
DE ABC Transporter; Drug Resistance; Molecular Chaperone; Multidrug
   Transporters; Protein Misfolding; Chemical Chaperones; P-glycoprotein
ID TRANSMEMBRANE CONDUCTANCE REGULATOR; NUCLEOTIDE-BINDING DOMAIN;
   MULTIDRUG TRANSPORTER; PHARMACOLOGICAL CHAPERONES; CATALYTIC CYCLE; ATP
   HYDROLYSIS; MONOCLONAL-ANTIBODIES; MAMMALIAN-CELLS; PROTEIN; ABCG2
AB P-glycoprotein (P-gp) is an ATP binding cassette transporter that effluxes a variety of structurally diverse compounds including anticancer drugs. Computational models of human P-gp in the apo- and nucleotide-bound conformation show that the adenine group of ATP forms hydrogen bonds with the conserved Asp-164 and Asp-805 in intracellular loops 1 and 3, respectively, which are located at the interface between the nucleotide binding domains and transmembrane domains. We investigated the role of Asp-164 and Asp-805 residues by substituting them with cysteine in a cysteine-less background. It was observed that the D164C/D805C mutant, when expressed in HeLa cells, led to misprocessing of P-gp, which thus failed to transport the drug substrates. The misfolded protein could be rescued to the cell surface by growing the cells at a lower temperature (27 degrees C) or by treatment with substrates (cyclosporine A, FK506), modulators (tariquidar), or small corrector molecules. We also show that short term (4-6 h) treatment with 15 m cyclosporine A or FK506 rescues the pre-formed immature protein trapped in the endoplasmic reticulum in an immunophilin-independent pathway. The intracellularly trapped misprocessed protein associates more with chaperone Hsp70, and the treatment with cyclosporine A reduces the association of mutant P-gp, thus allowing it to be trafficked to the cell surface. The function of rescued cell surface mutant P-gp is similar to that of wild-type protein. These data demonstrate that the Asp-164 and Asp-805 residues are not important for ATP binding, as proposed earlier, but are critical for proper folding and maturation of a functional transporter.
C1 [Kapoor, Khyati; Bhatnagar, Jaya; Chufan, Eduardo E.; Ambudkar, Suresh V.] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Ambudkar, SV (reprint author), NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bldg 37, Bethesda, MD 20892 USA.
EM ambudkar@mail.nih.gov
FU Research Program of the National Institutes of Health, Center for Cancer
   Research, NCI Grant [ZIA BC010030-13]
FX This work was supported, in whole or in part, by the Research Program of
   the National Institutes of Health, Center for Cancer Research, NCI Grant
   ZIA BC010030-13.
NR 43
TC 9
Z9 9
U1 0
U2 7
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 8
PY 2013
VL 288
IS 45
BP 32622
EP 32636
DI 10.1074/jbc.M113.498980
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 275MQ
UT WOS:000328681700044
PM 24064216
ER

PT J
AU Arumugam, A
   Weng, ZP
   Talwelkar, SS
   Chaudhary, SC
   Kopelovich, L
   Elmets, CA
   Afaq, F
   Athar, M
AF Arumugam, Aadithya
   Weng, Zhiping
   Talwelkar, Sarang S.
   Chaudhary, Sandeep C.
   Kopelovich, Levy
   Elmets, Craig A.
   Afaq, Farrukh
   Athar, Mohammad
TI Inhibiting Cycloxygenase and Ornithine Decarboxylase by Diclofenac and
   Alpha-Difluoromethylornithine Blocks Cutaneous SCCs by Targeting Akt-ERK
   Axis
SO PLOS ONE
LA English
DT Article
ID NONMELANOMA SKIN-CANCER; SQUAMOUS-CELL CARCINOMA; SIGNALING PATHWAYS;
   EPITHELIAL-CELLS; DOUBLE-BLIND; PHOTOCARCINOGENESIS; PREVENTION;
   EXPRESSION; APOPTOSIS; TUMORS
AB Non-melanoma skin cancer (NMSC) is the most common type of skin cancer in Caucasian populations. Its increasing incidence has been a major public health concern. Elevated expressions of ODC and COX-2 are associated with both murine and human NMSCs. Inhibition of these molecular targets singly employing their respective small molecule inhibitors showed limited success. Here, we show that combined blockade of ODC and COX-2 using their potent inhibitors, DFMO and diclofenac respectively abrogates growth of A431 epidermal xenograft tumors in nu/nu mice by more than 90%. The tumor growth inhibition was associated with a diminution in the proliferation and enhancement in apoptosis. The proliferation markers such as PCNA and cyclin D1 were reduced. TUNEL-positive apoptotic cells and cleaved caspase-3 were increased in the residual tumors. These agents also manifested direct target-unrelated effects. Reduced expression of phosphorylated MAPKAP-2, ERK, and Akt (ser(473) & thr(308)) were noticed. The mechanism by which combined inhibition of ODC/COX attenuated tumor growth and invasion involved reduction in EMT. Akt activation by ODC+COX-2 over-expression was the key player in this regard as Akt inhibition manifested effects similar to those observed by the combined inhibition of ODC+COX-2 whereas forced over-expression of Akt resisted against DFMO+diclofenac treatment. These data suggest that ODC+COX-2 over-expression together leads to pathogenesis of aggressive and invasive cutaneous carcinomas by activating Akt signaling pathway, which through augmenting EMT contributes to tumor invasion.
C1 [Arumugam, Aadithya; Weng, Zhiping; Talwelkar, Sarang S.; Chaudhary, Sandeep C.; Elmets, Craig A.; Afaq, Farrukh; Athar, Mohammad] Univ Alabama Birmingham, Dept Dermatol, Birmingham, AL 35294 USA.
   [Elmets, Craig A.; Athar, Mohammad] Univ Alabama Birmingham, Skin Dis Res Ctr, Birmingham, AL 35294 USA.
   [Kopelovich, Levy] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Athar, M (reprint author), Univ Alabama Birmingham, Dept Dermatol, Birmingham, AL 35294 USA.
EM mathar@uab.edu
RI Talwelkar, Sarang/C-8925-2015
FU NIH [R01 CA138998, NO1-CN-43300]
FX This work was supported in part by NIH grants R01 CA138998 and
   NO1-CN-43300. The funders had no role in study design, data collection
   and analysis, decision to publish, or preparation of the manuscript.
NR 46
TC 3
Z9 3
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 8
PY 2013
VL 8
IS 11
AR e80076
DI 10.1371/journal.pone.0080076
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255CG
UT WOS:000327216200101
PM 24260338
ER

PT J
AU ElZarrad, MK
   Mukhopadhyay, P
   Mohan, N
   Hao, EK
   Dokmanovic, M
   Hirsch, DS
   Shen, Y
   Pacher, P
   Wu, WJ
AF ElZarrad, M. Khair
   Mukhopadhyay, Partha
   Mohan, Nishant
   Hao, Enkui
   Dokmanovic, Milos
   Hirsch, Dianne S.
   Shen, Yi
   Pacher, Pal
   Wu, Wen Jin
TI Trastuzumab Alters the Expression of Genes Essential for Cardiac
   Function and Induces Ultrastructural Changes of Cardiomyocytes in Mice
SO PLOS ONE
LA English
DT Article
ID CONGESTIVE-HEART-FAILURE; DILATED CARDIOMYOPATHY; BREAST-CANCER; INDUCED
   CARDIOTOXICITY; INDUCED APOPTOSIS; BLOOD-PRESSURE; VENTRICULAR MYOCYTES;
   CIRCADIAN VARIATION; TROPONIN-I; STRESS
AB Treatment with trastuzumab, a humanized monoclonal antibody directed against the extracellular domain of Human Epidermal Growth Factor Receptor 2 (HER2), very successfully improves outcomes for women with HER2-positive breast cancer. However, trastuzumab treatment was recently linked to potentially irreversible serious cardiotoxicity, the mechanisms of which are largely elusive. This study reports that trastuzumab significantly alters the expression of myocardial genes essential for DNA repair, cardiac and mitochondrial functions, which is associated with impaired left ventricular performance in mice coupled with significant ultrastructural alterations in cardiomyocytes revealed by electron microscopy. Furthermore, trastuzumab treatment also promotes oxidative stress and apoptosis in myocardium of mice, and elevates serum levels of cardiac troponin-I (cTnI) and cardiac myosin light chain-1 (cMLC1). The elevated serum levels of cMLC1 in mice treated with trastuzumab highlights the potential that cMLC1 could be a useful biomarker for trastuzumab-induced cardiotoxicity.
C1 [ElZarrad, M. Khair; Mohan, Nishant; Dokmanovic, Milos; Hirsch, Dianne S.; Shen, Yi; Wu, Wen Jin] US FDA, Div Monoclonal Antibodies, Off Biotechnol Prod, Off Pharmaceut Sci,Ctr Drug Evaluat & Res, Bethesda, MD 20014 USA.
   [ElZarrad, M. Khair] NCI, Interagcy Oncol Task Force IOTF Fellowship Progra, NIH, Bethesda, MD 20892 USA.
   [Mukhopadhyay, Partha; Hao, Enkui; Pacher, Pal] NIAAA, Lab Physiol Studies, NIH, Bethesda, MD USA.
RP Wu, WJ (reprint author), US FDA, Div Monoclonal Antibodies, Off Biotechnol Prod, Off Pharmaceut Sci,Ctr Drug Evaluat & Res, Bethesda, MD 20014 USA.
EM wen.wu@fda.hhs.gov
RI MUKHOPADHYAY, PARTHA/G-3890-2010; Pacher, Pal/B-6378-2008
OI MUKHOPADHYAY, PARTHA/0000-0002-1178-1274; Pacher,
   Pal/0000-0001-7036-8108
FU Federal Drug Administration-Office of Women's Health Research Science
   Program Award [750912CDR]; Interagency Oncology Task Force Joint
   Fellowship Program; United States Food and Drug Administration; National
   Cancer Institute
FX This study is supported by Federal Drug Administration-Office of Women's
   Health Research Science Program Award to WJW (Project ID: 750912CDR) and
   the Interagency Oncology Task Force Joint Fellowship Program sponsored
   by the United States Food and Drug Administration and National Cancer
   Institute. The funders had no role in study design, data collection and
   analysis, decision to publish, or preparation of the manuscript.
NR 56
TC 16
Z9 16
U1 0
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 8
PY 2013
VL 8
IS 11
AR e79543
DI 10.1371/journal.pone.0079543
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255CG
UT WOS:000327216200073
PM 24255707
ER

PT J
AU Klabunde, CN
   Joseph, DA
   King, JB
   White, A
   Plescia, M
AF Klabunde, Carrie N.
   Joseph, Djenaba A.
   King, Jessica B.
   White, Arica
   Plescia, Marcus
TI Vital Signs: Colorectal Cancer Screening Test Use - United States, 2012
SO MMWR-MORBIDITY AND MORTALITY WEEKLY REPORT
LA English
DT Article
ID HEALTH; CARE; PREFERENCES; STRATEGIES; SYSTEM
AB Background: Strong evidence exists that screening with fecal occult blood testing (FOBT), sigmoidoscopy, or colonoscopy reduces the number of deaths from colorectal cancer (CRC). The percentage of the population up-to-date with recommended CRC screening increased from 54% in 2002 to 65% in 2010, primarily through increased use of colonoscopy.
   Methods: Data from the 2012 Behavioral Risk Factor Surveillance System survey were analyzed to estimate percentages of adults aged 50-75 years who reported CRC screening participation consistent with United States Preventive Services Task Force recommendations.
   Results: In 2012, 65.1% of U. S. adults were up-to-date with CRC screening, and 27.7% had never been screened. The proportion of respondents who had never been screened was greater among those without insurance (55.0%) and without a regular care provider (61.0%) than among those with health insurance (24.0%) and a regular care provider (23.5%). Colonoscopy was the most commonly used screening test (61.7%), followed by FOBT (10.4%). Colonoscopy was used by more than 53% of the population in every state. The percentages of blacks and whites up-to-date with CRC screening were equivalent. Compared with whites, a higher percentage of blacks across all income and education levels used FOBT.
   Conclusions: Many age-eligible adults did not use any type of CRC screening test as recommended. Organized, population-based approaches might increase CRC screening among those who have never been screened. Promoting both FOBT and colonoscopy as viable screening test options might increase CRC screening rates and reduce health disparities.
C1 [Klabunde, Carrie N.] NCI, Bethesda, MD 20892 USA.
   [Joseph, Djenaba A.; King, Jessica B.; White, Arica; Plescia, Marcus] CDC, Natl Ctr Chron Dis Prevent & Hlth Promot, Div Canc Prevent & Control, Atlanta, GA 30333 USA.
RP Joseph, DA (reprint author), CDC, Natl Ctr Chron Dis Prevent & Hlth Promot, Div Canc Prevent & Control, Atlanta, GA 30333 USA.
EM dajoseph@cdc.gov
NR 18
TC 106
Z9 107
U1 0
U2 5
PU CENTER DISEASE CONTROL & PREVENTION
PI ATLANTA
PA MAILSTOP E-90, ATLANTA, GA 30333 USA
SN 0149-2195
EI 1545-861X
J9 MMWR-MORBID MORTAL W
JI MMWR-Morb. Mortal. Wkly. Rep.
PD NOV 8
PY 2013
VL 62
IS 44
BP 881
EP 888
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 251NW
UT WOS:000326937500004
ER

PT J
AU D'Souza, L
   Cukras, C
   Antolik, C
   Craig, C
   Lee, JY
   He, H
   Li, SB
   Smaoui, N
   Hejtmancik, JF
   Sieving, PA
   Wang, XJ
AF D'Souza, Leera
   Cukras, Catherine
   Antolik, Christian
   Craig, Candice
   Lee, Ji-Yun
   He, Hong
   Li, Shibo
   Smaoui, Nizar
   Hejtmancik, James F.
   Sieving, Paul A.
   Wang, Xinjing
TI Characterization of novel RS1 exonic deletions in juvenile X-linked
   retinoschisis
SO MOLECULAR VISION
LA English
DT Article
ID XLRS1 GENE; CLINICAL-FEATURES; MUTATIONS; FAMILIES; PHENOTYPE; GENOTYPE
AB Purpose: X-linked juvenile retinoschisis (XLRS) is a vitreoretinal dystrophy characterized by schisis (splitting) of the inner layers of the neuroretina. Mutations within the retinoschisis (RS1) gene are responsible for this disease. The mutation spectrum consists of amino acid substitutions, splice site variations, small indels, and larger genomic deletions. Clinically, genomic deletions are rarely reported. Here, we characterize two novel full exonic deletions: one encompassing exon 1 and the other spanning exons 4-5 of the RS1 gene. We also report the clinical findings in these patients with XLRS with two different exonic deletions.
   Methods: Unrelated XLRS men and boys and their mothers (if available) were enrolled for molecular genetics evaluation. The patients also underwent ophthalmologic examination and in some cases electroretinogram (ERG) recording. All the exons and the flanking intronic regions of the RS1 gene were analyzed with direct sequencing. Two patients with exonic deletions were further evaluated with array comparative genomic hybridization to define the scope of the genomic aberrations. After the deleted genomic region was identified, primer walking followed by direct sequencing was used to determine the exact breakpoints.
   Results: Two novel exonic deletions of the RS1 gene were identified: one including exon 1 and the other spanning exons 4 and 5. The exon 1 deletion extends from the 5' region of the RS1 gene (including the promoter) through intron 1 (c.(-35)-1723_c.512664del4472). The exon 4-5 deletion spans introns 3 to intron 5 (c.185-1020_c.522+1844del5764).
   Conclusions: Here we report two novel exonic deletions within the RS1 gene locus. We have also described the clinical presentations and hypothesized the genomic mechanisms underlying these schisis phenotypes.
C1 [D'Souza, Leera; Cukras, Catherine; Antolik, Christian; Craig, Candice; He, Hong; Smaoui, Nizar; Hejtmancik, James F.; Wang, Xinjing] NEI, Ophthalm Genet & Visual Funct Branch, NIH, Bethesda, MD 20892 USA.
   [Lee, Ji-Yun; Li, Shibo] Univ Oklahoma, Dept Pediat, Oklahoma City, OK USA.
   [Sieving, Paul A.] NEI, Off Director, NIH, Bethesda, MD 20892 USA.
RP Wang, XJ (reprint author), NEI, Ophthalm Genet & Visual Funct Branch, NIH, 10D43,10 Ctr Dr, Bethesda, MD 20892 USA.
EM wangx6@nei.nih.gov
FU US National Institutes of Health (NIH), National Eye Institute (NEI)
FX This research was supported by the US National Institutes of Health
   (NIH), National Eye Institute (NEI) extramural, clinical, and intramural
   programs. The authors would like to thank the NEI/NIH eyeGENE (R)
   Coordinating Center, Kerry Goetz, Melissa Reeves, Vida Ndiforv, Sally
   Vitez, and Alexandra Garafalo for their assistance and technical support
   during the course of this study.
NR 22
TC 1
Z9 1
U1 1
U2 1
PU MOLECULAR VISION
PI ATLANTA
PA C/O JEFF BOATRIGHT, LAB B, 5500 EMORY EYE CENTER, 1327 CLIFTON RD, N E,
   ATLANTA, GA 30322 USA
SN 1090-0535
J9 MOL VIS
JI Mol. Vis.
PD NOV 7
PY 2013
VL 19
BP 2209
EP 2216
PG 8
WC Biochemistry & Molecular Biology; Ophthalmology
SC Biochemistry & Molecular Biology; Ophthalmology
GA 272LP
UT WOS:000328462400003
PM 24227916
ER

PT J
AU Gustchina, E
   Li, M
   Ghirlando, R
   Schuck, P
   Louis, JM
   Pierson, J
   Rao, P
   Subramaniam, S
   Gustchina, A
   Clore, GM
   Wlodawer, A
AF Gustchina, Elena
   Li, Mi
   Ghirlando, Rodolfo
   Schuck, Peter
   Louis, John M.
   Pierson, Jason
   Rao, Prashant
   Subramaniam, Sriram
   Gustchina, Alla
   Clore, G. Marius
   Wlodawer, Alexander
TI Complexes of Neutralizing and Non-Neutralizing Affinity Matured Fabs
   with a Mimetic of the Internal Trimeric Coiled-Coil of HIV-1 gp41
SO PLOS ONE
LA English
DT Article
ID ANALYTICAL ULTRACENTRIFUGATION; SEDIMENTATION-VELOCITY; ENVELOPE
   GLYCOPROTEIN; CRYSTAL-STRUCTURES; ANTIBODY; REGION; DESIGN; INHIBITORS;
   ACCURACY; SYSTEM
AB A series of mini-antibodies (monovalent and bivalent Fabs) targeting the conserved internal trimeric coiled-coil of the N-heptad repeat (N-HR) of HIV-1 gp41 has been previously constructed and reported. Crystal structures of two closely related monovalent Fabs, one (Fab 8066) broadly neutralizing across a wide panel of HIV-1 subtype B and C viruses, and the other (Fab 8062) non-neutralizing, representing the extremes of this series, were previously solved as complexes with 5-Helix, a gp41 pre-hairpin intermediate mimetic. Binding of these Fabs to covalently stabilized chimeric trimers of N-peptides of HIV1 gp41 (named (CCIZN36)(3) or 3-H) has now been investigated using X-ray crystallography, cryo-electron microscopy, and a variety of biophysical methods. Crystal structures of the complexes between 3-H and Fab 8066 and Fab 8062 were determined at 2.8 and 3.0 angstrom resolution, respectively. Although the structures of the complexes with the neutralizing Fab 8066 and its non-neutralizing counterpart Fab 8062 were generally similar, small differences between them could be correlated with the biological properties of these antibodies. The conformations of the corresponding CDRs of each antibody in the complexes with 3-H and 5-Helix are very similar. The adaptation to a different target upon complex formation is predominantly achieved by changes in the structure of the trimer of N-HR helices, as well as by adjustment of the orientation of the Fab molecule relative to the N-HR in the complex, via rigid-body movement. The structural data presented here indicate that binding of three Fabs 8062 with high affinity requires more significant changes in the structure of the N-HR trimer compared to binding of Fab 8066. A comparative analysis of the structures of Fabs complexed to different gp41 intermediate mimetics allows further evaluation of biological relevance for generation of neutralizing antibodies, as well as provides novel structural insights into immunogen design.
C1 [Gustchina, Elena; Louis, John M.; Clore, G. Marius] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
   [Li, Mi; Gustchina, Alla; Wlodawer, Alexander] NCI, Macromol Crystallog Lab, Frederick, MD 21701 USA.
   [Li, Mi] SAIC Frederick, Basic Res Program, Frederick, MD USA.
   [Ghirlando, Rodolfo] NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
   [Schuck, Peter] Natl Inst Biomed Imaging & Bioengn, NIH, Lab Cellular Imaging & Macromol Biophys, Bethesda, MD USA.
   [Pierson, Jason] FEI Co, Hillsboro, OR USA.
   [Rao, Prashant; Subramaniam, Sriram] NCI, Ctr Canc Res, Cell Biol Lab, Bethesda, MD USA.
RP Gustchina, A (reprint author), NCI, Macromol Crystallog Lab, Frederick, MD 21701 USA.
EM gustchia@mail.nih.gov; mariusc@mail.nih.gov; wlodawer@nih.gov
RI Clore, G. Marius/A-3511-2008; 
OI Clore, G. Marius/0000-0003-3809-1027; Schuck, Peter/0000-0002-8859-6966
FU U.S. Department of Energy, Office of Science, Office of Basic Energy
   Sciences [W-31-109-Eng-38]; Intramural Research Programs of the NIDDK;
   Intramural Research Programs of the NIBIB; National Cancer Institute,
   Center for Cancer Research; AIDS Targeted Antiviral Program of the
   Office of the Director of the NIH; Federal funds from the National
   Cancer Institute, NIH [HHSN261200800001E]
FX The authors acknowledge the use of beamline 22-ID of the Southeast
   Regional Collaborative Access Team (SER-CAT), located at the Advanced
   Photon Source, Argonne National Laboratory. Use of the APS was supported
   by the U.S. Department of Energy, Office of Science, Office of Basic
   Energy Sciences, under Contract No. W-31-109-Eng-38. This project was
   supported in part by the Intramural Research Programs of the NIDDK (to
   G. M. C), NIBIB (to P. S.), and the National Cancer Institute, Center
   for Cancer Research (to S. S. and A. W.), by the AIDS Targeted Antiviral
   Program of the Office of the Director of the NIH (to S. S. and G. M.
   C.), and with Federal funds from the National Cancer Institute, NIH,
   under Contract No. HHSN261200800001E (to M. L.). The content of this
   publication is solely the responsibility of the authors and does not
   necessarily represent the official views or policies of the Department
   of Health and Human Services, nor does the mention of trade names,
   commercial products, or organizations imply endorsement by the U. S.
   Government. The funders had no role in study design, data collection and
   analysis, decision to publish, or preparation of the manuscript.
NR 43
TC 8
Z9 8
U1 1
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 7
PY 2013
VL 8
IS 11
AR e78187
DI 10.1371/journal.pone.0078187
PG 15
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 254KD
UT WOS:000327162900010
PM 24244293
ER

PT J
AU Rozenberg, JM
   Bhattacharya, P
   Chatterjee, R
   Glass, K
   Vinson, C
AF Rozenberg, Julian M.
   Bhattacharya, Paramita
   Chatterjee, Raghunath
   Glass, Kimberly
   Vinson, Charles
TI Combinatorial Recruitment of CREB, C/EBP beta and c-Jun Determines
   Activation of Promoters upon Keratinocyte Differentiation
SO PLOS ONE
LA English
DT Article
ID ELEMENT-BINDING PROTEIN; INVOLUCRIN GENE PROMOTER; GENOME-WIDE ANALYSIS;
   TRANSCRIPTION FACTORS; IN-VITRO; CHROMATIN ACCESSIBILITY; MEDIATED
   TRANSCRIPTION; SKIN TUMORIGENESIS; CELL-SURVIVAL; ONCOGENIC RAS
AB Background: Transcription factors CREB, C/EBP beta and Jun regulate genes involved in keratinocyte proliferation and differentiation. We questioned if specific combinations of CREB, C/EBP beta and c-Jun bound to promoters correlate with RNA polymerase II binding, mRNA transcript levels and methylation of promoters in proliferating and differentiating keratinocytes.
   Results: Induction of mRNA and RNA polymerase II by differentiation is highest when promoters are bound by C/EBP beta alone, C/EBP beta together with c-Jun, or by CREB, C/EBP beta and c-Jun, although in this case CREB binds with low affinity. In contrast, RNA polymerase II binding and mRNA levels change the least upon differentiation when promoters are bound by CREB either alone or in combination with C/EBP beta or c-Jun. Notably, promoters bound by CREB have relatively high levels of RNA polymerase II binding irrespective of differentiation. Inhibition of C/EBP beta or c-Jun preferentially represses mRNA when gene promoters are bound by corresponding transcription factors and not CREB. Methylated promoters have relatively low CREB binding and, accordingly, those which are bound by C/EBP beta are induced by differentiation irrespective of CREB. Composite "Half and Half'' consensus motifs and co localizing consensus DNA binding motifs are overrepresented in promoters bound by the combination of corresponding transcription factors.
   Conclusion: Correlational and functional data describes combinatorial mechanisms regulating the activation of promoters. Colocalization of C/EBP beta and c-Jun on promoters without strong CREB binding determines high probability of activation upon keratinocyte differentiation.
C1 [Rozenberg, Julian M.] Univ N Carolina, Dept Pathol & Lab Med, Chapel Hill, NC USA.
   [Bhattacharya, Paramita] Saha Inst Nucl Phys, Crystallog & Mol Biol Div, Kolkata, W Bengal, India.
   [Chatterjee, Raghunath] Indian Stat Inst, Div Biol Sci, Human Genet Unit, Kolkata, India.
   [Glass, Kimberly] Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Boston, MA 02115 USA.
   [Vinson, Charles] NCI, Lab Metab, Bethesda, MD 20892 USA.
RP Vinson, C (reprint author), NCI, Lab Metab, Bethesda, MD 20892 USA.
EM vinsonc@dc37a.nci.nih.gov
FU National Institutes of Health, Bethesda, Maryland USA; NIH
FX This study was performed and funded by the National Institutes of
   Health, Bethesda, Maryland USA. The source of funding was intramural
   budget of the NIH. The funders had no role in study design, data
   collection and analysis, decision to publish, or preparation of the
   manuscript.
NR 53
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 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 7
PY 2013
VL 8
IS 11
AR e78179
DI 10.1371/journal.pone.0078179
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 254KD
UT WOS:000327162900009
PM 24244291
ER

PT J
AU Saeed, F
   Pisitkun, T
   Hoffert, JD
   Rashidian, S
   Wang, GH
   Gucek, M
   Knepper, MA
AF Saeed, Fahad
   Pisitkun, Trairak
   Hoffert, Jason D.
   Rashidian, Sara
   Wang, Guanghui
   Gucek, Marjan
   Knepper, Mark A.
TI PhosSA: Fast and accurate phosphorylation site assignment algorithm for
   mass spectrometry data
SO PROTEOME SCIENCE
LA English
DT Article
ID QUANTITATIVE PHOSPHOPROTEOMIC ANALYSIS; PROTEIN IDENTIFICATION;
   SIGNALING NETWORKS; SPECTRA; LOCALIZATION; PEPTIDE; CELLS; DISCOVERY;
   SEQUENCES; ALIGNMENT
AB Phosphorylation site assignment of high throughput tandem mass spectrometry (LC-MS/MS) data is one of the most common and critical aspects of phosphoproteomics. Correctly assigning phosphorylated residues helps us understand their biological significance. The design of common search algorithms (such as Sequest, Mascot etc.) do not incorporate site assignment; therefore additional algorithms are essential to assign phosphorylation sites for mass spectrometry data. The main contribution of this study is the design and implementation of a linear time and space dynamic programming strategy for phosphorylation site assignment referred to as PhosSA. The proposed algorithm uses summation of peak intensities associated with theoretical spectra as an objective function. Quality control of the assigned sites is achieved using a post-processing redundancy criteria that indicates the signal-to-noise ratio properties of the fragmented spectra. The quality assessment of the algorithm was determined using experimentally generated data sets using synthetic peptides for which phosphorylation sites were known. We report that PhosSA was able to achieve a high degree of accuracy and sensitivity with all the experimentally generated mass spectrometry data sets. The implemented algorithm is shown to be extremely fast and scalable with increasing number of spectra (we report up to 0.5 million spectra/hour on a moderate workstation). The algorithm is designed to accept results from both Sequest and Mascot search engines. An executable is freely available at http://helixweb.nih.gov/ESBL/PhosSA/ for academic research purposes.
C1 [Saeed, Fahad; Pisitkun, Trairak; Hoffert, Jason D.; Rashidian, Sara; Knepper, Mark A.] NHLBI, Epithelial Syst Biol Lab, NIH, Bethesda, MD 20892 USA.
   [Wang, Guanghui; Gucek, Marjan] NHLBI, Prote Core Facil, NIH, Bethesda, MD 20892 USA.
   [Rashidian, Sara] Catholic Univ Amer, Dept Elect Engn & Comp Sci, Washington, DC 20064 USA.
   [Pisitkun, Trairak] Chulalongkorn Univ, Fac Med, Bangkok 10330, Thailand.
RP Saeed, F (reprint author), NHLBI, Epithelial Syst Biol Lab, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM fahad.saeed@nih.gov
OI Pisitkun, Trairak/0000-0001-6677-2271
FU Division of Intramural Research, National Heart, Lung and Blood
   Institute, National Institutes of Health (NIH) [ZO1-HL001285]
FX This work and the publication cost for this manuscript was funded by the
   operating budget of Division of Intramural Research, National Heart,
   Lung and Blood Institute, National Institutes of Health (NIH), Project
   ZO1-HL001285.
NR 43
TC 4
Z9 4
U1 0
U2 7
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1477-5956
J9 PROTEOME SCI
JI Proteome Sci.
PD NOV 7
PY 2013
VL 11
SU 1
AR S14
DI 10.1186/1477-5956-11-S1-S14
PG 15
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 270OF
UT WOS:000328327300014
PM 24565028
ER

PT J
AU Barta, SK
   Xue, XN
   Wang, D
   Tamari, R
   Lee, JY
   Mounier, N
   Kaplan, LD
   Ribera, JM
   Spina, M
   Tirelli, U
   Weiss, R
   Galicier, L
   Boue, F
   Wilson, WH
   Wyen, C
   Oriol, A
   Navarro, JT
   Dunleavy, K
   Little, RF
   Ratner, L
   Garcia, O
   Morgades, M
   Remick, SC
   Noy, A
   Sparano, JA
AF Barta, Stefan K.
   Xue, Xiaonan
   Wang, Dan
   Tamari, Roni
   Lee, Jeannette Y.
   Mounier, Nicolas
   Kaplan, Lawrence D.
   Ribera, Josep-Maria
   Spina, Michele
   Tirelli, Umberto
   Weiss, Rudolf
   Galicier, Lionel
   Boue, Francois
   Wilson, Wyndham H.
   Wyen, Christoph
   Oriol, Albert
   Navarro, Jose-Tomas
   Dunleavy, Kieron
   Little, Richard F.
   Ratner, Lee
   Garcia, Olga
   Morgades, Mireia
   Remick, Scot C.
   Noy, Ariela
   Sparano, Joseph A.
TI Treatment factors affecting outcomes in HIV-associated non-Hodgkin
   lymphomas: a pooled analysis of 1546 patients
SO BLOOD
LA English
DT Article
ID ACTIVE ANTIRETROVIRAL THERAPY; B-CELL LYMPHOMA; PHASE-II TRIAL; ORAL
   COMBINATION CHEMOTHERAPY; VIRUS-INFECTION STATUS; DOSE-ADJUSTED EPOCH;
   INTENSIVE CHEMOTHERAPY; PLUS RITUXIMAB; INFUSIONAL CYCLOPHOSPHAMIDE;
   BURKITT-LYMPHOMA
AB Limited comparative data exist for the treatment of HIV-associated non-Hodgkin lymphoma. We analyzed pooled individual patient data for 1546 patients from 19 prospective clinical trials to assess treatment-specific factors (type of chemotherapy, rituximab, and concurrent combination antiretroviral [cART] use) and their influence on the outcomes complete response (CR), progression free survival (PFS), and overall survival (OS). In our analysis, rituximab was associated with a higher CR rate (odds ratio [OR] 2.89; P < .001), improved PFS (hazard ratio [HR] 0.50; P < .001), and OS (HR 0.51; P < .0001). Compared with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), initial therapy with more dose-intense regimens resulted in better CR rates (ACVBP [doxorubicin, cyclophosphamide, vindesine, bleomycin and prednisolone]: OR 1.70; P < .04), PFS (ACVBP: HR 0.72; P = .049; "intensive regimens": HR 0.35; P < .001) and OS ("intensive regimens": HR 0.54; P < .001). Infusional etoposide, prednisone, infusional vincristine, infusional doxorubicin, and cyclophosphamide (EPOCH) was associated with significantly better OS in diffuse large B-cell lymphoma (HR 0.33; P = .03). Concurrent use of cART was associated with improved CR rates (OR 1.89; P = .005) and trended toward improved OS (HR 0.78; P = .07). These findings provide supporting evidence for current patterns of care where definitive evidence is unavailable.
C1 [Barta, Stefan K.; Xue, Xiaonan; Wang, Dan; Sparano, Joseph A.] Albert Einstein Canc Ctr, Bronx, NY USA.
   [Tamari, Roni; Noy, Ariela] Mem Sloan Kettering Canc Ctr, Div Hematol Oncol, New York, NY 10021 USA.
   [Tamari, Roni; Noy, Ariela] Weill Cornell Med Coll, New York, NY USA.
   [Lee, Jeannette Y.] Univ Arkansas, Dept Biostat, Little Rock, AR 72204 USA.
   [Mounier, Nicolas] GELA, Midi Pyrenees, France.
   [Kaplan, Lawrence D.] Univ Calif San Francisco, Div Hematol Oncol, Adult Lymphoma Program, San Francisco, CA 94143 USA.
   [Ribera, Josep-Maria; Oriol, Albert; Navarro, Jose-Tomas; Garcia, Olga; Morgades, Mireia] ICO Hosp Germans Trias & Pujol, Jose Carreras Res Inst, Badalona, Spain.
   [Ribera, Josep-Maria; Oriol, Albert; Navarro, Jose-Tomas; Garcia, Olga; Morgades, Mireia] PETHEMA Grp, Badalona, Spain.
   [Spina, Michele; Tirelli, Umberto] Natl Canc Inst, Dept Med Oncol, Aviano, Italy.
   [Galicier, Lionel] Hop St Louis, AP HP, Dept Clin Immunol, Paris, France.
   [Boue, Francois] Hop Antoine Beclere, Serv Med Interne & Immunol, Clamart, France.
   [Wilson, Wyndham H.; Dunleavy, Kieron; Little, Richard F.] NCI, Metab Branch & Clin Invest Branch, Bethesda, MD 20892 USA.
   [Wyen, Christoph] Univ Hosp Cologne, Dept Med, Cologne, Germany.
   [Ratner, Lee] Washington Univ, Div Oncol, St Louis, MO USA.
   [Remick, Scot C.] W Virginia Univ, Mary Babb Randolph Canc Ctr, Morgantown, WV 26506 USA.
RP Barta, SK (reprint author), Montefiore Med Ctr, Albert Einstein Canc Ctr, Dept Oncol, 111 East 210th St, Bronx, NY 10467 USA.
EM sbarta@montefiore.org
OI Noy, Ariela/0000-0002-3001-4898
FU AIDS Malignancy Consortium [UO1CA121947]; Paul Calabresi Career
   Development Award for Clinical Oncology [K12CA132783-03]; American
   Society of Clinical Oncology Cancer Foundation
FX This work was supported in parts by the AIDS Malignancy Consortium
   (grant UO1CA121947), the Paul Calabresi Career Development Award for
   Clinical Oncology (grant K12CA132783-03), the American Society of
   Clinical Oncology Cancer Foundation 2010 Young Investigator Award, Red
   Tematica de Investigacion Cooperativa en Cancer grant RD12/0036/0029,
   Instituto de Salud Carlos III, Spain, Clinical and Translational Science
   Award grants UL1 RR025750 and KL2 RR025749, and TL1 RR025748 from the
   National Center for Research Resources, a component of the National
   Institutes of Health (NIH), and NIH Roadmap for Medical Research.
NR 49
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U1 0
U2 9
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD NOV 7
PY 2013
VL 122
IS 19
BP 3251
EP 3262
DI 10.1182/blood-2013-04-498964
PG 12
WC Hematology
SC Hematology
GA 258NN
UT WOS:000327466100009
PM 24014242
ER

PT J
AU Sumner, CJ
   d'Ydewalle, C
   Wooley, J
   Fawcett, KA
   Hernandez, D
   Gardiner, AR
   Kalmar, B
   Baloh, RH
   Gonzalez, M
   Zuchner, S
   Stanescu, HC
   Kleta, R
   Mankodi, A
   Cornblath, DR
   Boylan, KB
   Reilly, MM
   Greensmith, L
   Singleton, AB
   Harms, MB
   Rossor, AM
   Houlden, H
AF Sumner, Charlotte J.
   d'Ydewalle, Constantin
   Wooley, Joe
   Fawcett, Katherine A.
   Hernandez, Dena
   Gardiner, Alice R.
   Kalmar, Bernadett
   Baloh, Robert H.
   Gonzalez, Michael
   Zuechner, Stephan
   Stanescu, Horia C.
   Kleta, Robert
   Mankodi, Ami
   Cornblath, David R.
   Boylan, Kevin B.
   Reilly, Mary M.
   Greensmith, Linda
   Singleton, Andrew B.
   Harms, Matthew B.
   Rossor, Alexander M.
   Houlden, Henry
TI A Dominant Mutation in FBXO38 Causes Distal Spinal Muscular Atrophy with
   Calf Predominance
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID TRANSCRIPTION FACTOR KLF7; HEREDITARY MOTOR NEUROPATHIES; F-BOX
   PROTEINS; AXON REGENERATION; GENE-EXPRESSION; SENSORY NEURONS; KRUPPEL;
   RNA; IDENTIFICATION; COMPLEX
AB Spinal muscular atrophies (SMAs) are a heterogeneous group of inherited disorders characterized by degeneration of anterior horn cells and progressive muscle weakness. In two unrelated families affected by a distinct form of autosomal-dominant distal SMA initially manifesting with calf weakness, we identified by genetic linkage analysis and exome sequencing a heterozygous missense mutation, c.616T>C (p.Cys206Arg), in F-box protein 38 (FBXO38). FBXO38 is a known coactivator of the transcription factor Kruppel-like factor 7 (KLF7), which regulates genes required for neuronal axon outgrowth and repair. The p.Cys206Arg substitution did not alter the subcellular localization of FBXO38 but did impair KLF7-mediated transactivation of a KLF7-responsive promoter construct and endogenous KLF7 target genes in both heterologously expressing human embryonic kidney 293T cells and fibroblasts derived from individuals with the FBXO38 missense mutation. This transcriptional dysregulation was associated with an impairment of neurite outgrowth in primary motor neurons. Together, these results suggest that a transcriptional regulatory pathway that has a well-established role in axonal development could also be critical for neuronal maintenance and highlight the importance of FBXO38 and KLF7 activity in motor neurons.
C1 [Sumner, Charlotte J.; d'Ydewalle, Constantin; Wooley, Joe; Cornblath, David R.] Johns Hopkins Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
   [Sumner, Charlotte J.] Johns Hopkins Sch Med, Dept Neurosci, Baltimore, MD 21205 USA.
   [d'Ydewalle, Constantin] VIB, Vesalius Res Ctr, Neurobiol Lab, B-3000 Louvain, Belgium.
   [d'Ydewalle, Constantin] Katholieke Univ Leuven, B-3000 Louvain, Belgium.
   [Fawcett, Katherine A.; Gardiner, Alice R.; Reilly, Mary M.; Houlden, Henry] Natl Hosp Neurol & Neurosurg, Dept Mol Neurosci, London WC1N 3BG, England.
   [Fawcett, Katherine A.; Gardiner, Alice R.; Kalmar, Bernadett; Reilly, Mary M.; Greensmith, Linda; Rossor, Alexander M.; Houlden, Henry] UCL Inst Neurol, London WC1N 3BG, England.
   [Fawcett, Katherine A.; Gardiner, Alice R.; Kalmar, Bernadett; Reilly, Mary M.; Greensmith, Linda; Rossor, Alexander M.; Houlden, Henry] Natl Hosp Neurol & Neurosurg, MRC, Ctr Neuromuscular Dis, London WC1N 3BG, England.
   [Hernandez, Dena; Singleton, Andrew B.] NIA, NIH, Neurogenet Lab, Bethesda, MD 20892 USA.
   [Baloh, Robert H.] Cedars Sinai Med Ctr, Dept Neurol, Los Angeles, CA 90095 USA.
   [Gonzalez, Michael; Zuechner, Stephan] Univ Miami, Miller Sch Med, Dr John T MacDonald Dept Human Genet, Miami, FL 33136 USA.
   [Gonzalez, Michael; Zuechner, Stephan] Univ Miami, Miller Sch Med, Hussman Inst Human Genom, Miami, FL 33136 USA.
   [Stanescu, Horia C.; Kleta, Robert] UCL, Ctr Nephrol, London WC1N 3BG, England.
   [Mankodi, Ami] NINDS, Neurogenet Branch, Bethesda, MD 20892 USA.
   [Boylan, Kevin B.] Mayo Clin, Dept Neurol, Jacksonville, FL 32224 USA.
   [Harms, Matthew B.] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA.
RP Sumner, CJ (reprint author), Johns Hopkins Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
EM csumner1@jhmi.edu; h.houlden@ucl.ac.uk
RI Singleton, Andrew/C-3010-2009; Houlden, Henry/C-1532-2008
OI Houlden, Henry/0000-0002-2866-7777
FU National Institute of Neurological Disorders and Stroke (NINDS)
   [R01NS062869]; Research Council of KU Leuven; NINDS [K08-NS-075094];
   Office of Rare Diseases [U54NS065712]; Ipsen clinical research
   fellowship; Wellcome Trust; Muscular Dystrophy Campaign; Medical
   Research Council; French Muscular Dystrophy Association; National
   Institute on Aging, National Institutes of Health, Department of Health
   and Human Services [ZO1 AG000958-10]
FX The authors would like to thank Kenneth Fischbeck for advice about
   genetics, Vinay Chaudhry and Zeng Wang for clinical care, Chris Dorsey
   and Jamal Garrison for muscle histology, and Peggy Allred for aid in
   DNA-sample collection. C.J.S. is supported by National Institute of
   Neurological Disorders and Stroke (NINDS) grant R01NS062869. C.d.Y. is
   supported by the Research Council of KU Leuven (Special Research Fund).
   M.B.H. is funded by the NINDS (K08-NS-075094). A.M.R. is funded by the
   NINDS and Office of Rare Diseases (U54NS065712), as well as an Ipsen
   clinical research fellowship. H.H. is supported by The Wellcome Trust,
   the Muscular Dystrophy Campaign, the Medical Research Council, and The
   French Muscular Dystrophy Association. We would also like to thank the
   University College London Hospitals National Institute for Health
   Research Biomedical Research Centre funding scheme. This work was also
   supported in part by the Intramural Research Program of the National
   Institute on Aging, National Institutes of Health, Department of Health
   and Human Services (project ZO1 AG000958-10).
NR 35
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Z9 8
U1 1
U2 6
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 NOV 7
PY 2013
VL 93
IS 5
BP 976
EP 983
DI 10.1016/j.ajhg.2013.10.006
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 252HU
UT WOS:000326996600018
PM 24207122
ER

PT J
AU Fauci, AS
   Marston, HD
AF Fauci, Anthony S.
   Marston, Hilary D.
TI Achieving an AIDS-free World: Science and Implementation
SO CELL
LA English
DT Editorial Material
ID HIV-1 INFECTION; PREVENTION; ANTIBODIES; THERAPY; VACCINE
C1 [Fauci, Anthony S.; Marston, Hilary D.] NIAID, NIH, Bethesda, MD 20892 USA.
RP Fauci, AS (reprint author), NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM afauci@niaid.nih.gov
NR 12
TC 0
Z9 0
U1 0
U2 15
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
EI 1097-4172
J9 CELL
JI Cell
PD NOV 7
PY 2013
VL 155
IS 4
BP 733
EP 734
DI 10.1016/j.cell.2013.10.016
PG 2
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 251MW
UT WOS:000326934300001
PM 24157218
ER

PT J
AU Jablonski, KL
   Fedorova, OV
   Racine, ML
   Geolfos, CJ
   Gates, PE
   Chonchol, M
   Fleenor, BS
   Lakatta, EG
   Bagrov, AY
   Seals, DR
AF Jablonski, Kristen L.
   Fedorova, Olga V.
   Racine, Matthew L.
   Geolfos, Candace J.
   Gates, Phillip E.
   Chonchol, Michel
   Fleenor, Bradley S.
   Lakatta, Edward G.
   Bagrov, Alexei Y.
   Seals, Douglas R.
TI Dietary Sodium Restriction and Association with Urinary Marinobufagenin,
   Blood Pressure, and Aortic Stiffness
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID VASCULAR ENDOTHELIAL DYSFUNCTION; NACL-SENSITIVE HYPERTENSION; ARTERIAL
   STIFFNESS; INCIDENT HYPERTENSION; SALT SENSITIVITY; OLDER-ADULTS;
   NA/K-ATPASE; KAPPA-B; PUMP; HUMANS
AB Background and objectivesSystolic BP and large elastic artery stiffness both increase with age and are reduced by dietary sodium restriction. Production of the natriuretic hormone marinobufagenin, an endogenous 1 Na+,K+-ATPase inhibitor, is increased in salt-sensitive hypertension and contributes to the rise in systolic BP during sodium loading.Design, setting, participants, & measurementsThe hypothesis was that dietary sodium restriction performed in middle-aged/older adults (eight men and three women; 602 years) with moderately elevated systolic BP (1392/83 +/- 2 mmHg) would reduce urinary marinobufagenin excretion as well as systolic BP and aortic pulse-wave velocity (randomized, placebo-controlled, and crossover design). This study also explored the associations among marinobufagenin excretion with systolic BP and aortic pulse-wave velocity across conditions of 5 weeks of a low-sodium (77 +/- 9 mmol/d) and 5 weeks of a normal-sodium (144 +/- 7 mmol/d) diet.ResultsUrinary marinobufagenin excretion (weekly measurements; 25.4 +/- 1.8 versus 30.7 +/- 2.1 pmol/kg per day), systolic BP (127 +/- 3 versus 138 +/- 5 mmHg), and aortic pulse-wave velocity (700 +/- 40 versus 843 +/- 36 cm/s) were lower during the low- versus normal-sodium condition (all P<0.05). Across all weeks, marinobufagenin excretion was related with systolic BP (slope=0.61, P<0.001) and sodium excretion (slope=0.46, P<0.001). These associations persisted during the normal- but not the low-sodium condition (both P<0.005). Marinobufagenin excretion also was associated with aortic pulse-wave velocity (slope=0.70, P=0.02) and endothelial cell expression of NAD(P)H oxidase-p47phox (slope=0.64, P=0.006).ConclusionsThese results show, for the first time in humans, that dietary sodium restriction reduces urinary marinobufagenin excretion and that urinary marinobufagenin excretion is positively associated with systolic BP, aortic stiffness (aortic pulse-wave velocity), and endothelial cell expression of the oxidant enzyme NAD(P)H oxidase. Importantly, marinobufagenin excretion is positively related to systolic BP over ranges of sodium intake typical of an American diet, extending previous observations in rodents and humans fed experimentally high-sodium diets.
C1 [Jablonski, Kristen L.; Racine, Matthew L.; Geolfos, Candace J.; Fleenor, Bradley S.; Seals, Douglas R.] Univ Colorado, Dept Integrat Physiol, Boulder, CO 80309 USA.
   [Fedorova, Olga V.; Lakatta, Edward G.; Bagrov, Alexei Y.] NIA, Intramural Res Program, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA.
   [Gates, Phillip E.] Univ Exeter, Sch Med, Inst Biomed & Clin Sci, Exeter, Devon, England.
   [Chonchol, Michel] Univ Colorado Denver, Anschutz Med Ctr, Div Renal Dis & Hypertens, Aurora, CO USA.
RP Jablonski, KL (reprint author), Univ Colorado, Div Renal Dis & Hypertens, Aurora, CO 80220 USA.
EM Kristen.Nowak@ucdenver.edu
FU National Institutes of Health [AG013038, AG006537, AG031141, AG033994,
   TR000154]; Intramural Research Program, National Institute on Aging,
   National Institutes of Health
FX This work was supported by National Institutes of Health Awards
   AG013038, AG006537, AG031141, AG033994, and TR000154. This study was
   supported, in part, by the Intramural Research Program, National
   Institute on Aging, National Institutes of Health (O.V.F., E. G. L., and
   A.Y.B.).
NR 34
TC 18
Z9 18
U1 0
U2 5
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 NOV 7
PY 2013
VL 8
IS 11
BP 1952
EP 1959
DI 10.2215/CJN.00900113
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA 250FR
UT WOS:000326836400017
PM 23929930
ER

PT J
AU Grupi, A
   Minton, AP
AF Grupi, Asaf
   Minton, Allen P.
TI Concentration-Dependent Viscosity of Binary and Ternary Mixtures of
   Nonassociating Proteins: Measurement and Analysis
SO JOURNAL OF PHYSICAL CHEMISTRY B
LA English
DT Article
ID REVERSIBLE SELF-ASSOCIATION; MONOCLONAL-ANTIBODY; LIGHT-SCATTERING;
   ABSORPTION
AB Using a recently developed automated viscometer (Grupi, A.; Minton, A. P. Anal. Chem. 2012, 84, 10732-10736), the dependence of solution viscosity upon the concentrations of bovine serum albumin, hen egg ovomucoid, and human fibrinogen have been measured individually and in binary and ternary mixtures over a wide range of compositions and at total concentrations of up to 300 g/L. The concentration dependence of viscosity of all solutions is quantitatively described over the entire range of concentrations and compositions by a semiempirical equation requiring specification of only two composition-independent global parameters per protein.
C1 [Grupi, Asaf; Minton, Allen P.] NIDDK, Sect Phys Biochem, Lab Biochem & Genet, NIH,US Dept HHS, Bethesda, MD 20892 USA.
RP Grupi, A (reprint author), Bar Ilan Univ, Fac Life Sci, Ramat Gan, Israel.
EM grupia@gmail.com; minton@helix.nih.gov
OI Minton, Allen/0000-0001-8459-1247
FU Intramural Research Program of the National Institute of Diabetes and
   Digestive and Kidney Diseases
FX This research was supported by the Intramural Research Program of the
   National Institute of Diabetes and Digestive and Kidney Diseases.
NR 17
TC 0
Z9 0
U1 3
U2 17
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1520-6106
J9 J PHYS CHEM B
JI J. Phys. Chem. B
PD NOV 7
PY 2013
VL 117
IS 44
BP 13861
EP 13865
DI 10.1021/jp406530r
PG 5
WC Chemistry, Physical
SC Chemistry
GA 250IB
UT WOS:000326845100015
PM 24131130
ER

PT J
AU Schroder, S
   Herker, E
   Itzen, F
   He, D
   Thomas, S
   Gilchrist, DA
   Kaehlcke, K
   Cho, S
   Pollard, KS
   Capra, JA
   Schnolzer, M
   Cole, PA
   Geyer, M
   Bruneau, BG
   Adelman, K
   Ott, M
AF Schroeder, Sebastian
   Herker, Eva
   Itzen, Friederike
   He, Daniel
   Thomas, Sean
   Gilchrist, Daniel A.
   Kaehlcke, Katrin
   Cho, Sungyoo
   Pollard, Katherine S.
   Capra, John A.
   Schnoelzer, Martina
   Cole, Philip A.
   Geyer, Matthias
   Bruneau, Benoit G.
   Adelman, Karen
   Ott, Melanie
TI Acetylation of RNA Polymerase II Regulates Growth-Factor-Induced Gene
   Transcription in Mammalian Cells
SO MOLECULAR CELL
LA English
DT Article
ID C-TERMINAL DOMAIN; HISTONE H3; CHIP-SEQ; DROSOPHILA-MELANOGASTER;
   CHROMATIN TEMPLATES; HUMAN GENOME; DNA-BINDING; ELONGATION; PROMOTERS;
   PHOSPHORYLATION
AB Lysine acetylation regulates transcription by targeting histones and nonhistone proteins. Here we report that the central regulator of transcription, RNA polymerase II, is subject to acetylation in mammalian cells. Acetylation occurs at eight lysines within the C-terminal domain (CTD) of the largest polymerase subunit and is mediated by p300/KAT3B. CTD acetylation is specifically enriched downstream of the transcription start sites of polymerase-occupied genes genome-wide, indicating a role in early stages of transcription initiation or elongation. Mutation of lysines or p300 inhibitor treatment causes the loss of epidermal growth-factor-induced expression of c-Fos and Egr2, immediate-early genes with promoter-proximally paused polymerases, but does not affect expression or polymerase occupancy at housekeeping genes. Our studies identify acetylation as a new modification of the mammalian RNA polymerase II required for the induction of growth factor response genes.
C1 [Schroeder, Sebastian; Herker, Eva; He, Daniel; Thomas, Sean; Kaehlcke, Katrin; Cho, Sungyoo; Pollard, Katherine S.; Capra, John A.; Bruneau, Benoit G.; Ott, Melanie] Gladstone Inst, San Francisco, CA 94158 USA.
   [Schroeder, Sebastian; He, Daniel; Thomas, Sean; Kaehlcke, Katrin; Cho, Sungyoo; Pollard, Katherine S.; Capra, John A.; Bruneau, Benoit G.; Ott, Melanie] Univ Calif San Francisco, San Francisco, CA 94143 USA.
   [Herker, Eva] Heinrich Pette Inst, Leibniz Inst Expt Virol, D-20251 Hamburg, Germany.
   [Itzen, Friederike; Geyer, Matthias] Max Planck Inst Mol Physiol, D-44227 Dortmund, Germany.
   [Gilchrist, Daniel A.; Adelman, Karen] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC 27709 USA.
   [Schnoelzer, Martina] German Canc Res Ctr, D-69120 Heidelberg, Germany.
   [Cole, Philip A.] Johns Hopkins Univ, Baltimore, MD 21205 USA.
   [Geyer, Matthias] Res Ctr Caesar, D-53175 Bonn, Germany.
RP Ott, M (reprint author), Gladstone Inst, San Francisco, CA 94158 USA.
EM mott@gladstone.ucsf.edu
RI Herker, Eva/B-9699-2014; 
OI Herker, Eva/0000-0001-9644-2484; Ott, Melanie/0000-0002-5697-1274;
   Gilchrist, Daniel/0000-0003-1668-2790
FU Gladstone; NIH [AI083139-02, GM62437, GM82901, U01HL098179]; Intramural
   Research Program of the NIH, National Institute of Environmental Health
   Sciences [Z01 ES101987]; Deutsche Forschungsgemeinschaft [GE 976/5];
   Boehringer Ingelheim Fonds; Human Frontiers Science Program; E.G.G.
   fellowship; PhRMA Foundation
FX We thank Jeffrey Corden and Andrew Rice for sharing reagents; Alexander
   Williams, Kirsten Eilertson, Brian Egan, Pao-Chen Li, and Ginger Muse
   for advice and assistance with experiments; and Gary Howard and Anna
   Lisa Lucido for editorial assistance. We gratefully acknowledge funds
   from Gladstone, the NIH (AI083139-02 [M.O.], GM62437 [P.A.C.], GM82901
   [K.S.P. and J.A.C.], U01HL098179 [K.S.P. and B.G.B.]), the Intramural
   Research Program of the NIH, National Institute of Environmental Health
   Sciences (K.A., Z01 ES101987), the Deutsche Forschungsgemeinschaft
   (M.G., GE 976/5), the Boehringer Ingelheim Fonds (S.S.), the Human
   Frontiers Science Program and an E.G.G. fellowship (E.H.), and the PhRMA
   Foundation (J.A.C.).
NR 50
TC 33
Z9 35
U1 6
U2 24
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
J9 MOL CELL
JI Mol. Cell
PD NOV 7
PY 2013
VL 52
IS 3
BP 314
EP 324
DI 10.1016/j.molcel.2013.10.009
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 250KU
UT WOS:000326852500005
PM 24207025
ER

PT J
AU Huang, J
   Liu, S
   Bellani, MA
   Thazhathveetil, AK
   Ling, C
   de Winter, JP
   Wang, YS
   Wang, WD
   Seidman, MM
AF Huang, Jing
   Liu, Shuo
   Bellani, Marina A.
   Thazhathveetil, Arun Kalliat
   Ling, Chen
   de Winter, Johan P.
   Wang, Yinsheng
   Wang, Weidong
   Seidman, Michael M.
TI The DNA Translocase FANCM/MHF Promotes Replication Traverse of DNA
   Interstrand Crosslinks
SO MOLECULAR CELL
LA English
DT Article
ID FANCONI-ANEMIA PATHWAY; MAINTAIN GENOME STABILITY; COMPLEMENTATION
   GROUP-M; HUMAN-CELLS; ESCHERICHIA-COLI; MAMMALIAN-CELLS; UVA
   IRRADIATION; CORE COMPLEX; REPAIR; HELICASE
AB The replicative machinery encounters many impediments, some of which can be overcome by lesion bypass or replication restart pathways, leaving repair for a later time. However, interstrand crosslinks (ICLs), which preclude DNA unwinding, are considered absolute blocks to replication. Current models suggest that fork collisions, either from one or both sides of an ICL, initiate repair processes required for resumption of replication. To test these proposals, we developed a single-molecule technique for visualizing encounters of replication forks with ICLs as they occur in living cells. Surprisingly, the most frequent patterns were consistent with replication traverse of an ICL, without lesion repair. The traverse frequency was strongly reduced by inactivation of the translocase and DNA binding activities of the FANCM/MHF complex. The results indicate that translocase-based mechanisms enable DNA synthesis to continue past ICLs and that these lesions are not always absolute blocks to replication.
C1 [Huang, Jing; Bellani, Marina A.; Seidman, Michael M.] NIA, NIH, Lab Mol Gerontol, Baltimore, MD 21224 USA.
   [Liu, Shuo; Wang, Yinsheng] Univ Calif Riverside, Dept Chem, Riverside, CA 92521 USA.
   [Thazhathveetil, Arun Kalliat] Northwestern Univ, Dept Chem, Evanston, IL 60208 USA.
   [Ling, Chen; Wang, Weidong] NIA, NIH, Genet Lab, Baltimore, MD 21224 USA.
   [de Winter, Johan P.] Vrije Univ Amsterdam Med Ctr, Dept Clin Genet, NL-1081 BT Amsterdam, Netherlands.
RP Seidman, MM (reprint author), NIA, NIH, Lab Mol Gerontol, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM seidmanm@grc.nia.nih.gov
FU Intramural Research Program of the NIH, National Institute on Aging
   [AG000738-10, AG000688-07]
FX This research was supported in part by the Intramural Research Program
   of the NIH, National Institute on Aging (AG000738-10 and AG000688-07).
   We thank Dr. Kurt Andresen, Dr. John Wilson, Dr. Michael Leffak, and Dr.
   Ranjan Sen for helpful discussions and Dr. K.J. Patel, Dr. Wojciech
   Niedzwiedz, Dr. Minoru Takata, and Dr. Steve West for the generous gift
   of cell lines. This paper is dedicated to the memory of Johan de Winter,
   our friend and colleague.
NR 59
TC 35
Z9 35
U1 1
U2 9
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
J9 MOL CELL
JI Mol. Cell
PD NOV 7
PY 2013
VL 52
IS 3
BP 434
EP 446
DI 10.1016/j.molcel.2013.09.021
PG 13
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 250KU
UT WOS:000326852500014
PM 24207054
ER

PT J
AU Persaud, D
   Gay, H
   Ziemniak, C
   Chen, YH
   Piatak, M
   Chun, TW
   Strain, M
   Richman, D
   Luzuriaga, K
AF Persaud, Deborah
   Gay, Hannah
   Ziemniak, Carrie
   Chen, Ya Hui
   Piatak, Michael, Jr.
   Chun, Tae-Wook
   Strain, Matthew
   Richman, Douglas
   Luzuriaga, Katherine
TI Absence of Detectable HIV-1 Viremia after Treatment Cessation in an
   Infant
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; EFFECTIVE ANTIRETROVIRAL THERAPY;
   INFECTED INFANTS; DYNAMICS; CHILDREN; TRANSMISSION; REPLICATION;
   CLEARANCE; TIME; RESERVOIRS
AB An infant born to a woman with human immunodeficiency virus type 1 (HIV-1) infection began receiving antiretroviral therapy (ART) 30 hours after birth owing to high-risk exposure. ART was continued when detection of HIV-1 DNA and RNA on repeat testing met the standard diagnostic criteria for infection. After therapy was discontinued (when the child was 18 months of age), levels of plasma HIV-1 RNA, proviral DNA in peripheral-blood mononuclear cells, and HIV-1 antibodies, as assessed by means of clinical assays, remained undetectable in the child through 30 months of age. This case suggests that very early ART in infants may alter the establishment and long-term persistence of HIV-1 infection.
C1 [Persaud, Deborah; Ziemniak, Carrie; Chen, Ya Hui] Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21287 USA.
   [Piatak, Michael, Jr.] Leidos Biomed Res, Frederick Natl Lab Canc Res, Frederick, MD USA.
   [Chun, Tae-Wook] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
   [Gay, Hannah] Univ Mississippi, Dept Pediat, Med Ctr, Jackson, MS USA.
   [Strain, Matthew; Richman, Douglas] Univ Calif San Diego, La Jolla, CA 92093 USA.
   [Strain, Matthew; Richman, Douglas] Vet Affairs San Diego Healthcare Syst, San Diego, CA USA.
   [Luzuriaga, Katherine] Univ Massachusetts, Sch Med, Dept Pediat, Program Mol Med, Worcester, MA USA.
   [Luzuriaga, Katherine] Univ Massachusetts, Sch Med, Ctr Clin & Translat Sci, Worcester, MA USA.
RP Persaud, D (reprint author), Johns Hopkins Univ, Sch Med, 720 Rutland Ave,Ross Bldg,Rm 1170, Baltimore, MD 21287 USA.
EM dpers@jhmi.edu
FU NIH [AI93701, HD0577849]; American Foundation for AIDS Research;
   International Maternal Pediatric Adolescent AIDS Clinical Trials Network
   [U01-AI-068632, UM1-AI-068632]; University of Massachusetts Center for
   Clinical and Translational Science [UL1TR000161]; Collaboratory of AIDS
   Researchers for Eradication [AI080193, AI69432, AI047745, AI74621,
   AI306214, AI096113]; Department of Veterans Affairs; Johns Hopkins
   University Center for AIDS Research (CFAR) [P30-AI094189]; University of
   Massachusetts Medical School CFAR [P30-AI042845]; NIAID; National Cancer
   Institute [HHSN261200800001E]
FX Supported by grants from the NIH (AI93701 and HD0577849, to Dr.
   Persaud), by funding from the American Foundation for AIDS Research (to
   Drs. Persaud and Luzuriaga); by grants from the International Maternal
   Pediatric Adolescent AIDS Clinical Trials Network (U01-AI-068632 and
   UM1-AI-068632, to Drs. Persaud and Luzuriaga), the University of
   Massachusetts Center for Clinical and Translational Science
   (UL1TR000161, to Dr. Luzuriaga), and the Collaboratory of AIDS
   Researchers for Eradication (AI080193, AI69432, AI047745, AI74621,
   AI306214, and AI096113); and by funding from the Department of Veterans
   Affairs (to Drs. Strain and Richman). The research was also supported in
   part by grants from the Johns Hopkins University Center for AIDS
   Research (CFAR) (P30-AI094189) and the University of Massachusetts
   Medical School CFAR (P30-AI042845) and by the NIAID Intramural Research
   Program. Specific specialty viral-load testing was funded by a contract
   from the National Cancer Institute (HHSN261200800001E).
NR 32
TC 201
Z9 207
U1 2
U2 24
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 7
PY 2013
VL 369
IS 19
BP 1828
EP 1835
DI 10.1056/NEJMoa1302976
PG 8
WC Medicine, General & Internal
SC General & Internal Medicine
GA 247HF
UT WOS:000326607800011
PM 24152233
ER

PT J
AU Doroshow, JH
AF Doroshow, James H.
TI Overcoming Resistance to Targeted Anticancer Drugs
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
ID KINASE INHIBITORS; CHEMOTHERAPY
AB More than a decade ago, imatinib, an agent that has a specific inhibitory interaction with the BCR-ABL fusion protein, was introduced for the treatment of chronic myeloid leukemia (CML). The introduction of this agent dramatically changed researchers' understanding not only of the role of tyrosine kinases as targets for oncology drugs (despite the conserved status of protein kinase domains in nature), but also their ability to conceptualize and test novel molecular mechanisms of action and drug resistance in solid tumors such as adenocarcinoma of the lung as well as in hematopoietic cancers.(1),(2) The underlying genetic instability of most cancers ...
C1 NCI, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
RP Doroshow, JH (reprint author), NCI, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
NR 10
TC 6
Z9 7
U1 0
U2 11
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 7
PY 2013
VL 369
IS 19
BP 1852
EP 1853
DI 10.1056/NEJMe1311325
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 247HF
UT WOS:000326607800015
PM 24180495
ER

PT J
AU Antipov, AE
   Barzykin, AV
   Berezhkovskii, AM
   Makhnovskii, YA
   Zitserman, VY
   Aldoshin, SM
AF Antipov, Anatoly E.
   Barzykin, Alexander V.
   Berezhkovskii, Alexander M.
   Makhnovskii, Yurii A.
   Zitserman, Vladimir Yu
   Aldoshin, Sergei M.
TI Effective diffusion coefficient of a Brownian particle in a periodically
   expanded conical tube
SO PHYSICAL REVIEW E
LA English
DT Article
ID HOMOGENIZATION; SURFACES
AB Diffusion in a tube of periodically varying diameter occurs slower than that in a cylindrical tube because diffusing particles get trapped in wells of the periodic entropy potential which is due to variation of the tube cross-section area. To quantify the slowdown one has to establish a relation between the effective diffusion coefficient of the particle and the tube geometry, which is a very complicated problem. Here we show how to overcome the difficulties in the case of a periodically expanded conical tube, where we find an approximate solution for the effective diffusion coefficient as a function of the parameters determining the tube geometry.
C1 [Antipov, Anatoly E.] Moscow MV Lomonosov State Univ, Fac Fundamental Phys & Chem Engn, Moscow 119991, Russia.
   [Barzykin, Alexander V.] Royal Bank Scotland, London EC2M 4AA, England.
   [Berezhkovskii, Alexander M.] NIH, Math & Stat Comp Lab, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
   [Makhnovskii, Yurii A.] Russian Acad Sci, Topchiev Inst Petrochem Synth, Moscow 19991, Russia.
   [Zitserman, Vladimir Yu] Russian Acad Sci, Joint Inst High Temp, Moscow 125412, Russia.
   [Aldoshin, Sergei M.] Russian Acad Sci, Inst Problems Chem Phys, Chernogolovka 142432, Russia.
RP Makhnovskii, YA (reprint author), Russian Acad Sci, Topchiev Inst Petrochem Synth, Leninsky Prospect 29, Moscow 19991, Russia.
EM yuam@ips.ac.ru
RI Makhnovskii, Yurii/B-1223-2014; Aldoshin, Sergey/H-1647-2011
OI Makhnovskii, Yurii/0000-0002-1517-536X; 
FU Russian Ministry of Science and Education [G34.31.0055]; National
   Institutes of Health (NIH), the Center for Information Technology
FX A.E.A., Yu.A.M., and S.M.A. thank the Russian Ministry of Science and
   Education for support (project for financial support of leading
   scientists No. G34.31.0055). A.M.B. was supported by the Intramural
   Research Program of the National Institutes of Health (NIH), the Center
   for Information Technology.
NR 23
TC 7
Z9 7
U1 1
U2 15
PU AMER PHYSICAL SOC
PI COLLEGE PK
PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA
SN 1539-3755
EI 1550-2376
J9 PHYS REV E
JI Phys. Rev. E
PD NOV 7
PY 2013
VL 88
IS 5
AR 054101
DI 10.1103/PhysRevE.88.054101
PG 4
WC Physics, Fluids & Plasmas; Physics, Mathematical
SC Physics
GA 250VA
UT WOS:000326883000013
PM 24329385
ER

PT J
AU Rozhnova, G
   Metcalf, CJE
   Grenfell, BT
AF Rozhnova, Ganna
   Metcalf, C. Jessica E.
   Grenfell, Bryan T.
TI Characterizing the dynamics of rubella relative to measles: the role of
   stochasticity
SO JOURNAL OF THE ROYAL SOCIETY INTERFACE
LA English
DT Article
DE rubella and measles; stochasticity; recurrent epidemics; childhood
   diseases; spectral analysis
ID CONGENITAL-RUBELLA; METAPOPULATION DYNAMICS; RECURRENT OUTBREAKS;
   EPIDEMIC MODELS; VACCINATION; TIME; TRANSMISSION; SEASONALITY;
   EXTINCTION; PREDICTABILITY
AB Rubella is a completely immunizing and mild infection in children. Understanding its behaviour is of considerable public health importance because of congenital rubella syndrome, which results from infection with rubella during early pregnancy and may entail a variety of birth defects. The recurrent dynamics of rubella are relatively poorly resolved, and appear to show considerable diversity globally. Here, we investigate the behaviour of a stochastic seasonally forced susceptible-infected-recovered model to characterize the determinants of these dynamics and illustrate patterns by comparison with measles. We perform a systematic analysis of spectra of stochastic fluctuations around stable attractors of the corresponding deterministic model and compare them with spectra from full stochastic simulations in large populations. This approach allows us to quantify the effects of demographic stochasticity and to give a coherent picture of measles and rubella dynamics, explaining essential differences in the recurrent patterns exhibited by these diseases. We discuss the implications of our findings in the context of vaccination and changing birth rates as well as the persistence of these two childhood infections.
C1 [Rozhnova, Ganna] Univ Manchester, Sch Phys & Astron, Theoret Phys Div, Manchester M13 9PL, Lancs, England.
   [Rozhnova, Ganna] Univ Lisbon, Fac Ciencias, Ctr Fis Mat Condensada, P-1649003 Lisbon, Portugal.
   [Rozhnova, Ganna] Univ Lisbon, Fac Ciencias, Dept Fis, P-1649003 Lisbon, Portugal.
   [Metcalf, C. Jessica E.] Univ Oxford, Dept Zool, Oxford OX1 3PS, England.
   [Grenfell, Bryan T.] Princeton Univ, Dept Ecol & Evolutionary Biol, Princeton, NJ 08544 USA.
   [Grenfell, Bryan T.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Rozhnova, G (reprint author), Univ Manchester, Sch Phys & Astron, Theoret Phys Div, Manchester M13 9PL, Lancs, England.
EM ganna.rozhnova@manchester.ac.uk
FU Portuguese Foundation for Science and Technology [SFRH/BPD/69137/2010];
   RAPIDD programme of the Science and Technology Directorate, Department
   of Homeland Security; Fogarty International Center, National Institutes
   of Health; Bill and Melinda Gates Foundation
FX G.R. gratefully acknowledges the financial support from the Portuguese
   Foundation for Science and Technology under contract no.
   SFRH/BPD/69137/2010. B. T. G. was supported by the RAPIDD programme of
   the Science and Technology Directorate, Department of Homeland Security
   and the Fogarty International Center, National Institutes of Health.
   J.E.M. and B. T. G. were supported by the Bill and Melinda Gates
   Foundation.
NR 62
TC 4
Z9 4
U1 1
U2 11
PU ROYAL SOC
PI LONDON
PA 6-9 CARLTON HOUSE TERRACE, LONDON SW1Y 5AG, ENGLAND
SN 1742-5689
EI 1742-5662
J9 J R SOC INTERFACE
JI J. R. Soc. Interface
PD NOV 6
PY 2013
VL 10
IS 88
AR UNSP 20130643
DI 10.1098/rsif.2013.0643
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 298CK
UT WOS:000330301300020
PM 24026472
ER

PT J
AU Nansel, TR
   Haynie, DL
   Lipsky, LM
   Wang, J
   Mehta, SN
   Laffel, LMB
AF Nansel, Tonja R.
   Haynie, Denise L.
   Lipsky, Leah M.
   Wang, Jing
   Mehta, Sanjeev N.
   Laffel, Lori M. B.
TI Relationships among parent and youth healthful eating attitudes and
   youth dietary intake in a cross-sectional study of youth with type 1
   diabetes
SO INTERNATIONAL JOURNAL OF BEHAVIORAL NUTRITION AND PHYSICAL ACTIVITY
LA English
DT Article
DE Dietary intake; Social cognitive theory; Type 1 diabetes; Children;
   Adolescents
ID SOCIAL COGNITIVE THEORY; CARDIOVASCULAR RISK-FACTORS; VEGETABLE
   CONSUMPTION; SELF-EFFICACY; ENVIRONMENTAL-INFLUENCES; PHYSICAL-ACTIVITY;
   GLYCEMIC CONTROL; CHILDREN; FRUIT; ADOLESCENTS
AB Background: Constructs based on Social Cognitive Theory have shown utility in understanding dietary behavior; however, little research has examined these relations in youth and parents concurrently. Unique demands of dietary management among families of youth with type 1 diabetes (T1D) suggest the importance of investigation in this population. The purpose of this study was to develop and evaluate youth and parent measures of self-efficacy, outcome expectations, and barriers for healthful eating, and parent modeling of healthful eating, in a sample of youth with type 1 diabetes and their parents.
   Methods: Youth (n= 252) ages 8-18 years with diabetes duration = 1 year and parents completed self-report measures of healthful eating attitudes including self-efficacy, perceived barriers, positive and negative outcome expectations; youth reported parent modeling of healthful eating. Youth dietary intake from 3-day diet records was used to calculate the Healthy Eating Index 2005 and the Nutrient Rich Foods 9.3 index, measures of overall diet quality. The relations among parent and youth healthful eating attitudes, parent modeling, and youth diet quality were examined using structural equation modeling.
   Results: Internal consistency and test-retest reliability of the measures were acceptable. The structural equation model demonstrated acceptable fit (CFI/TLI= 0.94/0.94; RMSEA= 0.03), and items loaded the hypothesized factors. Parent modeling (beta) over cap = : 27; p = 02) and attitudes toward healthful eating (latent variable comprised of self-efficacy, barriers, outcome expectations) ((beta) over cap = : 16; p = 04) had direct effects on youth diet quality. Parent modeling had a direct effect on youth attitudes ((beta) over cap = : 49; p < : 001) ; parent attitudes had an indirect effect on youth attitudes through parent modeling (<(beta)over cap> =: 12; p;< : 001). Youth attitudes were not associated with youth diet quality. Overall, the model accounted for 20% of the variance in child diet quality.
   Conclusions: Parent diet-related behaviors demonstrated an impact on youth attitudes and diet quality, suggesting the importance of family-based clinical and public health efforts to improve diet.
C1 [Nansel, Tonja R.; Haynie, Denise L.; Lipsky, Leah M.; Wang, Jing] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Hlth Behav Branch, Div Intramural Populat Hlth Res, NIH,DHHS, Bethesda, MD 20892 USA.
   [Mehta, Sanjeev N.; Laffel, Lori M. B.] Joslin Diabet Ctr, Pediat Adolescent & Young Adult Sect, Genet & Epidemiol Sect, Boston, MA 02215 USA.
RP Nansel, TR (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Hlth Behav Branch, Div Intramural Populat Hlth Res, NIH,DHHS, 6100 Execut Blvd,Rm 7B13,MSC 7510, Bethesda, MD 20892 USA.
EM nanselt@mail.nih.gov
OI Nansel, Tonja/0000-0002-8298-7595; Haynie, Denise/0000-0002-8270-6079;
   Lipsky, Leah/0000-0003-2645-4388
FU intramural research program of the National Institutes of Health, Eunice
   Kennedy Shriver National Institute of Child Health and Human Development
   [HHSN267200703434C]
FX This research was supported by the intramural research program of the
   National Institutes of Health, Eunice Kennedy Shriver National Institute
   of Child Health and Human Development, contract number
   HHSN267200703434C.
NR 66
TC 4
Z9 4
U1 3
U2 9
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1479-5868
J9 INT J BEHAV NUTR PHY
JI Int. J. Behav. Nutr. Phys. Act.
PD NOV 6
PY 2013
VL 10
AR 125
DI 10.1186/1479-5868-10-125
PG 10
WC Nutrition & Dietetics; Physiology
SC Nutrition & Dietetics; Physiology
GA 290VX
UT WOS:000329787700001
PM 24195642
ER

PT J
AU Taha, AY
   Zahid, T
   Epps, T
   Trepanier, MO
   Burnham, WM
   Bazinet, RP
   Zhang, L
AF Taha, Ameer Y.
   Zahid, Tariq
   Epps, Tina
   Trepanier, Marc-Olivier
   Burnham, W. M.
   Bazinet, Richard P.
   Zhang, Liang
TI Selective reduction of excitatory hippocampal sharp waves by
   docosahexaenoic acid and its methyl ester analog ex-vivo
SO BRAIN RESEARCH
LA English
DT Article
DE Docosahexaenoic acid (DHA); Excitatory hippocampal sharp waves; Omega-3
   (n-3) polyunsaturated fatty acids (PUFAs); Seizures; Epilepsy;
   Docosahexaenoic acid methyl ester; GARA receptors
ID POLYUNSATURATED FATTY-ACIDS; TEMPORAL-LOBE EPILEPSY; VOLTAGE-GATED K+;
   BRAIN PHOSPHOLIPIDS; IN-VITRO; RAT; RECEPTOR; CELLS; MODULATION;
   CHANNELS
AB Excitatory sharp waves (SPWs) originating from the hippocampus are considered to model the interictal "spikes" that occur in people with temporal lobe epilepsy. Docosahexaenoic acid (DHA) is an omega-3 polyunsaturated fatty acid that has been reported to reduce neuronal excitability in vitro. The effect of DHA on hippocampal SPWs, however, is not known. Our goal was to determine whether DHA suppresses SPWs in thick mouse hippocampal slices, and to compare its effects with those of oleic acid (OA, control) and the standard anticonvulsant carbamazepine (CBZ). Also tested, were DHA's structural PUPA analogs n-3 docosapentaenoic acid (n-3 DPA), n-6 docosapentaenoic acid (n-6 DPA) and DHA-methyl ester (DHA-Me). The possible involvement of GABAergic activity was also examined using GABA receptor blockers. Extracellular recordings from CA1 and CA3 regions in hippocampal slices revealed that DHA reduced the incidence of SPWs. CBZ also reduced the incidence of SPWs and was 5 time more potent than DHA. DHA's effects on SPWs was abolished in the presence of GABA-receptor blockers, suggesting involvement of the GABA system in reducing excitatory SPWs. C-14 DHA application to the slices confirmed the incorporation of DHA into membrane phospholipids. N-3 DPA and n-6 DPA, however, which also incorporate into phospholipids, had no effect on SPWs, while DHA-Me, a DHA analog that does not incorporate into membrane phospholipids, was effective at reducing them. We conclude that DHA, but not its n-3 and n-6 analogs, reduces network excitability of the recurrent CA3 circuitry in the mouse hippocampus. This reduction may be mediated by DHA in its unesterified form, and is likely related to a modulatory effect of DHA on GABAergic activity. Crown Copyright (C) 2013 Published by Elsevier B.V. All rights reserved.
C1 [Taha, Ameer Y.; Zahid, Tariq; Epps, Tina; Zhang, Liang] Univ Hlth Network, Toronto Western Res Inst, Div Fundamental Neurobiol, Toronto, ON M5T 2S8, Canada.
   [Taha, Ameer Y.; Epps, Tina; Burnham, W. M.] Univ Toronto, Fac Med, Dept Pharmacol & Toxicol, Toronto, ON M5S 1A8, Canada.
   [Zahid, Tariq; Zhang, Liang] Univ Toronto, Fac Med, Dept Med, Toronto, ON M5S 3E2, Canada.
   [Trepanier, Marc-Olivier; Bazinet, Richard P.] Univ Toronto, Fac Med, Dept Nutr Sci, Toronto, ON M5S 3E2, Canada.
   [Taha, Ameer Y.; Epps, Tina; Trepanier, Marc-Olivier; Burnham, W. M.; Bazinet, Richard P.; Zhang, Liang] Univ Toronto, Fac Med, Epilepsy Res Program, Toronto, ON M5S 1A8, Canada.
RP Taha, AY (reprint author), NIA, Brain Physiol & Metab Sect, NIH, 9000 Rockville Pike,Room 1S-107, Bethesda, MD 20892 USA.
EM a.taha@utoronto.ca
FU Canadian Institutes of Health Research (CIHR); Natural Science and
   Engineering Research Council of Canada; CIHR
FX This study was funded by the Canadian Institutes of Health Research
   (CIHR) and Natural Science and Engineering Research Council of Canada to
   Drs. W.M.B., R.P.B. and L.Z. Dr. A.Y.T. was a recipient of a Canada
   Graduate Scholarships CIHR Doctoral Research Award. The authors thank
   Nisarg Patel for his technical assistance with some of the
   electrophysiology experiments.
NR 50
TC 6
Z9 7
U1 1
U2 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
EI 1872-6240
J9 BRAIN RES
JI Brain Res.
PD NOV 6
PY 2013
VL 1537
BP 9
EP 17
DI 10.1016/j.brainres.2013.09.004
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 264XV
UT WOS:000327915200002
PM 24036166
ER

PT J
AU Nadel, J
   Huang, TJ
   Xia, ZY
   Burlin, T
   Zametkin, A
   Smith, CB
AF Nadel, Jeffrey
   Huang, Tianjian
   Xia, Zengyan
   Burlin, Thomas
   Zametkin, Alan
   Smith, Carolyn Beebe
TI Voluntary exercise regionally augments rates of cerebral protein
   synthesis
SO BRAIN RESEARCH
LA English
DT Article
DE Protein synthesis; Exercise; Synaptic plasticity; Hippocampus;
   Paraventricular nucleus; Frontal cortex
ID CORTICOTROPIN-RELEASING HORMONE; LONG-TERM POTENTIATION; TISSUE
   AMINO-ACIDS; SYNAPTIC PLASTICITY; NEUROTROPHIC FACTOR;
   PHYSICAL-ACTIVITY; IMPROVES MEMORY; MESSENGER-RNA; GROWTH-FACTOR; BRAIN
   HEALTH
AB Exercise is a natural form of neurophysiologic stimulation that has known benefits for mental health, maintenance of cerebral function, and stress reduction. Exercise is known to induce an upregulation of brain-derived neurotrophic factor and this is thought to be involved in associated increases in neural plasticity. Protein synthesis is also an essential component of adaptive plasticity. We hypothesized that exercise may stimulate changes in brain protein synthesis as part of its effects on plasticity. Here, we applied the quantitative autoradiographic L-[1-C-14]leucine method to the in vivo determination of regional rates of cerebral protein synthesis (rCPS) in adult rats following a seven day period of voluntary wheel-running and their sedentary counterparts. In four of 21 brain regions examined, the mean values of rCPS in the exercised rats were statistically significantly higher than in sedentary controls; regions affected were paraventricular hypothalamic nucleus, ventral hippocampus as a whole, CA1 pyramidal cell layer in ventral hippocampus, and frontal cortex. Increases in rCPS approached statistical significance in dentate gyrus of the ventral hippocampus. Our results affirm the value of exercise in encouraging hippocampal and possibly cortical neuroplasticity, and also suggest that exercise may modulate stimulation of stress-response pathways. Ultimately, our study indicates that measurement of rCPS with PET might be used as a marker of brain response to exercise in human subjects. Published by Elsevier B.V.
C1 [Nadel, Jeffrey; Huang, Tianjian; Xia, Zengyan; Burlin, Thomas; Zametkin, Alan; Smith, Carolyn Beebe] NIMH, US Publ Hlth Serv, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Smith, CB (reprint author), NIMH, US Publ Hlth Serv, Dept Hlth & Human Serv, 10 Ctr Dr,MSC 1298, Bethesda, MD 20892 USA.
EM beebe@mail.nih.gov
FU Intramural Research Program, National Institute of Mental Health
FX We thank Dr. Michelle Reith, Mrs. Kathleen Schmidt, and Ms. Kate
   Turetsky of the Section on Neuroadaptation and Protein Metabolism,
   National Institute of Mental Health, for their helpful manuscript
   suggestions. This research was supported by the Intramural Research
   Program, National Institute of Mental Health.
NR 36
TC 4
Z9 4
U1 1
U2 9
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
EI 1872-6240
J9 BRAIN RES
JI Brain Res.
PD NOV 6
PY 2013
VL 1537
BP 125
EP 131
DI 10.1016/j.brainres.2013.09.001
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 264XV
UT WOS:000327915200014
PM 24016692
ER

PT J
AU Frank, CA
   Wang, XN
   Collins, CA
   Rodal, AA
   Yuan, Q
   Verstreken, P
   Dickman, DK
AF Frank, C. Andrew
   Wang, Xinnan
   Collins, Catherine A.
   Rodal, Avital A.
   Yuan, Quan
   Verstreken, Patrik
   Dickman, Dion K.
TI New Approaches for Studying Synaptic Development, Function, and
   Plasticity Using Drosophila as a Model System
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID PRESYNAPTIC TRANSMITTER RELEASE; SITE-SPECIFIC RECOMBINATION; MEDIATED
   ENHANCER DETECTION; NEUROTRANSMITTER RELEASE; NEUROMUSCULAR-JUNCTION;
   AXONAL-TRANSPORT; RETROGRADE SIGNAL; NERVOUS WRECK; ACTIVE ZONE;
   MITOCHONDRIAL PATHOLOGY
AB The fruit fly Drosophila melanogaster has been established as a premier experimental model system for neuroscience research. These organisms are genetically tractable, yet their nervous systems are sufficiently complex to study diverse processes that are conserved across metazoans, including neural cell fate determination and migration, axon guidance, synaptogenesis and function, behavioral neurogenetics, and responses to neuronal injury. For several decades, Drosophila neuroscientists have taken advantage of a vast toolkit of genetic and molecular techniques to reveal fundamental principles of neuroscience illuminating to all systems, including the first behavioral mutants from Seymour Benzer's pioneering work in the 1960s and 1970s, the cloning of the first potassium channel in the 1980s, and the identification of the core genes that orchestrate axon guidance and circadian rhythms in the 1990s. Over the past decade, new tools and innovations in genetic, imaging, and electrophysiological technologies have enabled the visualization, in vivo, of dynamic processes in synapses with unprecedented resolution. We will review some of the fresh insights into synaptic development, function, and plasticity that have recently emerged in Drosophila with an emphasis on the unique advantages of this model system.
C1 [Frank, C. Andrew] Univ Iowa, Carver Coll Med, Dept Anat & Cell Biol, Iowa City, IA 52242 USA.
   [Wang, Xinnan] Stanford Univ, Sch Med, Stanford Inst Neuroinnovat & Translat Neurosci, Palo Alto, CA 94305 USA.
   [Wang, Xinnan] Stanford Univ, Sch Med, Dept Neurosurg, Palo Alto, CA 94305 USA.
   [Collins, Catherine A.] Univ Michigan, Dept Mol Cellular & Dev Biol, Ann Arbor, MI 48109 USA.
   [Rodal, Avital A.] Brandeis Univ, Dept Biol, Waltham, MA 02453 USA.
   [Yuan, Quan] NINDS, NIH, Bethesda, MD 20892 USA.
   [Verstreken, Patrik] VIB, Ctr Biol Dis, B-3000 Louvain, Belgium.
   [Verstreken, Patrik] Katholieke Univ Leuven, Dept Human Genet, B-3000 Louvain, Belgium.
   [Dickman, Dion K.] Univ So Calif, Dept Biol, Los Angeles, CA 90089 USA.
RP Dickman, DK (reprint author), Univ So Calif, Dept Biol, HNB 309,3641 Watt Way, Los Angeles, CA 90089 USA.
EM dickman@usc.edu
OI Verstreken, Patrik/0000-0002-5073-5393; Collins,
   Catherine/0000-0002-1608-6692
FU National Institutes of Health [MH092351, NS062738, NS60947, NS082127,
   NS067066, NS069844]; New Scholar Award from the Ellison Medical
   Foundation; University of Iowa Carver Trust; Basil O'Connor Scholar
   award from the March of Dimes; European Research Counsel Starting Grant;
   Fonds voor Wetenschappelijk Onderzoek Vlaanderen; BELSPO
   interuniversitaire attractive pool; research fund KU Leuven; Instituut
   voor Wetenschap en Technologie Vlaanderen; Fundacao para a Ciencia e a
   Tecnologia; VIB; Bumpus Foundation; Sloan Foundation; Klingenstein
   Foundation; Michael J. Fox Foundation; National Science Foundation
   [IOS-0842701]; intramural research program of the National Institute of
   Neurological Disorders and Stroke
FX This work was supported by a National Institutes of Health Grant
   MH092351 and a New Scholar Award from the Ellison Medical Foundation to
   D.K.D.; National Institutes of Health Grant NS062738 and support from
   the University of Iowa Carver Trust to C.A.F.; National Institutes of
   Health Grants NS60947 and NS082127, and a Basil O'Connor Scholar award
   from the March of Dimes to A.A.R.; a European Research Counsel Starting
   Grant, the Fonds voor Wetenschappelijk Onderzoek Vlaanderen, BELSPO
   interuniversitaire attractive pool, the research fund KU Leuven, the
   Instituut voor Wetenschap en Technologie Vlaanderen, the Fundacao para a
   Ciencia e a Tecnologia, and VIB to P.V.; National Institutes of Health
   Grant NS067066 and fellowships from the Bumpus, Sloan, Klingenstein, and
   Michael J. Fox Foundations to X.W.; National Institutes of Health Grant
   NS069844 and National Science Foundation Grant IOS-0842701 to C.A.C.;
   and the intramural research program of the National Institute of
   Neurological Disorders and Stroke to Q.Y.
NR 154
TC 9
Z9 9
U1 2
U2 23
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 6
PY 2013
VL 33
IS 45
BP 17560
EP 17568
DI 10.1523/JNEUROSCI.3261-13.2013
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 252PI
UT WOS:000327019100003
PM 24198346
ER

PT J
AU Volman, SF
   Lammel, S
   Margolis, EB
   Kim, Y
   Richard, JM
   Roitman, MF
   Lobo, MK
AF Volman, Susan F.
   Lammel, Stephan
   Margolis, Elyssa B.
   Kim, Yunbok
   Richard, Jocelyn M.
   Roitman, Mitchell F.
   Lobo, Mary Kay
TI New Insights into the Specificity and Plasticity of Reward and Aversion
   Encoding in the Mesolimbic System
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID VENTRAL TEGMENTAL AREA; NUCLEUS-ACCUMBENS SHELL; SUBSECOND DOPAMINE
   RELEASE; MEDIUM SPINY NEURONS; CONDITIONED PLACE PREFERENCE; MEDIATING
   OPIATE REWARD; PREFRONTAL CORTEX; STRIATAL NEURONS; DISTINCT ROLES;
   BASAL GANGLIA
AB The mesocorticolimbic system, consisting, at its core, of the ventral tegmental area, the nucleus accumbens, and medial prefrontal cortex, has historically been investigated primarily for its role in positively motivated behaviors and reinforcement learning, and its dysfunction in addiction, schizophrenia, depression, and other mood disorders. Recently, researchers have undertaken a more comprehensive analysis of this system, including its role in not only reward but also punishment, as well as in both positive and negative reinforcement. This focus has been facilitated by new anatomical, physiological, and behavioral approaches to delineate functional circuits underlying behaviors and to determine how this system flexibly encodes and responds to positive and negative states and events, beyond simple associative learning. This review is a summary of topics covered in a mini-symposium at the 2013 Society for Neuroscience annual meeting.
C1 [Volman, Susan F.] NIDA, Div Basic Neurosci & Behav Res, Bethesda, MD 20892 USA.
   [Lammel, Stephan] Stanford Univ, Sch Med, Nancy Pritzker Lab, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA.
   [Margolis, Elyssa B.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA.
   [Kim, Yunbok] Univ Pittsburgh, Dept Neurosci, Pittsburgh, PA 15260 USA.
   [Richard, Jocelyn M.] Univ Michigan, Dept Psychol, Ann Arbor, MI 48109 USA.
   [Roitman, Mitchell F.] Univ Illinois, Dept Psychol, Chicago, IL 60607 USA.
   [Lobo, Mary Kay] Univ Maryland, Sch Med, Dept Anat & Neurobiol, Baltimore, MD 21230 USA.
RP Volman, SF (reprint author), NIDA, Div Basic Neurosci & Behav Res, 6001 Execut Blvd,Room 4282,MSC 9555, Bethesda, MD 20892 USA.
EM svolman@nida.nih.gov
RI Lobo, Mary Kay/K-7734-2015; 
OI Lobo, Mary Kay/0000-0002-9419-2079; Richard,
   Jocelyn/0000-0001-5750-0418; Lammel, Stephan/0000-0002-3350-3208
FU National Institute on Drug Abuse [R01 DA030529, R01 DA025634]; National
   Institute of Mental Health [R37 MH048404, F31 MH090602]
FX This work was supported by National Institute on Drug Abuse Grant R01
   DA030529 to E.B.M. and Grant R01 DA025634 to M.F.R., National Institute
   of Mental Health Grant R37 MH048404 to B. Mohgaddam, and Fellowship F31
   MH090602 to J.M.R. The order of the authors reflects the order of their
   presentations in the SfN Minisymposium.
NR 129
TC 52
Z9 52
U1 1
U2 27
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 6
PY 2013
VL 33
IS 45
BP 17569
EP 17576
DI 10.1523/JNEUROSCI.3250-13.2013
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 252PI
UT WOS:000327019100004
PM 24198347
ER

PT J
AU Reilly, MT
   Faulkner, GJ
   Dubnau, J
   Ponomarev, I
   Gage, FH
AF Reilly, Matthew T.
   Faulkner, Geoffrey J.
   Dubnau, Joshua
   Ponomarev, Igor
   Gage, Fred H.
TI The Role of Transposable Elements in Health and Diseases of the Central
   Nervous System
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID POSTTRAUMATIC-STRESS-DISORDER; L1 RETROTRANSPOSITION; HUMAN BRAIN;
   DROSOPHILA-MELANOGASTER; GENE-EXPRESSION; HUMAN GENOME; LINE-1
   RETROTRANSPOSITION; ENDOGENOUS RETROVIRUSES; ALCOHOL DEPENDENCE; HYBRID
   DYSGENESIS
AB First discovered in maize by Barbara McClintock in the 1940s, transposable elements (TEs) are DNA sequences that in some cases have the ability to move along chromosomes or "transpose" in the genome. This revolutionary finding was initially met with resistance by the scientific community and viewed by some as heretical. A large body of knowledge has accumulated over the last 60 years on the biology of TEs. Indeed, it is now known that TEs can generate genomic instability and reconfigure gene expression networks both in the germline and somatic cells. This review highlights recent findings on the role of TEs in health and diseases of the CNS, which were presented at the 2013 Society for Neuroscience meeting. The work of the speakers in this symposium shows that TEs are expressed and active in the brain, challenging the dogma that neuronal genomes are static and revealing that they are susceptible to somatic genomic alterations. These new findings on TE expression and function in the CNS have major implications for understanding the neuroplasticity of the brain, which could hypothetically have a role in shaping individual behavior and contribute to vulnerability to disease.
C1 [Reilly, Matthew T.] NIAAA, Bethesda, MD 20892 USA.
   [Faulkner, Geoffrey J.] Mater Med Res Inst, South Brisbane, Qld, Australia.
   [Dubnau, Joshua] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA.
   [Ponomarev, Igor] Univ Texas Austin, Waggoner Ctr Alcohol & Addict Res, Austin, TX 78712 USA.
   [Ponomarev, Igor] Univ Texas Austin, Coll Pharm, Austin, TX 78712 USA.
   [Gage, Fred H.] Salk Inst Biol Studies, Genet Lab, La Jolla, CA 92037 USA.
RP Reilly, MT (reprint author), NIAAA, NIH, MSC 9304, Bethesda, MD 20892 USA.
EM reillymt@mail.nih.gov; gage@salk.edu
RI Faulkner, Geoffrey/M-3168-2014; 
OI Faulkner, Geoffrey/0000-0001-5769-4494; Dubnau, Josh/0000-0002-9285-7444
FU Australian National Health and Medical Research Council [GNT1042449,
   GNT1045991, GNT1045237]; National Institutes of Health [R01NS067690,
   AA013517, AA013476, AA017234, R01MH088485, R01 MH095741]; DART
   Neuroscience LLC.; DoD-TATRC Grant; G. Harold & Leila Y. Mathers
   Foundation
FX G.J.F. was supported by Australian National Health and Medical Research
   Council Project Grants GNT1042449 and GNT1045991 and Career Development
   Fellowship GNT1045237. J.D. was supported by National Institutes of
   Health Grant R01NS067690 and DART Neuroscience LLC. I.P. was supported
   by National Institutes of Health Grants AA013517, AA013476, and
   AA017234, and a DoD-TATRC Grant. F.H.G. was supported by National
   Institutes of Health Grants R01MH088485 and R01 MH095741 and the G.
   Harold & Leila Y. Mathers Foundation. We thank M.L. Gage for editorial
   comments on the manuscript.
NR 138
TC 35
Z9 35
U1 0
U2 25
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 6
PY 2013
VL 33
IS 45
BP 17577
EP 17586
DI 10.1523/JNEUROSCI.3369-13.2013
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 252PI
UT WOS:000327019100005
PM 24198348
ER

PT J
AU Clark, L
   Averbeck, B
   Payer, D
   Sescousse, G
   Winstanley, CA
   Xue, G
AF Clark, Luke
   Averbeck, Bruno
   Payer, Doris
   Sescousse, Guillaume
   Winstanley, Catharine A.
   Xue, Gui
TI Pathological Choice: The Neuroscience of Gambling and Gambling Addiction
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID POSITRON-EMISSION-TOMOGRAPHY; VENTROMEDIAL PREFRONTAL CORTEX;
   DECISION-MAKING; DOPAMINE RELEASE; COGNITIVE DISTORTIONS; RECEPTOR
   AVAILABILITY; ORBITOFRONTAL CORTEX; BASOLATERAL AMYGDALA; REWARD
   ANTICIPATION; NICOTINE DEPENDENCE
AB Gambling is pertinent to neuroscience research for at least two reasons. First, gambling is a naturalistic and pervasive example of risky decision making, and thus gambling games can provide a paradigm for the investigation of human choice behavior and "irrationality." Second, excessive gambling involvement (i.e., pathological gambling) is currently conceptualized as a behavioral addiction, and research on this condition may provide insights into addictive mechanisms in the absence of exogenous drug effects. This article is a summary of topics covered in a Society for Neuroscience minisymposium, focusing on recent advances in understanding the neural basis of gambling behavior, including translational findings in rodents and nonhuman primates, which have begun to delineate neural circuitry and neurochemistry involved.
C1 [Clark, Luke] Univ Cambridge, Dept Psychol, Cambridge CB2 3EB, England.
   [Averbeck, Bruno] NIMH, Neuropsychol Lab, Bethesda, MD 20892 USA.
   [Payer, Doris] Ctr Addict & Mental Hlth, Res Imaging Ctr, Toronto, ON M5T 1R8, Canada.
   [Sescousse, Guillaume] Radboud Univ Nijmegen, Donders Inst Brain Cognit & Behav, NL-6525 HP Nijmegen, Netherlands.
   [Winstanley, Catharine A.] Univ British Columbia, Dept Psychol, Vancouver, BC V6T 1Z4, Canada.
   [Xue, Gui] Beijing Normal Univ, State Key Lab Cognit Neurosci & Learning, Beijing 100875, Peoples R China.
   [Xue, Gui] Beijing Normal Univ, IDG McGovern Inst Brain Res, Beijing 100875, Peoples R China.
RP Clark, L (reprint author), Univ Cambridge, Dept Psychol, Downing St, Cambridge CB2 3EB, England.
EM lc260@cam.ac.uk
RI Sescousse, Guillaume/J-1721-2012; Winstanley, Catharine/K-5003-2015;
   Xue, Gui/A-1762-2009; 
OI Winstanley, Catharine/0000-0001-7032-4471; Xue, Gui/0000-0001-7891-8151;
   Payer, Doris/0000-0001-9313-2587
FU Medical Research Council [G1100554]; Intramural Research Program of the
   National Institute of Mental Health; Canadian Institutes of Health
   Research (CIHR); Canadian Natural Sciences and Engineering Research
   Council; Parkinson Society Canada; Canadian Foundation for Innovation;
   Michael Smith Foundation for Health Research; CIHR New Investigator
   Award program; Natural Science Foundation of China [31130025];
   Netherlands Organization for Scientific Research; Ontario Problem
   Gambling Research Centre [2642]; Canadian Institutes of Health Research
   [CIHR/IRSC 258458]
FX L.C. was supported by the Medical Research Council (G1100554). B.A. was
   supported by the Intramural Research Program of the National Institute
   of Mental Health. C.A.W. was supported by the Canadian Institutes of
   Health Research (CIHR), the Canadian Natural Sciences and Engineering
   Research Council, Parkinson Society Canada, and the Canadian Foundation
   for Innovation and receives salary support through the Michael Smith
   Foundation for Health Research and the CIHR New Investigator Award
   program. G.X. was supported by the Natural Science Foundation of China
   (31130025). G.S. was supported by The Netherlands Organization for
   Scientific Research. D.P. was supported by Ontario Problem Gambling
   Research Centre 2642 and Canadian Institutes of Health Research
   (CIHR/IRSC 258458). B.A., D.P., G.S., C.A.W., and G.X. are listed
   alphabetically.
NR 98
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PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 6
PY 2013
VL 33
IS 45
BP 17617
EP 17623
DI 10.1523/JNEUROSCI.3231-13.2013
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 252PI
UT WOS:000327019100010
PM 24198353
ER

PT J
AU Niu, JW
   Ding, L
   Li, JJ
   Kim, H
   Liu, JK
   Li, HP
   Moberly, A
   Badea, TC
   Duncan, ID
   Son, YJ
   Scherer, SS
   Luo, WQ
AF Niu, Jingwen
   Ding, Long
   Li, Jian J.
   Kim, Hyukmin
   Liu, Jiakun
   Li, Haipeng
   Moberly, Andrew
   Badea, Tudor C.
   Duncan, Ian D.
   Son, Young-Jin
   Scherer, Steven S.
   Luo, Wenqin
TI Modality-Based Organization of Ascending Somatosensory Axons in the
   Direct Dorsal Column Pathway
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID EXTERNAL CUNEATE NUCLEI; PRIMARY AFFERENT-FIBERS; SPINAL-CORD;
   SOMATOTOPIC ORGANIZATION; FASCICULUS-GRACILIS; CENTRAL PROJECTION;
   POSTERIOR COLUMNS; SQUIRREL MONKEYS; MUSCLE AFFERENTS; CEREBRAL-CORTEX
AB The long-standing doctrine regarding the functional organization of the direct dorsal column (DDC) pathway is the "somatotopic map" model, which suggests that somatosensory afferents are primarily organized by receptive field instead of modality. Using modality-specific genetic tracing, here we show that ascending mechanosensory and proprioceptive axons, two main types of the DDC afferents, are largely segregated into a medial-lateral pattern in the mouse dorsal column and medulla. In addition, we found that this modality-based organization is likely to be conserved in other mammalian species, including human. Furthermore, we identified key morphological differences between these two types of afferents, which explains how modality segregation is formed and why a rough "somatotopic map" was previously detected. Collectively, our results establish a new functional organization model for the mammalian direct dorsal column pathway and provide insight into how somatotopic and modality-based organization coexist in the central somatosensory pathway.
C1 [Niu, Jingwen; Ding, Long; Liu, Jiakun; Li, Haipeng; Moberly, Andrew; Luo, Wenqin] Univ Penn, Dept Neurosci, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Li, Jian J.; Scherer, Steven S.] Univ Penn, Dept Neurol, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Kim, Hyukmin; Son, Young-Jin] Temple Univ, Sch Med, Shriners Hosp Pediat Res Ctr, Philadelphia, PA 19140 USA.
   [Kim, Hyukmin; Son, Young-Jin] Temple Univ, Sch Med, Dept Anat & Cell Biol, Philadelphia, PA 19140 USA.
   [Li, Haipeng] First Peoples Hosp Chenzhou, Dept Neurol, Chenzhou, Hunan, Peoples R China.
   [Badea, Tudor C.] NEI, Retinal Circuit Dev & Genet Unit, Bethesda, MD 20892 USA.
   [Duncan, Ian D.] Univ Wisconsin, Sch Vet Med, Dept Med Sci, Madison, WI 53706 USA.
RP Luo, WQ (reprint author), Univ Penn, Dept Neurosci, Perelman Sch Med, 145 Johnson Pavil,3610 Hamilton Walk, Philadelphia, PA 19104 USA.
EM luow@mail.med.upenn.edu
FU National Institutes of Health [R00NS069799, 1R01NS083702]; Thomas B.
   McCabe and Jeanette E. Laws McCabe Pilot Award; Basil O'Connor Starter
   Scholar Research Award; University of Pennsylvania; National Institutes
   of Health; Shriners Hospitals for the Children
FX W.L. was supported by National Institutes of Health Grants R00NS069799
   and 1R01NS083702, Thomas B. McCabe and Jeanette E. Laws McCabe Pilot
   Award, Basil O'Connor Starter Scholar Research Award, and the University
   of Pennsylvania. Y.-J.S. was supported by the National Institutes of
   Health and Shriners Hospitals for the Children.
NR 49
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U1 0
U2 2
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 6
PY 2013
VL 33
IS 45
BP 17691
EP 17709
DI 10.1523/JNEUROSCI.3429-13.2013
PG 19
WC Neurosciences
SC Neurosciences & Neurology
GA 252PI
UT WOS:000327019100019
PM 24198362
ER

PT J
AU Keeley, PW
   Luna, G
   Fariss, RN
   Skyles, KA
   Madsen, NR
   Raven, MA
   Poche, RA
   Swindell, EC
   Jamrich, M
   Oh, EC
   Swaroop, A
   Fisher, SK
   Reese, BE
AF Keeley, Patrick W.
   Luna, Gabriel
   Fariss, Robert N.
   Skyles, Kimberly A.
   Madsen, Nils R.
   Raven, Mary A.
   Poche, Ross A.
   Swindell, Eric C.
   Jamrich, Milan
   Oh, Edwin C.
   Swaroop, Anand
   Fisher, Steven K.
   Reese, Benjamin E.
TI Development and Plasticity of Outer Retinal Circuitry Following Genetic
   Removal of Horizontal Cells
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID DEVELOPING MOUSE RETINA; ROD BIPOLAR CELLS; SYNAPSE FORMATION; HOMOTYPIC
   NEIGHBORS; DENDRITIC GROWTH; MORPHOLOGY; DEGENERATION; SPECIFICITY;
   LAMINATION; EXPRESSION
AB The present study examined the consequences of eliminating horizontal cells from the outer retina during embryogenesis upon the organization and assembly of the outer plexiform layer (OPL). Retinal horizontal cells exhibit a migration defect in Lim1-conditional knock-out (Lim1-CKO) mice and become mispositioned in the inner retina before birth, redirecting their dendrites into the inner plexiform layer. The resultant (mature) OPL, developing in the absence of horizontal cells, shows a retraction of rod spherules into the outer nuclear layer and a sprouting of rod bipolar cell dendrites to reach ectopic ribbon-protein puncta. Cone pedicles and the dendrites of type 7 cone bipolar cells retain their characteristic stratification and colocalization within the collapsed OPL, although both are atrophic and the spatial distribution of the pedicles is disrupted. Developmental analysis of Lim1-CKO retina reveals that components of the rod and cone pathways initially co-assemble within their normal strata in the OPL, indicating that horizontal cells are not required for the correct targeting of photoreceptor terminals or bipolar cell dendrites. As the rod spherules begin to retract during the second postnatal week, rod bipolar cells initially show no signs of ectopic growth, sprouting only subsequently and continuing to do so well after the eighth postnatal week. These results demonstrate the critical yet distinctive roles for horizontal cells on the rod and cone pathways and highlight a unique and as-yet-unrecognized maintenance function of an inhibitory interneuron that is not required for the initial targeting and co-stratification of other components in the circuit.
C1 [Keeley, Patrick W.; Luna, Gabriel; Skyles, Kimberly A.; Madsen, Nils R.; Raven, Mary A.; Fisher, Steven K.; Reese, Benjamin E.] Univ Calif Santa Barbara, Neurosci Res Inst, Santa Barbara, CA 93106 USA.
   [Keeley, Patrick W.; Raven, Mary A.; Fisher, Steven K.] Univ Calif Santa Barbara, Dept Mol Cellular & Dev Biol, Santa Barbara, CA 93106 USA.
   [Luna, Gabriel] Univ Calif Santa Barbara, Ctr Bioimage Informat, Santa Barbara, CA 93106 USA.
   [Fisher, Steven K.] Univ Calif Santa Barbara, Dept Elect & Comp Engn, Santa Barbara, CA 93106 USA.
   [Reese, Benjamin E.] Univ Calif Santa Barbara, Dept Psychol & Brain Sci, Santa Barbara, CA 93106 USA.
   [Poche, Ross A.] Baylor Coll Med, Dept Mol Physiol & Biophys, Houston, TX 77030 USA.
   [Jamrich, Milan] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
   [Swindell, Eric C.] Univ Texas Houston, Sch Med, Dept Pediat, Houston, TX 77030 USA.
   [Oh, Edwin C.] Duke Univ, Med Ctr, Ctr Human Dis Modeling, Dept Med,Div Neurol, Durham, NC 27710 USA.
   [Fariss, Robert N.] NEI, Biol Imaging Core, NIH, Bethesda, MD 20892 USA.
   [Swaroop, Anand] NEI, Neurobiol Neurodegenerat & Repair Lab, NIH, Bethesda, MD 20892 USA.
RP Reese, BE (reprint author), Univ Calif Santa Barbara, Neurosci Res Inst, Santa Barbara, CA 93106 USA.
EM breese@psych.ucsb.edu
OI Swaroop, Anand/0000-0002-1975-1141; Swindell, Eric/0000-0002-1193-8200
FU National Institutes of Health [R01 EY-019968, S10 RR-022585, S10
   OD-010610]; National Science Foundation [OIA-0941717, IIS-0808772];
   National Eye Institute Intramural Research Program; Neuroscience
   Research Institute/Department of Molecular, Cellular; Developmental
   Biology Microscopy Facility at University of California, Santa Barbara
FX This research was supported by the National Institutes of Health (Grant
   R01 EY-019968 and Grant S10 RR-022585 to B.E.R.; Grant S10 OD-010610 to
   M.A.R.), the National Science Foundation (Grants OIA-0941717 and
   IIS-0808772 to S.K.F.), and the National Eye Institute Intramural
   Research Program (A.S.) and was facilitated by the Neuroscience Research
   Institute/Department of Molecular, Cellular, and Developmental Biology
   Microscopy Facility at University of California, Santa Barbara. We thank
   Dr. Richard Behringer for providing initial Lim1-flox mice for breeding.
NR 51
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U2 7
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 6
PY 2013
VL 33
IS 45
BP 17847
EP 17862
DI 10.1523/JNEUROSCI.1373-13.2013
PG 16
WC Neurosciences
SC Neurosciences & Neurology
GA 252PI
UT WOS:000327019100031
PM 24198374
ER

PT J
AU Crivat, G
   Lizunov, VA
   Li, CR
   Stenkula, KG
   Zimmerberg, J
   Cushman, SW
   Pick, L
AF Crivat, Georgeta
   Lizunov, Vladimir A.
   Li, Caroline R.
   Stenkula, Karin G.
   Zimmerberg, Joshua
   Cushman, Samuel W.
   Pick, Leslie
TI Insulin Stimulates Translocation of Human GLUT4 to the Membrane in Fat
   Bodies of Transgenic Drosophila melanogaster
SO PLOS ONE
LA English
DT Article
ID RAT ADIPOSE-CELLS; MANDUCA-SEXTA L; GLUCOSE-TRANSPORT; 3T3-L1
   ADIPOCYTES; PHOSPHATIDYLINOSITOL 3-KINASE; PLASMA-MEMBRANE; TRAFFICKING;
   GROWTH; RECEPTOR; PROTEIN
AB The fruit fly Drosophila melanogaster is an excellent model system for studies of genes controlling development and disease. However, its applicability to physiological systems is less clear because of metabolic differences between insects and mammals. Insulin signaling has been studied in mammals because of relevance to diabetes and other diseases but there are many parallels between mammalian and insect pathways. For example, deletion of Drosophila Insulin-Like Peptides resulted in 'diabetic' flies with elevated circulating sugar levels. Whether this situation reflects failure of sugar uptake into peripheral tissues as seen in mammals is unclear and depends upon whether flies harbor the machinery to mount mammalian-like insulin-dependent sugar uptake responses. Here we asked whether Drosophila fat cells are competent to respond to insulin with mammalian-like regulated trafficking of sugar transporters. Transgenic Drosophila expressing human glucose transporter-4 (GLUT4), the sugar transporter expressed primarily in insulin-responsive tissues, were generated. After expression in fat bodies, GLUT4 intracellular trafficking and localization were monitored by confocal and total internal reflection fluorescence microscopy (TIRFM). We found that fat body cells responded to insulin with increased GLUT4 trafficking and translocation to the plasma membrane. While the amplitude of these responses was relatively weak in animals reared on a standard diet, it was greatly enhanced in animals reared on sugar-restricted diets, suggesting that flies fed standard diets are insulin resistant. Our findings demonstrate that flies are competent to mobilize translocation of sugar transporters to the cell surface in response to insulin. They suggest that Drosophila fat cells are primed for a response to insulin and that these pathways are down-regulated when animals are exposed to constant, high levels of sugar. Finally, these studies are the first to use TIRFM to monitor insulin-signaling pathways in Drosophila, demonstrating the utility of TIRFM of tagged sugar transporters to monitor signaling pathways in insects.
C1 [Crivat, Georgeta; Li, Caroline R.; Pick, Leslie] Univ Maryland, Dept Entomol, College Pk, MD 20742 USA.
   [Lizunov, Vladimir A.; Zimmerberg, Joshua] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, NIH, Bethesda, MD USA.
   [Stenkula, Karin G.; Cushman, Samuel W.] NIDDK, Expt Diabet Metab & Nutr Sect, Diabet Endocrinol & Obes Branch, NIH, Bethesda, MD 20892 USA.
RP Pick, L (reprint author), Univ Maryland, Dept Entomol, College Pk, MD 20742 USA.
EM lpick@umd.edu
RI Bai, Li/N-8311-2013
FU March of Dimes Birth Defects Foundation [1-FY-10-368]; NICHD; NIDDK
FX This work was supported by the March of Dimes Birth Defects Foundation
   (grant # 1-FY-10-368 to L. P.,
   http://www.marchofdimes.com/research/research-grants.aspx) and
   Intramural Research Programs of NICHD and NIDDK. The funders had no role
   in study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
NR 67
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U1 0
U2 17
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 6
PY 2013
VL 8
IS 11
AR e77953
DI 10.1371/journal.pone.0077953
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 247XD
UT WOS:000326656200020
PM 24223128
ER

PT J
AU Murugan, RN
   Ahn, M
   Lee, WC
   Kim, HY
   Song, JH
   Cheong, C
   Hwang, E
   Seo, JH
   Shin, SY
   Choi, SH
   Park, JE
   Bang, JK
AF Murugan, Ravichandran N.
   Ahn, Mija
   Lee, Woo Cheol
   Kim, Hye-Yeon
   Song, Jung Hyun
   Cheong, Chaejoon
   Hwang, Eunha
   Seo, Ji-Hyung
   Shin, Song Yub
   Choi, Sun Ho
   Park, Jung-Eun
   Bang, Jeong Kyu
TI Exploring the Binding Nature of Pyrrolidine Pocket-Dependent
   Interactions in the Polo-Box Domain of Polo-Like Kinase 1
SO PLOS ONE
LA English
DT Article
ID PROTEIN-PROTEIN INTERFACE; PLK1; DISCOVERY; POSITION; AFFINITY; PEPTIDE
AB Background: Over the years, a great deal of effort has been focused on the design and synthesis of potent, linear peptide inhibitors targeting the polo-like kinase 1 (Plk1), which is critically involved in multiple mitotic processes and has been established as an adverse prognostic marker for tumor patients. Plk1 localizes to its intracellular anchoring sites via its polo-box domain, and inhibiting the Plk1 polo-box domain has been considered as an approach to circumvent the specificity problems associated with inhibiting the conserved adenosine triphosphate-binding pocket. The polo-box domain consists of two different binding regions, such as the unique, broader pyrrolidine-binding pocket and the conserved, narrow, Tyr-rich hydrophobic channel, among the three Plk polo-box domains (Plks 1-3), respectively. Therefore, the studies that provide insights into the binding nature of the unique, broader pyrrolidine-binding pocket might lead to the development of selective Plk1-inhibitory compounds.
   Methodology/Principal Findings: In an attempt to retain the monospecificity by targeting the unique, broader pyrrolidine-binding pocket, here, for the first time, a systematic approach was undertaken to examine the structure-activity relationship of N-terminal-truncated PLHSpTM derivatives, to apply a site-directed ligand approach using bulky aromatic and non-aromatic systems, and to characterize the binding nature of these analogues using X-ray crystallographic studies. We have identified a new mode of binding interactions, having improved binding affinity and retaining the Plk1 polo-box domain specificity, at the pyrrolidine-binding pocket. Furthermore, our data revealed that the pyrrolidine-binding pocket was very specific to recognize a short and bulky hydrophobic ligand like adamantane, whereas the Tyr-rich hydrophobic channel was specific with lengthy and small hydrophobic groups.
   Conclusion/Significance: The progress made using our site-directed ligands validated this approach to specifically direct the ligand into the unique pyrrolidine-binding region, and it extends the applicability of the strategy for discovering selective protein-protein interaction inhibitors.
C1 [Murugan, Ravichandran N.; Ahn, Mija; Lee, Woo Cheol; Kim, Hye-Yeon; Song, Jung Hyun; Cheong, Chaejoon; Hwang, Eunha; Seo, Ji-Hyung; Bang, Jeong Kyu] Korea Basic Sci Inst, Div Magnet Resonance, Ochang, Chung Buk, South Korea.
   [Shin, Song Yub] Chosun Univ, Grad Sch, Dept Biomat, Kwangju, South Korea.
   [Shin, Song Yub] Chosun Univ, Sch Med, Dept Cellular & Mol Med, Kwangju, South Korea.
   [Choi, Sun Ho] Dong A ST, Res Labs, Yongin, Gyeonggi Do, South Korea.
   [Choi, Sun Ho; Park, Jung-Eun] NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Park, JE (reprint author), NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM parkju@mail.nih.gov; bangjk@kbsi.re.kr
FU Korea Basic Science Institute's Research Program [T33418]
FX This work was supported by the Korea Basic Science Institute's Research
   Program grant T33418 (JKB). The funders had no role in study design,
   data collection and analysis, decision to publish, or preparation of the
   manuscript.
NR 21
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U1 0
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PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 6
PY 2013
VL 8
IS 11
AR e80043
DI 10.1371/journal.pone.0080043
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 247XD
UT WOS:000326656200104
PM 24223211
ER

PT J
AU Trucco, MM
   Awad, O
   Wilky, BA
   Goldstein, SD
   Huang, RL
   Walker, RL
   Shah, P
   Katuri, V
   Gul, N
   Zhu, YLJ
   McCarthy, EF
   Paz-Priel, I
   Meltzer, PS
   Austin, CP
   Xia, MH
   Loeb, DM
AF Trucco, Matteo M.
   Awad, Ola
   Wilky, Breelyn A.
   Goldstein, Seth D.
   Huang, Ruili
   Walker, Robert L.
   Shah, Preeti
   Katuri, Varalakshmi
   Gul, Naheed
   Zhu, Yuelin J.
   McCarthy, Edward F.
   Paz-Priel, Ido
   Meltzer, Paul S.
   Austin, Christopher P.
   Xia, Menghang
   Loeb, David M.
TI A Novel Chordoma Xenograft Allows In Vivo Drug Testing and Reveals the
   Importance of NF-kappa B Signaling in Chordoma Biology
SO PLOS ONE
LA English
DT Article
ID BREAST-CANCER; CELL-LINE; GENE-EXPRESSION; PHASE-II; BRACHYURY;
   IDENTIFICATION; ACTIVATION; ESTABLISHMENT; INDUCTION; TUMOR
AB Chordoma is a rare primary bone malignancy that arises in the skull base, spine and sacrum and originates from remnants of the notochord. These tumors are typically resistant to conventional chemotherapy, and to date there are no FDA-approved agents to treat chordoma. The lack of in vivo models of chordoma has impeded the development of new therapies for this tumor. Primary tumor from a sacral chordoma was xenografted into NOD/SCID/IL-2R gamma-null mice. The xenograft is serially transplantable and was characterized by both gene expression analysis and whole genome SNP genotyping. The NIH Chemical Genomics Center performed high-throughput screening of 2,816 compounds using two established chordoma cell lines, U-CH1 and U-CH2B. The screen yielded several compounds that showed activity and two, sunitinib and bortezomib, were tested in the xenograft. Both agents slowed the growth of the xenograft tumor. Sensitivity to an inhibitor of I kappa B, as well as inhibition of an NF-kappa B gene expression signature demonstrated the importance of NF-kappa B signaling for chordoma growth. This serially transplantable chordoma xenograft is thus a practical model to study chordomas and perform in vivo preclinical drug testing.
C1 [Trucco, Matteo M.; Awad, Ola; Wilky, Breelyn A.; Goldstein, Seth D.; Shah, Preeti; Katuri, Varalakshmi; Gul, Naheed; Paz-Priel, Ido; Loeb, David M.] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21218 USA.
   [Huang, Ruili; Austin, Christopher P.; Xia, Menghang] NIH, Natl Ctr Adv Translat Sci, Rockville, MD USA.
   [Walker, Robert L.; Zhu, Yuelin J.; Meltzer, Paul S.] NCI, Genet Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [McCarthy, Edward F.] Johns Hopkins Univ, Dept Pathol, Baltimore, MD USA.
RP Loeb, DM (reprint author), Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21218 USA.
EM loebda@jhmi.edu
FU The Chordoma Foundation; Sarcoma Foundation of America
FX The work was funded by grants from The Chordoma Foundation and from
   Sarcoma Foundation of America. The funders had no role in study design,
   data collection and analysis, decision to publish, or preparation of the
   manuscript.
NR 29
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U1 0
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PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 6
PY 2013
VL 8
IS 11
AR e79950
DI 10.1371/journal.pone.0079950
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 247XD
UT WOS:000326656200099
PM 24223206
ER

PT J
AU White, AA
   Danis, M
AF White, Amina A.
   Danis, Marion
TI Patient-Physician Interactions and Electronic Health Records Reply
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Letter
C1 [White, Amina A.; Danis, Marion] NIH, Dept Bioeth, Bethesda, MD 20892 USA.
RP White, AA (reprint author), NIH, 10 Ctr Dr,Bldg 10,Room 1C118, Bethesda, MD 20892 USA.
EM amina.white@nih.gov
FU Intramural NIH HHS [Z99 CL999999]
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 6
PY 2013
VL 310
IS 17
BP 1858
EP 1858
DI 10.1001/jama.2013.277990
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 246PH
UT WOS:000326550900025
PM 24193089
ER

PT J
AU Pindolia, DK
   Garcia, AJ
   Huang, Z
   Smith, DL
   Alegana, VA
   Noor, AM
   Snow, RW
   Tatem, AJ
AF Pindolia, Deepa K.
   Garcia, Andres J.
   Huang, Zhuojie
   Smith, David L.
   Alegana, Victor A.
   Noor, Abdisalan M.
   Snow, Robert W.
   Tatem, Andrew J.
TI The demographics of human and malaria movement and migration patterns in
   East Africa
SO MALARIA JOURNAL
LA English
DT Article
ID PLASMODIUM-FALCIPARUM MALARIA; HUMAN MOBILITY; TRANSMISSION; DISEASE;
   TRAVEL; RISK; ELIMINATION; EPIDEMIOLOGY; POPULATIONS; IMPORTATION
AB Introduction: The quantification of parasite movements can provide valuable information for control strategy planning across all transmission intensities. Mobile parasite carrying individuals can instigate transmission in receptive areas, spread drug resistant strains and reduce the effectiveness of control strategies. The identification of mobile demographic groups, their routes of travel and how these movements connect differing transmission zones, potentially enables limited resources for interventions to be efficiently targeted over space, time and populations.
   Methods: National population censuses and household surveys provide individual-level migration, travel, and other data relevant for understanding malaria movement patterns. Together with existing spatially referenced malaria data and mathematical models, network analysis techniques were used to quantify the demographics of human and malaria movement patterns in Kenya, Uganda and Tanzania. Movement networks were developed based on connectivity and magnitudes of flow within each country and compared to assess relative differences between regions and demographic groups. Additional malaria-relevant characteristics, such as short-term travel and bed net use, were also examined.
   Results: Patterns of human and malaria movements varied between demographic groups, within country regions and between countries. Migration rates were highest in 20-30 year olds in all three countries, but when accounting for malaria prevalence, movements in the 10-20 year age group became more important. Different age and sex groups also exhibited substantial variations in terms of the most likely sources, sinks and routes of migration and malaria movement, as well as risk factors for infection, such as short-term travel and bed net use.
   Conclusion: Census and survey data, together with spatially referenced malaria data, GIS and network analysis tools, can be valuable for identifying, mapping and quantifying regional connectivities and the mobility of different demographic groups. Demographically-stratified HPM and malaria movement estimates can provide quantitative evidence to inform the design of more efficient intervention and surveillance strategies that are targeted to specific regions and population groups.
C1 [Pindolia, Deepa K.; Garcia, Andres J.; Huang, Zhuojie] Univ Florida, Emerging Pathogens Inst, Gainesville, FL 32610 USA.
   [Pindolia, Deepa K.; Garcia, Andres J.; Huang, Zhuojie] Univ Florida, Dept Geog, Gainesville, FL 32611 USA.
   [Pindolia, Deepa K.; Alegana, Victor A.; Noor, Abdisalan M.; Snow, Robert W.] Univ Oxford, KEMRI Wellcome Trust, Malaria Publ Hlth Dept, Collaborat Programme, Nairobi, Kenya.
   [Huang, Zhuojie] Penn State Univ, Ctr Infect Dis Dynam, University Pk, PA 16802 USA.
   [Huang, Zhuojie] Penn State Univ, Dept Biol, University Pk, PA 16802 USA.
   [Smith, David L.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
   [Smith, David L.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
   [Smith, David L.] Ctr Dis Dynam Econ & Policy, Washington, DC USA.
   [Alegana, Victor A.; Tatem, Andrew J.] Univ Southampton, Dept Geog & Environm, Southampton, Hants, England.
   [Noor, Abdisalan M.; Snow, Robert W.] Univ Oxford, Ctr Trop Med, Nuffield Dept Clin Med, Oxford, England.
RP Pindolia, DK (reprint author), Univ Florida, Emerging Pathogens Inst, Gainesville, FL 32610 USA.
EM dpindolia@gmail.com
OI Snow, Robert/0000-0003-3725-6088; Alegana, Victor/0000-0001-5177-9227
FU Emerging Pathogens Institute, University of Florida; RAPIDD program of
   the Science and Technology Directorate, Department of Homeland Security;
   Fogarty International Center, National Institutes of Health; NIH/NIAID
   [U19AI089674]; Bill and Melinda Gates Foundation [49446, 1032350];
   Bloomberg Family Foundation; Wellcome Trust [079080]; Wellcome Trust
   Intermediate Research Fellowship [095127]; Wellcome Trust Major Overseas
   Programme [092654]
FX AJT & DLS acknowledge funding support from the Emerging Pathogens
   Institute, University of Florida, the RAPIDD program of the Science and
   Technology Directorate, Department of Homeland Security, and the Fogarty
   International Center, National Institutes of Health, and are also
   supported by grants from NIH/NIAID (U19AI089674) and the Bill and
   Melinda Gates Foundation (#49446 and #1032350). DLS acknowledges funding
   support from Bloomberg Family Foundation. RWS is supported by the
   Wellcome Trust as Principal Research Fellow (#079080). AMN is supported
   by a Wellcome Trust Intermediate Research Fellowship (##095127). Both
   RWS and AMN are also supported by Wellcome Trust Major Overseas
   Programme grant to the KEMRI/Wellcome Trust Research Programme
   (#092654). The funders had no role in study design, data collection and
   analysis, decision to publish, or preparation of the manuscript. This
   paper forms part of the output of the AfriPop population mapping project
   (www.afripop.org) and the human mobility mapping project
   (www.thummp.org).
NR 56
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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 NOV 5
PY 2013
VL 12
AR 397
DI 10.1186/1475-2875-12-397
PG 12
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 281LS
UT WOS:000329103600005
PM 24191976
ER

PT J
AU Gupta, K
   Jang, H
   Harlen, K
   Puri, A
   Nussinov, R
   Schneider, JP
   Blumenthal, R
AF Gupta, Kshitij
   Jang, Hyunbum
   Harlen, Kevin
   Puri, Anu
   Nussinov, Ruth
   Schneider, Joel P.
   Blumenthal, Robert
TI Mechanism of Membrane Permeation Induced by Synthetic beta-Hairpin
   Peptides
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID AMYLOID ION CHANNELS; SOLID-STATE NMR; ATOMIC-FORCE MICROSCOPY;
   ALL-D-ENANTIOMER; LIPID-BILAYERS; ANTIMICROBIAL PEPTIDE; PORE FORMATION;
   MOLECULAR-DYNAMICS; PROTEGRIN-1; VESICLES
AB We have investigated the membrane destabilizing properties of synthetic amphiphilic cationic peptides, MAX1 and MAX35, which have the propensity to form beta-hairpin structures under certain conditions, and a control non-beta-hairpin-forming peptide MAX8V16E. All three peptides bind to liposomes containing a mixture of zwitterionic POPC and negatively charged POPS lipids as determined by Zeta potential measurements. Circular dichroism measurements indicated folding of MAX1 and MAX35 in the presence of the POPC/POPS liposomes, whereas no such folding was observed with MAX8V16E. There was no binding or folding of these peptides to liposomes containing only POPC. MAX1 and MAX35 induced release of contents from negatively charged liposomes, whereas MAX8V16E failed to promote solute release under identical conditions. Thus, MAX1 and MAX35 bind to, and fold at the surface of negatively charged liposomes adopting a lytic conformation. We ruled out leaky fusion as a mechanism of release by including 2 mol% PEG-PE in the liposomes, which inhibits aggregation/fusion but not folding of MAX or MAX-induced leakage. Using a concentration-dependent quenching probe (calcein), we determined that MAX-induced leakage of liposome contents was an all-or-none process. At MAX1 concentrations, which cause release of similar to 50% of the liposomes that contain small (R-h<1.5 nm) markers, only similar to 15% of those liposomes release a fluorescent dextran of 40 kDa. A multimeric model of the pore is presented based on these results. Atomistic molecular dynamics simulations show that barrels consisting of 10 beta-hairpin MAXI and MAX35 peptides are relatively more stable than MAX8V16E barrels in the bilayer, suggesting that barrels of this size are responsible for the peptides lytic action.
C1 [Gupta, Kshitij; Puri, Anu; Blumenthal, Robert] NCI, Basic Res Lab, Ctr Canc Res, NIH, Frederick, MD 21701 USA.
   [Jang, Hyunbum; Nussinov, Ruth] NCI, Basic Sci Program, SAIC Frederick, NIH, Frederick, MD 21701 USA.
   [Harlen, Kevin; Schneider, Joel P.] NCI, Peptide Design & Mat Sect, Biol Chem Lab, NIH, Frederick, MD 21701 USA.
RP Blumenthal, R (reprint author), NCI, Basic Res Lab, Ctr Canc Res, NIH, Frederick, MD 21701 USA.
EM blumenthalr@mail.nih.gov
RI Schneider, Joel/N-2610-2014
FU Frederick National Laboratory for Cancer Research, National Institutes
   of Health [HHSN261200800001E]; NIH, Frederick National Lab, Center for
   Cancer Research
FX This project has been funded in whole or in part with Federal funds from
   the Frederick National Laboratory for Cancer Research, National
   Institutes of Health, under contract HHSN261200800001E. This research
   was supported [in part] by the Intramural Research Program of NIH,
   Frederick National Lab, Center for Cancer Research. All simulations had
   been performed using the high-performance computational facilities of
   the Biowulf PC/Linux cluster at the National Institutes of Health,
   Bethesda, MD (http://biowulf.nih.gov).
NR 55
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U1 4
U2 59
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 NOV 5
PY 2013
VL 105
IS 9
BP 2093
EP 2103
DI 10.1016/j.bpj.2013.09.040
PG 11
WC Biophysics
SC Biophysics
GA 250NB
UT WOS:000326858400019
PM 24209854
ER

PT J
AU Miranda, TB
   Morris, SA
   Hager, GL
AF Miranda, Tina B.
   Morris, Stephanie A.
   Hager, Gordon L.
TI Complex genomic interactions in the dynamic regulation of transcription
   by the glucocorticoid receptor
SO MOLECULAR AND CELLULAR ENDOCRINOLOGY
LA English
DT Article
DE Glucocorticoids; Nuclear receptor; Glucocorticoid receptor;
   Transcription dynamics; Assisted-loading; Chromatin structure
ID MAMMARY-TUMOR VIRUS; CHROMATIN-REMODELING COMPLEXES; LONG-RANGE
   INTERACTIONS; NF-KAPPA-B; MMTV PROMOTER; IN-VIVO; LIVING CELLS;
   MOLECULAR CHAPERONES; GENE-EXPRESSION; FACTOR ACCESS
AB The glucocorticoid receptor regulates transcriptional output through complex interactions with the genome. These events require continuous remodeling of chromatin, interactions of the glucocorticoid receptor with chaperones and other accessory factors, and recycling of the receptor by the proteasome. Therefore, the cohort of factors expressed in a particular cell type can determine the physiological outcome upon treatment with glucocorticoid hormones. In addition, circadian and ultradian cycling of hormones can also affect GR response. Here we will discuss revision of the classical static model of GR binding to response elements to incorporate recent findings from single cell and genome-wide analyses of GR regulation. We will highlight how these studies have changed our views on the dynamics of GR recruitment and its modulation of gene expression. Published by Elsevier Ireland Ltd.
C1 [Miranda, Tina B.; Morris, Stephanie A.; Hager, Gordon L.] NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA.
RP Hager, GL (reprint author), NCI, Lab Receptor Biol & Gene Express, NIH, Bldg 41,B602,41 Lib Dr, Bethesda, MD 20892 USA.
EM hagerg@exchange.nih.gov
FU Intramural Research Program of the National Institutes of Health,
   National Cancer Institute, Center for Cancer Research; National
   Institute of General Medical Science Pharmacological Research Training
   Fellowship; UNCF-Merck Postdoctoral Science Research Fellowship
FX This research was supported by the Intramural Research Program of the
   National Institutes of Health, National Cancer Institute, Center for
   Cancer Research, by the National Institute of General Medical Science
   Pharmacological Research Training Fellowship to T.B.M., and by a
   UNCF-Merck Postdoctoral Science Research Fellowship to S.A.M.
NR 94
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Z9 20
U1 1
U2 12
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0303-7207
J9 MOL CELL ENDOCRINOL
JI Mol. Cell. Endocrinol.
PD NOV 5
PY 2013
VL 380
IS 1-2
SI SI
BP 16
EP 24
DI 10.1016/j.mce.2013.03.002
PG 9
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 251FE
UT WOS:000326912400003
PM 23499945
ER

PT J
AU Burd, CJ
   Archer, TK
AF Burd, Craig J.
   Archer, Trevor K.
TI Chromatin architecture defines the glucocorticoid response
SO MOLECULAR AND CELLULAR ENDOCRINOLOGY
LA English
DT Article
DE Chromatin; Glucocorticoid receptor; Nuclear receptor
ID TUMOR VIRUS PROMOTER; RECEPTOR BINDING; MMTV PROMOTER;
   ESTROGEN-RECEPTOR; NUCLEAR RECEPTOR; ANDROGEN RECEPTOR; HUMAN GENOME;
   POSITIONED NUCLEOSOMES; DNA DEMETHYLATION; PROSTATE-CANCER
AB The glucocorticoid receptor (GR) functions to regulate a wide group of physiological processes through hormone inducible interaction with genomic loci and subsequent manipulation of the transcriptional output of target genes. Despite expression in a wide variety of tissues, the GR has diverse roles that are regulated tightly in a cell type specific manner. With the advent of whole genome approaches, the details of that diversity and the mechanisms regulating them are beginning to be elucidated. This review aims describe the recent advances detailing the role chromatin structure plays in dictating GR specificity. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
C1 [Burd, Craig J.] Ohio State Univ, Dept Mol Genet, Columbus, OH 43210 USA.
   [Archer, Trevor K.] NIEHS, Chromatin & Gene Express Sect, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Burd, CJ (reprint author), Ohio State Univ, Dept Mol Genet, 590 Biomed Res Tower,460 W 12th Ave, Columbus, OH 43210 USA.
EM craig.burd@osumc.edu
RI Burd, Craig/D-9500-2017; 
OI Burd, Craig/0000-0002-6899-6751
FU NIEHS NIH HHS [R00 ES019918]
NR 74
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U1 3
U2 12
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0303-7207
J9 MOL CELL ENDOCRINOL
JI Mol. Cell. Endocrinol.
PD NOV 5
PY 2013
VL 380
IS 1-2
SI SI
BP 25
EP 31
DI 10.1016/j.mce.2013.03.020
PG 7
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 251FE
UT WOS:000326912400004
PM 23545159
ER

PT J
AU Tsytlonok, M
   Craig, PO
   Sivertsson, E
   Serquera, D
   Perrett, S
   Best, RB
   Wolynes, PG
   Itzhaki, LS
AF Tsytlonok, Maksym
   Craig, Patricio O.
   Sivertsson, Elin
   Serquera, David
   Perrett, Sarah
   Best, Robert B.
   Wolynes, Peter G.
   Itzhaki, Laura S.
TI Complex Energy Landscape of a Giant Repeat Protein
SO STRUCTURE
LA English
DT Article
ID KAPPA-B-ALPHA; FLY-CASTING MECHANISM; FOLDING MECHANISM; MODULAR
   PROTEIN; ANKYRIN DOMAIN; HOLOENZYME; STABILITY; RECOGNITION; DELETION;
   REVEALS
AB Here, we reveal a remarkable complexity in the unfolding of giant HEAT-repeat protein PR65/A, a molecular adaptor for the heterotrimeric PP2A phosphatases. The repeat array ruptures at multiple sites, leading to intermediate states with noncontiguous folded subdomains. There is a dominant sequence of unfolding, which reflects a nonuniform stability distribution across the repeat array and can be rationalized by theoretical models accounting for heterogeneous contact density in the folded structure. Unfolding of certain intermediates is, however, competitive, leading to parallel unfolding pathways. The low-stability, central repeats sample unfolded conformations under physiological conditions, suggesting how folding directs function: certain regions present rigid motifs for molecular recognition, whereas others have the flexibility with which to broaden the search area, as in the fly-casting mechanism. Partial unfolding of PR65/A also impacts catalysis by altering the proximity of bound catalytic subunit and substrate. Thus, the repeat array orchestrates the assembly and activity of PP2A.
C1 [Tsytlonok, Maksym; Serquera, David] Hutchison MRC Res Ctr, MRC, Canc Cell Unit, Cambridge CB2 0XZ, England.
   [Tsytlonok, Maksym; Sivertsson, Elin; Best, Robert B.; Itzhaki, Laura S.] Univ Cambridge, Dept Chem, Cambridge CB2 1EW, England.
   [Craig, Patricio O.] Univ Calif San Diego, Dept Chem & Biochem, La Jolla, CA 92093 USA.
   [Craig, Patricio O.] Univ Calif San Diego, Ctr Theoret Biol Phys, La Jolla, CA 92093 USA.
   [Perrett, Sarah] Chinese Acad Sci, Inst Biophys, Natl Lab Biomacromol, Beijing 100101, Peoples R China.
   [Wolynes, Peter G.] Rice Univ, Ctr Theoret Biol Phys, Houston, TX 77251 USA.
   [Wolynes, Peter G.] Rice Univ, Dept Chem, Houston, TX 77251 USA.
   [Best, Robert B.] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Best, RB (reprint author), Univ Cambridge, Dept Chem, Lensfield Rd, Cambridge CB2 1EW, England.
EM robertbe@helix.nih.gov; pwolynes@rice.edu; lsi10@cam.ac.uk
RI Best, Robert/H-7588-2016
OI Best, Robert/0000-0002-7893-3543
FU National Institutes of Health [GM017862, R01 GM44557]; Medical Research
   Council of the UK [G1002329]; Medical Research Foundation; Royal Society
   University Research Fellowship while at Cambridge; National Institute of
   Diabetes and Digestive and Kidney Diseases while at the National
   Institutes of Health; 973 Program [2012CB911000, 2013CB910700]
FX We thank the Center of Theoretical Biological Physics for computational
   resources. We thank Dr. Stephen McLaughlin (Medical Research Council
   Laboratory of Molecular Biology) for help with analysis of PR65/A
   oligomers. P.G.W. and P.O.C. acknowledge grants (GM017862 and R01
   GM44557) from the National Institutes of Health. L.S.I., M.T., and E.S.
   are supported by the Medical Research Council of the UK (G1002329) and
   the Medical Research Foundation. R.B.B. is supported by a Royal Society
   University Research Fellowship while at Cambridge and by the Intramural
   Research Programme of the National Institute of Diabetes and Digestive
   and Kidney Diseases while at the National Institutes of Health. S.P. is
   supported by the 973 Program (2012CB911000 and 2013CB910700). This work
   was facilitated by a Royal Society International Joint-Project Grant (to
   L.S.I. and S.P.).
NR 39
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PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0969-2126
EI 1878-4186
J9 STRUCTURE
JI Structure
PD NOV 5
PY 2013
VL 21
IS 11
BP 1954
EP 1965
DI 10.1016/j.str.2013.08.028
PG 12
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 250JJ
UT WOS:000326848800008
PM 24120762
ER

PT J
AU Pals, J
   Attene-Ramos, MS
   Xia, MH
   Wagner, ED
   Plewa, MJ
AF Pals, Justin
   Attene-Ramos, Matias S.
   Xia, Menghang
   Wagner, Elizabeth D.
   Plewa, Michael J.
TI Human Cell Toxicogenomic Analysis Linking Reactive Oxygen Species to the
   Toxicity of Monohaloacetic Acid Drinking Water Disinfection Byproducts
SO ENVIRONMENTAL SCIENCE & TECHNOLOGY
LA English
DT Article
ID SELECTIVE COX-2 INHIBITOR; OXIDATIVE STRESS; COLON-CANCER; HALOACETIC
   ACIDS; URINARY-BLADDER; NADPH OXIDASE; DNA-DAMAGE; CYTOTOXICITY;
   ACTIVATION; GENOTOXICITY
AB Chronic exposure to drinking water disinfection byproducts has been linked to adverse health risks. The monohaloacetic acids (monoHAAs) are generated as byproducts during the disinfection of drinking water and are cytotoxic, genotoxic, mutagenic, and teratogenic. Iodoacetic acid toxicity was mitigated by antioxidants, suggesting the involvement of oxidative stress. Other monoHAAs may share a similar mode of action. Each monoHAA generated a significant concentration response increase in the expression of a beta-lactamase reporter under the control of the antioxidant response element (ARE). The monoHAAs generated oxidative stress with a rank order of iodoacetic acid (IAA) > bromoacetic acid (BAA) >> chloroacetic acid (CAA); this rank order was observed with other toxicological end points. Toxicogenomic analysis was conducted with a nontransformed human intestinal epithelial cell line (FHs 74 Int). Exposure to the monoHAAs altered the transcription levels of multiple oxidative stress responsive genes, indicating that each exposure generated oxidative stress. The transcriptome profiles showed an increase in thioredoxin reductase 1 (TXNRD1) and sulfiredoxin (SRXN1), suggesting peroxiredoxin proteins had been oxidized during monoHAA exposures. Three possible sources of reactive oxygen species were identified, the hypohalous acid generating peroxidase enzymes lactoperoxidase (LPO) and myeloperoxidase (MPO), nicotinamide adenine dinucleotide phosphate (NADPH)-dependent oxidase 5 (NOX5), and PTGS2 (COX-2) mediated arachidonic acid metabolism. Each monoHAA exposure caused an increase in COX-2 mRNA levels. These data provide a functional association between monoHAA exposure and adverse health outcomes such as oxidative stress, inflammation, and cancer.
C1 [Pals, Justin; Wagner, Elizabeth D.; Plewa, Michael J.] Univ Illinois, Dept Crop Sci, Urbana, IL USA.
   [Attene-Ramos, Matias S.; Xia, Menghang] NIH, Natl Ctr Adv Translat Sci, Bethesda, MD 20892 USA.
   [Wagner, Elizabeth D.; Plewa, Michael J.] Univ Illinois, Safe Global Water Inst, Ctr Adv Mat Purificat Water Syst, Urbana, IL USA.
   [Wagner, Elizabeth D.; Plewa, Michael J.] Univ Illinois, NSF Sci & Technol, Ctr Adv Mat Purificat Water Syst, Urbana, IL USA.
RP Plewa, MJ (reprint author), Univ Illinois, Dept Crop Sci, Urbana, IL USA.
EM mplewa@illinois.edu
FU Center of Advanced Materials for the Purification of Water with Systems
   (Water CAMPWS) a National Science Foundation Science and Technology
   Center [CTS-0120978]; NIEHS [T32 ES007326]; National Institute of
   Environmental Health Sciences/National Toxicology Program [IAG
   Y3-ES-7020-01]
FX We appreciate support by the Center of Advanced Materials for the
   Purification of Water with Systems (Water CAMPWS) a National Science
   Foundation Science and Technology Center, under Award CTS-0120978. J.P.
   was supported by a NIEHS Predoctoral Fellowship under Grant No. T32
   ES007326. This work was partially supported through an interagency
   agreement (IAG Y3-ES-7020-01) from the National Institute of
   Environmental Health Sciences/National Toxicology Program to the
   National Center for Advancing Translational Sciences, National
   Institutes of Health.
NR 74
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U1 3
U2 57
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0013-936X
EI 1520-5851
J9 ENVIRON SCI TECHNOL
JI Environ. Sci. Technol.
PD NOV 5
PY 2013
VL 47
IS 21
BP 12514
EP 12523
DI 10.1021/es403171b
PG 10
WC Engineering, Environmental; Environmental Sciences
SC Engineering; Environmental Sciences & Ecology
GA 248OP
UT WOS:000326711300078
PM 24050308
ER

PT J
AU Darbari, DS
   Wang, ZY
   Kwak, MJ
   Hildesheim, M
   Nichols, J
   Allen, D
   Seamon, C
   Peters-Lawrence, M
   Conrey, A
   Hall, MK
   Kato, GJ
   Taylor, JG
AF Darbari, Deepika S.
   Wang, Zhengyuan
   Kwak, Minjung
   Hildesheim, Mariana
   Nichols, James
   Allen, Darlene
   Seamon, Catherine
   Peters-Lawrence, Marlene
   Conrey, Anna
   Hall, Mary K.
   Kato, Gregory J.
   Taylor, James G.
TI Severe Painful Vaso-Occlusive Crises and Mortality in a Contemporary
   Adult Sickle Cell Anemia Cohort Study
SO PLOS ONE
LA English
DT Article
ID ACUTE CHEST SYNDROME; PULMONARY-HYPERTENSION; RISK-FACTORS; DISEASE;
   CHILDREN; HYDROXYUREA; DEATH; PREVENTION; STROKE; TRIAL
AB Background: Frequent painful vaso-occlusive crises (VOCs) were associated with mortality in the Cooperative Study of Sickle Cell Disease (CSSCD) over twenty years ago. Modern therapies for sickle cell anemia (SCA) like hydroxyurea are believed to have improved overall patient survival. The current study sought to determine the relevance of the association between more frequent VOCs and death and its relative impact upon overall mortality compared to other known risk factors in a contemporary adult SCA cohort.
   Methods: Two hundred sixty four SCA adults were assigned into two groups based on patient reported outcomes for emergency department (ED) visits or hospitalizations for painful VOC treatment during the 12 months prior to evaluation.
   Results: Higher baseline hematocrit (p = 0.0008), ferritin (p = 0.005), and HDL cholesterol (p = 0.01) were independently associated with 1 or more painful VOCs requiring an ED visit or hospitalization for acute pain. During a median follow-up of 5 years, mortality was higher in the ED visit/hospitalization group (relative risk [RR] 2.68, 95% CI 1.1-6.5, p = 0.03). Higher tricuspid regurgitatant jet velocity (TRV) (RR 2.41, 95% CI 1.5-3.9, p < 0.0001), elevated ferritin (RR 4.00, 95% CI 1.8-9.0, p = 0.001) and lower glomerular filtration rate (RR=2.73, 95% CI 1.6-4.6, p < 0.0001) were also independent risk factors for mortality.
   Conclusions: Severe painful VOCs remain a marker for SCA disease severity and premature mortality in a modern cohort along with other known risk factors for death including high TRV, high ferritin and lower renal function. The number of patient reported pain crises requiring healthcare utilization is an easily obtained outcome that could help to identify high risk patients for disease modifying therapies.
C1 [Darbari, Deepika S.] Childrens Natl Med Ctr, Ctr Canc & Blood Disorders, Washington, DC 20010 USA.
   [Darbari, Deepika S.; Wang, Zhengyuan; Taylor, James G.] NHLBI, NIH, Hematol Branch, Genom Med Sect, Bethesda, MD 20892 USA.
   [Kwak, Minjung] Natl Heart Lung & Blood Inst, NIH, Off Biostat Res, Bethesda, MD USA.
   [Hildesheim, Mariana; Nichols, James; Allen, Darlene; Seamon, Catherine; Peters-Lawrence, Marlene; Conrey, Anna; Kato, Gregory J.] Natl Heart Lung & Blood Inst, NIH, Hematol Branch, Sickle Cell Dis Vasc Sect, Bethesda, MD USA.
   [Hall, Mary K.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
RP Taylor, JG (reprint author), NHLBI, NIH, Hematol Branch, Genom Med Sect, Bethesda, MD 20892 USA.
EM jamesta@mail.nih.gov
RI Kato, Gregory/I-7615-2014; 
OI Kato, Gregory/0000-0003-4465-3217; Taylor, James/0000-0002-4421-1809
FU Division of Intramural Research, National Heart, Lung and Blood
   Institute [1ZIAHL006012-01]
FX This study was supported by the Division of Intramural Research,
   National Heart, Lung and Blood Institute (project 1ZIAHL006012-01). The
   funders had no role in study design, data collection and analysis,
   decision to publish, or preparation of the manuscript.
NR 31
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U1 0
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 5
PY 2013
VL 8
IS 11
AR UNSP e79923
DI 10.1371/journal.pone.0079923
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 247EE
UT WOS:000326597400095
PM 24224021
ER

PT J
AU Lear, BC
   Darrah, EJ
   Aldrich, BT
   Gebre, S
   Scott, RL
   Nash, HA
   Allada, R
AF Lear, Bridget C.
   Darrah, Eric J.
   Aldrich, Benjamin T.
   Gebre, Senetibeb
   Scott, Robert L.
   Nash, Howard A.
   Allada, Ravi
TI UNC79 and UNC80, Putative Auxiliary Subunits of the NARROW ABDOMEN Ion
   Channel, Are Indispensable for Robust Circadian Locomotor Rhythms in
   Drosophila
SO PLOS ONE
LA English
DT Article
ID CATION CHANNEL; SUPRACHIASMATIC NUCLEUS; NEURONAL EXCITABILITY; GENE;
   MELANOGASTER; EXPRESSION; PACEMAKER; ELEGANS; PROTEIN; GENOME
AB In the fruit fly Drosophila melanogaster, a network of circadian pacemaker neurons drives daily rhythms in rest and activity. The ion channel NARROW ABDOMEN (NA), orthologous to the mammalian sodium leak channel NALCN, functions downstream of the molecular circadian clock in pacemaker neurons to promote behavioral rhythmicity. To better understand the function and regulation of the NA channel, we have characterized two putative auxiliary channel subunits in Drosophila, unc79 (aka dunc79) and unc80 (aka CG18437). We have generated novel unc79 and unc80 mutations that represent strong or complete loss-of-function alleles. These mutants display severe defects in circadian locomotor rhythmicity that are indistinguishable from na mutant phenotypes. Tissue-specific RNA interference and rescue analyses indicate that UNC79 and UNC80 likely function within pacemaker neurons, with similar anatomical requirements to NA. We observe an interdependent, post-transcriptional regulatory relationship among the three gene products, as loss of na, unc79, or unc80 gene function leads to decreased expression of all three proteins, with minimal effect on transcript levels. Yet despite this relationship, we find that the requirement for unc79 and unc80 in circadian rhythmicity cannot be bypassed by increasing NA protein expression, nor can these putative auxiliary subunits substitute for each other. These data indicate functional requirements for UNC79 and UNC80 beyond promoting channel subunit expression. Immunoprecipitation experiments also confirm that UNC79 and UNC80 form a complex with NA in the Drosophila brain. Taken together, these data suggest that Drosophila NA, UNC79, and UNC80 function together in circadian clock neurons to promote rhythmic behavior.
C1 [Lear, Bridget C.; Darrah, Eric J.; Aldrich, Benjamin T.; Gebre, Senetibeb] Univ Iowa, Dept Biol, Iowa City, IA 52242 USA.
   [Scott, Robert L.; Nash, Howard A.] NIMH, Mol Biol Lab, Bethesda, MD 20892 USA.
   [Allada, Ravi] Northwestern Univ, Dept Neurobiol, Evanston, IL USA.
RP Lear, BC (reprint author), Univ Iowa, Dept Biol, Iowa City, IA 52242 USA.
EM bridget-lear@uiowa.edu
FU NIH [R00 GM080107, R01 NS052903]; NARSAD
FX This work was supported by NIH grant R00 GM080107 to B. C. L, NIH R01
   NS052903 to R. A., and a NARSAD Young Investigator Award to B. C. L. The
   funders had no role in study, design, data collection and analysis,
   decision to publish, or preparation of the manuscript.
NR 28
TC 12
Z9 13
U1 0
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 5
PY 2013
VL 8
IS 11
AR e78147
DI 10.1371/journal.pone.0078147
PG 13
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 247EE
UT WOS:000326597400018
PM 24223770
ER

PT J
AU Bea, S
   Valdes-Mas, R
   Navarro, A
   Salaverria, I
   Martin-Garcia, D
   Jares, P
   Gine, E
   Pinyol, M
   Royo, C
   Nadeu, F
   Conde, L
   Juan, M
   Clot, G
   Vizan, P
   Di Croce, L
   Puente, DA
   Lopez-Guerra, M
   Moros, A
   Roue, G
   Aymerich, M
   Villamor, N
   Colomo, L
   Martinez, A
   Valera, A
   Martin-Subero, JI
   Amador, V
   Hernandez, L
   Rozman, M
   Enjuanes, A
   Forcada, P
   Muntanola, A
   Hartmann, EM
   Calasanz, MJ
   Rosenwald, A
   Ott, G
   Hernandez-Rivas, JM
   Klapper, W
   Siebert, R
   Wiestner, A
   Wilson, WH
   Colomer, D
   Lopez-Guillermo, A
   Lopez-Otin, C
   Puente, XS
   Campo, E
AF Bea, Silvia
   Valdes-Mas, Rafael
   Navarro, Alba
   Salaverria, Itziar
   Martin-Garcia, David
   Jares, Pedro
   Gine, Eva
   Pinyol, Magda
   Royo, Cristina
   Nadeu, Ferran
   Conde, Laura
   Juan, Manel
   Clot, Guillem
   Vizan, Pedro
   Di Croce, Luciano
   Puente, Diana A.
   Lopez-Guerra, Monica
   Moros, Alexandra
   Roue, Gael
   Aymerich, Marta
   Villamor, Neus
   Colomo, Lluis
   Martinez, Antonio
   Valera, Alexandra
   Martin-Subero, Jose I.
   Amador, Virginia
   Hernandez, Luis
   Rozman, Maria
   Enjuanes, Anna
   Forcada, Pilar
   Muntanola, Ana
   Hartmann, Elena M.
   Calasanz, Maria J.
   Rosenwald, Andreas
   Ott, German
   Hernandez-Rivas, Jesus M.
   Klapper, Wolfram
   Siebert, Reiner
   Wiestner, Adrian
   Wilson, Wyndham H.
   Colomer, Dolors
   Lopez-Guillermo, Armando
   Lopez-Otin, Carlos
   Puente, Xose S.
   Campo, Elias
TI Landscape of somatic mutations and clonal evolution in mantle cell
   lymphoma
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE next-generation sequencing; cancer genetics; cancer heterogeneity
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; MARGINAL ZONE LYMPHOMA; GENE-EXPRESSION;
   MULTIPLE-MYELOMA; GOOD PROGNOSIS; CODING GENOME; C-MYC; NOTCH1;
   HETEROGENEITY; SIGNATURES
AB Mantle cell lymphoma (MCL) is an aggressive tumor, but a subset of patients may follow an indolent clinical course. To understand the mechanisms underlying this biological heterogeneity, we performed whole-genome and/or whole-exome sequencing on 29 MCL cases and their respective matched normal DNA, as well as 6 MCL cell lines. Recurrently mutated genes were investigated by targeted sequencing in an independent cohort of 172 MCL patients. We identified 25 significantly mutated genes, including known drivers such as ataxia-telangectasia mutated (ATM), cyclin D1 (CCND1), and the tumor suppressor TP53; mutated genes encoding the anti-apoptotic protein BIRC3 and Toll-like receptor 2 (TLR2); and the chromatin modifiers WHSC1, MLL2, and MEF2B. We also found NOTCH2 mutations as an alternative phenomenon to NOTCH1 mutations in aggressive tumors with a dismal prognosis. Analysis of two simultaneous or subsequent MCL samples by whole-genome/whole-exome (n = 8) or targeted (n = 19) sequencing revealed subclonal heterogeneity at diagnosis in samples from different topographic sites and modulation of the initial mutational profile at the progression of the disease. Some mutations were predominantly clonal or subclonal, indicating an early or late event in tumor evolution, respectively. Our study identifies molecular mechanisms contributing to MCL pathogenesis and offers potential targets for therapeutic intervention.
C1 [Bea, Silvia; Navarro, Alba; Salaverria, Itziar; Martin-Garcia, David; Jares, Pedro; Gine, Eva; Pinyol, Magda; Royo, Cristina; Nadeu, Ferran; Conde, Laura; Juan, Manel; Clot, Guillem; Lopez-Guerra, Monica; Moros, Alexandra; Roue, Gael; Aymerich, Marta; Villamor, Neus; Colomo, Lluis; Martinez, Antonio; Valera, Alexandra; Martin-Subero, Jose I.; Amador, Virginia; Hernandez, Luis; Rozman, Maria; Enjuanes, Anna; Colomer, Dolors; Lopez-Guillermo, Armando; Campo, Elias] Univ Barcelona, Hosp Clin, Inst Invest Biomed August Pi i Sunyer, E-08036 Barcelona, Spain.
   [Valdes-Mas, Rafael; Puente, Diana A.; Lopez-Otin, Carlos; Puente, Xose S.] Univ Oviedo, Inst Univ Oncol, E-33006 Oviedo, Spain.
   [Vizan, Pedro; Di Croce, Luciano] Ctr Genom Regulat, Barcelona 08003, Spain.
   [Vizan, Pedro; Di Croce, Luciano] Univ Pompeu Fabra, Barcelona 08003, Spain.
   [Forcada, Pilar; Muntanola, Ana] Mutua Terrassa, Terrassa 08221, Spain.
   [Hartmann, Elena M.; Rosenwald, Andreas] Univ Wurzburg, Inst Pathol, D-97080 Wurzburg, Germany.
   [Calasanz, Maria J.] Univ Navarra, Dept Genet, E-31080 Pamplona, Spain.
   [Ott, German] Robert Bosch Krankenhaus, D-70376 Stuttgart, Germany.
   [Ott, German] Dr Margarete Fischer Bosch Inst Clin Pharmacol, D-70376 Stuttgart, Germany.
   [Hernandez-Rivas, Jesus M.] Univ Salamanca, Ctr Invest Canc, Salamanca 37007, Spain.
   [Klapper, Wolfram] Univ Kiel, Hematopathol Sect, D-24105 Kiel, Germany.
   [Klapper, Wolfram] Univ Kiel, Lymph Node Registry, D-24105 Kiel, Germany.
   [Siebert, Reiner] Univ Kiel, Inst Human Genet, D-24105 Kiel, Germany.
   [Wiestner, Adrian] NHLBI, Bethesda, MD 20892 USA.
   [Wilson, Wyndham H.] NCI, Bethesda, MD 20892 USA.
RP Campo, E (reprint author), Univ Barcelona, Hosp Clin, Inst Invest Biomed August Pi i Sunyer, E-08036 Barcelona, Spain.
EM sbea@clinic.ub.es; xspuente@uniovi.es; ecampo@clinic.ub.es
RI Roue, Gael/D-4759-2014; Di Croce, Luciano/E-7759-2015; Navarro,
   Alba/H-2611-2015; Royo, Cristina/H-3193-2015; ENJUANES,
   Anna/H-3245-2015; SALAVERRIA, ITZIAR/L-2246-2015; Colomo,
   Luis/A-2259-2016; Siebert, Reiner/A-8049-2010; Lopez-Otin,
   Carlos/C-6657-2013; Calasanz, MJ/R-5813-2016; Klapper,
   Wolfram/S-6314-2016; Hernandez-Rivas, Jesus Maria/B-5459-2017; Bea,
   Silvia/K-7699-2014; 
OI Roue, Gael/0000-0003-0245-2257; Di Croce, Luciano/0000-0003-3488-6228;
   Navarro, Alba/0000-0002-4041-0974; Royo, Cristina/0000-0002-1214-4656;
   ENJUANES, Anna/0000-0002-4679-6687; SALAVERRIA,
   ITZIAR/0000-0002-2427-9822; Colomo, Luis/0000-0001-5236-5085;
   Lopez-Otin, Carlos/0000-0001-6964-1904; Calasanz,
   MJ/0000-0002-0374-3008; Hernandez-Rivas, Jesus
   Maria/0000-0002-9661-9371; COLOMER, DOLORS/0000-0001-7486-8484; Bea,
   Silvia/0000-0001-7192-2385; Martin-Subero, Jose
   Ignacio/0000-0001-8809-5195; Suarez-Puente, Xose/0000-0001-9525-1483;
   Rozman, Maria/0000-0002-2641-1110; Nadeu, Ferran/0000-0003-2910-9440;
   Vizan, Pedro/0000-0002-6787-9940; Campo, elias/0000-0001-9850-9793
FU Fondo de Investigaciones Sanitarias [PI11/01177, PI10/01404];
   Association for International Cancer Research [12-0142]; Lymphoma
   Research Foundation; Red Tematica de Investigacion Cooperativa en Cancer
   [RD06/0020/0039, RD12/0036/0036]; Plan Nacional [SAF08/03630,
   SAF10/21165, SAF12/38432]; Generalitat de Catalunya [2009-SGR-992];
   European Regional Development Fund; National Heart, Lung, and Blood
   Institute; National Cancer Institute
FX We thank M. Prieto, S. Guijarro, M. Sanchez, L. Pla, S. Martin, C.
   Capdevila, N. de Moner, N. Villahoz, and C. Muro for their assistance;
   and the Spanish Centro Nacional de Analisis Genomico, Centro Nacional de
   Genotipado, and Institut d'Investigacions Biomediques August Pi i Sunyer
   Genomic Unit for their services. This work was developed at the Centro
   Esther Koplowitz, Barcelona, Spain, and supported by the Fondo de
   Investigaciones Sanitarias (PI11/01177, PI10/01404); Association for
   International Cancer Research (12-0142); Lymphoma Research Foundation;
   Red Tematica de Investigacion Cooperativa en Cancer (RD06/0020/0039;
   RD12/0036/0036); Plan Nacional (SAF08/03630, SAF10/21165, SAF12/38432);
   Generalitat de Catalunya 2009-SGR-992; and the European Regional
   Development Fund. C.L-O. is a Botin Foundation investigator and E. C. is
   an Institucio Catalana de Recerca i Estudis Avancats-Academia
   investigator. A. W. and W. H. W. are supported by the intramural
   research program of National Heart, Lung, and Blood Institute and
   National Cancer Institute, respectively.
NR 43
TC 115
Z9 117
U1 2
U2 34
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 NOV 5
PY 2013
VL 110
IS 45
BP 18250
EP 18255
DI 10.1073/pnas.1314608110
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 246PG
UT WOS:000326550800057
PM 24145436
ER

PT J
AU Kang'ethe, W
   Bernstein, HD
AF Kang'ethe, Wanyoike
   Bernstein, Harris D.
TI Charge-dependent secretion of an intrinsically disordered protein via
   the autotransporter pathway
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE bacterial pathogenesis; membrane protein assembly; type Va secretion
ID ADENYLATE-CYCLASE TOXIN; OUTER-MEMBRANE; BACTERIAL AUTOTRANSPORTER;
   ESCHERICHIA-COLI; BORDETELLA-PERTUSSIS; BIOLOGICAL-MEMBRANES; VIRULENCE
   PROTEIN; PASSENGER DOMAIN; BETA-DOMAIN; IN-VITRO
AB Autotransporters are a large class of virulence proteins produced by Gram-negative bacteria. They contain an N-terminal extracellular ("passenger") domain that folds into a C-helical structure and a C-terminal beta-barrel ("beta") domain that anchors the protein to the outer membrane. Because the periplasm lacks ATP, the source of energy that drives passenger domain secretion is unknown. The prevailing model postulates that vectorial folding of the beta-helix in the extracellular space facilitates unidirectional secretion of the passenger domain. In this study we used a chimeric protein composed of the 675-residue receptor-binding domain (RD) of the Bordetella pertussis adenylate cyclase toxin CyaA fused to the C terminus of the Escherichia coli O157:H7 autotransporter EspP to test this hypothesis. The RD is a highly acidic, repetitive polypeptide that is intrinsically disordered in the absence of calcium. Surprisingly, we found that the RD moiety was efficiently secreted when it remained in an unfolded conformation. Furthermore, we found that neutralizing or reversing the charge of acidic amino acid clusters stalled translocation in the vicinity of the altered residues. These results challenge the vectorial folding model and, together with the finding that naturally occurring passenger domains are predominantly acidic, provide evidence that a net negative charge plays a significant role in driving the translocation reaction.
C1 [Kang'ethe, Wanyoike; Bernstein, Harris D.] Natl Inst Diabet & Digest & Kidney Dis, Genet & Biochem Branch, NIH, Bethesda, MD 20892 USA.
RP Bernstein, HD (reprint author), Natl Inst Diabet & Digest & Kidney Dis, Genet & Biochem Branch, NIH, Bethesda, MD 20892 USA.
EM harris_bernstein@nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases
FX We thank Qing Chen (Center for Biologics Evaluation and Research/ Food
   and Drug Administration) for helping to clone CyaA, Miguel Valvano for
   providing plasmid pSCrhaB2, Matt Wenham for generating the anti-EspP
   passenger domain polyclonal antibody, and Trevor Lithgow for sharing
   bioinformatic data. We also thank Olga Pavlova and Susan Buchanan for
   helpful comments on the manuscript. This work was supported by the
   Intramural Research Program of the National Institute of Diabetes and
   Digestive and Kidney Diseases.
NR 62
TC 12
Z9 12
U1 3
U2 14
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 NOV 5
PY 2013
VL 110
IS 45
BP E4246
EP E4255
DI 10.1073/pnas.1310345110
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 246PG
UT WOS:000326550800015
PM 24145447
ER

PT J
AU Subramaniam, S
AF Subramaniam, Sriram
TI Structure of trimeric HIV-1 envelope glycoproteins
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Letter
ID MOLECULAR ARCHITECTURE
C1 NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Subramaniam, S (reprint author), NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bldg 37, Bethesda, MD 20892 USA.
EM ss1@nih.gov
NR 7
TC 15
Z9 15
U1 1
U2 18
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 NOV 5
PY 2013
VL 110
IS 45
BP E4172
EP E4174
DI 10.1073/pnas.1313802110
PG 3
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 246PG
UT WOS:000326550800003
PM 24106302
ER

PT J
AU te Riele, ASJM
   Bhonsale, A
   James, CA
   Rastegar, N
   Murray, B
   Burt, JR
   Tichnell, C
   Madhavan, S
   Judge, DP
   Bluemke, DA
   Zimmerman, SL
   Kamel, IR
   Calkins, H
   Tandri, H
AF te Riele, Anneline S. J. M.
   Bhonsale, Aditya
   James, Cynthia A.
   Rastegar, Neda
   Murray, Brittney
   Burt, Jeremy R.
   Tichnell, Crystal
   Madhavan, Srinivasa
   Judge, Daniel P.
   Bluemke, David A.
   Zimmerman, Stefan L.
   Kamel, Ihab R.
   Calkins, Hugh
   Tandri, Harikrishna
TI Incremental Value of Cardiac Magnetic Resonance Imaging in Arrhythmic
   Risk Stratification of Arrhythmogenic Right Ventricular
   Dysplasia/Cardiomyopathy-Associated Desmosomal Mutation Carriers
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Article
DE cardiomyopathy; electrocardiography; magnetic resonance imaging; risk
   stratification; tachyarrhythmias
ID TASK-FORCE CRITERIA; CARDIOVERTER-DEFIBRILLATOR THERAPY; SUDDEN-DEATH;
   FOLLOW-UP; CARDIOMYOPATHY; DYSPLASIA; GENE; PLAKOPHILIN-2; PLAKOGLOBIN;
   PREVENTION
AB Objectives The aim of this study was to identify the incremental value and optimal role of cardiac magnetic resonance (CMR) imaging in arrhythmic risk stratification of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C)associated desmosomal mutation carriers without histories of sustained ventricular arrhythmia.
   Background Risk stratification of ARVD/C mutation carriers is challenging.
   Methods Sixty-nine patients (mean age 27.0 +/- 15.3 years, 42% men) harboring ARVD/C-associated pathogenic mutations (83% plakophilin 2) without prior sustained ventricular arrhythmias were included. Electrocardiographic and 24-h Holter monitoring findings closest to presentation were analyzed for electrical abnormalities per revised task force criteria. CMR studies were done to identify abnormal cardiac structure and function according to the revised task force criteria.
   Results Overall, 42 patients (61%) presented with electrical abnormalities on the basis of electrocardiography and Holter monitoring, of whom 20 (48%) had abnormal results on CMR. Only 1 of 27 patients (4%) without electrical abnormalities at initial evaluation had abnormal CMR results. Over a mean follow-up period of 5.8 +/- 4.4 years, 11 patients (16%) experienced sustained ventricular arrhythmias, exclusively in patients with both electrical abnormalities (electrocardiography and/or Holter monitoring) and abnormal CMR results.
   Conclusions These results suggest that electrical abnormalities on electrocardiography and Holter monitoring precede detectable structural abnormalities in ARVD/C mutation carriers. Therefore, evaluation of cardiac structure and function using CMR is probably not necessary in the absence of baseline electrical abnormalities. Among ARVD/C mutation carriers, the presence of both electrical and CMR abnormalities identifies patients at high risk for events and thus patients who might benefit from prophylactic implantable cardioverter-defibrillator placement. (C) 2013 by the American College of Cardiology Foundation
C1 [te Riele, Anneline S. J. M.] Univ Med Ctr Utrecht, Dept Med, Div Cardiol, Utrecht, Netherlands.
   [Bhonsale, Aditya; James, Cynthia A.; Murray, Brittney; Tichnell, Crystal; Madhavan, Srinivasa; Judge, Daniel P.; Calkins, Hugh; Tandri, Harikrishna] Johns Hopkins Univ, Sch Med, Dept Med, Div Cardiol, Baltimore, MD 21205 USA.
   [Rastegar, Neda; Burt, Jeremy R.; Bluemke, David A.; Zimmerman, Stefan L.; Kamel, Ihab R.] Johns Hopkins Univ, Sch Med, Dept Radiol, Baltimore, MD 21205 USA.
   [Bluemke, David A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
RP Tandri, H (reprint author), Johns Hopkins Univ Hosp, Dept Med, Div Cardiol, 600 North Wolfe St,Carnegie 565D, Baltimore, MD 21287 USA.
EM htandri1@jhmi.edu
OI te Riele, Anneline/0000-0003-1115-6193; Bluemke,
   David/0000-0002-8323-8086
FU Dutch Heart Foundation, the Netherlands [2011SB013]; Radiological
   Society of North America [RF1106]; National Heart, Lung, and Blood
   Institute [K23HL093350]; St. Jude Medical Foundation; Medtronic, Inc.;
   Bogle Foundation; Healing Hearts Foundation; Campanella family;
   Wilmerding Endowments; Dr. Francis P. Chiaramonte Private Foundation
FX This study was supported by funding from the Dutch Heart Foundation, the
   Netherlands (grant 2011SB013 to Ms. te Riele); the Radiological Society
   of North America (grant RF1106 to Dr. Burt); the National Heart, Lung,
   and Blood Institute (grant K23HL093350 to Dr. Tandri); the St. Jude
   Medical Foundation, and Medtronic, Inc. The Johns Hopkins ARVD/C Program
   is supported by the Bogle Foundation, the Healing Hearts Foundation, the
   Campanella family, the Wilmerding Endowments, and the Dr. Francis P.
   Chiaramonte Private Foundation. Dr. Calkins has received research
   support from Medtronic, Inc. and St. Jude Medical. All other authors
   have reported that they have no relationships relevant to the contents
   of this paper to disclose.
NR 34
TC 30
Z9 31
U1 0
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
EI 1558-3597
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 5
PY 2013
VL 62
IS 19
BP 1761
EP 1769
DI 10.1016/j.jacc.2012.11.087
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 242KI
UT WOS:000326239100007
PM 23810894
ER

PT J
AU Cheng, HM
   Chuang, SY
   Sung, SH
   Yu, WC
   Pearson, A
   Lakatta, EG
   Pan, WH
   Chen, CH
AF Cheng, Hao-Min
   Chuang, Shao-Yuan
   Sung, Shih-Hsien
   Yu, Wen-Chung
   Pearson, Alan
   Lakatta, Edward G.
   Pan, Wen-Harn
   Chen, Chen-Huan
TI Derivation and Validation of Diagnostic Thresholds for Central Blood
   Pressure Measurements Based on Long-Term Cardiovascular Risks
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Article
DE central blood pressure; diagnostic thresholds; high blood pressure;
   hypertension
ID CENTRAL AORTIC PRESSURE; SPURIOUS SYSTOLIC HYPERTENSION; CAROTID-ARTERY
   TONOMETRY; LEFT-VENTRICULAR MASS; PULSE PRESSURE; UPPER-LIMB;
   GENERAL-POPULATION; ISCHEMIC-STROKE; WAVE REFLECTION; ALL-CAUSE
AB Objectives This study sought to derive and validate outcome-driven thresholds of central blood pressure (CBP) for diagnosing hypertension.
   Background Current guidelines for managing patients with hypertension mainly rely on blood pressure (BP) measured at brachial arteries (cuff BP). However, BP measured at the central aorta (central BP [CBP]) may be a better prognostic factor for predicting future cardiovascular events than cuff BP.
   Methods In a derivation cohort (1,272 individuals and a median follow-up of 15 years), we determined diagnostic thresholds for CBP by using current guideline-endorsed cutoffs for cuff BP with a bootstrapping (resampling by drawing randomly with replacement) and an approximation method. To evaluate the discriminatory power in predicting cardiovascular outcomes, the derived thresholds were tested in a validation cohort (2,501 individuals with median follow-up of 10 years).
   Results The 2 analyses yielded similar diagnostic thresholds for CBP. After rounding, systolic/diastolic threshold was 110/80 mm Hg for optimal BP and 130/90 mm Hg for hypertension. Compared with optimal BP, the risk of cardiovascular mortality increased significantly in subjects with hypertension (hazard ratio: 3.08, 95% confidence interval: 1.05 to 9.05). Of the multivariate Cox proportional hazards model, incorporation of a dichotomous variable by defining hypertension as CBP >= 130/90 mm Hg was associated with the largest contribution to the predictive power.
   Conclusions CBP of 130/90 mm Hg was determined to be the cutoff limit for normality and was characterized by a greater discriminatory power for long-term events in our validation cohort. This report represents an important step toward the application of the CBP concept in clinical practice. (C) 2013 by the American College of Cardiology Foundation
C1 [Cheng, Hao-Min; Pearson, Alan] Univ Adelaide, Fac Hlth Sci, Joanna Briggs Inst, Adelaide, SA, Australia.
   [Cheng, Hao-Min; Chen, Chen-Huan] Taipei Vet Gen Hosp, Dept Med Res & Educ, Taipei 11221, Taiwan.
   [Cheng, Hao-Min; Sung, Shih-Hsien; Yu, Wen-Chung; Chen, Chen-Huan] Natl Yang Ming Univ, Cardiovasc Res Ctr, Taipei 112, Taiwan.
   [Cheng, Hao-Min; Sung, Shih-Hsien; Yu, Wen-Chung; Chen, Chen-Huan] Natl Yang Ming Univ, Dept Med, Taipei 112, Taiwan.
   [Chuang, Shao-Yuan; Pan, Wen-Harn] Natl Hlth Res Inst, Inst Populat Hlth Sci, Miaoli, Taiwan.
   [Sung, Shih-Hsien; Chen, Chen-Huan] Natl Yang Ming Univ, Inst Publ Hlth, Taipei 112, Taiwan.
   [Chuang, Shao-Yuan; Chen, Chen-Huan] Natl Yang Ming Univ, Community Med Res Ctr, Taipei 112, Taiwan.
   [Lakatta, Edward G.] NIA, Cardiovasc Sci Lab, Intramural Res Program Baltimore, Bethesda, MD 20892 USA.
   [Pan, Wen-Harn] Acad Sinica, Inst BioMed Sci, Taipei 115, Taiwan.
RP Chen, CH (reprint author), Taipei Vet Gen Hosp, Dept Med Res & Educ, 201,Sec 2,Shih Pai Rd, Taipei 11221, Taiwan.
EM pan@ibms.sinica.edu.tw; chench@vghtpe.gov.tw
RI Pan, Wen-Harn /F-9972-2010; Chuang, Shao-Yuan/B-3478-2011
FU National Science Council [NSC 96-2314-B-010-035-MY3]; Taipei Veterans
   General Hospital [V98C1-028]; Research Foundation of Cardiovascular
   Medicine (Taipei, Taiwan, Republic of China); Research and Development
   [NO1-AG-1-2118]; Intramural Research Program of the National Institute
   on Aging, National Institutes of Health, National Health Research
   Institutes in Taiwan [NHRI-EX93-9225PP, NHRI-EX94-9225PP, PH-102-PP-19,
   NSC 5-2314-B-001-012-MY3, NSC 102-2314-B-400-001]; Department of Health
   in Taiwan [DOH80-2, DOH81-021, DOH8202-1027, DOH83-TD-015, DOH-84TD-006]
FX This work was supported in part by a grant from the National Science
   Council (NSC 96-2314-B-010-035-MY3), an intramural grant from the Taipei
   Veterans General Hospital (grant V98C1-028), Grants-in-Aid from the
   Research Foundation of Cardiovascular Medicine (Taipei, Taiwan, Republic
   of China), Research and Development contract NO1-AG-1-2118, the
   Intramural Research Program of the National Institute on Aging, National
   Institutes of Health, National Health Research Institutes in Taiwan
   (NHRI-EX93-9225PP, NHRI-EX94-9225PP, PH-102-PP-19, NSC
   5-2314-B-001-012-MY3, NSC 102-2314-B-400-001), and by the Department of
   Health in Taiwan (DOH80-27, DOH81-021, DOH8202-1027, DOH83-TD-015, and
   DOH-84TD-006). Dr. Chen reports that Microlife Co., Ltd., and National
   Yang-Ming University have signed a contract for transfer of the
   noninvasive central blood pressure estimating technique. All other
   authors have reported that they have no relationships relevant to the
   contents of this paper to disclose. The first two authors contributed
   equally to this work.
NR 57
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Z9 39
U1 0
U2 11
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
EI 1558-3597
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 5
PY 2013
VL 62
IS 19
BP 1780
EP 1787
DI 10.1016/j.jacc.2013.06.029
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 242KI
UT WOS:000326239100010
PM 23850921
ER

PT J
AU Williams-DeVane, CR
   Reif, DM
   Hubal, EC
   Bushel, PR
   Hudgens, EE
   Gallagher, JE
   Edwards, SW
AF Williams-DeVane, ClarLynda R.
   Reif, David M.
   Hubal, Elaine Cohen
   Bushel, Pierre R.
   Hudgens, Edward E.
   Gallagher, Jane E.
   Edwards, Stephen W.
TI Decision tree-based method for integrating gene expression, demographic,
   and clinical data to determine disease endotypes
SO BMC SYSTEMS BIOLOGY
LA English
DT Article
DE Asthma; Endotypes; Gene Expression; Integrated analysis
ID SYSTEMS BIOLOGY APPROACH; GENOME-WIDE ASSOCIATION; ASTHMA
   RESEARCH-PROGRAM; HUMAN PERIPHERAL-BLOOD; REGULATORY NETWORKS;
   CLUSTER-ANALYSIS; MOLECULAR EPIDEMIOLOGY; COLORECTAL-CANCER; BAYESIAN
   NETWORKS; ADULT ASTHMA
AB Background: Complex diseases are often difficult to diagnose, treat and study due to the multi-factorial nature of the underlying etiology. Large data sets are now widely available that can be used to define novel, mechanistically distinct disease subtypes (endotypes) in a completely data-driven manner. However, significant challenges exist with regard to how to segregate individuals into suitable subtypes of the disease and understand the distinct biological mechanisms of each when the goal is to maximize the discovery potential of these data sets.
   Results: A multi-step decision tree-based method is described for defining endotypes based on gene expression, clinical covariates, and disease indicators using childhood asthma as a case study. We attempted to use alternative approaches such as the Student's t-test, single data domain clustering and the Modk-prototypes algorithm, which incorporates multiple data domains into a single analysis and none performed as well as the novel multi-step decision tree method. This new method gave the best segregation of asthmatics and non-asthmatics, and it provides easy access to all genes and clinical covariates that distinguish the groups.
   Conclusions: The multi-step decision tree method described here will lead to better understanding of complex disease in general by allowing purely data-driven disease endotypes to facilitate the discovery of new mechanisms underlying these diseases. This application should be considered a complement to ongoing efforts to better define and diagnose known endotypes. When coupled with existing methods developed to determine the genetics of gene expression, these methods provide a mechanism for linking genetics and exposomics data and thereby accounting for both major determinants of disease.
C1 [Williams-DeVane, ClarLynda R.; Edwards, Stephen W.] US EPA, Natl Hlth & Environm Effects Res Lab, Integrated Syst Toxicol Div, Durham, NC 27711 USA.
   [Reif, David M.; Hubal, Elaine Cohen] US EPA, Natl Ctr Computat Toxicol, Durham, NC 27711 USA.
   [Bushel, Pierre R.] NIEHS, Biostat Branch, Durham, NC 27709 USA.
   [Hudgens, Edward E.; Gallagher, Jane E.] US EPA, Natl Hlth & Environm Effects Res Lab, Environm Publ Hlth Div, Durham, NC 27711 USA.
RP Williams-DeVane, CR (reprint author), N Carolina Cent Univ, Julius L Chambers Biomed Biotechnol Res Inst, Dept Biol, Durham, NC 27707 USA.
EM clarlynda.williams@nccu.edu; edwards.stephen@epa.gov
OI Reif, David/0000-0001-7815-6767
FU National Health and Environmental Effects Research Laboratory; National
   Center for Computational Toxicology within the U.S. EPA's Office of
   Research and Development; Intramural Research Program of the National
   Institutes of Health (NIH); National Institute of Environmental Health
   Sciences (NIEHS) [Z01 ES102345-04, Z01 ES101744-04, U54 CA156735-02]
FX The authors wish to acknowledge the following for substantial
   contributions to this manuscript: Steve Siferd and Wendell Jones at
   Expression Analysis; the staff at Henry Ford Health System; all study
   volunteers and their families. We would like to thank Dr. Robert
   Hamilton of Johns Hopkins University, for the IgE measurements. We would
   also like to thank BJ George, Julian Preston, Lyle Burgoon, and Richard
   Judson for critical review of the manuscript. This study was funded by
   the National Health and Environmental Effects Research Laboratory and
   the National Center for Computational Toxicology within the U.S. EPA's
   Office of Research and Development, the Intramural Research Program of
   the National Institutes of Health (NIH) and National Institute of
   Environmental Health Sciences (NIEHS) [Z01 ES102345-04] and [Z01
   ES101744-04], and [U54 CA156735-02]. This manuscript has been subjected
   to review by the US Environmental Protection Agency, National Health and
   Environmental Effects Research Laboratory and approved for publication.
   Approval does not signify that the contents reflect the views of the
   Agency, nor does the mention of trade names or commercial products
   constitute endorsement or recommendation for use.
NR 79
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Z9 6
U1 4
U2 18
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1752-0509
J9 BMC SYST BIOL
JI BMC Syst. Biol.
PD NOV 4
PY 2013
VL 7
AR 119
DI 10.1186/1752-0509-7-119
PG 19
WC Mathematical & Computational Biology
SC Mathematical & Computational Biology
GA 259CH
UT WOS:000327504500001
PM 24188919
ER

PT J
AU Yucesoy, B
   Talzhanov, Y
   Johnson, VJ
   Wilson, NW
   Biagini, RE
   Wang, W
   Frye, B
   Weissman, DN
   Germolec, DR
   Luster, MI
   Barmada, MM
AF Yucesoy, Berran
   Talzhanov, Yerkebulan
   Johnson, Victor J.
   Wilson, Nevin W.
   Biagini, Raymond E.
   Wang, Wei
   Frye, Bonnie
   Weissman, David N.
   Germolec, Dori R.
   Luster, Michael I.
   Barmada, Michael M.
TI Genetic variants within the MHC region are associated with immune
   responsiveness to childhood vaccinations
SO VACCINE
LA English
DT Article
DE Major histocompatibility complex; Genetic polymorphism; Childhood
   vaccine; Immune response
ID HUMAN-LEUKOCYTE ANTIGEN; HEPATITIS-B-VACCINE; MEASLES-VACCINE; HLA-G;
   ANTIBODY-RESPONSE; SURFACE-ANTIGEN; NONRESPONSIVENESS; POLYMORPHISMS;
   HAPLOTYPES; VIRUS
AB The influence of genetic variability within the major histocompatibility complex (MHC) region on variations in immune responses to childhood vaccination was investigated. The study group consisted of 135 healthy infants who had been immunized with hepatitis B (HBV), 7-valent pneumococcal conjugate (PCV7), and diphtheria, tetanus, acellular pertussis (DTaP) vaccines according to standard childhood immunization schedules. Genotype analysis was performed on genomic DNA using Illumina Goldengate MHC panels (Mapping and Exon Centric). At the 1 year post vaccination check-up total, isotypic, and antigen-specific serum antibody levels were measured using multiplex immunoassays. A number of single nucleotide polymorphisms (SNPs) within MHC Class I and II genes were found to be associated with variations in the vaccine specific antibody responses and serum levels of immunoglobulins (IgG, IgM) and IgG isotypes (IgG1, IgG4) (all at p <0.001). Linkage disequilibrium patterns and functional annotations showed that significant SNPs were strongly correlated with other functional regulatory SNPs. These SNPs were found to regulate the expression of a group of genes involved in antigen processing and presentation including HLA-A, HLA-C, HLA-G, HLA-H, HLA-DRA, HLA-DRB1, HLA-DRB5, HLA-DQA1, HLA-DQB1, HLA-DOB, and TAP-2. The results suggest that genetic variations within particular MHC genes can influence immune response to common childhood vaccinations, which in turn may influence vaccine efficacy. Published by Elsevier Ltd.
C1 [Yucesoy, Berran; Wang, Wei; Frye, Bonnie] NIOSH, Toxicol & Mol Biol Branch, CDC, Morgantown, WV 26505 USA.
   [Talzhanov, Yerkebulan; Barmada, Michael M.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Human Genet, Pittsburgh, PA 15261 USA.
   [Johnson, Victor J.] BRT, Morrisville, NC USA.
   [Wilson, Nevin W.] Univ Nevada, Sch Med, Dept Pediat, Reno, NV 89557 USA.
   [Biagini, Raymond E.] NIOSH, Biomonitoring & Hlth Assessment Branch, CDC, Cincinnati, OH 45226 USA.
   [Weissman, David N.] NIOSH, Div Resp Dis Studies, CDC, Morgantown, WV 26505 USA.
   [Germolec, Dori R.] NIEHS, Toxicol Branch, DNTP, Res Triangle Pk, NC 27709 USA.
   [Luster, Michael I.] W Virginia Univ, Sch Publ Hlth, Morgantown, WV 26506 USA.
RP Yucesoy, B (reprint author), NIOSH, Toxicol & Mol Biol Branch, Hlth Effects Lab Div, 1095 Willowdale Rd, Morgantown, WV 26505 USA.
EM byucesoy@cdc.gov; yet5@pitt.edu; vjohnson@brt-labs.com;
   nwilson@medicine.nevada.edu; RBiagini@cdc.gov; WWang1@cdc.gov;
   BFrye@cdc.gov; DWeissman@cdc.gov; germolec@niehs.nih.gov;
   miklus22@comcast.net; barmada@pitt.edu
OI Barmada, M Michael/0000-0002-3604-6460
FU NIEHS [Y1-ES-0001]
FX This work was supported in part by an Interagency Agreement with the
   Intramural Research Program of the NIEHS (Y1-ES-0001).
NR 46
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U1 1
U2 7
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
EI 1873-2518
J9 VACCINE
JI Vaccine
PD NOV 4
PY 2013
VL 31
IS 46
BP 5381
EP 5391
DI 10.1016/j.vaccine.2013.09.026
PG 11
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 254NS
UT WOS:000327173000011
PM 24075919
ER

PT J
AU Sandrini, M
   Censor, N
   Mishoe, J
   Cohen, LG
AF Sandrini, Marco
   Censor, Nitzan
   Mishoe, Jonathan
   Cohen, Leonardo G.
TI Causal Role of Prefrontal Cortex in Strengthening of Episodic Memories
   through Reconsolidation
SO CURRENT BIOLOGY
LA English
DT Article
ID TRANSCRANIAL MAGNETIC STIMULATION; DECLARATIVE MEMORY;
   BRAIN-STIMULATION; RETRIEVAL; HUMANS; CONSOLIDATION; NEUROSCIENCE;
   INDIVIDUALS; DYNAMICS; IMPROVES
AB Memory consolidation is a dynamic process. Reactivation of consolidated memories triggers reconsolidation, a time-limited period during which memories can be modified [1-4]. Episodic memory refers to our ability to recall specific past events about what happened, including where and when [5]. However, it is unknown whether noninvasive stimulation of the neocortex during reconsolidation might strengthen existing episodic memories in humans. To modify these memories, we applied repetitive transcranial magnetic stimulation (rTMS) [6] over right lateral prefrontal cortex (PFC), a region involved in the reactivation of episodic memories [7, 8]. We report that rTMS of PFC after memory reactivation strengthened verbal episodic memories, an effect documented by improved recall 24 hr postreactivation compared to stimulation of PFC without reactivation and vertex (control site) after reactivation. In contrast, there was no effect of stimulation 1 hr postreactivation (control experiment), showing that memory strengthening is time dependent, consistent with the reconsolidation theory. Thus, we demonstrated that right lateral PFC plays a causal role in strengthening of episodic memories through reconsolidation in humans. Reconsolidation may serve as an opportunity to modify existing memories with noninvasive stimulation of a critical brain region, an issue of fundamental importance for memory research and clinical applications.
C1 [Sandrini, Marco; Censor, Nitzan; Mishoe, Jonathan; Cohen, Leonardo G.] NINDS, Human Cort Physiol & Stroke Neurorehabil Sect, Bethesda, MD 20892 USA.
   [Sandrini, Marco] Uniformed Serv Univ Hlth Sci, Ctr Neurosci & Regenerat Med, Bethesda, MD 20814 USA.
RP Sandrini, M (reprint author), NINDS, Human Cort Physiol & Stroke Neurorehabil Sect, Bethesda, MD 20892 USA.
EM marco.sandrini@nih.gov
RI Sandrini, Marco/J-2276-2014
OI Sandrini, Marco/0000-0002-1664-5722
FU Intramural Research Program of the NINDS, NIH; NINDS Ruth L. Kirschstein
   National Research Service Award (NRSA); Department of Defense in the
   Center for Neuroscience and Regenerative Medicine (CNRM)
FX This work was supported by the Intramural Research Program of the NINDS,
   NIH to J.M. and L.G.C., by an NINDS Ruth L. Kirschstein National
   Research Service Award (NRSA) to N.C., and by funding from Department of
   Defense in the Center for Neuroscience and Regenerative Medicine (CNRM)
   to M.S. We would like to thank Sook-Lei Liew for insightful comments and
   suggestions.
NR 23
TC 21
Z9 22
U1 3
U2 18
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0960-9822
EI 1879-0445
J9 CURR BIOL
JI Curr. Biol.
PD NOV 4
PY 2013
VL 23
IS 21
BP 2181
EP 2184
DI 10.1016/j.cub.2013.08.045
PG 4
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 252GR
UT WOS:000326993600031
PM 24206845
ER

PT J
AU Ozdemir, B
   Abd-Almageed, W
   Roessler, S
   Wang, XW
AF Ozdemir, Bahadir
   Abd-Almageed, Wael
   Roessler, Stephanie
   Wang, Xin Wei
TI iSubgraph: Integrative Genomics for Subgroup Discovery in Hepatocellular
   Carcinoma Using Graph Mining and Mixture Models
SO PLOS ONE
LA English
DT Article
ID REGULATORY MODULES; SYSTEMS BIOLOGY; MICRORNA TARGETS; PREDICTION;
   GENES; CLASSIFICATION; IDENTIFICATION; CANCER
AB The high tumor heterogeneity makes it very challenging to identify key tumorigenic pathways as therapeutic targets. The integration of multiple omics data is a promising approach to identify driving regulatory networks in patient subgroups. Here, we propose a novel conceptual framework to discover patterns of miRNA-gene networks, observed frequently up-or down-regulated in a group of patients and to use such networks for patient stratification in hepatocellular carcinoma (HCC). We developed an integrative subgraph mining approach, called iSubgraph, and identified altered regulatory networks frequently observed in HCC patients. The miRNA and gene expression profiles were jointly analyzed in a graph structure. We defined a method to transform microarray data into graph representation that encodes miRNA and gene expression levels and the interactions between them as well. The iSubgraph algorithm was capable to detect cooperative regulation of miRNAs and genes even if it occurred only in some patients. Next, the miRNA-mRNA modules were used in an unsupervised class prediction model to discover HCC subgroups via patient clustering by mixture models. The robustness analysis of the mixture model showed that the class predictions are highly stable. Moreover, the Kaplan-Meier survival analysis revealed that the HCC subgroups identified by the algorithm have different survival characteristics. The pathway analyses of the miRNA-mRNA co-modules identified by the algorithm demonstrate key roles of Myc, E2F1, let-7, TGFB1, TNF and EGFR in HCC subgroups. Thus, our method can integrate various omics data derived from different platforms and with different dynamic scales to better define molecular tumor subtypes. iSubgraph is available as MATLAB code at http://www.cs.umd.edu/similar to ozdemir/isubgraph/.
C1 [Ozdemir, Bahadir] Univ Maryland, Dept Comp Sci, College Pk, MD 20742 USA.
   [Ozdemir, Bahadir; Roessler, Stephanie; Wang, Xin Wei] Natl Canc Inst, Ctr Canc Res, Human Carcinogenesis Lab, Liver Carcinogenesis Sect, Bethesda, MD USA.
   [Abd-Almageed, Wael] Univ Maryland, Inst Adv Comp Studies, College Pk, MD 20742 USA.
   [Roessler, Stephanie] Univ Heidelberg Hosp, Inst Pathol, Heidelberg, Germany.
RP Roessler, S (reprint author), Natl Canc Inst, Ctr Canc Res, Human Carcinogenesis Lab, Liver Carcinogenesis Sect, Bethesda, MD USA.
EM stephanie.roessler@med.uni-heidelberg.de; xw3u@nih.gov
RI Wang, Xin/B-6162-2009
FU UMD-NCI Partnership for Cancer Technology; Intramural Research Program
   of the Center for Cancer Research, the National Cancer Institute [Z01-BC
   010313]
FX B.O. was supported by the UMD-NCI Partnership for Cancer Technology.
   This work was supported in part by grants (Z01-BC 010313) from the
   Intramural Research Program of the Center for Cancer Research, the
   National Cancer Institute. The funders had no role in study design, data
   collection and analysis, decision to publish, or preparation of the
   manuscript.
NR 40
TC 1
Z9 1
U1 0
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 4
PY 2013
VL 8
IS 11
AR e78624
DI 10.1371/journal.pone.0078624
PG 16
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 245ZC
UT WOS:000326503400079
PM 24223834
ER

PT J
AU Simpson, CL
   Wojciechowski, R
   Yee, SS
   Soni, P
   Bailey-Wilson, JE
   Stambolian, D
AF Simpson, Claire L.
   Wojciechowski, Robert
   Yee, Stephanie S.
   Soni, Poorva
   Bailey-Wilson, Joan E.
   Stambolian, Dwight
TI Regional replication of association with refractive error on 15q14 and
   15q25 in the Age-Related Eye Disease Study cohort
SO MOLECULAR VISION
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; HIGH-DOSE SUPPLEMENTATION;
   LINKAGE-DISEQUILIBRIUM; SUSCEPTIBILITY LOCUS; GENETIC ASSOCIATION;
   CLINICAL-TRIAL; BETA-CAROTENE; VISION LOSS; VITAMIN-C; MYOPIA
AB Purpose: Refractive error is a complex trait with multiple genetic and environmental risk factors, and is the most common cause of preventable blindness worldwide. The common nature of the trait suggests the presence of many genetic factors that individually may have modest effects. To achieve an adequate sample size to detect these common variants, large, international collaborations have formed. These consortia typically use meta-analysis to combine multiple studies from many different populations. This approach is robust to differences between populations; however, it does not compensate for the different haplotypes in each genetic background evidenced by different alleles in linkage disequilibrium with the causative variant. We used the Age-Related Eye Disease Study (AREDS) cohort to replicate published significant associations at two loci on chromosome 15 from two genome-wide association studies (GWASs). The single nucleotide polymorphisms (SNPs) that exhibited association on chromosome 15 in the original studies did not show evidence of association with refractive error in the AREDS cohort. This paper seeks to determine whether the non-replication in this AREDS sample may be due to the limited number of SNPs chosen for replication.
   Methods: We selected all SNPs genotyped on the Illumina Omni2.5v1_B array or custom TaqMan assays or imputed from the GWAS data, in the region surrounding the SNPs from the Consortium for Refractive Error and Myopia study. We analyzed the SNPs for association with refractive error using standard regression methods in PLINK. The effective number of tests was calculated using the Genetic Type I Error Calculator.
   Results: Although use of the same SNPs used in the Consortium for Refractive Error and Myopia study did not show any evidence of association with refractive error in this AREDS sample, other SNPs within the candidate regions demonstrated an association with refractive error. Significant evidence of association was found using the hyperopia categorical trait, with the most significant SNPs rs1357179 on 15q14 (p=1.69x10(-3)) and rs7164400 on 15q25 (p=8.39x10(-4)), which passed the replication thresholds.
   Conclusions: This study adds to the growing body of evidence that attempting to replicate the most significant SNPs found in one population may not be significant in another population due to differences in the linkage disequilibrium structure and/or allele frequency. This suggests that replication studies should include less significant SNPs in an associated region rather than only a few selected SNPs chosen by a significance threshold.
C1 [Simpson, Claire L.; Wojciechowski, Robert; Bailey-Wilson, Joan E.] NHGRI, Inherited Dis Res Branch, NIH, Baltimore, MD USA.
   [Wojciechowski, Robert] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
   [Yee, Stephanie S.; Soni, Poorva; Stambolian, Dwight] Univ Penn, Dept Ophthalmol, Philadelphia, PA 19104 USA.
RP Bailey-Wilson, JE (reprint author), NHGRI, Inherited Dis Res Branch, NIH, Baltimore, MD USA.
EM jebw@mail.nih.gov
OI Bailey-Wilson, Joan/0000-0002-9153-2920; Wojciechowski,
   Robert/0000-0002-9593-4652
FU NEI [R01EY020483, 1K08EY022943]; National Human Genome Research
   Institute, National Institutes of Health
FX This work was supported in part by NEI R01EY020483 (DS), NEI
   1K08EY022943 (RW) and by the intramural program of the National Human
   Genome Research Institute, National Institutes of Health. DS and JEBW
   planned the study and obtained funding for the study. DS, JEBW and RW
   chose the SNPs to be genotyped. SSY, PS and DS performed the Taqman
   genotyping. CLS, RW and JEBW performed data quality control and
   statistical analysis. CLS, DS, JEBW and RS contributed to interpretation
   of the results. All authors contributed to and commented on the final
   manuscript.
NR 41
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U1 1
U2 2
PU MOLECULAR VISION
PI ATLANTA
PA C/O JEFF BOATRIGHT, LAB B, 5500 EMORY EYE CENTER, 1327 CLIFTON RD, N E,
   ATLANTA, GA 30322 USA
SN 1090-0535
J9 MOL VIS
JI Mol. Vis.
PD NOV 2
PY 2013
VL 19
BP 2173
EP 2186
PG 14
WC Biochemistry & Molecular Biology; Ophthalmology
SC Biochemistry & Molecular Biology; Ophthalmology
GA 272LK
UT WOS:000328461900001
PM 24227913
ER

PT J
AU Fauci, AS
   Marston, HD
AF Fauci, Anthony S.
   Marston, Hilary D.
TI Achieving an AIDS-free world: science and implementation
SO LANCET
LA English
DT Editorial Material
ID HIV-1 INFECTION; PREVENTION; ANTIBODIES; THERAPY; VACCINE
C1 [Fauci, Anthony S.; Marston, Hilary D.] NIAID, NIH, Bethesda, MD 20892 USA.
RP Fauci, AS (reprint author), NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM afauci@niaid.nih.gov
NR 12
TC 8
Z9 8
U1 0
U2 13
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0140-6736
EI 1474-547X
J9 LANCET
JI Lancet
PD NOV 2
PY 2013
VL 382
IS 9903
BP 1461
EP 1462
DI 10.1016/S0140-6736(13)62042-5
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 247MR
UT WOS:000326622500004
PM 24152937
ER

PT J
AU Fujimoto, J
   Wistuba, II
   Moon, J
   Kalemkerian, G
   Redman, M
   Stewart, DJ
   Ivy, P
   Gandara, D
   Tsao, A
AF Fujimoto, Junya
   Wistuba, Ignacio I.
   Moon, James
   Kalemkerian, Gregory
   Redman, Mary
   Stewart, David J.
   Ivy, Percy
   Gandara, David
   Tsao, Anne
TI BIOMARKER RESULTS FROM A PHASE I STUDY OF CEDIRANIB (NSC #732208) IN
   COMBINATION WITH CISPLATIN AND PEMETREXED IN CHEMONAIVE PATIENTS WITH
   MALIGNANT PLEURAL MESOTHELIOMA (SWOG S0905)
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Meeting Abstract
DE PDGFR; VEGFR; S0905 biomarkers; mesothelioma
C1 [Fujimoto, Junya; Wistuba, Ignacio I.; Tsao, Anne] Univ Texas MD Anderson Canc Ctr, Houston, TX USA.
   [Moon, James; Redman, Mary] Swog Stat Ctr, Aurora, CO USA.
   [Kalemkerian, Gregory] Univ Michigan, Ann Arbor, MI 48109 USA.
   [Stewart, David J.] Univ Ottawa, Ottawa, ON K1N 6N5, Canada.
   [Ivy, Percy] NCI, Bethesda, MD 20892 USA.
   [Gandara, David] Univ Calif Davis Canc Ctr, Div Hematol Oncol, Sacramento, CA USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
EI 1556-1380
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD NOV
PY 2013
VL 8
SU 2
MA P1.14-009
BP S642
EP S642
PG 1
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA AM1RE
UT WOS:000339624903070
ER

PT J
AU Gomez, SL
   Cheng, I
   Gali, K
   Patel, MI
   Haile, R
   Noone, AM
   Wakelee, H
AF Gomez, Scarlett Lin
   Cheng, Iona
   Gali, Kathleen
   Patel, Manali I.
   Haile, Robert
   Noone, Anne-Michelle
   Wakelee, Heather
TI LUNG CANCER INCIDENCE TRENDS AMONG ASIAN-AMERICAN ETHNIC POPULATIONS IN
   THE UNITED STATES, 1990-2010
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Meeting Abstract
DE lung cancer; incidence trends; Asian-Americans
C1 [Gomez, Scarlett Lin; Cheng, Iona; Gali, Kathleen] Canc Prevent Inst Calif, Fremont, CA USA.
   [Patel, Manali I.; Haile, Robert; Wakelee, Heather] Stanford Univ, Stanford, CA 94305 USA.
   [Noone, Anne-Michelle] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
EI 1556-1380
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD NOV
PY 2013
VL 8
SU 2
MA O24.03
BP S233
EP S233
PG 1
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA AM1RE
UT WOS:000339624901043
ER

PT J
AU Hassan, R
   Miller, A
   Sharon, E
   Thomas, A
   Reynolds, JC
   Ling, A
   Kreitman, RJ
   Steinberg, S
   Fowler, DH
   Pastan, I
AF Hassan, Raffit
   Miller, Andrew
   Sharon, Elad
   Thomas, Anish
   Reynolds, James C.
   Ling, Alexander
   Kreitman, Robert J.
   Steinberg, Seth
   Fowler, Daniel H.
   Pastan, Ira
TI DURABLE CANCER REGRESSIONS IN CHEMOTHERAPY REFRACTORY MESOTHELIOMA
   PATIENTS WITH THE ANTI-MESOTHELIN IMMUNOTOXIN SS1P AND HOST IMMUNE
   DEPLETION WITH PENTOSTATIN (P) AND CYCLOPHOSPHAMIDE (C)
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Meeting Abstract
DE mesothelioma; Immunotoxin; Major tumor regressions; Neutralizing
   antibody
C1 [Hassan, Raffit; Miller, Andrew; Sharon, Elad; Thomas, Anish; Reynolds, James C.; Ling, Alexander; Kreitman, Robert J.; Steinberg, Seth; Fowler, Daniel H.; Pastan, Ira] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
EI 1556-1380
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD NOV
PY 2013
VL 8
SU 2
MA O22.03
BP S225
EP S225
PG 1
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA AM1RE
UT WOS:000339624901031
ER

PT J
AU Maltzman, JD
   Wallin, BA
   Gupta, A
   Wustner, J
   Hassan, R
AF Maltzman, Julia D.
   Wallin, Bruce A.
   Gupta, Anubha
   Wustner, Jason
   Hassan, Raffit
TI EXPOSURE-RESPONSE RELATIONSHIP OF AMATUXIMAB (AMA) IN COMBINATION WITH
   PEMETREXED AND CISPLATIN (P/C) IN PATIENTS WITH UNRESECTABLE PLEURAL
   MESOTHELIOMA
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Meeting Abstract
C1 [Maltzman, Julia D.; Wallin, Bruce A.; Wustner, Jason] Morphotek Inc, Clin Dev, Exton, PA USA.
   [Gupta, Anubha] Eisai & Co Ltd, Tokyo, Japan.
   [Hassan, Raffit] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
EI 1556-1380
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD NOV
PY 2013
VL 8
SU 2
MA O22.05
BP S226
EP S226
PG 1
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA AM1RE
UT WOS:000339624901032
ER

PT J
AU Pikor, L
   Lockwood, WW
   Thu, KL
   Vucic, EA
   Chari, R
   Gazdar, AF
   Lam, S
   Lam, WL
AF Pikor, Larissa
   Lockwood, William W.
   Thu, Kelsie L.
   Vucic, Emily A.
   Chari, Raj
   Gazdar, Adi F.
   Lam, Stephen
   Lam, Wan L.
TI AMPLIFICATION OF YEATS4, A NOVEL ONCOGENE IN NSCLC, INHIBITS THE P53
   PATHWAY AND INCREASES RESISTANCE TO CISPLATIN
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Meeting Abstract
DE p53 pathway; Integrative analysis; oncogene; YEATS4
C1 [Pikor, Larissa; Thu, Kelsie L.; Vucic, Emily A.; Lam, Stephen; Lam, Wan L.] BC Canc Res Ctr, Vancouver, BC, Canada.
   [Lockwood, William W.] NIH, Natl Human Genome Res Unit, Bethesda, MD USA.
   [Chari, Raj] Harvard Univ, Sch Med, Dept Genet, Cambridge, MA 02138 USA.
   [Gazdar, Adi F.] Univ Texas SW Med Ctr Dallas, Hamon Ctr Therapeut Oncol Res, Dallas, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
EI 1556-1380
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD NOV
PY 2013
VL 8
SU 2
MA MO15.09
BP S351
EP S351
PG 1
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA AM1RE
UT WOS:000339624901222
ER

PT J
AU Szabo, E
AF Szabo, Eva
TI STUDY DESIGN AND RESPONSE ASSESSMENT IN CHEMOPREVENTION TRIALS
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Meeting Abstract
DE atypical adenomatous hyperplasia; chemoprevention; bronchial dysplasia
C1 [Szabo, Eva] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
EI 1556-1380
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD NOV
PY 2013
VL 8
SU 2
MA E09.3
BP S28
EP S28
PG 1
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA AM1RE
UT WOS:000339624900033
ER

PT J
AU Thomas, A
   Rajan, A
   Berman, A
   Scepura, B
   Brzezniak, C
   Carter, CA
   Guha, U
   Wang, YS
   Szabo, E
   Loehrer, PJ
   Giaccone, G
AF Thomas, Anish
   Rajan, Arun
   Berman, Arlene
   Scepura, Barbara
   Brzezniak, Christina
   Carter, Corey A.
   Guha, Udayan
   Wang, Yisong
   Szabo, Eva
   Loehrer, Patrick J.
   Giaccone, Giuseppe
TI CLINICAL ACTIVITY OF SUNITINIB IN PATIENTS WITH THYMIC CARCINOMA
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Meeting Abstract
DE thymoma; Thymic carcinoma; Sunitinib; anti-angiogenesis
C1 [Thomas, Anish; Rajan, Arun; Berman, Arlene; Scepura, Barbara; Guha, Udayan; Wang, Yisong; Szabo, Eva] NCI, Bethesda, MD 20892 USA.
   [Brzezniak, Christina; Carter, Corey A.] Walter Reed Natl Mil Med Ctr, John P Murtha Canc Ctr, Bethesda, MD USA.
   [Loehrer, Patrick J.] Indiana Univ, Simon Canc Ctr, Bloomington, IN 47405 USA.
   [Giaccone, Giuseppe] Georgetown Univ, Lombardi Comprehens Canc Ctr, Washington, DC 20057 USA.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
EI 1556-1380
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD NOV
PY 2013
VL 8
SU 2
MA MO03.07
BP S268
EP S269
PG 2
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA AM1RE
UT WOS:000339624901099
ER

PT J
AU Travis, W
   Wilkerson, M
   Rekhtman, N
   Cheney, R
   Clarke, B
   Dacic, S
   Duhig, E
   Farver, C
   Funkhouser, WK
   Illei, P
   Sica, G
   Suh, J
   Tsao, MS
AF Travis, William
   Wilkerson, Matthew
   Rekhtman, Natasha
   Cheney, Richard
   Clarke, Belinda
   Dacic, Sanja
   Duhig, Edwina
   Farver, Carol
   Funkhouser, William K.
   Illei, Peter
   Sica, Gabriel
   Suh, James
   Tsao, Ming S.
CA Tcga Canc Genome Atlas Res Network
TI CORRELATING HISTOLOGIC AND MOLECULAR FEATURES IN THE LUNG ADENOCARCINOMA
   TCGA PROJECT
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Meeting Abstract
DE Lung cancer; genetics; Adenocarcinoma; histologic classification
C1 [Travis, William; Rekhtman, Natasha] Mem Sloan Kettering Canc Ctr, New York, NY USA.
   [Wilkerson, Matthew] Lineberger Comprehens Canc Ctr, Chapel Hill, NC USA.
   [Cheney, Richard] Roswell Pk Canc Inst, New York, NY USA.
   [Clarke, Belinda] Prince Charles Hosp, Dept Pathol, Chermside, Qld, Australia.
   [Dacic, Sanja] Univ Pittsburgh, Dept Pathol, Pittsburgh, PA 15260 USA.
   [Duhig, Edwina] Sullivan Nicolaides Pathol, Brisbane, Qld, Australia.
   [Farver, Carol] Cleveland Clin, Dept Pathol, Cleveland, OH USA.
   [Funkhouser, William K.] Univ N Carolina, Dept Pathol, Chapel Hill, NC 27515 USA.
   [Illei, Peter] Johns Hopkins, Dept Pathol, Baltimore, MD USA.
   [Sica, Gabriel] Emory Univ, Dept Pathol, Atlanta, GA 30322 USA.
   [Suh, James] NYU, Dept Pathol, New York, NY 10003 USA.
   [Tsao, Ming S.] Princess Margaret Canc Ctr, Dept Pathol, Toronto, ON, Canada.
   [Tcga Canc Genome Atlas Res Network] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
EI 1556-1380
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD NOV
PY 2013
VL 8
SU 2
MA P2.18-007
BP S957
EP S958
PG 2
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA AM1RE
UT WOS:000339624904276
ER

PT J
AU Xi, SC
   Shan, JG
   Guo, HL
   Xu, H
   Xiao, ZX
   Kunst, TF
   Mercedes, L
   Hong, JA
   Zhang, M
   Schrump, DS
AF Xi, Sichuan
   Shan, Jigui
   Guo, Hongliang
   Xu, Hong
   Xiao, Zuoxiang
   Kunst, Tricia F.
   Mercedes, Leandro
   Hong, Julie A.
   Zhang, Mary
   Schrump, David S.
TI LONG NON-CODING RNA BC070487 REPRESSES THE NOVEL TUMOR SUPPRESSOR GENE
   ZNFX1 DURING TOBACCO-INDUCED HUMAN PULMONARY CARCINOGENESIS
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Meeting Abstract
DE Lung cancer; Cigarette smoke; long non-coding RNA; epigenetics
C1 [Xi, Sichuan; Kunst, Tricia F.; Mercedes, Leandro; Hong, Julie A.; Zhang, Mary; Schrump, David S.] NCI, Thorac Oncol Sect, Surg Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Shan, Jigui] NCI, Adv Biomed Comp Ctr, Bethesda, MD 20892 USA.
   [Guo, Hongliang] Shandong Tumor Hosp & Inst, Jinan, Peoples R China.
   [Xu, Hong] NCI, Lab Canc Prevent, Bethesda, MD 20892 USA.
   [Xiao, Zuoxiang] NCI, Canc & Inflammat Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
EI 1556-1380
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD NOV
PY 2013
VL 8
SU 2
MA P2.02-012
BP S755
EP S755
PG 1
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA AM1RE
UT WOS:000339624903267
ER

PT J
AU Ahmed, MM
   Hodge, JW
   Guha, C
   Bernhard, EJ
   Vikram, B
   Coleman, CN
AF Ahmed, Mansoor M.
   Hodge, James W.
   Guha, Chandan
   Bernhard, Eric J.
   Vikram, Bhadrasain
   Coleman, C. Norman
TI Harnessing the Potential of Radiation-Induced Immune Modulation for
   Cancer Therapy
SO CANCER IMMUNOLOGY RESEARCH
LA English
DT Article
ID CYTOTOXIC T-LYMPHOCYTES; METASTATIC LUNG-CANCER; DENDRITIC CELLS;
   CROSS-PRESENTATION; TUMOR-CELLS; ANTIGENS; IMMUNOGENICITY;
   IMMUNOTHERAPY; CHEMOTHERAPY; RADIOTHERAPY
AB The conventional use of radiotherapy is for local tumor control. Radiotherapy of the primary tumor can prevent the development of distant metastases, but this modality is generally not effective for treating preexisting systemic disease. However, radiation-induced tumor destruction may be considered a novel strategy for in situ cancer vaccination, in which tumor antigens released from dying tumor cells may be presented in an immunostimulatory context. Moreover, radiation has been demonstrated to induce immunogenic modulation in various tumor types by altering the biology of surviving cells to render them more susceptible to T cell-mediated killing. Finally, radiotherapy typically has a favorable toxicity profile and is associated with the absence of systemic immunosuppression. Together, these properties suggest that radiotherapy may serve as an important component of combinatorial immunotherapies aimed at augmenting systemic antitumor immunity. Here, we provide an overview of the radiation-induced modulations of the immune system that may be harnessed for cancer therapy. (C) 2013 AACR.
C1 [Ahmed, Mansoor M.; Bernhard, Eric J.; Vikram, Bhadrasain; Coleman, C. Norman] NCI, Radiat Res Program, Div Canc Treatment & Diag, NIH, Rockville, MD 20850 USA.
   [Hodge, James W.] NCI, Recombinant Vaccine Grp, Lab Tumor Immunol & Biol, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
   [Guha, Chandan] Albert Einstein Coll Med, Montefiore Med Ctr, Dept Radiat Oncol, Bronx, NY 10467 USA.
RP Ahmed, MM (reprint author), NCI, Radiotherapy Dev Branch, Radiat Res Program, Div Canc Treatment & Diag,NIH, 9609 Med Ctr Dr,Room 3W224, Rockville, MD 20850 USA.
EM ahmedmm@mail.nih.gov
RI Hodge, James/D-5518-2015
OI Hodge, James/0000-0001-5282-3154
NR 29
TC 14
Z9 14
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2326-6066
EI 2326-6074
J9 CANCER IMMUNOL RES
JI Cancer Immunol. Res.
PD NOV
PY 2013
VL 1
IS 5
BP 280
EP 284
DI 10.1158/2326-6066.CIR-13-0141
PG 5
WC Oncology; Immunology
SC Oncology; Immunology
GA AM7FO
UT WOS:000340030400002
PM 24777964
ER

PT J
AU Purcell, RH
AF Purcell, Robert H.
TI Impact
SO NATIONAL MEDICAL JOURNAL OF INDIA
LA English
DT Editorial Material
ID NON-B HEPATITIS; NON-A; VIRUS; EPIDEMIC; INDIA
C1 NIAID, Hepatitis Viruses Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Purcell, RH (reprint author), NIAID, Hepatitis Viruses Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
NR 8
TC 0
Z9 0
U1 0
U2 0
PU ALL INDIA INST MEDICAL SCIENCES
PI NEW DELHI
PA ANSARI NAGAR, NEW DELHI 110 029, INDIA
SN 0970-258X
J9 NATL MED J INDIA
JI Natl. Med. J. India
PD NOV-DEC
PY 2013
VL 26
IS 6
BP 378
EP 379
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA AN1DK
UT WOS:000340322700018
PM 25141380
ER

PT J
AU Farooqui, MZH
   Wiestner, A
AF Farooqui, Mohammed Z. H.
   Wiestner, Adrian
TI Ibrutinib for the treatment of chronic lymphocytic leukemia
SO EXPERT OPINION ON ORPHAN DRUGS
LA English
DT Article
DE B-cell receptor; Bruton's tyrosine kinase; chronic lymphocytic leukemia;
   ibrutinib; kinase; microenvironment; PCI-32765; targeted therapy
ID B-CELL RECEPTOR; PHASE-II; TUMOR PROLIFERATION; THERAPEUTIC TARGET;
   SIGNALING PATHWAYS; ANTITUMOR-ACTIVITY; ANTIGEN RECEPTORS; T-CELLS;
   LENALIDOMIDE; ACTIVATION
AB Introduction: Chemoimmunotherapy has improved response rates and overall survival (OS) in patients with chronic lymphocytic leukemia (CLL). Despite these advances, CLL remains an incurable disease outside of stem cell transplantation. B-cell receptor (BCR) signaling is a pivotal pathway in the pathogenesis of CLL by promoting survival and proliferation of CLL cells. Bruton's tyrosine kinase (BTK) is essential for BCR signaling and can be irreversibly inhibited by ibrutinib (PCI 32765).
   Areas covered: The clinical presentation and current treatment of CLL are briefly reviewed before focusing on the role of BCR signaling in the pathogenesis of CLL. The development of ibrutinib and the preclinical and clinical experience with this targeted agent in CLL are discussed.
   Expert opinion: Ibrutinib and other kinase inhibitors targeting BCR signaling are heralding a new era in the treatment of CLL. Efficacy and tolerability of ibrutinib are equally impressive and make it the most active monotherapy in CLL. Ibrutinib does not appear to increase the risk of infections, and the development of drug resistance is uncommon, providing a foundation for possible long-term therapy with this agent. Treatment goals and strategies will become more evident as we learn more about duration of response, mechanisms of resistance, tolerability of chronic use, and results with combination therapies.
C1 [Farooqui, Mohammed Z. H.; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Wiestner, A (reprint author), NHLBI, Hematol Branch, NIH, Bld 10,CRC 3-5140,10 Ctr Dr, Bethesda, MD 20892 USA.
EM wiestnera@mail.nih.gov
FU Intramural Research Program of the National, Heart, Lung and Blood
   Institute
FX The authors' work and research was funded through the Intramural
   Research Program of the National, Heart, Lung and Blood Institute.
NR 90
TC 1
Z9 1
U1 1
U2 6
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 2167-8707
J9 EXPERT OPIN ORPHAN D
JI Exp. Opin. Orphan Drugs
PD NOV
PY 2013
VL 1
IS 11
BP 925
EP 933
DI 10.1517/21678707.2013.850413
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA AK2FK
UT WOS:000338234300008
ER

PT J
AU Pazmino, P
AF Pazmino, Patricio
TI Renal risk stratification with the new oral anticoagulantss
SO CLEVELAND CLINIC JOURNAL OF MEDICINE
LA English
DT Letter
ID ATRIAL-FIBRILLATION; DABIGATRAN; MANAGEMENT
C1 Nephrol Internal Med & Hypertens NIH Ctr, El Paso, TX 79902 USA.
RP Pazmino, P (reprint author), Nephrol Internal Med & Hypertens NIH Ctr, El Paso, TX 79902 USA.
NR 8
TC 1
Z9 1
U1 0
U2 0
PU CLEVELAND CLINIC
PI CLEVELAND
PA 9500 EUCLID AVE, CLEVELAND, OH 44106 USA
SN 0891-1150
EI 1939-2869
J9 CLEV CLIN J MED
JI Clevel. Clin. J. Med.
PD NOV
PY 2013
VL 80
IS 11
BP 733
EP 734
DI 10.3949/ccjm.80c.11001
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA AI2ZO
UT WOS:000336727900009
PM 24186892
ER

PT J
AU Krishnamurthi, RV
   Feigin, VL
   Forouzanfar, MH
   Mensah, GA
   Connor, M
   Bennett, DA
   Moran, AE
   Sacco, RL
   Anderson, LM
   Truelsen, T
   O'Donnell, M
   Venketasubramanian, N
   Barker-Collo, S
   Lawes, CMM
   Wang, WZ
   Shinohara, Y
   Witt, E
   Ezzati, M
   Naghavi, M
   Murray, C
AF Krishnamurthi, Rita V.
   Feigin, Valery L.
   Forouzanfar, Mohammad H.
   Mensah, George A.
   Connor, Myles
   Bennett, Derrick A.
   Moran, Andrew E.
   Sacco, Ralph L.
   Anderson, Laurie M.
   Truelsen, Thomas
   O'Donnell, Martin
   Venketasubramanian, Narayanaswamy
   Barker-Collo, Suzanne
   Lawes, Carlene M. M.
   Wang, Wenzhi
   Shinohara, Yukito
   Witt, Emma
   Ezzati, Majid
   Naghavi, Mohsen
   Murray, Christopher
CA Global Burden Dis
   Risk Factors Study 2010 GBD 2010
   Gbd Stroke Experts Grp
TI Global and regional burden of first-ever ischaemic and haemorrhagic
   stroke during 1990-2010: findings from the Global Burden of Disease
   Study 2010
SO LANCET GLOBAL HEALTH
LA English
DT Article
ID MIDDLE-INCOME COUNTRIES; EPIDEMIOLOGIC TRANSITION;
   CARDIOVASCULAR-DISEASES; SYSTEMATIC ANALYSIS; RISK-FACTORS; PREVENTION;
   MORTALITY; HEALTH; TRENDS; CHINA
AB Background The burden of ischaemic and haemorrhagic stroke varies between regions and over time. With differences in prognosis, prevalence of risk factors, and treatment strategies, knowledge of stroke pathological type is important for targeted region-specific health-care planning for stroke and could inform priorities for type-specific prevention strategies. We used data from the Global Burden of Diseases, Injuries, and Risk Factors Study 2010 (GBD 2010) to estimate the global and regional burden of first-ever ischaemic and haemorrhagic stroke during 1990-2010.
   Methods We searched Medline, Embase, LILACS, Scopus, PubMed, Science Direct, Global Health Database, the WHO library, and regional databases from 1990 to 2012 to identify relevant studies published between 1990 and 2010. We applied the GBD 2010 analytical technique (DisMod-MR) to calculate regional and country-specific estimates for ischaemic and haemorrhagic stroke incidence, mortality, mortality-to-incidence ratio, and disability-adjusted life-years (DALYs) lost, by age group (aged <75 years, >= 75 years, and in total) and country income level (high-income and low-income and middle-income) for 1990, 2005, and 2010.
   Findings We included 119 studies (58 from high-income countries and 61 from low-income and middle-income countries). Worldwide, the burden of ischaemic and haemorrhagic stroke increased significantly between 1990 and 2010 in terms of the absolute number of people with incident ischaemic and haemorrhagic stroke (37% and 47% increase, respectively), number of deaths (21% and 20% increase), and DALYs lost (18% and 14% increase). In the past two decades in high-income countries, incidence of ischaemic stroke reduced significantly by 13% (95% CI 6-18), mortality by 37% (19-39), DALYs lost by 34% (16-36), and mortality-to-incidence ratios by 21% (10-27). For haemorrhagic stroke, incidence reduced significantly by 19% (1-15), mortality by 38% (32-43), DALYs lost by 39% (32-44), and mortality-to-incidence ratios by 27% (19-35). By contrast, in low-income and middle-income countries, we noted a significant increase of 22% (5-30) in incidence of haemorrhagic stroke and a 6% (-7 to 18) non-significant increase in the incidence of ischaemic stroke. Mortality rates for ischaemic stroke fell by 14% (9-19), DALYs lost by 17% (-11 to 21%), and mortality-to-incidence ratios by 16% (-12 to 22). For haemorrhagic stroke in low-income and middle-income countries, mortality rates reduced by 23% (-18 to 25%), DALYs lost by 25% (-21 to 28), and mortality-to-incidence ratios by 36% (-34 to 28).
   Interpretation Although age-standardised mortality rates for ischaemic and haemorrhagic stroke have decreased in the past two decades, the absolute number of people who have these stroke types annually, and the number with related deaths and DALYs lost, is increasing, with most of the burden in low-income and middle-income countries. Further study is needed in these countries to identify which subgroups of the population are at greatest risk and who could be targeted for preventive efforts.
C1 [Krishnamurthi, Rita V.; Feigin, Valery L.; Witt, Emma] Auckland Univ Technol, Fac Hlth & Environm Studies, Natl Inst Stroke & Appl Neurosci, Auckland, New Zealand.
   [Forouzanfar, Mohammad H.; Naghavi, Mohsen; Murray, Christopher] Univ Washington, Dept Global Hlth, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
   [Mensah, George A.] NIH, NHLBI, Bethesda, MD 20892 USA.
   [Connor, Myles] Natl Hlth Serv Borders, Melrose, MA USA.
   [Connor, Myles] Univ Edinburgh, Div Clin Neurosci, Edinburgh EH8 9YL, Midlothian, Scotland.
   [Connor, Myles] Univ St Andrews, Bute Med Sch, St Andrews KY16 9AJ, Fife, Scotland.
   [Connor, Myles] Univ Witwatersrand, Sch Publ Hlth, ZA-2050 Johannesburg, South Africa.
   [Bennett, Derrick A.] Univ Oxford, Nuffield Dept Populat Hlth, Clin Trial Serv Unit, Oxford, England.
   [Bennett, Derrick A.] Univ Oxford, Nuffield Dept Populat Hlth, Epidemiol Studies Unit, Oxford, England.
   [Moran, Andrew E.] Columbia Univ, Med Ctr, Div Gen Med, New York, NY 10027 USA.
   [Sacco, Ralph L.] Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
   [Anderson, Laurie M.] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA.
   [Anderson, Laurie M.] Washington State Inst Publ Policy, Olympia, WA USA.
   [Truelsen, Thomas] Univ Copenhagen, Herlev Hosp, Dept Neurol, DK-2730 Herlev, Denmark.
   [Ezzati, Majid] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, Dept Epidemiol & Biostat, MRC HPA Ctr Environm & Hlth, London, England.
   [O'Donnell, Martin] Univ Ireland, Galway, Ireland.
   [Venketasubramanian, Narayanaswamy] Natl Univ Singapore, Yong Loo Lin Sch Med, Univ Med Cluster, Div Neurol, Singapore 117595, Singapore.
   [Venketasubramanian, Narayanaswamy] Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore 117595, Singapore.
   [Barker-Collo, Suzanne] Univ Auckland, Sch Psychol, Auckland 1, New Zealand.
   [Lawes, Carlene M. M.] Univ Auckland, Natl Inst Hlth Innovat, Auckland 1, New Zealand.
   [Wang, Wenzhi] Beijing Neurosurg Inst, Beijing, Peoples R China.
   [Shinohara, Yukito] Tachikawa Hosp, Federat Natl Publ Serv Personnel Mutual Aid Assoc, Tachikawa, Tokyo, Japan.
RP Feigin, VL (reprint author), Auckland Univ Technol Univ, Fac Hlth & Environm Studies, Sch Publ Hlth & Psychosocial Studies, Sch Rehabil & Occupat Studies,Natl Inst Stroke &, Auckland 1142, New Zealand.
EM valery.feigin@aut.ac.nz
FU Bill & Melinda Gates Foundation
FX Funding Bill & Melinda Gates Foundation.
NR 29
TC 163
Z9 164
U1 9
U2 27
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 2214-109X
J9 LANCET GLOB HEALTH
JI Lancet Glob. Health
PD NOV
PY 2013
VL 1
IS 5
BP E259
EP E281
DI 10.1016/S0140-6736(13)61953-4
PG 23
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA AH8YE
UT WOS:000336423300013
PM 25104492
ER

PT J
AU Gierasch, LM
   Lynn, DG
   Schneider, JP
AF Gierasch, Lila M.
   Lynn, David G.
   Schneider, Joel P.
TI The Sixth Peptide Engineering Meeting PEM6, Emory University Conference
   Center, Atlanta, Georgia, October 2 to 5, 2012
SO BIOPOLYMERS
LA English
DT Editorial Material
C1 [Gierasch, Lila M.] Univ Massachusetts Amherst, Amherst, MA 01003 USA.
   [Lynn, David G.] Emory Univ, Atlanta, GA 30322 USA.
   [Schneider, Joel P.] NCI, Bethesda, MD 20892 USA.
RP Gierasch, LM (reprint author), Univ Massachusetts Amherst, Amherst, MA 01003 USA.
NR 0
TC 0
Z9 0
U1 1
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0006-3525
EI 1097-0282
J9 BIOPOLYMERS
JI Biopolymers
PD NOV
PY 2013
VL 100
IS 6
SI SI
BP VII
EP VII
DI 10.1002/bip.22427
PG 1
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA AI0HZ
UT WOS:000336528700001
PM 24281724
ER

PT J
AU Veiga, AS
   Schneider, JP
AF Veiga, Ana Salome
   Schneider, Joel P.
TI Antimicrobial Hydrogels for the Treatment of Infection
SO BIOPOLYMERS
LA English
DT Review
DE hydrogels; antimicrobial; biomaterials
ID LINKED CHITOSAN HYDROGELS; SILVER NANOPARTICLES; ANTIBACTERIAL ACTIVITY;
   ESCHERICHIA-COLI; THERMOSENSITIVE HYDROGEL; NANOCOMPOSITE HYDROGELS;
   POLY(ETHYLENE GLYCOL); ANTIFOULING HYDROGELS; IMPLANT INFECTIONS; WOUND
   DRESSINGS
AB The increasing prevalence of microbial infections, especially those associated with impaired wound healing and biomedical implant failure has spurred the development of new materials having antimicrobial activity. Hydrogels are a class of highly hydrated material finding use in diverse medical applications such as drug delivery, tissue engineering, as wound fillers, and as implant coatings, to name a few. The biocompatible nature of many gels make them a convenient starting platform to develop selectively active antimicrobial materials. Hydrogels with antimicrobial properties can be obtained through the encapsulation or covalent immobilization of known antimicrobial agents, or the material itself can be designed to possess inherent antimicrobial activity. In this review we present an overview of antimicrobial hydrogels that have recently been developed and when possible provide a discussion relevant to their mechanism of action. (C) 2013 Wiley Periodicals, Inc.
C1 [Veiga, Ana Salome] Univ Lisbon, Fac Med, P-1649028 Lisbon, Portugal.
   [Schneider, Joel P.] NCI, Biol Chem Lab, Frederick, MD 21702 USA.
RP Schneider, JP (reprint author), NCI, Biol Chem Lab, Frederick, MD 21702 USA.
EM joel.schneider@nih.gov
RI Schneider, Joel/N-2610-2014; 
OI Veiga, Ana Salome/0000-0002-9892-2243
FU Fundacao para a Ciencia e a Tecnologia - Ministerio da Educacao e
   Ciencia (FCT-MEC, Portugal), FCT [IF/00803/2012]
FX Contract grant sponsor: Fundacao para a Ciencia e a Tecnologia -
   Ministerio da Educacao e Ciencia (FCT-MEC, Portugal), FCT Investigator
   Programme Contract grant number: IF/00803/2012
NR 88
TC 12
Z9 12
U1 30
U2 187
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0006-3525
EI 1097-0282
J9 BIOPOLYMERS
JI Biopolymers
PD NOV
PY 2013
VL 100
IS 6
SI SI
BP 637
EP 644
DI 10.1002/bip.22412
PG 8
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA AI0HZ
UT WOS:000336528700010
PM 24122459
ER

PT J
AU Roy, AK
   Klein, RG
   Angelosante, A
   Bar-Haim, Y
   Leibenluft, E
   Hulvershorn, L
   Dixon, E
   Dodds, A
   Spindel, C
AF Roy, Amy K.
   Klein, Rachel G.
   Angelosante, Aleta
   Bar-Haim, Yair
   Leibenluft, Ellen
   Hulvershorn, Leslie
   Dixon, Erica
   Dodds, Alice
   Spindel, Carrie
TI Clinical Features of Young Children Referred for Impairing Temper
   Outbursts
SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY
LA English
DT Article
ID SEVERE MOOD DYSREGULATION; PEDIATRIC BIPOLAR DISORDER; OPPOSITIONAL
   DEFIANT DISORDER; SCHOOL-AGE-CHILDREN; MATERNAL DEPRESSION; EXPRESSIVE
   BEHAVIOR; EMOTION REGULATION; CONDUCT DISORDER; YOUTH; CHILDHOOD
AB Objective: In light of the current controversy about whether severe temper outbursts are diagnostic of mania in young children, we conducted a study to characterize such children, focusing on mania and other mood disorders, emotion regulation, and parental psychiatric history.
   Methods: Study participants included 51 5-9-year-old children with frequent, impairing outbursts (probands) and 24 non-referred controls without outbursts. Parents completed a lifetime clinical interview about their child, and rated their child's current mood and behavior. Teachers completed a behavior rating scale. To assess emotion regulation, children were administered the Balloons Game, which assesses emotion expressivity in response to frustration, under demands of high and low regulation. Parental lifetime diagnoses were ascertained in blind clinical interviews.
   Results: No child had bipolar disorder, bipolar disorder not otherwise specified (NOS), or major depression (MDD). The most prevalent disorder was oppositional defiant disorder (88.2%), followed by attention-deficit/hyperactivity disorder (74.5%), anxiety disorders (49.0%), and non-MDD depressive disorders (33.3%). Eleven probands (21.6%) met criteria for severe mood dysregulation. During the Balloons Game, when there were no demands for self-regulation, children with severe outbursts showed reduced positive expressivity, and also showed significant deficits in controlling negative facial expressions when asked to do so. Anxiety disorders were the only diagnoses significantly elevated in probands' mothers.
   Conclusions: Overall, young children with severe temper outbursts do not present with bipolar disorder. Rather, disruptive behavior disorders with anxiety and depressive mood are common. In children with severe outbursts, deficits in regulating emotional facial expressions may reflect deficits controlling negative affect. This work represents a first step towards elucidating mechanisms underlying severe outbursts in young children.
C1 [Roy, Amy K.] Fordham Univ, Dept Psychol, Bronx, NY 10458 USA.
   [Klein, Rachel G.; Angelosante, Aleta; Spindel, Carrie] NYU, Ctr Child Study, New York, NY USA.
   [Bar-Haim, Yair] Tel Aviv Univ, Sch Psychol Sci, IL-69978 Tel Aviv, Israel.
   [Leibenluft, Ellen] NIMH, Sect Bipolar Spectrum Disorders, Emot & Dev Branch, Bethesda, MD 20892 USA.
   [Hulvershorn, Leslie] Indiana Univ Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA.
   [Dixon, Erica] Amer Univ, Dept Psychol, Washington, DC 20016 USA.
   [Dodds, Alice] Drexel Univ, Coll Med, Philadelphia, PA 19104 USA.
RP Roy, AK (reprint author), Fordham Univ, Dept Psychol, 441 E Fordham Rd, Bronx, NY 10458 USA.
EM aroy3@fordham.edu
OI Dixon, Erica/0000-0001-9125-2497
FU Seevak Family Foundation; National Institute of Mental Health [K23
   MH074821]
FX This study was supported by generous grants from the Seevak Family
   Foundation (Rachel G. Klein, P. I.). Amy Roy was supported by K23
   MH074821 (Amy Roy, P. I.) from the National Institute of Mental Health.
NR 37
TC 9
Z9 10
U1 5
U2 16
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 NOV
PY 2013
VL 23
IS 9
BP 588
EP 596
DI 10.1089/cap.2013.0005
PG 9
WC Pediatrics; Pharmacology & Pharmacy; Psychiatry
SC Pediatrics; Pharmacology & Pharmacy; Psychiatry
GA AI0FT
UT WOS:000336522300002
PM 24168713
ER

PT J
AU Bradley, C
   Yabroff, KR
   Warren, JL
   Chawla, N
   Zeruto, C
   Lamont, EB
AF Bradley, Cathy
   Yabroff, K. Robin
   Warren, Joan L.
   Chawla, Neetu
   Zeruto, Christopher
   Lamont, Elizabeth B.
TI Trends in chemotherapy-related treatment of advanced-stage colorectal
   (CRC) cancer.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT ASCO's Quality Care Symposium
CY NOV 01-02, 2013
CL San Diego, CA
SP ASCO
C1 Virginia Commonwealth Univ, Richmond, VA USA.
   NCI, NIH, Bethesda, MD 20892 USA.
   Informat Management Serv Inc, Calverton, MD USA.
   Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 1
PY 2013
VL 31
IS 31
SU S
MA 258
PG 1
WC Oncology
SC Oncology
GA AG6YR
UT WOS:000335565500251
ER

PT J
AU Castro, KM
   Friedman, EL
   Mack, N
   Siegel, RD
   Eisenstein, J
   Das, IP
   Clauser, S
AF Castro, Kathleen M.
   Friedman, Eliot Lawrence
   Mack, Nadesa
   Siegel, Robert D.
   Eisenstein, Jana
   Das, Irene Prabhu
   Clauser, Steven
TI Improving quality of care within the NCI Community Cancer Centers
   Program (NCCCP) network
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT ASCO's Quality Care Symposium
CY NOV 01-02, 2013
CL San Diego, CA
SP ASCO
C1 NCI, NIH, Rockville, MD USA.
   Lehigh Valley Hosp & Hlth Network, Allentown, PA USA.
   Hartford Hosp, Helen & Harry Gray Canc Ctr, Hartford, CT 06115 USA.
   NCI, NIH, Bethesda, MD 20892 USA.
   NCI, Div Canc Control & Populat Sci, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 1
PY 2013
VL 31
IS 31
SU S
MA 178
PG 1
WC Oncology
SC Oncology
GA AG6YR
UT WOS:000335565500175
ER

PT J
AU Das, IP
   Mallin, K
   Gay, EG
   Rozjabek, H
   Fennell, ML
   Stewart, AK
   Castro, KM
   Clauser, S
AF Das, Irene Prabhu
   Mallin, Katherine
   Gay, E. Greer
   Rozjabek, Heather
   Fennell, Mary L.
   Stewart, Andrew K.
   Castro, Kathleen M.
   Clauser, Steven
TI Expectations of discipline representation on multidisciplinary treatment
   planning (MTP) teams
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT ASCO's Quality Care Symposium
CY NOV 01-02, 2013
CL San Diego, CA
SP ASCO
C1 NCI, Div Canc Control & Populat Sci, NIH, Rockville, MD USA.
   Amer Coll Surg, Commiss Canc, Chicago, IL USA.
   NCI, Appl Res Program, NIH, Rockville, MD USA.
   Brown Univ, Providence, RI 02912 USA.
   Remedy Informat, Sandy, UT USA.
   NCI, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
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 NOV 1
PY 2013
VL 31
IS 31
SU S
MA 195
PG 1
WC Oncology
SC Oncology
GA AG6YR
UT WOS:000335565500192
ER

PT J
AU Das, IP
   Rozjabek, H
   Fennell, ML
   Mallin, K
   Gay, EG
   Castro, KM
   Stewart, AK
   Clauser, S
AF Das, Irene Prabhu
   Rozjabek, Heather
   Fennell, Mary L.
   Mallin, Katherine
   Gay, E. Greer
   Castro, Kathleen M.
   Stewart, Andrew K.
   Clauser, Steven
TI Patient involvement in multidisciplinary treatment planning (MTP).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT ASCO's Quality Care Symposium
CY NOV 01-02, 2013
CL San Diego, CA
SP ASCO
C1 NCI, Div Canc Control & Populat Sci, NIH, Rockville, MD USA.
   NCI, Appl Res Program, NIH, Rockville, MD USA.
   Brown Univ, Providence, RI 02912 USA.
   Amer Coll Surg, Commiss Canc, Chicago, IL USA.
   NCI, NIH, Rockville, MD USA.
   Remedy Informat, Sandy, UT USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
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 NOV 1
PY 2013
VL 31
IS 31
SU S
MA 145
PG 1
WC Oncology
SC Oncology
GA AG6YR
UT WOS:000335565500142
ER

PT J
AU Garfinkel, S
   Frentzel, E
   Evensen, C
   Keller, S
   Yost, KJ
   Sangl, J
   Arora, NK
AF Garfinkel, Steven
   Frentzel, Elizabeth
   Evensen, Christian
   Keller, San
   Yost, Kathleen J.
   Sangl, Judith
   Arora, Neeraj K.
TI Developing CAHPS for cancer care prototype: Progress and next steps.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT ASCO's Quality Care Symposium
CY NOV 01-02, 2013
CL San Diego, CA
SP ASCO
C1 Amer Inst Res, Chapel Hill, NC USA.
   Mayo Clin, Rochester, MN USA.
   Agcy Healthcare Res & Qual, Rockville, MD USA.
   NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 1
PY 2013
VL 31
IS 31
SU S
MA 134
PG 1
WC Oncology
SC Oncology
GA AG6YR
UT WOS:000335565500131
ER

PT J
AU Gorin, SS
   Haggstrom, D
   McDonald, K
   Han, P
   Fairfield, K
   Ganz, PA
   Cheung, WY
   Clauser, S
AF Gorin, Sherri Sheinfeld
   Haggstrom, David
   McDonald, Kathryn
   Han, Paul
   Fairfield, Kathleen
   Ganz, Patricia A.
   Cheung, Winson Y.
   Clauser, Steven
CA QCCC CCI Work Grp
TI Coordinating cancer care: Measurement and intervention approaches across
   the cancer continuum
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT ASCO's Quality Care Symposium
CY NOV 01-02, 2013
CL San Diego, CA
SP ASCO
C1 NCI, NIH, SAIC, Rockville, MD USA.
   Indiana Univ Sch Med, VA HSR&D Ctr Excellence Implementing Evidence Bas, Regenstrief Inst, IU Ctr Hlth Serv & Outcomes Res, Indianapolis, IN 46202 USA.
   Stanford Univ, Stanford, CA 94305 USA.
   Maine Med Ctr, Reseach Inst, Scarborough, ME USA.
   Maine Med Ctr, Scarborough, ME USA.
   Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA.
   Univ Calif Los Angeles, Sch Publ Hlth, Los Angeles, CA 90024 USA.
   British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada.
   NCI, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 1
PY 2013
VL 31
IS 31
SU S
MA 103
PG 1
WC Oncology
SC Oncology
GA AG6YR
UT WOS:000335565500103
ER

PT J
AU Wiggins, JL
   Monk, CS
AF Wiggins, Jillian Lee
   Monk, Christopher S.
TI A translational neuroscience framework for the development of
   socioemotional functioning in health and psychopathology
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Article
ID AUTISM SPECTRUM DISORDERS; SEROTONIN TRANSPORTER GENE; GENOME-WIDE
   ASSOCIATION; GENERALIZED ANXIETY DISORDER; MAJOR DEPRESSIVE DISORDER;
   MEDIAL PREFRONTAL CORTEX; EMOTIONAL FACIAL EXPRESSIONS; PROMOTER REGION
   POLYMORPHISM; BIAS MODIFICATION TREATMENT; BRAINS DEFAULT NETWORK
AB The development of socioemotional functioning is a complex process that occurs over a protracted time period and requires coordinating affective, cognitive, and social faculties. At many points in development, the trajectory of socioemotional development can be deleteriously altered due to a combination of environmental insults and individual vulnerabilities. The result can be psychopathology. However, researchers are just beginning to understand the neural and genetic mechanisms involved in the development of healthy and disordered socioemotional functioning. We propose a translational developmental neuroscience framework to understand the transactional process that results in socioemotional functioning in both healthy and disordered populations. We then apply this framework to healthy socioemotional development, pediatric anxiety, pediatric depression, and autism spectrum disorder, selectively reviewing current literature in light of the framework. Finally, we examine ways that the framework can help to frame future directions of research on socioemotional development and translational implications for intervention.
C1 [Wiggins, Jillian Lee; Monk, Christopher S.] Univ Michigan, Ann Arbor, MI 48109 USA.
RP Wiggins, JL (reprint author), NIMH, Sect Bipolar Spectrum Disorders, Emot & Dev Branch, Bldg 15K,MSC-2670, Bethesda, MD 20892 USA.
EM jillian.wiggins@nih.gov
RI Monk, Christopher/J-1805-2014
NR 167
TC 2
Z9 2
U1 7
U2 14
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0954-5794
EI 1469-2198
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD NOV
PY 2013
VL 25
IS 4
SI SI
BP 1293
EP 1309
DI 10.1017/S095457941300062X
PN 2
PG 17
WC Psychology, Developmental
SC Psychology
GA AC2YP
UT WOS:000332382500008
PM 24342841
ER

PT J
AU Leibenluft, E
   Stoddard, J
AF Leibenluft, Ellen
   Stoddard, Joel
TI The developmental psychopathology of irritability
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Article
ID OPPOSITIONAL DEFIANT DISORDER; SEVERE MOOD DYSREGULATION; PEDIATRIC
   BIPOLAR DISORDER; INFORMATION-PROCESSING MECHANISMS; PROACTIVE
   AGGRESSION; CONDUCT DISORDER; EMOTION REGULATION; BEHAVIOR PROBLEMS;
   TRAIT ANGER; MALTREATED CHILDREN
AB Chronic, severe irritability is common in childhood and is very impairing. Furthermore, childhood irritability predicts suicidality, social impairment, and depressive and anxiety disorders in adulthood. Focusing on both normative and pathologic development, we review the construct of irritability from its origins in aggression and disruptive behavior research to its contemporary relevance for affective psychopathology. We then describe two broad neurocognitive systems that show promise in differentiating irritable from nonirritable youths: aberrant processing of emotional stimuli and impaired context-sensitive regulation. We suggest behavioral, neurocognitive, and physiologic measures that may aid in studying severe irritability and assessing its therapeutics. Finally, we argue for therapeutic trials targeting severe irritability that address emotional aspects of irritability in addition to the associated disruptive behavior.
C1 [Leibenluft, Ellen; Stoddard, Joel] NIMH, Bethesda, MD 20892 USA.
RP Stoddard, J (reprint author), NIMH, NIH, Sect Bipolar Spectrum Disorders, Emot & Dev Branch,Dept Hlth & Human Serv, Bldg 15K,Room 208,15K North Dr,MSC 2670, Bethesda, MD 20892 USA.
EM joel.stoddard@nih.gov
OI Stoddard, Joel/0000-0003-4070-4566
FU Intramural NIH HHS [Z01 MH002786-06]
NR 172
TC 25
Z9 25
U1 6
U2 31
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0954-5794
EI 1469-2198
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD NOV
PY 2013
VL 25
IS 4
SI SI
BP 1473
EP 1487
DI 10.1017/S0954579413000722
PN 2
PG 15
WC Psychology, Developmental
SC Psychology
GA AC2YP
UT WOS:000332382500018
PM 24342851
ER

PT J
AU Baratz-Goldstein, R
   Rubovitch, V
   Tweedie, D
   Benromano, T
   Lin, R
   Greig, NH
   Pick, CG
AF Baratz-Goldstein, R.
   Rubovitch, V
   Tweedie, D.
   Benromano, T.
   Lin, R.
   Greig, N. H.
   Pick, C. G.
TI Thalidomide analog, 3 ' 6, dithiothalidomide, as a neuroprotective
   treatment for minimal traumatic brain injury - possible mechanisms
SO JOURNAL OF MOLECULAR NEUROSCIENCE
LA English
DT Meeting Abstract
CT 21st Annual Meeting of the Israel-Society-for-Neuroscience / 1st
   Binational Australian-Israeli Meeting on Neuroscience
CY DEC 15-15, 2012
CL Eilat, ISRAEL
SP Israel Soc Neuroscience
C1 [Baratz-Goldstein, R.; Rubovitch, V; Benromano, T.; Lin, R.; Pick, C. G.] Tel Aviv Univ, Sackler Sch Med, Dept Anat & Anthropol, IL-69978 Tel Aviv, Israel.
   [Tweedie, D.; Greig, N. H.] NIA, Neurosci Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RI Pick, Chaim/D-4789-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0895-8696
EI 1559-1166
J9 J MOL NEUROSCI
JI J. Mol. Neurosci.
PD NOV
PY 2013
VL 51
SU 1
BP S16
EP S16
PG 1
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA AC9DF
UT WOS:000332833800034
ER

PT J
AU Baruch, K
   Ron-Harel, N
   Gal, H
   Deczkowska, A
   Shifrut, E
   Ndifon, W
   Mirlas-Neisberg, N
   Cardon, C
   Mattson, MP
   Gomez-Pinilla, F
   Friedman, N
   Schwartz, M
AF Baruch, K.
   Ron-Harel, N.
   Gal, H.
   Deczkowska, A.
   Shifrut, E.
   Ndifon, W.
   Mirlas-Neisberg, N.
   Cardon, C.
   Mattson, M. P.
   Gomez-Pinilla, F.
   Friedman, N.
   Schwartz, M.
TI CNS-specific immunity at the choroid plexus: a shift towards destructive
   Th2-inflammation in brain aging
SO JOURNAL OF MOLECULAR NEUROSCIENCE
LA English
DT Meeting Abstract
CT 21st Annual Meeting of the Israel-Society-for-Neuroscience / 1st
   Binational Australian-Israeli Meeting on Neuroscience
CY DEC 15-15, 2012
CL Eilat, ISRAEL
SP Israel Soc Neuroscience
C1 [Baruch, K.; Deczkowska, A.; Mirlas-Neisberg, N.; Cardon, C.; Schwartz, M.] Weizmann Inst Sci, Dept Neurobiol, IL-76100 Rehovot, Israel.
   [Ron-Harel, N.] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
   [Gal, H.; Shifrut, E.; Ndifon, W.; Friedman, N.] Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel.
   [Mattson, M. P.] NIA, Neurosci Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
   [Gomez-Pinilla, F.] Univ Calif Los Angeles, Dept Physiol Sci, Brain Injury Res Ctr, Los Angeles, CA 90095 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0895-8696
EI 1559-1166
J9 J MOL NEUROSCI
JI J. Mol. Neurosci.
PD NOV
PY 2013
VL 51
SU 1
BP S31
EP S32
PG 2
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA AC9DF
UT WOS:000332833800074
ER

PT J
AU Mocchetti, I
   Rozzi, S
   Borelli, G
   Steiner, J
   Reglodi, D
   Avdoshina, V
AF Mocchetti, I
   Rozzi, S.
   Borelli, G.
   Steiner, J.
   Reglodi, D.
   Avdoshina, V
TI PACAP27 IS NEUROPROTECTIVE AGAINST HIV-TAT NEUROTOXICITY
SO JOURNAL OF MOLECULAR NEUROSCIENCE
LA English
DT Meeting Abstract
CT 21st Annual Meeting of the Israel-Society-for-Neuroscience / 1st
   Binational Australian-Israeli Meeting on Neuroscience
CY DEC 15-15, 2012
CL Eilat, ISRAEL
SP Israel Soc Neuroscience
C1 [Mocchetti, I; Rozzi, S.; Borelli, G.; Avdoshina, V] Georgetown Univ, Med Ctr, Dept Neurosci, Washington, DC 20007 USA.
   [Steiner, J.] Natl Inst Neurol Disorders, NIH, Bethesda, MD USA.
   [Reglodi, D.] Univ Pecs, Dept Anat, PTE MTA Lendulet PACAP Res Team, Pecs, Hungary.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0895-8696
EI 1559-1166
J9 J MOL NEUROSCI
JI J. Mol. Neurosci.
PD NOV
PY 2013
VL 51
SU 1
BP S200
EP S200
PG 1
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA AC9DF
UT WOS:000332833800444
ER

PT J
AU Ravni, A
   Seaborn, T
   Au, R
   Chow, BKC
   Fournier, A
   Wurtz, O
   Vaudry, H
   Eiden, LE
   Vaudry, D
AF Ravni, A.
   Seaborn, T.
   Au, R.
   Chow, B. K. C.
   Fournier, A.
   Wurtz, O.
   Vaudry, H.
   Eiden, L. E.
   Vaudry, D.
TI PACAP AND NGF INCREASE SERPINB1A EXPRESSION THROUGH THE CALCINEURIN AND
   MAP-KINASE PATHWAYS TO PROTECT PC12 CELLS FROM APOPTOSIS
SO JOURNAL OF MOLECULAR NEUROSCIENCE
LA English
DT Meeting Abstract
CT 21st Annual Meeting of the Israel-Society-for-Neuroscience / 1st
   Binational Australian-Israeli Meeting on Neuroscience
CY DEC 15-15, 2012
CL Eilat, ISRAEL
SP Israel Soc Neuroscience
C1 [Ravni, A.; Seaborn, T.; Chow, B. K. C.; Wurtz, O.; Vaudry, H.; Vaudry, D.] INSERM, DC2N, Neurotroph Factor & Neuronal Differentiat Team, U982, F-76821 Mont St Aignan, France.
   [Ravni, A.; Seaborn, T.; Au, R.; Chow, B. K. C.; Wurtz, O.; Vaudry, H.; Vaudry, D.] Univ Rouen, Int Associated Lab Samuel Champlain, F-76821 Mont St Aignan, France.
   [Ravni, A.; Wurtz, O.; Vaudry, H.; Vaudry, D.] Univ Rouen, IRIB, PRIMACEN, F-76821 Mont St Aignan, France.
   [Seaborn, T.] Univ Laval, Ctr Hosp Univ Quebec CRCHUQ, Ctr Rech, Dept Pediat,Hop St Francois dAssise, Quebec City, PQ, Canada.
   [Au, R.; Chow, B. K. C.] Univ Hong Kong, Dept Zool, Hong Kong, Hong Kong, Peoples R China.
   [Fournier, A.] Univ Quebec, Inst Natl Rech Sci, Inst Armand Frappier, Pointe Claire, PQ H9R 1G6, Canada.
   [Eiden, L. E.] NIMH, Lab Cellular & Mol Regulat, Bethesda, MD 20892 USA.
RI Chow, Billy/D-3064-2009; Wurtz, Olivier/H-5494-2015
OI Chow, Billy/0000-0003-3390-0307; Wurtz, Olivier/0000-0003-2628-4745
NR 0
TC 0
Z9 0
U1 0
U2 6
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0895-8696
EI 1559-1166
J9 J MOL NEUROSCI
JI J. Mol. Neurosci.
PD NOV
PY 2013
VL 51
SU 1
BP S213
EP S213
PG 1
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA AC9DF
UT WOS:000332833800471
ER

PT J
AU Serebro, IS
   Barak, B
   Modai, S
   Gilam, A
   Okun, E
   Belinson, H
   Michaelson, DM
   Mattson, M
   Shomron, N
   Ashery, U
AF Serebro, Shvarts, I
   Barak, B.
   Modai, S.
   Gilam, A.
   Okun, E.
   Belinson, H.
   Michaelson, D. M.
   Mattson, M.
   Shomron, N.
   Ashery, U.
TI Elucidating the role of environmental enrichment in mitigating
   Alzheimer's disease pathology through microRNAs regulation
SO JOURNAL OF MOLECULAR NEUROSCIENCE
LA English
DT Meeting Abstract
CT 21st Annual Meeting of the Israel-Society-for-Neuroscience / 1st
   Binational Australian-Israeli Meeting on Neuroscience
CY DEC 15-15, 2012
CL Eilat, ISRAEL
SP Israel Soc Neuroscience
C1 [Serebro, Shvarts, I; Barak, B.; Belinson, H.; Michaelson, D. M.; Ashery, U.] Tel Aviv Univ, Fac Life Sci, Dept Neurobiol, IL-69978 Tel Aviv, Israel.
   [Barak, B.; Shomron, N.; Ashery, U.] Tel Aviv Univ, Sagol Sch Neurosci, IL-69978 Tel Aviv, Israel.
   [Modai, S.; Gilam, A.; Shomron, N.] Tel Aviv Univ, Sackler Fac Med, Dept Cell & Dev Biol, IL-69978 Tel Aviv, Israel.
   [Okun, E.] Bar Ilan Univ, Mina & Everard Goodman Fac Life Sci, IL-52900 Ramat Gan, Israel.
   [Okun, E.] Bar Ilan Univ, Gonda Goldschmidt Multidisciplinary Brain Res Ctr, IL-52900 Ramat Gan, Israel.
   [Mattson, M.] NIA, Lab Neurosci, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0895-8696
EI 1559-1166
J9 J MOL NEUROSCI
JI J. Mol. Neurosci.
PD NOV
PY 2013
VL 51
SU 1
BP S115
EP S115
PG 1
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA AC9DF
UT WOS:000332833800296
ER

PT J
AU Shaham, Y
AF Shaham, Y.
TI Incubation of craving and fear: behavioral and neuronal mechanisms
SO JOURNAL OF MOLECULAR NEUROSCIENCE
LA English
DT Meeting Abstract
CT 21st Annual Meeting of the Israel-Society-for-Neuroscience / 1st
   Binational Australian-Israeli Meeting on Neuroscience
CY DEC 15-15, 2012
CL Eilat, ISRAEL
SP Israel Soc Neuroscience
C1 [Shaham, Y.] NIDA, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0895-8696
EI 1559-1166
J9 J MOL NEUROSCI
JI J. Mol. Neurosci.
PD NOV
PY 2013
VL 51
SU 1
BP S110
EP S110
PG 1
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA AC9DF
UT WOS:000332833800282
ER

PT J
AU Li, KG
   Simons-Morton, BG
   Hingson, R
AF Li, Kaigang
   Simons-Morton, Bruce G.
   Hingson, Ralph
TI Impaired-Driving Prevalence Among US High School Students: Associations
   With Substance Use and Risky Driving Behaviors
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Article
ID ROAD TRAFFIC CRASHES; ADOLESCENT DRINKING; YOUNG-ADULTS; ALCOHOL-USE;
   CHECKPOINTS PROGRAM; COLLEGE-STUDENTS; UNITED-STATES; DRIVERS;
   INVOLVEMENT; DRUGS
AB Objectives. We examined the prevalence of impaired driving among US high school students and associations with substance use and risky driving behavior.
   Methods. We assessed driving while alcohol or drug impaired (DWI) and riding with alcohol-or drug-impaired drivers (RWI) in a nationally representative sample of 11th-grade US high school students (n = 2431). We examined associations with drinking and binge drinking, illicit drug use, risky driving, and demographic factors using multivariate sequential logistic regression analysis.
   Results. Thirteen percent of 11th-grade students reported DWI at least 1 of the past 30 days, and 24% reported RWI at least once in the past year. Risky driving was positively associated with DWI (odds ratio [OR] = 1.25; P < .001) and RWI (OR = 1.09; P < .05), controlling for binge drinking (DWI: OR = 3.17; P < .01; RWI: OR = 6.12; P < .001) and illicit drug use (DWI: OR = 5.91; P < .001; RWI: OR = 2.29; P = .05). DWI was higher for adolescents who drove after midnight (OR = 15.7), drove while sleepy or drowsy (OR = 8.6), read text messages (OR = 11.8), sent text messages (OR = 5.0), and made cell phone calls (OR = 3.2) while driving.
   Conclusions. Our findings suggest the need for comprehensive approaches to the prevention of DWI, RWI, and other risky driving behavior.
C1 [Li, Kaigang; Simons-Morton, Bruce G.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Hlth Behav Branch, Div Intramural Populat Hlth Res, Bethesda, MD USA.
   [Hingson, Ralph] NIAAA, Epidemiol & Prevent Res Div, Bethesda, MD USA.
RP Simons-Morton, BG (reprint author), NICHD, Hlth Behav Branch, DIPHR, 6100 Execut Blvd 7B13M, Bethesda, MD 20892 USA.
EM mortonb@exchange.nih.gov
OI Simons-Morton, Bruce/0000-0003-1099-6617
FU Eunice Kennedy Shriver National Institute of Child Health and Human
   Development [HHSN267200800009C]; National Heart, Lung and Blood
   Institute; National Institute on Alcohol Abuse and Alcoholism; Maternal
   and Child Health Bureau of the Health Resources and Services
   Administration
FX This project (contract no. HHSN267200800009C) was supported in part by
   the intramural research program of the Eunice Kennedy Shriver National
   Institute of Child Health and Human Development, and the National Heart,
   Lung and Blood Institute, the National Institute on Alcohol Abuse and
   Alcoholism, and the Maternal and Child Health Bureau of the Health
   Resources and Services Administration, with supplemental support from
   the National Institute on Drug Abuse.
NR 55
TC 13
Z9 13
U1 2
U2 17
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 NOV
PY 2013
VL 103
IS 11
BP E71
EP E77
DI 10.2105/AJPH.2013.301296
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA AA4BG
UT WOS:000331038500022
PM 24028236
ER

PT J
AU York, AG
   Chandris, P
   Nogare, DD
   Head, J
   Wawrzusin, P
   Fischer, RS
   Chitnis, A
   Shroff, H
AF York, Andrew G.
   Chandris, Panagiotis
   Nogare, Damian Dalle
   Head, Jeffrey
   Wawrzusin, Peter
   Fischer, Robert S.
   Chitnis, Ajay
   Shroff, Hari
TI Instant super-resolution imaging in live cells and embryos via analog
   image processing
SO NATURE METHODS
LA English
DT Article
ID STRUCTURED-ILLUMINATION MICROSCOPY; FIELD OPTICAL NANOSCOPY; RESOLUTION;
   EXCITATION; MOVEMENT; REVEALS; EXPORT
AB Existing super-resolution fluorescence microscopes compromise acquisition speed to provide subdiffractive sample information. We report an analog implementation of structured illumination microscopy that enables three-dimensional (3D) super-resolution imaging with a lateral resolution of 145 nm and an axial resolution of 350 nm at acquisition speeds up to 100 Hz. By using optical instead of digital image-processing operations, we removed the need to capture, store and combine multiple camera exposures, increasing data acquisition rates 10- to 100-fold over other super-resolution microscopes and acquiring and displaying super-resolution images in real time. Low excitation intensities allow imaging over hundreds of 2D sections, and combined physical and computational sectioning allow similar depth penetration to spinning-disk confocal microscopy. We demonstrate the capability of our system by imaging fine, rapidly moving structures including motor-driven organelles in human lung fibroblasts and the cytoskeleton of flowing blood cells within developing zebrafish embryos.
C1 [York, Andrew G.; Wawrzusin, Peter; Shroff, Hari] Natl Inst Biomed Imaging & Bioengn, Sect High Resolut Opt Imaging, NIH, Bethesda, MD USA.
   [Chandris, Panagiotis] NIDDK, NIH, Bethesda, MD 20892 USA.
   [Nogare, Damian Dalle; Head, Jeffrey; Chitnis, Ajay] NICHHD, NIH, Bethesda, MD 20892 USA.
   [Fischer, Robert S.] NHLBI, NIH, Bethesda, MD 20892 USA.
RP York, AG (reprint author), Natl Inst Biomed Imaging & Bioengn, Sect High Resolut Opt Imaging, NIH, Bethesda, MD USA.
EM andrew.g.york+naturemethods@gmail.com
RI Shroff, Hari/E-7247-2016
OI Shroff, Hari/0000-0003-3613-8215
FU Intramural Research Programs of the US National Institute of Biomedical
   Imaging and Bioengineering; National Institute of Diabetes and Digestive
   and Kidney Diseases; National Heart, Lung, and Blood Institute; National
   Institute of Child Health and Human Development
FX We thank G. Patterson for encouragement and the use of his cell culture
   facilities, L. Maldonado-Baez (US National Heart, Lung, and Blood
   Institute) for the mCherry-tagged Rab8A plasmid, C. Combs for lending us
   his objective lenses, S. Parekh for useful discussions and for help in
   sample preparation, E. Tyler and A. Hoofring for help with illustrations
   and Y. Wu for help with Huygens deconvolution software. This work was
   supported by the Intramural Research Programs of the US National
   Institute of Biomedical Imaging and Bioengineering (to A.G.Y., P.W. and
   H.S.); the National Institute of Diabetes and Digestive and Kidney
   Diseases (to P.C.); the National Heart, Lung, and Blood Institute (to
   R.S.F.) and the National Institute of Child Health and Human Development
   (to D.D.N., J.H. and A.C.).
NR 36
TC 65
Z9 67
U1 9
U2 49
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1548-7091
EI 1548-7105
J9 NAT METHODS
JI Nat. Methods
PD NOV
PY 2013
VL 10
IS 11
BP 1122
EP 1126
DI 10.1038/NMETH.2687
PG 5
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 246AK
UT WOS:000326507600030
PM 24097271
ER

PT J
AU Memoli, MJ
   Harvey, H
   Morens, DM
   Taubenberger, JK
AF Memoli, Matthew J.
   Harvey, Hillery
   Morens, David M.
   Taubenberger, Jeffery K.
TI Influenza in pregnancy
SO INFLUENZA AND OTHER RESPIRATORY VIRUSES
LA English
DT Review
ID UNITED-STATES; H1N1 INFLUENZA; NEURAMINIDASE INHIBITORS; SEASONAL
   INFLUENZA; A(H1N1) VIRUS; A H1N1; RHEUMATOID-ARTHRITIS; VACCINATION
   COVERAGE; EMERGING INFECTIONS; PANDEMIC INFLUENZA
AB The 2009 pandemic served as a strong reminder that influenza-induced disease can have a great impact on certain at-risk populations and that pregnant women are one such important population. The increased risk of fatal and severe disease in these women was appreciated more than 500 years ago, and during the last century, pregnant women and their newborns have continued to be greatly affected by both seasonal and pandemic influenza. In this review, we briefly discuss the data collected both before and after the 2009 pandemic as it relates to the impact of influenza on pregnant women and their fetuses/newborns, as well as risk variables, clinical features, clues to pathophysiologic mechanisms, and approaches to treatment and prevention.
C1 [Memoli, Matthew J.; Taubenberger, Jeffery K.] NIH, Viral Pathogenesis & Evolut Sect, Infect Dis Lab, Bethesda, MD 20892 USA.
   [Harvey, Hillery; Morens, David M.] NIAID, Off Director, NIH, Bethesda, MD 20892 USA.
RP Memoli, MJ (reprint author), NIH, Viral Pathogenesis & Evolut Sect, Infect Dis Lab, Bldg 10, Bethesda, MD 20892 USA.
FU Intramural Research Program of the NIH
FX This research was supported by the Intramural Research Program of the
   NIH.
NR 82
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Z9 7
U1 1
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1750-2640
EI 1750-2659
J9 INFLUENZA OTHER RESP
JI Influenza Other Respir. Viruses
PD NOV
PY 2013
VL 7
IS 6
BP 1033
EP 1039
DI 10.1111/irv.12055
PG 7
WC Infectious Diseases; Virology
SC Infectious Diseases; Virology
GA AA3OG
UT WOS:000331001400024
PM 23170853
ER

PT J
AU Yu, HJ
   Feng, LZ
   Viboud, CG
   Shay, DK
   Jiang, Y
   Zhou, H
   Zhou, MG
   Xu, Z
   Hu, N
   Yang, WZ
   Nie, SF
AF Yu, Hongjie
   Feng, Luzhao
   Viboud, Cecile G.
   Shay, David K.
   Jiang, Yong
   Zhou, Hong
   Zhou, Maigeng
   Xu, Zhen
   Hu, Nan
   Yang, Weizhong
   Nie, Shaofa
TI Regional variation in mortality impact of the 2009 A (H1N1) influenza
   pandemic in China
SO INFLUENZA AND OTHER RESPIRATORY VIRUSES
LA English
DT Article
DE A(H1N1) pandemic; China; influenza; mortality; negative binomial model;
   regional variation
ID RESPIRATORY SYNCYTIAL VIRUS; A H1N1; UNITED-STATES; SEASONAL INFLUENZA;
   GLOBAL MORTALITY; RISK-FACTORS; HONG-KONG; DEATHS; POPULATION; INFECTION
AB Background Laboratory-confirmed deaths grossly underestimate influenza mortality burden, so that reliable burden estimates are derived from indirect statistical studies, which are scarce in low- and middle-income settings.
   Objectives Here, we used statistical excess mortality models to estimate the burden of seasonal and pandemic influenza in China.
   Methods We modeled data from a nationally representative population-based death registration system, combined with influenza virological surveillance data, to estimate influenza-associated excess mortality for the 2004-2005 through 2009-2010 seasons, by age and region.
   Results The A(H1N1) pandemic was associated with 11.4-12.1 excess respiratory and circulatory (R&C) deaths per 100 000 population in rural sites of northern and southern China during 2009-2010; these rates were 2.2-2.8 times higher than those of urban sites (P < 0.01). Influenza B accounted for a larger proportion of deaths than pandemic A(H1N1) in 2009-2010 in some regions. Nationally, we attribute 126 200 (95% CI, 61 000-248 400) excess R&C deaths (rate of 9.4/100 000) and 2 323 000 (1 166 000-4 533 000) years of life lost (YLL) to the first year of A (H1N1) pdm circulation.
   Conclusions The A(H1N1) pandemic posed a mortality and YLL burden comparable to that of interpandemic influenza in China. Our high burden estimates in rural areas highlight the need to enhance epidemiological surveillance and healthcare services, in underdeveloped and remote areas.
C1 [Yu, Hongjie; Nie, Shaofa] Huazhong Univ Sci & Technol, Tongji Med Coll, Sch Publ Hlth, Dept Epidemiol & Stat, Wuhan 430030, Peoples R China.
   [Yu, Hongjie; Feng, Luzhao; Xu, Zhen; Yang, Weizhong] Chinese Ctr Dis Control & Prevent, Div Infect Dis, Key Lab Surveillance & Early Warning Infect Dis, Beijing, Peoples R China.
   [Viboud, Cecile G.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
   [Shay, David K.] Ctr Dis Control & Prevent, Influenza Div, Natl Ctr Immunizat & Resp Dis, Atlanta, GA USA.
   [Jiang, Yong; Hu, Nan] Chinese Ctr Dis Control & Prevent, Natl Ctr Chron & Noncommunicable Dis Control & Pr, Beijing, Peoples R China.
   [Zhou, Hong] Ctr Dis Control & Prevent, Natl Ctr Chron Dis Prevent & Hlth Promot, Atlanta, GA USA.
   [Zhou, Maigeng] Chinese Ctr Dis Control & Prevent, Ctr Publ Hlth Surveillance & Informat Serv, Beijing, Peoples R China.
RP Nie, SF (reprint author), Huazhong Univ Sci & Technol, Tongji Med Coll, Sch Publ Hlth, Dept Epidemiol & Stat, 13 Hangkong Rd, Wuhan 430030, Peoples R China.
EM sf_nie@mails.tjmu.edu.cn
OI Shay, David/0000-0001-9619-4820
FU China-U.S. Collaborative Program on Emerging and Re-emerging Infectious
   Diseases; Ministry of Science and Technology, China [2012 ZX10004-201]
FX We thank the local Centers for Disease Control and Prevention in the
   Disease Surveillance Points sites and National Influenza Surveillance
   Network. The views expressed are those of the authors and do not
   necessarily represent the policy of the China CDC or the U.S. Centers
   for Disease Control and Prevention. This study was supported by the
   China-U.S. Collaborative Program on Emerging and Re-emerging Infectious
   Diseases and the Grants of the Ministry of Science and Technology, China
   (2012 ZX10004-201).
NR 36
TC 10
Z9 15
U1 1
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1750-2640
EI 1750-2659
J9 INFLUENZA OTHER RESP
JI Influenza Other Respir. Viruses
PD NOV
PY 2013
VL 7
IS 6
BP 1350
EP 1360
DI 10.1111/irv.12121
PG 11
WC Infectious Diseases; Virology
SC Infectious Diseases; Virology
GA AA3OG
UT WOS:000331001400063
PM 23668477
ER

PT J
AU Hales, CM
   Rees, H
   Seyfried, NT
   Dammer, EB
   Duong, DM
   Gearing, M
   Montine, TJ
   Troncoso, JC
   Thambisetty, M
   Levey, AI
   Lah, JJ
   Wingo, TS
AF Hales, Chadwick M.
   Rees, Howard
   Seyfried, Nicholas T.
   Dammer, Eric B.
   Duong, Duc M.
   Gearing, Marla
   Montine, Thomas J.
   Troncoso, Juan C.
   Thambisetty, Madhav
   Levey, Allan I.
   Lah, James J.
   Wingo, Thomas S.
TI Abnormal Gephyrin Immunoreactivity Associated With Alzheimer Disease
   Pathologic Changes
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Article
DE beta-amyloid; Alzheimer disease; GABA; Gephyrin; Presenilin; Synapse
ID MILD COGNITIVE IMPAIRMENT; AMYLOID PRECURSOR PROTEIN; GLYCINE RECEPTOR;
   BRAIN; PREVALENCE; VARIANTS; BETA; MICE
AB Many neurodegenerative disorders involve the abnormal accumulation of proteins. In addition to the pathologic hallmarks of neurofibrillary tangles and A-amyloid plaques in Alzheimer disease (AD), here we show that abnormal accumulations of gephyrin, an inhibitory receptorYanchoring protein, are highly correlated with the neuropathologic diagnosis of AD in 17 AD versus 14 control cases. Furthermore, gephyrin accumulations were specific for AD and not seen in normal controls or other neurodegenerative diseases including Parkinson disease, corticobasal degeneration, and frontotemporal degeneration. Gephyrin accumulations in AD overlapped with A-amyloid plaques and, more rarely, neurofibrillary tangles. Biochemical and proteomic studies of AD and control brain samples suggested alterations in gephyrin solubility and reveal elevated levels of gephyrin lower-molecular- weight species in the AD insoluble fraction. Because gephyrin is involved in synaptic organization and synaptic dysfunction is an early event in AD, these findings point to its possible role in the pathogenesis of AD.
C1 [Hales, Chadwick M.; Rees, Howard; Levey, Allan I.; Lah, James J.; Wingo, Thomas S.] Emory Univ, Sch Med, Dept Neurol, Atlanta, GA 30322 USA.
   [Hales, Chadwick M.; Rees, Howard; Seyfried, Nicholas T.; Dammer, Eric B.; Duong, Duc M.; Gearing, Marla; Levey, Allan I.; Lah, James J.; Wingo, Thomas S.] Emory Univ, Sch Med, Ctr Neurodegenerat Dis, Atlanta, GA 30322 USA.
   [Seyfried, Nicholas T.] Emory Univ, Sch Med, Dept Biochem, Atlanta, GA 30322 USA.
   [Dammer, Eric B.; Wingo, Thomas S.] Emory Univ, Sch Med, Dept Human Genet, Atlanta, GA 30322 USA.
   [Gearing, Marla] Emory Univ, Sch Med, Dept Pathol & Lab Med, Atlanta, GA 30322 USA.
   [Montine, Thomas J.] Univ Washington, Dept Pathol, Seattle, WA 98195 USA.
   [Troncoso, Juan C.] Johns Hopkins Sch Med, Dept Pathol, Baltimore, MD USA.
   [Troncoso, Juan C.] Johns Hopkins Sch Med, Dept Neurol, Baltimore, MD USA.
   [Thambisetty, Madhav] NIA, NIH, Bethesda, MD 20892 USA.
   [Wingo, Thomas S.] Atlanta Vet Adm Med Ctr, Atlanta, GA USA.
RP Wingo, TS (reprint author), Emory Univ, Sch Med, Dept Neurol, Ctr Neurodegenerat Dis, Whitehead Res Bldg,615 Michael St, Atlanta, GA 30322 USA.
EM thomas.wingo@emory.edu
OI Dammer, Eric/0000-0003-2947-7606
FU American Brain Foundation Clinical Research Training Fellowship; Emory
   Alzheimer's Disease Research Center [NIA-AG025688, NIAP01AG1449]; Emory
   Neuroscience NINDS Core Facility [P30NS055077]; John's Hopkins
   University Alzheimer's Disease Research Center [NIA-AG05146];
   Alzheimer's Association [IIRG-09-134090]; Department of Veteran Affairs
   [CDA1-002-09F, 1IK2BX001820]; Department of Veterans Affairs; NIA
   intramural Research Program of the National Institutes of Health
FX This work was funded by the American Brain Foundation Clinical Research
   Training Fellowship (Chadwick Hales), Emory Alzheimer's Disease Research
   Center-NIA-AG025688 (Allan Levey) and NIAP01AG1449, Emory Neuroscience
   NINDS Core Facility-P30NS055077 (James Lah), John's Hopkins University
   Alzheimer's Disease Research Center-NIA-AG05146 and Alzheimer's
   Association-IIRG-09-134090 (Juan Troncoso), and The Department of
   Veteran Affairs-CDA1-002-09F and 1IK2BX001820 (Thomas Wingo). This work
   was supported in part by the Department of Veterans Affairs and the NIA
   intramural Research Program of the National Institutes of Health. This
   work does not represent the views of the Department of Veterans Affairs
   or the US Government.
NR 32
TC 9
Z9 9
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-3069
EI 1554-6578
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD NOV
PY 2013
VL 72
IS 11
BP 1009
EP 1015
PG 7
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 299ZA
UT WOS:000330433000002
PM 24128675
ER

PT J
AU Nair, G
   Absinta, M
   Reich, DS
AF Nair, G.
   Absinta, M.
   Reich, D. S.
TI Optimized T1-MPRAGE Sequence for Better Visualization of Spinal Cord
   Multiple Sclerosis Lesions at 3T
SO AMERICAN JOURNAL OF NEURORADIOLOGY
LA English
DT Article
ID PULSE SEQUENCES; STIR SEQUENCE; BRAIN MRI; ECHO; MS; ABNORMALITIES; T-1
AB BACKGROUND AND PURPOSE: Spinal cord lesions are highly prevalent in MS, and their visualization can help both in diagnosis and patient follow-up. However, the sensitivity of MR imaging to spinal cord lesions remains poor, primarily because of suboptimal contrast between lesions and a normal-appearing cord. Here, we propose an optimized 3D MPRAGE sequence for improved detection of MS lesions in the spinal cord at 3T.
   MATERIALS AND METHODS: Images were acquired by use of T2 FSE, STIR, T1-gradient recalled-echo (for T1 mapping), and T1-MPRAGE in the sagittal plane, and T2*-weighted scans in the axial plane, on 40 patients with MS and 7 healthy volunteers. Two observers qualitatively evaluated the images for lesion conspicuity. Lesions seen between the C1 and C4 segments in 10 randomly selected patients with MS were further evaluated quantitatively for contrast-to-noise ratio between the lesion and normal-appearing cord, and for lesion burden.
   RESULTS: Spinal cord lesions were more conspicuous on the optimized T1-MPRAGE sequence than on any other sequence tested. Detailed analysis revealed that lesions were almost 3 times more conspicuous (P < .01), and the total lesion volume was 2 times greater (P < .05, n=10), in the T1-MPRAGE sequence compared with the standard STIR sequence. Correlation of clinical disability (Expanded Disability Status Score) with lesion load from each sequence also demonstrated the importance of the improved lesion conspicuity with T1-MPRAGE.
   CONCLUSIONS: The optimized T1-MPRAGE sequence described here improves the reliability of lesion visualization and estimation of lesion burden, especially when used in conjunction with other well-established clinical sequences.
C1 [Nair, G.; Absinta, M.; Reich, D. S.] Natl Inst Neurol Disorders & Stroke, NIH, Bethesda, MD 20892 USA.
   [Absinta, M.] Univ Vita Salute San Raffaele, San Raffaele Sci Inst, Inst Expt Neurol, Div Neurosci,NeuroImaging Res Unit, Milan, Italy.
   Univ Vita Salute San Raffaele, San Raffaele Sci Inst, Inst Expt Neurol, Dept Neurol,Div Neurosci, Milan, Italy.
   [Reich, D. S.] Johns Hopkins Univ, Dept Radiol & Neurol, Baltimore, MD USA.
RP Nair, G (reprint author), Natl Inst Neurol Disorders & Stroke, Translat Neuroradiol Unit, NIH, Bldg 10,Rm 5C103,10 Ctr Dr,MSC 1400, Bethesda, MD 20892 USA.
EM reichds@ninds.nih.gov
RI Reich, Daniel/E-5701-2010
OI Reich, Daniel/0000-0002-2628-4334
FU Intramural Research Program of the National Institute of Neurologic
   Disorders and Stroke (NINDS), National Institutes of Health
FX This study was supported by the Intramural Research Program of the
   National Institute of Neurologic Disorders and Stroke (NINDS), National
   Institutes of Health. We also thank the National Institute of Mental
   Health (NIMH)/NINDS Functional Magnetic Resonance Facility, John Ostuni
   (NINDS), Souheil Inati (NIMH), and the Neuroimmunology Branch clinical
   group for their help.
NR 28
TC 13
Z9 13
U1 0
U2 0
PU AMER SOC NEURORADIOLOGY
PI DENVILLE
PA PO BOX 3000, DENVILLE, NJ 07834-9349 USA
SN 0195-6108
EI 1936-959X
J9 AM J NEURORADIOL
JI Am. J. Neuroradiol.
PD NOV
PY 2013
VL 34
IS 11
BP 2215
EP 2222
DI 10.3174/ajnr.A3637
PG 8
WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical
   Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 297DD
UT WOS:000330234700028
PM 23764721
ER

PT J
AU Tellez-Plaza, M
   Guallar, E
   Fabsitz, RR
   Howard, BV
   Umans, JG
   Francesconi, KA
   Goessler, W
   Devereux, RB
   Navas-Acien, A
AF Tellez-Plaza, Maria
   Guallar, Eliseo
   Fabsitz, Richard R.
   Howard, Barbara V.
   Umans, Jason G.
   Francesconi, Kevin A.
   Goessler, Walter
   Devereux, Richard B.
   Navas-Acien, Ana
TI Cadmium Exposure and Incident Peripheral Arterial Disease
SO CIRCULATION-CARDIOVASCULAR QUALITY AND OUTCOMES
LA English
DT Article
DE cadmium; peripheral arterial disease
ID NUTRITION EXAMINATION SURVEY; AMERICAN-HEART-ASSOCIATION;
   CARDIOVASCULAR-DISEASE; URINARY CADMIUM; ESTROGEN-RECEPTOR;
   NATIONAL-HEALTH; US ADULTS; METALS; POPULATION; ATHEROSCLEROSIS
AB Background-Cadmium has been associated with peripheral arterial disease (PAD) in cross-sectional studies, but prospective evidence is lacking. Our goal was to evaluate the association of urine cadmium concentrations with incident PAD in a large population-based cohort.
   Methods and Results-A prospective cohort study was performed with 2864 adult American Indians 45 to 74 years of age from Arizona, Oklahoma, and North and South Dakota who participated in the Strong Heart Study from 1989 to 1991 and were followed through 2 follow-up examination visits in 1993 to 1995 and 1997 to 1999. Participants were free of PAD, defined as an ankle brachial index <0.9 or >1.4 at baseline, and had complete baseline information on urine cadmium, potential confounders, and ankle brachial index determinations in the follow-up examinations. Urine cadmium was measured using inductively coupled plasma mass spectrometry and corrected for urinary dilution by normalization to urine creatinine. Multivariable-adjusted hazard ratios were computed using Cox-proportional hazards models for interval-censored data. A total of 470 cases of incident PAD, defined as an ankle brachial index <0.9 or >1.4, were identified. After adjustment for cardiovascular disease risk factors including smoking status and pack-years, the hazard ratio comparing the 80th to the 20th percentile of urine cadmium concentrations was 1.41 (1.05-1.81). The hazard ratio comparing the highest to the lowest tertile was 1.96 (1.32-2.81). The association persisted after excluding participants with ankle brachial index >1.4 only as well as in subgroups defined by sex and smoking status.
   Conclusions-Urine cadmium, a biomarker of long-term cadmium exposure, was independently associated with incident PAD, providing further support for cadmium as a cardiovascular disease risk factor.
C1 [Tellez-Plaza, Maria; Navas-Acien, Ana] Johns Hopkins Univ, Dept Environm Hlth Sci, Bloomberg Sch Publ Hlth, Baltimore, MD 21205 USA.
   [Tellez-Plaza, Maria; Guallar, Eliseo; Navas-Acien, Ana] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
   [Tellez-Plaza, Maria; Guallar, Eliseo; Navas-Acien, Ana] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD USA.
   [Tellez-Plaza, Maria; Guallar, Eliseo] Natl Ctr Cardiovasc Res CNIC, Div Epidemiol & Populat Genet, Madrid, Spain.
   [Tellez-Plaza, Maria] Fdn Invest Hosp Clin Valencia INCLIVA, Valencia, Spain.
   [Guallar, Eliseo] Johns Hopkins Med Inst, Dept Med, Baltimore, MD 21205 USA.
   [Fabsitz, Richard R.] NHLBI, Epidemiol Branch, Bethesda, MD 20892 USA.
   [Howard, Barbara V.; Umans, Jason G.] MedStar Hlth Res Inst, Hyattsville, MD USA.
   [Howard, Barbara V.; Umans, Jason G.] Georgetown Univ, Hyattsville, MD USA.
   [Francesconi, Kevin A.; Goessler, Walter] Karl Franzens Univ Graz, Inst Chem Analyt Chem, Graz, Austria.
   [Devereux, Richard B.] Weill Cornell Med Coll, New York, NY USA.
RP Tellez-Plaza, M (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, 615 N Wolfe St,Room W7513D, Baltimore, MD 21205 USA.
EM mtellezp@jhsph.edu
RI Guallar, Eliseo/D-3807-2014; 
OI Guallar, Eliseo/0000-0002-4471-9565; Tellez-Plaza,
   Maria/0000-0002-3850-1228; Goessler, Walter/0000-0002-0142-9373
FU National Heart, Lung, and Blood Institute [R01 HL090863, HL41642,
   HL41652, HL41654, HL65521]; Rio Hortega training grant (Funds for
   Research in Health Sciences, Ministry of Science and Innovation, Spain)
FX This work was supported by the National Heart, Lung, and Blood Institute
   (grant R01 HL090863, SHS grants HL41642, HL41652, HL41654, and HL65521).
   M.T.-P. was supported by a Rio Hortega training grant (Funds for
   Research in Health Sciences, Ministry of Science and Innovation, Spain).
NR 64
TC 14
Z9 15
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-7705
EI 1941-7713
J9 CIRC-CARDIOVASC QUAL
JI Circ.-Cardiovasc. Qual. Outcomes
PD NOV
PY 2013
VL 6
IS 6
BP 626
EP +
DI 10.1161/CIRCOUTCOMES.112.000663
PG 11
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 298ZA
UT WOS:000330362400009
PM 24255048
ER

PT J
AU Hayashi, K
   Hooper, LC
   Shimomura, Y
AF Hayashi, Kozaburo
   Hooper, Laura C.
   Shimomura, Yoshikazu
TI Who Pays the Toll for Solving the Enigma of Corneal Herpes?
SO CORNEA
LA English
DT Article; Proceedings Paper
CT 18th Annual Meeting of the Kyoto-Cornea-Club
CY DEC 07-08, 2012
CL Kyoto, JAPAN
SP Kyoto Cornea Club
DE HSK; cytokines; chemokines; neovascularization; PMNs
ID SIMPLEX STROMAL KERATITIS; ENDOTHELIAL GROWTH-FACTOR; COLONY-STIMULATING
   FACTOR; VIRUS TYPE-1 DNA; OCULAR INFECTION; EYE DISEASE; T-CELLS;
   INFLAMMATORY CELLS; EPITHELIAL-CELLS; HSV-1 DNA
AB In herpetic stromal keratitis (HSK), herpes simplex virus type-1 DNA fragments and herpes simplex virus-immunoglobulin G immune complexes are present in corneas long after the infective virus has disappeared. These viral components are highly immunogenic and potentiate the production of proinflammatory cytokines and chemokines via Toll-like receptors expressed on corneal cells and macrophages. In addition, angiogenic factors, such as the vascular endothelium growth factor and the tissue-damaging enzyme, matrix metalloproteinase 9, are induced by corneal cells and macrophages through the recognition of these viral components in the pathogenesis of HSK. Upon neovascularization, robust infiltration of leukocytes via leaky new vessels is elicited. Activated polymorphonuclear leukocytes (PMNs) secrete hydrogen peroxide and myeloperoxidase, which inhibit viral growth. PMNs also produce tumor necrosis factor, monokine-induced by interferon-gamma (CXCL9), and nitric oxide. These factors provide a local environment that can induce the differentiation of peripheral CD4(+) T cells to induce Th1-predominant immunopathology. Thus, strategies developed to alter these pathways should lead to new preventative and therapeutic measures for the treatment of HSK.
C1 [Hayashi, Kozaburo; Hooper, Laura C.] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
   [Shimomura, Yoshikazu] Kinki Univ, Sch Med, Dept Ophthalmol, Osaka 589, Japan.
RP Hayashi, K (reprint author), 1-26-8 Chofugaoka, Chofu, Tokyo 1820021, Japan.
EM kozaburo@yc4.so-net.ne.jp
NR 76
TC 1
Z9 1
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0277-3740
EI 1536-4798
J9 CORNEA
JI Cornea
PD NOV
PY 2013
VL 32
SU 1
BP S3
EP S12
PG 10
WC Ophthalmology
SC Ophthalmology
GA 298XC
UT WOS:000330356800002
PM 24104930
ER

PT J
AU Bornstein, MH
   Manian, N
AF Bornstein, Marc H.
   Manian, Nanmathi
TI Maternal responsiveness and sensitivity reconsidered: Some is more
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Article
ID INFANT-MOTHER ATTACHMENT; TO-FACE INTERACTION; INTERACTIONAL SYNCHRONY;
   DEVELOPMENTAL PSYCHOPATHOLOGY; NATURALISTIC EXCHANGES; EMOTIONAL
   AVAILABILITY; INTERACTION PATTERNS; SOCIAL CONTINGENCY; PARENTING
   BEHAVIOR; CHILD INTERACTION
AB Is it always or necessarily the case that common and important parenting practices are better, insofar as they occur more often, or worse, because they occur less often? Perhaps, less is more, or some is more. To address this question, we studied mothers' microcoded contingent responsiveness to their infants (M = 5.4 months, SD = 0.2) in relation to independent global judgments of the same mothers' parenting sensitivity. In a community sample of 335 European American dyads, videorecorded infant and maternal behaviors were timed microanalytically throughout an extended home observation; separately and independently, global maternal sensitivity was rated macroanalytically. Sequential analysis and spline regression showed that, as maternal contingent responsiveness increased, judged maternal sensitivity increased to significance on the contingency continuum, after which mothers who were even more contingent were judged less sensitive. Just significant levels of maternal responsiveness are deemed optimally sensitive. Implications of these findings for typical and atypical parenting, child development, and intervention science are discussed.
C1 [Bornstein, Marc H.; Manian, Nanmathi] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA.
RP Bornstein, MH (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Suite 8030,6705 Rockledge Dr, Bethesda, MD 20892 USA.
EM Marc_H_Bornstein@nih.gov
FU Intramural NIH HHS [ZIA HD001119-25]
NR 126
TC 15
Z9 16
U1 7
U2 37
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0954-5794
EI 1469-2198
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD NOV
PY 2013
VL 25
IS 4
BP 957
EP 971
DI 10.1017/S0954579413000308
PN 1
PG 15
WC Psychology, Developmental
SC Psychology
GA 298XT
UT WOS:000330358700007
PM 24229542
ER

PT J
AU Klimes-Dougan, B
   Desjardins, CD
   James, MG
   Narayan, AJ
   Long, JD
   Cullen, KR
   Gold, PW
   Martinez, PE
AF Klimes-Dougan, Bonnie
   Desjardins, Christopher David
   James, Matthew G.
   Narayan, Angela J.
   Long, Jeffrey D.
   Cullen, Kathryn R.
   Gold, Philip W.
   Martinez, Pedro E.
TI The development of thought problems: A longitudinal family risk study of
   offspring of bipolar, unipolar, and well parents
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Article
ID OBSESSIVE-COMPULSIVE-DISORDER; CHILD-BEHAVIOR CHECKLIST; DEPRESSED
   MOTHERS; SUICIDAL IDEATION; ADOLESCENT; PSYCHOPATHOLOGY; SYMPTOMS;
   METAANALYSIS; ASSOCIATION; PSYCHOSIS
AB There is growing evidence that many offspring of parents with bipolar disorder (BD) will develop moderate to severe forms of psychopathology during childhood and adolescence, including thought problems. The purpose of this study was to evaluate the developmental progression of thought problems within the context of a family risk study. Repeated assessments of thought problems, spanning approximately 15 years, were conducted in offspring (N = 192 from 98 families) of parents diagnosed with BD (O-BD), unipolar depression (O-UNI), or no significant psychiatric or medical problems (O-WELL). Survival analysis showed that the O-BD group had the greatest estimated probability of developing thought problems over time, followed by O-UNI, and then O-WELL and O-BD exhibiting higher levels of persistence than O-WELL. Parent-reported thought problems in childhood and adolescence predicted a range of problems in young adulthood. Disturbances in reality testing and other atypical behaviors are likely to disrupt progression through important developmental periods and to associate with poor outcomes. These findings are likely relevant to preventing the occurrence or progression of problems in offspring of bipolar parents. The study of thought problems across development represents an important area of continued research in children at risk for development of affective disorders.
C1 [Klimes-Dougan, Bonnie; Desjardins, Christopher David; James, Matthew G.; Narayan, Angela J.; Cullen, Kathryn R.] Univ Minnesota, Minneapolis, MN 55455 USA.
   [Long, Jeffrey D.] Univ Iowa, Iowa City, IA 52242 USA.
   [Gold, Philip W.; Martinez, Pedro E.] NIMH, Bethesda, MD 20892 USA.
RP Klimes-Dougan, B (reprint author), Univ Minnesota, Dept Psychol, 75 E River Rd,412 Elliot Hall, Minneapolis, MN 55455 USA.
EM klimes@umn.edu
NR 70
TC 3
Z9 3
U1 0
U2 6
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0954-5794
EI 1469-2198
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD NOV
PY 2013
VL 25
IS 4
BP 1079
EP 1091
DI 10.1017/S0954579413000382
PN 1
PG 13
WC Psychology, Developmental
SC Psychology
GA 298XT
UT WOS:000330358700015
PM 24229550
ER

PT J
AU Tarbox, SI
   Addington, J
   Cadenhead, KS
   Cannon, TD
   Cornblatt, BA
   Perkins, DO
   Seidman, LJ
   Tsuang, MT
   Walker, EF
   Heinssen, R
   McGlashan, TH
   Woods, SW
AF Tarbox, Sarah I.
   Addington, Jean
   Cadenhead, Kristin S.
   Cannon, Tyrone D.
   Cornblatt, Barbara A.
   Perkins, Diana O.
   Seidman, Larry J.
   Tsuang, Ming T.
   Walker, Elaine F.
   Heinssen, Robert
   McGlashan, Thomas H.
   Woods, Scott W.
TI Premorbid functional development and conversion to psychosis in clinical
   high-risk youths
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Article
ID 1ST EPISODE PSYCHOSIS; ULTRA-HIGH-RISK; PREDICTIVE-VALIDITY; PRODROMAL
   SYMPTOMS; ADJUSTMENT SCALE; 1ST-EPISODE SCHIZOPHRENIA; NONAFFECTIVE
   PSYCHOSIS; INTERRATER RELIABILITY; NEGATIVE SYMPTOMS; PATTERNS
AB Deterioration in premorbid functioning is a common feature of schizophrenia, but sensitivity to psychosis conversion among clinical high-risk samples has not been examined. This study evaluates premorbid functioning as a predictor of psychosis conversion among a clinical high-risk sample, controlling for effects of prior developmental periods. Participants were 270 clinical high-risk individuals in the North American Prodrome Longitudinal Study-I, 78 of whom converted to psychosis over the next 2.5 years. Social, academic, and total maladjustment in childhood, early adolescence, and late adolescence were rated using the Cannon-Spoor Premorbid Adjustment Scale. Early adolescent social dysfunction significantly predicted conversion to psychosis (hazard ratio = 1.30, p = .014), independently of childhood social maladjustment and independently of severity of most baseline positive and negative prodromal symptoms. Baseline prodromal symptoms of disorganized communication, social anhedonia, suspiciousness, and diminished ideational richness mediated this association. Early adolescent social maladjustment and baseline suspiciousness together demonstrated moderate positive predictive power (59%) and high specificity (92.1%) in predicting conversion. Deterioration of academic and total functioning, although observed, did not predict conversion to psychosis. Results indicate early adolescent social dysfunction to be an important early predictor of conversion. As such, it may be a good candidate for inclusion in prediction algorithms and could represent an advantageous target for early intervention.
C1 [Tarbox, Sarah I.; McGlashan, Thomas H.; Woods, Scott W.] Yale Univ, Sch Med, New Haven, CT 06519 USA.
   [Addington, Jean] Univ Calgary, Calgary, AB T2N 1N4, Canada.
   [Cadenhead, Kristin S.; Tsuang, Ming T.] Univ Calif San Diego, San Diego, CA 92103 USA.
   [Cannon, Tyrone D.] Univ Calif Los Angeles, Los Angeles, CA USA.
   [Cornblatt, Barbara A.] Zucker Hillside Hosp, Glen Oaks, NY USA.
   [Cornblatt, Barbara A.] Albert Einstein Coll Med, Bronx, NY USA.
   [Cornblatt, Barbara A.] Feinstein Inst Med Res, Manhasset, NY USA.
   [Perkins, Diana O.] Univ N Carolina, Chapel Hill, NC USA.
   [Seidman, Larry J.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
   [Walker, Elaine F.] Emory Univ, Atlanta, GA 30322 USA.
   [Heinssen, Robert] NIMH, Bethesda, MD USA.
RP Tarbox, SI (reprint author), Yale Univ, Sch Med, PRIME Res Clin, Connecticut Mental Hlth Ctr, 34 Pk St,B-38, New Haven, CT 06519 USA.
EM sarah.tarbox@yale.edu
FU NIMH NIH HHS [R01 MH065562, K05 MH001654, K05 MH01654, K24 MH076191, K24
   MH76191, P50 MH064065, P50 MH080272, R01 MH060720, R01 MH061523, R01
   MH062066, R01 MH065079, R01MH065079, R21 MH075027, U01 MH066069, U01
   MH066134, U01 MH066160, U01 MH081984, U01MH066134]
NR 61
TC 17
Z9 17
U1 3
U2 10
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0954-5794
EI 1469-2198
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD NOV
PY 2013
VL 25
IS 4
BP 1171
EP 1186
DI 10.1017/S0954579413000448
PN 1
PG 16
WC Psychology, Developmental
SC Psychology
GA 298XT
UT WOS:000330358700021
PM 24229556
ER

PT J
AU Raviprakash, K
   Sun, PF
   Raviv, Y
   Luke, T
   Martin, N
   Kochel, T
AF Raviprakash, Kanakatte
   Sun, Peifang
   Raviv, Yossef
   Luke, Thomas
   Martin, Nicholas
   Kochel, Tadeusz
TI Dengue virus photo-inactivated in presence of 1,5-iodonaphthylazide
   (INA) or AMT, a psoralen compound (4 '-aminomethyl-trioxsalen) is highly
   immunogenic in mice
SO HUMAN VACCINES & IMMUNOTHERAPEUTICS
LA English
DT Article
DE dengue virus; virus inactivation; vaccine; immunogenicity; mouse
ID PHOTOCHEMICAL INACTIVATION; RECOMBINANT SUBUNIT; HEMORRHAGIC-FEVER;
   VACCINE PROTOTYPE; IMMUNE-RESPONSES; RHESUS MACAQUES; DNA; PROTECTION;
   ENVELOPE; ANTIBODY
AB Two novel methods of dengue virus inactivation using iodonaphthyl azide (INA) and aminomethyl trioxsalen (AMT) were compared with traditional virus inactivation by formaldehyde. The AMT inactivated dengue-2 virus retained its binding to a panel of 5 monoclonal antibodies specific for dengue-2 envelope protein, whereas inactivation by formaldehyde and INA led to 30-50% decrease in binding. All three inactivated viruses elicited high level virus neutralizing antibodies in vaccinated mice. However, only mice vaccinated with AMT inactivated virus mounted T cell responses similar to live, uninactivated virus.
C1 [Raviprakash, Kanakatte; Sun, Peifang; Luke, Thomas; Martin, Nicholas; Kochel, Tadeusz] Naval Med Res Ctr, Viral & Rickettsial Dis Dept, Silver Spring, MD 20910 USA.
   [Sun, Peifang; Luke, Thomas] Henry M Jackson Fdn, Bethesda, MD USA.
   [Raviv, Yossef] NCI, Basic Res Program, SAIC Frederick, Frederick, MD 21701 USA.
RP Raviprakash, K (reprint author), Naval Med Res Ctr, Viral & Rickettsial Dis Dept, Silver Spring, MD 20910 USA.
EM Kanakatte.raviprakas@med.navy.mil
FU Office of Naval Research, NMRC work unit [A0311]; Frederick National
   Laboratory for Cancer Research; National Institutes of Health
   [HHSN26120080001E]
FX This work was funded by a research grant from the Office of Naval
   Research, NMRC work unit # A0311. This work was supported in whole or in
   part by the Frederick National Laboratory for Cancer Research, and the
   Intramural Research Program of the National Institutes of Health
   (contract HHSN26120080001E). We thank Dan Ewing, Karla Block, Liang
   Zhaodong, and Susana Widjaja for excellent technical assistance. Authors
   Raviprakash, Martin and Kochel are employees of the United States
   government or military service members. This work was prepared as part
   of their official duties. Title 17 U.S.C. section 101 defines a US.
   Government work as a work prepared by a military service member or
   employee of the US. Government as part of that person's official duties.
   The views expressed in this article are those of the authors and do not
   necessarily reflect the official policy or position of the Department of
   the Navy, Department of Defense, the Department of Health and Human
   Services, nor the United States Government.
NR 39
TC 4
Z9 4
U1 0
U2 1
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 2164-5515
EI 2164-554X
J9 HUM VACC IMMUNOTHER
JI Human Vaccines Immunother.
PD NOV
PY 2013
VL 9
IS 11
BP 2336
EP 2341
DI 10.4161/hv.25602
PG 6
WC Biotechnology & Applied Microbiology; Immunology
SC Biotechnology & Applied Microbiology; Immunology
GA 299FW
UT WOS:000330382300016
PM 23835446
ER

PT J
AU AlGhatrif, M
   Strait, JB
   Morrell, CH
   Canepa, M
   Wright, J
   Elango, P
   Scuteri, A
   Najjar, SS
   Ferrucci, L
   Lakatta, EG
AF AlGhatrif, Majd
   Strait, James B.
   Morrell, Chris H.
   Canepa, Marco
   Wright, Jeanette
   Elango, Palchamy
   Scuteri, Angelo
   Najjar, Samer S.
   Ferrucci, Luigi
   Lakatta, Edward G.
TI Longitudinal Trajectories of Arterial Stiffness and the Role of Blood
   Pressure The Baltimore Longitudinal Study of Aging
SO HYPERTENSION
LA English
DT Article
DE aging; blood pressure; vascular stiffness
ID PULSE-WAVE-VELOCITY; TREATED HYPERTENSIVE SUBJECTS; AORTIC STIFFNESS;
   INDEPENDENT PREDICTOR; CARDIOVASCULAR MORTALITY; ACCELERATED
   PROGRESSION; INCIDENT HYPERTENSION; NORMOTENSIVE SUBJECTS; 6-YEAR
   PERIOD; RISK-FACTORS
AB Carotid-femoral pulse wave velocity (PWV), a marker of arterial stiffness, is an established independent cardiovascular risk factor. Little information is available on the pattern and determinants of the longitudinal change in PWV with aging. Such information is crucial to elucidating mechanisms underlying arterial stiffness and the design of interventions to retard it. Between 1988 and 2013, we collected 2 to 9 serial measures of PWV in 354 men and 423 women of the Baltimore Longitudinal Study of Aging, who were 21 to 94 years of age and free of clinically significant cardiovascular disease. Rates of PWV increase accelerated with advancing age in men more than women, leading to sex differences in PWV after the age of 50 years. In both sexes, not only systolic blood pressure (SBP) 140 mmHg but also SBP of 120 to 139 mmHg was associated with steeper rates of PWV increase compared with SBP<120 mmHg. Furthermore, there was a dose-dependent effect of SBP in men with marked acceleration in PWV rate of increase with age at SBP 140 mmHg compared with SBP of 120 to 139 mmHg. Except for waist circumference in women, no other traditional cardiovascular risk factors predicted longitudinal PWV increase. In conclusion, the steeper longitudinal increase of PWV in men than women led to the sex difference that expanded with advancing age. Age and SBP are the main longitudinal determinants of PWV, and the effect of SBP on PWV trajectories exists even in the prehypertensive range.
C1 [AlGhatrif, Majd; Strait, James B.; Morrell, Chris H.; Canepa, Marco; Wright, Jeanette; Scuteri, Angelo; Lakatta, Edward G.] NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA.
   [Elango, Palchamy; Ferrucci, Luigi] NIA, Longitudinal Studies Sect, NIH, Baltimore, MD 21224 USA.
   [AlGhatrif, Majd] Johns Hopkins Sch Med, Dept Med, Baltimore, MD USA.
   [Scuteri, Angelo] Hosp San Raffaele Pisana IRCCS, Rome, Italy.
   [Najjar, Samer S.] MedStar Res Inst, Div Cardiol, Washington, DC USA.
   [Canepa, Marco] Univ Genoa, Div Cardiol, Genoa, Italy.
RP AlGhatrif, M (reprint author), Biomed Res Ctr, Lab Cardiovasc Sci, 251 Bayview Blvd,Suite 100,Room 09B116, Baltimore, MD 21224 USA.
EM majd.alghatrif@nih.gov
FU National Institutes of Health; National Institute on Aging (USA);
   Medstar Research Institute
FX This research was supported by the Intramural Research Program of the
   National Institutes of Health, National Institute on Aging (USA), and
   Medstar Research Institute.
NR 36
TC 68
Z9 69
U1 0
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0194-911X
EI 1524-4563
J9 HYPERTENSION
JI Hypertension
PD NOV
PY 2013
VL 62
IS 5
BP 934
EP 941
DI 10.1161/HYPERTENSIONAHA.113.01445
PG 8
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 295IO
UT WOS:000330110000033
PM 24001897
ER

PT J
AU West, SK
   Bates, MN
   Lee, JS
   Schaumberg, DA
   Lee, DJ
   Adair-Rohani, H
   Chen, DF
   Araj, H
AF West, Sheila K.
   Bates, Michael N.
   Lee, Jennifer S.
   Schaumberg, Debra A.
   Lee, David J.
   Adair-Rohani, Heather
   Chen, Dong Feng
   Araj, Houmam
TI Is Household Air Pollution a Risk Factor for Eye Disease?
SO INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH
LA English
DT Review
DE biomass; blindness; cataract; trachoma; dry eye disease; household air
   pollution
ID CIGARETTE-SMOKE EXPOSURE; MACULAR DEGENERATION; OCULAR SURFACE;
   OXIDATIVE STRESS; DRY EYE; DEVELOPING-COUNTRIES; BIOMASS FUELS; BBQ
   CHARCOAL; SOUTH-INDIA; WOOD SMOKE
AB In developing countries, household air pollution (HAP) resulting from the inefficient burning of coal and biomass (wood, charcoal, animal dung and crop residues) for cooking and heating has been linked to a number of negative health outcomes, mostly notably respiratory diseases and cancers. While ocular irritation has been associated with HAP, there are sparse data on adverse ocular outcomes that may result from acute and chronic exposures. We consider that there is suggestive evidence, and biological plausibility, to hypothesize that HAP is associated with some of the major blinding, and painful, eye conditions seen worldwide. Further research on this environmental risk factor for eye diseases is warranted.
C1 [West, Sheila K.; Lee, Jennifer S.] Johns Hopkins Univ Hosp, Wilmer Eye Inst, Baltimore, MD 21287 USA.
   [Bates, Michael N.] Univ Calif Berkeley, Sch Publ Hlth, Div Epidemiol, Berkeley, CA 94720 USA.
   [Bates, Michael N.] Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA.
   [Schaumberg, Debra A.] Univ Utah, Sch Med, Dept Ophthalmol & Visual Sci, John A Moran Eye Ctr, Salt Lake City, UT 84132 USA.
   [Schaumberg, Debra A.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02215 USA.
   [Schaumberg, Debra A.; Chen, Dong Feng] Harvard Univ, Sch Med, Dept Ophthalmol, Schepens Eye Res Inst,Massachusetts Eye & Ear, Boston, MA 02114 USA.
   [Lee, David J.] Univ Miami, Miller Sch Med, Dept Epidemiol & Publ Hlth, Miami, FL 33101 USA.
   [Adair-Rohani, Heather] WHO, CH-1211 Geneva, Switzerland.
   [Araj, Houmam] NEI, Bethesda, MD 20892 USA.
RP West, SK (reprint author), Johns Hopkins Univ Hosp, Wilmer Eye Inst, Baltimore, MD 21287 USA.
EM shwest@jhmi.edu; m_bates@berkeley.edu; jenleesf@gmail.com;
   debra.schaumberg@utah.edu; dlee@med.miami.edu; hradair@gmail.com;
   dongfeng_chen@meei.harvard.edu; arajh@mail.nih.gov
FU Department of Health and Human Services; National Institutes of Health;
   U.S. State Department; U.S. Environmental Protection Agency; U.S. Agency
   for International Development; Global Alliance for Clean Cookstoves
FX This publication arose from deliberations at a workshop: "Health Burden
   of Indoor Air Pollution on Women and Children in Developing Countries",
   held in Washington DC, USA, 9-11 May 2011, and sponsored by several U.S.
   Federal Agencies (Department of Health and Human Services, National
   Institutes of Health, U.S. State Department, U.S. Environmental
   Protection Agency, and the U.S. Agency for International Development)
   and the Global Alliance for Clean Cookstoves. Co-authors of the report
   comprised the Ocular Health Subgroup at the workshop. The paper
   represents the views of the authors and not necessarily those of their
   employers.; The authors acknowledge the assistance of William Martin,
   National Institute of Child Health and Development and Nigel Bruce,
   University of Liverpool, in organizing and overseeing the workshop, and
   Henry Falk, Centers for Disease Control and Prevention, for helpful
   discussions.
NR 83
TC 8
Z9 9
U1 2
U2 12
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1660-4601
J9 INT J ENV RES PUB HE
JI Int. J. Environ. Res. Public Health
PD NOV
PY 2013
VL 10
IS 11
BP 5378
EP 5398
DI 10.3390/ijerph10115378
PG 21
WC Environmental Sciences; Public, Environmental & Occupational Health
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
   Health
GA 301GM
UT WOS:000330520800008
PM 24284355
ER

PT J
AU Stein, SM
   Tiersten, A
   Hochster, HS
   Blank, SV
   Pothuri, B
   Curtin, J
   Shapira, I
   Levinson, B
   Ivy, P
   Joseph, B
   Guddati, AK
   Muggia, F
AF Stein, Stacey M.
   Tiersten, Amy
   Hochster, Howard S.
   Blank, Stephanie V.
   Pothuri, Bhavana
   Curtin, John
   Shapira, Ilan
   Levinson, Benjamin
   Ivy, Percy
   Joseph, Benson
   Guddati, Achuta Kumar
   Muggia, Franco
TI A Phase 2 Study of Oxaliplatin Combined With Continuous Infusion
   Topotecan for Patients With Previously Treated Ovarian Cancer
SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER
LA English
DT Article
DE Phase 2; Oxalipatin; Topotecan; Continuous infusion; Ovarian cancer
ID PEGYLATED LIPOSOMAL DOXORUBICIN; RECURRENT EPITHELIAL OVARIAN;
   PLATINUM-BASED CHEMOTHERAPY; TRIAL; GEMCITABINE; CARBOPLATIN;
   COMBINATION; STATISTICS; PACLITAXEL; RESISTANT
AB Background: Phase 2 trials suggest that prolonged intravenous (IV) infusion of the topoisomerase 1 inhibitor topotecan may be less toxic than when given by standard IV bolus 5-day administration. Oxaliplatin exhibits efficacy in platinum-pretreated disease and shows preclinical synergy with topoisomerase 1 inhibitors. We sought to determine the efficacy and safety of oxaliplatin plus infusion topotecan in recurrent platinum-pretreated ovarian cancer.
   Methods: Patients with recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancers previously treated with 1 to 2 prior regimens including platinum and taxane received oxaliplatin (85 mg/m(2) day 1 and day 15) and topotecan (0.4 mg/m(2) per day) by continuous IV infusion over 14 days every 4 weeks. The primary objective of the trial was to estimate the objective response rate in platinum-resistant disease (stratum 1) and in platinum-sensitive disease (stratum 2). Toxicities were assessed in all patients.
   Results: Thirty-eight patients received 144 cycles of therapy (median, 4; range, 1-6). The most common grade 3 and grade 4 toxicities included thrombocytopenia (grade 3, 37%; and grade 4, 19%), neutropenia (grade 3, 37%; grade 4, 11%), and anemia (grade 3, 15%). Response occurred in 4 of 19 patients in stratum I (21%; 95% confidence intervals, 6%-46%) and 9 of 19 patients in stratum 2 (47%; 95% CI, 24%-71%). Three in each stratum had lengthy complete responses.
   Conclusions: Biweekly oxaliplatin plus a 14-day continuous IV infusion of topotecan, given monthly, is an active regimen in platinum-pretreated ovarian cancer and merits additional evaluation.
C1 [Stein, Stacey M.; Hochster, Howard S.] Yale Univ, Sch Med, Dept Med, Div Med Oncol, New Haven, CT 06510 USA.
   [Tiersten, Amy; Joseph, Benson; Muggia, Franco] NYU, Sch Med, Dept Med, Div Med Oncol, New York, NY USA.
   [Blank, Stephanie V.; Pothuri, Bhavana; Curtin, John] NYU, Sch Med, Dept Obstet & Gynecol, Div Gynecol Oncol, New York, NY USA.
   [Shapira, Ilan] Albert Einstein Coll Med, Beth Israel Canc Ctr, Bronx, NY USA.
   NYU, Sch Med, New York, NY USA.
   [Levinson, Benjamin] NYU, Sch Med, Dept Populat Hlth, Div Biostat, New York, NY USA.
   [Ivy, Percy] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
   [Guddati, Achuta Kumar] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Internal Med, Boston, MA 02115 USA.
RP Guddati, AK (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Internal Med, Boston, MA 02115 USA.
EM drgakumar@yahoo.com
OI Curtin, John/0000-0002-9370-5119; Muggia, Franco/0000-0003-0703-9146
FU Department of Health and Human Services, National Cancer Institute
   [N01-CM-62204]
FX Supported by the Department of Health and Human Services, National
   Cancer Institute contract number N01-CM-62204, New York Cancer
   Consortium (PI: Joseph A. Sparano, MD)
NR 27
TC 7
Z9 7
U1 2
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1048-891X
EI 1525-1438
J9 INT J GYNECOL CANCER
JI Int. J. Gynecol. Cancer
PD NOV
PY 2013
VL 23
IS 9
BP 1577
EP 1582
DI 10.1097/IGC.0b013e3182a809e0
PG 6
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 299DC
UT WOS:000330374300007
PM 24172094
ER

PT J
AU Adiseshaiah, P
   Dellinger, A
   MacFarland, D
   Stern, S
   Dobrovolskaia, M
   Ileva, L
   Patri, AK
   Bernardo, M
   Brooks, DB
   Zhou, ZG
   McNeil, S
   Kepley, C
AF Adiseshaiah, Pavan
   Dellinger, Anthony
   MacFarland, Darren
   Stern, Stephan
   Dobrovolskaia, Marina
   Ileva, Lilia
   Patri, Anil K.
   Bernardo, Marcelino
   Brooks, D. Bradford
   Zhou, Zhiguo
   McNeil, Scott
   Kepley, Christopher
TI A Novel Gadolinium-Based Trimetasphere Metallofullerene for Application
   as a Magnetic Resonance Imaging Contrast Agent
SO INVESTIGATIVE RADIOLOGY
LA English
DT Article
DE trimetasphere metallofullerene; magnetic resonance imaging;
   gadolinium-based contrast agent; blood compatibility; nanoparticle
ID NEPHROGENIC SYSTEMIC FIBROSIS; IN-VITRO ANALYSIS; BREAST-CANCER;
   GD-DTPA; COMPLEMENT ACTIVATION; MRI; NANOPARTICLES; RELAXIVITY; MODEL;
   RATS
AB Objective: Macromolecular contrast agents for magnetic resonance imaging (MRI) are useful blood-pool agents because of their long systemic half-life and have found applications in monitoring tumor vasculature and angiogenesis. Macromolecular contrast agents have been able to overcome some of the disadvantages of the conventional small-molecule contrast agent Magnevist (gadolinium-diethylenetriaminepentaacetic acid), such as rapid extravasation and quick renal clearance, which limits the viable MRI time. There is an urgent need for new MRI contrast agents that increase the sensitivity of detection with a higher relaxivity, longer blood half-life, and reduced toxicity from free Gd3+ ions. Here, we report on the characterization of a novel water-soluble, derivatized, gadolinium-enclosed metallofullerene nanoparticle (Hydrochalarone-1) in development as an MRI contrast agent.
   Materials and Methods: The physicochemical properties of Hydrochalarone-1 were characterized by dynamic light scattering (hydrodynamic diameter), atomic force microscopy (particle height), X potential analysis (surface charge), and inductively coupled plasma-mass spectrometry (gadolinium concentration). The blood compatibility of Hydrochalarone-1 was also assessed in vitro through analysis of hemolysis, platelet aggregation, and complement activation of human blood. In vitro relaxivities, in vivo pharmacokinetics, and a pilot in vivo acute toxicity study were also performed.
   Results: An extensive in vitro and in vivo characterization of Hydrochalarone-1 is described here. The hydrodynamic size of Hydrochalarone-1 was 5 to 7 nm depending on the dispersing media, and it was negatively charged at physiological pH. Hydrochalarone-1 showed compatibility with blood cells in vitro, and no significant hemolysis, platelet aggregation, or complement activation was observed in vitro. In addition, Hydrochalarone-1 had significantly higher r(1) and r(2) in vitro relaxivities in human plasma in comparison with Magnevist and was not toxic at the doses administered in an in vivo pilot acute-dose toxicity study in mice.
   In vivo MRI pharmacokinetic analysis after a single intravenous injection of Hydrochalarone-1 (0.2 mmol Gd/kg) showed that the volume of distribution at steady state was approximately 100 mL/kg, suggesting prolonged systemic circulation. Hydrochalarone-1 also had a long blood half-life (88 minutes) and increased relaxivity, suggesting application as a promising blood-pool MRI contrast agent.
   Conclusions: The evidence suggests that Hydrochalarone-1, with its long systemic half-life, may have significant utility as a blood-pool MRI contrast agent.
C1 [Adiseshaiah, Pavan; Stern, Stephan; Dobrovolskaia, Marina; Patri, Anil K.; McNeil, Scott] SAIC Frederick Inc, Nanotechnol Characterizat Lab, Adv Technol Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
   [Dellinger, Anthony; MacFarland, Darren; Brooks, D. Bradford; Zhou, Zhiguo] Luna Innovat Inc, Luna nanoWorks, Danville, VA USA.
   [Dellinger, Anthony; Kepley, Christopher] Joint Sch Nanosci & Nanoengn, Dept Nanosci, Greensboro, NC USA.
   [Ileva, Lilia; Bernardo, Marcelino] SAIC Frederick Inc, Small Anim Imaging Program, Lab Anim Sci Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
   [Bernardo, Marcelino] NCI, Mol Imaging Program, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Adiseshaiah, P (reprint author), SAIC Frederick Inc, Nanotechnol Characterizat Lab, Adv Technol Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
EM adiseshaiahp@mail.nih.gov
RI Nanotechnology Characterization Lab, NCL/K-8454-2012
FU National Cancer Institute, National Institutes of Health
   [HHSN261200800001E]
FX This project has been funded in whole or in part with federal funds from
   the National Cancer Institute, National Institutes of Health, under
   contract no. HHSN261200800001E. The content of this publication does not
   necessarily reflect the views or policies of the Department of Health
   and Human Services, nor does mention of trade names, commercial
   products, or organizations imply endorsement by the US Government.
NR 73
TC 8
Z9 8
U1 1
U2 41
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0020-9996
EI 1536-0210
J9 INVEST RADIOL
JI Invest. Radiol.
PD NOV
PY 2013
VL 48
IS 11
BP 745
EP 754
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 300EO
UT WOS:000330447400001
PM 23748228
ER

PT J
AU Watts, DH
   Brown, ER
   Maldonado, Y
   Herron, C
   Chipato, T
   Reddy, L
   Moodley, D
   Nakabiito, C
   Manji, K
   Fawzi, W
   George, K
   Richardson, P
   Zwerski, S
   Coovadia, H
   Fowler, M
AF Watts, D. Heather
   Brown, Elizabeth R.
   Maldonado, Yvonne
   Herron, Casey
   Chipato, Tsungai
   Reddy, Leanne
   Moodley, Dhayendre
   Nakabiito, Clemensia
   Manji, Karim
   Fawzi, Wafaie
   George, Kathleen
   Richardson, Paul
   Zwerski, Sheryl
   Coovadia, Hoosen
   Fowler, MaryGlenn
CA HPTN 046 Protocol Team
TI HIV Disease Progression in the First Year After Delivery Among African
   Women Followed in the HPTN 046 Clinical Trial
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE HIV; postpartum; disease progression
ID TO-CHILD TRANSMISSION; ANTIRETROVIRAL THERAPY; PREGNANT-WOMEN;
   PREVENTION; MORTALITY; INFECTION; ADHERENCE; PROGRAM; MALAWI; COUNT
AB Background: Starting lifelong antiretroviral therapy (ART) in HIV infected pregnant women may decrease HIV progression and transmission, but adherence after delivery may be difficult, especially for asymptomatic women. We evaluated disease progression among HIV-infected women not on ART with CD4(+) lymphocyte counts above 200 cells per microliter at delivery.
   Methods: We analyzed risk of death, progression to AIDS (stage IV or CD4 <200 cells per microliter), or to CD4(+) count <350 1 year after delivery among postpartum women enrolled to a prevention of breastfeeding transmission trial using the Kaplan-Meier method. In the primary analysis, women were censored if ART was initiated.
   Results: Among 1285 women who were not WHO stage IV or less at 6 weeks postpartum, 49 (4.3%) progressed to stage IV/CD4 <200 cells per microliter or death by 1 year. Progression to CD4 <200 cells per microliter or death occurred among 16 (4.3%) of 441 women with CD4 count of 350-549 cells per microliter and 10 (1.6%) of 713 with CD4 counts >550 cells per microliter at delivery. CD4 <350 cells per microliter by 12 months postpartum occurred among 116 (37.0%) of 350 women with CD4 count 400-549 cells per microliter and 48 (7.4%) of 713 with CD4 count >550 cells per microliter at delivery.
   Conclusions: Progression to AIDS or CD4 count <350 cells per microliter is uncommon through 1 year postpartum for women with CD4 counts over 550 cells per microliter at delivery, but occurred in over one third of those with CD4 counts under 550 cells per microliter. ART should be continued after delivery or breastfeeding among women with CD4 counts <550 cells per microliter if follow-up and antiretroviral adherence can be maintained.
C1 [Watts, D. Heather] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Maternal & Pediat Infect Dis Branch, NIH, Bethesda, MD 20892 USA.
   [Brown, Elizabeth R.; Herron, Casey] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
   [Maldonado, Yvonne] Stanford Univ, Sch Med, Dept Pediat, Palo Alto, CA 94304 USA.
   [Chipato, Tsungai] Univ Zimbabwe, Coll Med, Harare, Zimbabwe.
   [Reddy, Leanne; Moodley, Dhayendre] Univ KwaZulu Natal, CAPRISA, Nelson R Mandela Sch Med, Durban, South Africa.
   [Nakabiito, Clemensia] Johns Hopkins Univ, Res Collaborat, Makerere Univ, Kampala, Uganda.
   [Manji, Karim] Muhimbili Univ Hlth & Allied Sci, Dar Es Salaam, Tanzania.
   [Fawzi, Wafaie] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
   [George, Kathleen] Family Hlth Int, Chapel Hill, NC USA.
   [Richardson, Paul; Fowler, MaryGlenn] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
   [Zwerski, Sheryl] NIAID, NIH, Bethesda, MD 20892 USA.
   [Coovadia, Hoosen] Univ Witwatersrand, Maternal Adolescent & Child Hlth, Johannesburg, South Africa.
   [Brown, Elizabeth R.; Herron, Casey; Zwerski, Sheryl] SCHARP, Seattle, WA USA.
RP Watts, DH (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Maternal & Pediat Infect Dis Branch, 6100 Execut Blvd,Room 4B11,MSC 7510, Bethesda, MD 20892 USA.
EM wattsh@mail.nih.gov
FU HIV Prevention Trials Network (HPTN); National Institute of Allergy and
   Infectious Diseases of the National Institutes of Health; National
   Institute of Child Health and Human Development of the National
   Institutes of Health; National Institute on Drug Abuse of the National
   Institutes of Health; National Institute of Mental Health of the
   National Institutes of Health; Office of AIDS Research of the National
   Institutes of Health; NICHD [N01-DK-9-001/HHSN267200800001C]; US
   Department of Health and Human Services [U01 AI046749]
FX This study was supported by the HIV Prevention Trials Network (HPTN) and
   sponsored by the National Institute of Allergy and Infectious Diseases,
   National Institute of Child Health and Human Development, National
   Institute on Drug Abuse, National Institute of Mental Health, and Office
   of AIDS Research, of the National Institutes of Health, US Department of
   Health and Human Services under award U01 AI046749. Overall support for
   the International Maternal Pediatric Adolescent AIDS Clinical Trials
   Group (IMPAACT) was provided by the National Institute of Allergy and
   Infectious Diseases (NIAID) (U01 AI068632), the Eunice Kennedy Shriver
   National Institute of Child Health and Human Development (NICHD), and
   the National Institute of Mental Health (NIMH) (AI068632). The content
   is solely the responsibility of the authors and does not necessarily
   represent the official views of the NIH. Support of the sites was
   provided by the National Institute of Allergy and Infectious Diseases
   (NIAID) and the NICHD International and Domestic Pediatric and Maternal
   HIV Clinical Trials Network funded by NICHD (contract number
   N01-DK-9-001/HHSN267200800001C). The study products were provided for
   free by Boehringer-Ingelheim.
NR 21
TC 4
Z9 4
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
EI 1077-9450
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD NOV 1
PY 2013
VL 64
IS 3
BP 299
EP 306
PG 8
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 300GY
UT WOS:000330453600011
PM 23846568
ER

PT J
AU Greenberg, AE
   Purcell, DW
   Gordon, CM
   Flores, S
   Grossman, C
   Fisher, HH
   Barasky, RJ
AF Greenberg, Alan E.
   Purcell, David W.
   Gordon, Christopher M.
   Flores, Stephen
   Grossman, Cynthia
   Fisher, Holly H.
   Barasky, Rebecca J.
TI NIH Support of Centers for AIDS Research and Department of Health
   Collaborative Public Health Research: Advancing CDC's Enhanced
   Comprehensive HIV Prevention Planning Project
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE Centers for AIDS Research; Enhanced Comprehensive HIV Prevention
   Planning; National HIV/AIDS Strategy; HIV care continuum; HIV treatment
   cascade
ID CARE; RECOMMENDATIONS
C1 [Greenberg, Alan E.; Barasky, Rebecca J.] George Washington Univ, Sch Publ Hlth & Hlth Serv, Dept Epidemiol & Biostat, Washington, DC 20037 USA.
   [Greenberg, Alan E.; Barasky, Rebecca J.] Dist Columbia Dev Ctr AIDS Res, Washington, DC USA.
   [Purcell, David W.; Flores, Stephen; Fisher, Holly H.] Ctr Dis Control & Prevent, Atlanta, GA USA.
   [Gordon, Christopher M.; Grossman, Cynthia] NIMH, Bethesda, MD 20892 USA.
RP Greenberg, AE (reprint author), George Washington Univ, Sch Publ Hlth & Hlth Serv, Dept Epidemiol & Biostat, 2100-W Penn Ave NW,8th Floor, Washington, DC 20037 USA.
EM aeg1@gwu.edu
FU National Institutes of Health [5P30AI087714]
FX Supported by supplemental funds to the National Institutes of Health
   funded District of Columbia Developmental Center for AIDS Research
   (CFAR) grant (5P30AI087714) for the CFAR Enhanced Comprehensive HIV
   Prevention Planning initiative.
NR 28
TC 4
Z9 4
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
EI 1077-9450
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD NOV 1
PY 2013
VL 64
SU 1
BP S1
EP S6
PG 6
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 300JW
UT WOS:000330461200001
PM 23982663
ER

PT J
AU Tsutsui, Y
   Ramakrishnan, B
   Qasba, PK
AF Tsutsui, Yuko
   Ramakrishnan, Boopathy
   Qasba, Pradman K.
TI Crystal Structures of beta-1,4-Galactosyltransferase 7 Enzyme Reveal
   Conformational Changes and Substrate Binding
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID EHLERS-DANLOS-SYNDROME; HEPARAN-SULFATE; COMPLEX; PROTEOGLYCANS;
   BIOSYNTHESIS; RECOGNITION; SNAPSHOTS; DONOR; GENE
AB The beta-1,4-galactosyltransferase 7 (beta 4GalT7) enzyme is involved in proteoglycan synthesis. In the presence of a manganese ion, it transfers galactose from UDP-galactose to xylose on a proteoglycan acceptor substrate. We present here the crystal structures of human beta 4GalT7 in open and closed conformations. A comparison of these crystal structures shows that, upon manganese and UDP or UDP-Gal binding, the enzyme undergoes conformational changes involving a small and a long loop. We also present the crystal structures of Drosophila wild-type beta 4GalT7 and D211N beta 4GalT7 mutant enzymes in the closed conformation in the presence of the acceptor substrate xylobiose and the donor substrate UDP-Gal, respectively. To understand the catalytic mechanism, we have crystallized the ternary complex of D211N beta 4GalT7 mutant enzyme in the presence of manganese with the donor and the acceptor substrates together in the same crystal structure. The galactose moiety of the bound UDP-Gal molecule forms seven hydrogen bonds with the protein molecule. The nonreducing end of the xylose moiety of xylobiose binds to the hydrophobic acceptor sugar binding pocket created by the conformational changes, whereas its extended xylose moiety forms hydrophobic interactions with a Tyr residue. In the ternary complex crystal structure, the nucleophile O4 oxygen atom of the xylose molecule is found in close proximity to the C1 and O5 atoms of the galactose moiety. This is the first time that a Michaelis complex of a glycosyltransferase has been described, and it clearly suggests an S(N)2 type catalytic mechanism for the beta 4GalT7 enzyme.
C1 NCI, Struct Glycobiol Sect, NIH, Frederick, MD 21702 USA.
   NCI, Basic Res Program, SAIC Frederick Inc, Nanobiol Program,Ctr Canc Res,NIH, Frederick, MD 21702 USA.
RP Qasba, PK (reprint author), Frederick Natl Lab Canc Res, Struct Glycobiol Sect, Bldg 469,Rm 221,POB B, Frederick, MD 21702 USA.
EM qasba@helix.nih.gov
FU National Cancer Institute, National Institutes of Health
   [HHSN261200800001E]; Intramural Research Program of the National
   Institutes of Health, NCI, National Institutes of Health
FX This project has been funded in whole or in part with federal funds from
   the National Cancer Institute, National Institutes of Health, under
   contract HHSN261200800001E (to P. K. Q.). This research was supported
   (in part) by the Intramural Research Program of the National Institutes
   of Health, NCI, National Institutes of Health.
NR 37
TC 12
Z9 13
U1 3
U2 17
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 1
PY 2013
VL 288
IS 44
BP 31963
EP 31970
DI 10.1074/jbc.M113.509984
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 302HX
UT WOS:000330596200049
PM 24052259
ER

PT J
AU Hall, BE
   Wankhade, UD
   Konkel, JE
   Cherukuri, K
   Nagineni, CN
   Flanders, KC
   Arany, PR
   Chen, WJ
   Rane, SG
   Kulkarni, AB
AF Hall, Bradford E.
   Wankhade, Umesh D.
   Konkel, Joanne E.
   Cherukuri, Karthik
   Nagineni, Chandrasekharam N.
   Flanders, Kathleen C.
   Arany, Praveen R.
   Chen, Wanjun
   Rane, Sushil G.
   Kulkarni, Ashok B.
TI Transforming Growth Factor-beta 3 (TGF-beta 3) Knock-in Ameliorates
   Inflammation Due to TGF-beta 1 Deficiency While Promoting Glucose
   Tolerance
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID MESENCHYMAL STEM-CELLS; FACTOR-BETA; TGF-BETA; TARGETED DISRUPTION;
   EXPRESSION PATTERNS; CRYSTAL-STRUCTURE; TRANSGENIC MICE; PALATE FUSION;
   ADULT TISSUES; CLEFT-PALATE
AB Three homologues of TGF-beta exist in mammals as follows: TGF-beta 1, TGF-beta 2, and TGF-beta 3. All three proteins share high homology in their amino acid sequence, yet each TGF-beta isoform has unique heterologous motifs that are highly conserved during evolution. Although these TGF-beta proteins share similar properties in vitro, isoform-specific properties have been suggested through in vivo studies and by the unique phenotypes for each TGF-beta knock-out mouse. To test our hypothesis that each of these homologues has nonredundant functions, and to identify such isoform-specific roles, we genetically exchanged the coding sequence of the mature TGF-beta 1 ligand with a sequence from TGF-beta 3 using targeted recombination to create chimeric TGF-beta 1/3 knock-in mice (TGF-beta 1(L beta 3/L beta 3)). In the TGF-beta 1(L beta 3/L beta 3) mouse, localization and activation still occur through the TGF-beta 1 latent associated peptide, but cell signaling is triggered through the TGF-beta 3 ligand that binds to TGF-beta receptors. Unlike TGF-beta 1(-/-) mice, the TGF-beta 1(L beta 3/L beta 3) mice show neither embryonic lethality nor signs of multifocal inflammation, demonstrating that knock-in of the TGF-beta 3 ligand can prevent the vasculogenesis defects and autoimmunity associated with TGF-beta 1 deficiency. However, the TGF-beta 1(L beta 3/L beta 3) mice have a shortened life span and display tooth and bone defects, indicating that the TGF-beta homologues are not completely interchangeable. Remarkably, the TGF-beta 1(L beta 3/L beta 3) mice display an improved metabolic phenotype with reduced body weight gain and enhanced glucose tolerance by induction of beneficial changes to the white adipose tissue compartment. These findings reveal both redundant and unique nonoverlapping functional diversity in TGF-beta isoform signaling that has relevance to the design of therapeutics aimed at targeting the TGF-beta pathway in human disease.
C1 [Hall, Bradford E.; Cherukuri, Karthik; Kulkarni, Ashok B.] NIDCR, Funct Genom Sect, Lab Cell & Dev Biol, NIH, Bethesda, MD 20892 USA.
   [Konkel, Joanne E.; Chen, Wanjun] NIDCR, Mucosal Immunol Sect, NIH, Bethesda, MD 20892 USA.
   [Arany, Praveen R.] NIDCR, Cell Regulat & Control Unit, NIH, Bethesda, MD 20892 USA.
   [Wankhade, Umesh D.; Rane, Sushil G.] NIDDK, Cell Growth & Metab Sect, NIH, Bethesda, MD 20892 USA.
   [Nagineni, Chandrasekharam N.] NEI, NIH, Bethesda, MD 20892 USA.
   [Flanders, Kathleen C.] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
RP Kulkarni, AB (reprint author), NIDCR, Funct Genom Sect, Lab Cell & Dev Biol, NIH, 30 Convent Dr,Bldg 30,Rm 130, Bethesda, MD 20892 USA.
EM ak40m@nih.gov
FU National Institutes of Health [ZO1 DE000698-13]; Divisions of Intramural
   Research, NIDCR; Divisions of Intramural Research, NCI; Divisions of
   Intramural Research, NIDDK
FX This work was supported, in whole or in part, by National Institutes of
   Health Grant ZO1 DE000698-13 and grants from Divisions of Intramural
   Research, NIDCR, NCI, and NIDDK.
NR 66
TC 7
Z9 8
U1 0
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 1
PY 2013
VL 288
IS 44
BP 32074
EP 32092
DI 10.1074/jbc.M113.480764
PG 19
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 302HX
UT WOS:000330596200058
PM 24056369
ER

PT J
AU Arora, NK
   Jensen, RE
   Sulayman, N
   Hamilton, AS
   Potosky, AL
AF Arora, Neeraj K.
   Jensen, Roxanne E.
   Sulayman, Nadiyah
   Hamilton, Ann S.
   Potosky, Arnold L.
TI Patient-Physician Communication About Health-Related Quality-of-Life
   Problems: Are Non-Hodgkin Lymphoma Survivors Willing to Talk?
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID RANDOMIZED CONTROLLED-TRIAL; CANCER-PATIENTS; ONCOLOGY; ASSESSMENTS;
   CARE; PROFESSIONALS; INTERVENTION; SATISFACTION; RECOGNITION; CHALLENGES
AB Purpose
   To investigate non-Hodgkin lymphoma (NHL) survivors' willingness to discuss health-related quality-of-life (HRQOL) problems with their follow-up care physician.
   Patients and Methods
   Willingness to discuss HRQOL problems (physical, daily, emotional, social, and sexual functioning) was examined among 374 NHL survivors, 2 to 5 years postdiagnosis. Survivors were asked if they would bring up HRQOL problems with their physician and indicate reasons why not. Logistic regression models examined the association of patient sociodemographics, clinical characteristics, follow-up care variables, and current HRQOL scores with willingness to discuss HRQOL problems.
   Results
   Overall, 94%, 82%, 76%, 43%, and 49% of survivors would initiate discussions of physical, daily, emotional, social, and sexual functioning, respectively. Survivors who indicated their physician "always" spent enough time with them or rated their care as "excellent" were more willing to discuss HRQOL problems (P < .05). Survivors reporting poorer physical health were less willing to discuss their daily functioning problems (P < .001). Men were more willing to discuss sexual problems than women (P < .001). One in three survivors cited "nothing can be done" as a reason for not discussing daily functioning problems, and at least one in four cited "this was not their doctor's job" and a preference to "talk to another clinician" as reasons for not discussing emotional, social, and sexual functioning.
   Conclusion
   NHL survivors' willingness to raise HRQOL problems with their physician varied by HRQOL domain. For some domains, even when survivors were experiencing problems, they may not discuss them. To deliver cancer care for the whole patient, interventions that facilitate survivor-clinician communication about survivors' HRQOL are needed. (C) 2013 by American Society of Clinical Oncology
C1 [Arora, Neeraj K.] NCI, Bethesda, MD 20892 USA.
   [Jensen, Roxanne E.; Sulayman, Nadiyah; Potosky, Arnold L.] Georgetown Univ, Washington, DC USA.
   [Hamilton, Ann S.] Univ So Calif, Los Angeles, CA USA.
RP Arora, NK (reprint author), NCI, Div Canc Control & Populat Sci, 9606 Med Ctr Dr,3E514,MSC 9762, Bethesda, MD 20892 USA.
EM aroran@mail.nih.gov
FU California Department of Health Services as part of the statewide cancer
   reporting program [103885]; National Cancer Institute's Surveillance,
   Epidemiology, and End Results Program [N01-PC-35139]; Centers for
   Disease Control and Prevention's National Program of Cancer Registries
   [N02-PC-15105, U55/CCR921930-02]
FX Supported by the California Department of Health Services as part of the
   statewide cancer reporting program mandated by California Health and
   Safety Code Section 103885, Contract No. N01-PC-35139 from the National
   Cancer Institute's Surveillance, Epidemiology, and End Results Program
   awarded to the University of Southern California, Contract No.
   N02-PC-15105 awarded to the Public Health Institute (PHI), and Agreement
   No. U55/CCR921930-02 awarded to the PHI from the Centers for Disease
   Control and Prevention's National Program of Cancer Registries.
NR 44
TC 5
Z9 5
U1 1
U2 8
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 NOV 1
PY 2013
VL 31
IS 31
BP 3964
EP 3970
DI 10.1200/JCO.2012.47.6705
PG 7
WC Oncology
SC Oncology
GA 301OD
UT WOS:000330540700020
PM 24062408
ER

PT J
AU Wolff, AC
   Hammond, MEH
   Hicks, DG
   Dowsett, M
   McShane, LM
   Allison, KH
   Allred, DC
   Bartlett, JMS
   Bilous, M
   Fitzgibbons, P
   Hanna, W
   Jenkins, RB
   Mangu, PB
   Paik, S
   Perez, EA
   Press, MF
   Spears, PA
   Vance, GH
   Viale, G
   Hayes, DF
AF Wolff, Antonio C.
   Hammond, M. Elizabeth H.
   Hicks, David G.
   Dowsett, Mitch
   McShane, Lisa M.
   Allison, Kimberly H.
   Allred, Donald C.
   Bartlett, John M. S.
   Bilous, Michael
   Fitzgibbons, Patrick
   Hanna, Wedad
   Jenkins, Robert B.
   Mangu, Pamela B.
   Paik, Soonmyung
   Perez, Edith A.
   Press, Michael F.
   Spears, Patricia A.
   Vance, Gail H.
   Viale, Giuseppe
   Hayes, Daniel F.
TI Recommendations for Human Epidermal Growth Factor Receptor 2 Testing in
   Breast Cancer: American Society of Clinical Oncology/College of American
   Pathologists Clinical Practice Guideline Update
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID IN-SITU HYBRIDIZATION; HER2 GENE AMPLIFICATION; RABBIT
   MONOCLONAL-ANTIBODY; CORE NEEDLE-BIOPSY; TIME RT-PCR; ASCO/CAP
   HER2-POSITIVITY CRITERIA; ADJUVANT TRASTUZUMAB BENEFIT; TISSUE
   MICROARRAY TECHNOLOGY; POLYMERASE CHAIN-REACTION; ESTROGEN-RECEPTOR
AB Purpose
   To update the American Society of Clinical Oncology (ASCO)/College of American Pathologists (CAP) guideline recommendations for human epidermal growth factor receptor 2 (HER2) testing in breast cancer to improve the accuracy of HER2 testing and its utility as a predictive marker in invasive breast cancer.
   Methods
   ASCO/CAP convened an Update Committee that included coauthors of the 2007 guideline to conduct a systematic literature review and update recommendations for optimal HER2 testing.
   Results
   The Update Committee identified criteria and areas requiring clarification to improve the accuracy of HER2 testing by immunohistochemistry (IHC) or in situ hybridization (ISH). The guideline was reviewed and approved by both organizations.
   Recommendations
   The Update Committee recommends that HER2 status (HER2 negative or positive) be determined in all patients with invasive (early stage or recurrence) breast cancer on the basis of one or more HER2 test results (negative, equivocal, or positive). Testing criteria define HER2-positive status when (on observing within an area of tumor that amounts to > 10% of contiguous and homogeneous tumor cells) there is evidence of protein overexpression (IHC) or gene amplification (HER2 copy number or HER2/CEP17 ratio by ISH based on counting at least 20 cells within the area). If results are equivocal (revised criteria), reflex testing should be performed using an alternative assay (IHC or ISH). Repeat testing should be considered if results seem discordant with other histopathologic findings. Laboratories should demonstrate high concordance with a validated HER2 test on a sufficiently large and representative set of specimens. Testing must be performed in a laboratory accredited by CAP or another accrediting entity. The Update Committee urges providers and health systems to cooperate to ensure the highest quality testing.
C1 [Wolff, Antonio C.] Johns Hopkins Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
   [McShane, Lisa M.] NCI, Bethesda, MD 20892 USA.
   [Hammond, M. Elizabeth H.] Univ Utah, Sch Med & Intermt Healthcare, Salt Lake City, UT USA.
   [Hicks, David G.] Univ Rochester, Med Ctr, Rochester, NY 14642 USA.
   [Dowsett, Mitch] Royal Marsden Hosp, London SW3 6JJ, England.
   [Allison, Kimberly H.] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
   [Fitzgibbons, Patrick] St Jude Med Ctr, Fullerton, CA USA.
   [Press, Michael F.] Univ So Calif, Los Angeles, CA USA.
   [Allred, Donald C.] Washington Univ, Sch Med, St Louis, MO USA.
   [Bartlett, John M. S.] Ontario Canc Inst Res, Toronto, ON, Canada.
   [Hanna, Wedad] Sunnybrook Hlth Sci Ctr, Toronto, ON M4N 3M5, Canada.
   [Bilous, Michael] Univ Western Sydney & Healthscope Pathol, Sydney, NSW, Australia.
   [Jenkins, Robert B.] Mayo Clin, Rochester, MN USA.
   [Mangu, Pamela B.] Amer Soc Clin Oncol, Alexandria, VA 22314 USA.
   [Paik, Soonmyung] Natl Surg Adjuvant Breast & Bowel Project, Pittsburgh, PA USA.
   [Perez, Edith A.] Mayo Clin, Jacksonville, FL 32224 USA.
   [Spears, Patricia A.] N Carolina State Univ, Raleigh, NC 27695 USA.
   [Vance, Gail H.] Indiana Univ, Med Ctr, Indianapolis, IN USA.
   [Viale, Giuseppe] Univ Milan, European Inst Oncol, Milan, Italy.
   [Hayes, Daniel F.] Univ Michigan, Comprehens Canc Care Ctr, Ann Arbor, MI 48109 USA.
RP Wolff, AC (reprint author), Amer Soc Clin Oncol, 2318 Mill Rd,Suite 800, Alexandria, VA 22314 USA.
EM guidelines@asco.org
OI Wolff, Antonio/0000-0003-3734-1063
NR 154
TC 749
Z9 786
U1 8
U2 44
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 NOV 1
PY 2013
VL 31
IS 31
BP 3997
EP +
DI 10.1200/JCO.2013.50.9984
PG 18
WC Oncology
SC Oncology
GA 301OD
UT WOS:000330540700024
PM 24101045
ER

PT J
AU Lambert, BL
   Bann, CM
   Bauer, CR
   Shankaran, S
   Bada, HS
   Lester, BM
   Whitaker, TM
   LaGasse, LL
   Hammond, J
   Higgins, RD
AF Lambert, Brittany L.
   Bann, Carla M.
   Bauer, Charles R.
   Shankaran, Seetha
   Bada, Henrietta S.
   Lester, Barry M.
   Whitaker, Toni M.
   LaGasse, Linda L.
   Hammond, Jane
   Higgins, Rosemary D.
TI Risk-Taking Behavior Among Adolescents with Prenatal Drug Exposure and
   Extrauterine Environmental Adversity
SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS
LA English
DT Article
DE prenatal drug exposure; cocaine; adolescence; risk-taking behavior
ID INTRAUTERINE COCAINE EXPOSURE; SUBSTANCE USE; NEUROBEHAVIORAL
   DISINHIBITION; SEXUAL INTERCOURSE; IMPULSE CONTROL; HEALTH-RISK;
   CHILDREN; CHILDHOOD; VIOLENCE; GENDER
AB Objective: High-risk environments characterized by familial substance use, poverty, inadequate parental monitoring, and violence exposure are associated with an increased propensity for adolescents to engage in risk-taking behaviors (e. g., substance use, sexual behavior, and delinquency). However, additional factors such as drug exposure in utero and deficits in inhibitory control among drug-exposed youth may further influence the likelihood that adolescents in high-risk environments will engage in risk-taking behavior. This study examined the influence of prenatal substance exposure, inhibitory control, and sociodemographic/environmental risk factors on risk-taking behaviors in a large cohort of adolescents with and without prenatal cocaine exposure (PCE). Method: Risk-taking behavior (delinquency, substance use, and sexual activity) was assessed in 963 adolescents (433 cocaine-exposed, 530 nonexposed) at 15 years of age. Results: Prenatal cocaine exposure predicted later arrests and early onset of sexual behavior in controlled analyses. Associations were partially mediated, however, by adolescent inhibitory control problems. PCE was not associated with substance use at this age. In addition, male gender, low parental involvement, and violence exposure were associated with greater odds of engaging in risk-taking behavior across the observed domains. Conclusions: Study findings substantiate concern regarding the association between prenatal substance exposure and related risk factors and the long-term outcomes of exposed youth. Access to the appropriate social, educational, and medical services is essential in preventing and intervening with risk-taking behaviors and the potential consequences (e. g., adverse health outcomes and incarceration), especially among high-risk adolescent youth and their families.
C1 [Lambert, Brittany L.] Univ Miami, Dept Psychol, Coral Gables, FL 33146 USA.
   [Bann, Carla M.; Hammond, Jane] RTI Int, Dept Stat & Epidemiol, Res Triangle Pk, NC USA.
   [Bauer, Charles R.] Univ Miami, Miller Sch Med, Dept Pediat, Miami, FL 33136 USA.
   [Shankaran, Seetha] Wayne State Univ, Sch Med, Dept Pediat, Detroit, MI 48201 USA.
   [Bada, Henrietta S.] Univ Kentucky Hosp, Dept Pediat, Lexington, KY USA.
   [Lester, Barry M.; LaGasse, Linda L.] Brown Univ, Dept Pediat, Brown Ctr Study Children Risk, Warren Alpert Med Sch,Women & Infants Hosp Rhode, Providence, RI 02912 USA.
   [Whitaker, Toni M.] Univ Tennessee, Hlth Sci Ctr, Dept Pediat, Boling Ctr Dev Disabil, Memphis, TN USA.
   [Higgins, Rosemary D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Lambert, BL (reprint author), Univ Miami, Dept Psychol, Flipse Bldg,5665 Ponce de Leon Blvd,Room 116, Coral Gables, FL 33146 USA.
EM blambert@psy.miami.edu
FU National Institutes of Health through the National Institute on Drug
   Abuse; Eunice Kennedy Shriver National Institute of Child Health and
   Human Development; National Institute of Mental Health; Administration
   on Children, Youth, and Families; Center for Substance Abuse and
   Treatment, US Department of Health and Human Services
FX This investigation was supported by the National Institutes of Health
   through the National Institute on Drug Abuse and the Eunice Kennedy
   Shriver National Institute of Child Health and Human Development, with
   supplemental funding from the National Institute of Mental Health, the
   Administration on Children, Youth, and Families and the Center for
   Substance Abuse and Treatment, US Department of Health and Human
   Services. We are indebted to our medical and nursing colleagues and the
   infants and their parents who agreed to take part in this study.
NR 48
TC 7
Z9 8
U1 2
U2 15
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0196-206X
EI 1536-7312
J9 J DEV BEHAV PEDIATR
JI J. Dev. Behav. Pediatr.
PD NOV-DEC
PY 2013
VL 34
IS 9
BP 669
EP 679
PG 11
WC Behavioral Sciences; Psychology, Developmental; Pediatrics
SC Behavioral Sciences; Psychology; Pediatrics
GA 298YB
UT WOS:000330359500005
PM 24220515
ER

PT J
AU Olivera, A
   Kitamura, Y
   Wright, LD
   Allende, ML
   Chen, WP
   Kaneko-Goto, T
   Yoshihara, Y
   Proia, RL
   Rivera, J
AF Olivera, Ana
   Kitamura, Yoshiaki
   Wright, Laurel D.
   Allende, Maria L.
   Chen, Weiping
   Kaneko-Goto, Tomomi
   Yoshihara, Yoshihiro
   Proia, Richard L.
   Rivera, Juan
TI Sphingosine-1-phosphate can promote mast cell hyper-reactivity through
   regulation of contactin-4 expression
SO JOURNAL OF LEUKOCYTE BIOLOGY
LA English
DT Article
DE Fc epsilon RI; mast cell degranulation; cytokine production; anaphylaxis
ID MEMBRANE-PROTEIN SLMAP; SPHINGOSINE 1-PHOSPHATE; MYELINATED AXONS; K+
   CHANNELS; CA2+ INFLUX; ACTIVATION; IMMUNITY; KINASE; LYASE; RESPONSES
AB Both genes and the environment are determinants in the susceptibility to allergies and may alter the severity of the disease. We explored whether an increase in the levels of the lipid mediator S1P in vivo, a condition found during allergic asthma, could affect the sensitivity or the response of MCs to IgE/Ag and the onset of allergic disease. We found that increasing S1P levels by genetic deletion of S1P lyase, the enzyme catabolizing S1P, led to elevated activity of circulating tryptase. Accordingly, MCs of S1P lyase-deficient mice were mostly degranulated in the tissues and showed enhanced calcium levels, degranulation, and cytokine production in response to IgE/Ag in vitro. Th 1-skewed mice (C57BL/6) had lower levels of S1P in circulation and histamine responses than did Th 2-skewed (129/Sv) mice. However, when S1P levels were increased by pharmacologic inhibition of S1P lyase, the C57BL/6 mice showed increased histamine release into the circulation and anaphylactic responses similar to those in the 129/Sv mice. Culturing of MCs in the presence of S1P enhanced their degranulation responses, and when the S1P-treated MCs were used to reconstitute MC-deficient (Kit(W-sh)) mice, they caused enhanced anaphylaxis. Gene expression arrays in S1P lyase-deficient MCs and MCs treated with S1P continuously revealed increased expression of numerous genes, including the adhesion molecule CNTN4, which contributed to the enhanced responses. Our findings argue that dysregulation in the metabolism of S1P is a contributing factor in modulating MC responsiveness and the allergic response.
C1 [Olivera, Ana; Kitamura, Yoshiaki; Wright, Laurel D.; Rivera, Juan] NIAMSD, Immunogenet Mol Lab, NIH, Bethesda, MD 20892 USA.
   [Allende, Maria L.; Proia, Richard L.] NIDDK, Genet Dev & Dis Branch, NIH, Bethesda, MD 20892 USA.
   [Chen, Weiping] NIDDK, Genom Core, NIH, Bethesda, MD 20892 USA.
   [Kaneko-Goto, Tomomi; Yoshihara, Yoshihiro] RIKEN Brain Sci Inst, Lab Neurobiol Synapse, Saitama, Japan.
RP Olivera, A (reprint author), NIAMS, Immunogenet Mol Lab, NIH, Bldg 10,Room 13C103, Bethesda, MD 20892 USA.
EM oliveraa@ep.niams.nih.gov; juan_rivera@nih.gov
RI Yoshihara, Yoshihiro/N-6481-2015
FU Intramural Research Program of the NIAMS; NIDDK of the U.S. National
   Institutes of Health; Laboratory Animal Care and Use Section of the
   Office of Science and Technology, NIAMS
FX This work was supported by the Intramural Research Program of the NIAMS
   and the NIDDK of the U.S. National Institutes of Health. We are grateful
   for the support of the Laboratory Animal Care and Use Section of the
   Office of Science and Technology, NIAMS. We are also grateful to Dr.
   Barbara Dema for help with statistical analysis.
NR 75
TC 6
Z9 6
U1 0
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0741-5400
EI 1938-3673
J9 J LEUKOCYTE BIOL
JI J. Leukoc. Biol.
PD NOV
PY 2013
VL 94
IS 5
BP 1013
EP 1024
DI 10.1189/jlb.0313163
PG 12
WC Cell Biology; Hematology; Immunology
SC Cell Biology; Hematology; Immunology
GA 301MZ
UT WOS:000330537700018
PM 23904439
ER

PT J
AU Fessler, MB
   Rose, K
   Zhang, YM
   Jaramillo, R
   Zeldin, DC
AF Fessler, Michael B.
   Rose, Kathryn
   Zhang, Yanmei
   Jaramillo, Renee
   Zeldin, Darryl C.
TI Relationship between serum cholesterol and indices of erythrocytes and
   platelets in the US population
SO JOURNAL OF LIPID RESEARCH
LA English
DT Article
DE high density lipoprotein-cholesterol; non-high density
   lipoprotein-cholesterol; hematocrit; National Health and Nutrition
   Examination Survey
ID HIGH-DENSITY-LIPOPROTEIN; CORONARY-HEART-DISEASE; SCAVENGER RECEPTOR BI;
   METABOLIC SYNDROME; TYPE-2 HYPERCHOLESTEROLEMIA;
   CARDIOVASCULAR-DISEASES; SEDIMENTATION-RATE; DIABETES-MELLITUS;
   HEMOLYTIC-ANEMIA; LEUKOCYTE COUNT
AB Whereas dyslipidemia has been associated with leukocytosis, the relationship between serum cholesterol and other hematopoietic lineages is poorly defined. Erythrocytes and platelets, anucleate cells relegated to nonspecific diffusional exchange of cholesterol with serum, have been proposed to have a distinct relationship to cholesterol from leukocytes. We examined the relationship between serum cholesterol and circulating erythrocyte/platelet indices in 4,469 adult participants of the National Health and Nutrition Examination Survey (NHANES) 2005-2006. In linear regression analyses, serum non-high density lipoprotein-cholesterol (non-HDL-C) was positively associated with mean erythrocyte number, hematocrit, hemoglobin concentration, platelet count, and platelet crit independently of age, gender, race/ethnicity, smoking, body mass index, serum folate, and C-reactive protein. The magnitude of the relationship was most marked for platelets, with lowest versus highest non-HDL-C quartile subjects having geometric mean platelet counts of 258,000/mu l versus 281,000/mu l, respectively (adjusted model, P < 0.001 for trend). These associations persisted in a sensitivity analysis excluding several conditions that affect erythrocyte/platelet and/or serum cholesterol levels, and were also noted in an independent analysis of 5,318 participants from NHANES 2007-2008. As non-HDL-C, erythrocytes, and platelets all impact cardiovascular disease risk, there is a need for advancing understanding of the underlying interactions that govern levels of these three blood components.
C1 [Fessler, Michael B.; Zeldin, Darryl C.] NIEHS, Biol Res Lab, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA.
   [Rose, Kathryn; Zhang, Yanmei; Jaramillo, Renee] SRA Int, Durham, NC 27713 USA.
RP Fessler, MB (reprint author), NIEHS, Biol Res Lab, NIH, US Dept HHS, POB 12233, Res Triangle Pk, NC 27709 USA.
EM fesslerm@niehs.nih.gov
FU Intramural Research Program of the National Institute of Environmental
   Health Sciences, National Institutes of Health [Z01 ES-102005, Z01
   ES-025041]
FX This work was supported in part by the Intramural Research Program of
   the National Institute of Environmental Health Sciences, National
   Institutes of Health Grants Z01 ES-102005 and Z01 ES-025041.
NR 59
TC 6
Z9 6
U1 0
U2 8
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0022-2275
EI 1539-7262
J9 J LIPID RES
JI J. Lipid Res.
PD NOV
PY 2013
VL 54
IS 11
BP 3177
EP 3188
DI 10.1194/jlr.P037614
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 301LS
UT WOS:000330534400025
PM 23999863
ER

PT J
AU Kim, P
   Arizpe, J
   Rosen, BH
   Razdan, V
   Haring, CT
   Jenkins, SE
   Deveney, CM
   Brotman, MA
   Blair, JR
   Pine, DS
   Baker, CI
   Leibenluft, E
AF Kim, Pilyoung
   Arizpe, Joseph
   Rosen, Brooke H.
   Razdan, Varun
   Haring, Catherine T.
   Jenkins, Sarah E.
   Deveney, Christen M.
   Brotman, Melissa A.
   Blair, James R.
   Pine, Daniel S.
   Baker, Chris I.
   Leibenluft, Ellen
TI Impaired fixation to eyes during facial emotion labelling in children
   with bipolar disorder or severe mood dysregulation
SO JOURNAL OF PSYCHIATRY & NEUROSCIENCE
LA English
DT Article
ID VISUAL SCAN PATHS; AMYGDALA ACTIVATION; NEURAL CIRCUITRY; FACE
   RECOGNITION; RATING-SCALE; SCHIZOPHRENIA; EXPRESSIONS; GAZE; PERCEPTION;
   AUTISM
AB Background: Children with bipolar disorder (BD) or severe mood dysregulation (SMD) show behavioural and neural deficits during facial emotion processing. In those with other psychiatric disorders, such deficits have been associated with reduced attention to eye regions while looking at faces. Methods: We examined gaze fixation patterns during a facial emotion labelling task among children with pediatric BD and SMD and among healthy controls. Participants viewed facial expressions with varying emotions (anger, fear, sadness, happiness, neutral) and emotional levels (60%, 80%, 100%) and labelled emotional expressions. Results: Our study included 22 children with BD, 28 with SMD and 22 controls. Across all facial emotions, children with BD and SMD made more labelling errors than controls. Compared with controls, children with BD spent less time looking at eyes and made fewer eye fixations across emotional expressions. Gaze patterns in children with SMD tended to fall between those of children with BD and controls, although they did not differ significantly from either of these groups on most measures. Decreased fixations to eyes correlated with lower labelling accuracy in children with BD, but not in those with SMD or in controls. Limitations: Most children with BD were medicated, which precluded our ability to evaluate medication effects on gaze patterns. Conclusion: Facial emotion labelling deficits in children with BD are associated with impaired attention to eyes. Future research should examine whether impaired attention to eyes is associated with neural dysfunction. Eye gaze deficits in children with BD during facial emotion labelling may also have treatment implications. Finally, children with SMD exhibited decreased attention to eyes to a lesser extent than those with BD, and these equivocal findings are worthy of further study.
C1 [Kim, Pilyoung; Rosen, Brooke H.; Razdan, Varun; Haring, Catherine T.; Jenkins, Sarah E.; Deveney, Christen M.; Brotman, Melissa A.; Blair, James R.; Pine, Daniel S.; Leibenluft, Ellen] NIMH, Emot & Dev Branch, NIH, US Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
   [Kim, Pilyoung] Univ Denver, Dept Psychol, Denver, CO 80208 USA.
   [Arizpe, Joseph; Baker, Chris I.] NIMH, Lab Brain & Cognit, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Kim, P (reprint author), Univ Denver, Dept Psychol, 2155 South Race St, Denver, CO 80208 USA.
EM pilyoung.kim@du.edu
RI Brotman, Melissa/H-7409-2013; Arizpe, Joseph/N-1399-2014; 
OI Arizpe, Joseph/0000-0001-8958-7757; Baker, Chris/0000-0001-6861-8964
FU Intramural Research Program of the National Institute of Mental Health
   (NIMH), National Institutes of Health
FX Funding for this study was provided exclusively by the Intramural
   Research Program of the National Institute of Mental Health (NIMH),
   National Institutes of Health. We thank the staff of the Emotion and
   Development Branch at NIMH and the children and families for their
   participation.
NR 59
TC 2
Z9 2
U1 5
U2 16
PU CMA-CANADIAN MEDICAL ASSOC
PI OTTAWA
PA 1867 ALTA VISTA DR, OTTAWA, ONTARIO K1G 5W8, CANADA
SN 1180-4882
EI 1488-2434
J9 J PSYCHIATR NEUROSCI
JI J. Psychiatry Neurosci.
PD NOV
PY 2013
VL 38
IS 6
BP 407
EP 416
DI 10.1503/jpn.120232
PG 10
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 301IM
UT WOS:000330526000008
PM 23906351
ER

PT J
AU Fleischhacker, SE
   Flournoy, R
   Moore, LV
AF Fleischhacker, Sheila E.
   Flournoy, Rebecca
   Moore, Latetia V.
TI Meaningful, Measurable, and Manageable Approaches to Evaluating Healthy
   Food Financing Initiatives: An Overview of Resources and Approaches
SO JOURNAL OF PUBLIC HEALTH MANAGEMENT AND PRACTICE
LA English
DT Article
DE community and economic development; food access; healthy food financing
   initiatives; healthy food retail; policy evaluation
ID COMMUNITY-DEVELOPMENT; PHYSICAL-ACTIVITY; UNITED-STATES; ENVIRONMENTS;
   OBESITY; POLICY; ADOLESCENTS; RESTAURANTS; VALIDATION; ACCESS
AB More than 23 million Americans have limited access to grocery stores. Healthy food financing initiatives have been emerging at local, state, and federal levels to address grocery gaps. Through public-private partnerships, retailers have been awarded funding to open or renovate a variety of food outlets. Preliminary findings have reported increased access to healthy foods, as well as improved community and economic development. As policy makers continue to consider enacting or expanding these initiatives and as all program stakeholders increasingly seek information on program impacts, this article provides guidance on using meaningful, measurable, and manageable methods to evaluate program's multifaceted outcomes.
C1 [Fleischhacker, Sheila E.] NIH, NIH Div Nutr Res Coordinat, US Dept HHS, Bethesda, MD 20892 USA.
   [Flournoy, Rebecca] Alameda Cty Publ Hlth Dept, Oakland, CA USA.
   [Moore, Latetia V.] Ctr Dis Control & Prevent, Nutr Branch, Div Nutr Phys Act & Obes, Natl Ctr Chron Dis Prevent & Hlth Promot, Atlanta, GA USA.
RP Fleischhacker, SE (reprint author), NIH, NIH Div Nutr Res Coordinat, US Dept HHS, Two Democracy Plaza,Room 635,6707 Democracy Blvd, Bethesda, MD 20892 USA.
EM sheila.fleischhacker@nih.gov
NR 43
TC 6
Z9 6
U1 4
U2 14
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1078-4659
EI 1550-5022
J9 J PUBLIC HEALTH MAN
JI J. Public Health Manag. Pract.
PD NOV-DEC
PY 2013
VL 19
IS 6
BP 541
EP 549
DI 10.1097/PHH.0b013e318271c6eb
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 300ED
UT WOS:000330446300012
PM 23073081
ER

PT J
AU Moreland, J
   Nakashima, Y
   Alldredge, JW
   Zabow, G
AF Moreland, John
   Nakashima, Yoshihiro
   Alldredge, Jacob W.
   Zabow, Gary
TI Novel methods for in situ characterization of individual micro- and
   nanoscale magnetic particles
SO MRS BULLETIN
LA English
DT Article
ID SUSCEPTIBILITY ARTIFACTS; CONTRAST AGENTS; SPIN-ECHO; SIMULATION;
   BIOSENSORS; SPHERES; FIELDS; MODEL
AB New instrumentation is being developed to better understand the in vivo properties of magnetic particles suspended in solution or lodged in tissue. We describe three novel methods with the necessary sensitivity to measure the microscopic magnetic properties of individual magnetic particles and complexes quantitatively. The first method is based on proton nuclear magnetic resonance of a magnetic particle suspended in water in a microcapillary probe; the second method uses high-resolution magnetic resonance imaging of water surrounding a magnetic particle; and the third method is based on AC susceptometry with a magnetic cantilever that combines magnetic particle imaging concepts with probe microscopy. We present the physical basis for the measurements, estimate sensitivity limits, and discuss future impacts on the development of magnetic particles for bioimaging and bioassays.
C1 [Moreland, John] NIST, Phys Measurement Lab, Microsyst Project, Boulder, CO 80305 USA.
   [Nakashima, Yoshihiro; Alldredge, Jacob W.] NIST, Boulder, CO USA.
   [Zabow, Gary] NINDS, Bethesda, MD 20892 USA.
RP Moreland, J (reprint author), NIST, Phys Measurement Lab, Microsyst Project, Boulder, CO 80305 USA.
EM moreland@boulder.nist.gov; yoshihiro.nakashima@nist.gov;
   alldredg@boulder.nist.gov; zabowg@mail.nih.gov
NR 29
TC 0
Z9 0
U1 1
U2 5
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0883-7694
EI 1938-1425
J9 MRS BULL
JI MRS Bull.
PD NOV
PY 2013
VL 38
IS 11
BP 933
EP 937
DI 10.1557/mrs.2013.258
PG 5
WC Materials Science, Multidisciplinary; Physics, Applied
SC Materials Science; Physics
GA 298SU
UT WOS:000330345500020
ER

PT J
AU Grobman, WA
   Gilbert, SA
   Iams, JD
   Spong, CY
   Saade, G
   Mercer, BM
   Tita, ATN
   Rouse, DJ
   Sorokin, Y
   Leveno, KJ
   Tolosa, JE
   Thorp, JM
   Caritis, SN
   Van Dorsten, JP
AF Grobman, William A.
   Gilbert, Sharon A.
   Iams, Jay D.
   Spong, Catherine Y.
   Saade, George
   Mercer, Brian M.
   Tita, Alan T. N.
   Rouse, Dwight J.
   Sorokin, Yoram
   Leveno, Kenneth J.
   Tolosa, Jorge E.
   Thorp, John M.
   Caritis, Steve N.
   Van Dorsten, J. Peter
CA Eunice Kennedy Shriver Natl Inst C
TI Activity Restriction Among Women With a Short Cervix EDITORIAL COMMENT
SO OBSTETRICAL & GYNECOLOGICAL SURVEY
LA English
DT Editorial Material
C1 [Grobman, William A.] Northwestern Univ, Dept Obstet, Chicago, IL 60611 USA.
   Northwestern Univ, Dept Gynecol, Chicago, IL 60611 USA.
   Ohio State Univ, Columbus, OH 43210 USA.
   Univ Texas Med Branch, Galveston, TX 77555 USA.
   Case Western Reserve Univ, Metrohlth Med Ctr, Cleveland, OH USA.
   Univ Alabama Birmingham, Birmingham, AL USA.
   Brown Univ, Providence, RI 02912 USA.
   Wayne State Univ, Detroit, MI USA.
   Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
   Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
   Univ N Carolina, Chapel Hill, NC USA.
   Univ Pittsburgh, Pittsburgh, PA USA.
   Med Univ S Carolina, Charleston, SC 29425 USA.
   George Washington Univ, Ctr Biostat, Washington, DC USA.
   Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Grobman, WA (reprint author), Northwestern Univ, Dept Obstet, Chicago, IL 60611 USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7828
EI 1533-9866
J9 OBSTET GYNECOL SURV
JI Obstet. Gynecol. Surv.
PD NOV
PY 2013
VL 68
IS 11
BP 727
EP 728
PG 2
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 301DO
UT WOS:000330513200002
ER

PT J
AU Schietinger, A
   Arina, A
   Liu, RB
   Wells, S
   Huang, JH
   Engels, B
   Bindokas, V
   Bartkowiak, T
   Lee, D
   Herrmann, A
   Piston, DW
   Pittet, MJ
   Lin, PC
   Zal, T
   Schreiber, H
AF Schietinger, Andrea
   Arina, Ainhoa
   Liu, Rebecca B.
   Wells, Sam
   Huang, Jianhua
   Engels, Boris
   Bindokas, Vytas
   Bartkowiak, Todd
   Lee, David
   Herrmann, Andreas
   Piston, David W.
   Pittet, Mikael J.
   Lin, P. Charles
   Zal, Tomasz
   Schreiber, Hans
TI Longitudinal confocal microscopy imaging of solid tumor destruction
   following adoptive T cell transfer
SO ONCOIMMUNOLOGY
LA English
DT Article
DE imaging; cancer; tumor microenvironment; tumor immunology; CD8 T cell;
   stroma
ID ANTIGENIC CANCER-CELLS; SUPPRESSOR-CELLS; STROMAL FIBROBLASTS;
   ESTABLISHED TUMORS; IMMUNE SUPPRESSION; CROSS-PRESENTATION;
   INTERFERON-GAMMA; LOSS VARIANTS; EXPRESSION; ERADICATION
AB A fluorescence-based, high-resolution imaging approach was used to visualize longitudinally the cellular events unfolding during T cell-mediated tumor destruction. The dynamic interplay of T cells, cancer cells, cancer antigen loss variants, and stromal cells-all color-coded in vivo-was analyzed in established, solid tumors that had developed behind windows implanted on the backs of mice. Events could be followed repeatedly within precisely the same tumor region-before, during and after adoptive T cell therapy-thereby enabling for the first time a longitudinal in vivo evaluation of protracted events, an analysis not possible with terminal imaging of surgically exposed tumors. T cell infiltration, stromal interactions, and vessel destruction, as well as the functional consequences thereof, including the elimination of cancer cells and cancer cell variants were studied. Minimal perivascular T cell infiltrates initiated vascular destruction inside the tumor mass eventually leading to macroscopic central tumor necrosis. Prolonged engagement of T cells with tumor antigen-crosspresenting stromal cells correlated with high IFN gamma cytokine release and bystander elimination of antigen-negative cancer cells. The high-resolution, longitudinal, in vivo imaging approach described here will help to further a better mechanistic understanding of tumor eradication by T cells and other anti-cancer therapies.
C1 [Schietinger, Andrea; Arina, Ainhoa; Liu, Rebecca B.; Engels, Boris; Schreiber, Hans] Univ Chicago, Dept Pathol, Chicago, IL 60637 USA.
   [Wells, Sam; Piston, David W.] Vanderbilt Univ, Sch Med, Dept Physiol & Biophys, Nashville, TN 37212 USA.
   [Huang, Jianhua; Lin, P. Charles] Vanderbilt Univ, Sch Med, Dept Radiat Oncol, Nashville, TN 37212 USA.
   [Huang, Jianhua; Lin, P. Charles] Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr, Nashville, TN 37212 USA.
   [Bindokas, Vytas] Univ Chicago, Chicago, IL USA.
   [Bartkowiak, Todd; Zal, Tomasz] Univ Texas MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA.
   [Lee, David] Univ Chicago, Sch Med, Chicago, IL 60637 USA.
   [Herrmann, Andreas] Dept Canc Immunotherapeut, Duarte, CA USA.
   [Herrmann, Andreas] Dept Tumor Immunol, Duarte, CA USA.
   [Pittet, Mikael J.] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
   [Pittet, Mikael J.] Harvard Univ, Sch Med, Boston, MA USA.
   [Lin, P. Charles] NCI, Ctr Canc Res, NIH, Frederick, MD 21701 USA.
RP Schreiber, H (reprint author), Univ Chicago, Dept Pathol, 5841 S Maryland Ave, Chicago, IL 60637 USA.
EM hszz@uchicago.edu
FU National Institute of Health; NCI;  [R01-CA22677];  [R01-CA37516]; 
   [P01-CA97296];  [R01-CA137059]
FX We thank Ann Schue for excellent help in arranging the mouse transfers
   from University of Chicago to Vanderbilt University; Laura DeBusk,
   Kimberly Boelte, and CarolAnn Bonner for help and technical assistance,
   Anita Chong, Alexander Chervonsky, Maki Motobu, Karin Schreiber, Heather
   Booras, David Binder, and Christian Idel for technical advice and
   helpful discussions, and at the University of Texas MD Anderson Cancer
   Center, Anna Zal and Felix Nwajei for help with the contextual analysis
   of cell motility. We thank Mary Philip for critical reading of the
   manuscript and valuable suggestions. We thank the University of Chicago
   Cancer Research Center Core facilities, especially R Duggan, D Leclerc
   and M Olson for expert assistance with cell sorting and flow cytometric
   analysis, the Vanderbilt Cell Imaging Shared Resource, and Christine
   Labno, University of Chicago Light Microscopy Core, for technical
   assistance. This work was supported by National Institute of Health,
   Activities to Promote Research Collaborations (APRC) program from the
   NCI, and grants, R01-CA22677, R01-CA37516 and P01-CA97296 to H.S, as
   well as R01-CA137059 to T.Z.
NR 64
TC 20
Z9 20
U1 1
U2 8
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 2162-4011
EI 2162-402X
J9 ONCOIMMUNOLOGY
JI OncoImmunology
PD NOV
PY 2013
VL 2
IS 11
AR e26677
DI 10.4161/onci.26677
PG 14
WC Oncology; Immunology
SC Oncology; Immunology
GA 299VU
UT WOS:000330424600003
PM 24482750
ER

PT J
AU Andersen, DK
   Andren-Sandberg, A
   Duell, EJ
   Goggins, M
   Korc, M
   Petersen, GM
   Smith, JP
   Whitcomb, DC
AF Andersen, Dana K.
   Andren-Sandberg, Ake
   Duell, Eric J.
   Goggins, Michael
   Korc, Murray
   Petersen, Gloria M.
   Smith, Jill P.
   Whitcomb, David C.
TI Pancreatitis-Diabetes-Pancreatic Cancer Summary of an NIDDK-NCI Workshop
SO PANCREAS
LA English
DT Article
AB A workshop sponsored by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and the National Cancer Institute (NCI) on "Pancreatitis-Diabetes-Pancreatic Cancer" focused on the risk factors of chronic pancreatitis (CP) and diabetes mellitus (DM) on the development of pancreatic ductal adenocarcinoma (PDAC). Sessions were held on (a) an overview of the problem of PDAC; (b) CP as a risk factor of PDAC; (c) DM as a risk factor of PDAC; (d) pancreatogenic, or type 3c, DM; (e) genomic associations of CP, DM, and PDAC; (f) surveillance of high-risk populations and early detection of PDAC; and (g) effects of DM treatment on PDAC. Recent data and current understandings of the mechanisms of CP- and DM-associated factors on PDAC development were discussed, and a detailed review of the possible risks of DM treatment on the development of PDAC was provided by representatives from academia, industry, and the Food and Drug Administration. The current status of possible biomarkers of PDAC and surveillance strategies for high-risk populations were discussed, and the gaps in knowledge and opportunities for further research were elucidated. A broad spectrum of expertise of the speakers and the discussants provided an unusually productive workshop, the highlights of which are summarized in the accompanying article.
C1 [Andersen, Dana K.; Smith, Jill P.] NIDDK, Div Digest Dis & Nutr, NIH, Bethesda, MD 20892 USA.
   [Andren-Sandberg, Ake] Karolinska Inst, Dept Surg, Stockholm, Sweden.
   [Duell, Eric J.] Catalan Inst Oncol, Unit Nutr Environm & Canc, Barcelona, Spain.
   [Goggins, Michael] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
   [Goggins, Michael] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
   [Korc, Murray] Indiana Univ Sch Med, Dept Med, Indianapolis, IN 46202 USA.
   [Korc, Murray] Indiana Univ Sch Med, Dept Biochem & Mol Biol, Indianapolis, IN 46202 USA.
   [Petersen, Gloria M.] Mayo Clin & Mayo Grad Sch Med, Dept Epidemiol, Rochester, MN USA.
   [Whitcomb, David C.] Univ Pittsburgh, Sch Med, Dept Med, Pittsburgh, PA 15213 USA.
   [Whitcomb, David C.] Univ Pittsburgh, Sch Med, Dept Cell Biol & Physiol, Pittsburgh, PA USA.
   [Whitcomb, David C.] Univ Pittsburgh, Sch Med, Dept Human Genet, Pittsburgh, PA USA.
RP Andersen, DK (reprint author), NIDDK, Div Digest Dis & Nutr, NIH, 6707 Democracy Blvd,Rom 659, Bethesda, MD 20892 USA.
EM dana.andersen@nih.gov
FU Intramural NIH HHS [Z99 DK999999]; NCI NIH HHS [R01 CA075059]
NR 0
TC 34
Z9 34
U1 0
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD NOV
PY 2013
VL 42
IS 8
BP 1227
EP 1237
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 300MQ
UT WOS:000330468400006
PM 24152948
ER

PT J
AU Caulfield, T
   Evans, J
   McGuire, A
   McCabe, C
   Bubela, T
   Cook-Deegan, R
   Fishman, J
   Hogarth, S
   Miller, FA
   Ravitsky, V
   Biesecker, B
   Borry, P
   Cho, MK
   Carroll, JC
   Etchegary, H
   Joly, Y
   Kato, K
   Lee, SSJ
   Rothenberg, K
   Sankar, P
   Szego, MJ
   Ossorio, P
   Pullman, D
   Rousseau, F
   Ungar, WJ
   Wilson, B
AF Caulfield, Timothy
   Evans, Jim
   McGuire, Amy
   McCabe, Christopher
   Bubela, Tania
   Cook-Deegan, Robert
   Fishman, Jennifer
   Hogarth, Stuart
   Miller, Fiona A.
   Ravitsky, Vardit
   Biesecker, Barbara
   Borry, Pascal
   Cho, Mildred K.
   Carroll, June C.
   Etchegary, Holly
   Joly, Yann
   Kato, Kazuto
   Lee, Sandra Soo-Jin
   Rothenberg, Karen
   Sankar, Pamela
   Szego, Michael J.
   Ossorio, Pilar
   Pullman, Daryl
   Rousseau, Francois
   Ungar, Wendy J.
   Wilson, Brenda
TI Reflections on the Cost of "Low-Cost" Whole Genome Sequencing: Framing
   the Health Policy Debate
SO PLOS BIOLOGY
LA English
DT Article
ID CANCER; HYPE; MEDICINE; SCIENCE; TESTS
AB The cost of whole genome sequencing is dropping rapidly. There has been a great deal of enthusiasm about the potential for this technological advance to transform clinical care. Given the interest and significant investment in genomics, this seems an ideal time to consider what the evidence tells us about potential benefits and harms, particularly in the context of health care policy. The scale and pace of adoption of this powerful new technology should be driven by clinical need, clinical evidence, and a commitment to put patients at the centre of health care policy.
C1 [Caulfield, Timothy] Univ Alberta, Hlth Law Inst, Edmonton, AB, Canada.
   [Evans, Jim] UNC Sch Med, Dept Genet, Chapel Hill, NC USA.
   [McGuire, Amy] Baylor Coll Med, Ctr Med Eth & Hlth Policy, Houston, TX 77030 USA.
   [McCabe, Christopher] Univ Alberta, Dept Emergency Med, Edmonton, AB, Canada.
   [Bubela, Tania] Univ Alberta, Sch Publ Hlth, Edmonton, AB, Canada.
   [Cook-Deegan, Robert] Duke Univ, Inst Genome Sci & Policy, Durham, NC USA.
   [Cook-Deegan, Robert] Duke Univ, Sanford Sch Publ Policy, Durham, NC USA.
   [Fishman, Jennifer] McGill Univ, Biomed Eth Unit, Montreal, PQ, Canada.
   [Hogarth, Stuart] Kings Coll London, Dept Social Sci Hlth & Med, London WC2R 2LS, England.
   [Miller, Fiona A.; Ungar, Wendy J.] Univ Toronto, Inst Hlth Policy Management & Evaluat, Toronto, ON, Canada.
   [Ravitsky, Vardit] Univ Montreal, Fac Med, Bioeth Programs, Montreal, PQ H3C 3J7, Canada.
   [Biesecker, Barbara] Johns Hopkins Univ JHU, Genet Counseling Program, Bethesda, MD USA.
   [Biesecker, Barbara] Natl Human Genome Res Inst NHGRI, Social & Behav Res Branch SBRB, Bethesda, MD USA.
   [Biesecker, Barbara] NHGRI, Natl Inst Hlth NIH, Bethesda, MD 20892 USA.
   [Borry, Pascal] Katholieke Univ Leuven, Dept Publ Hlth & Primary Care, Louvain, Belgium.
   [Cho, Mildred K.; Lee, Sandra Soo-Jin] Stanford Univ, Stanford Ctr Biomed Eth, Stanford, CA 94305 USA.
   [Carroll, June C.] Univ Toronto, Dept Family & Community Med, Toronto, ON M5S 1A1, Canada.
   [Carroll, June C.] Mt Sinai Hosp, Granovsky Gluskin Family Med Ctr, Toronto, ON M5G 1X5, Canada.
   [Etchegary, Holly; Pullman, Daryl] Mem Univ Newfoundland, Fac Med, St John, NF, Canada.
   [Joly, Yann] McGill Univ, Fac Med, Dept Human Genet, Montreal, PQ, Canada.
   [Kato, Kazuto] Osaka Univ, Grad Sch Med, Dept Biomed Eth & Publ Policy, Suita, Osaka, Japan.
   [Kato, Kazuto] Kyoto Univ, Inst Integrated Cell Mat Sci, Kyoto, Japan.
   [Lee, Sandra Soo-Jin] Stanford Univ, Program Sci Technol & Soc, Stanford, CA 94305 USA.
   [Rothenberg, Karen] NHGRI, Natl Inst Hlth, Bethesda, MD 20892 USA.
   [Sankar, Pamela] Univ Penn, Dept Med Eth & Hlth Policy, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Szego, Michael J.] Univ Toronto, McLaughlin Ctr, Ctr Clin Eth, Toronto, ON, Canada.
   [Szego, Michael J.] Joint Ctr Bioeth, Ctr Clin Eth, Toronto, ON, Canada.
   [Szego, Michael J.] Hosp Sick Children, Ctr Appl Gen, Toronto, ON M5G 1X8, Canada.
   [Ossorio, Pilar] Univ Wisconsin, Sch Law, Madison, WI 53706 USA.
   [Ossorio, Pilar] Morgridge Inst Res, Madison, WI USA.
   [Rousseau, Francois] CHU, Quebec Res Ctr, Quebec City, PQ, Canada.
   [Rousseau, Francois] Univ Laval, Fac Med, Quebec City, PQ G1K 7P4, Canada.
   [Ungar, Wendy J.] Hosp Sick Children, Program Child Hlth Evaluat Sci, Toronto, ON M5G 1X8, Canada.
   [Wilson, Brenda] Univ Ottawa, Dept Epidemiol & Community Med, Ottawa, ON, Canada.
RP Caulfield, T (reprint author), Univ Alberta, Hlth Law Inst, Edmonton, AB, Canada.
EM caulfield@ualberta.ca
RI Bubela, Tania/F-4860-2014; McCabe, Christopher/E-2051-2016; 
OI Bubela, Tania/0000-0002-0807-2899; Miller, Fiona/0000-0003-4953-6255;
   Cook-Deegan, Robert/0000-0002-8251-4237
FU Canadian Institutes of Health Research; Intramural NIH HHS; NHGRI NIH
   HHS [P50 HG003391]
NR 58
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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 NOV
PY 2013
VL 11
IS 11
AR UNSP e1001699
DI 10.1371/journal.pbio.1001699
PG 6
WC Biochemistry & Molecular Biology; Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics
GA 298VI
UT WOS:000330352200001
PM 24223516
ER

PT J
AU Cui, C
   Chatterjee, B
   Lozito, TP
   Zhang, Z
   Francis, RJ
   Yagi, H
   Swanhart, LM
   Sanker, S
   Francis, D
   Yu, Q
   San Agustin, JT
   Puligilla, C
   Chatterjee, T
   Tansey, T
   Liu, XQ
   Kelley, MW
   Spiliotis, ET
   Kwiatkowski, AV
   Tuan, R
   Pazour, GJ
   Hukriede, NA
   Lo, CW
AF Cui, Cheng
   Chatterjee, Bishwanath
   Lozito, Thomas P.
   Zhang, Zhen
   Francis, Richard J.
   Yagi, Hisato
   Swanhart, Lisa M.
   Sanker, Subramaniam
   Francis, Deanne
   Yu, Qing
   San Agustin, Jovenal T.
   Puligilla, Chandrakala
   Chatterjee, Tania
   Tansey, Terry
   Liu, Xiaoqin
   Kelley, Matthew W.
   Spiliotis, Elias T.
   Kwiatkowski, Adam V.
   Tuan, Rocky
   Pazour, Gregory J.
   Hukriede, Neil A.
   Lo, Cecilia W.
TI Wdpcp, a PCP Protein Required for Ciliogenesis, Regulates Directional
   Cell Migration and Cell Polarity by Direct Modulation of the Actin
   Cytoskeleton
SO PLOS BIOLOGY
LA English
DT Article
ID NON-CILIARY MECHANISMS; NEURAL-TUBE CLOSURE; PRIMARY CILIUM; CONVERGENT
   EXTENSION; PLANAR POLARITY; HAIR-CELLS; INNER-EAR; MOUSE; ZEBRAFISH;
   PATHWAY
AB Planar cell polarity (PCP) regulates cell alignment required for collective cell movement during embryonic development. This requires PCP/PCP effector proteins, some of which also play essential roles in ciliogenesis, highlighting the long-standing question of the role of the cilium in PCP. Wdpcp, a PCP effector, was recently shown to regulate both ciliogenesis and collective cell movement, but the underlying mechanism is unknown. Here we show Wdpcp can regulate PCP by direct modulation of the actin cytoskeleton. These studies were made possible by recovery of a Wdpcp mutant mouse model. Wdpcp-deficient mice exhibit phenotypes reminiscent of Bardet-Biedl/Meckel-Gruber ciliopathy syndromes, including cardiac outflow tract and cochlea defects associated with PCP perturbation. We observed Wdpcp is localized to the transition zone, and in Wdpcp-deficient cells, Sept2, Nphp1, and Mks1 were lost from the transition zone, indicating Wdpcp is required for recruitment of proteins essential for ciliogenesis. Wdpcp is also found in the cytoplasm, where it is localized in the actin cytoskeleton and in focal adhesions. Wdpcp interacts with Sept2 and is colocalized with Sept2 in actin filaments, but in Wdpcp-deficient cells, Sept2 was lost from the actin cytoskeleton, suggesting Wdpcp is required for Sept2 recruitment to actin filaments. Significantly, organization of the actin filaments and focal contacts were markedly changed in Wdpcp-deficient cells. This was associated with decreased membrane ruffling, failure to establish cell polarity, and loss of directional cell migration. These results suggest the PCP defects in Wdpcp mutants are not caused by loss of cilia, but by direct disruption of the actin cytoskeleton. Consistent with this, Wdpcp mutant cochlea has normal kinocilia and yet exhibits PCP defects. Together, these findings provide the first evidence, to our knowledge, that a PCP component required for ciliogenesis can directly modulate the actin cytoskeleton to regulate cell polarity and directional cell migration.
C1 [Cui, Cheng; Chatterjee, Bishwanath; Zhang, Zhen; Francis, Richard J.; Yagi, Hisato; Swanhart, Lisa M.; Sanker, Subramaniam; Liu, Xiaoqin; Hukriede, Neil A.; Lo, Cecilia W.] Univ Pittsburgh, Sch Med, Dept Dev Biol, Pittsburgh, PA 15260 USA.
   [Cui, Cheng; Chatterjee, Bishwanath; Francis, Richard J.; Francis, Deanne; Yu, Qing; Chatterjee, Tania; Tansey, Terry; Lo, Cecilia W.] Natl Heart Lung & Blood Inst, Natl Inst Hlth, Dev Biol Lab, Bethesda, MD USA.
   [Lozito, Thomas P.; Tuan, Rocky] Univ Pittsburgh, Sch Med, Dept Orthopaed Surg, Ctr Cellular & Mol Engn, Pittsburgh, PA 15261 USA.
   [San Agustin, Jovenal T.; Pazour, Gregory J.] Univ Massachusetts, Med Ctr, Program Mol Med, Worcester, MA 01605 USA.
   [Puligilla, Chandrakala; Kelley, Matthew W.] Natl Inst Deafness & Other Commun Disorders, Natl Inst Hlth, Sect Dev Neurosci, Bethesda, MD USA.
   [Spiliotis, Elias T.] Drexel Univ, Dept Biol, Philadelphia, PA 19104 USA.
   [Kwiatkowski, Adam V.] Univ Pittsburgh, Sch Med, Dept Cell Biol, Pittsburgh, PA USA.
RP Cui, C (reprint author), Univ Pittsburgh, Sch Med, Dept Dev Biol, Pittsburgh, PA 15260 USA.
EM cel36@pitt.edu
RI Francis, Richard/P-2524-2015; 
OI Francis, Deanne/0000-0002-4158-1521; Pazour,
   Gregory/0000-0002-6285-8796; Zhang, Zhen/0000-0002-9898-054X
FU NIH [HL098180, GM060992, GM097664]
FX This work was supported by NIH grants HL098180 (CWL), GM060992 (GJP) and
   GM097664 (ETS) at http://www.nih.gov/. The funders had no role in study
   design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
NR 54
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PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1545-7885
J9 PLOS BIOL
JI PLoS. Biol.
PD NOV
PY 2013
VL 11
IS 11
AR e1001720
DI 10.1371/journal.pbio.1001720
PG 17
WC Biochemistry & Molecular Biology; Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics
GA 298VI
UT WOS:000330352200022
PM 24302887
ER

PT J
AU Patsopoulos, NA
   Barcellos, LF
   Hintzen, RQ
   Schaefer, C
   Van Duijn, CM
   Noble, JA
   Raj, T
   Gourraud, PA
   Stranger, BE
   Oksenberg, J
   Olsson, T
   Taylor, BV
   Sawcer, S
   Hafler, DA
   Carrington, M
   De Jager, PL
   De Bakker, PIW
AF Patsopoulos, Nikolaos A.
   Barcellos, Lisa F.
   Hintzen, Rogier Q.
   Schaefer, Catherine
   Van Duijn, Cornelia M.
   Noble, Janelle A.
   Raj, Towfique
   Gourraud, Pierre-Antoine
   Stranger, Barbara E.
   Oksenberg, Jorge
   Olsson, Tomas
   Taylor, Bruce V.
   Sawcer, Stephen
   Hafler, David A.
   Carrington, Mary
   De Jager, Philip L.
   De Bakker, Paul I. W.
CA Imsgc
   Anzgene
TI Fine-Mapping the Genetic Association of the Major Histocompatibility
   Complex in Multiple Sclerosis: HLA and Non-HLA Effects
SO PLOS GENETICS
LA English
DT Article
ID SUSCEPTIBILITY LOCI; RHEUMATOID-ARTHRITIS; RISK ALLELES; DISEASE;
   GENOME; HLA-DRB1; MHC; POPULATION; SELECTION; MICB
AB The major histocompatibility complex (MHC) region is strongly associated with multiple sclerosis (MS) susceptibility. HLADRB1* 15: 01 has the strongest effect, and several other alleles have been reported at different levels of validation. Using SNP data from genome-wide studies, we imputed and tested classical alleles and amino acid polymorphisms in 8 classical human leukocyte antigen (HLA) genes in 5,091 cases and 9,595 controls. We identified 11 statistically independent effects overall: 6 HLA-DRB1 and one DPB1 alleles in class II, one HLA-A and two B alleles in class I, and one signal in a region spanning from MICB to LST1. This genomic segment does not contain any HLA class I or II genes and provides robust evidence for the involvement of a non-HLA risk allele within the MHC. Interestingly, this region contains the TNF gene, the cognate ligand of the well-validated TNFRSF1A MS susceptibility gene. The classical HLA effects can be explained to some extent by polymorphic amino acid positions in the peptide-binding grooves. This study dissects the independent effects in the MHC, a critical region for MS susceptibility that harbors multiple risk alleles.
C1 [Patsopoulos, Nikolaos A.; Raj, Towfique; De Jager, Philip L.] Brigham & Womens Hosp, Dept Neurol, Inst Neurosci, Program Translat NeuroPsychiatr Genom, Boston, MA 02115 USA.
   [Patsopoulos, Nikolaos A.; De Bakker, Paul I. W.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med,Div Genet, Boston, MA USA.
   [Patsopoulos, Nikolaos A.; Raj, Towfique; De Jager, Philip L.; De Bakker, Paul I. W.] Harvard Med Sch, Boston, MA USA.
   [Patsopoulos, Nikolaos A.; Raj, Towfique; Hafler, David A.; De Jager, Philip L.; De Bakker, Paul I. W.] Broad Inst Harvard, Cambridge, MA USA.
   [Patsopoulos, Nikolaos A.; Raj, Towfique; Hafler, David A.; De Jager, Philip L.; De Bakker, Paul I. W.] MIT, Cambridge, MA 02139 USA.
   [Barcellos, Lisa F.] Univ Calif Berkeley, Sch Publ Hlth, Genet Epidemiol & Genom Lab, Div Epidemiol, Berkeley, CA 94720 USA.
   [Barcellos, Lisa F.; Schaefer, Catherine] Kaiser Permanente Div Res, Oakland, CA USA.
   [Hintzen, Rogier Q.] Erasmus MC, MS Ctr ErasMS, Dept Neurol, Rotterdam, Netherlands.
   [Van Duijn, Cornelia M.] Erasmus MC, Dept Epidemiol & Biostat & Clin Genet, Genet Epidemiol Unit, Rotterdam, Netherlands.
   [Noble, Janelle A.] Childrens Hosp, Oakland Res Inst, Oakland, CA 94609 USA.
   [Gourraud, Pierre-Antoine; Oksenberg, Jorge] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA.
   [Stranger, Barbara E.] Univ Chicago, Dept Med, Med Genet Sect, Chicago, IL 60637 USA.
   [Stranger, Barbara E.] Univ Chicago, Inst Genom & Syst Biol, Chicago, IL USA.
   [Olsson, Tomas] Karolinska Inst, Dept Clin Neurosci CMM, Stockholm, Sweden.
   [Taylor, Bruce V.] Univ Tasmania, Menzies Res Inst Tasmania, Hobart, Tas, Australia.
   [Sawcer, Stephen] Univ Cambridge, Addenbrookes Hosp, Dept Clin Neurosci, Cambridge CB2 2QQ, England.
   [Hafler, David A.] Yale Univ, Sch Med, Dept Neurol, New Haven, CT USA.
   [Hafler, David A.] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT USA.
   [Carrington, Mary] Frederick Natl Lab Canc Res, SAIC Frederick, Expt Immunol Lab, Canc & Inflammat Program, Frederick, MD USA.
   [Carrington, Mary] Ragon Inst MGH, MIT & Harvard, Charlestown, MA USA.
   [De Bakker, Paul I. W.] Univ Med Ctr, Div Biomed Genet, Dept Med Genet, Utrecht, Netherlands.
   [De Bakker, Paul I. W.] Univ Med Ctr, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands.
RP Patsopoulos, NA (reprint author), Brigham & Womens Hosp, Dept Neurol, Inst Neurosci, Program Translat NeuroPsychiatr Genom, 75 Francis St, Boston, MA 02115 USA.
EM pdejager@rics.bwh.harvard.edu; pdebakker@umcutrecht.nl
RI de Bakker, Paul/B-8730-2009; D'Alfonso, Sandra/K-7295-2014; MOSCATO,
   PABLO/G-7668-2013; Zipp, Frauke/C-9968-2015; Gourraud,
   Pierre-Antoine/O-3024-2015; 
OI de Bakker, Paul/0000-0001-7735-7858; D'Alfonso,
   Sandra/0000-0002-3983-9925; Zipp, Frauke/0000-0002-1231-1928; Saarela,
   Janna/0000-0002-0853-6219; Field, Judith/0000-0002-7089-0999;
   Butzkueven, Helmut/0000-0003-3940-8727; Stranger,
   Barbara/0000-0001-9021-7331
FU National Multiple Sclerosis Society; NIH/NINDS [R01NS049510,
   R01NS0495103]; NIH/NIAID [R01AI076544]; Dutch MS Research foundation;
   Bibbi and Niels Jensens Foundation; Swedish Brain Foundation; Swedish
   research council; Stockholm County Council [562183]; Swedish Council for
   Working life and Social Research; Knut and Alice Wallenbergs foundation;
   MS research Australia (MSRA); John T. Reid Charitable Trusts; Trish MS
   Research Foundation; Australian Research Council [LP0776744]; Cambridge
   NIHR Biomedical Research Centre; Frederick National Laboratory for
   Cancer Research [HHSN261200800001E]; NIH, Frederick National Lab, Center
   for Cancer Research; Netherlands Organization for Scientific Research
   (NWO) [016.126.354];  [R01NS049477];  [R01NS026799]
FX This investigation was supported (in part) by a Postdoctoral Fellowship
   from the National Multiple Sclerosis Society to NAP, and by R01NS049477,
   R01NS026799, NIH/NINDS R01NS049510, R01NS0495103, NIH/NIAID R01AI076544,
   Dutch MS Research foundation, Bibbi and Niels Jensens Foundation, The
   Swedish Brain Foundation and Swedish research council, Stockholm County
   Council (562183), Swedish Council for Working life and Social Research,
   Knut and Alice Wallenbergs foundation, MS research Australia (MSRA),
   John T. Reid Charitable Trusts, Trish MS Research Foundation and the
   Australian Research Council, under the Linkage Projects Scheme
   (LP0776744), the Cambridge NIHR Biomedical Research Centre. This project
   has been funded in whole or in part with federal funds from the
   Frederick National Laboratory for Cancer Research, 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 Intramural Research Program of the NIH,
   Frederick National Lab, Center for Cancer Research. PLDJ is a Harry
   Weaver neuroscience scholar of the National MS Society (JF2138A1). PIWdB
   is the recipient of a VIDI Award from the Netherlands Organization for
   Scientific Research (NWO project 016.126.354). The funders had no role
   in study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
NR 48
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U1 3
U2 18
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 NOV
PY 2013
VL 9
IS 11
AR e1003926
DI 10.1371/journal.pgen.1003926
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 299BG
UT WOS:000330369000021
PM 24278027
ER

PT J
AU Vaisman, A
   McDonald, JP
   Huston, D
   Kuban, W
   Liu, LL
   Van Houten, B
   Woodgate, R
AF Vaisman, Alexandra
   McDonald, John P.
   Huston, Donald
   Kuban, Wojciech
   Liu, Lili
   Van Houten, Bennett
   Woodgate, Roger
TI Removal of Misincorporated Ribonucleotides from Prokaryotic Genomes: An
   Unexpected Role for Nucleotide Excision Repair
SO PLOS GENETICS
LA English
DT Article
ID TRANSLESION DNA-SYNTHESIS; SOS MUTATOR ACTIVITY; ESCHERICHIA-COLI;
   MISMATCH REPAIR; DAMAGE RECOGNITION; BACILLUS-SUBTILIS; RECA PROTEIN;
   BASE-PAIR; RNASE-H; MUTAGENESIS
AB Stringent steric exclusion mechanisms limit the misincorporation of ribonucleotides by high-fidelity DNA polymerases into genomic DNA. In contrast, low-fidelity Escherichia coli DNA polymerase V (pol V) has relatively poor sugar discrimination and frequently misincorporates ribonucleotides. Substitution of a steric gate tyrosine residue with alanine (umuC_Y11A) reduces sugar selectivity further and allows pol V to readily misincorporate ribonucleotides as easily as deoxynucleotides, whilst leaving its poor base-substitution fidelity essentially unchanged. However, the mutability of cells expressing the steric gate pol V mutant is very low due to efficient repair mechanisms that are triggered by the misincorporated rNMPs. Comparison of the mutation frequency between strains expressing wild-type and mutant pol V therefore allows us to identify pathways specifically directed at ribonucleotide excision repair (RER). We previously demonstrated that rNMPs incorporated by umuC_Y11A are efficiently removed from DNA in a repair pathway initiated by RNase HII. Using the same approach, we show here that mismatch repair and base excision repair play minimal back-up roles in RER in vivo. In contrast, in the absence of functional RNase HII, umuC_Y11A-dependent mutagenesis increases significantly in Delta uvrA, uvrB5 and Delta uvrC strains, suggesting that rNMPs misincorporated into DNA are actively repaired by nucleotide excision repair (NER) in vivo. Participation of NER in RER was confirmed by reconstituting ribonucleotide-dependent NER in vitro. We show that UvrABC nuclease-catalyzed incisions are readily made on DNA templates containing one, two, or five rNMPs and that the reactions are stimulated by the presence of mispaired bases. Similar to NER of DNA lesions, excision of rNMPs proceeds through dual incisions made at the 8th phosphodiester bond 5' and 4th-5th phosphodiester bonds 3' of the ribonucleotide. Ribonucleotides misinserted into DNA can therefore be added to the broad list of helix-distorting modifications that are substrates for NER.
C1 [Vaisman, Alexandra; McDonald, John P.; Huston, Donald; Kuban, Wojciech; Woodgate, Roger] Natl Inst Child Hlth & Human Dev, Lab Genom Integr, NIH, Bethesda, MD 20892 USA.
   [Liu, Lili; Van Houten, Bennett] Univ Pittsburgh, Inst Canc, Dept Pharmacol & Chem Biol, Pittsburgh, PA USA.
RP Vaisman, A (reprint author), Natl Inst Child Hlth & Human Dev, Lab Genom Integr, NIH, Bethesda, MD 20892 USA.
EM woodgate@nih.gov
FU National Institute of Child Health and Human Development/National
   Institutes of Health Intramural Research Program; National Institutes of
   Health [R01ES019566]
FX This work was supported by funds from the National Institute of Child
   Health and Human Development/National Institutes of Health Intramural
   Research Program to RW and National Institutes of Health grant
   R01ES019566 to BVH. The funders had no role in study design, data
   collection and analysis, decision to publish, or preparation of the
   manuscript.
NR 71
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U2 6
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 NOV
PY 2013
VL 9
IS 11
AR e1003878
DI 10.1371/journal.pgen.1003878
PG 15
WC Genetics & Heredity
SC Genetics & Heredity
GA 299BG
UT WOS:000330369000004
PM 24244177
ER

PT J
AU Yu, HJ
   Alonso, WJ
   Feng, LZ
   Tan, Y
   Shu, YL
   Yang, WZ
   Viboud, C
AF Yu, Hongjie
   Alonso, Wladimir J.
   Feng, Luzhao
   Tan, Yi
   Shu, Yuelong
   Yang, Weizhong
   Viboud, Cecile
TI Characterization of Regional Influenza Seasonality Patterns in China and
   Implications for Vaccination Strategies: Spatio-Temporal Modeling of
   Surveillance Data
SO PLOS MEDICINE
LA English
DT Article
ID RESPIRATORY SYNCYTIAL VIRUS; UNITED-STATES; ABSOLUTE-HUMIDITY;
   MORTALITY; TRANSMISSION; TEMPERATURE; SYNCHRONY; AFRICA; BRAZIL
AB Background: The complexity of influenza seasonal patterns in the inter-tropical zone impedes the establishment of effective routine immunization programs. China is a climatologically and economically diverse country, which has yet to establish a national influenza vaccination program. Here we characterize the diversity of influenza seasonality in China and make recommendations to guide future vaccination programs.
   Methods and Findings: We compiled weekly reports of laboratory-confirmed influenza A and B infections from sentinel hospitals in cities representing 30 Chinese provinces, 2005-2011, and data on population demographics, mobility patterns, socio-economic, and climate factors. We applied linear regression models with harmonic terms to estimate influenza seasonal characteristics, including the amplitude of annual and semi-annual periodicities, their ratio, and peak timing. Hierarchical Bayesian modeling and hierarchical clustering were used to identify predictors of influenza seasonal characteristics and define epidemiologically-relevant regions. The annual periodicity of influenza A epidemics increased with latitude (mean amplitude of annual cycle standardized by mean incidence, 140% [95% CI 128%-151%] in the north versus 37% [95% CI 27%-47%] in the south, p<0.0001). Epidemics peaked in January-February in Northern China (latitude >= 33 degrees N) and April-June in southernmost regions (latitude <27 degrees N). Provinces at intermediate latitudes experienced dominant semi-annual influenza A periodicity with peaks in January-February and June-August (periodicity ratio >0.6 in provinces located within 27.4 degrees N-31.3 degrees N, slope of latitudinal gradient with latitude -0.016 [95% CI -0.025 to -0.008], p < 0.001). In contrast, influenza B activity predominated in colder months throughout most of China. Climate factors were the strongest predictors of influenza seasonality, including minimum temperature, hours of sunshine, and maximum rainfall. Our main study limitations include a short surveillance period and sparse influenza sampling in some of the southern provinces.
   Conclusions: Regional-specific influenza vaccination strategies would be optimal in China; in particular, annual campaigns should be initiated 4-6 months apart in Northern and Southern China. Influenza surveillance should be strengthened in mid-latitude provinces, given the complexity of seasonal patterns in this region. More broadly, our findings are consistent with the role of climatic factors on influenza transmission dynamics.
C1 [Yu, Hongjie; Feng, Luzhao; Yang, Weizhong] Chinese Ctr Dis Control & Prevent, Div Infect Dis, Key Lab Surveillance & Early Warning Infect Dis, Beijing, Peoples R China.
   [Alonso, Wladimir J.; Tan, Yi; Viboud, Cecile] Fogarty Int Ctr, NIH, Bethesda, MD USA.
   [Shu, Yuelong] China CDC, Natl Inst Viral Dis Control & Prevent, Key Lab Med Virol, Natl Hlth & Family Planning Commiss, Beijing, Peoples R China.
RP Yu, HJ (reprint author), Chinese Ctr Dis Control & Prevent, Div Infect Dis, Key Lab Surveillance & Early Warning Infect Dis, Beijing, Peoples R China.
EM yangwz@chinacdc.cn; viboudc@mail.nih.gov
FU US National Institutes of Health [U19 AI51915]; Ministry of Science and
   Technology, China [2012 ZX10004-201]; Pandemic Emergent Threats Unit,
   Office of Global Affairs, Department of Health and Human Services
FX This work was supported by the US National Institutes of Health
   (Comprehensive International Program for Research on AIDS grant U19
   AI51915); the China-U.S. Collaborative Program on Emerging and
   Re-emerging Infectious Diseases; grants from the Ministry of Science and
   Technology, China (2012 ZX10004-201); and the in-house Influenza
   Research Program of the Division of International Epidemiology and
   Population Studies, Fogarty International Center, National Institutes of
   Health, which is funded by the Pandemic Emergent Threats Unit, Office of
   Global Affairs, Department of Health and Human Services. The funders had
   no role in study design, data collection and analysis, decision to
   publish, or preparation of the manuscript.
NR 53
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PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1549-1676
J9 PLOS MED
JI PLos Med.
PD NOV
PY 2013
VL 10
IS 11
AR e1001552
DI 10.1371/journal.pmed.1001552
PG 16
WC Medicine, General & Internal
SC General & Internal Medicine
GA 299CD
UT WOS:000330371600009
PM 24348203
ER

PT J
AU Barker, CM
   Niu, TC
   Reisen, WK
   Hartley, DM
AF Barker, Christopher M.
   Niu, Tianchan
   Reisen, William K.
   Hartley, David M.
TI Data-Driven Modeling to Assess Receptivity for Rift Valley Fever Virus
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID WEST NILE VIRUS; LOUIS ENCEPHALITIS-VIRUS; SALIVARY-GLAND ANTIGENS;
   HOST-FEEDING PATTERNS; VECTOR COMPETENCE; CULEX-TARSALIS;
   DIPTERA-CULICIDAE; KERN-COUNTY; ANTIBODY-RESPONSE;
   ENVIRONMENTAL-TEMPERATURE
AB Rift Valley Fever virus (RVFV) is an enzootic virus that causes extensive morbidity and mortality in domestic ruminants in Africa, and it has shown the potential to invade other areas such as the Arabian Peninsula. Here, we develop methods for linking mathematical models to real-world data that could be used for continent-scale risk assessment given adequate data on local host and vector populations. We have applied the methods to a well-studied agricultural region of California with >1 million dairy cattle, abundant and competent mosquito vectors, and a permissive climate that has enabled consistent transmission of West Nile virus and historically other arboviruses. Our results suggest that RVFV outbreaks could occur from February-November, but would progress slowly during winter-early spring or early fall and be limited spatially to areas with early increases in vector abundance. Risk was greatest in summer, when the areas at risk broadened to include most of the dairy farms in the study region, indicating the potential for considerable economic losses if an introduction were to occur. To assess the threat that RVFV poses to North America, including what-if scenarios for introduction and control strategies, models such as this one should be an integral part of the process; however, modeling must be paralleled by efforts to address the numerous remaining gaps in data and knowledge for this system.
C1 [Barker, Christopher M.; Reisen, William K.] Univ Calif Davis, Sch Vet Med, Ctr Vectorborne Dis, Davis, CA 95616 USA.
   [Barker, Christopher M.; Reisen, William K.] Univ Calif Davis, Sch Vet Med, Dept Pathol Microbiol & Immunol, Davis, CA 95616 USA.
   [Barker, Christopher M.; Niu, Tianchan; Reisen, William K.; Hartley, David M.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
   [Niu, Tianchan; Hartley, David M.] Georgetown Univ, Med Ctr, Div Integrated Biodef, Washington, DC 20007 USA.
   [Hartley, David M.] Georgetown Univ, Med Ctr, Dept Microbiol & Immunol, Washington, DC 20007 USA.
RP Barker, CM (reprint author), Univ Calif Davis, Sch Vet Med, Ctr Vectorborne Dis, Davis, CA 95616 USA.
EM cmbarker@ucdavis.edu
OI , David/0000-0003-2589-2538
FU Research and Policy for Infectious Disease Dynamics (RAPIDD) program of
   the Science and Technology Directorate, Department of Homeland Security;
   Fogarty International Center, National Institutes of Health; Centers for
   Disease Control and Prevention [U01EH000418]; National Institutes of
   Allergy and Infectious Diseases, National Institues of Health [R01
   AI55607]
FX This study was supported by the Research and Policy for Infectious
   Disease Dynamics (RAPIDD) program of the Science and Technology
   Directorate, Department of Homeland Security and the Fogarty
   International Center, National Institutes of Health. CMB also
   acknowledges financial support from Centers for Disease Control and
   Prevention grant U01EH000418 to study the impacts of climate change on
   mosquitoborne virus transmission. WKR acknowledges financial support
   from National Institutes of Allergy and Infectious Diseases, National
   Institues of Health grant R01 AI55607 to model arboviral amplification.
   The funders had no role in study design, data collection and analysis,
   decision to publish, or preparation of the manuscript.
NR 73
TC 9
Z9 9
U1 0
U2 11
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 NOV
PY 2013
VL 7
IS 11
AR e2515
DI 10.1371/journal.pntd.0002515
PG 10
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 299EM
UT WOS:000330378400015
PM 24244769
ER

PT J
AU de-la-Torre, A
   Sauer, A
   Pfaff, AW
   Bourcier, T
   Brunet, J
   Speeg-Schatz, C
   Ballonzoli, L
   Villard, O
   Ajzenberg, D
   Sundar, N
   Grigg, ME
   Gomez-Marin, JE
   Candolfi, E
AF de-la-Torre, Alejandra
   Sauer, Arnaud
   Pfaff, Alexander W.
   Bourcier, Tristan
   Brunet, Julie
   Speeg-Schatz, Claude
   Ballonzoli, Laurent
   Villard, Odile
   Ajzenberg, Daniel
   Sundar, Natarajan
   Grigg, Michael E.
   Gomez-Marin, Jorge E.
   Candolfi, Ermanno
TI Severe South American Ocular Toxoplasmosis Is Associated with Decreased
   Ifn-gamma/Il-17 alpha and Increased Il-6/Il-13 Intraocular Levels
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID CONGENITAL TOXOPLASMOSIS; GENETIC-CHARACTERIZATION; IMMUNE-SYSTEM;
   GONDII; RETINOCHOROIDITIS; INFECTION; COLOMBIA; OUTBREAK; DISEASE;
   UVEITIS
AB In a cross sectional study, 19 French and 23 Colombian cases of confirmed active ocular toxoplasmosis (OT) were evaluated. The objective was to compare clinical, parasitological and immunological responses and relate them to the infecting strains. A complete ocular examination was performed in each patient. The infecting strain was characterized by genotyping when intraocular Toxoplasma DNA was detectable, as well as by peptide-specific serotyping for each patient. To characterize the immune response, we assessed Toxoplasma protein recognition patterns by intraocular antibodies and the intraocular profile of cytokines, chemokines and growth factors. Significant differences were found for size of active lesions, unilateral macular involvement, unilateral visual impairment, vitreous inflammation, synechiae, and vasculitis, with higher values observed throughout for Colombian patients. Multilocus PCR-DNA sequence genotyping was only successful in three Colombian patients revealing one type I and two atypical strains. The Colombian OT patients possessed heterogeneous atypical serotypes whereas the French were uniformly reactive to type II strain peptides. The protein patterns recognized by intraocular antibodies and the cytokine patterns were strikingly different between the two populations. Intraocular IFN-gamma and IL-17 expression was lower, while higher levels of IL-13 and IL-6 were detected in aqueous humor of Colombian patients. Our results are consistent with the hypothesis that South American strains may cause more severe OT due to an inhibition of the protective effect of IFN-gamma.
C1 [de-la-Torre, Alejandra; Gomez-Marin, Jorge E.] Univ Quindio, Ctr Invest Biomed, GEPAMOL, Armenia, Colombia.
   [de-la-Torre, Alejandra; Sauer, Arnaud; Pfaff, Alexander W.; Brunet, Julie; Villard, Odile; Candolfi, Ermanno] Univ Strasbourg, Inst Parasitol & Pathol Trop, Strasbourg, France.
   [de-la-Torre, Alejandra] Univ Rosario, Escuela Med & Ciencias Salud, Dept Inmunol, Bogota, Colombia.
   [Sauer, Arnaud; Bourcier, Tristan; Speeg-Schatz, Claude; Ballonzoli, Laurent] Hop Univ Strasbourg, Serv Ophtalmol, Strasbourg, France.
   [Ajzenberg, Daniel] Ctr Hosp Univ Dupuytren, Ctr Natl Reference CNR Toxoplasmose, Toxoplasma Biol Resource Ctr BRC, Limoges, France.
   [Ajzenberg, Daniel] Univ Limoges, INSERM, Lab Parasitol Mycol, Fac Med,UMR 1094, Limoges, France.
   [Sundar, Natarajan; Grigg, Michael E.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP de-la-Torre, A (reprint author), Univ Quindio, Ctr Invest Biomed, GEPAMOL, Armenia, Colombia.
EM candolfi@unistra.fr
RI Gomez-Marin, Jorge/L-9793-2013; de-la-Torre, Alejandra/G-6436-2016
OI Gomez-Marin, Jorge/0000-0001-6472-3329; de-la-Torre,
   Alejandra/0000-0003-0684-1989
FU Colciencias [111345921861]; Ecos Nord Program; Intramural Research
   Program of the National Institutes of Health; NIAID; Fondation Nationale
   pour la Recherche [DPR20121125433]; Universidad del Quindio, Hopitaux
   Universitaires de Strasbourg [2007-3964]; Universite de Strasbourg
FX This work was supported by Colciencias, Grant 111345921861, the Ecos
   Nord Program, the Intramural Research Program of the National Institutes
   of Health and NIAID and the Fondation Nationale pour la Recherche, Grant
   Retinal Physiopathology DPR20121125433. We would like to thank the
   Universidad del Quindio, Hopitaux Universitaires de Strasbourg for the
   PHRC grant 2007-3964, and Universite de Strasbourg for additional
   financial support. The funders had no role in study design, data
   collection and analysis, decision to publish, or preparation of the
   manuscript.
NR 55
TC 21
Z9 22
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 NOV
PY 2013
VL 7
IS 11
AR e2541
DI 10.1371/journal.pntd.0002541
PG 11
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 299EM
UT WOS:000330378400026
PM 24278490
ER

PT J
AU Majerciak, V
   Ni, T
   Yang, WJ
   Meng, BW
   Zhu, J
   Zheng, ZM
AF Majerciak, Vladimir
   Ni, Ting
   Yang, Wenjing
   Meng, Bowen
   Zhu, Jun
   Zheng, Zhi-Ming
TI A Viral Genome Landscape of RNA Polyadenylation from KSHV Latent to
   Lytic Infection
SO PLOS PATHOGENS
LA English
DT Article
ID SARCOMA-ASSOCIATED HERPESVIRUS; DEPENDENT DNA-REPLICATION;
   KAPOSIS-SARCOMA; GENE-EXPRESSION; DOWNSTREAM ELEMENTS; PROTEIN
   EXPRESSION; NUCLEAR-RNA; SEQUENCE; CELLS; ORF57
AB RNA polyadenylation (pA) is one of the major steps in regulation of gene expression at the posttranscriptional level. In this report, a genome landscape of pA sites of viral transcripts in B lymphocytes with Kaposi sarcoma-associated herpesvirus (KSHV) infection was constructed using a modified PA-seq strategy. We identified 67 unique pA sites, of which 55 could be assigned for expression of annotated,90 KSHV genes. Among the assigned pA sites, twenty are for expression of individual single genes and the rest for multiple genes (average 2.7 genes per pA site) in cluster-gene loci of the genome. A few novel viral pA sites that could not be assigned to any known KSHV genes are often positioned in the antisense strand to ORF8, ORF21, ORF34, K8 and ORF50, and their associated antisense mRNAs to ORF21, ORF34 and K8 could be verified by 3'RACE. The usage of each mapped pA site correlates to its peak size, the larger (broad and wide) peak size, the more usage and thus, the higher expression of the pA site-associated gene(s). Similar to mammalian transcripts, KSHV RNA polyadenylation employs two major poly(A) signals, AAUAAA and AUUAAA, and is regulated by conservation of cis-elements flanking the mapped pA sites. Moreover, we found two or more alternative pA sites downstream of ORF54, K2 (vIL6), K9 (vIRF1), K10.5 (vIRF3), K11 (vIRF2), K12 (Kaposin A), T1.5, and PAN genes and experimentally validated the alternative polyadenylation for the expression of KSHV ORF54, K11, and T1.5 transcripts. Together, our data provide not only a comprehensive pA site landscape for understanding KSHV genome structure and gene expression, but also the first evidence of alternative polyadenylation as another layer of posttranscriptional regulation in viral gene expression.
C1 [Majerciak, Vladimir; Meng, Bowen; Zheng, Zhi-Ming] NCI, Tumor Virus RNA Biol Sect, Gene Regulat & Chromosome Biol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
   [Ni, Ting; Yang, Wenjing; Zhu, Jun] NHLBI, DNA Sequencing & Genom Core, NIH, Bethesda, MD 20892 USA.
RP Majerciak, V (reprint author), NCI, Tumor Virus RNA Biol Sect, Gene Regulat & Chromosome Biol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
EM zhuj4@mail.nih.gov; zhengt@exchange.nih.gov
FU National Institutes of Health, National Cancer Institute, Center for
   Cancer Research and National Heart, Lung, and Blood Institute
FX This work was supported by the Intramural Programs of the National
   Institutes of Health, National Cancer Institute, Center for Cancer
   Research and National Heart, Lung, and Blood Institute. The funders had
   no role in study design, data collection and analysis, decision to
   publish, or preparation of the manuscript.
NR 67
TC 11
Z9 11
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD NOV
PY 2013
VL 9
IS 11
AR e1003749
DI 10.1371/journal.ppat.1003749
PG 15
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 299HN
UT WOS:000330386900023
PM 24244170
ER

PT J
AU Sakakibara, N
   Chen, D
   Jang, MK
   Kang, DW
   Luecke, HF
   Wu, SY
   Chiang, CM
   McBride, AA
AF Sakakibara, Nozomi
   Chen, Dan
   Jang, Moon Kyoo
   Kang, Dong Wook
   Luecke, Hans F.
   Wu, Shwu-Yuan
   Chiang, Cheng-Ming
   McBride, Alison A.
TI Brd4 Is Displaced from HPV Replication Factories as They Expand and
   Amplify Viral DNA
SO PLOS PATHOGENS
LA English
DT Article
ID HUMAN-PAPILLOMAVIRUS TYPE-16; E2 PROTEIN; LIFE-CYCLE; TRANSCRIPTIONAL
   ACTIVATION; EPITHELIAL DIFFERENTIATION; BROMODOMAIN PROTEIN; DAMAGE
   RESPONSE; CELL-LINES; EPISOMAL MAINTENANCE; MITOTIC CHROMOSOMES
AB Replication foci are generated by many viruses to concentrate and localize viral DNA synthesis to specific regions of the cell. Expression of the HPV16 E1 and E2 replication proteins in keratinocytes results in nuclear foci that recruit proteins associated with the host DNA damage response. We show that the Brd4 protein localizes to these foci and is essential for their formation. However, when E1 and E2 begin amplifying viral DNA, Brd4 is displaced from the foci and cellular factors associated with DNA synthesis and homologous recombination are recruited. Differentiated HPV-infected keratinocytes form similar nuclear foci that contain amplifying viral DNA. We compare the different foci and show that, while they have many characteristics in common, there is a switch between early Brd4-dependent foci and mature Brd4-independent replication foci. However, HPV genomes encoding mutated E2 proteins that are unable to bind Brd4 can replicate and amplify the viral genome. We propose that, while E1, E2 and Brd4 might bind host chromatin at early stages of infection, there is a temporal and functional switch at later stages and increased E1 and E2 levels promote viral DNA amplification, displacement of Brd4 and growth of a replication factory. The concomitant DNA damage response recruits proteins required for DNA synthesis and repair, which could then be utilized for viral DNA replication. Hence, while Brd4 can enhance replication by concentrating viral processes in specific regions of the host nucleus, this interaction is not absolutely essential for HPV replication.
C1 [Sakakibara, Nozomi; Chen, Dan; Jang, Moon Kyoo; McBride, Alison A.] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
   [Kang, Dong Wook; Luecke, Hans F.] NIDDK, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
   [Wu, Shwu-Yuan; Chiang, Cheng-Ming] Univ Texas SW Med Ctr Dallas, Simmons Comprehens Canc Ctr, Dallas, TX 75390 USA.
   [Wu, Shwu-Yuan; Chiang, Cheng-Ming] Univ Texas SW Med Ctr Dallas, Dept Biochem, Dallas, TX 75390 USA.
   [Chiang, Cheng-Ming] Univ Texas SW Med Ctr Dallas, Dept Pharmacol, Dallas, TX 75390 USA.
RP Sakakibara, N (reprint author), NIAID, Viral Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM amcbride@nih.gov
OI McBride, Alison/0000-0001-5607-5157
FU Intramural Research Program of the NIAID; NIDDK, NIH; NIH [CA103867];
   CPRIT [RP110471]; Welch Foundation [I-1805]
FX This work was funded by the Intramural Research Program of the NIAID,
   and NIDDK, NIH. This work was also supported in part by NIH grant
   CA103867, CPRIT grant RP110471, and Welch Foundation grant I-1805 (to
   CMC). The funders had no role in study design, data collection and
   analysis, decision to publish, or preparation of the manuscript.
NR 71
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Z9 24
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD NOV
PY 2013
VL 9
IS 11
AR e1003777
DI 10.1371/journal.ppat.1003777
PG 23
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 299HN
UT WOS:000330386900036
PM 24278023
ER

PT J
AU Tedbury, PR
   Ablan, SD
   Freed, EO
AF Tedbury, Philip R.
   Ablan, Sherimay D.
   Freed, Eric O.
TI Global Rescue of Defects in HIV-1 Envelope Glycoprotein Incorporation:
   Implications for Matrix Structure
SO PLOS PATHOGENS
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; GP41 CYTOPLASMIC TAIL; TYPE-1 MATRIX;
   PLASMA-MEMBRANE; ASSEMBLY SITES; CRYSTAL-STRUCTURES; LIPID RAFTS;
   PROTEIN; GAG; ENV
AB The matrix (MA) domain of HIV-1 Gag plays key roles in membrane targeting of Gag, and envelope (Env) glycoprotein incorporation into virions. Although a trimeric MA structure has been available since 1996, evidence for functional MA trimers has been elusive. The mechanism of HIV-1 Env recruitment into virions likewise remains unclear. Here, we identify a point mutation in MA that rescues the Env incorporation defects imposed by an extensive panel of MA and Env mutations. Mapping the mutations onto the putative MA trimer reveals that the incorporation-defective mutations cluster at the tips of the trimer, around the perimeter of a putative gap in the MA lattice into which the cytoplasmic tail of gp41 could insert. By contrast, the rescue mutation is located at the trimer interface, suggesting that it may confer rescue of Env incorporation via modification of MA trimer interactions, a hypothesis consistent with additional mutational analysis. These data strongly support the existence of MA trimers in the immature Gag lattice and demonstrate that rescue of Env incorporation defects is mediated by modified interactions at the MA trimer interface. The data support the hypothesis that mutations in MA that block Env incorporation do so by imposing a steric clash with the gp41 cytoplasmic tail, rather than by disrupting a specific MA-gp41 interaction. The importance of the trimer interface in rescuing Env incorporation suggests that the trimeric arrangement of MA may be a critical factor in permitting incorporation of Env into the Gag lattice.
C1 [Tedbury, Philip R.; Ablan, Sherimay D.; Freed, Eric O.] NCI, Ctr Canc Res, HIV Drug Resistance Program, Virus Cell Interact Sect, Frederick, MD 21702 USA.
RP Tedbury, PR (reprint author), NCI, Ctr Canc Res, HIV Drug Resistance Program, Virus Cell Interact Sect, Frederick, MD 21702 USA.
EM efreed@nih.gov
OI Tedbury, Philip/0000-0001-8151-4967
FU NIH, National Cancer Institute, Center for Cancer Research; Intramural
   AIDS targeted Antiviral Program
FX Research in the Freed lab is supported by the Intramural Research
   Program of the NIH, National Cancer Institute, Center for Cancer
   Research and by the Intramural AIDS targeted Antiviral Program. The
   funders had no role in study design, data collection and analysis,
   decision to publish, or preparation of the manuscript.
NR 69
TC 19
Z9 19
U1 0
U2 0
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD NOV
PY 2013
VL 9
IS 11
AR e1003739
DI 10.1371/journal.ppat.1003739
PG 13
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 299HN
UT WOS:000330386900016
PM 24244165
ER

PT J
AU Bressler, SB
   Almukhtar, T
   Aiello, LP
   Bressler, NM
   Ferris, FL
   Glassman, AR
   Greven, CM
AF Bressler, Susan B.
   Almukhtar, Talat
   Aiello, Lloyd P.
   Bressler, Neil M.
   Ferris, Frederick L., III
   Glassman, Adam R.
   Greven, Craig M.
CA Diabet Retinopathy Clinical Res Ne
TI GREEN OR YELLOW LASER TREATMENT FOR DIABETIC MACULAR EDEMA Exploratory
   Assessment Within the Diabetic Retinopathy Clinical Research Network
SO RETINA-THE JOURNAL OF RETINAL AND VITREOUS DISEASES
LA English
DT Article
DE diabetic macular edema; laser photocoagulation; laser wavelength
ID ARGON BLUE-GREEN; WAVELENGTH SELECTION; PHOTOCOAGULATION; RANIBIZUMAB;
   KRYPTON
AB Purpose: Explore differences in green compared with yellow focal/grid laser treatment on functional and anatomical endpoints in eyes with diabetic macular edema. Methods: Data from two randomized clinical trials were evaluated for differences in visual acuity and optical coherence tomography parameters for eyes assigned to sham injection + prompt laser, ranibizumab + prompt laser, or prompt laser only: among subgroups of eyes treated exclusively and electively with either green or yellow laser. Results: In the sham injection + prompt laser group, the mean visual acuity letter score change for eyes receiving green and yellow laser treatment, respectively, was + 2.4 +/- 14 and + 5.1 +/- 13 at the 52-week visit (P = 0.06) and + 2.4 +/- 15 and + 6.0 +/- 13 at the 104-week visit (P = 0.13), with no corresponding evidence of differences in optical coherence tomography thickness. When comparing wavelength groups in the ranibizumab + prompt laser and prompt laser-only groups, meaningful differences in visual acuity and optical coherence tomography thickness were not detected at 1 year or 2 years. Conclusion: A trend toward improved vision outcome with yellow laser observed in one trial was not corroborated by anatomical outcomes or by the other trial. In this study, without random assignment to different wavelengths controlling for bias and confounding, it is not possible to determine whether one wavelength is better than the other.
C1 [Bressler, Susan B.; Bressler, Neil M.] Johns Hopkins Univ, Sch Med, Wilmer Eye Inst, Dept Ophthalmol, Baltimore, MD 21205 USA.
   [Almukhtar, Talat; Glassman, Adam R.] Jaeb Ctr Hlth Res, Tampa, FL 33647 USA.
   [Aiello, Lloyd P.] Harvard Univ, Sch Med, Joslin Diabet Ctr, Dept Ophthalmol,Beetham Eye Inst, Boston, MA 02115 USA.
   [Ferris, Frederick L., III] NEI, Div Epidemiol & Clin Applicat, Bethesda, MD 20892 USA.
   [Ferris, Frederick L., III] NIH, Bethesda, MD 20892 USA.
   [Greven, Craig M.] Wake Forest Univ, Ctr Eye, Dept Ophthalmol, Winston Salem, NC 27109 USA.
RP Almukhtar, T (reprint author), Jaeb Ctr Hlth Res, 15310 Amberly Dr,Suite 350, Tampa, FL 33647 USA.
EM drcrstat6@jaeb.org
FU National Eye Institute; National Institute of Diabetes and Digestive and
   Kidney Diseases; National Institutes of Health; Department of Health and
   Human Services [EY14231, EY14229, EY18817]; Office of Research
   Administration; Abbott Medical Optics; Allergan; Bausch Lomb;
   Bristol-Meyer-Squibb; Carl Zeiss Meditec; EMMES Corporation; ForSight
   Labs; LLC Genentech; Genzyme Corporation; Lumenis; Notal Vision;
   Novartis; Regeneron
FX Supported by the National Eye Institute and the National Institute of
   Diabetes and Digestive and Kidney Diseases, National Institutes of
   Health, Department of Health and Human Services EY14231, EY14229,
   EY18817 through cooperative agreements. The funding organization
   (National Institutes of Health) participated in oversight of the conduct
   of the study and review of the article but not directly in the design or
   conduct of the study or in the collection, management, analysis, or
   interpretation of the data or in the preparation of the article.
   Genentech provided ranibizumab for the study. In addition, Genentech
   provided funds to DRCR. net to defray the study's clinical site costs.
   As described in the Diabetic Retinopathy Clinical Research Network
   (DRCR.net) Industry Collaboration Guidelines (available at:
   www.drcr.net), the DRCR.net had complete control over the design of the
   protocol, ownership of the data, and all editorial content of
   presentations and publications related to the protocol. A complete list
   of all DRCR. net investigator financial disclosures can be found at www.
   drcr. net. Writing committee financial disclosures: N. M. Bressler:
   Grants to investigators at The Johns Hopkins University are negotiated
   and administered by the institution (such as the School of Medicine)
   that receives the grants, typically through the Office of Research
   Administration. Individual investigators who participate in the
   sponsored projects are not directly compensated by the sponsor but may
   receive salary or other support from the institution to support their
   effort on the projects. Dr. N. M. Bressler is the Principal Investigator
   of grants at The Johns Hopkins University sponsored by the following
   entities (not including the National Institutes of Health): Abbott
   Medical Optics, Allergan, Bausch & Lomb, Bristol-Meyer-Squibb, Carl
   Zeiss Meditec, EMMES Corporation, ForSight Labs, LLC Genentech, Genzyme
   Corporation, Lumenis, Notal Vision, Novartis, and Regeneron. A complete
   list of all DRCR.net investigator financial disclosures can be found at
   www.drcr.net.
NR 23
TC 2
Z9 3
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0275-004X
EI 1539-2864
J9 RETINA-J RET VIT DIS
JI Retin.-J. Retin. Vitr. Dis.
PD NOV-DEC
PY 2013
VL 33
IS 10
BP 2080
EP 2088
PG 9
WC Ophthalmology
SC Ophthalmology
GA 297EI
UT WOS:000330237900012
PM 23792486
ER

PT J
AU Bokanovic, D
   Aberer, W
   Hemmer, W
   Heinemann, A
   Komericki, P
   Scheffel, J
   Sturm, GJ
AF Bokanovic, D.
   Aberer, W.
   Hemmer, W.
   Heinemann, A.
   Komericki, P.
   Scheffel, J.
   Sturm, G. J.
TI Determination of sIgE to rPhl p 1 is sufficient to diagnose grass pollen
   allergy
SO ALLERGY
LA English
DT Article
DE basophil activation test; component-resolved diagnosis; conjunctival
   provocation test; grass pollen allergy; immuno solid-phase allergen chip
   (ISAC)
ID HYMENOPTERA VENOM ALLERGY; BASOPHIL ACTIVATION TEST; IN-VITRO DIAGNOSIS;
   RVES V 5; SKIN PRICK; IGE; IMMUNOTHERAPY; SENSITIVITY; EFFICACY; RELEASE
AB BackgroundNew diagnostic tools such as the basophil activation test (BAT) and component-resolved diagnosis (CRD) are promising for hymenoptera venom or food allergy. A clear benefit for inhalant allergens has not yet been shown. Our aim was to compare new and established tests for grass pollen allergy.
   MethodsForty-nine patients with grass pollen allergy and 47 controls were prospectively enrolled in the study. A symptom score was calculated for each patient. Conjunctival provocation tests (CPT), skin prick tests (SPT), BAT, and sIgE determination including CRD were performed. Sensitivity and specificity were compared and results were correlated with the symptom score.
   ResultsSingle determination of sIgE to rPhlp1 showed the best balance between sensitivity (98%) and specificity (92%). Use of additional components, such as rPhl p 2 and 5, did not increase sensitivity. Generally, sensitivity of tests was high: SPT 100%, ISAC-112 100%, sIgE to timothy grass 98%, BAT 98%, ISAC-103 84%, and CPT 83%. Specificity ranged from 79% (SPT) to 96% (CPT). All test results and calculated values (e.g. ratio sIgE/tIgE) did not correlate with symptom severity. Asymptomatic sensitization to timothy grass in controls was rare in the CAP (11%) and predominantly due to Phlp1 sensitization.
   ConclusionrPhlp1 was sufficient to diagnose grass pollen allergy, and sIgE patterns were the same in symptomatically and asymptomatically sensitized subjects. The testing of multiple components was of minor importance, and no test correlated with symptom severity.
C1 [Bokanovic, D.; Aberer, W.; Komericki, P.; Sturm, G. J.] Med Univ Graz, Dept Dermatol & Venereol, A-8036 Graz, Austria.
   [Hemmer, W.] Floridsdorf Allergy Ctr, Vienna, Austria.
   [Heinemann, A.] Med Univ Graz, Inst Expt & Clin Pharmacol, A-8036 Graz, Austria.
   [Scheffel, J.] NIAMSD, Lab Mol Immunogenet, NIH, Bethesda, MD 20892 USA.
RP Sturm, GJ (reprint author), Med Univ Graz, Dept Dermatol & Venereol, Auenbruggerpl 8, A-8036 Graz, Austria.
EM gunter.sturm@medunigraz.at
OI Heinemann, Akos/0000-0002-8554-2372
NR 31
TC 7
Z9 7
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0105-4538
EI 1398-9995
J9 ALLERGY
JI Allergy
PD NOV
PY 2013
VL 68
IS 11
BP 1403
EP 1409
DI 10.1111/all.12263
PG 7
WC Allergy; Immunology
SC Allergy; Immunology
GA 294IP
UT WOS:000330039100008
PM 24117513
ER

PT J
AU McGuire, JL
   Bergstrom, HC
   Parker, CC
   Le, T
   Morgan, M
   Tang, HY
   Selwyn, RG
   Silva, AC
   Choi, K
   Ursano, RJ
   Palmer, AA
   Johnson, LR
AF McGuire, Jennifer L.
   Bergstrom, Hadley C.
   Parker, Clarissa C.
   Le, Thien
   Morgan, Maria
   Tang, Haiying
   Selwyn, Reed G.
   Silva, Afonso C.
   Choi, Kwang
   Ursano, Robert J.
   Palmer, Abraham A.
   Johnson, Luke R.
TI Traits of fear resistance and susceptibility in an advanced intercross
   line
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE AIL; fear conditioning; fear generalisation; hippocampus; HPA axis;
   manganese-enhanced MRI
ID POSTTRAUMATIC-STRESS-DISORDER; PITUITARY-ADRENAL AXIS;
   MANGANESE-ENHANCED MRI; CONDITIONED FEAR; MINERALOCORTICOID RECEPTOR;
   FUNCTIONAL CONNECTIVITY; HIPPOCAMPAL SUBREGIONS; GENE-EXPRESSION; COMBAT
   VETERANS; MEMORY
AB Genetic variability in the strength and precision of fear memory is hypothesised to contribute to the etiology of anxiety disorders, including post-traumatic stress disorder. We generated fear-susceptible (F-S) or fear-resistant (F-R) phenotypes from an F-8 advanced intercross line (AIL) of C57BL/6J and DBA/2J inbred mice by selective breeding. We identified specific traits underlying individual variability in Pavlovian conditioned fear learning and memory. Offspring of selected lines differed in the acquisition of conditioned fear. Furthermore, F-S mice showed greater cued fear memory and generalised fear in response to a novel context than F-R mice. F-S mice showed greater basal corticosterone levels and hypothalamic corticotrophin-releasing hormone (CRH) mRNA levels than F-R mice, consistent with higher hypothalamic-pituitary-adrenal (HPA) axis drive. Hypothalamic mineralocorticoid receptor and CRH receptor 1 mRNA levels were decreased in F-S mice as compared with F-R mice. Manganese-enhanced magnetic resonance imaging (MEMRI) was used to investigate basal levels of brain activity. MEMRI identified a pattern of increased brain activity in F-S mice that was driven primarily by the hippocampus and amygdala, indicating excessive limbic circuit activity in F-S mice as compared with F-R mice. Thus, selection pressure applied to the AIL population leads to the accumulation of heritable trait-relevant characteristics within each line, whereas non-behaviorally relevant traits remain distributed. Selected lines therefore minimise false-positive associations between behavioral phenotypes and physiology. We demonstrate that intrinsic differences in HPA axis function and limbic excitability contribute to phenotypic differences in the acquisition and consolidation of associative fear memory. Identification of system-wide traits predisposing to variability in fear memory may help in the direction of more targeted and efficacious treatments for fear-related pathology.
C1 [McGuire, Jennifer L.; Bergstrom, Hadley C.; Le, Thien; Morgan, Maria; Choi, Kwang; Ursano, Robert J.; Johnson, Luke R.] Uniformed Serv Univ Hlth Sci, Sch Med, Dept Psychiat, Bethesda, MD USA.
   [McGuire, Jennifer L.; Bergstrom, Hadley C.; Le, Thien; Morgan, Maria; Choi, Kwang; Ursano, Robert J.; Johnson, Luke R.] Uniformed Serv Univ Hlth Sci, Sch Med, Program Neurosci, Bethesda, MD USA.
   [Bergstrom, Hadley C.; Le, Thien; Choi, Kwang; Ursano, Robert J.; Johnson, Luke R.] Ctr Study Traumat Stress, Bethesda, MD USA.
   [Parker, Clarissa C.; Palmer, Abraham A.] Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA.
   [Tang, Haiying; Selwyn, Reed G.] Uniformed Serv Univ Hlth Sci, Sch Med, Dept Radiol, Bethesda, MD USA.
   [Silva, Afonso C.] NINDS, NIH, Bethesda, MD 20892 USA.
   [Palmer, Abraham A.] Univ Chicago, Dept Psychiat & Behav Neurosci, Chicago, IL 60637 USA.
   [Johnson, Luke R.] Queensland Univ Technol, Translat Res Inst, Inst Hlth & Biomed Innovat, Dept Psychol, Brisbane, Qld 4059, Australia.
RP Johnson, LR (reprint author), Translat Res Inst, Brisbane, Qld, Australia.
EM LukeJohnsonPhD@gmail.com
RI Palmer, Abraham/L-2158-2014; 
OI Palmer, Abraham/0000-0003-3634-0747; Bergstrom,
   Hadley/0000-0003-3677-1619
FU CSTS [G188NW]; NIH [R01MH079103];  [T32DA007255]
FX We would like to thank Dr Laura Tucker, Dr Asamoah Bosomti, Ann Schue,
   Sumajari Das, Smita Dey, Maj Robert Long, Rose Arditi and Alice Fladung
   for excellent assistance with aspects of this project. Aspects of this
   work were presented at the Society for Neuroscience Annual Meeting, 14
   October 2012, the Amygdala, Stress and PTSD Conference, 24 April 2012,
   and in the following Nature News article: Stress: the roots of
   resilience. Nature 490, 165-167 (11 October 2012),
   http://www.nature.com/news/stress-the-roots-of-resilience-1.11570. This
   project was funded by CSTS grant G188NW to L. R. Johnson, by NIH
   R01MH079103 to A. A. Palmer, and by T32DA007255 to C. C. Parker. The
   authors declare no conflicts of interest.
NR 80
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Z9 6
U1 2
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0953-816X
EI 1460-9568
J9 EUR J NEUROSCI
JI Eur. J. Neurosci.
PD NOV
PY 2013
VL 38
IS 9
BP 3314
EP 3324
DI 10.1111/ejn.12337
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 295FF
UT WOS:000330101300006
PM 23968228
ER

PT J
AU Ruiz, MO
   Kelly, AC
   Brown, WM
   Novakofski, JE
   Mateus-Pinilla, NE
AF Ruiz, Marilyn O'Hara
   Kelly, Amy C.
   Brown, William M.
   Novakofski, Jan E.
   Mateus-Pinilla, Nohra E.
TI Influence of landscape factors and management decisions on spatial and
   temporal patterns of the transmission of chronic wasting disease in
   white-tailed deer
SO GEOSPATIAL HEALTH
LA English
DT Article
DE chronic wasting disease; landscape epidemiology; white-tailed deer;
   environmental transmission; prion; USA
ID PATHOGENIC PRION PROTEIN; RANGING MULE DEER; SPONGIFORM ENCEPHALOPATHY;
   ODOCOILEUS-VIRGINIANUS; ENVIRONMENTAL SOURCES; SOIL; WISCONSIN;
   ILLINOIS; EPIDEMIOLOGY; PREVALENCE
AB Chronic wasting disease (CWD) has been reported in white-tailed deer at the border of the US states of Illinois and Wisconsin since 2002. Transmission of infectious prions between animals and from the environment has resulted in spatial and temporal structure observable in the spatio-temporal patterns of reported cases. Case locations of 382 positive cases from 28,954 deer tested between 2002 and 2009 provided insight into the potential risk factors and landscape features associated with transmission using a combination of clustering, generalised linear modelling and descriptive evaluations of a risk map of predicted cases of CWD. A species distribution map of white-tailed deer developed using MaxEnt provided an estimate of deer locations. We found that deer probability increased in areas with larger forests and less urban and agricultural lands. Spatial clustering analysis revealed a core area of persistent CWD transmission in the northern part of the region. The regression model indicated that larger and more compact forests were associated with higher risk for CWD. High risk areas also had soils with less clay and more sand than other parts of the region. The transmission potential was higher where landscape features indicated the potential for higher deer concentrations. The inclusion of spatial lag variables improved the model. Of the 102 cases reported in the study area in the two years following the study period, 89 (87%) of those were in the 32% of the study area with the highest 50% of predicted risk of cases.
C1 [Ruiz, Marilyn O'Hara; Brown, William M.] Univ Illinois, Dept Pathobiol, Urbana, IL 61802 USA.
   [Kelly, Amy C.] NIDDK, NIH, Bethesda, MD 20892 USA.
   [Novakofski, Jan E.] Univ Illinois, Dept Anim Sci, Urbana, IL 61802 USA.
   [Mateus-Pinilla, Nohra E.] Univ Illinois, Illinois Nat Hist Survey, Prairie Res Inst, Champaign, IL 61820 USA.
RP Ruiz, MO (reprint author), Univ Illinois, Dept Pathobiol, 2001 South Lincoln Ave, Urbana, IL 61802 USA.
EM moruiz@illinois.edu
FU The Illinois Department of Natural Resources, the United States
   Geological Survey, United States Department of Agriculture and the US
   Fish and Wildlife Service Federal Aid in Wildlife Restoration [W-146-R]
FX The Illinois Department of Natural Resources, the United States
   Geological Survey, United States Department of Agriculture and the US
   Fish and Wildlife Service Federal Aid in Wildlife Restoration Project
   W-146-R provided funds for this work. Paul Shelton at the Illinois
   Department of Natural Resources provided insight on the collection of
   data on CWD in Illinois.
NR 51
TC 4
Z9 4
U1 9
U2 31
PU UNIV NAPLES FEDERICO II
PI NAPLES
PA FAC VET MED, DEP PATHOLOGY & ANIMAL HEALTH, VET PARASITOLOGY, VIA DELLA
   VETERINARIA 1, NAPLES, 80137, ITALY
SN 1827-1987
EI 1970-7096
J9 GEOSPATIAL HEALTH
JI Geospatial Health
PD NOV
PY 2013
VL 8
IS 1
BP 215
EP 227
PG 13
WC Health Care Sciences & Services; Public, Environmental & Occupational
   Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
   Health
GA 296UI
UT WOS:000330210500020
PM 24258897
ER

PT J
AU Kapogiannis, D
   Sutin, A
   Davatzikos, C
   Costa, P
   Resnick, S
AF Kapogiannis, Dimitrios
   Sutin, Angelina
   Davatzikos, Christos
   Costa, Paul, Jr.
   Resnick, Susan
TI The Five Factors of Personality and Regional Cortical Variability in the
   Baltimore Longitudinal Study of Aging
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE individual differences; trait; neuroticism; extraversion; openness;
   agreeableness; conscientiousness; anterior cingulate; orbitofrontal
   cortex; frontopolar cortex
ID VOXEL-BASED MORPHOMETRY; ANTERIOR CINGULATE; INDIVIDUAL-DIFFERENCES;
   ORBITOFRONTAL CORTEX; DECISION-MAKING; FUNCTIONAL CONNECTIVITY;
   FRONTOTEMPORAL DEMENTIA; PREFRONTAL CORTEX; BRAIN ASYMMETRY;
   SOCIAL-BEHAVIOR
AB Although personality changes have been associated with brain lesions and atrophy caused by neurodegenerative diseases and aging, neuroanatomical correlates of personality in healthy individuals and their stability over time have received relatively little investigation. In this study, we explored regional gray matter (GM) volumetric associations of the five-factor model of personality. Eighty-seven healthy older adults took the NEO Personality Inventory and had brain MRI at two time points 2 years apart. We performed GM segmentation followed by regional analysis of volumes examined in normalized space map creation and voxel based morphometry-type statistical inference in SPM8. We created a regression model including all five factors and important covariates. Next, a conjunction analysis identified associations between personality scores and GM volumes that were replicable across time, also using cluster-level Family-Wise-Error correction. Larger right orbitofrontal and dorsolateral prefrontal cortices and rolandic operculum were associated with lower Neuroticism; larger left temporal, dorsolateral prefrontal, and anterior cingulate cortices with higher Extraversion; larger right frontopolar and smaller orbitofrontal and insular cortices with higher Openness; larger right orbitofrontal cortex with higher Agreeableness; larger dorsolateral prefrontal and smaller frontopolar cortices with higher Conscientiousness. In summary, distinct personality traits were associated with stable individual differences in GM volumes. As expected for higher-order traits, regions performing a large number of cognitive and affective functions were implicated. Our findings highlight personality-related variation that may be related to individual differences in brain structure that merit additional attention in neuroimaging research. Hum Brain Mapp 34:2829-2840, 2013. (c) 2012 Wiley Periodicals, Inc.
C1 [Kapogiannis, Dimitrios] NIA, NIH, Clin Res Branch, Baltimore, MD 21224 USA.
   [Sutin, Angelina; Costa, Paul, Jr.; Resnick, Susan] NIA, NIH, Lab Behav Neurosci, Baltimore, MD 21224 USA.
   [Davatzikos, Christos] Univ Penn, Dept Radiol, Philadelphia, PA 19104 USA.
RP Kapogiannis, D (reprint author), NIA, NIH, Clin Res Branch, Baltimore, MD 21224 USA.
EM kapogiannisd@mail.nih.gov
OI Costa, Paul/0000-0003-4375-1712
FU Intramural Research Program of the NIH; National Institute on Aging
   (NIA) [N01-AG-3-2124]
FX Contract grant sponsors: Intramural Research Program of the NIH and
   National Institute on Aging (NIA); Contract grant number: N01-AG-3-2124.
NR 87
TC 17
Z9 17
U1 5
U2 14
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 NOV
PY 2013
VL 34
IS 11
BP 2829
EP 2840
DI 10.1002/hbm.22108
PG 12
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
   Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 295FG
UT WOS:000330101400008
PM 22610513
ER

PT J
AU Barakat, M
   Carrier, J
   Debas, K
   Lungu, O
   Fogel, S
   Vandewalle, G
   Hoge, RD
   Bellec, P
   Karni, A
   Ungerleider, LG
   Benali, H
   Doyon, J
AF Barakat, Marc
   Carrier, Julie
   Debas, Karen
   Lungu, Ovidiu
   Fogel, Stuart
   Vandewalle, Gilles
   Hoge, Richard D.
   Bellec, Pierre
   Karni, Avi
   Ungerleider, Leslie G.
   Benali, Habib
   Doyon, Julien
TI Sleep Spindles Predict Neural and Behavioral Changes in Motor Sequence
   Consolidation
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE motor sequence consolidation; cortico-striatal system; sleep spindles;
   EEG; fMRI
ID EXPERIENCE-DEPENDENT CHANGES; EYE-MOVEMENT SLEEP; MEMORY CONSOLIDATION;
   REM-SLEEP; CEREBRAL ACTIVATION; BASAL GANGLIA; STAGE-2 SLEEP;
   REACTION-TIME; PLASTICITY; BRAIN
AB The purpose of this study was to investigate the predictive function of sleep spindles in motor sequence consolidation. BOLD responses were acquired in 10 young healthy subjects who were trained on an explicitly known 5-item sequence using their left nondominant hand, scanned at 9:00 pm while performing that same task and then were retested and scanned 12 h later after a night of sleep during which polysomnographic measures were recorded. An automatic algorithm was used to detect sleep spindles and to quantify their characteristics (i.e., density, amplitude, and duration). Analyses revealed significant positive correlations between gains in performance and the amplitude of spindles. Moreover, significant increases in BOLD signal were observed in several motor-related areas, most of which were localized in the right hemisphere, particularly in the right cortico-striatal system. Such increases in BOLD signal also correlated positively with the amplitude of spindles at several derivations. Taken together, our results show that sleep spindles predict neural and behavioral changes in overnight motor sequence consolidation. Hum Brain Mapp 34:2918-2928, 2013. (c) 2012 Wiley Periodicals, Inc.
C1 [Barakat, Marc; Carrier, Julie; Debas, Karen; Lungu, Ovidiu; Fogel, Stuart; Vandewalle, Gilles; Hoge, Richard D.; Doyon, Julien] Univ Montreal, Inst Geriatr, Ctr Rech, Funct Neuroimaging Unit, Montreal, PQ H3C 3J7, Canada.
   [Barakat, Marc; Carrier, Julie; Vandewalle, Gilles] Hop Sacre Coeur, Ctr Adv Res Sleep Med, Montreal, PQ H4J 1C5, Canada.
   [Barakat, Marc; Carrier, Julie; Debas, Karen; Doyon, Julien] Univ Montreal, Dept Psychol, Ctr Rech Neuropsychol & Cognit, Montreal, PQ H3C 3J7, Canada.
   [Bellec, Pierre] McGill Univ, Montreal Neurol Inst, McConnell Brain Imaging Ctr, Montreal, PQ H3A 2B4, Canada.
   [Karni, Avi] Univ Haifa, Brain Behav Ctr, Lab Funct Brain Imaging & Learning Res, IL-31999 Haifa, Israel.
   [Ungerleider, Leslie G.; Doyon, Julien] NIMH, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
   [Benali, Habib; Doyon, Julien] Univ Paris 06, CHU Pitie Salpetriere, INSERM, Unite Mixte Rech S 678, Paris, France.
RP Doyon, J (reprint author), Funct Neuroimaging Unit, 4565,Queen Mary St,Room M-7836, Montreal, PQ H3W 1W5, Canada.
EM julien.doyon@umontreal.ca
OI Bellec, Pierre/0000-0002-9111-0699
FU Canadian Institutes of Health Research, FRSQ
FX Contract grant sponsors: Canadian Institutes of Health Research, FRSQ.
NR 58
TC 22
Z9 22
U1 1
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 NOV
PY 2013
VL 34
IS 11
BP 2918
EP 2928
DI 10.1002/hbm.22116
PG 11
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
   Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 295FG
UT WOS:000330101400015
PM 22674673
ER

PT J
AU Phillips, W
   Piller, LB
   Williamson, JD
   Whittle, J
   Jafri, SZA
   Ford, CE
   Einhorn, PT
   Oparil, S
   Furberg, CD
   Grimm, RH
   Alderman, MH
   Davis, BR
   Probstfield, JL
AF Phillips, William
   Piller, Linda B.
   Williamson, Jeff D.
   Whittle, Jeffrey
   Jafri, Syed Z. A.
   Ford, Charles E.
   Einhorn, Paula T.
   Oparil, Suzanne
   Furberg, Curt D.
   Grimm, Richard H., Jr.
   Alderman, Michael H.
   Davis, Barry R.
   Probstfield, Jeffrey L.
CA ALLHAT Collaborative Res Grp
TI Risk of Hospitalized Gastrointestinal Bleeding in Persons Randomized to
   Diuretic, ACE-Inhibitor, or Calcium-Channel Blocker in ALLHAT
SO JOURNAL OF CLINICAL HYPERTENSION
LA English
DT Article
ID LIPID-LOWERING TREATMENT; HEART-ATTACK TRIAL; CONVERTING
   ENZYME-INHIBITOR; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; ANTIHYPERTENSIVE
   DRUGS; HYPERTENSIVE PATIENTS; ELDERLY-PATIENTS; CLINICAL EVENTS; OLDER
   PATIENTS; ANTAGONISTS
AB Calcium channel blockers (CCBs) are an important class of medication useful in the treatment of hypertension. Several observational studies have suggested an association between CCB therapy and gastrointestinal (GI) hemorrhage. Using administrative databases, the authors re-examined in a post-hoc analysis whether the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) participants randomized to the CCB amlodipine had a greater risk of hospitalized GI bleeding (a prespecified outcome) compared with those randomized to the diuretic chlorthalidone or the angiotensin-converting enzyme inhibitor lisinopril. Participants randomized to chlorthalidone did not have a reduced risk for GI bleeding hospitalizations compared with participants randomized to amlodipine (hazard ratio [HR], 1.09; 95% confidence interval [CI], 0.92-1.28). Those randomized to lisinopril were at increased risk of GI bleeding compared with those randomized to chlorthalidone (HR, 1.16; 95% CI, 1.00-1.36). In a post-hoc comparison, participants assigned to lisinopril therapy had a higher risk of hospitalized GI hemorrhage (HR, 1.27; 95% CI, 1.06-1.51) vs those assigned to amlodipine. In-study use of atenolol prior to first GI hemorrhage was related to a lower incidence of GI bleeding (HR, 0.69; 95% CI, 0.57-0.83). Hypertensive patients on amlodipine do not have an increased risk of GI bleeding hospitalizations compared with those taking either chlorthalidone or lisinopril.
C1 [Phillips, William] Univ Calif Davis, Davis, CA 95616 USA.
   [Piller, Linda B.; Ford, Charles E.; Davis, Barry R.] Univ Texas Houston, Sch Publ Hlth, Houston, TX 77030 USA.
   [Williamson, Jeff D.; Furberg, Curt D.] Wake Forest Univ, Sch Med, Winston Salem, NC 27109 USA.
   [Whittle, Jeffrey] Clement J Zablocki VA Med Ctr, Milwaukee, WI USA.
   [Jafri, Syed Z. A.] CrystalRun HealthCare, Middletown, NY USA.
   [Einhorn, Paula T.] NHLBI, Bethesda, MD 20892 USA.
   [Oparil, Suzanne] Univ Alabama Birmingham, Birmingham, AL USA.
   [Grimm, Richard H., Jr.] Berman Ctr Outcomes & Clin Res, Minneapolis, MN USA.
   [Alderman, Michael H.] Albert Einstein Coll Med, Bronx, NY 10467 USA.
   [Probstfield, Jeffrey L.] Univ Washington, Med Ctr, Seattle, WA 98195 USA.
RP Piller, LB (reprint author), Univ Texas Houston, Sch Publ Hlth, 1200 Pressler St,W-906, Houston, TX 77030 USA.
EM Linda.B.Piller@uth.tmc.edu
FU Health and Human Services from the National Heart, Lung, and Blood
   Institute, National Institutes of Health, US Department of Health and
   Human Services, Bethesda, MD [N01-HC-35130, HHSN268201100036C]; Pfizer,
   Inc.; Daiichi Sankyo; Gilead; Merck; Amgen; Abbott Laboratories;
   GlaxoSmithKline; Sanofi Aventis; NHLBI
FX This research was supported by Health and Human Services contracts
   N01-HC-35130 and HHSN268201100036C from the National Heart, Lung, and
   Blood Institute, National Institutes of Health, US Department of Health
   and Human Services, Bethesda, MD. The ALLHAT investigators acknowledge
   contributions of study medications supplied by Pfizer, Inc (amlodipine
   and doxazosin), AstraZeneca (atenolol and lisinopril), and Bristol-Myers
   Squibb (pravastatin) and financial support provided by Pfizer, Inc. Dr
   Alderman has received research support from Daiichi Sankyo. Dr Davis has
   consulted for Amgen and Takeda. Dr Grimm has consulted for Merck,
   Pfizer, and Roche, and has received honoraria from Takeda. Dr Oparil has
   consulted for Schering Plough, Eli Lilly, Daiichi Sankyo, Boehringer
   Ingelheim, Novartis, NicOx, Pfizer, Omron Healthcare, and Forest
   Laboratories, and has received research support from Gilead, Daiichi
   Sankyo, Merck, and Amgen. Dr Probstfield has received research support
   from Abbott Laboratories, GlaxoSmithKline, and Sanofi Aventis. Drs
   Einhorn, Ford, Furberg, Jafri, Phillips, Piller, Whittle, and Williamson
   have no financial interests to report. Editorial assistance was provided
   by Ellen Breckenridge, PhD, of The University of Texas School of Public
   Health, Houston, TX, and was funded by NHLBI.
NR 46
TC 1
Z9 1
U1 1
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1524-6175
EI 1751-7176
J9 J CLIN HYPERTENS
JI J. Clin. Hypertens.
PD NOV
PY 2013
VL 15
IS 11
BP 825
EP 832
DI 10.1111/jch.12180
PG 8
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 295FO
UT WOS:000330102200013
PM 24283598
ER

PT J
AU Johnson, HL
   Fontelo, P
   Olsen, CH
   Jones, MAJKD
   Gimbel, RW
AF Johnson, Heather L.
   Fontelo, Paul
   Olsen, Cara H.
   Jones, M. A. J. Kenneth D., II
   Gimbel, Ronald W.
TI Family nurse practitioner student perception of journal abstract
   usefulness in clinical decision making: A randomized controlled trial
SO JOURNAL OF THE AMERICAN ASSOCIATION OF NURSE PRACTITIONERS
LA English
DT Article
DE Advanced practice nurse (APN); clinical decision making; decision
   making; computers; evidence-based practice; information technology;
   nurse practitioners
ID PRIMARY-CARE; QUESTIONS; INFORMATION; ACCURACY; ARTICLES; OUTCOMES
AB Purpose To assess family nurse practitioner (FNP) student perception of research abstract usefulness in clinical decision making. Data sources A randomized controlled trial conducted in a simulated environment with graduate FNP students of the Graduate School of Nursing, Uniformed Services University of the Health Sciences. Given a clinical case study and modified MEDLINE search tool accessible via an iPad device, participants were asked to develop a treatment plan and complete a data collection form. The primary measure was perceived usefulness of the research abstracts in clinical decision making regarding a simulated obese patient seeking to prevent type 2 diabetes. Secondary measures related to participant demographics and accessibility and usefulness of full-text manuscripts. Conclusions The majority of NP students identified readily available research abstracts as useful in shaping their clinical decision making. The presence or absence of full-text manuscripts associated with the abstracts did not appear to influence the perceived abstract usefulness. The majority of students with full-text manuscript access in the timed simulated clinical encounter read at least one paper, but cited insufficient time to read full-text as a constraint. Implications for practice Research abstracts at point of care may be valuable to FNPs if easily accessible and integrated into clinical workflow.
C1 [Johnson, Heather L.] Uniformed Serv Univ Hlth Sci, Grad Sch Nursing, Bethesda, MD 20814 USA.
   [Fontelo, Paul] Natl Lib Med, Lister Hill Ctr Biomed Commun, Bethesda, MD USA.
   [Olsen, Cara H.] Uniformed Serv Univ Hlth Sci, Dept Prevent Med & Biometr, Bethesda, MD USA.
   [Jones, M. A. J. Kenneth D., II] Uniformed Serv Univ Hlth Sci, Bethesda, MD USA.
   [Gimbel, Ronald W.] Uniformed Serv Univ Hlth Sci, Biomed Informat Dept, Bethesda, MD USA.
RP Johnson, HL (reprint author), Uniformed Serv Univ Hlth Sci, Grad Sch Nursing, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM heather.johnson@usuhs.edu
FU USUHS [R02930.2]
FX This work is supported by USUHS Protocol #R02930.2. The opinions or
   assertions contained herein are the private ones of the authors and are
   not to be construed as official or reflecting the views of the Uniformed
   Services University of the Health Sciences, the U. S. Department of
   Defense, the National Library of Medicine, or the National Institutes of
   Health.
NR 21
TC 0
Z9 0
U1 1
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2327-6886
EI 2327-6924
J9 J AM ASSOC NURSE PRA
JI J. Am. Assoc. Nurs. Pract.
PD NOV
PY 2013
VL 25
IS 11
BP 597
EP 603
DI 10.1111/1745-7599.12013
PG 7
WC Health Care Sciences & Services; Nursing
SC Health Care Sciences & Services; Nursing
GA 296HN
UT WOS:000330176000005
PM 24170534
ER

PT J
AU He, BJ
   Zempel, JM
AF He, Biyu J.
   Zempel, John M.
TI Average Is Optimal: An Inverted-U Relationship between Trial-to-Trial
   Brain Activity and Behavioral Performance
SO PLOS COMPUTATIONAL BIOLOGY
LA English
DT Article
ID STOCHASTIC RESONANCE; NEURAL VARIABILITY; EVOKED-RESPONSES; FUNCTIONAL
   CONNECTIVITY; ACTIVITY FLUCTUATIONS; PERCEPTUAL DECISIONS; TRANSIENT
   DYNAMICS; PREFRONTAL CORTEX; MOTOR PREPARATION; CORTICAL ACTIVITY
AB It is well known that even under identical task conditions, there is a tremendous amount of trial-to-trial variability in both brain activity and behavioral output. Thus far the vast majority of event-related potential (ERP) studies investigating the relationship between trial-to-trial fluctuations in brain activity and behavioral performance have only tested a monotonic relationship between them. However, it was recently found that across-trial variability can correlate with behavioral performance independent of trial-averaged activity. This finding predicts a U-or inverted-U-shaped relationship between trial-to-trial brain activity and behavioral output, depending on whether larger brain variability is associated with better or worse behavior, respectively. Using a visual stimulus detection task, we provide evidence from human electrocorticography (ECoG) for an inverted-U brain-behavior relationship: When the raw fluctuation in broadband ECoG activity is closer to the across-trial mean, hit rate is higher and reaction times faster. Importantly, we show that this relationship is present not only in the post-stimulus task-evoked brain activity, but also in the pre-stimulus spontaneous brain activity, suggesting anticipatory brain dynamics. Our findings are consistent with the presence of stochastic noise in the brain. They further support attractor network theories, which postulate that the brain settles into a more confined state space under task performance, and proximity to the targeted trajectory is associated with better performance.
C1 [He, Biyu J.] NINDS, NIH, Bethesda, MD 20892 USA.
   [Zempel, John M.] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA.
   [Zempel, John M.] Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA.
RP He, BJ (reprint author), NINDS, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM biyu.he@nih.gov
OI He, Biyu/0000-0003-1549-1351
FU Intramural Research Program of the NIH/NINDS
FX This research was supported by the Intramural Research Program of the
   NIH/NINDS. The funders had no role in study design, data collection and
   analysis, decision to publish, or preparation of the manuscript.
NR 75
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Z9 10
U1 0
U2 11
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7358
J9 PLOS COMPUT BIOL
JI PLoS Comput. Biol.
PD NOV
PY 2013
VL 9
IS 11
AR e1003348
DI 10.1371/journal.pcbi.1003348
PG 14
WC Biochemical Research Methods; Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology
GA 298XG
UT WOS:000330357200044
PM 24244146
ER

PT J
AU Wang, XX
   Panchanathan, S
   Chowell, G
AF Wang, Xiaoxia
   Panchanathan, Sarada
   Chowell, Gerardo
TI A Data-Driven Mathematical Model of CA-MRSA Transmission among Age
   Groups: Evaluating the Effect of Control Interventions
SO PLOS COMPUTATIONAL BIOLOGY
LA English
DT Article
ID RESISTANT-STAPHYLOCOCCUS-AUREUS; ACQUIRED METHICILLIN-RESISTANT;
   SOFT-TISSUE INFECTIONS; INTRANASAL MUPIROCIN; RISK-FACTORS; DISEASE
   TRANSMISSION; COMMUNITY; COLONIZATION; HOSPITALS; EMERGENCE
AB Community associated methicillin-resistant Staphylococcus aureus (CA-MRSA) has become a major cause of skin and soft tissue infections (SSTIs) in the US. We developed an age-structured compartmental model to study the spread of CA-MRSA at the population level and assess the effect of control intervention strategies. We used Monte-Carlo Markov Chain (MCMC) techniques to parameterize our model using monthly time series data on SSTIs incidence in children (<= 19 years) during January 2004 -December 2006 in Maricopa County, Arizona. Our model-based forecast for the period January 2007-December 2008 also provided a good fit to data. We also carried out an uncertainty and sensitivity analysis on the control reproduction number, R-c which we estimated at 1.3 (95% CI [1.2,1.4]) based on the model fit to data. Using our calibrated model, we evaluated the effect of typical intervention strategies namely reducing the contact rate of infected individuals owing to awareness of infection and decolonization strategies targeting symptomatic infected individuals on both Rc and the long-term disease dynamics. We also evaluated the impact of hypothetical decolonization strategies targeting asymptomatic colonized individuals. We found that strategies focused on infected individuals were not capable of achieving disease control when implemented alone or in combination. In contrast, our results suggest that decolonization strategies targeting the pediatric population colonized with CA-MRSA have the potential of achieving disease elimination.
C1 [Wang, Xiaoxia; Chowell, Gerardo] Arizona State Univ, Sch Human Evolut & Social Change, Math Computat & Modeling Sci Ctr, Tempe, AZ 85287 USA.
   [Panchanathan, Sarada] Maricopa Integrated Hlth Syst, Dept Pediat, Phoenix, AZ USA.
   [Chowell, Gerardo] NIH, Div Int Epidemiol & Populat Studies Fogarty, Int Ctr, Bethesda, MD 20892 USA.
   [Panchanathan, Sarada] Arizona State Univ, Dept Biomed Informat, Tempe, AZ USA.
RP Wang, XX (reprint author), Arizona State Univ, Sch Human Evolut & Social Change, Math Computat & Modeling Sci Ctr, Tempe, AZ 85287 USA.
EM xwang248@asu.edu
RI Barley, Kamal/F-9579-2011
OI Barley, Kamal/0000-0003-1874-9813
FU Arizona Biomedical Research Commission [1216]
FX This work was supported by the Arizona Biomedical Research Commission
   (http://azdhs.gov/biomedical/) with Commission Contract No. 1216. The
   funders had no role in study design, data collection and analysis,
   decision to publish, or preparation of the manuscript.
NR 50
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U1 1
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7358
J9 PLOS COMPUT BIOL
JI PLoS Comput. Biol.
PD NOV
PY 2013
VL 9
IS 11
AR e1003328
DI 10.1371/journal.pcbi.1003328
PG 13
WC Biochemical Research Methods; Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology
GA 298XG
UT WOS:000330357200028
PM 24277998
ER

PT J
AU Gonsalves, SG
   Ng, D
   Johnston, JJ
   Teer, JK
   Stenson, PD
   Cooper, DN
   Mullikin, JC
   Biesecker, LG
AF Gonsalves, Stephen G.
   Ng, David
   Johnston, Jennifer J.
   Teer, Jamie K.
   Stenson, Peter D.
   Cooper, David N.
   Mullikin, James C.
   Biesecker, Leslie G.
CA NISC Comparative Sequencing Progra
TI Using Exome Data to Identify Malignant Hyperthermia Susceptibility
   Mutations
SO ANESTHESIOLOGY
LA English
DT Article
ID RYANODINE RECEPTOR; CONGENITAL MYOPATHIES; MISSENSE VARIANTS; CORE
   MYOPATHIES; CLASSIFICATION; GENES; RYR1; RECOMMENDATIONS;
   IDENTIFICATION; RISK
AB Background: Malignant hyperthermia susceptibility (MHS) is a life-threatening, inherited disorder of muscle calcium metabolism, triggered by anesthetics and depolarizing muscle relaxants. An unselected cohort was screened for MHS mutations using exome sequencing. The aim of this study was to pilot a strategy for the RYR1 and CACNA1S genes.
   Methods: Exome sequencing was performed on 870 volunteers not ascertained for MHS. Variants in RYR1 and CACNA1S were annotated using an algorithm that filtered results based on mutation type, frequency, and information in mutation databases. Variants were scored on a six-point pathogenicity scale. Medical histories and pedigrees were reviewed for malignant hyperthermia and related disorders.
   Results: The authors identified 70 RYR1 and 53 CACNA1S variants among 870 exomes. Sixty-three RYR1 and 41 CACNA1S variants passed the quality and frequency metrics but the authors excluded synonymous variants. In RYR1, the authors identified 65 missense mutations, one nonsense, two that affected splicing, and one non-frameshift indel. In CACNA1S, 48 missense, one frameshift deletion, one splicing, and one non-frameshift indel were identified. RYR1 variants predicted to be pathogenic for MHS were found in three participants without medical or family histories of MHS. Numerous variants, previously described as pathogenic in mutation databases, were reclassified by the authors as being of unknown pathogenicity.
   Conclusions: Exome sequencing can identify asymptomatic patients at risk for MHS, although the interpretation of exome variants can be challenging. The use of exome sequencing in unselected cohorts is an important tool to understand the prevalence and penetrance of MHS, a critical challenge for the field.
C1 [Gonsalves, Stephen G.; Ng, David; Johnston, Jennifer J.; Biesecker, Leslie G.] NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA.
   [Mullikin, James C.] NHGRI, Natl Inst Hlth Intramural Sequencing Ctr, NIH, Bethesda, MD 20892 USA.
   [Stenson, Peter D.; Cooper, David N.] Cardiff Univ, Inst Med Genet, Sch Med, Cardiff CF10 3AX, S Glam, Wales.
   [Teer, Jamie K.] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
   [Gonsalves, Stephen G.; Ng, David; Johnston, Jennifer J.; Teer, Jamie K.; Stenson, Peter D.; Cooper, David N.; Mullikin, James C.; Biesecker, Leslie G.; NISC Comparative Sequencing Progra] Natl Human Genome Inst, NIH, Genet Dis Res Branch, Bethesda, MD USA.
RP Biesecker, LG (reprint author), NHGRI, Genet Dis Res Branch, NIH, 49 Convent Dr,4A56, Bethesda, MD 20892 USA.
EM lesb@mail.nih.gov
OI Cooper, David N./0000-0002-8943-8484
FU Division of Intramural Research of the National Human Genome Research
   Institute, National Institutes of Health, Bethesda, Maryland
FX Funding was provided by the Division of Intramural Research of the
   National Human Genome Research Institute, National Institutes of Health,
   Bethesda, Maryland. The laboratory has an agreement with the Illumina
   Corporation (San Diego, California) to provide some in-kind research
   support for an experiment on the ClinSeq (R) cohort that is separate
   from the work presented here.
NR 32
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U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-3022
EI 1528-1175
J9 ANESTHESIOLOGY
JI Anesthesiology
PD NOV
PY 2013
VL 119
IS 5
BP 1043
EP 1053
DI 10.1097/ALN.0b013e3182a8a8e7
PG 11
WC Anesthesiology
SC Anesthesiology
GA 290ZS
UT WOS:000329797900011
PM 24195946
ER

PT J
AU Curriero, FC
   Pinchoff, J
   van Landingham, SW
   Ferrucci, L
   Friedman, DS
   Ramulu, PY
AF Curriero, Frank C.
   Pinchoff, Jessie
   van Landingham, Suzanne W.
   Ferrucci, Luigi
   Friedman, David S.
   Ramulu, Pradeep Y.
TI Alteration of Travel Patterns With Vision Loss From Glaucoma and Macular
   Degeneration
SO JAMA OPHTHALMOLOGY
LA English
DT Article
ID SALISBURY EYE EVALUATION; QUALITY-OF-LIFE; AGE-RELATED MACULOPATHY;
   OLDER-ADULTS; VISUAL IMPAIRMENT; PHYSICAL-ACTIVITY; SEE PROJECT; FIELD
   LOSS; MOBILITY; DISABILITY
AB IMPORTANCE The distance patients can travel outside the home influences how much of the world they can sample and to what extent they can live independently. Recent technological advances have allowed travel outside the home to be directly measured in patients' real-world routines.
   OBJECTIVE To determine whether decreased visual acuity (VA) from age-related macular degeneration (AMD) and visual field (VF) loss from glaucoma are associated with restricted travel patterns in older adults. DESIGN Cross-sectional study.
   SETTING Patients were recruited from an eye clinic, while travel patterns were recorded during their real-world routines using a cellular tracking device.
   PARTICIPANTS Sixty-one control subjects with normal vision, 84 subjects with glaucoma with bilateral VF loss, and 65 subjects with AMD with bilateral or severe unilateral loss of VA had their location tracked every 15 minutes between 7 AM and 11 PM for 7 days using a tracking device.
   MAIN OUTCOMES AND MEASURES Average daily excursion size (defined as maximum distance away from home) and average daily excursion span (defined as maximum span of travel) were defined for each individual. The effects of vision loss on travel patterns were evaluated after controlling for individual and geographic factors.
   RESULTS In multivariable models comparing subjects with AMD and control subjects, average excursion size and span decreased by approximately one-quarter mile for each line of better-eye VA loss (P < .03 for both). Similar but not statistically significant associations were observed between average daily excursion size and span for severity of better-eye VF loss in subjects with glaucoma and control subjects. Being married or living with someone and younger age were associated with more distant travel, while less-distant travel was noted for older individuals, African Americans, and those living in more densely populated regions.
   CONCLUSIONS AND RELEVANCE Age-related macular degeneration-related loss of VA, but not glaucoma-related loss of VF, is associated with restriction of travel to more nearby locations. This constriction of life space may impact quality of life and restrict access to services.
C1 [Curriero, Frank C.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD USA.
   [Curriero, Frank C.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Biostat, Baltimore, MD USA.
   [Pinchoff, Jessie] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Int Hlth, Baltimore, MD USA.
   [van Landingham, Suzanne W.; Friedman, David S.; Ramulu, Pradeep Y.] Johns Hopkins Sch Med, Wilmer Eye Inst, Baltimore, MD USA.
   [Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Clin Res Branch, NIH, Bethesda, MD 20892 USA.
RP Curriero, FC (reprint author), Dept Environm Hlth Sci, 615 N Wolfe St E6614, Baltimore, MD 21205 USA.
EM fcurrier@jhsph.edu
FU Dennis W. Jahnigen Memorial Award, National Institutes of Health
   [EY018595]; Research to Prevent Blindness Robert and Helen Schaub
   Special Scholar Award; Intramural Research Program of the National
   Institutes of Health
FX This work was supported by the Dennis W. Jahnigen Memorial Award,
   National Institutes of Health grant EY018595, the Research to Prevent
   Blindness Robert and Helen Schaub Special Scholar Award, and the
   Intramural Research Program of the National Institutes of Health
NR 38
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Z9 3
U1 2
U2 7
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6165
EI 2168-6173
J9 JAMA OPHTHALMOL
JI JAMA Ophthalmol.
PD NOV
PY 2013
VL 131
IS 11
BP 1420
EP 1426
DI 10.1001/jamaophthalmol.2013.4471
PG 7
WC Ophthalmology
SC Ophthalmology
GA 291RZ
UT WOS:000329848300007
PM 24030033
ER

PT J
AU Hingson, RW
   White, A
AF Hingson, Ralph W.
   White, Aaron
TI Trends in Extreme Binge Drinking Among US High School Seniors
SO JAMA PEDIATRICS
LA English
DT Editorial Material
ID YOUNG-ADULTS; ALCOHOL; CONSUMPTION; ETHANOL; DEATHS; RISK
C1 [Hingson, Ralph W.; White, Aaron] NIAAA, Div Epidemiol & Prevent Res, Bethesda, MD 20892 USA.
RP Hingson, RW (reprint author), NIAAA, Div Epidemiol & Prevent Res, 5635 Fishers Ln, Bethesda, MD 20892 USA.
EM rhingson@mail.nih.gov
NR 19
TC 8
Z9 8
U1 0
U2 2
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6203
EI 2168-6211
J9 JAMA PEDIATR
JI JAMA Pediatr.
PD NOV
PY 2013
VL 167
IS 11
BP 996
EP 998
DI 10.1001/jamapediatrics.2013.3083
PG 3
WC Pediatrics
SC Pediatrics
GA 291PX
UT WOS:000329842300006
PM 24042186
ER

PT J
AU Oh, W
   Raju, TNK
AF Oh, William
   Raju, Tonse N. K.
TI Not All "Term" Infants Are Created Equal
SO JAMA PEDIATRICS
LA English
DT Editorial Material
ID LATE-PRETERM; NEONATAL OUTCOMES; MORTALITY
C1 [Oh, William] Women & Infants Hosp Rhode Isl, Dept Pediat, Providence, RI 02905 USA.
   [Raju, Tonse N. K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Oh, W (reprint author), Women & Infants Hosp Rhode Isl, Dept Pediat, 101 Dudley St, Providence, RI 02905 USA.
EM woh@wihri.org
NR 11
TC 2
Z9 2
U1 0
U2 2
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6203
EI 2168-6211
J9 JAMA PEDIATR
JI JAMA Pediatr.
PD NOV
PY 2013
VL 167
IS 11
BP 1001
EP 1002
DI 10.1001/jamapediatrics.2013.2593
PG 3
WC Pediatrics
SC Pediatrics
GA 291PX
UT WOS:000329842300009
PM 24080941
ER

PT J
AU Huang, Y
   Hauck, FR
   Signore, C
   Yu, AR
   Raju, TNK
   Huang, TTK
   Fein, SB
AF Huang, Yi
   Hauck, Fern R.
   Signore, Caroline
   Yu, Airong
   Raju, Tonse N. K.
   Huang, Terry T. -K.
   Fein, Sara B.
TI Influence of Bedsharing Activity on Breastfeeding Duration Among US
   Mothers
SO JAMA PEDIATRICS
LA English
DT Article
ID INFANT-DEATH-SYNDROME; UNITED-STATES; SLEEPING ENVIRONMENT;
   RECOMMENDATIONS; EXPANSION; TRENDS; RISK; SIDS
AB IMPORTANCE Some professional associations advocate bedsharing to facilitate breastfeeding, while others recommend against it to reduce the risk of sudden infant death syndrome and suffocation deaths. A better understanding of the quantitative influence of bedsharing on breastfeeding duration is needed to guide policy.
   OBJECTIVE To quantify the influence of bedsharing on breastfeeding duration.
   DESIGN, SETTING, AND PARTICIPANTS Longitudinal data were from the Infant Feeding Practices Study II, which enrolled mothers while pregnant and followed them through the first year of infant life. Questionnaires were sent at infant ages 1 to 7,9,10, and 12 months, and 1846 mothers answered at least 1 question regarding bedsharing and were breastfeeding at infant age 2 weeks.
   EXPOSURES Bedsharing, defined as the mother lying down and sleeping with her infant on the same bed or other sleeping surfaces for nighttime sleep or during the major sleep period.
   MAIN OUTCOMES AND MEASURES Survival analysis to investigate the effect of bedsharing on duration of any and exclusive breastfeeding.
   RESULTS Longer duration of bedsharing, indicated by a larger cumulative bedsharing score, was associated with a longer duration of any breastfeeding but not exclusive breastfeeding, after adjusting for covariates. Breastfeeding duration was longer among women who were better educated, were white, had previously breastfed, had planned to breastfeed, and had not returned to work in the first year postpartum.
   CONCLUSIONS AND RELEVANCE Multiple factors were associated with breastfeeding, including bedsharing. Given the risk of sudden infant death syndrome related to bedsharing, multipronged strategies to promote breastfeeding should be developed and tested.
C1 [Huang, Yi] Univ Maryland Baltimore Cty, Dept Math & Stat, Baltimore, MD 21228 USA.
   [Hauck, Fern R.] Univ Virginia, Sch Med, Dept Family Med, Charlottesville, VA 22908 USA.
   [Hauck, Fern R.] Univ Virginia, Sch Med, Dept Publ Hlth Sci, Charlottesville, VA 22908 USA.
   [Signore, Caroline; Raju, Tonse N. K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pregnancy & Perinatol Branch, NIH, US Dept HHS, Bethesda, MD USA.
   [Yu, Airong] Johns Hopkins Med Inst, Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD 21205 USA.
   [Huang, Terry T. -K.] Univ Nebraska Med Ctr, Coll Publ Hlth, Dept Hlth Promot Social & Behav Hlth, Omaha, NE USA.
   [Fein, Sara B.] US FDA, Ctr Food Safety & Appl Nutr, College Pk, MD USA.
RP Hauck, FR (reprint author), Univ Virginia, Sch Med, Dept Family Med, POB 800729, Charlottesville, VA 22908 USA.
EM frh8e@virginia.edu
FU US Department of Health and Human Services
FX The data collection was supported by several agencies in the US
   Department of Health and Human Services.
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U1 1
U2 13
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6203
EI 2168-6211
J9 JAMA PEDIATR
JI JAMA Pediatr.
PD NOV
PY 2013
VL 167
IS 11
BP 1038
EP 1044
DI 10.1001/jamapediatrics.2013.2632
PG 7
WC Pediatrics
SC Pediatrics
GA 291PX
UT WOS:000329842300016
PM 24061708
ER

PT J
AU King, BH
   Dukes, K
   Donnelly, CL
   Sikich, L
   McCracken, JT
   Scahill, L
   Hollander, E
   Bregman, JD
   Anagnostou, E
   Robinson, F
   Sullivan, L
   Hirtz, D
AF King, Bryan H.
   Dukes, Kimberly
   Donnelly, Craig L.
   Sikich, Linmarie
   McCracken, James T.
   Scahill, Lawrence
   Hollander, Eric
   Bregman, Joel D.
   Anagnostou, Evdokia
   Robinson, Fay
   Sullivan, Lisa
   Hirtz, Deborah
TI Baseline Factors Predicting Placebo Response to Treatment in Children
   and Adolescents With Autism Spectrum Disorders A Multisite Randomized
   Clinical Trial
SO JAMA PEDIATRICS
LA English
DT Article
ID PERVASIVE DEVELOPMENTAL DISORDERS; DOUBLE-BLIND; REPETITIVE BEHAVIOR;
   ABERRANT BEHAVIOR; SECRETIN; RISPERIDONE; IRRITABILITY; METAANALYSIS;
   HYPERACTIVITY; ARIPIPRAZOLE
AB IMPORTANCE The finding of factors that differentially predict the likelihood of response to placebo over that of an active drug could have a significant impact on study design in this population.
   OBJECTIVE To identify possible nonspecific, baseline predictors of response to intervention in a large randomized clinical trial of children and adolescents with autism spectrum disorders.
   DESIGN, SETTING, AND PARTICIPANTS Randomized clinical trial of citalopram hydrobromide for children and adolescents with autism spectrum disorders and prominent repetitive behavior. Baseline data at study entry were examined with respect to final outcome to determine if response predictors could be identified. A total of 149 children and adolescents 5 to 17 years of age (mean [SD] age, 9.4 [3.1] years) from 6 academic centers were randomly assigned to citalopram (n = 73) or placebo (n = 76). Participants had autistic disorder, Asperger syndrome, or pervasive developmental disorder, not otherwise specified; had illness severity ratings that were moderate or more than moderate on the Clinical Global Impression-Severity scale; and scored moderate or more than moderate on compulsive behaviors measured with the modified Children's Yale-Brown Obsessive-Compulsive Scale.
   INTERVENTIONS Twelveweeks of treatment with citalopram (10 mg/5 mL) or placebo. The mean (SD) maximum dose of citalopramwas 16.5 (6.5) mg by mouth daily (maximum dose, 20 mg/d).
   MAIN OUTCOMES AND MEASURES A positive response was defined as having a score of at least much improved on the Clinical Global Impression-Improvement scale at week 12. Baseline measures included demographic (sex, age, weight, and pubertal status), clinical, and family measures. Clinical variables included baseline illness severity ratings (the Aberrant Behavior Checklist, the Child and Adolescent Symptom Inventory, the Vineland Adaptive Behavior Scales, the Repetitive Behavior Scale-Revised, and the Children's Yale-Brown Obsessive-Compulsive Scale). Family measures included the Caregiver Strain Questionnaire.
   RESULTS Several baseline predictors of response were identified, and a principal component analysis yielded 3 composite measures (disruptive behavior, autism/mood, and caregiver strain) that significantly predicted response at week 12. Specifically, participants in the placebo group were significantly less likely than participants in the citalopram group to respond at week 12 if they entered the study more symptomatic on each of the 3 composite measures, and they were at least 2 times less likely to be responders.
   CONCLUSIONS AND RELEVANCE This analysis suggests strategies that may be useful in anticipating and potentially mitigating the nonspecific response in randomized clinical trials of children and adolescents with autism spectrum disorders.
C1 [King, Bryan H.] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
   [King, Bryan H.] Seattle Childrens Hosp, Dept Psychiat & Behav Med, Seattle, WA 98105 USA.
   [Dukes, Kimberly; Robinson, Fay] DM STAT Inc, Malden, MA USA.
   [Donnelly, Craig L.] Dartmouth Hitchcock Med Ctr, Lebanon, NH 03766 USA.
   [Sikich, Linmarie] Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA.
   [McCracken, James T.] Univ Calif Los Angeles, Jane & Terry Semel Inst Neurosci & Human Behav, Los Angeles, CA 90024 USA.
   [Scahill, Lawrence] Emory Univ, Dept Pediat, Atlanta, GA 30322 USA.
   [Hollander, Eric] Yeshiva Univ, Albert Einstein Coll Med, Bronx, NY USA.
   [Bregman, Joel D.] Ctr Autism, Philadelphia, PA USA.
   [Anagnostou, Evdokia] Univ Toronto, Dept Pediat, Toronto, ON M5S 1A1, Canada.
   [Sullivan, Lisa] Boston Univ, Sch Publ Hlth, Boston, MA 02215 USA.
   [Hirtz, Deborah] NINDS, Bethesda, MD 20892 USA.
RP King, BH (reprint author), Seattle Childrens Hosp, Dept Psychiat & Behav Med, 4800 Sand Point Way NE, Seattle, WA 98105 USA.
EM bhking@uw.edu
OI Scahill, Lawrence/0000-0001-5073-1707
FU National Institute of Mental Health; Eunice Kennedy Shriver National
   Institute of Child Health and Human Development; National Institute of
   Neurological Disorders and Stroke; National Institute on Deafness and
   Other Communication Disorders; National Institute of Environmental
   Health Sciences via STAART Center contract Boston University/Dartmouth
   [U54-MH066398]; National Institute of Environmental Health Sciences via
   STAART Center contract DM-STAT, Inc [U01-HD045023]; National Institute
   of Environmental Health Sciences via STAART Center contract Mount Sinai
   [U54-MH066673]; National Institute of Environmental Health Sciences via
   STAART Center contract UCLA [U54-MH068172]; National Institute of
   Environmental Health Sciences via STAART Center contract University of
   North Carolina [U54-MH066418]; National Institute of Environmental
   Health Sciences via STAART Center contract Yale University
   [U54-MH066494]
FX This work was funded by the National Institute of Mental Health, the
   Eunice Kennedy Shriver National Institute of Child Health and Human
   Development, the National Institute of Neurological Disorders and
   Stroke, the National Institute on Deafness and Other Communication
   Disorders, and the National Institute of Environmental Health Sciences
   via the following STAART Center contracts: Boston University/Dartmouth
   (U54-MH066398), Helen Tager-Flusberg, principal investigator (PI);
   DM-STAT, Inc (U01-HD045023), Kimberly Dukes, PI; Mount Sinai
   (U54-MH066673), Eric Hollander, PI; UCLA (U54-MH068172), Marian Sigman,
   PI; University of North Carolina (U54-MH066418), Joseph Piven, PI; and
   Yale University (U54-MH066494), Fred Volkmar, PI.
NR 46
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Z9 13
U1 0
U2 15
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6203
EI 2168-6211
J9 JAMA PEDIATR
JI JAMA Pediatr.
PD NOV
PY 2013
VL 167
IS 11
BP 1045
EP 1052
DI 10.1001/jamapediatrics.2013.2698
PG 8
WC Pediatrics
SC Pediatrics
GA 291PX
UT WOS:000329842300017
PM 24061784
ER

PT J
AU Sandoval, PC
   Slentz, DH
   Pisitkun, T
   Saeed, F
   Hoffert, JD
   Knepper, MA
AF Sandoval, Pablo C.
   Slentz, Dane H.
   Pisitkun, Trairak
   Saeed, Fahad
   Hoffert, Jason D.
   Knepper, Mark A.
TI Proteome-Wide Measurement of Protein Half-Lives and Translation Rates in
   Vasopressin-Sensitive Collecting Duct Cells
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID AMINO-ACID-SEQUENCES; MASS-SPECTROMETRY; GENE-EXPRESSION; WATER CHANNEL;
   AQUAPORIN-2 ABUNDANCE; PLASMA-MEMBRANE; DEGRADATION; KIDNEY;
   QUANTIFICATION; GLYCOSYLATION
AB Vasopressin regulates water excretion, in part, by controlling the abundances of the water channel aquaporin-2 (AQP2) protein and regulatory proteins in the renal collecting duct. To determine whether vasopressin-induced alterations in protein abundance result from modulation of protein production, protein degradation, or both, we used protein mass spectrometry with dynamic stable isotope labeling in cell culture to achieve a proteome-wide determination of protein half-lives and relative translation rates in mpkCCD cells. Measurements were made at steady state in the absence or presence of the vasopressin analog, desmopressin (dDAVP). Desmopressin altered the translation rate rather than the stability of most responding proteins, but it significantly increased both the translation rate and the half-life of AQP2. In addition, proteins associated with vasopressin action, including Mal2, Akap12, gelsolin, myosin light chain kinase, annexin-2, and Hsp70, manifested altered translation rates. Interestingly, desmopressin increased the translation of seven glutathione S-transferase proteins and enhanced protein S-glutathionylation, uncovering a previously unexplored vasopressin-induced post-translational modification. Additional bioinformatic analysis of the mpkCCD proteome indicated a correlation between protein function and protein half-life. In particular, processes that are rapidly regulated, such as transcription, endocytosis, cell cycle regulation, and ubiquitylation are associated with proteins with especially short half-lives. These data extend our understanding of the mechanisms underlying vasopressin signaling and provide a broad resource for additional investigation of collecting duct function (http://helixweb.nih.gov/ESBL/Database/ProteinHalfLives/index.html).
C1 [Sandoval, Pablo C.; Slentz, Dane H.; Pisitkun, Trairak; Saeed, Fahad; Hoffert, Jason D.; Knepper, Mark A.] NHLBI, Epithelial Syst Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Knepper, MA (reprint author), NIH, Bldg 10,Room 6N260,10 Ctr Dr,MSC 1603, Bethesda, MD 20892 USA.
EM knepperm@nhlbi.nih.gov
OI Pisitkun, Trairak/0000-0001-6677-2271
FU Division of Intramural Research, NHLBI [ZO1-HL001285]
FX This work was funded by the operating budget of the Division of
   Intramural Research, NHLBI (Project ZO1-HL001285; to M.A.K.).
NR 40
TC 27
Z9 27
U1 0
U2 1
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 NOV
PY 2013
VL 24
IS 11
BP 1793
EP 1805
DI 10.1681/ASN.2013030279
PG 13
WC Urology & Nephrology
SC Urology & Nephrology
GA 292OJ
UT WOS:000329911300012
PM 24029424
ER

PT J
AU Burghardt, T
   Kastner, J
   Suleiman, H
   Rivera-Milla, E
   Stepanova, N
   Lottaz, C
   Kubitza, M
   Boger, CA
   Schmidt, S
   Gorski, M
   de Vries, U
   Schmidt, H
   Hertting, I
   Kopp, J
   Rascle, A
   Moser, M
   Heid, IM
   Warth, R
   Spang, R
   Wegener, J
   Mierke, CT
   Englert, C
   Witzgall, R
AF Burghardt, Tillmann
   Kastner, Juergen
   Suleiman, Hani
   Rivera-Milla, Eric
   Stepanova, Natalya
   Lottaz, Claudio
   Kubitza, Marion
   Boeger, Carsten A.
   Schmidt, Sarah
   Gorski, Mathias
   de Vries, Uwe
   Schmidt, Helga
   Hertting, Irmgard
   Kopp, Jeffrey
   Rascle, Anne
   Moser, Markus
   Heid, Iris M.
   Warth, Richard
   Spang, Rainer
   Wegener, Joachim
   Mierke, Claudia T.
   Englert, Christoph
   Witzgall, Ralph
TI LMX1B is Essential for the Maintenance of Differentiated Podocytes in
   Adult Kidneys
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID NAIL-PATELLA SYNDROME; FOCAL SEGMENTAL GLOMERULOSCLEROSIS; TRANSCRIPTION
   FACTOR; ACTIN CYTOSKELETON; GENE-EXPRESSION; CRUCIAL ROLE; MUTANT MICE;
   IN-VIVO; PROTEIN; NEPHRIN
AB Mutations of the LMX1B gene cause nail-patella syndrome, a rare autosomal-dominant disorder affecting the development of the limbs, eyes, brain, and kidneys. The characterization of conventional Lmx1b knockout mice has shown that LMX1B regulates the development of podocyte foot processes and slit diaphragms, but studies using podocyte-specific Lmx1b knockout mice have yielded conflicting results regarding the importance of LMX1B for maintaining podocyte structures. In order to address this question, we generated inducible podocyte-specific Lmx1b knockout mice. One week of Lmx1b inactivation in adult mice resulted in proteinuria with only minimal foot process effacement. Notably, expression levels of slit diaphragm and basement membrane proteins remained stable at this time point, and basement membrane charge properties also did not change, suggesting that alternative mechanisms mediate the development of proteinuria in these mice. Cell biological and biophysical experiments with primary podocytes isolated after 1 week of Lmx1b inactivation indicated dysregulation of actin cytoskeleton organization, and time-resolved DNA microarray analysis identified the genes encoding actin cytoskeleton-associated proteins, including Abra and Arl4c, as putative LMX1B targets. Chromatin immunoprecipitation experiments in conditionally immortalized human podocytes and gel shift assays showed that LMX1B recognizes AT-rich binding sites (FLAT elements) in the promoter regions of ABRA and ARL4C, and knockdown experiments in zebrafish support a model in which LMX1B and ABRA act in a common pathway during pronephros development. Our report establishes the importance of LMX1B in fully differentiated podocytes and argues that LMX1B is essential for the maintenance of an appropriately structured actin cytoskeleton in podocytes.
C1 [Burghardt, Tillmann; Kastner, Juergen; Suleiman, Hani; Stepanova, Natalya; Kubitza, Marion; de Vries, Uwe; Schmidt, Helga; Hertting, Irmgard; Rascle, Anne; Witzgall, Ralph] Univ Regensburg, Inst Mol & Cellular Anat, D-93053 Regensburg, Germany.
   [Lottaz, Claudio; Spang, Rainer] Univ Regensburg, Inst Funct Genom, D-93053 Regensburg, Germany.
   [Warth, Richard] Univ Regensburg, Inst Med Cell Biol, D-93053 Regensburg, Germany.
   [Wegener, Joachim] Univ Regensburg, Inst Analyt Chem, D-93053 Regensburg, Germany.
   [Rivera-Milla, Eric; Englert, Christoph] Fritz Lipmann Inst, Leibniz Inst Age Res, Jena, Germany.
   [Boeger, Carsten A.] Univ Regensburg, Univ Hosp Regensburg, Dept Internal Med 2, D-93053 Regensburg, Germany.
   [Gorski, Mathias; Heid, Iris M.] Univ Regensburg, Univ Hosp Regensburg, Dept Epidemiol & Prevent Med, D-93053 Regensburg, Germany.
   [Schmidt, Sarah; Moser, Markus] Max Planck Inst Biochem, Dept Mol Med, D-82152 Martinsried, Germany.
   [Kopp, Jeffrey] NIDDK, Kidney Dis Sect, NIH, Bethesda, MD 20892 USA.
   [Heid, Iris M.] Helmholtz Zentrum Munchen, Inst Epidemiol, Neuherberg, Germany.
   [Mierke, Claudia T.] Univ Leipzig, Inst Expt Phys 1, D-04109 Leipzig, Germany.
RP Witzgall, R (reprint author), Univ Regensburg, Inst Mol & Cellular Anat, Univ Str 31, D-93053 Regensburg, Germany.
EM ralph.witzgall@vkl.uni-regensburg.de
RI Wegener, Joachim/A-1234-2011; Warth, Richard/N-7119-2014; 
OI Warth, Richard/0000-0001-6084-0659; Witzgall, Ralph/0000-0002-5283-4846;
   Kopp, Jeffrey/0000-0001-9052-186X
FU German Research Council [SFB 699]
FX Financial support from German Research Council Grant SFB 699 is
   gratefully acknowledged.
NR 81
TC 17
Z9 17
U1 0
U2 7
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 NOV
PY 2013
VL 24
IS 11
BP 1830
EP 1848
DI 10.1681/ASN.2012080788
PG 19
WC Urology & Nephrology
SC Urology & Nephrology
GA 292OJ
UT WOS:000329911300015
PM 23990680
ER

PT J
AU O'Seaghdha, CM
   Hwang, SJ
   Larson, MG
   Meigs, JB
   Vasan, RS
   Fox, CS
AF O'Seaghdha, Conall M.
   Hwang, Shih-Jen
   Larson, Martin G.
   Meigs, James B.
   Vasan, Ramachandran S.
   Fox, Caroline S.
TI Analysis of a Urinary Biomarker Panel for Incident Kidney Disease and
   Clinical Outcomes
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID GENERAL-POPULATION; HEART-FAILURE; NONCARDIOVASCULAR MORTALITY;
   NONVASCULAR MORTALITY; MULTIPLE BIOMARKERS; CARDIOVASCULAR RISK; INJURY
   MOLECULE-1; EPITHELIAL-CELLS; EXPRESSION; PREDICTION
AB Whether novel biomarkers improve the assessment of incident kidney disease and related adverse outcomes remains to be tested in longitudinal observational studies. We tested 14 urinary biomarkers for association with incident kidney, cardiovascular, and mortality outcomes in 2948 Framingham Heart Study participants. Baseline examinations were performed between 1995 and 1998; mean follow-up was 10.1 years for renal outcomes and 11.2 years for survival analyses. Primary outcomes were incident CKD, incident albuminuria, incident cardiovascular disease, and all-cause mortality. Secondary analyses assessed incident congestive heart failure (CHF) and mortality with coexistent kidney disease. Biomarkers were tested for association with renal end points using logistic regression and incident cardiovascular and mortality outcomes in proportional hazards models; 1-microglobulin, Kim-1, and TFF-3 predicted all-cause mortality (hazard ratio per SD increase in log-transformed biomarker [HR] range, 1.15 to 1.21; 95% confidence interval [CI] range, 1.04 to 1.34; P values=0.007 to <0.001), whereas 1-microglobulin, 2-microglobulin, KIM-1, and TFF-3 associated with death with coexistent kidney disease (HR range, 1.72-2.25; 95% CI, 1.17 to 3.24; P values<0.01). KIM-1 also associated with the risk of incident CHF (HR, 1.32; 95% CI, 1.07 to 1.63; P=0.008). CTGF associated nominally with CKD (HR, 0.83; 95% CI, 0.71 to 0.98; P=0.03), but no other biomarkers associated with incident CKD or albuminuria. Addition of 1-microglobulin and TFF-3 resulted in a nonsignificant net reclassification index (NRI) of 3% for all-cause mortality beyond clinical risk factors. In conclusion, components of a panel of 14 subclinical biomarkers of kidney injury were associated with important clinical outcomes and merit additional investigation.
C1 [O'Seaghdha, Conall M.; Hwang, Shih-Jen; Larson, Martin G.; Vasan, Ramachandran S.; Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA 01702 USA.
   [O'Seaghdha, Conall M.; Hwang, Shih-Jen; Fox, Caroline S.] Ctr Populat Studies, Framingham, MA USA.
   [O'Seaghdha, Conall M.] Massachusetts Gen Hosp, Div Renal, Boston, MA 02114 USA.
   [Meigs, James B.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
   [Fox, Caroline S.] Harvard Univ, Sch Med, Boston, MA USA.
   [O'Seaghdha, Conall M.] Beaumont Hosp, Div Renal, Dublin 9, Ireland.
   [Vasan, Ramachandran S.] Boston Univ, Sch Med, Prevent Med & Epidemiol Sect, Boston, MA 02118 USA.
   [Fox, Caroline S.] Brigham & Womens Hosp, Div Endocrinol, Boston, MA 02115 USA.
RP Fox, CS (reprint author), NHLBI, Framingham Heart Study, 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA.
EM foxca@nhlbi.nih.gov
OI Ramachandran, Vasan/0000-0001-7357-5970
FU National Heart, Lung, and Blood Institute [N01-HC-25195]
FX The Framingham Heart Study is supported by National Heart, Lung, and
   Blood Institute Grant N01-HC-25195.
NR 46
TC 21
Z9 22
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 NOV
PY 2013
VL 24
IS 11
BP 1880
EP 1888
DI 10.1681/ASN.2013010019
PG 9
WC Urology & Nephrology
SC Urology & Nephrology
GA 292OJ
UT WOS:000329911300019
PM 23990678
ER

PT J
AU Sharma, K
   Karl, B
   Mathew, AV
   Gangoiti, JA
   Wassel, CL
   Saito, R
   Pu, MY
   Sharma, S
   You, YH
   Wang, L
   Diamond-Stanic, M
   Lindenmeyer, MT
   Forsblom, C
   Wu, W
   Ix, JH
   Ideker, T
   Kopp, JB
   Nigam, SK
   Cohen, CD
   Groop, PH
   Barshop, BA
   Natarajan, L
   Nyhan, WL
   Naviaux, RK
AF Sharma, Kumar
   Karl, Bethany
   Mathew, Anna V.
   Gangoiti, Jon A.
   Wassel, Christina L.
   Saito, Rintaro
   Pu, Minya
   Sharma, Shoba
   You, Young-Hyun
   Wang, Lin
   Diamond-Stanic, Maggie
   Lindenmeyer, Maja T.
   Forsblom, Carol
   Wu, Wei
   Ix, Joachim H.
   Ideker, Trey
   Kopp, Jeffrey B.
   Nigam, Sanjay K.
   Cohen, Clemens D.
   Groop, Per-Henrik
   Barshop, Bruce A.
   Natarajan, Loki
   Nyhan, William L.
   Naviaux, Robert K.
TI Metabolomics Reveals Signature of Mitochondrial Dysfunction in Diabetic
   Kidney Disease
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID ORGANIC ANION; NEPHROPATHY; GENES; TRANSPORTERS; BIOMARKERS; DISCOVERY;
   URINE; RISK; DRUG; OAT1
AB Diabetic kidney disease is the leading cause of ESRD, but few biomarkers of diabetic kidney disease are available. This study used gas chromatography-mass spectrometry to quantify 94 urine metabolites in screening and validation cohorts of patients with diabetes mellitus (DM) and CKD(DM+CKD), in patients with DM without CKD (DM-CKD), and in healthy controls. Compared with levels in healthy controls, 13 metabolites were significantly reduced in the DM+CKD cohorts (P0.001), and 12 of the 13 remained significant when compared with the DM-CKD cohort. Many of the differentially expressed metabolites were water-soluble organic anions. Notably, organic anion transporter-1 (OAT1) knockout mice expressed a similar pattern of reduced levels of urinary organic acids, and human kidney tissue from patients with diabetic nephropathy demonstrated lower gene expression of OAT1 and OAT3. Analysis of bioinformatics data indicated that 12 of the 13 differentially expressed metabolites are linked to mitochondrial metabolism and suggested global suppression of mitochondrial activity in diabetic kidney disease. Supporting this analysis, human diabetic kidney sections expressed less mitochondrial protein, urine exosomes from patients with diabetes and CKD had less mitochondrial DNA, and kidney tissues from patients with diabetic kidney disease had lower gene expression of PGC1 (a master regulator of mitochondrial biogenesis). We conclude that urine metabolomics is a reliable source for biomarkers of diabetic complications, and our data suggest that renal organic ion transport and mitochondrial function are dysregulated in diabetic kidney disease.
C1 [Sharma, Kumar; Karl, Bethany; Saito, Rintaro; You, Young-Hyun; Diamond-Stanic, Maggie; Barshop, Bruce A.; Natarajan, Loki; Nyhan, William L.; Naviaux, Robert K.] Univ Calif San Diego, Inst Metabol Med, San Diego, CA 92103 USA.
   [Sharma, Kumar; Karl, Bethany; Mathew, Anna V.; Saito, Rintaro; Sharma, Shoba; You, Young-Hyun; Diamond-Stanic, Maggie; Ix, Joachim H.] Univ Calif San Diego, Ctr Renal Translat Med, Div Nephrol Hypertens, San Diego, CA 92103 USA.
   [Sharma, Kumar; Saito, Rintaro; Ideker, Trey; Naviaux, Robert K.] Univ Calif San Diego, Dept Med, Div Med Genet, San Diego, CA 92103 USA.
   [Wassel, Christina L.; Pu, Minya; Natarajan, Loki] Univ Calif San Diego, Dept Family & Prevent Med, San Diego, CA 92103 USA.
   [Wu, Wei; Nigam, Sanjay K.] Univ Calif San Diego, Dept Pediat, San Diego, CA 92103 USA.
   [Wu, Wei; Nigam, Sanjay K.] Univ Calif San Diego, Dept Med, San Diego, CA 92103 USA.
   [Wu, Wei; Nigam, Sanjay K.] Univ Calif San Diego, Dept Cell & Mol Med, San Diego, CA 92103 USA.
   [Sharma, Kumar; Karl, Bethany; Mathew, Anna V.; Diamond-Stanic, Maggie; Ix, Joachim H.] Vet Affairs San Diego Healthcare Syst, Div Nephrol Hypertens, San Diego, CA USA.
   [Gangoiti, Jon A.; Barshop, Bruce A.; Nyhan, William L.; Naviaux, Robert K.] Univ Calif San Diego, Dept Pediat, Div Genet, Biochem Genet Program, La Jolla, CA 92093 USA.
   [Wang, Lin; Naviaux, Robert K.] Univ Calif San Diego, Mitochondrial & Metab Dis Ctr, Dept Med, La Jolla, CA 92093 USA.
   [Wang, Lin; Naviaux, Robert K.] Univ Calif San Diego, Mitochondrial & Metab Dis Ctr, Dept Pediat, La Jolla, CA 92093 USA.
   [Wang, Lin; Naviaux, Robert K.] Univ Calif San Diego, Mitochondrial & Metab Dis Ctr, Dept Pathol, La Jolla, CA 92093 USA.
   [Lindenmeyer, Maja T.; Cohen, Clemens D.] Univ Zurich Hosp, Div Nephrol, Zurich, Switzerland.
   [Forsblom, Carol; Groop, Per-Henrik] Univ Helsinki, Cent Hosp, Folkhalsan Res Ctr, Folkhalsan Inst Genet, Helsinki, Finland.
   [Forsblom, Carol; Groop, Per-Henrik] Univ Helsinki, Cent Hosp, Dept Med, Div Nephrol, Helsinki, Finland.
   [Kopp, Jeffrey B.] NIDDK, Kidney Dis Sect, NIH, Bethesda, MD 20892 USA.
   [Groop, Per-Henrik] IDI Baker Heart & Diabet Inst, Melbourne, Vic, Australia.
RP Sharma, K (reprint author), Univ Calif San Diego, Inst Metabol Med, Ctr Renal Translat Med, Div Nephrol Hypertens, 405 Stein Clin Res Bldg,MC 0711, La Jolla, CA 92093 USA.
EM kumarsharma@ucsd.edu
OI Mathew, Anna/0000-0002-7043-4221; Kopp, Jeffrey/0000-0001-9052-186X
FU Juvenile Diabetes Research Foundation (VAMerit Award) [5101BX000277];
   National Institute of Diabetes and Digestive and Kidney Diseases
   [1DP3DK094352]; National Institutes of Health [T32]; Folkhalsan Research
   Foundation; Wilhelm and Else Stockmann Foundation; Liv och Halsa
   Foundation; Folkhausen Research Foundation; UCSD Christini Fund; Wright
   Family Foundation; Lennox Foundation; Else Kroner-Fresenius Foundation
   [A62/04]; NCCR Kidney; National Resource for Network Biology
   [P41GM103504]; San Diego Center for Systems Biology [P50 GM085764]
FX K.S. was supported by grants from the Juvenile Diabetes Research
   Foundation (VAMerit Award 5101BX000277) and National Institute of
   Diabetes and Digestive and Kidney Diseases (1DP3DK094352). B. K. and A.
   V. M. were supported by a National Institutes of Health T32 Training
   Grant. The Finnish Diabetic Nephropathy Study was supported by grants
   from the Folkhalsan Research Foundation, the Wilhelm and Else Stockmann
   Foundation, and the Liv och Halsa Foundation. P. G. and C. F. were
   supported by the Folkhausen Research Foundation. R.K.N. and L. W. were
   supported in part by the UCSD Christini Fund, the Wright Family
   Foundation, and the Lennox Foundation. C. D. C. was supported by grants
   from the Else Kroner-Fresenius Foundation (A62/04) and the NCCR Kidney.
   T. I. was funded by the National Resource for Network Biology
   (P41GM103504) and the San Diego Center for Systems Biology (P50
   GM085764).
NR 29
TC 87
Z9 89
U1 5
U2 32
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 NOV
PY 2013
VL 24
IS 11
BP 1901
EP 1912
DI 10.1681/ASN.2013020126
PG 12
WC Urology & Nephrology
SC Urology & Nephrology
GA 292OJ
UT WOS:000329911300021
PM 23949796
ER

PT J
AU Lemieux, JE
   Kyes, SA
   Otto, TD
   Feller, AI
   Eastman, RT
   Pinches, RA
   Berriman, M
   Su, XZ
   Newbold, CI
AF Lemieux, Jacob E.
   Kyes, Sue A.
   Otto, Thomas D.
   Feller, Avi I.
   Eastman, Richard T.
   Pinches, Robert A.
   Berriman, Matthew
   Su, Xin-Zhuan
   Newbold, Chris I.
TI Genome-wide profiling of chromosome interactions in Plasmodium
   falciparum characterizes nuclear architecture and reconfigurations
   associated with antigenic variation
SO MOLECULAR MICROBIOLOGY
LA English
DT Article
ID MUTUALLY EXCLUSIVE EXPRESSION; MALARIA PARASITES; VAR GENES; VIRULENCE
   GENES; CHROMATIN-STRUCTURE; RECEPTOR GENES; RIBOSOMAL DNA;
   TRANSCRIPTION; REVEALS; MOUSE
AB Spatial relationships within the eukaryotic nucleus are essential for proper nuclear function. In Plasmodium falciparum, the repositioning of chromosomes has been implicated in the regulation of the expression of genes responsible for antigenic variation, and the formation of a single, peri-nuclear nucleolus results in the clustering of rDNA. Nevertheless, the precise spatial relationships between chromosomes remain poorly understood, because, until recently, techniques with sufficient resolution have been lacking. Here we have used chromosome conformation capture and second-generation sequencing to study changes in chromosome folding and spatial positioning that occur during switches in var gene expression. We have generated maps of chromosomal spatial affinities within the P.falciparum nucleus at 25Kb resolution, revealing a structured nucleolus, an absence of chromosome territories, and confirming previously identified clustering of heterochromatin foci. We show that switches in var gene expression do not appear to involve interaction with a distant enhancer, but do result in local changes at the active locus. These maps reveal the folding properties of malaria chromosomes, validate known physical associations, and characterize the global landscape of spatial interactions. Collectively, our data provide critical information for a better understanding of gene expression regulation and antigenic variation in malaria parasites.
C1 [Lemieux, Jacob E.; Kyes, Sue A.; Pinches, Robert A.; Newbold, Chris I.] Weatherall Inst Mol Med, Oxford OX3 9DS, England.
   [Lemieux, Jacob E.; Eastman, Richard T.; Su, Xin-Zhuan] NIAID, NIH, Bethesda, MD 20892 USA.
   [Otto, Thomas D.; Berriman, Matthew; Newbold, Chris I.] Wellcome Trust Sanger Inst, Cambridge CB10 1SA, England.
   [Feller, Avi I.] Harvard Univ, Dept Stat, Cambridge, MA 02138 USA.
RP Newbold, CI (reprint author), Weatherall Inst Mol Med, Oxford OX3 9DS, England.
EM xsu@niaid.nih.gov; chris.newbold@imm.ox.ac.uk
OI Newbold, Chris/0000-0002-9274-3789; Otto, Thomas/0000-0002-1246-7404;
   Su, Xinzhuan/0000-0003-3246-3248
FU European Union; Wellcome Trust [098051, 082130/Z/07/Z]; Rhodes Trust;
   Division of Intramural Research, NIAID, NIH
FX We would like to thank Mike Quail for library preparation, Mandy Sanders
   for help with sample preparation, Professor Kirk Deitsch for generously
   sharing the strains DCJ and B15C2 and Dr Thomas Wellems for helpful
   advice throughout the project. T.D.O. was supported by the European
   Union 7th framework EVIMalaR and M. B. by the Wellcome Trust (Grant
   number: 098051). We would like to acknowledge the support of the
   Wellcome Trust (C.I.N., S. A. K. and R. A. P.; Programme Grant No.:
   082130/Z/07/Z), the Rhodes Trust (J.E.L.) and the Division of Intramural
   Research, NIAID, NIH (X.S.) for financing this work.
NR 81
TC 16
Z9 16
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0950-382X
EI 1365-2958
J9 MOL MICROBIOL
JI Mol. Microbiol.
PD NOV
PY 2013
VL 90
IS 3
BP 519
EP 537
DI 10.1111/mmi.12381
PG 19
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA 295HO
UT WOS:000330107400005
PM 23980881
ER

PT J
AU Anderson, AL
   Thomason, ME
AF Anderson, Amy L.
   Thomason, Moriah E.
TI Functional plasticity before the cradle: A review of neural functional
   imaging in the human fetus
SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
LA English
DT Review
DE Default mode network; Fetal; Fetus; fMRI; Functional connectivity; MEG;
   Plasticity; Resting state
ID AUDITORY-EVOKED RESPONSES; FETAL-BRAIN ACTIVITY; RESTING-STATE NETWORKS;
   PRIMARY VISUAL-CORTEX; INFANT BRAIN; IN-UTERO; SPATIOTEMPORAL ATLAS;
   COCHLEAR IMPLANTS; BEHAVIORAL STATES; CORTICAL NETWORKS
AB The organization of the brain is highly plastic in fetal life. Establishment of healthy neural functional systems during the fetal period is essential to normal growth and development. Across the last several decades, remarkable progress has been made in understanding the development of human fetal functional brain systems. This is largely due to advances in imaging methodologies. Fetal neuroimaging began in the 1950-1970's with fetal electroencephalography (EEG) applied during labor. Later, in the 1980's, magnetoencephalography (MEG) emerged as an effective approach for investigating fetal brain function. Most recently, functional magnetic resonance imaging (fMRI) has arisen as an additional powerful approach for examining fetal brain function. This review will discuss major developmental findings from fetal imaging studies such as the maturation of prenatal sensory system functions, functional hemispheric asymmetry, and sensory-driven neurodevelopment. We describe how with improved imaging and analysis techniques, functional imaging of the fetus has the potential to assess the earliest point of neural maturation and provide insight into the patterning and sequence of normal and abnormal brain development. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Anderson, Amy L.; Thomason, Moriah E.] Wayne State Univ, Merrill Palmer Skillman Inst Child & Family Dev, Detroit, MI 48202 USA.
   [Anderson, Amy L.; Thomason, Moriah E.] NICHD NIH DHHS, Perinatol Res Branch, Detroit, MI USA.
   [Thomason, Moriah E.] Wayne State Univ, Sch Med, Dept Pediat, Detroit, MI 48202 USA.
RP Thomason, ME (reprint author), Wayne State Univ, Sch Med, Merrill Palmer Skillman Inst, 71 E Ferry St, Detroit, MI 48202 USA.
EM moriah@wayne.edu
FU Merrill Palmer Skillman Institute for Child and Family Development;
   Department of Pediatrics; Wayne State University (WSU) School of
   Medicine; WSU Perinatal Initiative; WSU's Perinatology Virtual Discovery
   Grant; W. K. Kellogg Foundation [P3018205]; Perinatology Research
   Branch, Division of Intramural Research, Eunice Kennedy Shriver NICHD,
   NIH, DHHS; Wayne State University Research Grant Program
FX This research was supported, in part, by the Merrill Palmer Skillman
   Institute for Child and Family Development; the Department of
   Pediatrics; Wayne State University (WSU) School of Medicine; the WSU
   Perinatal Initiative; WSU's Perinatology Virtual Discovery Grant (made
   possible by W. K. Kellogg Foundation award P3018205); and by the
   Perinatology Research Branch, Division of Intramural Research, Eunice
   Kennedy Shriver NICHD, NIH, DHHS. This project was also supported by an
   award from the Wayne State University Research Grant Program to MET. The
   content is solely the responsibility of the authors and does not
   necessarily represent the official views of the National Institute of
   Mental Health or the National Institutes of Health. The authors thank
   Cheryl Deep and Catherine Blasio at the Institute of Gerontology, Wayne
   State University for their assistance in obtaining images of our fetal
   MRI studies at Wayne State University. The authors acknowledge the
   critical analysis provided by the Reviewers and thank them for their
   contribution to the work.
NR 120
TC 14
Z9 15
U1 4
U2 26
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0149-7634
EI 1873-7528
J9 NEUROSCI BIOBEHAV R
JI Neurosci. Biobehav. Rev.
PD NOV
PY 2013
VL 37
IS 9
BP 2220
EP 2232
DI 10.1016/j.neubiorev.2013.03.013
PN B
PG 13
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 292EC
UT WOS:000329884000013
PM 23542738
ER

PT J
AU Igarashi, M
   Chang, LS
   Ma, KZ
   Rapoport, SI
AF Igarashi, Miki
   Chang, Lisa
   Ma, Kaizong
   Rapoport, Stanley I.
TI Kinetics of eicosapentaenoic acid in brain, heart and liver of conscious
   rats fed a high n-3 PUFA containing diet
SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS
LA English
DT Article
DE Eicosapentaenoic acid; Turnover; Kinetics; Metabolism; Brain; Rat
   docosahexaenoic
ID POLYUNSATURATED FATTY-ACIDS; ALPHA-LINOLENIC ACID; TRIACYLGLYCEROL-RICH
   LIPOPROTEINS; DOCOSAHEXAENOIC ACID; ARACHIDONIC-ACID; ADULT RATS;
   IN-VIVO; PHOSPHOLIPIDS; METABOLISM; DEPRIVATION
AB Eicosapentaenoic acid (EPA, 20:5n-3), a precursor of docosahexaenoic acid (DHA), may benefit cardiovascular and brain health. Quantifying EPA's in vivo kinetics might elucidate these effects. [1-C-14] EPA was infused i.v. for 5 min in unanesthetized male rats fed a standard EPA-DHA diet. Plasma and microwaved tissue were analyzed. Kinetic parameters were calculated using our compartmental model. At 5 min, 31-48% of labeled EPA in brain and heart was oxidized, 7% in liver. EPA incorporation rates from brain and liver precursor EPA-CoA pools into lipids, mainly phospholipids, were 36 and 2529 nmol/s/g x 10(-4), insignificant for heart. Deacylation-reacylation half-lives were 22 h and 38-128 min. Conversion rates to DHA equaled 0.65 and 25.1 nmol/s/g x 10(-4), respectively. The low brain concentration and incorporation rate and high oxidation of EPA suggest that, if EPA has a beneficial effect in brain, it might result from its suppression of peripheral inflammation and hepatic conversion to bioactive DHA. (C) 2013 Published by Elsevier Ltd.
C1 [Igarashi, Miki; Chang, Lisa; Ma, Kaizong; Rapoport, Stanley I.] NIA, Brain Physiol & Metab Sect, NIH, Bethesda, MD 20892 USA.
RP Igarashi, M (reprint author), Univ Calif Irvine, Dept Anat & Neurobiol, 3216 Gillespie Neurosci Res Facil, Irvine, CA 92697 USA.
EM miki.i@uci.edu
FU National Institute on Aging
FX This research was supported entirely by the Intramural Research Program
   of the National Institute on Aging. The authors declare no conflict of
   interest.
NR 67
TC 7
Z9 7
U1 0
U2 9
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0952-3278
EI 1532-2823
J9 PROSTAG LEUKOTR ESS
JI Prostaglandins Leukot. Essent. Fatty Acids
PD NOV-DEC
PY 2013
VL 89
IS 6
BP 403
EP 412
DI 10.1016/j.plefa.2013.09.004
PG 10
WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology &
   Metabolism
SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology &
   Metabolism
GA 294AA
UT WOS:000330013600003
PM 24209500
ER

PT J
AU Greten, TF
   Malek, NP
   Schmidt, S
   Arends, J
   Bartenstein, P
   Bechstein, W
   Bernatik, T
   Bitzer, M
   Chavan, A
   Dollinger, M
   Domagk, D
   Drognitz, O
   Dux, M
   Farkas, S
   Folprecht, G
   Galle, P
   Geissler, M
   Gerken, G
   Habermehl, D
   Helmberger, T
   Herfarth, K
   Hoffmann, RT
   Holtmann, M
   Huppert, P
   Jakobs, T
   Keller, M
   Klempnauer, J
   Kolligs, F
   Korber, J
   Lang, H
   Lehner, F
   Lordick, F
   Lubienski, A
   Manns, MP
   Mahnken, A
   Mohler, M
   Monch, C
   Neuhaus, P
   Niederau, C
   Ocker, M
   Otto, G
   Pereira, P
   Pott, G
   Riemer, J
   Ringe, K
   Ritterbusch, U
   Rummeny, E
   Schirmacher, P
   Schlitt, HJ
   Schlottmann, K
   Schmitz, V
   Schuler, A
   Schulze-Bergkamen, H
   von Schweinitz, D
   Seehofer, D
   Sitter, H
   Strassburg, CP
   Stroszczynski, C
   Strobel, D
   Tannapfel, A
   Trojan, J
   van Thiel, I
   Vogel, A
   Wacker, F
   Wedemeyer, H
   Wege, H
   Weinmann, A
   Wittekind, C
   Wormann, B
   Zech, CJ
AF Greten, T. F.
   Malek, N. P.
   Schmidt, S.
   Arends, J.
   Bartenstein, P.
   Bechstein, W.
   Bernatik, T.
   Bitzer, M.
   Chavan, A.
   Dollinger, M.
   Domagk, D.
   Drognitz, O.
   Duex, M.
   Farkas, S.
   Folprecht, G.
   Galle, P.
   Geissler, M.
   Gerken, G.
   Habermehl, D.
   Helmberger, T.
   Herfarth, K.
   Hoffmann, R. T.
   Holtmann, M.
   Huppert, P.
   Jakobs, T.
   Keller, M.
   Klempnauer, J.
   Kolligs, F.
   Koerber, J.
   Lang, H.
   Lehner, F.
   Lordick, F.
   Lubienski, A.
   Manns, M. P.
   Mahnken, A.
   Moehler, M.
   Moench, C.
   Neuhaus, P.
   Niederau, C.
   Ocker, M.
   Otto, G.
   Pereira, P.
   Pott, G.
   Riemer, J.
   Ringe, K.
   Ritterbusch, U.
   Rummeny, E.
   Schirmacher, P.
   Schlitt, H. J.
   Schlottmann, K.
   Schmitz, V.
   Schuler, A.
   Schulze-Bergkamen, H.
   von Schweinitz, D.
   Seehofer, D.
   Sitter, H.
   Strassburg, C. P.
   Stroszczynski, C.
   Strobel, D.
   Tannapfel, A.
   Trojan, J.
   van Thiel, I.
   Vogel, A.
   Wacker, F.
   Wedemeyer, H.
   Wege, H.
   Weinmann, A.
   Wittekind, C.
   Woermann, B.
   Zech, C. J.
TI Diagnosis of and Therapy for Hepatocellular Carcinoma
SO ZEITSCHRIFT FUR GASTROENTEROLOGIE
LA German
DT Article
DE viral hepatitis; hepatitis B; hepatitis C
ID RANDOMIZED CONTROLLED-TRIAL; QUALITY-OF-LIFE; HEPATITIS-B-VIRUS; CHRONIC
   LIVER-DISEASE; PERCUTANEOUS ETHANOL INJECTION;
   CONTRAST-ENHANCED-ULTRASOUND; PHASE-II TRIAL; TRANSCATHETER ARTERIAL
   CHEMOEMBOLIZATION; SIROLIMUS-BASED IMMUNOSUPPRESSION; RADIOFREQUENCY
   THERMAL ABLATION
AB The interdisciplinary guidelines at the S3 level on the diagnosis of and therapy for hepatocellular carcinoma (HCC) constitute an evidence- and consensus-based instrument that is aimed at improving the diagnosis of and therapy for HCC since these are very challenging tasks. The purpose of the guidelines is to offer the patient (with suspected or confirmed HCC) adequate, scientifically based and up-to-date procedures in diagnosis, therapy and rehabilitation. This holds not only for locally limited or focally advanced disease but also for the existence of recurrences or distant metastases. Besides making a contribution to an appropriate health-care service, the guidelines should also provide the foundation for an individually adapted, high-quality therapy. The explanatory background texts should also enable non-specialist but responsible colleagues to give sound advice to their patients concerning specialist procedures, side effects and results. In the medium and long-term this should reduce the morbidity and mortality of patients with HCC and improve their quality of life.
RP Greten, TF (reprint author), NCI, Bldg 10 Rm 12N266,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM gretentf@mail.nih.gov
RI Folprecht, Gunnar/F-8638-2011; Vogel, Arndt/A-8437-2012; Greten,
   Tim/B-3127-2015
OI Folprecht, Gunnar/0000-0002-9321-9911; Greten, Tim/0000-0002-0806-2535
NR 573
TC 31
Z9 32
U1 3
U2 15
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0044-2771
EI 1439-7803
J9 Z GASTROENTEROL
JI Z. Gastroent.
PD NOV
PY 2013
VL 51
IS 11
BP 1269
EP 1326
DI 10.1055/s-0033-1355841
PG 58
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 292XL
UT WOS:000329935900020
PM 24243572
ER

PT J
AU Hricik, D
   Nickerson, P
   Formica, R
   Poggio, E
   Rush, D
   Newell, K
   Goebel, J
   Gibson, I
   Fairchild, R
   Riggs, M
   Ikle, D
   Bridges, N
   Heeger, P
AF Hricik, Donald
   Nickerson, Peter
   Formica, Richard
   Poggio, Emilio
   Rush, David
   Newell, Kenneth
   Goebel, Jens
   Gibson, Ian
   Fairchild, Robert
   Riggs, Michael
   Ikle, David
   Bridges, Nancy
   Heeger, Peter
TI MULTICENTER VALIDATION OF URINARY CXCL9 AS A RISK-STRATIFYING BIOMARKER
   FOR ONGOING AND INCIPIENT KIDNEY TRANSPLANT INJURY
SO TRANSPLANT INTERNATIONAL
LA English
DT Meeting Abstract
C1 [Hricik, Donald] Univ Hosp Case Med Ctr, Cleveland, OH USA.
   [Nickerson, Peter; Rush, David; Gibson, Ian] Univ Manitoba, Winnipeg, MB R3T 2N2, Canada.
   [Formica, Richard] Yale Univ, New Haven, CT 06520 USA.
   [Poggio, Emilio; Fairchild, Robert] Cleveland Clin, Cleveland, OH USA.
   [Newell, Kenneth] Emory Univ, Atlanta, GA 30322 USA.
   [Goebel, Jens] Cincinnati Childrens Hosp, Cincinnati, OH USA.
   [Bridges, Nancy] NIH, Bethesda, MD USA.
   [Heeger, Peter] Mt Sinai Sch Med, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0934-0874
EI 1432-2277
J9 TRANSPL INT
JI Transpl. Int.
PD NOV
PY 2013
VL 26
SU 2
SI SI
BP 63
EP 63
PG 1
WC Surgery; Transplantation
SC Surgery; Transplantation
GA 269HJ
UT WOS:000328232000232
ER

PT J
AU Ezzat, R
   Okasha, H
   Moustafa, H
   Ashry, M
   Naguib, M
   Elgemeie, E
AF Ezzat, Reem
   Okasha, Hussein
   Moustafa, Hala
   Ashry, Mahmoud
   Naguib, Mohamed
   Elgemeie, Emad
TI ROLE OF ABDOMINAL ULTRASOUND, ENDOSCOPIC ULTRASOUND (EUS) AND FINE
   NEEDLE ASPIRATION (FNA) IN DIAGNOSIS OF CYSTIC PANCREATIC LESIONS
SO TRANSPLANT INTERNATIONAL
LA English
DT Meeting Abstract
C1 [Ezzat, Reem; Moustafa, Hala; Ashry, Mahmoud] Assuit Univ Hosp, Assiut, Egypt.
   [Okasha, Hussein; Naguib, Mohamed] Cairo Univ Hosp, Giza, Egypt.
   [Elgemeie, Emad] Natl Canc Inst, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0934-0874
EI 1432-2277
J9 TRANSPL INT
JI Transpl. Int.
PD NOV
PY 2013
VL 26
SU 2
SI SI
BP 326
EP 326
PG 1
WC Surgery; Transplantation
SC Surgery; Transplantation
GA 269HJ
UT WOS:000328232002326
ER

PT J
AU Pratt, CA
   Boyington, J
   Esposito, L
   Pemberton, VL
   Bonds, D
   Kelley, M
   Yang, S
   Murray, D
   Stevens, J
AF Pratt, Charlotte A.
   Boyington, Josephine
   Esposito, Layla
   Pemberton, Victoria L.
   Bonds, Denise
   Kelley, Melinda
   Yang, Song
   Murray, David
   Stevens, June
TI Childhood Obesity Prevention and Treatment Research (COPTR):
   Interventions addressing multiple influences in childhood and adolescent
   obesity
SO CONTEMPORARY CLINICAL TRIALS
LA English
DT Article
DE Childhood obesity; Prevention; Treatment; Multi-site trial; Research
   consortium
ID RANDOMIZED CONTROLLED-TRIAL; PHYSICAL-ACTIVITY; YOUNG ADULTHOOD; US
   CHILDREN; OVERWEIGHT; PREVALENCE; COMMUNITY; TRENDS; FAMILY; GIRLS
AB This paper is the first of five papers in this issue that describes a new research consortium funded by the National Institutes of Health. It describes the design characteristics of the Childhood Obesity Prevention and Treatment Research (COPTR) trials and common measurements across the trials. The COPTR Consortium is conducting interventions to prevent obesity in pre-schoolers and treat overweight or obese 7-13 year olds. Four randomized controlled trials will enroll a total of 1700 children and adolescents (similar to 50% female, 70% minorities), and will test innovative multi-level and multi-component interventions in multiple settings involving primary tare physicians, parks and recreational centers, family advocates, and schools. For all the studies, the primary outcome measure is body mass index; secondary outcomes, moderators and mediators of intervention include diet, physical activity, home and neighborhood influences, and psychosocial factors. COPTR is being conducted collaboratively among four participating field centers, a coordinating center, and NIH project offices. Outcomes from COPTR have the potential to enhance our knowledge of interventions to prevent and treat childhood obesity. Published by Elsevier Inc.
C1 [Pratt, Charlotte A.; Boyington, Josephine; Esposito, Layla; Pemberton, Victoria L.; Bonds, Denise; Kelley, Melinda; Yang, Song; Murray, David] NIH, Bethesda, MD USA.
   [Stevens, June] Univ N Carolina, Chapel Hill, NC USA.
RP Pratt, CA (reprint author), NHLBI, Div Cardiovasc Sci, Prevent & Populat Sci Program, Clin Applicat & Prevent Branch,NIH, 6701 Rockledge Dr MSC 7936,Room 10118, Bethesda, MD 20892 USA.
EM prattc@nhlbi.nih.gov
FU National Heart, Lung, and Blood Institute [U01 HL103561, U01 HL103620,
   U01 HL103622, U01 HL103629, U01 HD068890]; Eunice Kennedy Shriver
   National Institute of Child Health and Development; NIH Office of
   Behavioral and Social Sciences Research
FX This research is being supported by grant numbers: U01 HL103561, U01
   HL103620, U01 HL103622, U01 HL103629, and U01 HD068890 from the National
   Heart, Lung, and Blood Institute, the Eunice Kennedy Shriver National
   Institute of Child Health and Development, and the NIH Office of
   Behavioral and Social Sciences Research.
NR 38
TC 9
Z9 9
U1 2
U2 19
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1551-7144
EI 1559-2030
J9 CONTEMP CLIN TRIALS
JI Contemp. Clin. Trials
PD NOV
PY 2013
VL 36
IS 2
BP 406
EP 413
DI 10.1016/j.cct.2013.08.010
PG 8
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 283RS
UT WOS:000329265300010
PM 23999502
ER

PT J
AU Domanchuk, K
   Ferrucci, L
   Guralnik, JM
   Criqui, MH
   Tian, L
   Liu, KA
   Losordo, D
   Stein, J
   Green, D
   Kibbe, M
   Zhao, LH
   Annex, B
   Perlman, H
   Lloyd-Jones, D
   Pearce, W
   Taylor, D
   McDermott, MM
AF Domanchuk, Kathryn
   Ferrucci, Luigi
   Guralnik, Jack M.
   Criqui, Michael H.
   Tian, Lu
   Liu, Kiang
   Losordo, Douglas
   Stein, James
   Green, David
   Kibbe, Melina
   Zhao, Lihui
   Annex, Brian
   Perlman, Harris
   Lloyd-Jones, Donald
   Pearce, William
   Taylor, Doris
   McDermott, Mary M.
TI Progenitor cell release plus exercise to improve functional performance
   in peripheral artery disease: The PROPEL Study
SO CONTEMPORARY CLINICAL TRIALS
LA English
DT Article
DE Intermittent claudication; Physical functioning; GM-CSF; Stem cells;
   Peripheral vascular disease
ID COLONY-STIMULATING FACTOR; RANDOMIZED CONTROLLED-TRIAL; ANKLE BRACHIAL
   INDEX; INTERMITTENT CLAUDICATION; OCCLUSIVE DISEASE; TREADMILL WALKING;
   PHYSICAL-ACTIVITY; VASCULAR-DISEASE; ELDERLY-PATIENTS; 6-MINUTE WALK
AB Functional impairment, functional decline, and mobility loss are major public health problems in people with lower extremity peripheral artery disease (PAD). Few medical therapies significantly improve walking performance in PAD. We describe methods for the PROgenitor cell release Plus Exercise to improve functionaL performance in PAD (PROPEL) Study, a randomized controlled clinical trial designed to determine whether granulocyte-macrophage colony stimulating factor (GM-CSF) combined with supervised treadmill walking exercise improves six-minute walk distance more than GM-CSF alone, more than supervised treadmill exercise alone, and more than placebo plus attention control in participants with PAD, respectively. PROPEL Study participants are randomized to one of four arms in a 2 by 2 factorial design. The four study arms are GM-CSF plus supervised treadmill exercise, GM-CSF plus attention control, placebo plus supervised exercise therapy, or placebo plus attention control. The primary outcome is change in six-minute walk distance at 12-week follow-up. Secondary outcomes include change in brachial artery flow-mediated dilation (FMD), change in maximal treadmill walking time, and change in circulating CD34+ cells at 12-week follow-up. Outcomes are also measured at six-week and six-month follow-up. Results of the PROPEL Study will have important implications for understanding mechanisms of improving walking performance and preventing mobility loss in the large and growing number of men and women with PAD. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Domanchuk, Kathryn; Losordo, Douglas; Green, David; Perlman, Harris; McDermott, Mary M.] Northwestern Univ, Feinberg Sch Med, Dept Med, Chicago, IL 60611 USA.
   [Ferrucci, Luigi] Natl Inst Aging, Bethesda, MD 20892 USA.
   [Guralnik, Jack M.] Univ Maryland, Sch Med, Dept Epidemiol & Publ Hlth, Baltimore, MD 21201 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.
   [Liu, Kiang; Zhao, Lihui; Lloyd-Jones, Donald] Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
   [Stein, James] Univ Wisconsin, Dept Med, Madison, WI 53792 USA.
   [Kibbe, Melina; Pearce, William] Northwestern Univ, Feinberg Sch Med, Dept Surg, Chicago, IL 60611 USA.
   [Kibbe, Melina] Jesse Brown Vet Affairs Med Ctr, Chicago, IL 60612 USA.
   [Annex, Brian] Univ Virginia, Robert M Berne Cardiovasc Ctr, Charlottesville, VA 22908 USA.
   [Annex, Brian] Univ Virginia, Dept Med, Charlottesville, VA 22908 USA.
   [Taylor, Doris] Texas Heart Inst, Dept Regenerat Med Res, Houston, TX 77225 USA.
RP McDermott, MM (reprint author), 750 N Lake Shore Dr,10th Floor, Chicago, IL 60611 USA.
EM mdm608@northwestern.edu
FU National Heart, Lung, and Blood Institute [R01HL107510]
FX This study is supported by the National Heart, Lung, and Blood Institute
   (grant number R01HL107510).
NR 54
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Z9 8
U1 2
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1551-7144
EI 1559-2030
J9 CONTEMP CLIN TRIALS
JI Contemp. Clin. Trials
PD NOV
PY 2013
VL 36
IS 2
BP 502
EP 509
DI 10.1016/j.cct.2013.09.011
PG 8
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 283RS
UT WOS:000329265300019
PM 24080099
ER

PT J
AU Millum, J
   Grady, C
AF Millum, Joseph
   Grady, Christine
TI The ethics of placebo-controlled trials: Methodological justifications
SO CONTEMPORARY CLINICAL TRIALS
LA English
DT Article
DE Ethics; Placebo control; Randomized controlled trial
ID HUMAN-IMMUNODEFICIENCY-VIRUS; EARLY INTERVENTION PROJECT;
   DEVELOPING-COUNTRIES; CLINICAL-RESEARCH; CARE DEBATE; TRANSMISSION;
   ZIDOVUDINE; STANDARD
AB The use of placebo controls in clinical trials remains controversial. Ethical analysis and international ethical guidance permit the use of placebo controls in randomized trials when scientifically indicated in four cases: (1) when there is no proven effective treatment for the condition under study; (2) when withholding treatment poses negligible risks to participants; (3) when there are compelling methodological reasons for using placebo, and withholding treatment does not pose a risk of serious harm to participants; and, more controversially, (4) when there are compelling methodological reasons for using placebo, and the research is intended to develop interventions that can be implemented in the population from which trial participants are drawn, and the trial does not require participants to forgo treatment they would otherwise receive. The concept of methodological reasons is essential to assessing the ethics of placebo controls in these controversial last two cases. This article sets out key considerations relevant to considering whether methodological reasons for a placebo control are compelling. Published by Elsevier Inc.
C1 [Millum, Joseph; Grady, Christine] NIH, Ctr Clin, Dept Bioeth, Bethesda, MD 20892 USA.
   [Millum, Joseph] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Millum, J (reprint author), NIH, Ctr Clin, Dept Bioeth, 10-1C118,10 Ctr Dr, Bethesda, MD 20892 USA.
EM joseph.millum@nih.gov
FU Intramural NIH HHS [Z99 CL999999]
NR 31
TC 7
Z9 7
U1 2
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1551-7144
EI 1559-2030
J9 CONTEMP CLIN TRIALS
JI Contemp. Clin. Trials
PD NOV
PY 2013
VL 36
IS 2
BP 510
EP 514
DI 10.1016/j.cct.2013.09.003
PG 5
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 283RS
UT WOS:000329265300020
PM 24035802
ER

PT J
AU Berger, VW
AF Berger, Vance W.
TI A unifying framework for standard and covariate-adaptive randomization
   procedures based on minimizing suitable imbalance functions
SO CONTEMPORARY CLINICAL TRIALS
LA English
DT Article
DE Adaptive randomization; Allocation concealment; Imbalance function
ID CLINICAL-TRIALS; SELECTION BIAS; ALLOCATION; MINIMIZATION; DESIGNS
AB Minimization is based on minimizing an imbalance function defined in terms of one or more covariates. Standard (non-adaptive) randomization procedures, on the other hand, generally do not specify or try to minimize an imbalance function. However, it turns out that they may be formulated in this manner. Doing so places adaptive and standard randomization procedures within the same framework, and also suggests novel randomization procedures that combine the best elements of both. Published by Elsevier Inc.
C1 [Berger, Vance W.] NCI, Biometry Res Grp, Rockville, MD 20850 USA.
   [Berger, Vance W.] Univ Maryland Baltimore Cty, Baltimore, MD 21228 USA.
RP Berger, VW (reprint author), NCI, Biometry Res Grp, 9609 Med Ctr Dr, Rockville, MD 20850 USA.
EM vb78c@nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 16
TC 1
Z9 1
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1551-7144
EI 1559-2030
J9 CONTEMP CLIN TRIALS
JI Contemp. Clin. Trials
PD NOV
PY 2013
VL 36
IS 2
BP 527
EP 530
DI 10.1016/j.cct.2013.09.017
PG 4
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 283RS
UT WOS:000329265300022
PM 24120653
ER

PT J
AU Subramanian, J
   Simon, R
AF Subramanian, Jyothi
   Simon, Richard
TI Overfitting in prediction models - Is it a problem only in high
   dimensions?
SO CONTEMPORARY CLINICAL TRIALS
LA English
DT Article
DE Classifiers; Prediction accuracy; Overfitting; Clinical trials; Patient
   selection
ID GENE-EXPRESSION DATA; CLASSIFICATION; EVENTS
AB The growing recognition that human diseases are molecularly heterogeneous has stimulated interest in the development of prognostic and predictive classifiers for patient selection and stratification. In the process of classifier development, it has been repeatedly emphasized that in situations where the number of candidate predictor variables is much larger than the number of observations, the apparent (training set, resubstitution) accuracy of the classifiers can be highly optimistically biased and hence, classification accuracy should be reported based on evaluation of the classifier on a separate test set or using complete cross-validation. Such evaluation methods have however not been the norm in the case of low-dimensional, p < n data that arise, for example, in clinical trials when a classifier is developed on a combination of clinico-pathological variables and a small number of genetic biomarkers selected from an understanding of the biology of the disease. We undertook simulation studies to investigate the existence and extent of the problem of overfitting with low-dimensional data. The results indicate that overfitting can be a serious problem even for low-dimensional data, especially if the relationship of outcome to the set of predictor variables is not strong. We hence encourage the adoption of either a separate test set or complete cross-validation to evaluate classifier accuracy, even when the number of candidate predictor variables is substantially smaller than the number of cases. Published by Elsevier Inc.
C1 [Subramanian, Jyothi] Emmes Corp, Rockville, MD 20850 USA.
   [Simon, Richard] Natl Canc Inst, Biometr Res Branch, Bethesda, MD 20892 USA.
RP Simon, R (reprint author), Natl Canc Inst, Biometr Res Branch, Bethesda, MD 20892 USA.
EM rsimon@mail.nih.gov
NR 15
TC 13
Z9 13
U1 2
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1551-7144
EI 1559-2030
J9 CONTEMP CLIN TRIALS
JI Contemp. Clin. Trials
PD NOV
PY 2013
VL 36
IS 2
BP 636
EP 641
DI 10.1016/j.cct.2013.06.011
PG 6
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 283RS
UT WOS:000329265300033
PM 23811117
ER

PT J
AU Rahimpour, S
   Yang, CZ
   Frerich, J
   Zhuang, ZP
AF Rahimpour, Shervin
   Yang, Chunzhang
   Frerich, Jason
   Zhuang, Zhengping
TI GLIAL-TUMOR INTERFACE IN METASTATIC AND PRIMARY BRAIN NEOPLASMS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 4th Quadrennial Meeting of the World-Federation-of-Neuro-Oncology (WFNO)
   held in conjunction with the 18th Annual Meeting of the
   Society-for-Neuro-Oncology (SNO)
CY NOV 21-24, 2013
CL San Francisco, CA
SP World Federat Neuro Oncol, Soc Neuro Oncol
C1 [Rahimpour, Shervin; Yang, Chunzhang; Frerich, Jason; Zhuang, Zhengping] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV
PY 2013
VL 15
SU 3
BP 9
EP 9
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 258JT
UT WOS:000327456200036
ER

PT J
AU Choi, YA
   Pandya, H
   Gibo, DM
   Fokt, I
   Priebe, W
   Debinski, W
AF Choi, Young A.
   Pandya, Hetal
   Gibo, Denise M.
   Fokt, Isabela
   Priebe, Waldemar
   Debinski, Waldemar
TI NUCLEUS-TARGETED DOXORUBICIN AS A POTENTIAL THERAPY FOR GLIOBLASTOMA
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 4th Quadrennial Meeting of the World-Federation-of-Neuro-Oncology (WFNO)
   held in conjunction with the 18th Annual Meeting of the
   Society-for-Neuro-Oncology (SNO)
CY NOV 21-24, 2013
CL San Francisco, CA
SP World Federat Neuro Oncol, Soc Neuro Oncol
C1 [Choi, Young A.; Gibo, Denise M.; Debinski, Waldemar] Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA.
   [Pandya, Hetal] NIH, Bethesda, MD 20892 USA.
   [Fokt, Isabela; Priebe, Waldemar] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
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 NOV
PY 2013
VL 15
SU 3
BP 40
EP 40
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 258JT
UT WOS:000327456200167
ER

PT J
AU Grasso, C
   Liu, LN
   Becher, O
   Berlow, N
   Davis, L
   Fouladi, M
   Gajjar, A
   Hawkins, C
   Huang, E
   Hulleman, E
   Hutt, M
   Keller, C
   Li, XN
   Meltzer, P
   Quezado, M
   Quist, M
   Raabe, E
   Spellman, P
   Truffaux, N
   van Vurden, D
   Wang, N
   Warren, K
   Pal, R
   Grill, J
   Monje, M
AF Grasso, Catherine
   Liu, Lining
   Becher, Oren
   Berlow, Noah
   Davis, Lara
   Fouladi, Maryam
   Gajjar, Amar
   Hawkins, Cynthia
   Huang, Elaine
   Hulleman, Esther
   Hutt, Marianne
   Keller, Charles
   Li, Xiao-Nan
   Meltzer, Paul
   Quezado, Martha
   Quist, Michael
   Raabe, Eric
   Spellman, Paul
   Truffaux, Nathalene
   van Vurden, Dannis
   Wang, Nicholas
   Warren, Katherine
   Pal, Ranadip
   Grill, Jacques
   Monje, Michelle
TI THERAPEUTIC OPPORTUNITIES IN DIFFUSE INTRINSIC PONTINE GLIOMAS
   DETERMINED BY FUNCTIONAL CHEMICAL SCREENS AND MUTATIONAL PROFILING
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 4th Quadrennial Meeting of the World-Federation-of-Neuro-Oncology (WFNO)
   held in conjunction with the 18th Annual Meeting of the
   Society-for-Neuro-Oncology (SNO)
CY NOV 21-24, 2013
CL San Francisco, CA
SP World Federat Neuro Oncol, Soc Neuro Oncol
C1 [Hawkins, Cynthia] Univ Toronto, Toronto, ON, Canada.
   [Liu, Lining; Monje, Michelle] Stanford Univ, Stanford, CA 94305 USA.
   [Grasso, Catherine; Davis, Lara; Huang, Elaine; Keller, Charles; Quist, Michael; Spellman, Paul; Wang, Nicholas] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
   [Hulleman, Esther; van Vurden, Dannis] VU Canc Ctr, Amsterdam, Netherlands.
   [Hutt, Marianne; Raabe, Eric] Johns Hopkins Univ, Baltimore, MD USA.
   [Truffaux, Nathalene; Grill, Jacques] Inst Gustave Roussy, Villejuif, France.
   [Becher, Oren] Duke Univ, Durham, NC USA.
   [Berlow, Noah; Pal, Ranadip] Texas Tech Univ, Lubbock, TX 79409 USA.
   [Li, Xiao-Nan] Texas Childrens Canc Ctr, Waco, TX USA.
   [Fouladi, Maryam] Cincinnati Childrens Hosp, Cincinnati, OH USA.
   [Gajjar, Amar] St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
   [Meltzer, Paul; Quezado, Martha; Warren, Katherine] Natl Inst Hlth, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV
PY 2013
VL 15
SU 3
BP 44
EP 44
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 258JT
UT WOS:000327456200184
ER

PT J
AU Warren, K
   McCully, C
   Bacher, J
   Thomas, T
   Murphy, R
   Steffen-Smith, E
   McAllister, R
   Pastakia, D
   Widemann, B
AF Warren, Katherine
   McCully, Cynthia
   Bacher, John
   Thomas, Thomas
   Murphy, Robert
   Steffen-Smith, Emilie
   McAllister, Rhonda
   Pastakia, Devang
   Widemann, Brigitte
TI GEOGRAPHIC VARIABILITY OF DRUG PENETRATION INTO THE CENTRAL NERVOUS
   SYSTEM
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 4th Quadrennial Meeting of the World-Federation-of-Neuro-Oncology (WFNO)
   held in conjunction with the 18th Annual Meeting of the
   Society-for-Neuro-Oncology (SNO)
CY NOV 21-24, 2013
CL San Francisco, CA
SP World Federat Neuro Oncol, Soc Neuro Oncol
C1 [Warren, Katherine; McCully, Cynthia; Bacher, John; Thomas, Thomas; Murphy, Robert; Steffen-Smith, Emilie; McAllister, Rhonda; Pastakia, Devang; Widemann, Brigitte] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV
PY 2013
VL 15
SU 3
BP 60
EP 60
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 258JT
UT WOS:000327456200250
ER

PT J
AU Choi, YA
   Pandya, H
   Gibo, DM
   Debinski, W
AF Choi, Young A.
   Pandya, Hetal
   Gibo, Denise M.
   Debinski, Waldemar
TI TARGETING (KLAKLAK)(2), A PRO-APOPTOTIC PEPTIDE TO GBM CELLS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 4th Quadrennial Meeting of the World-Federation-of-Neuro-Oncology (WFNO)
   held in conjunction with the 18th Annual Meeting of the
   Society-for-Neuro-Oncology (SNO)
CY NOV 21-24, 2013
CL San Francisco, CA
SP World Federat Neuro Oncol, Soc Neuro Oncol
C1 [Choi, Young A.; Gibo, Denise M.; Debinski, Waldemar] Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA.
   [Pandya, Hetal] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV
PY 2013
VL 15
SU 3
BP 69
EP 69
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 258JT
UT WOS:000327456200285
ER

PT J
AU Pandya, H
   Choi, Y
   Park, J
AF Pandya, Hetal
   Choi, Yong
   Park, John
TI DIFFERENTIATION AND GENERATION OF MICROGLIA-LIKE CELLS FROM HUMAN
   INDUCED PLURIPOTENT STEM CELLS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 4th Quadrennial Meeting of the World-Federation-of-Neuro-Oncology (WFNO)
   held in conjunction with the 18th Annual Meeting of the
   Society-for-Neuro-Oncology (SNO)
CY NOV 21-24, 2013
CL San Francisco, CA
SP World Federat Neuro Oncol, Soc Neuro Oncol
C1 [Pandya, Hetal; Choi, Yong; Park, John] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
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 NOV
PY 2013
VL 15
SU 3
BP 71
EP 71
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 258JT
UT WOS:000327456200294
ER

PT J
AU Sul, J
   Hilf, N
   Kutscher, S
   Schoor, O
   Lindner, J
   Reinhardt, C
   Kreisl, T
   Iwamoto, F
   Fine, H
   Singh-Jasuja, H
AF Sul, Joohee
   Hilf, Norbert
   Kutscher, Sarah
   Schoor, Oliver
   Lindner, Juha
   Reinhardt, Carsten
   Kreisl, Teri
   Iwamoto, Fabio
   Fine, Howard
   Singh-Jasuja, Harpreet
TI A PHASE I TRIAL OF PEPTIDE-BASED GLIOMA VACCINE IMA950 IN PATIENTS WITH
   GLIOBLASTOMA: STUDY DESIGN AND PRELIMINARY RESULTS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 4th Quadrennial Meeting of the World-Federation-of-Neuro-Oncology (WFNO)
   held in conjunction with the 18th Annual Meeting of the
   Society-for-Neuro-Oncology (SNO)
CY NOV 21-24, 2013
CL San Francisco, CA
SP World Federat Neuro Oncol, Soc Neuro Oncol
C1 [Sul, Joohee; Kreisl, Teri] NCI, Neurooncol Branch, Bethesda, MD 20892 USA.
   [Hilf, Norbert; Kutscher, Sarah; Schoor, Oliver; Lindner, Juha; Reinhardt, Carsten; Singh-Jasuja, Harpreet] Immat Biotechnol GmbH, Tubingen, Germany.
   [Fine, Howard] NYU, Langone Med Ctr, New York, NY USA.
   [Iwamoto, Fabio] Columbia Univ, Neurooncol Div, Brain Tumor Ctr, New York, NY USA.
NR 0
TC 0
Z9 0
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 NOV
PY 2013
VL 15
SU 3
BP 73
EP 73
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 258JT
UT WOS:000327456200302
ER

PT J
AU Blakeley, J
   Ye, XB
   Bergner, A
   Dombi, E
   Zalewski, C
   Follmer, K
   Halpin, C
   Fayad, L
   Jacobs, M
   Baldwin, A
   Langmead, S
   Whitcomb, T
   Jennings, D
   Widemann, B
   Plotkin, S
AF Blakeley, Jaishri
   Ye, Xiaobu
   Bergner, Amanda
   Dombi, Eva
   Zalewski, Christopher
   Follmer, Krista
   Halpin, Chris
   Fayad, Laura
   Jacobs, Michael
   Baldwin, Andrea
   Langmead, Shannon
   Whitcomb, Trish
   Jennings, Dominique
   Widemann, Brigitte
   Plotkin, Scott
TI BEVACIZUMAB IN CHILDREN AND ADULTS WITH NEUROFIBROMATOSIS TYPE 2 AND
   SYMPTOMATIC VESTIBULAR SCHWANNOMAS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 4th Quadrennial Meeting of the World-Federation-of-Neuro-Oncology (WFNO)
   held in conjunction with the 18th Annual Meeting of the
   Society-for-Neuro-Oncology (SNO)
CY NOV 21-24, 2013
CL San Francisco, CA
SP World Federat Neuro Oncol, Soc Neuro Oncol
C1 [Blakeley, Jaishri; Ye, Xiaobu; Bergner, Amanda; Follmer, Krista; Fayad, Laura; Jacobs, Michael; Langmead, Shannon] Johns Hopkins Univ, Baltimore, MD USA.
   [Halpin, Chris; Jennings, Dominique] Massachusetts Gen Hosp, Boston, MA 02114 USA.
   [Dombi, Eva; Zalewski, Christopher; Baldwin, Andrea; Whitcomb, Trish; Widemann, Brigitte; Plotkin, Scott] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV
PY 2013
VL 15
SU 3
BP 101
EP 101
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 258JT
UT WOS:000327456200405
ER

PT J
AU Jain, R
   Poisson, L
   Scarpace, L
   Mikkelsen, T
   Kirby, J
   Freymann, J
   Hwang, S
   Gutman, D
   Jaffe, C
   Brat, D
   Flanders, A
AF Jain, Rajan
   Poisson, Laila
   Scarpace, Lisa
   Mikkelsen, Tom
   Kirby, Justin
   Freymann, John
   Hwang, Scott
   Gutman, David
   Jaffe, Carl
   Brat, Daniel
   Flanders, Adam
TI OUTCOME PREDICTION IN PATIENTS WITH GLIOBLASTOMA USING IMAGING, CLINICAL
   AND GENOMIC BIOMARKERS: FOCUS ON THE NON-ENHANCING COMPONENT OF THE
   TUMOR
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 4th Quadrennial Meeting of the World-Federation-of-Neuro-Oncology (WFNO)
   held in conjunction with the 18th Annual Meeting of the
   Society-for-Neuro-Oncology (SNO)
CY NOV 21-24, 2013
CL San Francisco, CA
SP World Federat Neuro Oncol, Soc Neuro Oncol
C1 [Jain, Rajan; Poisson, Laila; Scarpace, Lisa; Mikkelsen, Tom] Henry Ford Hosp, Detroit, MI 48202 USA.
   [Kirby, Justin; Freymann, John] SAIC Frederick Inc, NCI Frederick, Bethedsa, MD USA.
   [Hwang, Scott; Gutman, David; Brat, Daniel] Emory Univ, Sch Med, Atlanta, GA USA.
   [Jaffe, Carl] Boston Univ, Boston, MA 02215 USA.
   [Flanders, Adam] Thomas Jefferson Univ Hosp, Philadelphia, PA 19107 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
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 NOV
PY 2013
VL 15
SU 3
BP 112
EP 112
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 258JT
UT WOS:000327456200449
ER

PT J
AU Colen, R
   Vangel, M
   Gutman, D
   Hwang, S
   Wintermark, M
   Jain, R
   Jilwan-Nicolas, M
   Chen, J
   Raghavan, P
   Holder, C
   Rubin, D
   Huang, E
   Kirby, J
   Freymann, J
   Jaffe, C
   Flanders, A
   Zinn, P
AF Colen, Rivka
   Vangel, Mark
   Gutman, David
   Hwang, Scott
   Wintermark, Max
   Jain, Rajan
   Jilwan-Nicolas, Manal
   Chen, James
   Raghavan, Prashant
   Holder, Chad
   Rubin, Daniel
   Huang, Eric
   Kirby, Justin
   Freymann, John
   Jaffe, Carl
   Flanders, Adam
   Zinn, Pascal
TI IMAGING GENOMIC CORRELATION OF INVASIVE GENOMIC COMPOSITION AND PATIENT
   SURVIVAL DEMONSTRATES METABOLIC DYSFUNCTION: A TCGA GLIOMA PHENOTYPE
   RESEARCH GROUP PROJECT
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 4th Quadrennial Meeting of the World-Federation-of-Neuro-Oncology (WFNO)
   held in conjunction with the 18th Annual Meeting of the
   Society-for-Neuro-Oncology (SNO)
CY NOV 21-24, 2013
CL San Francisco, CA
SP World Federat Neuro Oncol, Soc Neuro Oncol
C1 [Colen, Rivka] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
   [Vangel, Mark] Massachusetts Gen Hosp, Boston, MA 02114 USA.
   [Gutman, David; Hwang, Scott; Holder, Chad] Emory Univ, Atlanta, GA 30322 USA.
   [Wintermark, Max; Jilwan-Nicolas, Manal; Raghavan, Prashant] Univ Virginia, Charlottesville, VA USA.
   [Jain, Rajan] Henry Ford, Detroit, MI USA.
   [Chen, James] Univ Calif San Diego Hlth Syst, San Diego, CA USA.
   [Chen, James] Univ Calif San Diego, San Diego Med Ctr, San Diego, CA 92103 USA.
   [Rubin, Daniel] Stanford Univ, Stanford, CA 94305 USA.
   [Huang, Eric; Kirby, Justin; Freymann, John] NCI, NIH, Bethesda, MD 20892 USA.
   [Jaffe, Carl] NCI, NIH, Rockville, MD USA.
   [Flanders, Adam] Thomas Jefferson Univ Hosp, Philadelphia, PA 19107 USA.
   [Zinn, Pascal] Baylor Coll Med, Dept Neurosurg, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
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 NOV
PY 2013
VL 15
SU 3
BP 193
EP 193
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 258JT
UT WOS:000327456200755
ER

PT J
AU Frerich, JM
   Rahimpour, S
   Zhuang, ZP
   Heiss, JD
AF Frerich, Jason M.
   Rahimpour, Shervin
   Zhuang, Zhengping
   Heiss, John D.
TI INDUCTION OF IMMUNOGENIC CANCER TESTIS ANTIGENS IN TUMOR-INITIATING
   GLIOMA STEM CELLS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 4th Quadrennial Meeting of the World-Federation-of-Neuro-Oncology (WFNO)
   held in conjunction with the 18th Annual Meeting of the
   Society-for-Neuro-Oncology (SNO)
CY NOV 21-24, 2013
CL San Francisco, CA
SP World Federat Neuro Oncol, Soc Neuro Oncol
C1 [Frerich, Jason M.; Rahimpour, Shervin; Zhuang, Zhengping; Heiss, John D.] NINDS, NIH, Surg Neurol Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV
PY 2013
VL 15
SU 3
BP 208
EP 208
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 258JT
UT WOS:000327456200817
ER

PT J
AU Yong, RL
   Wu, TX
   Mihatov, N
   Shen, MJ
   Brown, MA
   Zaghloul, KA
   Park, GE
   Park, JK
AF Yong, Raymund L.
   Wu, Tianxia
   Mihatov, Nino
   Shen, Michael J.
   Brown, M. Anthony
   Zaghloul, Kareem A.
   Park, Grace E.
   Park, John K.
TI RE-OPERATION FOR RECURRENT GLIOBLASTOMA MULTIFORME
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 4th Quadrennial Meeting of the World-Federation-of-Neuro-Oncology (WFNO)
   held in conjunction with the 18th Annual Meeting of the
   Society-for-Neuro-Oncology (SNO)
CY NOV 21-24, 2013
CL San Francisco, CA
SP World Federat Neuro Oncol, Soc Neuro Oncol
C1 [Yong, Raymund L.; Wu, Tianxia; Mihatov, Nino; Shen, Michael J.; Brown, M. Anthony; Zaghloul, Kareem A.; Park, John K.] NINDS, Bethesda, MD 20892 USA.
   [Park, Grace E.] NHGRI, Bethesda, MD 20892 USA.
   [Yong, Raymund L.] Mt Sinai Sch Med, New York, NY USA.
NR 0
TC 0
Z9 0
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 NOV
PY 2013
VL 15
SU 3
BP 224
EP 225
PG 2
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 258JT
UT WOS:000327456200883
ER

PT J
AU Wenger, C
   Miranda, PC
   Mekonnen, A
   Salvador, R
   Basser, P
AF Wenger, Cornelia
   Miranda, Pedro Cavaleiro
   Mekonnen, Abeye
   Salvador, Ricardo
   Basser, Peter
TI ELECTRIC FIELDS FOR THE TREATMENT OF GLIOBLASTOMAS: A MODELING STUDY
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 4th Quadrennial Meeting of the World-Federation-of-Neuro-Oncology (WFNO)
   held in conjunction with the 18th Annual Meeting of the
   Society-for-Neuro-Oncology (SNO)
CY NOV 21-24, 2013
CL San Francisco, CA
SP World Federat Neuro Oncol, Soc Neuro Oncol
C1 [Wenger, Cornelia; Miranda, Pedro Cavaleiro; Mekonnen, Abeye; Salvador, Ricardo] Univ Lisbon, Fac Sci, IBEB, P-1699 Lisbon, Portugal.
   [Basser, Peter] NICHD, STBB, NIH, Bethesda, MD USA.
RI Miranda, Pedro/A-5643-2013
OI Miranda, Pedro/0000-0002-6793-8111
NR 0
TC 1
Z9 1
U1 0
U2 5
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 NOV
PY 2013
VL 15
SU 3
BP 241
EP 241
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 258JT
UT WOS:000327456200943
ER

PT J
AU Abrami, L
   Brandi, L
   Moayeri, M
   Brown, MJ
   Krantz, BA
   Leppla, SH
   van der Goot, FG
AF Abrami, Laurence
   Brandi, Lucia
   Moayeri, Mahtab
   Brown, Michael J.
   Krantz, Bryan A.
   Leppla, Stephen H.
   van der Goot, F. Gisou
TI Hijacking Multivesicular Bodies Enables Long-Term and Exosome-Mediated
   Long-Distance Action of Anthrax Toxin
SO CELL REPORTS
LA English
DT Article
ID LETHAL FACTOR; PROTEIN TRANSLOCATION; PATHWAY; VESICLES; DELIVERY;
   SURFACE; CELLS; ALIX
AB Anthrax lethal toxin is a classical AB toxin comprised of two components: protective antigen (PA) and lethal factor (LF). Here, we show that following assembly and endocytosis, PA forms a channel that translocates LF, not only into the cytosol, but also into the lumen of endosomal intraluminal vesicles (ILVs). These ILVs can fuse and release LF into the cytosol, where LF can proteolyze and disable host targets. We find that LF can persist in ILVs for days, fully sheltered from proteolytic degradation, both in vitro and in vivo. During this time, ILV-localized LF can be transmitted to daughter cells upon cell division. In addition, LF-containing ILVs can be delivered to the extracellular medium as exosomes. These can deliver LF to the cytosol of naive cells in a manner that is independent of the typical anthrax toxin receptor-mediated trafficking pathway, while being sheltered from neutralizing extracellular factors of the immune system.
C1 [Abrami, Laurence; Brandi, Lucia; van der Goot, F. Gisou] Ecole Polytech Fed Lausanne, Global Hlth Inst, Stn 19, CH-1015 Lausanne, Switzerland.
   [Brown, Michael J.; Krantz, Bryan A.] Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA.
   [Krantz, Bryan A.] Univ Calif Berkeley, Dept Chem, Berkeley, CA 94720 USA.
   [Moayeri, Mahtab; Leppla, Stephen H.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP van der Goot, FG (reprint author), Ecole Polytech Fed Lausanne, Global Hlth Inst, Stn 19, CH-1015 Lausanne, Switzerland.
EM gisou.vandergoot@epfl.ch
FU Swiss National Science Foundation; NCCR Chemical Biology; NIAID [2R01
   AI077703-05]; NHLBI, NIH
FX We thank Nuria Reig for early experiments; Laura Symul for generating
   the models; J. Gruenberg for reagents, advice, and critical reading of
   the manuscript; Reika Watanabe for the SAR1a-GTP cDNA; and all the
   members of the F.G.v.d.G. laboratory for their helpful suggestions and
   discussions. This work was supported by the Swiss National Science
   Foundation and the NCCR Chemical Biology (to F.G.v.d.G.), NIAID grant
   2R01 AI077703-05 (to B. A. K.), and the intramural research programs of
   the NIAID and the NHLBI, NIH (to S. H. L.).
NR 34
TC 36
Z9 37
U1 1
U2 17
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 NOV
PY 2013
VL 5
IS 4
BP 986
EP 996
DI 10.1016/j.celrep.2013.10.019
PG 11
WC Cell Biology
SC Cell Biology
GA 269TY
UT WOS:000328266000014
PM 24239351
ER

PT J
AU Jellusova, J
   Miletic, AV
   Cato, MH
   Lin, WW
   Hu, YL
   Bishop, GA
   Shlomchik, MJ
   Rickert, RC
AF Jellusova, Julia
   Miletic, Ana V.
   Cato, Matthew H.
   Lin, Wai-Wai
   Hu, Yinling
   Bishop, Gail A.
   Shlomchik, Mark J.
   Rickert, Robert C.
TI Context-Specific BAFF-R Signaling by the NF-kappa B and PI3K Pathways
SO CELL REPORTS
LA English
DT Article
ID CLASS-SWITCH RECOMBINATION; CELL SURVIVAL; CUTTING EDGE; IKK-ALPHA;
   RECEPTOR SIGNALS; PHOSPHATIDYLINOSITOL 3-KINASE; NF-KAPPA-B2 P100;
   GERMINAL-CENTERS; T-LYMPHOCYTES; MARGINAL ZONE
AB BAFF is a soluble factor required for B cell maturation and survival. BAFF-R signals via the noncanonical NF-kappa B pathway regulated by the TRAF3/NIK/IKK1 axis. We show that deletion of Ikk1 during early B cell development causes a partial impairment in B cell maturation and BAFF-dependent survival, but inactivation of Ikk1 in mature B cells does not affect survival. We further show that BAFF-R employs CD19 to promote survival via phosphatidylinositol 3-kinase (PI3K), and that coinactivation of Cd19 and Ikk1 causes a profound block in B cell maturation at the transitional stage. Consistent with a role for PI3K in BAFF-R function, inactivation of PTEN mediates a partial rescue of B cell maturation and function in Baff(-/-) animals. Elevated PI3K signaling also circumvents BAFF-dependent survival in a spontaneous B cell lymphoma model. These findings indicate that the combined activities of PI3K and IKK1 drive peripheral B cell differentiation and survival in a context-dependent manner.
C1 [Jellusova, Julia; Miletic, Ana V.; Cato, Matthew H.; Rickert, Robert C.] Sanford Burnham Med Res Inst, Infect & Inflammatory Dis Ctr, Program Inflammatory Dis, La Jolla, CA 92037 USA.
   [Lin, Wai-Wai; Bishop, Gail A.] Univ Iowa, Grad Program Immunol, Iowa City, IA 52242 USA.
   [Lin, Wai-Wai; Bishop, Gail A.] VA Med Ctr, Iowa City, IA 52242 USA.
   [Bishop, Gail A.] Univ Iowa, Dept Microbiol, Iowa City, IA 52242 USA.
   [Bishop, Gail A.] Univ Iowa, Dept Internal Med, Iowa City, IA 52242 USA.
   [Hu, Yinling] NCI, Canc & Inflammat Program, Ctr Canc Res, NIH, Frederick, MD 21701 USA.
   [Shlomchik, Mark J.] Univ Pittsburgh, Sch Med, Dept Immunol, Pittsburgh, PA 15261 USA.
RP Rickert, RC (reprint author), Sanford Burnham Med Res Inst, Infect & Inflammatory Dis Ctr, Program Inflammatory Dis, 10901 North Torrey Pines Rd, La Jolla, CA 92037 USA.
EM robert@sanfordburnham.org
FU NIH [AI041649, HL088686, RR026280, AI043603, AR44077, AI49993]; NIH F32
   fellowship [CA132350]; Deutsche Forschungsgemeinschaft; Arthritis
   National Research Foundation
FX We thank the members of the Rickert laboratory for discussions, and Dr.
   D. Nemazee (TSRI, La Jolla, CA) for facilitating the transfer of the
   Baff<SUP>-/-</SUP> mice. This work was supported by NIH grants AI041649,
   HL088686, and RR026280 (to R. C. R); AI043603 and AR44077 (to M.J.S.);
   and AI49993 (to G. A. B). G. A. B. received resources and use of
   facilities from the Iowa City VAMC. A. V. M. was supported by NIH F32
   fellowship CA132350. J.J. was supported by fellowships from the Deutsche
   Forschungsgemeinschaft and the Arthritis National Research Foundation.
NR 65
TC 18
Z9 18
U1 0
U2 3
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 NOV
PY 2013
VL 5
IS 4
BP 1022
EP 1035
DI 10.1016/j.celrep.2013.10.022
PG 14
WC Cell Biology
SC Cell Biology
GA 269TY
UT WOS:000328266000017
PM 24239354
ER

PT J
AU Han, JC
   Thurm, A
   Williams, CG
   Joseph, LA
   Zein, WM
   Brooks, BP
   Butman, JA
   Brady, SM
   Fuhr, SR
   Hicks, MD
   Huey, AE
   Hanish, AE
   Danley, KM
   Raygada, MJ
   Rennert, OM
   Martinowich, K
   Sharp, SJ
   Tsao, JW
   Swedo, SE
AF Han, Joan C.
   Thurm, Audrey
   Williams, Christine Golden
   Joseph, Lisa A.
   Zein, Wadih M.
   Brooks, Brian P.
   Butman, John A.
   Brady, Sheila M.
   Fuhr, Shannon R.
   Hicks, Melanie D.
   Huey, Amanda E.
   Hanish, Alyson E.
   Danley, Kristen M.
   Raygada, Margarita J.
   Rennert, Owen M.
   Martinowich, Keri
   Sharp, Stephen J.
   Tsao, Jack W.
   Swedo, Susan E.
TI Association of brain-derived neurotrophic factor (BDNF)
   haploinsufficiency with lower adaptive behaviour and reduced cognitive
   functioning in WAGR/11p13 deletion syndrome
SO CORTEX
LA English
DT Article
DE Brain-derived neurotrophic factor; WAGR syndrome; 11p Deletion; IQ;
   Autism
ID MESSENGER-RNA EXPRESSION; INTELLECTUAL DISABILITY; WAGR SYNDROME;
   MENTAL-RETARDATION; VISUAL IMPAIRMENT; CHRONIC DISEASES; AUTISM;
   CHILDREN; SPECTRUM; ADOLESCENTS
AB In animal studies, brain-derived neurotrophic factor (BDNF) is an important regulator of central nervous system development and synaptic plasticity. WAGR (Wilms tumour, Aniridia, Genitourinary anomalies, and mental Retardation) syndrome is caused by 11p13 deletions of variable size near the BDNF locus and can serve as a model for studying human BDNF haploinsufficiency (+/-). We hypothesized that BDNF+/- would be associated with more severe cognitive impairment in subjects with WAGR syndrome. Twenty-eight subjects with WAGR syndrome (6-28 years), 12 subjects with isolated aniridia due to PAX6 mutations/microdeletions (7-54 years), and 20 healthy controls (4-32 years) received neurocognitive assessments. Deletion boundaries for the subjects in the WAGR group were determined by high-resolution oligonucleotide array comparative genomic hybridization. Within the WAGR group, BDNF+/- subjects (n = 15), compared with BDNF intact (+/+) subjects (n = 13), had lower adaptive behaviour (p = .02), reduced cognitive functioning (p = .04), higher levels of reported historical (p = .02) and current (p = .02) social impairment, and higher percentage meeting cut-off score for autism (p = .047) on Autism Diagnostic Interview-Revised. These differences remained nominally significant after adjusting for visual acuity. Using diagnostic measures and clinical judgement, 3 subjects (2 BDNF+/- and 1 BDNF+/+) in the WAGR group (10.7%) were classified with autism spectrum disorder. A comparison group of visually impaired subjects with isolated aniridia had cognitive functioning comparable to that of healthy controls. In summary, among subjects with WAGR syndrome, BDNF+/- subjects had a mean Vineland Adaptive Behaviour Compose score that was 14-points lower and a mean intelligence quotient (IQ) that was 20-points lower than BDNF+/+ subjects. Our findings support the hypothesis that BDNF plays an important role in human neurocognitive development. Published by Elsevier Ltd.
C1 [Han, Joan C.; Fuhr, Shannon R.; Hicks, Melanie D.; Huey, Amanda E.; Hanish, Alyson E.; Danley, Kristen M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Unit Metab & Neuroendocrinol, NIH, Bethesda, MD USA.
   [Han, Joan C.; Brady, Sheila M.] NICHD, Program Dev Endocrinol & Genet, Sect Growth & Obes, NIH, Bethesda, MD 20892 USA.
   [Thurm, Audrey; Williams, Christine Golden; Joseph, Lisa A.; Swedo, Susan E.] NIH, Pediat & Dev Neurosci Branch, Bethesda, MD 20892 USA.
   [Zein, Wadih M.] NEI, Ophthalm Genet & Visual Funct Branch, NIH, Bethesda, MD 20892 USA.
   [Butman, John A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
   [Hanish, Alyson E.] NINR, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
   [Raygada, Margarita J.; Rennert, Owen M.] NICHD, Sect Clin & Dev Genom, NIH, Bethesda, MD 20892 USA.
   [Martinowich, Keri] Lieber Inst Brain Dev, Baltimore, MD USA.
   [Sharp, Stephen J.; Tsao, Jack W.] Uniformed Serv Univ Hlth Sci, Dept Neurol, Bethesda, MD 20814 USA.
RP Han, JC (reprint author), NICHD, Unit Metab & Neuroendocrinol, NIH, 10 Ctr Dr,Bldg 10-CRC,Room 1-3330,MSC 1103, Bethesda, MD 20892 USA.
EM hanjo@mail.nih.gov
RI Butman, John/J-2780-2013; Martinowich, Keri/F-9841-2012; 
OI Butman, John/0000-0002-1547-9195; Martinowich, Keri/0000-0002-5237-0789
FU Intramural Research Programs of the Eunice Kennedy Shriller National
   Institute of Child Health and Human Development [ZIAHD008898,
   Z1AHD00641]; National Institute of Mental Health of the National
   Institutes of Health (NIH) [ZIAMH002868]; NIH Bench-to-Bedside Program
FX This study was funded by the Intramural Research Programs of the Eunice
   Kennedy Shriller National Institute of Child Health and Human
   Development (ZIAHD008898 and Z1AHD00641) and the National Institute of
   Mental Health (ZIAMH002868) of the National Institutes of Health (NIH),
   and by the NIH Bench-to-Bedside Program. We thank the members of
   International WAGR Syndrome Association for assistance in identifying
   families who were willing to participate in this study. We thank Jack
   Yanovski and Daniel Weinberger for helpful discussions. We thank
   Margaret Pekar, Miriya Tune, Mark Lee, Matthew Tsang, Tanvee Singh,
   Emily Yin, Jamila Grossman, and Rachel Kim for assistance with
   psychological testing and administrative support. Disclaimer: the
   opinions or assertions contained herein are the private views of the
   authors and are not to be construed as official or as reflecting the
   views of the Department of the Navy or the Department of Defense.
NR 53
TC 7
Z9 7
U1 2
U2 12
PU ELSEVIER MASSON
PI MILANO
PA VIA PALEOCAPA 7, 20121 MILANO, ITALY
SN 0010-9452
EI 1973-8102
J9 CORTEX
JI Cortex
PD NOV-DEC
PY 2013
VL 49
IS 10
BP 2700
EP 2710
DI 10.1016/j.cortex.2013.02.009
PG 11
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 282AM
UT WOS:000329142500011
PM 23517654
ER

PT J
AU Turk, GC
   Sharpless, KE
   Cleveland, D
   Jongsma, C
   Mackey, EA
   Marlow, AF
   Oflaz, R
   Paul, RL
   Sieber, JR
   Thompson, RQ
   Wood, LJ
   Yu, LL
   Zeisler, R
   Wise, SA
   Yen, JH
   Christopher, SJ
   Day, RD
   Long, SE
   Greene, E
   Harnly, J
   Ho, IP
   Betz, JM
AF Turk, Gregory C.
   Sharpless, Katherine E.
   Cleveland, Danielle
   Jongsma, Candice
   Mackey, Elizabeth A.
   Marlow, Anthony F.
   Oflaz, Rabia
   Paul, Rick L.
   Sieber, John R.
   Thompson, Robert Q.
   Wood, Laura J.
   Yu, Lee L.
   Zeisler, Rolf
   Wise, Stephen A.
   Yen, James H.
   Christopher, Steven J.
   Day, Russell D.
   Long, Stephen E.
   Greene, Ella
   Harnly, James
   Ho, I-Pin
   Betz, Joseph M.
TI Certification of Elements in and Use of Standard Reference Material 3280
   Multivitamin/Multielement Tablets
SO JOURNAL OF AOAC INTERNATIONAL
LA English
DT Article
ID SUPPLEMENT INGREDIENT DATABASE; DIETARY-SUPPLEMENTS; NIH OFFICE; ICP-MS;
   CADMIUM; VITAMINS; PROGRESS; LEAD
AB Standard Reference Material 3280 Multivitamin/ Multielement Tablets was issued by the National Institute of Standards and Technology in 2009, and has certified and reference mass fraction values for 13 vitamins, 26 elements, and two carotenoids. Elements were measured using two or more analytical methods at NIST with additional data contributed by collaborating laboratories. This reference material is expected to serve a dual purpose: to provide quality assurance in support of a database of dietary supplement products and to provide a means for analysts, dietary supplement manufacturers, and researchers to assess the appropriateness and validity of their analytical methods and the accuracy of their results.
C1 [Turk, Gregory C.; Sharpless, Katherine E.; Cleveland, Danielle; Jongsma, Candice; Mackey, Elizabeth A.; Marlow, Anthony F.; Oflaz, Rabia; Paul, Rick L.; Sieber, John R.; Thompson, Robert Q.; Wood, Laura J.; Yu, Lee L.; Zeisler, Rolf; Wise, Stephen A.; Yen, James H.] NIST, Gaithersburg, MD 20899 USA.
   [Christopher, Steven J.; Day, Russell D.; Long, Stephen E.] NIST, Charleston, SC 29412 USA.
   [Greene, Ella; Harnly, James] USDA, Food Composit Methods Dev Lab, Beltsville, MD 20705 USA.
   [Ho, I-Pin] Grocery Manufacturers Assoc, Washington, DC 20005 USA.
   [Betz, Joseph M.] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
RP Sharpless, KE (reprint author), NIST, 100 Bur Dr, Gaithersburg, MD 20899 USA.
EM katherine.sharpless@nist.gov
RI Yu, Lee/N-7263-2015; 
OI Yu, Lee/0000-0002-8043-6853; Cleveland, Danielle/0000-0003-3880-4584
FU National Institutes of Health, Office of Dietary Supplements through
   Interagency [Y1-OD-4147-01]
FX We extend our thanks to Brandi S. Benford and Barbara J. Porter, both
   formerly of NIST, for their contributions to this effort. Partial
   funding for this work was provided by the National Institutes of Health,
   Office of Dietary Supplements through Interagency Agreement No.
   Y1-OD-4147-01.
NR 13
TC 1
Z9 1
U1 0
U2 9
PU AOAC INT
PI GAITHERSBURG
PA 481 N FREDRICK AVE, STE 500, GAITHERSBURG, MD 20877-2504 USA
SN 1060-3271
EI 1944-7922
J9 J AOAC INT
JI J. AOAC Int.
PD NOV-DEC
PY 2013
VL 96
IS 6
BP 1281
EP 1287
DI 10.5740/jaoacint.13-135
PG 7
WC Chemistry, Analytical; Food Science & Technology
SC Chemistry; Food Science & Technology
GA 278YR
UT WOS:000328926300016
PM 24645505
ER

PT J
AU Celik, H
   Bouhrara, M
   Reiter, DA
   Fishbein, KW
   Spencer, RG
AF Celik, Hasan
   Bouhrara, Mustapha
   Reiter, David A.
   Fishbein, Kenneth W.
   Spencer, Richard G.
TI Stabilization of the inverse Laplace transform of multiexponential decay
   through introduction of a second dimension
SO JOURNAL OF MAGNETIC RESONANCE
LA English
DT Article
DE Inverse problems; NMR relaxometry; Fredholm integral
ID TIME-CORRELATION RELAXOMETRY; T-2
AB We propose a new approach to stabilizing the inverse Laplace transform of a multiexponential decay signal, a classically ill-posed problem, in the context of nuclear magnetic resonance relaxometry. The method is based on extension to a second, indirectly detected, dimension, that is, use of the established framework of two-dimensional relaxometry, followed by projection onto the desired axis. Numerical results for signals comprised of discrete T-1 and T-2 relaxation components and experiments performed on agarose gel phantoms are presented. We find markedly improved accuracy, and stability with respect to noise, as well as insensitivity to regularization in quantifying underlying relaxation components through use of the two-dimensional as compared to the one-dimensional inverse Laplace transform. This improvement is demonstrated separately for two different inversion algorithms, non-negative least squares and non-linear least squares, to indicate the generalizability of this approach. These results may have wide applicability in approaches to the Fredholm integral equation of the first kind. Published by Elsevier Inc.
C1 [Celik, Hasan; Bouhrara, Mustapha; Reiter, David A.; Fishbein, Kenneth W.; Spencer, Richard G.] NIA, Clin Invest Lab, NIH, Baltimore, MD 21224 USA.
RP Spencer, RG (reprint author), NIA, Clin Invest Lab, NIH, Baltimore, MD 21224 USA.
EM spencerri@mail.nih.gov
OI Fishbein, Kenneth/0000-0002-6353-4603
FU Intramural Research Program of the National Institute on Aging of the
   NIH
FX This work was supported by the Intramural Research Program of the
   National Institute on Aging of the NIH. The authors thank Professors
   John Benedetto and Wojciech Czaja of the University of Maryland for
   useful discussions and encouragement.
NR 11
TC 7
Z9 7
U1 0
U2 9
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1090-7807
EI 1096-0856
J9 J MAGN RESON
JI J. Magn. Reson.
PD NOV
PY 2013
VL 236
BP 134
EP 139
DI 10.1016/j.jmr.2013.07.008
PG 6
WC Biochemical Research Methods; Physics, Atomic, Molecular & Chemical;
   Spectroscopy
SC Biochemistry & Molecular Biology; Physics; Spectroscopy
GA 282CZ
UT WOS:000329149200017
PM 24035004
ER

PT J
AU Broccolo, F
   Drago, F
   Cassina, G
   Fava, A
   Fusetti, L
   Matteoli, B
   Ceccherini-Nelli, L
   Sabbadini, MG
   Lusso, P
   Parodi, A
   Malnati, MS
AF Broccolo, Francesco
   Drago, Francesco
   Cassina, Giulia
   Fava, Andrea
   Fusetti, Lisa
   Matteoli, Barbara
   Ceccherini-Nelli, Luca
   Sabbadini, Maria Grazia
   Lusso, Paolo
   Parodi, Aurora
   Malnati, Mauro S.
TI Selective Reactivation of Human Herpesvirus 6 in Patients With
   Autoimmune Connective Tissue Diseases
SO JOURNAL OF MEDICAL VIROLOGY
LA English
DT Article
DE HHV-6; viral reactivation; viral load; autoimmune connective tissue
   diseases; herpesviruses; plasma viremia
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; EPSTEIN-BARR-VIRUS; TIME PCR ASSAY;
   STEM-CELL TRANSPLANTATION; HUMAN-HERPESVIRUS-6 DNA; CYTOMEGALOVIRUS
   REACTIVATION; INCREASED PREVALENCE; MOLECULAR MIMICRY; SEVERITY INDEX;
   INFECTION
AB Viral infections have been associated with autoimmune connective tissue diseases. To evaluate whether active infection by Epstein-Barr virus (EBV), cytomegalovirus (CMV), human herpesvirus (HHV)-6, -7, -8, as well as parvovirus B19 (B19V) occur in patients with autoimmune connective tissue diseases, viral DNA loads were assessed in paired samples of serum and peripheral blood mononuclear cells (PBMCs) of 115 patients affected by different disorders, including systemic sclerosis, systemic, and discoid lupus erythematosus, rheumatoid arthritis, and dermatomyositis. Two additional groups, patients affected by inflammatory diseases (n=51) and healthy subjects (n=58) were studied as controls. The titers of anti-HHV-6 and anti-EBV antibodies were also evaluated. Cell-free HHV-6 serum viremia was detected in a significantly higher proportion of connective tissue diseases patients compared to controls (P<0.0002); a significant association between HHV-6 reactivation and the active disease state was found only for lupus erythematosus (P=0.021). By contrast, the rate of cell-free EBV viremia was similar in patients and controls groups. Cell-free CMV, HHV-8, and B19V viremia was not detected in any subject. Anti-HHV-6 and anti-EBV early antigen IgG titers were both significantly higher in autoimmune diseases patients as compared to healthy controls, although they were not associated with the presence of viremia. EBV, HHV-6, -7 prevalence and viral load in PBMCs of patients with connective tissue diseases and controls were similar. These data suggest that HHV-6 may act as a pathogenic factor predisposing patients to the development of autoimmune connective tissue diseases or, conversely, that these disorders may predispose patients to HHV-6 reactivation. J Med. Virol. 85:1925-1934, 2013. (c) 2013 Wiley Periodicals, Inc.
C1 [Broccolo, Francesco] Univ Milano Bicocca, Dept Hlth Sci, Milan, Italy.
   [Drago, Francesco; Parodi, Aurora] Univ Genoa, Dermatol Sect, Dept Endocrinol & Metab Sci, DiSEM, I-16132 Genoa, Italy.
   [Cassina, Giulia; Malnati, Mauro S.] Ist Sci San Raffaele, Unit Human Virol, I-20132 Milan, Italy.
   [Fava, Andrea; Sabbadini, Maria Grazia] Ist Sci San Raffaele, Unit Med & Clin Immunol, Div Immunol Transplantat & Infect Dis, I-20132 Milan, Italy.
   [Fusetti, Lisa; Matteoli, Barbara; Ceccherini-Nelli, Luca] Univ Pisa, Dept Expt Pathol, BMIE, Pisa, Italy.
   [Lusso, Paolo] NIAID, Sect Viral Pathogenesis, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
RP Broccolo, F (reprint author), Univ Milano Bicocca, Dept Publ Hlth, Lab Mol Microbiol & Virol, Via Cadore 48, I-20900 Monza, Italy.
EM francesco.broccolo@unimib.it; frdrago@libero.it
OI Parodi, Aurora/0000-0002-6622-2226; Broccolo,
   Francesco/0000-0002-9737-0459
NR 43
TC 9
Z9 11
U1 1
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0146-6615
EI 1096-9071
J9 J MED VIROL
JI J. Med. Virol.
PD NOV
PY 2013
VL 85
IS 11
BP 1925
EP 1934
DI 10.1002/jmv.23670
PG 10
WC Virology
SC Virology
GA 282UG
UT WOS:000329198500009
PM 23983182
ER

PT J
AU Kozmin, SG
   Stepchenkova, EI
   Chow, SC
   Schaaper, RM
AF Kozmin, Stanislav G.
   Stepchenkova, Elena I.
   Chow, Stephen C.
   Schaaper, Roel M.
TI A Critical Role for the Putative NCS2 Nucleobase Permease YjcD in the
   Sensitivity of Escherichia coli to Cytotoxic and Mutagenic Purine
   Analogs
SO MBIO
LA English
DT Article
ID BASE ANALOGS; GENE; K-12; 6-N-HYDROXYLAMINOPURINE; TRANSPORT; ADENINE;
   RESISTANCE; DEAMINASE; MUTATION; MUTANTS
AB The base analogs 6-N-hydroxylaminopurine (HAP) and 2-amino-HAP (AHAP) are potent mutagens in bacteria and eukaryotic organisms. Previously, we demonstrated that a defect in the Escherichia coli ycbX gene, encoding a molybdenum cofactor-dependent oxidoreductase, dramatically enhances sensitivity to the toxic and mutagenic action of these agents. In the present study, we describe the discovery and properties of a novel suppressor locus, yjcD, that strongly reduces the HAP sensitivity of the ycbX strain. Suppressor effects are also observed for other purine analogs, like AHAP, 6-mercaptopurine, 6-thioguanine, and 2-aminopurine. In contrast, the yjcD defect did not affect the sensitivity to the pyrimidine analog 5-fluorouracil. Homology searches have predicted that yjcD encodes a putative permease of the NCS2 family of nucleobase transporters. We further investigated the effects of inactivation of all other members of the NCS2 family, XanQ, XanP, PurP, UacT, UraA, RutG, YgfQ, YicO, and YbbY, and of the NCS1 family nucleobase permeases CodB and YbbW. None of these other defects significantly affected sensitivity to either HAP or AHAP. The combined data strongly suggest that YjcD is the primary importer for modified purine bases. We also present data showing that this protein may, in fact, also be a principal permease involved in transport of the normal purines guanine, hypoxanthine, and/or xanthine.
   IMPORTANCE Nucleotide metabolism is a critical aspect of the overall metabolism of the cell, as it is central to the core processes of RNA and DNA synthesis. At the same time, nucleotide metabolism can be subverted by analogs of the normal DNA or RNA bases, leading to highly toxic and mutagenic effects. Thus, understanding how cells process both normal and modified bases is of fundamental importance. This work describes a novel suppressor of the toxicity of certain modified purine bases in the bacterium Escherichia coli. This suppressor encodes a putative high-affinity nucleobase transporter that mediates the import of the modified purine bases. It is also a likely candidate for the long-sought high-affinity importer for the normal purines, like guanine and hypoxanthine.
C1 [Kozmin, Stanislav G.; Stepchenkova, Elena I.; Chow, Stephen C.; Schaaper, Roel M.] NIEHS, Mol Genet Lab, Res Triangle Pk, NC 27709 USA.
   [Kozmin, Stanislav G.] Duke Univ, Med Ctr, Dept Mol Genet & Microbiol, Durham, NC USA.
   [Stepchenkova, Elena I.] St Petersburg State Univ, Dept Genet & Biotechnol, St Petersburg 199034, Russia.
   [Stepchenkova, Elena I.] Russian Acad Sci, Inst Gen Genet, St Petersburg Branch, St Petersburg 196140, Russia.
RP Schaaper, RM (reprint author), NIEHS, Mol Genet Lab, Res Triangle Pk, NC 27709 USA.
EM schaaper@niehs.nih.gov
RI Kozmin, Stanislav/J-6849-2012; Stepchenkova, Elena/F-9931-2014
OI Kozmin, Stanislav/0000-0002-4128-4447; Stepchenkova,
   Elena/0000-0002-5854-8701
FU Intramural Research Program of the National Institute of Environmental
   Health Sciences (NIEHS) [ES050170]
FX This work was supported by project ES050170 of the Intramural Research
   Program of the National Institute of Environmental Health Sciences
   (NIEHS).
NR 34
TC 2
Z9 3
U1 1
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 2150-7511
J9 MBIO
JI mBio
PD NOV-DEC
PY 2013
VL 4
IS 6
AR e00661-13
DI 10.1128/mBio.00661-13
PG 7
WC Microbiology
SC Microbiology
GA 282LZ
UT WOS:000329174500012
PM 24169576
ER

PT J
AU Stepp, WH
   Meyers, JM
   McBride, AA
AF Stepp, Wesley H.
   Meyers, Jordan M.
   McBride, Alison A.
TI Sp100 Provides Intrinsic Immunity against Human Papillomavirus Infection
SO MBIO
LA English
DT Article
ID PML NUCLEAR-BODIES; HUMAN-CYTOMEGALOVIRUS-INFECTION;
   PROMYELOCYTIC-LEUKEMIA-PROTEIN; MINOR CAPSID PROTEIN; BOVINE
   PAPILLOMAVIRUS; MEDIATED REPRESSION; REPLICATION CYCLE; ANTIVIRAL
   DEFENSE; ONCOGENIC DOMAINS; ND10
AB Most DNA viruses associate with, and reorganize, nuclear domain 10 (ND10) bodies upon entry into the host nucleus. In this study, we examine the roles of the ND10 components PML, Sp100, and Daxx in the establishment of human papillomavirus type 18 (HPV18) infection of primary human keratinocytes. HPV18 DNA or HPV18 quasivirus was introduced into primary human keratinocytes depleted of each ND10 protein by small interfering RNA technology, and genome establishment was determined by using a quantitative immortalization assay and measurements of viral transcription and DNA replication. Keratinocyte depletion of Sp100 resulted in a substantial increase in the number of HPV18-immortalized colonies and a corresponding increase in viral transcription and DNA replication. However, Sp100 repressed viral transcription and replication only during the initial stages of viral establishment, suggesting that Sp100 acts as a repressor of incoming HPV DNA.
   IMPORTANCE The intrinsic immune system provides a first-line defense against invading pathogens. Host cells contain nuclear bodies (ND10) that are important for antiviral defense, yet many DNA viruses localize here upon cell entry. However, viruses also disrupt, reorganize, and modify individual components of the bodies. In this study, we show that one of the ND10 components, Sp100, limits the infection of human skin cells by human papillomavirus (HPV). HPVs are important pathogens that cause many types of infection of the cutaneous and mucosal epithelium and are the causative agents of several human cancers. Understanding how host cells counteract HPV infection could provide insight into antimicrobial therapies that could limit initial infection.
C1 [Stepp, Wesley H.; Meyers, Jordan M.; McBride, Alison A.] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
   [Stepp, Wesley H.] Georgetown Univ, Sch Med, Dept Microbiol & Immunol, Washington, DC USA.
RP McBride, AA (reprint author), NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
EM amcbride@nih.gov
OI McBride, Alison/0000-0001-5607-5157
FU Intramural Research Program of the NIAID, NIH
FX This work was funded by the Intramural Research Program of the NIAID,
   NIH.
NR 52
TC 11
Z9 11
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 2150-7511
J9 MBIO
JI mBio
PD NOV-DEC
PY 2013
VL 4
IS 6
AR e00845-13
DI 10.1128/mBio.00845-13
PG 13
WC Microbiology
SC Microbiology
GA 282LZ
UT WOS:000329174500028
PM 24194542
ER

PT J
AU Yao, YG
   Kajigaya, S
   Samsel, L
   McCoy, JP
   Torelli, G
   Young, NS
AF Yao, Yong-Gang
   Kajigaya, Sachiko
   Samsel, Leigh
   McCoy, J. Philip, Jr.
   Torelli, Giuseppe
   Young, Neal S.
TI Apparent mtDNA sequence heterogeneity in single human blood CD34(+)
   cells is markedly affected by storage and transport
SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS
LA English
DT Article
DE mtDNA; Single cell analysis; Mutation; Hematopoietic stem cell;
   Committed progenitors
ID FREE-RADICAL THEORY; MITOCHONDRIAL-DNA; VIABILITY; TRANSPLANTATION;
   GRANULOCYTES; TEMPERATURE; DISEASE
AB Single CD34(+) cells from adult human peripheral blood show mtDNA sequence heterogeneity. In this study, we compared mtDNA sequence variation in single CD34(+) cells from peripheral blood (PB) mononuclear cells (MNCs) from the same donors but under different conditions of storage and transport: group I, MNCs from heparinized PB that inadvertently required six days to be transported to the testing laboratory; group II, MNCs which were isolated from PB within a day of phlebotomy and frozen prior to transportation and storage. We observed more cell death for MNCs of group I than group II. Concordantly, group I CD34(+) cells had a very low potential for hematopoietic colony formation in vitro compared with group II cells. CD34(+) cells of group II showed an unexpectedly higher level of mtDNA sequence heterogeneity than was present in group I cells. These observations suggest that reduced mtDNA sequence heterogeneity in single CD34(+) cells of group I was likely due to elimination of cells harboring mutations. CD34+ cells that survive stress ex vivo may be more enriched in quiescent primitive hematopoietic stem cells, with fewer mtDNA mutations than are present in committed progenitors. Technically, attention is required to conditions of preparation of human blood samples for single cell mtDNA analysis. Published by Elsevier B.V.
C1 [Yao, Yong-Gang] Chinese Acad Sci & Yunnan Prov, Kunming Inst Zool, Key Lab Anim Models & Human Dis Mech, Kunming 650223, Yunnan, Peoples R China.
   [Yao, Yong-Gang; Kajigaya, Sachiko; Samsel, Leigh; McCoy, J. Philip, Jr.; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Yao, Yong-Gang; Kajigaya, Sachiko; Samsel, Leigh; McCoy, J. Philip, Jr.; Young, Neal S.] NHLBI, Flow Cytometry Core Facil, NIH, Bethesda, MD 20892 USA.
   [Torelli, Giuseppe] Univ Modena & Reggio Emilia, Dipartimento Oncol & Ematol, I-41100 Modena, Italy.
RP Yao, YG (reprint author), Chinese Acad Sci, Kunming Inst Zool, Key Lab Anim Models & Human Dis Mech, Kunming 650223, Yunnan, Peoples R China.
EM ygyaozh@gmail.com
FU NIH Research Program; National Natural Science Foundation of China
   [30925021, 31171225]; Yunnan Province [2009CI119]; Chinese Academy of
   Sciences
FX This study was supported by NIH Research Program. Y.-G.Y. was supported
   by the National Natural Science Foundation of China (30925021 and
   31171225), Yunnan Province (2009CI119) and the Chinese Academy of
   Sciences. Y.-G.Y. and N.S.Y. designed the research, Y.-G.Y., L.S., S.K.
   and J.P.M. performed the research, Y.-G.Y. and L.S. analyzed the data.
   Y.-G.Y., S.K. and N.S.Y. wrote the paper, G.T. contributed essential
   samples.
NR 22
TC 1
Z9 1
U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0027-5107
EI 1873-135X
J9 MUTAT RES-FUND MOL M
JI Mutat. Res.-Fundam. Mol. Mech. Mutagen.
PD NOV-DEC
PY 2013
VL 751
BP 36
EP 41
DI 10.1016/j.mrfmmm.2013.09.001
PG 6
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
GA 278FL
UT WOS:000328874500006
PM 24044942
ER

PT J
AU Papoti, D
   Yen, CCC
   Mackel, JB
   Merkle, H
   Silva, AC
AF Papoti, Daniel
   Yen, Cecil Chern-Chyi
   Mackel, Julie B.
   Merkle, Hellmut
   Silva, Afonso C.
TI An embedded four-channel receive-only RF coil array for fMRI experiments
   of the somatosensory pathway in conscious awake marmosets
SO NMR IN BIOMEDICINE
LA English
DT Article
DE animal models; marmosets; MRI; phased arrays; receive-only RF coils
ID ISOFLURANE-ANESTHETIZED RAT; FUNCTIONAL MRI; CONTRAST AGENT;
   RHESUS-MONKEYS; BRAIN ACTIVITY; IN-VIVO; CORTEX; NEUROSCIENCE;
   ACTIVATION; PRIMATES
AB fMRI has established itself as the main research tool in neuroscience and brain cognitive research. The common marmoset (Callithrix jacchus) is a non-human primate model of increasing interest in biomedical research. However, commercial MRI coils for marmosets are not generally available. The present work describes the design and construction of a four-channel receive-only surface RF coil array with excellent signal-to-noise ratio (SNR) specifically optimized for fMRI experiments in awake marmosets in response to somatosensory stimulation. The array was designed as part of a helmet-based head restraint system used to prevent motion during the scans. High SNR was obtained by building the coil array using a thin and flexible substrate glued to the inner surface of the restraint helmet, so as to minimize the distance between the array elements and the somatosensory cortex. Decoupling between coil elements was achieved by partial geometrical overlapping and by connecting them to home-built low-input-impedance preamplifiers. In vivo images show excellent coverage of the brain cortical surface with high sensitivity near the somatosensory cortex. Embedding the coil elements within the restraint helmet allowed fMRI data in response to somatosensory stimulation to be collected with high sensitivity and reproducibility in conscious, awake marmosets. Published 2013. This article is a U.S. Government work and is in the public domain in the USA.
C1 [Papoti, Daniel; Yen, Cecil Chern-Chyi; Mackel, Julie B.; Merkle, Hellmut; Silva, Afonso C.] NINDS, Cerebral Microcirculat Unit, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20892 USA.
RP Silva, AC (reprint author), NINDS, Cerebral Microcirculat Unit, Lab Funct & Mol Imaging, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM SilvaA@ninds.nih.gov
RI Yen, Cecil/C-2212-2009
OI Yen, Cecil/0000-0002-1519-9791
FU Intramural Research Program of the NIH, NINDS; Brazilian National
   Council for Scientific and Technological Development (CNPq)
   [207982/2012-0]
FX The authors are grateful to Xianfeng (Lisa) Zhang for her excellent
   technical skills, and to Dr Stephen Dodd for his help with assembly of
   the preamplifiers. This research was supported by the Intramural
   Research Program of the NIH, NINDS and partially supported by the
   Brazilian National Council for Scientific and Technological Development
   (CNPq) through the Science without Borders program (process No
   207982/2012-0).
NR 43
TC 6
Z9 6
U1 1
U2 12
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 NOV
PY 2013
VL 26
IS 11
BP 1395
EP 1402
DI 10.1002/nbm.2965
PG 8
WC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy
SC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy
GA 283DK
UT WOS:000329225200007
PM 23696219
ER

PT J
AU Hennekam, RC
   Biesecker, LG
   Allanson, JE
   Hall, JG
   Opitz, JM
   Temple, IK
   Carey, JC
AF Hennekam, Raoul C.
   Biesecker, Leslie G.
   Allanson, Judith E.
   Hall, Judith G.
   Opitz, John M.
   Temple, I. Karen
   Carey, John C.
CA Elements Morphology Consortium
TI Elements of Morphology: General Terms for Congenital Anomalies
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE nomenclature; definitions; genotype; phenotype; anomaly; variant;
   malformation; deformation; dysplasia; disruption; syndrome; sequence;
   association; morphology; dysmorphology
ID FETAL HEAD CONSTRAINT; STANDARD TERMINOLOGY; MALFORMATION SYNDROMES;
   FACIAL DIFFERENCES; CHARGE-SYNDROME; OLIGOHYDRAMNIOS; RECOMMENDATIONS;
   CLASSIFICATION; CRANIOSTENOSIS; NOMENCLATURE
AB An international group of clinicians working in the field of dysmorphology has established a process for the standardization of terms used to describe human morphology. The goals are to standardize these terms and develop consensus regarding their definitions. This project will increase the usefulness and precision of descriptions of the human phenotype and facilitate reliable comparisons of phenotypic findings among clinicians and researchers in medicine, developmental biology, and genetics. Here we define and illustrate the general terms that describe congenital anomalies as related to human conditions. (c) 2013 Wiley Periodicals, Inc.
C1 [Hennekam, Raoul C.] Univ Amsterdam, Acad Med Ctr, Dept Pediat, NL-1105 AZ Amsterdam, Netherlands.
   [Hennekam, Raoul C.] Univ Amsterdam, Acad Med Ctr, Dept Clin Genet, NL-1105 AZ Amsterdam, Netherlands.
   [Biesecker, Leslie G.] NHGRI, NIH, Bethesda, MD 20892 USA.
   [Allanson, Judith E.] Childrens Hosp Eastern Ontario, Dept Genet, Ottawa, ON K1H 8L1, Canada.
   [Hall, Judith G.] Univ British Columbia, Dept Med Genet, Vancouver, BC, Canada.
   [Hall, Judith G.] Univ British Columbia, Dept Pediat, Vancouver, BC V6T 1W5, Canada.
   [Hall, Judith G.] BC Childrens Hosp, Vancouver, BC, Canada.
   [Opitz, John M.; Carey, John C.] Univ Utah, Div Med Genet Human Genet Pathol Obstet & Gynecol, Salt Lake City, UT USA.
   [Temple, I. Karen] Univ Southampton, Fac Med, Southampton SO9 5NH, Hants, England.
   [Temple, I. Karen] Southampton Univ Hosp, Wessex Clin Genet Serv, Southampton, Hants, England.
RP Hennekam, RC (reprint author), AMC, Dept Pediat, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands.
EM r.c.hennekam@amc.uva.nl
RI temple, isabel/K-2391-2015
FU Intramural Research Program of the National Human
FX Grant sponsor: Intramural Research Program of the National Human
NR 54
TC 23
Z9 23
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
EI 1552-4833
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD NOV
PY 2013
VL 161
IS 11
SI SI
BP 2726
EP 2733
DI 10.1002/ajmg.a.36249
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 267ZP
UT WOS:000328137500009
PM 24124000
ER

PT J
AU Lin, AE
   Traum, AZ
   Sahai, I
   Keppler-Noreuil, K
   Kukolich, MK
   Adam, MP
   Westra, SJ
   Arts, HH
AF Lin, Angela E.
   Traum, Avram Z.
   Sahai, Inderneel
   Keppler-Noreuil, Kim
   Kukolich, Mary K.
   Adam, Margaret P.
   Westra, Sjirk J.
   Arts, Heleen H.
TI Sensenbrenner Syndrome (Cranioectodermal Dysplasia): Clinical and
   Molecular Analyses of 39 Patients Including Two New Patients
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE asphyxiating thoracic dystrophy; ciliopathy; cranioectodermal dysplasia;
   Jeune syndrome; sagittal craniosynostosis; Sensenbrenner syndrome; short
   rib-polydactyly syndromes
ID ASPHYXIATING THORACIC DYSTROPHY; TUBULOINTERSTITIAL NEPHROPATHY; JOUBERT
   SYNDROME; GAPO SYNDROME; MUTATIONS; PHENOTYPE; CILIOPATHIES; DISEASE;
   CRANIOSYNOSTOSIS; ABNORMALITIES
AB Sensenbrenner syndrome, also known as cranioectodermal dysplasia, is a rare multiple anomaly syndrome with distinctive craniofacial appearance, skeletal, ectodermal, connective tissue, renal, and liver anomalies. Dramatic advances with next-generation sequencing have expanded its phenotypic variability and molecular heterogeneity. We review 39 patients including two new patients, one with compound heterozygous novel mutations in WDR35 and a previously unreported multisutural craniosynostosis that may be a part of Sensenbrenner syndrome. In 14 of 25 (56.0%) patients pathogenic mutations have been identified in 4 different genes that regulate (intraflagellar) cilia transport. We compared Sensenbrenner syndrome to asphyxiating thoracic dystrophy-Jeune syndrome (ATD-JS) and other ciliopathies. Our analyses showed that the high anterior hairline, forehead bossing and dolichocephaly (accompanied by sagittal craniosynostosis in more than half of the patients) occur in almost all patients with Sensenbrenner syndrome. Metaphyseal dysplasia with narrow thorax, proximal limb shortness, and short fingers are typical of Sensenbrenner syndrome and ATD-JS. Respiratory complications have been reported in both syndromes, usually less severe with Sensenbrenner syndrome. Proposed diagnostic criteria for Sensenbrenner syndrome include the distinctive craniofacial appearance, ubiquitous brachydactyly and ectodermal anomalies, and sagittal craniosynostosis. Mild heart defects have been noted, but there have been no atrioventricular canal or heterotaxy defects that are common in Ellis-Van Creveld syndrome. We anticipate that the steady identification of molecularly defined patients may allow correlation of phenotype and genotype. Additional natural history data will improve genetic counseling and current guidelines. (c) 2013 Wiley Periodicals, Inc.
C1 [Lin, Angela E.; Sahai, Inderneel] MassGen Hosp Children, Boston, MA USA.
   [Traum, Avram Z.] MassGeneral Hosp Children, Dept Pediat, Pediat Nephrol Unit, Boston, MA USA.
   [Keppler-Noreuil, Kim] NHGRI, Genet Dis Res Branch, Human Dev Sect, NIH, Bethesda, MD 20892 USA.
   [Kukolich, Mary K.] Cook Childrens Hosp, Clin Genet Serv, Ft Worth, TX USA.
   [Adam, Margaret P.] Univ Washington, Div Med Genet, Seattle, WA 98195 USA.
   [Westra, Sjirk J.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
   [Arts, Heleen H.] Radboud Univ Nijmegen, Med Ctr, Dept Human Genet, NL-6525 ED Nijmegen, Netherlands.
RP Lin, AE (reprint author), Genet Unit, 185 Cambridge St,CPZN 2222, Boston, MA 02114 USA.
EM lin.angela@mgh.harvard.edu
FU Dutch Kidney Foundation [CP11.18]; Netherlands Organization for
   Scientific Research [NWO Veni-91613008]
FX H.H.A. is supported by grants from Dutch Kidney Foundation (CP11.18) and
   the Netherlands Organization for Scientific Research (NWO
   Veni-91613008). We express our deep gratitude to Dr. Friedhelm
   Hildebrandt from the Department of Pediatrics, University of Michigan
   (currently, Boston Children's Hospital, Boston, Massachusetts) for
   performing the molecular studies on the new patient 1. We thank Dr.
   Harald Jueppner, MD (Nephrology) and Barbara Luby, LICSW (Social
   Services) from the Mass-General Hospital for Children, and Meaghan Muir
   and her staff for research assistance at the Brigham and Women's
   Hospital. We thank Dr. Carlos Bacino from the Department of Molecular
   and Human Genetics, Baylor College of Medicine for assistance in
   interpreting the WES data on new patient 2.
NR 38
TC 15
Z9 15
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
EI 1552-4833
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD NOV
PY 2013
VL 161
IS 11
SI SI
BP 2762
EP 2776
DI 10.1002/ajmg.a.36265
PG 15
WC Genetics & Heredity
SC Genetics & Heredity
GA 267ZP
UT WOS:000328137500014
PM 24123776
ER

PT J
AU Absinta, M
   Sati, P
   Gaitan, MI
   Maggi, P
   Cortese, ICM
   Filippi, M
   Reich, DS
AF Absinta, Martina
   Sati, Pascal
   Gaitan, Maria I.
   Maggi, Pietro
   Cortese, Irene C. M.
   Filippi, Massimo
   Reich, Daniel S.
TI Seven-Tesla Phase Imaging of Acute Multiple Sclerosis Lesions: A New
   Window into the Inflammatory Process
SO ANNALS OF NEUROLOGY
LA English
DT Article
ID PYOGENIC BRAIN ABSCESSES; IN-VIVO; BIOPHYSICAL MECHANISMS; CORTICAL
   DEMYELINATION; 7 TESLA; PATHOLOGY; ANISOTROPY; CONTRAST; BARRIER; IRON
AB ObjectiveIn multiple sclerosis (MS), accurate, in vivo characterization of dynamic inflammatory pathological changes occurring in newly forming lesions could have major implications for understanding disease pathogenesis and mechanisms of tissue destruction. Here, we investigated the potential of ultrahigh-field magnetic resonance imaging (MRI; 7T), particularly phase imaging combined with dynamic contrast enhancement, to provide new insights in acute MS lesions.
   MethodsSixteen active MS patients were studied at 7T. Noncontrast, high-resolution T2* magnitude and phase scans, T1 scans before/after gadolinium contrast injection, and dynamic contrast-enhanced (DCE) T1 scans were acquired. T2*/phase features and DCE pattern were determined for acute and chronic lesions. When possible, 1-year follow-up 7T MRI was performed.
   ResultsOf 49 contrast-enhancing lesions, 44 could be analyzed. Centrifugal DCE lesions appeared isointense or hypointense on phase images, whereas centripetal DCE lesions showed thin, hypointense phase rims that clearly colocalized with the initial site of contrast enhancement. This pattern generally disappeared once enhancement resolved. Conversely, in 43 chronic lesions also selected for the presence of hypointense phase rims, the findings were stable over time, and the rims were typically thicker and darker. These considerations suggest different underlying pathological processes in the 2 lesion types.
   InterpretationUltrahigh-field MRI and, especially, phase contrast, are highly sensitive to tissue changes in acute MS lesions, which differ from the patterns seen in chronic lesions. In acute lesions, the hypointense phase rim reflects the expanding inflammatory edge and may directly correspond to inflammatory byproducts and sequelae of blood-brain barrier opening. Ann Neurol 2013;74:669-678
C1 [Absinta, Martina; Sati, Pascal; Gaitan, Maria I.; Maggi, Pietro; Cortese, Irene C. M.; Reich, Daniel S.] NINDS, Translat Neuroradiol Unit, NIH, Bethesda, MD 20852 USA.
   [Absinta, Martina; Filippi, Massimo] Univ Vita Salute San Raffaele, Inst Expt Neurol, San Raffaele Sci Inst, Neuroimaging Res Unit,Div Neurosci, Milan, Italy.
   [Maggi, Pietro] Univ Florence, Dept Neurosci Drug Res & Childs Hlth, Florence, Italy.
RP Reich, DS (reprint author), NINDS, Translat Neuroradiol Unit, NIH, 10 Ctr Dr MSC 1400,Bldg 10 Room 5C103, Bethesda, MD 20852 USA.
EM daniel.reich@nih.gov
RI Reich, Daniel/E-5701-2010
OI Reich, Daniel/0000-0002-2628-4334
FU NIH National Institute of Neurological Diseases and Stroke
FX The Intramural Research Program of the NIH National Institute of
   Neurological Diseases and Stroke supported this study.
NR 33
TC 33
Z9 33
U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0364-5134
EI 1531-8249
J9 ANN NEUROL
JI Ann. Neurol.
PD NOV
PY 2013
VL 74
IS 5
BP 669
EP 678
DI 10.1002/ana.23959
PG 10
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 273NX
UT WOS:000328543200007
PM 23813441
ER

PT J
AU Burbelo, PD
   Ragheb, JA
   Kapoor, A
   Zhang, YJ
AF Burbelo, Peter D.
   Ragheb, Jack A.
   Kapoor, Amit
   Zhang, Yanjin
TI The serological evidence in humans supports a negligible risk of
   zoonotic infection from porcine circovirus type 2
SO BIOLOGICALS
LA English
DT Article
DE Antibodies; Porcine circovirus; PCV-2; Seroepidemiology; Porcine-derived
   supplements
ID CATTLE; SEROCONVERSION; ANTIBODIES; VACCINES; DISEASE; ABSENCE; CANADA;
   PCV-2; FECES; ASSAY
AB There are two porcine circovirus (PCV) genotypes, PCV-1 and PCV-2. In pigs, PCV-1 infection is asymptomatic but PCV-2 infection can cause severe respiratory disease and other pathology. Although humans ingest PCV-contaminated foods and are exposed to PCV through other sources, the potential of PCV-2 as a zoonotic agent in humans and other species has not been fully explored. Here, four recombinant proteins derived from the PCV-2 capsid gene were examined as antigens using the Luciferase Immunoprecipitation System (LIPS) assay for serological analysis of PCV-2 infection. PCV-2-CAP-Delta 1 was the optimum recombinant protein in the LIPS assay with a sensitivity of 93% and specificity of 100% using porcine samples. Testing of healthy human blood donors, equine and bovine serum samples failed to demonstrate the presence of anti-PCV-2 antibodies. Additionally, analysis of two high-risk human groups, cystic fibrosis patients taking porcine derived oral supplements and type I diabetes patients who had undergone porcine islet cell transplantation, showed no evidence of anti-PCV-2 antibodies. These results extend the extensively demonstrated use of LIPS as a robust approach for identifying humoral responses and provide evidence that PCV-2 is likely not infectious in humans. Published by Elsevier Ltd on behalf of The International Alliance for Biological Standardization.
C1 [Burbelo, Peter D.] Natl Inst Dent & Craniofacial Res, Clin Dent Res Core, NIH, Bethesda, MD 20892 USA.
   [Ragheb, Jack A.] US FDA, Div Therapeut Prot, OBP OPS, CDER, Bethesda, MD 20892 USA.
   [Kapoor, Amit] Columbia Univ, Ctr Infect & Immun, New York, NY 10032 USA.
   [Zhang, Yanjin] Univ Maryland, Dept Vet Med, College Pk, MD 20742 USA.
RP Burbelo, PD (reprint author), NIH, 10 Ctr Dr,Bldg 10,Rm 1N102, Bethesda, MD 20892 USA.
EM burbelop@nidcr.nih.gov
FU Division of Intramural Research, National Institute of Dental and
   Craniofacial Research, NIH; CDER, Food and Drug Administration; NIH
   [AI090196, AI081132]; University of Maryland
FX This work was supported by the Division of Intramural Research, National
   Institute of Dental and Craniofacial Research, NIH and the CDER, Food
   and Drug Administration and from NIH grants AI090196, AI081132 and
   funding from the University of Maryland. We thank Haicheng Song and
   Chinta Lamichhane at Synbiotics for supplying the porcine serum samples
   and ELISA results for the samples. We are indebted to Michael Konstan
   (Case Western Reserve University) for making available the cystic
   fibrosis serum samples and to Annika Tibell (Karolinska Univ), Bill
   Switzer and Walid Heneine (CDC) for the xenotransplant serum samples. We
   also thank Shasta McClenahan and Phil Krause (FDA) for the PCV-1
   anti-serum.
NR 30
TC 5
Z9 5
U1 0
U2 3
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1045-1056
EI 1095-8320
J9 BIOLOGICALS
JI Biologicals
PD NOV
PY 2013
VL 41
IS 6
BP 430
EP 434
DI 10.1016/j.biologicals.2013.09.005
PG 5
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
   Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Pharmacology & Pharmacy
GA 274HG
UT WOS:000328596800013
PM 24120888
ER

PT J
AU Mahnke, YD
   Brodie, TM
   Sallusto, F
   Roederer, M
   Lugli, E
AF Mahnke, Yolanda D.
   Brodie, Tess M.
   Sallusto, Federica
   Roederer, Mario
   Lugli, Enrico
TI The who's who of T-cell differentiation: Human memory T-cell subsets
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Review
DE Flow cytometry; Human T-cell subsets; Memory T-cell differentiation;
   Naive T cells
ID CHEMOKINE RECEPTOR EXPRESSION; FLOW-CYTOMETRY; HUMAN NAIVE; PHENOTYPIC
   CLASSIFICATION; LYMPHOCYTE RECIRCULATION; MONOCLONAL-ANTIBODY; EFFECTOR
   FUNCTIONS; NONHUMAN-PRIMATES; HOMING RECEPTOR; GENE-EXPRESSION
AB Following antigen encounter and subsequent resolution of the immune response, a single naive T cell is able to generate multiple subsets of memory T cells with different phenotypic and functional properties and gene expression profiles. Single-cell technologies, first and foremost flow cytometry, have revealed the complex heterogeneity of the memory T-cell compartment and its organization into subsets. However, a consensus has still to be reached, both at the semantic (nomenclature) and phenotypic level, regarding the identification of these subsets. Here, we review recent developments in the characterization of the heterogeneity of the memory T-cell compartment, and propose a unified classification of both human and nonhuman primate T cells on the basis of phenotypic traits and in vivo properties. Given that vaccine studies and adoptive cell transfer immunotherapy protocols are influenced by these recent findings, it is important to use uniform methods for identifying and discussing functionally distinct subsets of T cells.
C1 [Mahnke, Yolanda D.] Univ Penn, Perelman Sch Med, Abramson Family Canc Res Ctr, Translat & Correlat Studies Lab, Philadelphia, PA 19104 USA.
   [Brodie, Tess M.; Sallusto, Federica] Inst Res Biomed, Bellinzona, Switzerland.
   [Roederer, Mario] NIAID, ImmunoTechnol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
   [Lugli, Enrico] Humanitas Clin & Res Ctr, Unit Clin & Expt Immunol, I-20089 Rozzano, MI, Italy.
RP Lugli, E (reprint author), Humanitas Clin & Res Ctr, Unit Clin & Expt Immunol, Via Manzoni 56, I-20089 Rozzano, MI, Italy.
EM roederer@nih.gov; enrico.lugli@humanitasresearch.it
RI Chiang, Vincent, Ming-Hsien/D-4312-2016
OI Chiang, Vincent, Ming-Hsien/0000-0002-2029-7863
FU Associazione Italiana per la Ricerca sul Cancro [MFAG10607]; Fondazione
   Cariplo [2012/0683]; European Community [322093]; NIAID Intramural
   Research Programs at the NIH; Swiss National Science Foundation
   [131092]; European Commission [FP7-HEALTH-F3-2009-241745]
FX We would like to apologize to those colleagues whose work could not be
   cited due to space constraints. The work in the authors' laboratories is
   supported by grants from the Associazione Italiana per la Ricerca sul
   Cancro (MFAG10607 to E.L.), Fondazione Cariplo (2012/0683 to E.L.), the
   European Community (Marie Curie Career Integration Grant 322093 to
   E.L.), the NIAID Intramural Research Programs at the NIH, and the Swiss
   National Science Foundation (131092 to F.S.) and the European Commission
   (FP7-HEALTH-F3-2009-241745 to F.S.).
NR 111
TC 87
Z9 91
U1 6
U2 23
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2980
EI 1521-4141
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD NOV
PY 2013
VL 43
IS 11
BP 2797
EP 2809
DI 10.1002/eji.201343751
PG 13
WC Immunology
SC Immunology
GA 267CL
UT WOS:000328074000020
PM 24258910
ER

PT J
AU Hickman, HD
   Yewdell, JW
AF Hickman, Heather D.
   Yewdell, Jonathan W.
TI Going Pro to enhance T-cell immunogenicity: Easy as pi?
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Editorial Material
DE Altered peptide ligand; MHC class I; Peptide; Tumor-associated Ag
ID MHC CLASS-I; NON-ANCHOR RESIDUES; PEPTIDE GENERATION; ANTIGENIC
   PEPTIDES; PROTEIN-SYNTHESIS; BINDING; RECOGNITION; TRANSLATION;
   MOLECULES; AFFINITY
AB MHC class I molecules bind intracellular oligopeptides and present them on the cell surface for CD8(+) T-cell activation and recognition. Strong peptide/MHC class I (pMHC) interactions typically induce the best CD8(+) T-cell responses; however, many immunotherapeutic tumor-specific peptides bind MHC with low affinity. To overcome this, immunologists can carefully alter peptides for enhanced MHC affinity but often at the cost of decreased T-cell recognition. A new report published in this issue of the European Journal of Immunology [Eur. J. Immunol. 2013. 43:3051-3060] shows that the substitution of proline at the third residue (p3P) of a common tumor peptide increases pMHC affinity and complex stability while enhancing T-cell receptor recognition. X-ray crystallography indicates that stability is generated through newly introduced CH-pi bonding between p3P and a conserved residue (Y159) in the MHC heavy chain. This finding highlights a previously unappreciated role for CH-pi bonding in MHC peptide binding, and importantly, arms immunologists with a novel and possibly general approach for increasing pMHC stability without compromising T-cell recognition.
C1 [Hickman, Heather D.; Yewdell, Jonathan W.] NIAID, Viral Dis Lab, Bethesda, MD 20892 USA.
RP Yewdell, JW (reprint author), NIAID, Viral Dis Lab, NIH Bldg 33,Room 2E13C-1,33 North Dr,MSTP 3209, Bethesda, MD 20892 USA.
EM jwyewdell@mail.nih.gov
FU Intramural NIH HHS [Z01 AI000542-20]
NR 26
TC 3
Z9 3
U1 1
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2980
EI 1521-4141
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD NOV
PY 2013
VL 43
IS 11
BP 2814
EP 2817
DI 10.1002/eji.201344095
PG 4
WC Immunology
SC Immunology
GA 267CL
UT WOS:000328074000002
PM 24155147
ER

PT J
AU Novelli, EM
   Kato, GJ
   Hildesheim, ME
   Barge, S
   Meyer, MP
   Lozier, J
   Hassett, AC
   Ragni, MV
   Isenberg, JS
   Gladwin, MT
AF Novelli, Enrico M.
   Kato, Gregory J.
   Hildesheim, Mariana E.
   Barge, Suchitra
   Meyer, Michael P.
   Lozier, Jay
   Hassett, Andrea Cortese
   Ragni, Margaret V.
   Isenberg, Jeffrey S.
   Gladwin, Mark T.
TI Thrombospondin-1 inhibits ADAMTS13 activity in sickle cell disease
SO HAEMATOLOGICA
LA English
DT Letter
DE sickle cell disease; ADAMTS13; acute chest syndrome
ID THROMBOTIC THROMBOCYTOPENIC PURPURA; ACUTE CHEST SYNDROME; PLASMA;
   PATIENT; CRISIS; VWF
C1 [Novelli, Enrico M.] Univ Pittsburgh, Vasc Med Inst, Div Hematol Oncol, Pittsburgh, PA 15260 USA.
   [Kato, Gregory J.; Lozier, Jay] NHLBI, Sickle Cell Vasc Dis Sect, NIH, Bethesda, MD 20892 USA.
   [Hildesheim, Mariana E.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Barge, Suchitra; Ragni, Margaret V.; Isenberg, Jeffrey S.; Gladwin, Mark T.] Univ Pittsburgh, Vasc Med Inst, Div Pulm Allergy Crit Care Med, Pittsburgh, PA USA.
   [Meyer, Michael P.; Hassett, Andrea Cortese] ITXM Diagnost, Pittsburgh, PA USA.
RP Novelli, EM (reprint author), Univ Pittsburgh, Vasc Med Inst, Div Hematol Oncol, Pittsburgh, PA 15260 USA.
EM novellie@upmc.edu
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
FU NHLBI NIH HHS [K23 HL112848]
NR 15
TC 6
Z9 6
U1 1
U2 2
PU FERRATA STORTI FOUNDATION
PI PAVIA
PA VIA GIUSEPPE BELLI 4, 27100 PAVIA, ITALY
SN 0390-6078
J9 HAEMATOLOGICA
JI Haematologica
PD NOV
PY 2013
VL 98
IS 11
BP E132
EP E134
DI 10.3324/haematol.2013.092635
PG 3
WC Hematology
SC Hematology
GA 273OF
UT WOS:000328544100001
PM 24186313
ER

PT J
AU Johnson, RA
   Barrett, MS
   Sisti, DA
AF Johnson, Rebecca A.
   Barrett, Marna S.
   Sisti, Dominic A.
TI The Ethical Boundaries of Patient and Advocate Influence on DSM-5
SO HARVARD REVIEW OF PSYCHIATRY
LA English
DT Article
DE Diagnostic and Statistical Manual of Mental Disorders; ethics; mental
   disorders; patient advocacy; social stigma
ID PSYCHOSIS RISK SYNDROME; MENTAL-ILLNESS; DIAGNOSTIC-CRITERIA;
   DECISION-MAKING; UNITED-STATES; HEALTH; DISORDER; HEBEPHILIA; POLICY;
   CLASSIFICATION
AB This article discusses the relationship between disease-advocacy groups and the revision process for the Diagnostic and Statistical Manual of Mental Disorders. We discuss three examples in which patient-advocacy groups engaged with the DSM-5 revision process: Autism Speaks' worries about the contraction of the autism diagnostic category, the National Alliance on Mental Illness's support for the inclusion of psychosis risk syndrome, and B4U-ACT's critique of the expansion of pedophilia. After a descriptive examination of the cases, we address two prescriptive questions. First, what is the ethical basis for patient and advocate influence on DSM diagnoses? Second, how should the American Psychiatric Association proceed when this influence comes into conflict with other goals of the revision process? We argue that the social effects of, and values embedded in, psychiatric classification, combined with patient and advocates' experiential knowledge about those aspects of diagnosis, ethically justify advocate influence in relation to those particular matters. However, this advocate influence ought to have limits, which we briefly explore. Our discussion has implications for discussions of disease categories as loci for social movements, for analyses of the expanding range of processes and institutions that advocacy groups target, and for broader questions regarding the aims of the DSM revision process.
C1 [Johnson, Rebecca A.] Univ Penn, Perelman Sch Med, Dept Bioeth, NIH, Philadelphia, PA 19104 USA.
   [Johnson, Rebecca A.; Sisti, Dominic A.] Univ Penn, Perelman Sch Med, Scattergood Program Appl Eth Behav Healthcare, Dept Med Eth & Hlth Policy, Philadelphia, PA 19104 USA.
   [Barrett, Marna S.] Univ Penn, Perelman Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA.
RP Johnson, RA (reprint author), 10 Ctr Dr,Rm 1C118, Bethesda, MD 20892 USA.
EM BJohnson88@gmail.com
OI Sisti, Dominic/0000-0002-2282-9253
NR 68
TC 3
Z9 3
U1 3
U2 17
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1067-3229
EI 1465-7309
J9 HARVARD REV PSYCHIAT
JI Harv. Rev. Psychiatr.
PD NOV-DEC
PY 2013
VL 21
IS 6
BP 334
EP 344
DI 10.1097/HRP.0000000000000010
PG 11
WC Psychiatry
SC Psychiatry
GA 273BE
UT WOS:000328507000004
PM 24201823
ER

PT J
AU Bornstein, MH
   Hendricks, C
AF Bornstein, Marc H.
   Hendricks, Charlene
TI Screening for developmental disabilities in developing countries
SO SOCIAL SCIENCE & MEDICINE
LA English
DT Article
DE Child development; Developmental disabilities; Developing countries;
   Risk factors; Policy making; Human development index
ID CHILDHOOD DISABILITY; 10 QUESTIONS; CHILDREN; RELIABILITY; PREVENTION;
   BANGLADESH; VALIDITY
AB Despite waxing international interest in child disability, little information exists about the situation of children with disabilities in developing countries. Using a culture-free screen for child disability from the 2005-2007 Multiple Indicator Cluster Survey, this study reports percentages of children in 16 developing countries who screened positive for cognitive, language, sensory, and motor disabilities, covariation among disabilities, deviation contrasts that compare each country to the overall effect of country (including effects of age and gender and their interactions), and associations of disabilities with the Human Development Index. Developmental disabilities vary by child age and country, and younger children in developing countries with lower standards of living are more likely to screen positive for disabilities. The discussion of these findings revolves around research and policy implications. Published by Elsevier Ltd.
C1 [Bornstein, Marc H.; Hendricks, Charlene] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Publ Hlth Serv, Bethesda, MD USA.
RP Bornstein, MH (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Suite 8030,6705 Rockledge Dr, Bethesda, MD 20892 USA.
EM Marc_H_Bornstein@nih.gov
FU NIH, NICHD
FX We thank D. Breakstone, P. Horn, and C. Padilla. The authors contributed
   equally to the work, and authorship is alphabetical. This research was
   supported by the Intramural Research Program of the NIH, NICHD.
NR 42
TC 7
Z9 7
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0277-9536
J9 SOC SCI MED
JI Soc. Sci. Med.
PD NOV
PY 2013
VL 97
SI SI
BP 307
EP 315
DI 10.1016/j.socscimed.2012.09.049
PG 9
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA 264WG
UT WOS:000327911100036
PM 23294875
ER

PT J
AU Belle, SH
   Berk, PD
   Chapman, WH
   Christian, NJ
   Courcoulas, AP
   Dakin, GF
   Flum, DR
   Horlick, M
   King, WC
   McCloskey, CA
   Mitchell, JE
   Patterson, EJ
   Pender, JR
   Steffen, KJ
   Thirlby, RC
   Wolfe, BM
   Yanovski, SZ
AF Belle, Steven H.
   Berk, Paul D.
   Chapman, William H.
   Christian, Nicholas J.
   Courcoulas, Anita P.
   Dakin, Greg F.
   Flum, David R.
   Horlick, Mary
   King, Wendy C.
   McCloskey, Carol A.
   Mitchell, James E.
   Patterson, Emma J.
   Pender, John R.
   Steffen, Kristine J.
   Thirlby, Richard C.
   Wolfe, Bruce M.
   Yanovski, Susan Z.
CA LABS Consortium
TI Baseline characteristics of participants in the Longitudinal Assessment
   of Bariatric Surgery-2 (LABS-2) study
SO SURGERY FOR OBESITY AND RELATED DISEASES
LA English
DT Article
DE Obesity; Bariatric surgery; Sex differences
ID GASTRIC BYPASS-SURGERY; QUALITY-OF-LIFE; PHYSICAL-ACTIVITY; OBESITY;
   HEALTH; PREVALENCE; TRENDS; CANDIDATES; DEPRESSION; INVENTORY
C1 [Belle, Steven H.; Christian, Nicholas J.; King, Wendy C.] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA 15261 USA.
   [Berk, Paul D.] Columbia Univ, Med Ctr, New York, NY USA.
   [Chapman, William H.; Pender, John R.] E Carolina Univ, Greenville, NC USA.
   [Courcoulas, Anita P.; McCloskey, Carol A.] Univ Pittsburgh, Med Ctr, Pittsburgh, PA 15261 USA.
   [Dakin, Greg F.] Weill Cornell Univ, Med Ctr, New York, NY USA.
   [Flum, David R.] Univ Washington, Seattle, WA 98195 USA.
   [Horlick, Mary; Yanovski, Susan Z.] NIDDK, Bethesda, MD 20892 USA.
   [Mitchell, James E.; Steffen, Kristine J.] Neuropsychiat Res Inst, Fargo, ND USA.
   [Patterson, Emma J.] Legacy Good Samaritan Hosp, Portland, OR USA.
   [Thirlby, Richard C.] Virginia Mason Med Ctr, Seattle, WA 98101 USA.
   [Wolfe, Bruce M.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
RP Belle, SH (reprint author), Univ Pittsburgh, Epidemiol Data Ctr, 127 Parran Hall,130 DeSoto St, Pittsburgh, PA 15261 USA.
EM belle@edc.pitt.edu
OI King, Wendy/0000-0002-0740-0029
FU National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
   [DCC -U01 DK066557, U01-DK66667]; Cornell University Medical Center CTSC
   [UL1-RR024996, U01-DK66568]; CTRC [M01RR-00037, UL1-RR024153];
   Neuropsychiatric Research Institute [U01-DK66471]; East Carolina
   University [U01-DK66526]; University of Pittsburgh Medical Center
   [U01-DK66585]; Oregon Health & Science University [U01-DK66555]
FX This clinical study was a cooperative agreement funded by the National
   Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Grant
   numbers: DCC -U01 DK066557; Columbia - U01-DK66667 (in collaboration
   with Cornell University Medical Center CTSC, Grant UL1-RR024996);
   University of Washington - U01-DK66568 (in collaboration with CTRC,
   Grant M01RR-00037); Neuropsychiatric Research Institute - U01-DK66471;
   East Carolina University U01-DK66526; University of Pittsburgh Medical
   Center U01-DK66585 (in collaboration with CTRC, Grant UL1-RR024153);
   Oregon Health & Science University U01-DK66555.
NR 36
TC 33
Z9 33
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1550-7289
EI 1878-7533
J9 SURG OBES RELAT DIS
JI Surg. Obes. Relat. Dis.
PD NOV-DEC
PY 2013
VL 9
IS 6
BP 926
EP 935
DI 10.1016/j.soard.2013.01.023
PG 10
WC Surgery
SC Surgery
GA 275ZV
UT WOS:000328718800019
PM 23602493
ER

PT J
AU Magill, SS
   Klompas, M
   Balk, R
   Burns, SM
   Deutschman, CS
   Diekema, D
   Fridkin, S
   Greene, L
   Guh, A
   Gutterman, D
   Hammer, B
   Henderson, D
   Hess, DR
   Hill, NS
   Horan, T
   Kollef, M
   Levy, M
   Septimus, E
   VanAntwerpen, C
   Wright, D
   Lipsett, P
AF Magill, Shelley S.
   Klompas, Michael
   Balk, Robert
   Burns, Suzanne M.
   Deutschman, Clifford S.
   Diekema, Daniel
   Fridkin, Scott
   Greene, Linda
   Guh, Alice
   Gutterman, David
   Hammer, Beth
   Henderson, David
   Hess, Dean R.
   Hill, Nicholas S.
   Horan, Teresa
   Kollef, Marin
   Levy, Mitchell
   Septimus, Edward
   VanAntwerpen, Carole
   Wright, Don
   Lipsett, Pamela
TI DEVELOPING A NEW, NATIONAL APPROACH TO SURVEILLANCE FOR
   VENTILATOR-ASSOCIATED EVENTS
SO AMERICAN JOURNAL OF CRITICAL CARE
LA English
DT Article
AB This article is an executive summary of a report from the Centers for Disease Control and Prevention Ventilator-Associated Pneumonia Surveillance Definition Working Group, entitled "Developing a New, National Approach to Surveillance for Ventilator-Associatied Events,"
C1 [Magill, Shelley S.; Fridkin, Scott; Guh, Alice; Horan, Teresa] Ctr Dis Control & Prevent, Div Healthcare Qual Promot, Atlanta, GA 30329 USA.
   [Klompas, Michael] Harvard Univ, Sch Med, Dept Populat Med, Boston, MA USA.
   [Klompas, Michael] Harvard Pilgrim Hlth Care Inst, Boston, MA USA.
   [Klompas, Michael] Brigham & Womens Hosp, Infect Control Dept, Boston, MA 02115 USA.
   [Klompas, Michael] Soc Healthcare Epidemiol Amer, Arlington, VA USA.
   [Balk, Robert] Rush Univ, Sch Med, Div Pulm & Crit Care Med, Chicago, IL 60612 USA.
   [Burns, Suzanne M.] Univ Virginia, Sch Nursing Crit & Acute Care, Charlottesville, VA USA.
   [Deutschman, Clifford S.] Univ Penn, Dept Anesthesiol & Crit Care, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Diekema, Daniel] Univ Iowa, Carver Coll Med, Div Infect Dis, Iowa City, IA USA.
   [Diekema, Daniel] Healthcare Infect Control Practices Advisory Comm, Atlanta, GA USA.
   [Greene, Linda] Rochester Gen Hlth Syst, Infect Prevent & Control Dept, Rochester, NY USA.
   [Greene, Linda] Assoc Profess Infect Control & Epidemiol, Washington, DC USA.
   [Gutterman, David] Med Coll Wisconsin, Dept Med, Milwaukee, WI 53226 USA.
   [Hammer, Beth] Zablocki VA Med Ctr, Dept Cardiol, Milwaukee, WI USA.
   [Henderson, David] NIH, Hosp Epidemiol & Qual Improvement, Ctr Clin, Bethesda, MD 20892 USA.
   [Hess, Dean R.] Massachusetts Gen Hosp, Dept Resp Care, Boston, MA 02114 USA.
   [Hess, Dean R.] Harvard Univ, Sch Med, Dept Anesthesia, Boston, MA 02115 USA.
   [Hess, Dean R.] Amer Assoc Resp Care, Irving, TX USA.
   [Hill, Nicholas S.] Tufts Med Ctr, Div Pulm & Crit Care Med, Boston, MA USA.
   [Kollef, Marin] Washington Univ, Div Pulm & Crit Care Med, St Louis, MO USA.
   [Levy, Mitchell] Brown Univ, Rhode Isl Hosp, Warren Alpert Med Sch, Div Pulm Crit Care & Sleep, Providence, RI 02903 USA.
   [Septimus, Edward] Texas A&M Hlth Sci Ctr, Dept Internal Med, College Stn, TX USA.
   [Septimus, Edward] Infect Dis Soc Amer, Arlington, VA USA.
   [VanAntwerpen, Carole] New York State Dept Hlth, Bur Healthcare Associated Infect, Albany, NY 12237 USA.
   [VanAntwerpen, Carole] Council State & Terr Epidemiologists, Atlanta, GA USA.
   [Wright, Don] US Dept HHS, Off Dis Prevent & Hlth Promot, Washington, DC 20201 USA.
   [Lipsett, Pamela] Johns Hopkins Univ, Sch Med, Dept Surg Anesthesiol & Crit Care Med, Baltimore, MD USA.
RP Magill, SS (reprint author), Ctr Dis Control & Prevent, Div Healthcare Qual Promot, 1600 Clifton Rd,MS A-24, Atlanta, GA 30329 USA.
EM smagill@cdc.gov
FU Centers for Disease Control and Prevention (CDC), Atlanta, Georgia; CDC;
   US Food and Drug Administration; Office of the National Coordinator for
   Health Information Technology; National Institute of General Medical
   Sciences; Merck; Cerexa; bioMeriuex; PurThread Technologies; Pfizer;
   Society of Healthcare Epidemiologists of America; Elsevier; McGraw-Hill;
   Up-To-Date; Jones and Bartlett
FX This work was supported by the Centers for Disease Control and
   Prevention (CDC), Atlanta, Georgia. Dr Klompas received grant support
   from the CDC, US Food and Drug Administration, and the Office of the
   National Coordinator for Health Information Technology. Dr Balk received
   grant support from the CDC and bioMerieux for participation in the EPIC
   CAP study (CDC) and the Procalcitonin in ICU antibiotic stewardship
   study (CDC and bioMerieux). Dr Deutschman received grant support from
   the National Institute of General Medical Sciences. Dr Diekema received
   grant support from Merck, Cerexa, bioMeriuex, PurThread Technologies,
   and Pfizer. Ms Greene consults for INC. Dr. Hess consulted for Philips
   Respironics, ResMed, Pari, and Breathe and received honoraria from
   Covidien and Maquet. Ms Greene lectured for Premier, Advanced
   Sterilization Products, and APIC. Dr Burns lectured for AACN. Ms Greene
   presented speeches for Covidien and Maquet. Dr Septimus received an
   honorarium for a lecture. Dr. Klompas received support from the Society
   of Healthcare Epidemiologists of America for the development of
   educational presentations. Dr Deutschman received royalties from
   Elsevier for the textbook, Evidence-based Practice of Critical Care
   Medicine. Dr Burns receives royalties from McGraw-Hill for books
   endorsed by AACN. Ms Greene receives royalties from Up-To-Date, Jones
   and Bartlett, and McGraw-Hill. The remaining authors have disclosed that
   they do not have any potential conflicts of interest.
NR 2
TC 10
Z9 10
U1 1
U2 3
PU AMER ASSOC CRITICAL CARE NURSES
PI ALISO VIEJO
PA 101 COLUMBIA, ALISO VIEJO, CA 92656 USA
SN 1062-3264
EI 1937-710X
J9 AM J CRIT CARE
JI Am. J. Crit. Care
PD NOV 1
PY 2013
VL 22
IS 6
BP 469
EP 473
DI 10.4037/ajcc2013893
PG 5
WC Critical Care Medicine; Nursing
SC General & Internal Medicine; Nursing
GA 268KB
UT WOS:000328167700007
PM 24186816
ER

PT J
AU Xiao, Q
   Yang, HP
   Wentzensen, N
   Hollenbeck, A
   Matthews, CE
AF Xiao, Qian
   Yang, Hannah P.
   Wentzensen, Nicolas
   Hollenbeck, Albert
   Matthews, Charles E.
TI Physical Activity in Different Periods of Life, Sedentary Behavior, and
   the Risk of Ovarian Cancer in the NIH-AARP Diet and Health Study
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID BREAST-CANCER; LARGE COHORT; WOMEN; PROGESTERONE; PREVENTION; EXERCISE;
   EPIDEMIOLOGY; ASSOCIATION; MECHANISMS; ANDROGENS
AB Background: Physical activity and sedentary behavior may influence ovarian cancer risk, but clear evidence is lacking.
   Methods: We prospectively investigated the relations of self-reported physical activity and sedentary behavior to ovarian cancer incidence in a cohort of 148,892 U.S. women ages 50-71 years at baseline (1995-1996), who were followed through 2006. Multivariate Cox proportional hazard models were used to estimate relative risks (RR) and 95% confidence intervals (CI). We also conducted analysis by hormone use, body mass index (BMI), and cancer subtype.
   Results: We identified 753 incident epithelial ovarian cancers. Overall, neither physical activity nor sedentary behavior at baseline was associated with ovarian cancer risk. Compared with women who never or rarely engaged in vigorous physical activity in the past year, women who reported more than 5 times/week of vigorous physical activity had an RR of 1.05 (95% CI, 0.84-1.32). Women who sat 7+ hours/day had an RR of 1.05 (95% CI, 0.80-1.37) compared with those reporting <3 hours of sitting. The associations were not modified by hormone use or BMI and were similar for both serous and non-serous subtypes.
   Conclusions: Physical activity and sedentary behavior in middle and older ages were not associated with ovarian cancer risk.
   Impact: We found no clear support for a role of physical activity and sedentary behavior in ovarian cancer risk. (C) 2013 AACR.
C1 [Xiao, Qian; Matthews, Charles E.] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Yang, Hannah P.; Wentzensen, Nicolas] NCI, Hormonal & Reprod Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Hollenbeck, Albert] AARP, Washington, DC USA.
RP Xiao, Q (reprint author), NCI, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr, Rockville, MD 20850 USA.
EM qian.xiao@nih.gov
RI matthews, Charles/E-8073-2015
OI matthews, Charles/0000-0001-8037-3103
FU Intramural Research Program of the NIH, National Cancer Institute,
   Department of Health and Human Services
FX This research was supported by the Intramural Research Program of the
   NIH, National Cancer Institute, Department of Health and Human Services.
NR 45
TC 11
Z9 11
U1 1
U2 9
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 NOV
PY 2013
VL 22
IS 11
BP 2000
EP 2008
DI 10.1158/1055-9965.EPI-13-0154
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 262ID
UT WOS:000327726800009
PM 23966580
ER

PT J
AU Hernandez, BY
   Zhu, XM
   Kwee, S
   Chan, OTM
   Tsai, N
   Okimoto, G
   Horio, D
   McGlynn, KA
   Altekruse, S
   Wong, LL
AF Hernandez, Brenda Y.
   Zhu, Xuemei
   Kwee, Sandi
   Chan, Owen T. M.
   Tsai, Naoky
   Okimoto, Gordon
   Horio, David
   McGlynn, Katherine A.
   Altekruse, Sean
   Wong, Linda L.
TI Viral Hepatitis Markers in Liver Tissue in Relation to Serostatus in
   Hepatocellular Carcinoma
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID B-VIRUS-INFECTION; UNITED-STATES; C VIRUS; INCREASING INCIDENCE;
   INSULIN-RESISTANCE; SUSTAINED RESPONSE; METABOLIC FACTORS;
   SURFACE-ANTIGEN; RISK-FACTORS; OCCULT
AB Background: Hepatocellular carcinoma (HCC) incidence is increasing in the United States. Hepatitis B virus (HBV) and hepatitis C virus (HCV) are major causes of HCC. Hepatitis infection in patients with HCC is generally diagnosed by serology, which is not always consistent with the presence of HBV and HCV in the liver. The relationship of liver viral status to serostatus in hepatocarcinogenesis is not fully understood.
   Methods: HBV and HCV were evaluated in formalin-fixed, paraffin-embedded liver tissue specimens in a retrospective study of 61 U. S. HCC cases of known serologic status. HBV DNA and HCV RNA were detected by PCR, reverse transcription PCR (RT-PCR), and pyrosequencing, and HBsAg and HBcAg were evaluated by immunohistochemistry.
   Results: Viral markers were detected in the liver tissue of 25 of 61 (41%) HCC cases. Tissue viral and serologic status were discordant in 27 (44%) cases, including those with apparent "occult" infection. Specifically, HBV DNA was detected in tissue of 4 of 39 (10%) serum HBsAg (-) cases, including 1 anti-HCV(+) case; and HCV RNA was detected in tissue of 3 of 42 (7%) anti-HCV seronegative cases, including two with serologic evidence of HBV.
   Conclusions: Viral hepatitis, including HBV-HCV coinfection, may be unrecognized in up to 17% of patients with HCC when based on serology alone. Further research is needed to understand the clinical significance of viral makers in liver tissue of patients with HCC in the absence of serologic indices.
   Impact: The contribution of HBV and HCV to the increasing incidence of HCC in the United States may be underestimated. (C) 2013 AACR.
C1 [Hernandez, Brenda Y.; Zhu, Xuemei; Kwee, Sandi; Chan, Owen T. M.; Okimoto, Gordon; Wong, Linda L.] Univ Hawaii, Ctr Canc, Honolulu, HI 96813 USA.
   [Kwee, Sandi] Queens Med Ctr, Honolulu, HI USA.
   [Chan, Owen T. M.; Tsai, Naoky; Horio, David; Wong, Linda L.] Univ Hawaii, John A Burns Sch Med, Honolulu, HI 96813 USA.
   [McGlynn, Katherine A.] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
   [Altekruse, Sean] NCI, Div Canc Control & Populat Sci, Rockville, MD USA.
RP Hernandez, BY (reprint author), Univ Hawaii, Ctr Canc, 701 Ilalo St, Honolulu, HI 96813 USA.
EM brenda@cc.hawaii.edu
FU National Cancer Institute [3P30CA071789-12S7]; NIH [HHSN-261200900299P]
FX This research was supported in part by National Cancer Institute
   3P30CA071789-12S7 (to M. Carbone) and NIH contract # HHSN-261200900299P
   (to K.A. McGlynn).
NR 55
TC 4
Z9 4
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD NOV
PY 2013
VL 22
IS 11
BP 2016
EP 2023
DI 10.1158/1055-9965.EPI-13-0397
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 262ID
UT WOS:000327726800011
PM 23983238
ER

PT J
AU Hiraki, LT
   Qu, CH
   Hutter, CM
   Baron, JA
   Berndt, SI
   Bezieau, S
   Brenner, H
   Caan, BJ
   Casey, G
   Chang-Claude, J
   Chanock, SJ
   Conti, DV
   Duggan, D
   Fuchs, CS
   Gallinger, S
   Giovannucci, EL
   Harrison, TA
   Hayes, RB
   Hazra, A
   Henderson, B
   Hoffmeister, M
   Hopper, JL
   Hudson, TJ
   Jenkins, MA
   Kury, SE
   Le Marchand, L
   Lemire, M
   Ma, J
   Manson, JE
   Nan, HM
   Newcomb, PA
   Ng, K
   Potter, JD
   Schoen, RE
   Schumacher, FR
   Seminara, D
   Slattery, ML
   Wactawski-Wende, J
   White, E
   Wu, KN
   Zanke, BW
   Kraft, P
   Peters, U
   Chan, AT
AF Hiraki, Linda T.
   Qu, Conghui
   Hutter, Carolyn M.
   Baron, John A.
   Berndt, Sonja I.
   Bezieau, Stephane
   Brenner, Hermann
   Caan, Bette J.
   Casey, Graham
   Chang-Claude, Jenny
   Chanock, Stephen J.
   Conti, David V.
   Duggan, David
   Fuchs, Charles S.
   Gallinger, Steven
   Giovannucci, Edward L.
   Harrison, Tabitha A.
   Hayes, Richard B.
   Hazra, Aditi
   Henderson, Brian
   Hoffmeister, Michael
   Hopper, John L.
   Hudson, Thomas J.
   Jenkins, Mark A.
   Kuery, S. Ebastien
   Le Marchand, Loic
   Lemire, Mathieu
   Ma, Jing
   Manson, JoAnn E.
   Nan, Hongmei
   Newcomb, Polly A.
   Ng, Kimmie
   Potter, John D.
   Schoen, Robert E.
   Schumacher, Fredrick R.
   Seminara, Daniela
   Slattery, Martha L.
   Wactawski-Wende, Jean
   White, Emily
   Wu, Kana
   Zanke, Brent W.
   Kraft, Peter
   Peters, Ulrike
   Chan, Andrew T.
TI Genetic Predictors of Circulating 25-Hydroxyvitamin D and Risk of
   Colorectal Cancer
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; VITAMIN-D-RECEPTOR; D-BINDING PROTEIN;
   COLON-CANCER; SUSCEPTIBILITY LOCI; ENVIRONMENT INTERACTIONS; CALCIUM
   SUPPLEMENTATION; METAANALYSIS; PREVENTION; GENOTYPE
AB Background: Experimental evidence has demonstrated an antineoplastic role for vitamin D in the colon, and higher circulating 25-hydroxyvitamin D [25(OH)D] levels are consistently associated with a lower risk of colorectal cancer. Genome-wide association studies have identified loci associated with levels of circulating 25(OH)D. The identified single-nucleotide polymorphisms (SNPs) from four gene regions collectively explain approximately 5% of the variance in circulating 25(OH)D.
   Methods: We investigated whether five polymorphisms in GC, CYP2R1, CYP24A1, and DHCR7/NADSYN1, genes previously shown to be associated with circulating 25(OH)D levels, were associated with colorectal cancer risk in 10,061 cases and 12,768 controls drawn from 13 studies included in the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO) and Colon Cancer Family Registry (CCFR). We conducted a meta-analysis of crude and multivariate-adjusted logistic regression models to calculate odds ratios and associated confidence intervals for SNPs individually, SNPs simultaneously, and for a vitamin D additive genetic risk score (GRS).
   Results: We did not observe a statistically significant association between the 25(OH)D-associated SNPs and colorectal cancer marginally, conditionally, or as a GRS, or for colon or rectal cancer separately.
   Conclusions: Our findings do not support an association between SNPs associated with circulating 25(OH)D and risk of colorectal cancer. Additional work is warranted to investigate the complex relationship between 25 (OH)D and colorectal cancer risk.
   Impact: There was no association observed between genetic markers of circulating 25(OH)D and colorectal cancer. These genetic markers account for a small proportion of the variance in 25(OH)D. (C) 2013 AACR.
C1 [Hiraki, Linda T.; Giovannucci, Edward L.; Hazra, Aditi; Kraft, Peter] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Program Mol & Genet Epidemiol, Boston, MA 02114 USA.
   [Giovannucci, Edward L.; Wu, Kana] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02114 USA.
   [Kraft, Peter] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02114 USA.
   [Fuchs, Charles S.; Manson, JoAnn E.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
   [Giovannucci, Edward L.; Ma, Jing; Chan, Andrew T.] Brigham & Womens Hosp, Channing Div Network Med, Boston, MA 02115 USA.
   [Chan, Andrew T.] Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02114 USA.
   [Fuchs, Charles S.; Hazra, Aditi; Manson, JoAnn E.; Ng, Kimmie] Harvard Univ, Sch Med, Dept Med, Boston, MA 02114 USA.
   [Fuchs, Charles S.] Dana Farber Canc Inst, Gastrointestinal Malignancy Program, Boston, MA 02115 USA.
   [Ng, Kimmie] Dana Farber Canc Inst, Boston, MA 02115 USA.
   [Qu, Conghui; Hutter, Carolyn M.; Harrison, Tabitha A.; Newcomb, Polly A.; Potter, John D.; White, Emily; Peters, Ulrike] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.
   [Newcomb, Polly A.; Potter, John D.; White, Emily; Peters, Ulrike] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA.
   [Baron, John A.] Univ N Carolina, Sch Med, Div Gastroenterol & Hepatol, Chapel Hill, NC USA.
   [Berndt, Sonja I.; Chanock, Stephen J.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Seminara, Daniela] NCI, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
   [Nan, Hongmei] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
   [Bezieau, Stephane; Kuery, S. Ebastien] CHU Nantes, Serv Genet Med, F-44035 Nantes 01, France.
   [Brenner, Hermann; Chang-Claude, Jenny; Hoffmeister, Michael] German Canc Res Ctr, Heidelberg, Germany.
   [Caan, Bette J.] Kaiser Permanente Med Care Program, Div Res, Oakland, CA 94611 USA.
   [Casey, Graham; Conti, David V.; Henderson, Brian; Schumacher, Fredrick R.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
   [Duggan, David] Translat Genom Res Inst, Phoenix, AZ USA.
   [Gallinger, Steven] Toronto Gen Hosp, Dept Surg, Toronto, ON, Canada.
   [Hudson, Thomas J.; Lemire, Mathieu] Ontario Inst Canc Res, Toronto, ON, Canada.
   [Hudson, Thomas J.] Univ Toronto, Dept Med Biophys, Toronto, ON, Canada.
   [Hudson, Thomas J.] Univ Toronto, Dept Mol Genet, Toronto, ON, Canada.
   [Zanke, Brent W.] Univ Ottawa, Fac Med, Ottawa, ON, Canada.
   [Hayes, Richard B.] NYU, Sch Med, Dept Environm Med, Div Epidemiol, New York, NY USA.
   [Wactawski-Wende, Jean] SUNY Buffalo, Dept Social & Prevent Med, New York, NY USA.
   [Hopper, John L.; Jenkins, Mark A.] Univ Melbourne, Melborne Sch Populat Hlth, Melbourne, Vic, Australia.
   [Le Marchand, Loic] Canc Res Ctr Hawaii, Program Epidemiol, Honolulu, HI USA.
   [Schoen, Robert E.] Univ Pittsburgh, Med Ctr, Dept Epidemiol, Pittsburgh, PA USA.
   [Slattery, Martha L.] Univ Utah, Hlth Sci Ctr, Dept Internal Med, Salt Lake City, UT USA.
   [Potter, John D.] Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand.
RP Chan, AT (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Gastroenterol,Gastroenterol Associates, 55 Fruit St, Boston, MA 02114 USA.
EM achan@partners.org
RI Gallinger, Steven/E-4575-2013; Hoffmeister, Michael/B-5745-2012; KURY,
   Sebastien/G-5971-2015; Bezieau, stephane/G-5621-2015; Jenkins,
   Mark/P-7803-2015; Brenner, Hermann/B-4627-2017
OI Potter, John/0000-0001-5439-1500; Hayes, Richard/0000-0002-0918-661X;
   Hoffmeister, Michael/0000-0002-8307-3197; KURY,
   Sebastien/0000-0001-5497-0465; Bezieau, stephane/0000-0003-0095-1319;
   Jenkins, Mark/0000-0002-8964-6160; Brenner, Hermann/0000-0002-6129-1572
FU regional Programme Hospitalier de Recherche Clinique (PHRC); Regional
   Council of Pays de la Loire; Groupement des Entreprises Francaises dans
   la Lutte contre le Cancer (GEFLUC); Association Anne de Bretagne
   Genetique; Ligue Regionale Contre le Cancer (LRCC); National Cancer
   Institute, NIH under RFA [CA-95-011]; Australasian Colorectal Cancer
   Family Registry [U01 CA097735]; Seattle Colorectal Cancer Family
   Registry [U01 CA074794]; Ontario Registry for Studies of Familial
   Colorectal Cancer [U01 CA074783]; NIH [U01 CA074783, P01 CA 055075, UM1
   CA167552, P50CA127003, R01 137178, P01 CA087969, CA42182]; Ontario
   Research Fund; Canadian Institutes of Health Research; Cancer Risk
   Evaluation (CaRE) Program grant from the Canadian Cancer Society
   Research Institute; Senior Investigator Awards from the Ontario
   Institute for Cancer Research , through Ontario Ministry of Research and
   Innovation; National Cancer Institute [R01 CA60987]; German Research
   Council (Deutsche Forschungsgemeinschaft) [BR 1704/6-1, BR 1704/6-3, BR
   1704/6-4, CH 117/1-1]; German Federal Ministry of Education and Research
   [01KH0404, 01ER0814]; National Cancer Institute, NIH, U. S. Department
   of Health and Human Services [R01 CA48998]; National Cancer Institute,
   NIH, U.S. Department of Health and Human Services [U01 CA137088, R01
   CA059045]; Canadian Institute of Health Research (CIHR) Fellowship
   Award; Intramural Research Program of the Division of Cancer
   Epidemiology and Genetics; Division of Cancer Prevention, National
   Cancer Institute, NIH, DHHS; NIH, Genes, Environment and Health
   Initiative [NIH GEI] [Z01 CP 010200]; intramural resources of the
   National Cancer Institute; NIH GEI [U01 HG 004438]; NIH from the
   National Cancer Institute [K05 CA154337]; Office of Dietary Supplements;
   National Heart, Lung, and Blood Institute, NIH, U.S. Department of
   Health and Human Services [HHSN268201100046C, HHSN268201100001C,
   HHSN268201100002C, HHSN268201100003C, HHSN268201100004C,
   HHSN271201100004C];  [R37 CA54281];  [P01 CA033619];  [R01 CA63464]; 
   [K24 DK098311]
FX S. Bezieau and S. Kury are affiliated with ASTERISK which was funded by
   a regional Programme Hospitalier de Recherche Clinique (PHRC) and
   supported by the Regional Council of Pays de la Loire, the Groupement
   des Entreprises Francaises dans la Lutte contre le Cancer (GEFLUC), the
   Association Anne de Bretagne Genetique, and the Ligue Regionale Contre
   le Cancer (LRCC).; J.A. Baron, G. Casey, D.V. Conti, J.L. Hopper, M. A.
   Jenkins, P. A. Newcomb, and F.R. Schumacher are affiliated with CCFR
   which is supported by the National Cancer Institute, NIH under RFA #
   CA-95-011 and through cooperative agreements with members of the CCFR
   and principal investigators (P.I.s). This genome wide scan was supported
   by the National Cancer Institute, NIH by U01 CA122839. The content of
   this article does not necessarily reflect the views or policies of the
   National Cancer Institute or any of the collaborating centers in the
   CFRs, nor does mention of trade names, commercial products, or
   organizations imply endorsement by the U.S. Government or the CFR. The
   following CCFR centers contributed data to this article and were
   supported by the following sources: Australasian Colorectal Cancer
   Family Registry (U01 CA097735), Seattle Colorectal Cancer Family
   Registry (U01 CA074794), and Ontario Registry for Studies of Familial
   Colorectal Cancer (U01 CA074783).; S. Gallinger, T.J. Hudson, M. Lemire,
   and B.W. Zanke are affiliated with OFCCR which is supported by the NIH,
   through funding allocated to the Ontario Registry for Studies of
   Familial Colorectal Cancer (U01 CA074783); see CCFR section above. As
   subset of ARCTIC, OFCCR is supported by a GL2 grant from the Ontario
   Research Fund, the Canadian Institutes of Health Research, and the
   Cancer Risk Evaluation (CaRE) Program grant from the Canadian Cancer
   Society Research Institute. T.J. Hudson and B. W. Zanke are recipients
   of Senior Investigator Awards from the Ontario Institute for Cancer
   Research, through generous support from the Ontario Ministry of Research
   and Innovation.; B. Henderson and L. Le Marchand are affiliated with
   COLO2&3/MEC. COLO2&3 is supported by the National Cancer Institute (R01
   CA60987). MEC is supported by R37 CA54281, P01 CA033619, and R01
   CA63464.; H. Brenner, J. Chang-Claude, and M. Hoffmeister are affiliated
   with DACHS which was supported by grants from the German Research
   Council (Deutsche Forschungsgemeinschaft, BR 1704/6-1, BR 1704/6-3, BR
   1704/6-4, and CH 117/1-1), and the German Federal Ministry of Education
   and Research (01KH0404 and 01ER0814).; B.J. Caan, J.D. Potter, and M.L.
   Slattery are affiliated with DALS which was supported by the National
   Cancer Institute, NIH, U. S. Department of Health and Human Services
   (R01 CA48998 to M. L. Slattery).; T.A. Harrison, C.M. Hutter, U. Peters,
   and C. Qu are affiliated with GECCO which is supported by National
   Cancer Institute, NIH, U.S. Department of Health and Human Services (U01
   CA137088). Funding for the genome-wide scan of DALS, PLCO, and WHI was
   provided by the National Cancer Institute, NIH, U. S. Department of
   Health and Human Services (R01 CA059045).; A.T. Chan, C.S. Fuchs, E.L.
   Giovannucci, L.T. Hiraki, A. Hazra, P. Kraft, H. Nan, K. Ng, and K. Wu
   are affiliated with HPFS, NHS, and PHS. HPFS was supported by the NIH
   (P01 CA 055075, UM1 CA167552, R01 137178, and P50CA127003), NHS by the
   NIH (R01 137178, P50CA127003, and P01 CA087969) and PHS by the NIH
   (CA42182). A.T. Chan is a Damon Runyon Clinical Investigator and also
   supported by K24 DK098311. L.T. Hiraki was supported by a Canadian
   Institute of Health Research (CIHR) Fellowship Award.; S.I. Berndt, S.J.
   Chanock, R.B. Hayes, and R.E. Schoen are affiliated with PLCO which was
   supported by the Intramural Research Program of the Division of Cancer
   Epidemiology and Genetics and supported by contracts from the Division
   of Cancer Prevention, National Cancer Institute, NIH, DHHS. Control
   samples were genotyped as part of the Cancer Genetic Markers of
   Susceptibility (CGEMS) prostate cancer scan, supported by the Intramural
   Research Program of the National Cancer Institute. The datasets used in
   this analysis were accessed with appropriate approval through the dbGaP
   online resource (http://www.cgems.cancer.gov/data_acess.html) through
   dbGaP accession number 000207v.1p1.c1. [National Cancer Institute (2009)
   CGEMS data website. http://cgems.cancer.gov/data_access.html; ref. 75].
   Control samples were also genotyped as part of the GWAS of Lung Cancer
   and Smoking [76]. Funding for this work was provided through the NIH,
   Genes, Environment and Health Initiative [NIH GEI] (Z01 CP 010200). The
   human subjects participating in the GWAS are derived from the Prostate,
   Lung, Colon and Ovarian Screening Trial and the study is supported by
   intramural resources of the National Cancer Institute. Assistance with
   genotype cleaning, as well as with general study coordination, was
   provided by the Gene Environment Association Studies, GENEVA
   Coordinating Center (U01 HG004446). Assistance with data cleaning was
   provided by the National Center for Biotechnology Information. Funding
   support for genotyping, which was conducted at the Center for Inherited
   Disease Research, Johns Hopkins University (Baltimore, MD) was provided
   by the NIH GEI (U01 HG 004438). The datasets used for the analyses
   described in this article were obtained from dbGaP at
   http://www.ncbi.nlm.nih.gov/gap through dbGaP accession number
   phs000093.; E. White is affiliated with VITAL which is supported in part
   by the NIH (K05 CA154337) from the National Cancer Institute and Office
   of Dietary Supplements.; J. Manson and J. Wactawski-Wende are affiliated
   with WHI. The WHI program is funded by the National Heart, Lung, and
   Blood Institute, NIH, U.S. Department of Health and Human Services
   through contracts HHSN268201100046C, HHSN268201100001C,
   HHSN268201100002C, HHSN268201100003C, HHSN268201100004C, and
   HHSN271201100004C.
NR 76
TC 11
Z9 11
U1 0
U2 13
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 NOV
PY 2013
VL 22
IS 11
BP 2037
EP 2046
DI 10.1158/1055-9965.EPI-13-0209
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 262ID
UT WOS:000327726800013
PM 23983240
ER

PT J
AU Hamilton, JG
   Birmingham, WC
   Tehranifar, P
   Irwin, ML
   Klein, WMP
   Nebeling, L
   Chubak, J
AF Hamilton, Jada G.
   Birmingham, Wendy C.
   Tehranifar, Parisa
   Irwin, Melinda L.
   Klein, William M. P.
   Nebeling, Linda
   Chubak, Jessica
TI Transitioning to Independence and Maintaining Research Careers in a New
   Funding Climate: American Society of Preventive Oncology Junior Members
   Interest Group Report
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
AB The American Society of Preventive Oncology (ASPO) is a professional society for multi-disciplinary investigators in cancer prevention and control. The ASPO Junior Members Interest Group promotes the interests of predoctoral, postdoctoral, and junior faculty members within the Society, and provides them with career development and training opportunities. To this end, as part of the 37th ASPO Annual Meeting held in Memphis, Tennessee in March 2013, the Junior Members Interest Group organized a session designed to address issues faced by early-career investigators as they navigate the transition to become an independent, well-funded scientist with a sustainable program of research in the current climate of reduced and limited resources. Four speakers were invited to provide their complementary but distinct perspectives on this topic based on their personal experiences in academic, research-intensive positions and in federal funding agencies. This report summarizes the main themes that emerged from the speakers' presentations and audience questions related to mentoring; obtaining grant funding; publishing; developing expertise; navigating appointments, promotion, and tenure; and balancing demands. These lessons can be used by early-career investigators in cancer prevention and control as they transition to independence and build programs of fundable research. (C)2013 AACR.
C1 [Hamilton, Jada G.] NCI, Canc Prevent Fellowship Program, Canc Prevent Div, Rockville, MD USA.
   [Hamilton, Jada G.] NCI, Proc Care Res Branch, Behav Res Program, Rockville, MD USA.
   [Nebeling, Linda] NCI, Hlth Behav Res Branch, Behav Res Program, Rockville, MD USA.
   [Klein, William M. P.] NCI, Behav Res Program, Div Canc Control & Populat Sci, Rockville, MD USA.
   [Birmingham, Wendy C.] Brigham Young Univ, Dept Psychol, Provo, UT 84602 USA.
   [Tehranifar, Parisa] Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY USA.
   [Irwin, Melinda L.] Yale Univ, Sch Publ Hlth, Dept Chron Dis Epidemiol, New Haven, CT USA.
   [Chubak, Jessica] Univ Washington, Grp Hlth Res Inst, Seattle, WA 98195 USA.
   [Chubak, Jessica] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
RP Hamilton, JG (reprint author), Mem Sloan Kettering Canc Ctr, Dept Psychiat & Behav Sci, 641 Lexington Ave,7th Floor, New York, NY 10022 USA.
EM hamiltoj@mskcc.org
FU Intramural NIH HHS [Z99 CA999999]; NCI NIH HHS [K07 CA151777]
NR 6
TC 2
Z9 2
U1 0
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD NOV
PY 2013
VL 22
IS 11
BP 2138
EP 2142
DI 10.1158/1055-9965.EPI-13-0807
PG 5
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 262ID
UT WOS:000327726800028
PM 24190867
ER

PT J
AU Jin, DJ
   Cagliero, C
   Zhou, YN
AF Jin, Ding Jun
   Cagliero, Cedric
   Zhou, Yan Ning
TI Role of RNA Polymerase and Transcription in the Organization of the
   Bacterial Nucleoid
SO CHEMICAL REVIEWS
LA English
DT Review
ID ESCHERICHIA-COLI CHROMOSOME; HISTONE-LIKE PROTEINS; DNA-BINDING PROTEIN;
   DIFFERENT PHYSIOLOGICAL STATES; RIBONUCLEIC-ACID SYNTHESIS; LEU-500
   PROMOTER MUTATION; RATE-DEPENDENT REGULATION; OSMOTIC-STRESS RESPONSE;
   SEPARATE CELL HALVES; GROWTH-RATE CONTROL
C1 [Jin, Ding Jun; Cagliero, Cedric; Zhou, Yan Ning] NCI, Transcript Control Sect, Gene Regulat & Chromosome Biol Lab, NIH, Frederick, MD 21702 USA.
RP Jin, DJ (reprint author), NCI, Transcript Control Sect, Gene Regulat & Chromosome Biol Lab, NIH, POB B, Frederick, MD 21702 USA.
EM jind@mail.nih.gov
FU NIH, National Cancer Institute, Center for Cancer Research
FX We thank Dr. Julio E. Cabrera who initiated the cell biology of RNAP in
   the laboratory and Mr. Bo Xiao who introduced the MatLab tools. Also, we
   thank our colleagues and reviewers for helpful comments on the
   manuscript. This research was supported by the Intramural Research
   Program of the NIH, National Cancer Institute, Center for Cancer
   Research.
NR 320
TC 24
Z9 24
U1 1
U2 19
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0009-2665
EI 1520-6890
J9 CHEM REV
JI Chem. Rev.
PD NOV
PY 2013
VL 113
IS 11
BP 8662
EP 8682
DI 10.1021/cr4001429
PG 21
WC Chemistry, Multidisciplinary
SC Chemistry
GA 253QA
UT WOS:000327103200016
PM 23941620
ER

PT J
AU Pacak, K
AF Pacak, Karel
TI A 12-cm Mass with No Symptoms and Unremarkable Laboratory Results
   Commentary
SO CLINICAL CHEMISTRY
LA English
DT Editorial Material
ID PHEOCHROMOCYTOMA; NORMETANEPHRINE; METANEPHRINE
C1 [Pacak, Karel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
RP Pacak, K (reprint author), NICHD, Sect Med Neuroendocrinol, Program Reprod & Adult Endocrinol, CRC, NIH Bldg 10,1 East,Rm 1-3140,10 Ctr Dr,MSC-1109, Bethesda, MD 20892 USA.
EM karel@mail.nih.gov
NR 2
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 NOV
PY 2013
VL 59
IS 11
BP 1565
EP 1565
DI 10.1373/clinchem.2013.208009
PG 1
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 269YT
UT WOS:000328281800006
PM 24167187
ER

PT J
AU Ho, JE
   Hwang, SJ
   Wollert, KC
   Larson, MG
   Cheng, S
   Kempf, T
   Vasan, RS
   Januzzi, JL
   Wang, TJ
   Fox, CS
AF Ho, Jennifer E.
   Hwang, Shih-Jen
   Wollert, Kai C.
   Larson, Martin G.
   Cheng, Susan
   Kempf, Tibor
   Vasan, Ramachandran S.
   Januzzi, James L.
   Wang, Thomas J.
   Fox, Caroline S.
TI Biomarkers of Cardiovascular Stress and Incident Chronic Kidney Disease
SO CLINICAL CHEMISTRY
LA English
DT Article
ID GROWTH-DIFFERENTIATION FACTOR-15; AMERICAN-HEART-ASSOCIATION; RECEPTOR
   FAMILY-MEMBER; SOLUBLE ST2; MYOCARDIAL-INFARCTION; BETA SUPERFAMILY;
   MORTALITY; MICROALBUMINURIA; ATHEROSCLEROSIS; COMMUNITY
AB BACKGROUND: Growth differentiation factor-15 (GDF-15), soluble ST2 (sST2), and high-sensitivity troponin I (hsTnI) are emerging predictors of adverse clinical outcomes. We examined whether circulating concentrations are related to the development of kidney disease in the community.
   METHODS: Plasma GDF-15, sST2, and hsTnI concentrations were measured in 2614 Framingham Offspring cohort participants (mean age 57 years, 54% women) at the sixth examination cycle (1995-1998). Associations of biomarkers with incident chronic kidney disease [CKD, eGFR <60 mL . min(-1) . (1.73 m(2))(-1), n = 276], microalbuminuria (urinary albumin to creatinine ratio >= 25 mg/g in women and 17 mg/g in men, n = 191), and rapid decline in renal function [decline in eGFR >= 3 mL . min(-1) . (1.73 m(2))(-1) per year, n = 237], were evaluated using multivariable logistic regression; P < 0.006 was considered statistically significant in primary analyses.
   RESULTS: Participants were followed over a mean of 9.5 years. Higher plasma GDF-15 was associated with incident CKD [multivariable-adjusted odds ratio (OR) 1.9 per 1-U increase in log-GDF-15, 95% CI 1.6 -2.3, P < 0.0001] and rapid decline in renal function (OR, 1.6; 95% CI, 1.3-1.8; P < 0.0001). GDF-15, sST2, and hsTnI had suggestive associations with incident microalbuminuria but did not meet the prespecified P-value threshold after multivariable adjustment. Adding plasma GDF-15 to clinical covariates improved risk prediction of incident CKD: the c-statistic increased from 0.826 to 0.845 (P = 0.0007), and categorical net reclassification was 6.3% (95% CI, 2.7-9.9%).
   CONCLUSIONS: Higher circulating GDF-15 is associated with incident renal outcomes and improves risk prediction of incident CKD. These findings may provide insights into the mechanisms of renal injury. (C) 2013 American Association for Clinical Chemistry
C1 [Ho, Jennifer E.; Hwang, Shih-Jen; Larson, Martin G.; Cheng, Susan; Vasan, Ramachandran S.; Wang, Thomas J.; Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
   [Ho, Jennifer E.; Hwang, Shih-Jen; Larson, Martin G.; Cheng, Susan; Vasan, Ramachandran S.; Wang, Thomas J.; Fox, Caroline S.] Boston Univ, Sch Med, Framingham, MA USA.
   [Ho, Jennifer E.; Hwang, Shih-Jen; Fox, Caroline S.] NHLBI, Ctr Populat Studies, Bethesda, MD 20892 USA.
   [Ho, Jennifer E.] Boston Univ, Med Ctr, Cardiovasc Med Sect, Dept Med, Boston, MA 02118 USA.
   [Wollert, Kai C.; Kempf, Tibor] Hannover Med Sch, Dept Cardiol & Angiol, Div Mol & Translat Cardiol, Hannover, Germany.
   [Larson, Martin G.] Boston Univ, Dept Math & Stat, Boston, MA 02118 USA.
   [Cheng, Susan] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Cardiol,Dept Med, Boston, MA 02115 USA.
   [Vasan, Ramachandran S.] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
   [Januzzi, James L.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiol Div,Dept Med, Boston, MA USA.
   [Wang, Thomas J.] Vanderbilt Univ, Dept Med, Div Cardiovasc Med, Nashville, TN USA.
   [Fox, Caroline S.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Metab & Diabet,Dept Med, Boston, MA 02115 USA.
RP Ho, JE (reprint author), Boston Univ, Med Ctr, Cardiovasc Med Sect, 88 East Newton St,C-818, Boston, MA 02118 USA.
EM jennifer.ho@bmc.org
OI Ramachandran, Vasan/0000-0001-7357-5970
FU American Diabetes Association; Roche Diagnostics, Inc.; American Heart
   Association; National Institutes of Health [1K23-HL116780]; Roche
   Diagnostics; German Ministry of Education and Research (BMBF,
   BioChancePlus); Ellison Foundation; DeSanctis Clinical Scholar
   Endowment, Roche Diagnostics, and Critical Diagnostics; National Heart,
   Lung and Blood Institute's Framingham Heart Study [N01-HC-25195]; Roche
   Diagnostics, Inc; Critical Diagnostics, Inc
FX The urinary albumin excretion assays were supported by a grant from the
   American Diabetes Association (Dr. James Meigs, not a co-author on this
   paper) and by donation of reagents by Roche Diagnostics, Inc.
   (Framingham Heart Study); J.E. Ho, American Heart Association, the
   National Institutes of Health (1K23-HL116780); K.C. Wollert, Roche
   Diagnostics and the German Ministry of Education and Research (BMBF,
   BioChancePlus); S. Cheng, the Ellison Foundation; J.L. Januzzi, the
   DeSanctis Clinical Scholar Endowment, Roche Diagnostics, and Critical
   Diagnostics. The National Heart, Lung and Blood Institute's Framingham
   Heart Study (contract no. N01-HC-25195 to Boston University).
   Measurement of sST2 was performed by Critical Diagnostics, Inc; GDF-15
   assays were provided by Roche Diagnostics, Inc; measurement of hsTnI was
   performed by Singulex, Inc (T.J. Wang, J.L. Januzzi, R.S. Vasan, and
   K.C. Wollert).
NR 39
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U1 2
U2 8
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 NOV
PY 2013
VL 59
IS 11
BP 1613
EP 1620
DI 10.1373/clinchem.2013.205716
PG 8
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 269YT
UT WOS:000328281800012
PM 23873716
ER

PT J
AU Wohlfarth, A
   Pang, SK
   Zhu, MS
   Gandhi, AS
   Scheidweiler, KB
   Liu, HF
   Huestis, MA
AF Wohlfarth, Ariane
   Pang, Shaokun
   Zhu, Mingshe
   Gandhi, Adarsh S.
   Scheidweiler, Karl B.
   Liu, Hua-fen
   Huestis, Marilyn A.
TI First Metabolic Profile of XLR-11, a Novel Synthetic Cannabinoid,
   Obtained by Using Human Hepatocytes and High-Resolution Mass
   Spectrometry
SO CLINICAL CHEMISTRY
LA English
DT Article
ID ACUTE KIDNEY INJURY; URINARY METABOLITES; IDENTIFICATION; MIXTURES; GAS
AB BACKGROUND: Since the mid-2000s synthetic cannabinoids have been abused as recreational drugs, prompting scheduling of these substances in many countries. To circumvent legislation, manufacturers constantly market new compounds; [1-(5-fluoropentyl)indol-3-yl]( 2,2,3,3-tetramethylcyclopropyl) methanone (XLR-11), the fluorinated UR-144 analog, is one of the most recent and widely abused drugs, and its use is now linked with acute kidney injury. Our goal was to investigate XLR-11 metabolism for identification of major urinary targets in analytical methods and to clarify the origin of metabolites when one or more parent synthetic cannabinoids can be the source.
   METHODS: We incubated 10 mu mol/L XLR-11 with pooled human hepatocytes and sampled after 1 and 3 h. Samples were analyzed by high-resolution mass spectrometry with a TOF scan followed by information-dependent acquisition triggered product ion scans with dynamic background subtraction and mass defect filters. Scans were thoroughly data mined with different data processing algorithms (Metabolite Pilot 1.5).
   RESULTS: XLR-11 underwent phase I and II metabolism, producing more than 25 metabolites resulting from hydroxylation, carboxylation, hemiketal and hemiacetal formation, internal dehydration, and further glucuronidation of some oxidative metabolites. No sulfate or glutathione conjugation was observed. XLR-11 also was defluorinated, forming UR-144 metabolites. On the basis of mass spectrometry peak areas, we determined that the major metabolites were 2'-carboxy-XLR-11, UR-144 pentanoic acid, 5-hydroxy-UR-144, hydroxy-XLR-11 glucuronides, and 2'-carboxy-UR-144 pentanoic acid. Minor metabolites were combinations of the biotransformations mentioned above, often glucuronidated.
   CONCLUSIONS: These are the first data defining major urinary targets of XLR-11 metabolism that could document XLR-11 intake in forensic and clinical investigations. (C) 2013 American Association for Clinical Chemistry
C1 [Wohlfarth, Ariane; Gandhi, Adarsh S.; Scheidweiler, Karl B.; Huestis, Marilyn A.] NIDA, IRP, NIH, Baltimore, MD 21224 USA.
   [Pang, Shaokun; Liu, Hua-fen] AB SCIEX, Foster City, CA USA.
   [Zhu, Mingshe] Bristol Myers Squibb Res & Dev, Dept Biotransformat, Princeton, NJ USA.
RP Huestis, MA (reprint author), NIDA, IRP, NIH, 251 Bayview Blvd Suite 200 Rm 05A-721, Baltimore, MD 21224 USA.
EM mhuestis@intra.nida.nih.gov
FU National Institutes of Health; AB Sciex; Intramural Research Program,
   National Institute on Drug Abuse
FX Materials transfer agreement between National Institutes of Health and
   AB Sciex and the Intramural Research Program, National Institute on Drug
   Abuse, and National Institutes of Health.
NR 23
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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 NOV
PY 2013
VL 59
IS 11
BP 1638
EP 1648
DI 10.1373/clinchem.2013.209965
PG 11
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 269YT
UT WOS:000328281800015
PM 24014837
ER

PT J
AU Levens, D
AF Levens, David
TI Cellular MYCro Economics: Balancing MYC Function with MYC Expression
SO COLD SPRING HARBOR PERSPECTIVES IN MEDICINE
LA English
DT Article
ID RNA-POLYMERASE-II; HUMAN C-MYC; AVIAN MYELOCYTOMATOSIS VIRUS; NUCLEOSOME
   CORE PARTICLE; GENE-EXPRESSION; DNA-BINDING; IN-VIVO; TRANSCRIPTIONAL
   CONTROL; ANGSTROM RESOLUTION; COLORECTAL-CANCER
AB The expression levels of the MYC oncoprotein have long been recognized to be associated with the outputs of major cellular processes including proliferation, cell growth, apoptosis, differentiation, and metabolism. Therefore, to understand how MYC operates, it is important to define quantitatively the relationship between MYC input and expression output for its targets as well as the higher-order relationships between the expression levels of subnetwork components and the flow of information and materials through those networks. Two different views of MYC are considered, first as a molecular microeconomic manager orchestrating specific positive and negative responses at individual promoters in collaboration with other transcription and chromatin components, and second, as a macroeconomic czar imposing an overarching rule onto all active genes. In either case, c-myc promoter output requires multiple inputs and exploits diverse mechanisms to tune expression to the appropriate levels relative to the thresholds of expression that separate health and disease.
C1 NCI, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Levens, D (reprint author), NCI, Pathol Lab, Ctr Canc Res, Bldg 10, Bethesda, MD 20892 USA.
EM levens@helix.nih.gov
NR 92
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U1 0
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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 NOV
PY 2013
VL 3
IS 11
AR a014233
DI 10.1101/cshperspect.a014233
PG 15
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 269XO
UT WOS:000328277500007
ER

PT J
AU Volkow, ND
   Normand, J
AF Volkow, Nora D.
   Normand, Jacques
TI Supplement: HIV and People Who Use Drugs in Central Asia: Confronting
   the Perfect Storm Preface
SO DRUG AND ALCOHOL DEPENDENCE
LA English
DT Editorial Material
C1 [Volkow, Nora D.; Normand, Jacques] NIDA, NIH, Rockville, MD USA.
RP Volkow, ND (reprint author), NIDA, NIH, Rockville, MD USA.
EM nvolkow@nida.nih.gov
NR 2
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0376-8716
EI 1879-0046
J9 DRUG ALCOHOL DEPEN
JI Drug Alcohol Depend.
PD NOV
PY 2013
VL 132
SU 1
BP S1
EP S1
DI 10.1016/j.drugalcdep.2013.07.019
PG 1
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 269KU
UT WOS:000328241000001
PM 23993084
ER

PT J
AU Shardell, M
   Hicks, G
   Ferrucci, L
AF Shardell, M.
   Hicks, G.
   Ferrucci, L.
TI CAUSAL INFERENCE IN STUDIES OF OLDER ADULTS WITH DROPOUT AND DEATH:
   VITAMIN D AND GAIT SPEED IN INCHIANTI
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Shardell, M.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
   [Hicks, G.] Univ Delaware, Newark, DE USA.
   [Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
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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 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 30
EP 30
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442101151
ER

PT J
AU Bernard, M
AF Bernard, M.
TI TRANSLATING AGING BIOLOGY TO CLINICAL APPLICATIONS - THE NIA/NIH
   PERSPECTIVE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Bernard, M.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 102
EP 102
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442101458
ER

PT J
AU Gudlaugsson, JF
   Johannsson, E
   Arngrimsson, SA
   Gudnason, V
   Aspelund, T
   Harris, T
   Jonsson, PV
   Olafsdottir, AS
AF Gudlaugsson, J. F.
   Johannsson, E.
   Arngrimsson, S. A.
   Gudnason, V.
   Aspelund, T.
   Harris, T.
   Jonsson, P. V.
   Olafsdottir, A. S.
TI WALKING, STRENGTH TRAINING, AND NUTRITION COUNSELLING IMPROVES PHYSICAL
   HEALTH IN OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Gudlaugsson, J. F.; Johannsson, E.; Arngrimsson, S. A.; Gudnason, V.; Aspelund, T.; Jonsson, P. V.; Olafsdottir, A. S.] Univ Iceland, Reykjavik, Iceland.
   [Gudnason, V.; Aspelund, T.] Iceland Heart Assoc, Kopavogur, Iceland.
   [Harris, T.] NIA, Washington, DC USA.
   [Jonsson, P. V.] Univ Hosp Iceland, Reykjavik, Iceland.
RI Aspelund, Thor/C-5983-2008; Gudnason, Vilmundur/K-6885-2015;
   Olafsdottir, Anna/A-8804-2013
OI Aspelund, Thor/0000-0002-7998-5433; Gudnason,
   Vilmundur/0000-0001-5696-0084; Olafsdottir, Anna/0000-0002-7258-1727
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 113
EP 113
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442102054
ER

PT J
AU Schrack, JA
   Glass, T
   Ferrucci, L
AF Schrack, J. A.
   Glass, T.
   Ferrucci, L.
TI ASSESSING THE "PHYSICAL CLIFF": DETAILED QUANTIFICATION METHODS TO
   ASSESS AGING AND PHYSICAL ACTIVITY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Schrack, J. A.; Glass, T.] Johns Hopkins Sch Publ Hlth, Baltimore, MD USA.
   [Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 117
EP 117
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442102072
ER

PT J
AU Schrack, JA
   Zipunnikov, V
   Goldsmith, J
   Bai, J
   Simonsick, EM
   Crainiceanu, C
   Ferrucci, L
AF Schrack, J. A.
   Zipunnikov, V.
   Goldsmith, J.
   Bai, J.
   Simonsick, E. M.
   Crainiceanu, C.
   Ferrucci, L.
TI MODELING THE "PHYSICAL CLIFF" WITH OBJECTIVE ACTIVITY ASSESSMENT:
   FINDINGS FROM THE BLSA
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Schrack, J. A.; Zipunnikov, V.; Bai, J.; Crainiceanu, C.] Johns Hopkins Sch Publ Hlth, Baltimore, MD USA.
   [Schrack, J. A.; Simonsick, E. M.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
   [Goldsmith, J.] Columbia Univ, Sch Publ Hlth, New York, NY USA.
NR 0
TC 0
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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 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 117
EP 117
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442102073
ER

PT J
AU Crainiceanu, C
   Bai, J
   Glass, T
   Schrack, JA
   Harris, T
AF Crainiceanu, C.
   Bai, J.
   Glass, T.
   Schrack, J. A.
   Harris, T.
TI DETAILED QUANTITATIVE ASSESSMENT OF HUMAN MOVEMENT USING HIGH-DENSITY
   ACCELEROMETER DATA
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Crainiceanu, C.; Bai, J.] Johns Hopkins Univ, Baltimore, MD USA.
   [Glass, T.; Schrack, J. A.] Johns Hopkins Univ Epidemiol, Baltimore, MD USA.
   [Harris, T.] NIA, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 118
EP 118
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442102075
ER

PT J
AU Goldsmith, J
   Schrack, JA
   Zipunnikov, V
   Ferrucci, L
   Crainiceanu, C
AF Goldsmith, J.
   Schrack, J. A.
   Zipunnikov, V.
   Ferrucci, L.
   Crainiceanu, C.
TI ESTIMATING ENERGY EXPENDITURE FROM HEART RATE AND ACTIVITY COUNTS: A
   BAYESIAN APPROACH
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Goldsmith, J.] Columbia Univ, New York, NY USA.
   [Schrack, J. A.; Zipunnikov, V.; Crainiceanu, C.] Johns Hopkins Univ, Baltimore, MD USA.
   [Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 118
EP 118
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442102077
ER

PT J
AU Mener, DJ
   Betz, J
   Yaffe, K
   Harris, T
   Helzner, E
   Strotmeyer, ES
   Simonsick, EM
   Lin, FR
AF Mener, D. J.
   Betz, J.
   Yaffe, K.
   Harris, T.
   Helzner, E.
   Strotmeyer, E. S.
   Simonsick, E. M.
   Lin, F. R.
TI APOLIPOPROTEIN E ALLELE AND HEARING LOSS IN OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Mener, D. J.; Lin, F. R.] Johns Hopkins Sch Med, Dept Otolaryngol Head & Neck Surg, Baltimore, MD USA.
   [Betz, J.; Lin, F. R.] Johns Hopkins Sch Med, Dept Epidemiol, Baltimore, MD USA.
   [Betz, J.; Lin, F. R.] Bloomberg Sch Publ Hlth, Baltimore, MD USA.
   [Betz, J.; Lin, F. R.] Johns Hopkins Med Inst, Ctr Aging & Hlth, Baltimore, MD 21205 USA.
   [Yaffe, K.] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
   [Yaffe, K.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA.
   [Yaffe, K.] Univ Calif San Francisco, Dept Epidemiol, San Francisco, CA 94143 USA.
   [Yaffe, K.] Univ Calif San Francisco, Dept Biostat, San Francisco, CA 94143 USA.
   [Harris, T.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
   [Helzner, E.] Suny Downstate Med Ctr, Dept Epidemiol, Brooklyn, NY 11203 USA.
   [Helzner, E.] Suny Downstate Med Ctr, Dept Biostat, Brooklyn, NY 11203 USA.
   [Simonsick, E. M.] NIA, Intramural Res Program, Bethesda, MD 20892 USA.
   [Strotmeyer, E. S.] Univ Pittsburgh, Ctr Aging & Populat Hlth, Pittsburgh, PA USA.
RI Strotmeyer, Elsa/F-3015-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 123
EP 123
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442102103
ER

PT J
AU Armstrong, JJ
   Mitnitski, AB
   Launer, LJ
   White, L
   Rockwood, K
AF Armstrong, J. J.
   Mitnitski, A. B.
   Launer, L. J.
   White, L.
   Rockwood, K.
TI A LIMIT TO FRAILTY IN OLDER JAPANESE-AMERICAN MEN IN RELATION TO
   MORTALITY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Armstrong, J. J.; Mitnitski, A. B.; Rockwood, K.] Dalhousie Univ, Halifax, NS, Canada.
   [Launer, L. J.] NIA, Bethesda, MD 20892 USA.
   [White, L.] Univ Hawaii, Honolulu, HI 96822 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 167
EP 168
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442102294
ER

PT J
AU Martin, KR
AF Martin, K. R.
TI CONSIDERATIONS FOR USING A HIP OR WAIST WORN ACCELEROMETER TO CAPTURE
   PHYSICAL ACTIVITY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Martin, K. R.] NIA, Lab Epidemiol & Populat Sci, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 206
EP 206
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442103020
ER

PT J
AU Caserotti, P
   Koster, A
   Harris, T
   Hvid, L
AF Caserotti, P.
   Koster, A.
   Harris, T.
   Hvid, L.
TI WRIST-WORN ACCELEROMETERS FOR PRESCRIBING PHYSICAL ACTIVITY IN OLDER
   PEOPLE WITH REDUCED MOBILITY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Caserotti, P.; Hvid, L.] Univ Southern Denmark, Odense, Denmark.
   [Koster, A.] Maastricht Univ, Maastricht, Netherlands.
   [Harris, T.] NIA, Intramural Res Program, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 207
EP 207
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442103022
ER

PT J
AU Ferrucci, L
AF Ferrucci, L.
TI USE OF THE ACTIHEART ACCELEROMETER IN THE BALTIMORE LONGITUDINAL STUDY
   ON AGING (BLSA)
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ferrucci, L.] NIA, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 207
EP 207
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442103023
ER

PT J
AU Hung, M
   Harris, T
   Caserotti, P
   Chen, KY
   Lange-Maia, B
   Glynn, NW
   Van Domelen, DR
   Koster, A
AF Hung, M.
   Harris, T.
   Caserotti, P.
   Chen, K. Y.
   Lange-Maia, B.
   Glynn, N. W.
   Van Domelen, D. R.
   Koster, A.
TI AGING RESEARCH EVALUATING ACCELEROMETRY (AREA): COMPARISON OF
   ACCELEROMETRY PERFORMANCE IN OLDER PEOPLE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Hung, M.; Harris, T.] NIA, IRP, Bethesda, MD 20892 USA.
   [Caserotti, P.] Univ Southern Denmark, Odensve, Denmark.
   [Chen, K. Y.] NIDDK, Bethesda, MD 20892 USA.
   [Lange-Maia, B.; Glynn, N. W.] Univ Pittsburgh, Pittsburgh, PA USA.
   [Van Domelen, D. R.] Emory Univ, Atlanta, GA 30322 USA.
   [Koster, A.] Maastricht Univ, Maastricht, Netherlands.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 207
EP 207
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442103024
ER

PT J
AU Palta, P
   Carlson, M
   Yasar, S
   Nahin, R
   DeKosky, ST
   Snitz, BE
   Williamson, JD
   Golden, SH
AF Palta, P.
   Carlson, M.
   Yasar, S.
   Nahin, R.
   DeKosky, S. T.
   Snitz, B. E.
   Williamson, J. D.
   Golden, S. H.
TI DIABETES AND COGNITIVE FUNCTIONING IN OLDER ADULTS: THE GINKGO
   EVALUATION OF MEMORY STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Palta, P.; Carlson, M.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
   [Yasar, S.; Golden, S. H.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
   [Nahin, R.] NIH, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
   [DeKosky, S. T.] Univ Virginia, Charlottesville, VA USA.
   [Snitz, B. E.] Univ Pittsburgh, Pittsburgh, PA USA.
   [Williamson, J. D.] Wake Forest Univ, Sch Med, Winston Salem, NC 27109 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 207
EP 207
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442103025
ER

PT J
AU Leroux, M
   Cohen, AA
   Milot, E
   Poirier, R
   Li, Q
   Fried, LP
   Ferrucci, L
AF Leroux, M.
   Cohen, A. A.
   Milot, E.
   Poirier, R.
   Li, Q.
   Fried, L. P.
   Ferrucci, L.
TI REFERENCE POPULATIONS FOR STATISTICAL DISTANCE OF PHYSIOLOGICAL
   DYSREGULATION DEMONSTRATE WITHIN-COUNTRY HOMOGENEITY BUT INTER-COUNTRY
   HETEROGENEITY OF BIOMARKER PATTERNS IN AGING
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Leroux, M.; Cohen, A. A.; Milot, E.; Poirier, R.; Li, Q.] Ctr Hosp Univ Sherbrooke, Grp Primus, Sherbrooke, PQ, Canada.
   [Fried, L. P.] Columbia Univ, New York, NY USA.
   [Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 221
EP 221
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442103091
ER

PT J
AU Milot, E
   Cohen, AA
   Li, Q
   Fried, LP
   Ferrucci, L
AF Milot, E.
   Cohen, A. A.
   Li, Q.
   Fried, L. P.
   Ferrucci, L.
TI BAYESIAN ANALYSIS OF PHYSIOLOGICAL DYSREGULATION TRAJECTORIES DURING
   AGING
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Milot, E.; Cohen, A. A.; Li, Q.] Ctr Hosp Univ Sherbrooke, Grp Rech Primus, Sherbrooke, PQ, Canada.
   [Fried, L. P.] Columbia Univ, Mailman Sch Publ Hlth, New York, NC USA.
   [Ferrucci, L.] NIA, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 222
EP 222
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442103093
ER

PT J
AU Morissette-Thomas, V
   Cohen, AA
   Dusseault-Belanger, F
   Legault, V
   Ferrucci, L
AF Morissette-Thomas, V.
   Cohen, A. A.
   Dusseault-Belanger, F.
   Legault, V.
   Ferrucci, L.
TI MULTIVARIATE ANALYSIS OF INFLAMMATORY MARKERS AND THEIR RELATIONSHIP
   WITH AGE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Morissette-Thomas, V.; Cohen, A. A.; Dusseault-Belanger, F.] Univ Sherbrooke, Sherbrooke, PQ J1K 2R1, Canada.
   [Morissette-Thomas, V.; Cohen, A. A.; Dusseault-Belanger, F.; Legault, V.] Ctr Hosp Univ Sherbrooke, Sherbrooke, PQ, Canada.
   [Ferrucci, L.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 222
EP 222
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442103092
ER

PT J
AU Rebok, G
   Ball, K
   Jones, R
   King, JW
   Marsiske, M
   Tennstedt, S
   Unverzagt, F
   Willis, SL
AF Rebok, G.
   Ball, K.
   Jones, R.
   King, J. W.
   Marsiske, M.
   Tennstedt, S.
   Unverzagt, F.
   Willis, S. L.
TI COGNITIVE TRAINING: RESULTS FROM THE ACTIVE STUDY AT 10 YEARS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Rebok, G.] Johns Hopkins Univ, Baltimore, MD USA.
   [Ball, K.] Univ Alabama Birmingham, Birmingham, AL USA.
   [Jones, R.] Hebrew SeniorLife, Boston, MA USA.
   [King, J. W.] NIA, Bethesda, MD 20892 USA.
   [Marsiske, M.] Univ Florida, Gainesville, FL USA.
   [Tennstedt, S.] New England Res Inst, Watertown, MA 02172 USA.
   [Unverzagt, F.] Indiana Univ Sch Med, Indianapolis, IN 46202 USA.
   [Willis, S. L.] Univ Washington, Seattle, WA 98195 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 222
EP 223
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442103096
ER

PT J
AU Bellizzi, K
   Breslau, ES
AF Bellizzi, K.
   Breslau, E. S.
TI COLORECTAL CANCER SCREENING IN OLDER ADULTS BY 5 YEAR LIFE EXPECTANCY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Bellizzi, K.] UConn, HDFS, Storrs, CT USA.
   [Breslau, E. S.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 232
EP 232
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442103145
ER

PT J
AU Moore, AZ
   Makrogiannis, S
   Simonsick, EM
   Ferrucci, L
AF Moore, A. Z.
   Makrogiannis, S.
   Simonsick, E. M.
   Ferrucci, L.
TI MUSCLE STRENGTH, MUSCLE AREA, AND TRAJECTORIES OF GAIT SPEED IN OLDER
   ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Moore, A. Z.; Makrogiannis, S.; Simonsick, E. M.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 259
EP 259
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442103280
ER

PT J
AU Schrack, JA
   Simonsick, EM
   Ferrucci, L
AF Schrack, J. A.
   Simonsick, E. M.
   Ferrucci, L.
TI GREATER ENERGETIC COST OF WALKING PREDICTS LONGITUDINAL GAIT SPEED
   DECLINE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Schrack, J. A.] Johns Hopkins Sch Publ Hlth, Baltimore, MD USA.
   [Schrack, J. A.; Simonsick, E. M.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 259
EP 260
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442103281
ER

PT J
AU Jerome, GJ
   Simonsick, EM
   Ko, S
   Moore, AZ
   Ferrucci, L
AF Jerome, G. J.
   Simonsick, E. M.
   Ko, S.
   Moore, A. Z.
   Ferrucci, L.
TI GAIT LABORATORY PARAMETERS AND MEANINGFUL GAIT SPEED DECLINE IN THE BLSA
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Jerome, G. J.] Towson Univ, Towson, MD USA.
   [Simonsick, E. M.; Moore, A. Z.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
   [Ko, S.] Chonnam Natl Univ, Yeosu, South Korea.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 260
EP 260
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442103283
ER

PT J
AU Ko, S
   Simonsick, EM
   Ferrucci, L
AF Ko, S.
   Simonsick, E. M.
   Ferrucci, L.
TI SHORT-TERM CHANGE IN GAIT LABORATORY PARAMETERS IN THE BLSA
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ko, S.] Chonnam Natl Univ, Yeosu, South Korea.
   [Simonsick, E. M.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 260
EP 260
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442103284
ER

PT J
AU Simonsick, EM
   Schrack, JA
   Moore, AZ
   Ko, S
   Ferrucci, L
AF Simonsick, E. M.
   Schrack, J. A.
   Moore, A. Z.
   Ko, S.
   Ferrucci, L.
TI BALANCE, PROPRIOCEPTION AND GAIT SPEED DECLINE IN THE BLSA
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Simonsick, E. M.; Moore, A. Z.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
   [Schrack, J. A.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
   [Ko, S.] Chonnam Natl Univ, Seoul, South Korea.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 260
EP 260
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442103282
ER

PT J
AU von Bonsdorff, M
   Groffen, DA
   Rantanen, T
   Jonsson, PV
   Aspelund, T
   Launer, LJ
   Gudnason, V
   Harris, T
AF von Bonsdorff, M.
   Groffen, D. A.
   Rantanen, T.
   Jonsson, P. V.
   Aspelund, T.
   Launer, L. J.
   Gudnason, V.
   Harris, T.
TI CORONARY ARTERY CALCIUM AND PHYSICAL PERFORMANCE AS DETERMINANTS OF
   MORTALITY: AGES-REYKJAVIK STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [von Bonsdorff, M.; Groffen, D. A.; Rantanen, T.] Univ Jyvaskyla, Gerontol Res Ctr & Hlth Sci, SF-40351 Jyvaskyla, Finland.
   [von Bonsdorff, M.; Launer, L. J.; Harris, T.] NIA, Bethesda, MD 20892 USA.
   [Groffen, D. A.] Maastricht Univ, Maastricht, Netherlands.
   [Jonsson, P. V.; Aspelund, T.; Gudnason, V.] Iceland Heart Assoc, Kopavogur, Iceland.
   [Jonsson, P. V.; Gudnason, V.] Univ Iceland, Reykjavik, Iceland.
RI Aspelund, Thor/C-5983-2008; Gudnason, Vilmundur/K-6885-2015
OI Aspelund, Thor/0000-0002-7998-5433; Gudnason,
   Vilmundur/0000-0001-5696-0084
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 262
EP 262
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442103295
ER

PT J
AU Sierra, F
   Kohanski, RA
AF Sierra, F.
   Kohanski, R. A.
TI THE TRANS-NIH GEROSCIENCE INTEREST GROUP
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Sierra, F.; Kohanski, R. A.] NIA, Div Aging Biol, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 348
EP 348
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442104226
ER

PT J
AU Chuang, Y
   Varma, VR
   Harris, G
   Fried, LP
   Rebok, G
   Xue, Q
   Carlson, M
AF Chuang, Y.
   Varma, V. R.
   Harris, G.
   Fried, L. P.
   Rebok, G.
   Xue, Q.
   Carlson, M.
TI THE ASSOCIATION BETWEEN AGGREGATE CARDIOVASCULAR RISK AND BRAIN FUNCTION
   IN AT-RISK COMMUNITY-DWELLING OLDER ADULTS: AN FMRI STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Chuang, Y.; Varma, V. R.; Harris, G.; Rebok, G.; Xue, Q.; Carlson, M.] Johns Hopkins Sch Publ Hlth, Baltimore, MD USA.
   [Chuang, Y.] NIA, Lab Behav Neurosci, Baltimore, MD 21224 USA.
   [Fried, L. P.] Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 355
EP 355
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442104263
ER

PT J
AU Li, Q
   Wang, S
   Cohen, AA
   Milot, E
   Ferrucci, L
AF Li, Q.
   Wang, S.
   Cohen, A. A.
   Milot, E.
   Ferrucci, L.
TI DATA MINING AND INFORMATICS APPROACHES TO BIOMARKER ANALYSIS DURING
   AGING
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Li, Q.; Wang, S.; Cohen, A. A.; Milot, E.] Univ Sherbrooke, Sherbrooke, PQ J1K 2R1, Canada.
   [Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 373
EP 373
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442104353
ER

PT J
AU Poirier, R
   Cohen, AA
   Leroux, M
   Dusseault-Belanger, F
   Fried, LP
   Ferrucci, L
AF Poirier, R.
   Cohen, A. A.
   Leroux, M.
   Dusseault-Belanger, F.
   Fried, L. P.
   Ferrucci, L.
TI PCA IDENTIFIES STABLE BIOLOGICAL PROCESSES THAT PREDICT FRAILTY, DEATH,
   AND CHRONIC DISEASES
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Poirier, R.; Cohen, A. A.; Leroux, M.; Dusseault-Belanger, F.] CHU Sherbrooke, Grp Rech PRIMUS, Sherbrooke, PQ J1H 5N4, Canada.
   [Poirier, R.] Univ Sherbrooke, Sherbrooke, PQ J1K 2R1, Canada.
   [Fried, L. P.] Columbia Univ, New York, NY USA.
   [Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 373
EP 373
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442104352
ER

PT J
AU Espeland, MA
   Brancati, FL
   Evans, M
   Gregg, E
   Kahn, SE
   Lewis, CE
   Pi-Sunyer, X
   Wing, R
AF Espeland, M. A.
   Brancati, F. L.
   Evans, M.
   Gregg, E.
   Kahn, S. E.
   Lewis, C. E.
   Pi-Sunyer, X.
   Wing, R.
TI DESIGN AND PRIMARY FINDINGS OF THE ACTION FOR HEALTH IN DIABETES TRIAL
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Espeland, M. A.] Wake Forest Sch Med, Dept Biostat Sci, Winston Salem, NC USA.
   [Brancati, F. L.] Johns Hopkins Sch Med, Baltimore, MD USA.
   [Evans, M.] NIDDK, Bethesda, MD 20892 USA.
   [Gregg, E.] Ctr Dis Control & Prevent, Atlanta, GA USA.
   [Kahn, S. E.] Univ Washington, Seattle, WA 98195 USA.
   [Lewis, C. E.] Univ Alabama Birmingham, Birmingham, AL USA.
   [Pi-Sunyer, X.] Columbia Univ, St Lukes Roosevelt Hosp Ctr, New York, NY USA.
   [Wing, R.] Miriam Hosp, Providence, RI 02906 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 388
EP 388
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442104429
ER

PT J
AU Hazuda, HP
   Gaussoin, SA
   Peters, AL
   Van Dorsten, B
   Wadden, TA
   Yanovski, SZ
   Zhang, P
   Rubin, R
AF Hazuda, H. P.
   Gaussoin, S. A.
   Peters, A. L.
   Van Dorsten, B.
   Wadden, T. A.
   Yanovski, S. Z.
   Zhang, P.
   Rubin, R.
TI BENEFITS OF INTENSIVE LIFESTYLE INTERVENTION ON DEPRESSION AND HEALTH
   RELATED QUALITY OF LIFE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Gaussoin, S. A.] Wake Forest Sch Med, Dept Biostat Sci, Winston Salem, NC USA.
   [Hazuda, H. P.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
   [Peters, A. L.] Roybal Comprehens Hlth Ctr, Los Angeles, CA USA.
   [Van Dorsten, B.] Univ Colorado, Denver Sch Med, Denver, CO 80202 USA.
   [Wadden, T. A.] Univ Penn, Philadelphia, PA 19104 USA.
   [Yanovski, S. Z.] NIDDK, Bethesda, MD 20892 USA.
   [Zhang, P.] Ctr Dis Control, Atlanta, GA 30333 USA.
   [Rubin, R.] Johns Hopkins Sch Med, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 389
EP 389
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442104431
ER

PT J
AU Lakatta, E
AF Lakatta, E.
TI REALITY OF AGING VIEWED FROM THE ARTERIAL WALL
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Lakatta, E.] Natl Inst Aging Intramural Res Program, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 399
EP 399
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442104486
ER

PT J
AU Buchowski, M
   Powers, JS
   Schnelle, J
   Chen, KY
AF Buchowski, M.
   Powers, J. S.
   Schnelle, J.
   Chen, K. Y.
TI PERFORMANCE FATIGABILITY AS A FUNCTION OF PHYSICAL ACTIVITY ENERGY
   EXPENDITURE IN OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Buchowski, M.; Powers, J. S.; Schnelle, J.] Vanderbilt Univ, Nashville, TN 37235 USA.
   [Chen, K. Y.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 3
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 418
EP 418
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442105052
ER

PT J
AU Glynn, NW
   Santanasto, AJ
   Simonsick, EM
   Harris, T
   Koster, A
   Caserotti, P
   Strotmeyer, ES
   Newman, AB
AF Glynn, N. W.
   Santanasto, A. J.
   Simonsick, E. M.
   Harris, T.
   Koster, A.
   Caserotti, P.
   Strotmeyer, E. S.
   Newman, A. B.
TI ASSOCIATION OF PERCEIVED FATIGABILITY AND ACTIVITY LEVELS ON PHYSICAL
   FUNCTION OF OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Glynn, N. W.; Santanasto, A. J.; Strotmeyer, E. S.; Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
   [Simonsick, E. M.] NIA, Baltimore, MD 21224 USA.
   [Harris, T.] NIA, Bethesda, MD 20892 USA.
   [Koster, A.] Maastricht Univ, Maastricht, Netherlands.
   [Caserotti, P.] Univ Southern Denmark, Odense, Denmark.
RI Strotmeyer, Elsa/F-3015-2014
NR 0
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 418
EP 419
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442105054
ER

PT J
AU Schrack, JA
   Simonsick, EM
   Zipunnikov, V
   Goldsmith, J
   Crainiceanu, C
   Ferrucci, L
AF Schrack, J. A.
   Simonsick, E. M.
   Zipunnikov, V.
   Goldsmith, J.
   Crainiceanu, C.
   Ferrucci, L.
TI INSIGHT INTO FATIGABILITY THROUGH ENERGETIC EFFICIENCY AND FREE LIVING
   ACTIVITY IN MID-TO-LATE LIFE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Schrack, J. A.; Zipunnikov, V.; Crainiceanu, C.] Johns Hopkins Sch Publ Hlth, Baltimore, MD USA.
   [Schrack, J. A.; Simonsick, E. M.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
   [Goldsmith, J.] Columbia Univ Sch Publ Hlth, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 418
EP 418
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442105051
ER

PT J
AU Simonsick, EM
   Schrack, JA
   Glynn, NW
   Ferrucci, L
AF Simonsick, E. M.
   Schrack, J. A.
   Glynn, N. W.
   Ferrucci, L.
TI PERFORMANCE FATIGABILITY AND MOBILITY DECLINE: DATA FROM THE BALTIMORE
   LONGITUDINAL STUDY OF AGING
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Simonsick, E. M.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
   [Schrack, J. A.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
   [Glynn, N. W.] Univ Pittsburgh, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 419
EP 419
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442105055
ER

PT J
AU Gamaldo, A
   Thorpe, R
   Whitfield, KE
AF Gamaldo, A.
   Thorpe, R.
   Whitfield, K. E.
TI RELATIONSHIP BETWEEN SLEEP QUALITY AND ACTIVITIES OF DAILY LIVING IN
   BLACKS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Gamaldo, A.] NIA, Baltimore, MD 21224 USA.
   [Thorpe, R.] Johns Hopkins Univ, Baltimore, MD USA.
   [Whitfield, K. E.] Duke Univ, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 432
EP 432
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442105124
ER

PT J
AU Ashida, S
   Schafer, EJ
   Marcum, CS
   Koehly, LM
AF Ashida, S.
   Schafer, E. J.
   Marcum, C. S.
   Koehly, L. M.
TI FAMILY PARTICIPATION IN ALZHEIMER'S CAREGIVING AND SELF-REPORTED HEALTH
   STATUS OF FAMILY MEMBERS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ashida, S.; Schafer, E. J.] Univ Iowa Coll Publ Hlth, Iowa City, IA USA.
   [Marcum, C. S.; Koehly, L. M.] NHGRI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 438
EP 439
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442105157
ER

PT J
AU Koster, A
   van der Berg, J
   Bosma, H
   Caserotti, P
   Martin, KR
   Stehouwer, C
   Harris, T
AF Koster, A.
   van der Berg, J.
   Bosma, H.
   Caserotti, P.
   Martin, K. R.
   Stehouwer, C.
   Harris, T.
TI MIDLIFE DETERMINANTS OF SEDENTARY BEHAVIOR IN OLD AGE: THE
   AGES-REYKJAVIK STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Koster, A.; van der Berg, J.; Bosma, H.] Maastricht Univ, Maastricht, Netherlands.
   [Caserotti, P.] Univ Southern Denmark, Odense, Denmark.
   [Martin, K. R.; Harris, T.] NIA, Bethesda, MD 20892 USA.
   [Stehouwer, C.] Maastricht Univ Med Ctr, Maastricht, Netherlands.
RI Bosma, Hans/A-6184-2013
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 442
EP 443
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442105177
ER

PT J
AU Martin, KR
   Koster, A
   Murphy, RA
   Van Domelen, DR
   Hung, M
   Brychta, RJ
   Chen, KY
   Harris, T
AF Martin, K. R.
   Koster, A.
   Murphy, R. A.
   Van Domelen, D. R.
   Hung, M.
   Brychta, R. J.
   Chen, K. Y.
   Harris, T.
TI CHANGES IN SEDENTARY PATTERNS WITH ADVANCING AGE AMONG US MEN AND WOMEN
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Martin, K. R.; Murphy, R. A.; Van Domelen, D. R.; Hung, M.; Harris, T.] NIA, NIH, Lab Epidemiol & Populat Sci, Bethesda, MD 20892 USA.
   [Koster, A.] Maastricht Univ, Dept Social Med, CAPHRI, Sch Publ Hlth & Primary Care, Maastricht, Netherlands.
   [Brychta, R. J.; Chen, K. Y.] NIDDK, NIH, Diabet Endocrinol & Obes Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 442
EP 442
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442105175
ER

PT J
AU Mingo, CA
   O'Connor, ML
   Moreira, RO
   McIlvane, JM
AF Mingo, C. A.
   O'Connor, M. L.
   Moreira, R. O.
   McIlvane, J. M.
TI PREDICTORS OF PERCEIVED DAILY STRESS AMONG OLDER BLACK AND WHITE WOMEN
   WITH ARTHRITIS: A DAILY DIARY STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Mingo, C. A.] Georgia State Univ, Inst Gerontol, Atlanta, GA 30303 USA.
   [O'Connor, M. L.; Moreira, R. O.] N Dakota State Univ, Dept Human Dev & Family Sci, Fargo, ND 58105 USA.
   [McIlvane, J. M.] NINR, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 460
EP 461
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442105258
ER

PT J
AU Boudreau, R
   Province, MA
   Elo, IT
   Sebastiani, P
   Newman, AB
   Hadley, E
AF Boudreau, R.
   Province, M. A.
   Elo, I. T.
   Sebastiani, P.
   Newman, A. B.
   Hadley, E.
TI PREDICTING FUTURE LONGEVITY IN LLFS OFFSPRING BASED ON THE
   CARDIOVASCULAR HEALTH STUDY (CHS) COHORT
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Boudreau, R.; Newman, A. B.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
   [Province, M. A.] Washington Univ, St Louis, MO USA.
   [Elo, I. T.] Univ Penn, Philadelphia, PA 19104 USA.
   [Sebastiani, P.] Boston Univ, Boston, MA 02215 USA.
   [Hadley, E.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 506
EP 506
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442105449
ER

PT J
AU Ward, RE
   Caserotti, P
   Harris, T
   Vinik, AI
   Simonsick, EM
   Cauley, JA
   Newman, AB
   Strotmeyer, ES
AF Ward, R. E.
   Caserotti, P.
   Harris, T.
   Vinik, A. I.
   Simonsick, E. M.
   Cauley, J. A.
   Newman, A. B.
   Strotmeyer, E. S.
TI LONGITUDINAL SENSORY AND MOTOR PERIPHERAL NERVE FUNCTION AND INCIDENT
   MOBILITY LIMITATION
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ward, R. E.; Cauley, J. A.; Newman, A. B.; Strotmeyer, E. S.] Univ Pittsburgh, Pittsburgh, PA USA.
   [Caserotti, P.] Univ Southern Denmark, Odense, Denmark.
   [Harris, T.] NIA, Lab Epidemiol Biometry & Demog, NIH, Bethesda, MD 20892 USA.
   [Vinik, A. I.] Eastern Virginia Med Sch, Dept Neurobiol, Norfolk, VA 23501 USA.
   [Simonsick, E. M.] NIA, Clin Res Branch, NIH, Baltimore, MD 21224 USA.
RI Strotmeyer, Elsa/F-3015-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 520
EP 520
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442105517
ER

PT J
AU Shea, K
   Kritchevsky, SB
   Hsu, F
   Booth, SL
   Nevitt, M
   Kwoh, K
   Harrris, TB
   Loeser, RF
AF Shea, K.
   Kritchevsky, S. B.
   Hsu, F.
   Booth, S. L.
   Nevitt, M.
   Kwoh, K.
   Harrris, T. B.
   Loeser, R. F.
TI VITAMIN K STATUS AND KNEE OSTEOARTHRITIS PROGRESSION IN OLDER ADULTS:
   THE HEALTH ABC STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Shea, K.; Kritchevsky, S. B.; Hsu, F.; Loeser, R. F.] Wake Forest Univ, Winston Salem, NC 27109 USA.
   [Booth, S. L.] Tufts Univ, Boston, MA 02111 USA.
   [Nevitt, M.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
   [Kwoh, K.] Univ Pittsburgh, Pittsburgh, PA USA.
   [Harrris, T. B.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 521
EP 521
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442105520
ER

PT J
AU Thorpe, R
   Spira, AP
   Kay, N
   Ayonayon, HN
   Garcia, M
   Satterfield, S
   Simonsick, EM
AF Thorpe, R.
   Spira, A. P.
   Kay, N.
   Ayonayon, H. N.
   Garcia, M.
   Satterfield, S.
   Simonsick, E. M.
TI SLEEP, RACE, AND MOBILITY LIMITATION: FINDINGS FROM THE HEALTH AGING AND
   BODY COMPOSITION STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Thorpe, R.; Spira, A. P.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
   [Garcia, M.; Simonsick, E. M.] NIA, Baltimore, MD 21224 USA.
   [Kay, N.] Univ Florida, Gainesville, FL USA.
   [Satterfield, S.] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA.
   [Ayonayon, H. N.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 521
EP 521
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442105519
ER

PT J
AU Bernard, M
AF Bernard, M.
TI UPDATE ON NIA RESEARCH IN WOMEN'S HEALTH
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Bernard, M.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 522
EP 522
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442105526
ER

PT J
AU Maggio, M
   Lauretani, F
   Ceda, G
   Ferrucci, L
AF Maggio, M.
   Lauretani, F.
   Ceda, G.
   Ferrucci, L.
TI THE MULTI-DOMAIN MOBILITY LAB IN OLDER PERSONS: FROM BENCH TO BEDSIDE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Maggio, M.; Ceda, G.] Univ Parma, I-43100 Parma, Italy.
   [Maggio, M.; Lauretani, F.; Ceda, G.] Univ Hosp Parma, Parma, Italy.
   [Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 538
EP 538
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442106043
ER

PT J
AU Hohman, TJ
   Pacheco, J
   Thornton-Wells, T
   Resnick, S
AF Hohman, T. J.
   Pacheco, J.
   Thornton-Wells, T.
   Resnick, S.
TI SUBJECTIVE COGNITIVE COMPLAINTS PREDICT CHANGES IN BRAIN STRUCTURE
   DURING NORMAL AGING AND DEMENTIA
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Hohman, T. J.; Thornton-Wells, T.] Vanderbilt Univ Sch Med, Nashville, TN USA.
   [Hohman, T. J.; Pacheco, J.; Resnick, S.] NIA, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 567
EP 567
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442106196
ER

PT J
AU Marcum, CS
   Koehly, L
   Ashida, S
AF Marcum, C. S.
   Koehly, L.
   Ashida, S.
TI WHO GIVES AND WHO CARES? IDENTIFYING PRIMARY CAREGIVERS IN ALZHEIMER'S
   DISEASE PATIENTS' NETWORKS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Marcum, C. S.; Koehly, L.; Ashida, S.] NHGRI, SBRB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 570
EP 570
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442106210
ER

PT J
AU Caserotti, P
   Ward, RE
   Glynn, NW
   Harris, T
   Strotmeyer, ES
AF Caserotti, P.
   Ward, R. E.
   Glynn, N. W.
   Harris, T.
   Strotmeyer, E. S.
TI LEG PRESS AND TASK BASED POWER MEASURES DIFFERENTIALLY ASSOCIATED WITH
   PHYSICAL PERFORMANCE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Caserotti, P.] Univ Southern Denamrk, Inst Sports Sci & Clin Biomech, Odense, Denmark.
   [Ward, R. E.; Glynn, N. W.; Strotmeyer, E. S.] Univ Pittsburgh, Pittsburgh, PA USA.
   [Harris, T.] NIA, Intramural Res Program, Bethesda, MD 20892 USA.
RI Strotmeyer, Elsa/F-3015-2014
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 572
EP 573
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442106220
ER

PT J
AU Correa-de-Araujo, R
AF Correa-de-Araujo, R.
TI CRAFTING A NEW TERMINOLOGY FOR SARCOPENIA
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Correa-de-Araujo, R.] NIA, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 573
EP 573
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442106225
ER

PT J
AU Glynn, NW
   Santanasto, AJ
   Boudreau, R
   Koster, A
   Caserotti, P
   Lange-Maia, B
   Harris, T
   Newman, AB
AF Glynn, N. W.
   Santanasto, A. J.
   Boudreau, R.
   Koster, A.
   Caserotti, P.
   Lange-Maia, B.
   Harris, T.
   Newman, A. B.
TI CHOOSING AN OPTIMAL SELF-REPORT PHYSICAL ACTIVITY MEASURE FOR OLDER
   ADULTS: DOES FUNCTION MATTER?
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Glynn, N. W.; Santanasto, A. J.; Boudreau, R.; Lange-Maia, B.; Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
   [Koster, A.] Maastricht Univ, Maastricht, Netherlands.
   [Caserotti, P.] Univ Southern Denmark, Odense, Denmark.
   [Harris, T.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 573
EP 573
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442106223
ER

PT J
AU Hvid, L
   Ward, RE
   Strotmeyer, ES
   Glynn, NW
   Harris, T
   Caserotti, P
AF Hvid, L.
   Ward, R. E.
   Strotmeyer, E. S.
   Glynn, N. W.
   Harris, T.
   Caserotti, P.
TI POWER MEASURES ARE DIFFERENTIALLY RELATED TO USUAL AND FAST 400M WALK
   INDEPENDENT OF STRENGTH
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Hvid, L.; Caserotti, P.] Univ Southern Denmark, Inst Sports Sci & Clin Biomech, Odense, Denmark.
   [Ward, R. E.; Strotmeyer, E. S.; Glynn, N. W.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
   [Harris, T.] NIA, Intramural Res Program, Bethesda, MD 20892 USA.
RI Strotmeyer, Elsa/F-3015-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 573
EP 573
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442106221
ER

PT J
AU Genther, DJ
   Betz, J
   Harris, T
   Purchase-Helzner, E
   Xue, Q
   Yaffe, K
   Simonsick, EM
   Lin, FR
AF Genther, D. J.
   Betz, J.
   Harris, T.
   Purchase-Helzner, E.
   Xue, Q.
   Yaffe, K.
   Simonsick, E. M.
   Lin, F. R.
TI ASSOCIATION OF HEARING LOSS AND MORTALITY IN OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Genther, D. J.; Lin, F. R.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
   [Betz, J.; Xue, Q.; Lin, F. R.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD USA.
   [Harris, T.; Simonsick, E. M.] NIA, Bethesda, MD 20892 USA.
   [Genther, D. J.; Betz, J.; Xue, Q.; Lin, F. R.] Johns Hopkins Ctr Aging & Hlth, Baltimore, MD USA.
   [Purchase-Helzner, E.] SUNY Downstate, Brooklyn, NY USA.
   [Yaffe, K.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 591
EP 592
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442106320
ER

PT J
AU Chen, DS
   Betz, J
   Yaffe, K
   Harris, T
   Purchase-Helzner, E
   Xue, Q
   Simonsick, EM
   Lin, FR
AF Chen, D. S.
   Betz, J.
   Yaffe, K.
   Harris, T.
   Purchase-Helzner, E.
   Xue, Q.
   Simonsick, E. M.
   Lin, F. R.
TI ASSOCIATION OF HEARING LOSS WITH PHYSICAL FUNCTIONAL DECLINE IN OLDER
   ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Chen, D. S.] Johns Hopkins Sch Med, Baltimore, MD USA.
   [Betz, J.; Xue, Q.; Lin, F. R.] Johns Hopkins Med Inst, Ctr Aging & Hlth, Baltimore, MD 21205 USA.
   [Simonsick, E. M.] NIA, Intramural Res Program, Baltimore, MD 21224 USA.
   [Harris, T.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
   [Purchase-Helzner, E.] Suny Downstate Med Ctr, Dept Epidemiol & Biostat, Brooklyn, NY 11203 USA.
   [Yaffe, K.] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
   [Yaffe, K.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA.
   [Lin, F. R.] Johns Hopkins Univ, Sch Med, Dept Otolaryngol Head & Neck Surg, Baltimore, MD 21205 USA.
   [Lin, F. R.] Johns Hopkins Univ, Dept Geriatr Med, Baltimore, MD USA.
   [Lin, F. R.] Johns Hopkins Univ, Dept Mental Hlth, Baltimore, MD USA.
   [Lin, F. R.] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA.
   [Yaffe, K.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 592
EP 592
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442106321
ER

PT J
AU Evans, J
AF Evans, J.
TI RESEARCH AND PRACTICE PRIORITIES FOR SUICIDE PREVENTION IN LATER LIFE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Evans, J.] NIMH, Geriatr Res Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2013
VL 53
SU 1
BP 593
EP 594
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 258EN
UT WOS:000327442106331
ER

PT J
AU Amorosa, VK
   Luetkemeyer, A
   Kang, M
   Johnson, VA
   Umbleja, T
   Haas, DW
   Yesmin, S
   Bardin, MC
   Chung, RT
   Alston-Smith, B
   Tebas, P
   Peters, MG
AF Amorosa, Valerianna K.
   Luetkemeyer, Anne
   Kang, Minhee
   Johnson, Victoria A.
   Umbleja, Triin
   Haas, David W.
   Yesmin, Suria
   Bardin, Matthew C.
   Chung, Ray T.
   Alston-Smith, Beverly
   Tebas, Pablo
   Peters, Marion G.
TI Addition of Nitazoxanide to PEG-IFN and Ribavirin to Improve HCV
   Treatment Response in HIV-1 and HCV Genotype 1 Coinfected Persons Naive
   to HCV Therapy: Results of the ACTG A5269 Trial
SO HIV CLINICAL TRIALS
LA English
DT Article
DE genotype 1; hepatitis C; HIV; nitazoxanide; pegylated interferon;
   ribavirin
ID CHRONIC HEPATITIS-C; HOMEOSTASIS MODEL ASSESSMENT; SIMPLE NONINVASIVE
   INDEX; VIROLOGICAL RESPONSE; SIGNIFICANT FIBROSIS; INSULIN-RESISTANCE;
   VIRUS; PROGRAM; PREDICT; PLASMA
AB Background: We hypothesized that nitazoxanide (NTZ) added to pegylated interferon alfa-2a (PEG-IFN) and weight-based ribavirin (WBR) would improve hepatitis C virus (HCV) virologic responses in HCV treatment-nave HIV-1/HCV genotype 1 coinfected persons. Methods: Prospective, single-arm study in which subjects received 4-week lead-in (NTZ 500 mg twice daily) followed by 48 weeks of NTZ, PEG-IFN, and WBR. We compared the HCV virologic responses of these subjects to historical controls from the completed ACTG study A5178 who received PEG-IFN and WBR and had similar subject characteristics. Primary endpoints were early virologic response and complete early virologic response (EVR and cEVR). Results: Among 67 subjects (78% male; 48% Black; median age, 50 years), EVR was achieved in 65.7% (90% CI, 55.0%-75.3%), cEVR in 38.8% (28.8%-49.6%). and SVR in 32.8% (23.4%-43.5%). EVR was higher with NTZ (51.4% in A5178; P = .03), but the sustained virologic response (SVR) proportion was similar (27.3% in A5178; P = .24). In contrast to A5178, SVR was similar across IL28B genotypes. Overall, NTZ was safe and well-tolerated. Conclusion: Whereas EVR proportion improved significantly in this pilot study, the addition of NTZ to PEG-IFN/WBR did not significantly improve SVR compared to historical controls. NTZ may be associated with an attenuation of the effect of IL28B on HCV treatment response.
C1 [Amorosa, Valerianna K.] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA USA.
   [Amorosa, Valerianna K.; Tebas, Pablo] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Luetkemeyer, Anne; Peters, Marion G.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
   [Kang, Minhee; Umbleja, Triin] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
   [Johnson, Victoria A.] Birmingham Vet Affairs Med Ctr, Birmingham, AL USA.
   [Johnson, Victoria A.] Univ Alabama Birmingham, Sch Med, Birmingham, AL USA.
   [Haas, David W.] Vanderbilt Univ Sch Med, Nashville, TN USA.
   [Yesmin, Suria] ACTG Operat Ctr, Silver Spring, MD USA.
   [Bardin, Matthew C.] Romark Labs LC, Tampa, FL USA.
   [Chung, Ray T.] Harvard Univ, Sch Med, Boston, MA USA.
   [Alston-Smith, Beverly] NIAID, Div Aids, NIH, Bethesda, MD 20892 USA.
RP Amorosa, VK (reprint author), Philadelphia VAMC, Dept Med, Univ & Woodlawn Ave,8th Floor, Philadelphia, PA 19010 USA.
EM valerianna.amorosa@uphs.upenn.edu
FU National Center for Advancing Translational Sciences (NCATS) component
   of the National Institutes of Health [UL1RR024989]; NIH Roadmap for
   Medical Research
FX This publication was made possible by the Clinical and Translational
   Science Collaborative of Cleveland grant UL1RR024989 from the National
   Center for Advancing Translational Sciences (NCATS) component of the
   National Institutes of Health and NIH Roadmap for Medical Research. Its
   contents are solely the responsibility of the authors and do not
   necessarily represent the official views of the NIH.
NR 17
TC 3
Z9 3
U1 0
U2 2
PU THOMAS LAND PUBLISHERS, INC
PI ST LOUIS
PA 255 JEFFERSON RD, ST LOUIS, MO 63119-3627 USA
SN 1528-4336
EI 1945-5771
J9 HIV CLIN TRIALS
JI HIV Clin. Trials
PD NOV-DEC
PY 2013
VL 14
IS 6
BP 274
EP 283
DI 10.1310/hct1408-274
PG 10
WC Infectious Diseases; Pharmacology & Pharmacy
SC Infectious Diseases; Pharmacology & Pharmacy
GA 272EQ
UT WOS:000328443500002
PM 24334180
ER

PT J
AU Dossou, KSS
   Devkota, KP
   Morton, C
   Egan, JM
   Lu, GH
   Beutler, JA
   Moaddel, R
AF Dossou, Katina S. S.
   Devkota, Krishna P.
   Morton, Cynthia
   Egan, Josephine M.
   Lu, Guanghua
   Beutler, John A.
   Moaddel, Ruin
TI Identification of CB1/CB2 Ligands from Zanthoxylum bungeanum
SO JOURNAL OF NATURAL PRODUCTS
LA English
DT Article
ID CANNABINOID RECEPTOR; ACID-AMIDES; ALKYLAMIDES; INHIBITION; ACTIVATION;
   EXPRESSION; CELLS
AB In order to study cannabinoid receptor ligands, a novel plate-based assay was developed previously to measure internalization of CB1/CB2 receptors by determining the change in the intracellular levels of the radiolabeled agonists. This plate-based assay was also used for screening against complex matrices, specifically, in the present study screening for CB1/CB2 receptor activity of extracts for several species of the plant genus Zanthoxylum. The objective of this screen was to identify novel antagonists of the 031 receptor, which simultaneously displayed agonist activity against the CB2 receptor, since compounds matching this criterion could be potential candidates for the treatment of type-1 diabetes. As a result, two Z. bungeanum extracts were deemed active, leading to the identification of eight compounds, of which compound 7 [(2E,4E,8E,10E,12E)-N-isobutyl-2,4,8,10,12-tetradecapentaenamide, gamma-sanshool] was obtained as a promising lead compound.
C1 [Dossou, Katina S. S.; Egan, Josephine M.; Moaddel, Ruin] NIA, Biomed Res Ctr, NIH, Baltimore, MD 21224 USA.
   [Devkota, Krishna P.; Beutler, John A.] NCI, Mol Targets Lab, Ctr Canc Res, Frederick, MD 21702 USA.
   [Morton, Cynthia] Carnegie Museum Nat Hist, Sect Bot, Pittsburgh, PA 15213 USA.
   [Lu, Guanghua] Chengdu Univ Tradit Chinese Med, Sch Pharm, Key Lab Minist Educ China Standardizat Chinese Ma, Chengdu 611137, Peoples R China.
RP Moaddel, R (reprint author), NIA, Biomed Res Ctr, NIH, 251 Bayview Blvd,Suite 100, Baltimore, MD 21224 USA.
EM moaddelru@grc.nia.nih.gov
FU National Institute of Aging, NIH; NIH, National Cancer Institute, Center
   for Cancer Research; NIH Office of Dietary Supplements
   [OD-Y2-OD-1557-01]
FX This research was supported by the Intramural Research Program of the
   National Institute of Aging, NIH, and, in part, by the Intramural
   Research Program of the NIH, National Cancer Institute, Center for
   Cancer Research. The work was supported, in part, by funds from the NIH
   Office of Dietary Supplements, grant OD-Y2-OD-1557-01. We thank Dr.
   C.-T. Che of the University of Illinois at Chicago for arranging for the
   collections of the Chinese Zanthoxylum species. We thank Drs. S. Tarasov
   and M. Dyba (Biophysics Resource Core, Structural Biophysics Laboratory,
   CCR) for assistance with mass spectrometry. We thank Drs. A. Tucker and
   R. J. Sahraoui (Delaware State University) for the image of Z. bungeanum
   in the graphical abstract.
NR 26
TC 11
Z9 11
U1 2
U2 14
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 NOV
PY 2013
VL 76
IS 11
BP 2060
EP 2064
DI 10.1021/np400478c
PG 5
WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy
SC Plant Sciences; Pharmacology & Pharmacy
GA 261PT
UT WOS:000327677800008
PM 24175626
ER

PT J
AU Sekula, RF
   Frederickson, AM
   Arnone, GD
   Quigley, MR
   Hallett, M
AF Sekula, Raymond F., Jr.
   Frederickson, Andrew M.
   Arnone, Gregory D.
   Quigley, Matthew R.
   Hallett, Mark
TI MICROVASCULAR DECOMPRESSION FOR HEMIFACIAL SPASM IN PATIENTS > 65 YEARS
   OF AGE: AN ANALYSIS OF OUTCOMES AND COMPLICATIONS
SO MUSCLE & NERVE
LA English
DT Article
DE botulinum toxin; cranial nerve; elderly; hemifacial spasm; microvascular
   decompression
ID QUALITY-OF-LIFE; DELAYED FACIAL PALSY; TRIGEMINAL NEURALGIA;
   ELDERLY-PATIENTS; CONSECUTIVE PATIENTS; CLINICAL ARTICLE; SAFETY;
   SERIES; NERVE; SCALE
AB Introduction: Few data are available to quantify the risks and benefits of microvascular decompression (MVD) in elderly patients with hemifacial spasm. Methods: Twenty-seven patients >65 years of age and 104 younger patients who underwent MVD for hemifacial spasm (HFS) over a 3-year period were analyzed retrospectively and compared. Results: Twenty-six (96.3%) elderly patients and 93 of 104 (89.4%) young patients reported a spasm-free status at a mean follow-up of 26.5 months after MVD. No significant difference in spasm-free status was noted. Cranial nerve complications and other major complications were compared, with no significant differences observed. Conclusions: Although this study does not offer definitive inclusion or exclusion criteria or clearly establish the safety of MVD for HFS in the elderly, our experience suggests that many elderly patients with HFS can undergo MVD safely, with outcomes and risk profiles similar to those of younger patients.
C1 [Sekula, Raymond F., Jr.; Frederickson, Andrew M.] Univ Pittsburgh, Med Ctr, Hamot Hosp, Erie, PA USA.
   [Arnone, Gregory D.] Univ Illinois, Dept Neurosurg, Chicago, IL 60612 USA.
   [Quigley, Matthew R.] Carnegie Mellon Univ, Dept Biomed Engn, Pittsburgh, PA 15213 USA.
   [Hallett, Mark] NINDS, Human Motor Control Sect, Bethesda, MD 20892 USA.
RP Sekula, RF (reprint author), Univ Pittsburgh, Med Ctr, Dept Neurol Surg, 200 Lothrop St, Pittsburgh, PA 15213 USA.
EM sekularf@upmc.edu
NR 42
TC 5
Z9 6
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0148-639X
EI 1097-4598
J9 MUSCLE NERVE
JI Muscle Nerve
PD NOV
PY 2013
VL 48
IS 5
BP 770
EP 776
DI 10.1002/mus.23800
PG 7
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 268BA
UT WOS:000328141600013
PM 24000070
ER

PT J
AU Maynard, S
   Keijzers, G
   Gram, M
   Desler, C
   Bendix, L
   Budtz-Jorgensen, E
   Molbo, D
   Croteau, DL
   Osler, M
   Stevnsner, T
   Rasmussen, LJ
   Dela, F
   Avlund, K
   Bohr, VA
AF Maynard, Scott
   Keijzers, Guido
   Gram, Martin
   Desler, Claus
   Bendix, Laila
   Budtz-Jorgensen, Esben
   Molbo, Drude
   Croteau, Deborah L.
   Osler, Merete
   Stevnsner, Tinna
   Rasmussen, Lene Juel
   Dela, Flemming
   Avlund, Kirsten
   Bohr, Vilhelm A.
TI Relationships between human vitality and mitochondrial respiratory
   parameters, reactive oxygen species production and dNTP levels in
   peripheral blood mononuclear cells
SO AGING-US
LA English
DT Article
DE vitality; mitochondrial respiration; reactive oxygen species;
   deoxyribonucleotides
ID CHRONIC-FATIGUE-SYNDROME; OXIDATIVE STRESS; REDOX REGULATION;
   FREE-RADICALS; DYSFUNCTION; DAMAGE; FIBROMYALGIA; SYMPTOMS; DISORDER;
   SF-36
AB Low vitality (a component of fatigue) in middle-aged and older adults is an important complaint often identified as a symptom of a disease state or side effect of a treatment. No studies to date have investigated the potential link between dysfunctional mitochondrial ATP production and low vitality. Therefore, we measured a number of cellular parameters related to mitochondrial activity in peripheral blood mononuclear cells (PBMCs) isolated from middle-aged men, and tested for association with vitality. These parameters estimate mitochondrial respiration, reactive oxygen species (ROS) production, and deoxyribonucleotide (dNTP) balance in PBMCs. The population was drawn from the Metropolit cohort of men born in 1953. Vitality level was estimated from the Medical Outcomes Study Short Form 36 (SF-36) vitality scale. We found that vitality score had no association with any of the mitochondrial respiration parameters. However, vitality score was inversely associated with cellular ROS production and cellular deoxythymidine triphosphate (dTTP) levels and positively associated with deoxycytidine triphosphate (dCTP) levels. We conclude that self-reported persistent low vitality is not associated with specific aspects of mitochondrial oxidative phosphorylation capacity in PBMCs, but may have other underlying cellular dysfunctions that contribute to dNTP imbalance and altered ROS production.
C1 [Maynard, Scott; Keijzers, Guido; Gram, Martin; Desler, Claus; Molbo, Drude; Rasmussen, Lene Juel; Dela, Flemming; Avlund, Kirsten] Univ Copenhagen, Ctr Hlth Aging, DK-2200 Copenhagen N, Denmark.
   [Maynard, Scott; Keijzers, Guido; Desler, Claus; Rasmussen, Lene Juel] Univ Copenhagen, Dept Cellular & Mol Med, DK-2200 Copenhagen N, Denmark.
   [Keijzers, Guido; Bendix, Laila; Osler, Merete; Stevnsner, Tinna; Avlund, Kirsten] Univ Aarhus, Danish Aging Res Ctr, DK-8000 Aarhus C, Denmark.
   [Keijzers, Guido; Bendix, Laila; Osler, Merete; Stevnsner, Tinna; Avlund, Kirsten] Univ Southern Denmark, Danish Aging Res Ctr, Odense, Denmark.
   [Keijzers, Guido; Bendix, Laila; Osler, Merete; Stevnsner, Tinna; Avlund, Kirsten] Univ Copenhagen, Danish Aging Res Ctr, DK-1168 Copenhagen, Denmark.
   [Gram, Martin; Dela, Flemming] Univ Copenhagen, Dept Biomed Sci, DK-2200 Copenhagen N, Denmark.
   [Bendix, Laila; Budtz-Jorgensen, Esben; Molbo, Drude; Avlund, Kirsten] Univ Copenhagen, Dept Publ Hlth, DK-1014 Copenhagen K, Denmark.
   [Croteau, Deborah L.; Bohr, Vilhelm A.] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
   [Osler, Merete] Glostrup Univ Hosp, Res Ctr Prevent & Hlth, DK-2600 Glostrup, Denmark.
   [Stevnsner, Tinna] Univ Aarhus, Dept Mol Biol & Genet, DK-8000 Aarhus C, Denmark.
RP Bohr, VA (reprint author), NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
EM bohr@nih.gov
OI Budtz-Jorgensen, Esben/0000-0002-5551-0724; Osler,
   Merete/0000-0002-6921-220X
FU Nordea-fonden; VELUX FOUNDATION
FX This work was supported by grants from Nordea-fonden and the VELUX
   FOUNDATION. The authors thank the staff at the Department of Public
   Health and the National Research Center for the Working Environment who
   undertook the CAMB data collection. Further thanks to Helle Bruunsgaard,
   Nils-Erik Fiehn, Poul Holm-Pedersen, and Erik Lykke Mortensen who
   initiated and established the Copenhagen Aging and Midlife Biobank from
   2009-2011 together with Kirsten Avlund, Ase Marie Hansen, Rikke Lund and
   Merete Osler. The authors thank Miriam Sander, PhD, and Morten
   Scheibye-Knudsen, MD, for their careful review of the manuscript. We
   also thank David Ferrick, PhD, Martin Brand, PhD, and Victor M.
   Darley-Usmar, PhD, for their constructive comments.
NR 58
TC 13
Z9 13
U1 0
U2 4
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 NOV
PY 2013
VL 5
IS 11
BP 850
EP 864
PG 15
WC Cell Biology
SC Cell Biology
GA 268TV
UT WOS:000328194300008
PM 24304678
ER

PT J
AU Haberzettl, R
   Bert, B
   Fink, H
   Fox, MA
AF Haberzettl, Robert
   Bert, Bettina
   Fink, Heidrun
   Fox, Meredith A.
TI Animal models of the serotonin syndrome: A systematic review
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Review
DE 5-HT-enhancing drug; 5-HT agonist; Animal model; Core response; Mouse;
   Rat; Serotonin; Serotonin syndrome; Validity
ID MONOAMINE-OXIDASE INHIBITOR; HEAD-TWITCH BEHAVIOR; BETA-ADRENOCEPTOR
   AGONISTS; CENTRAL 5-HT1A RECEPTORS; CENTRAL-NERVOUS-SYSTEM; WET-DOG
   SHAKES; INCREASED BRAIN 5-HYDROXYTRYPTAMINE; TRANSPORTER
   (SERT)-DEFICIENT MICE; NEUROLEPTIC MALIGNANT SYNDROME; NORADRENALINE
   RE-UPTAKE
AB The serotonin syndrome (SS) is a potentially life-threatening disorder in humans which is induced by ingestion of an overdose or by combination of two or more serotonin (5-HT)-enhancing drugs. In animals, acute administration of direct and indirect 5-HT agonists also leads to a set of behavioral and autonomic responses. In the current review, we provide an overview of the existing versions of the animal model of the SS. With a focus on studies in rats and mice, we analyze the frequency of behavioral and autonomic responses following administration of 5-HT-enhancing drugs and direct 5-HT agonists administered alone or in combination, and we briefly discuss the receptor mediation of these responses. Considering species differences, we identify a distinct set of behavioral and autonomic responses that are consistently observed following administration of direct and indirect 5-HT agonists. Finally, we discuss the importance of a standardized assessment of SS responses in rodents and the utility of animal models of the SS in translational studies, and provide suggestions for future research. (C) 2013 The Authors. Published by Elsevier B.V. All rights reserved.
C1 [Haberzettl, Robert; Bert, Bettina; Fink, Heidrun] Free Univ Berlin, Sch Vet Med, Inst Pharmacol & Toxicol, D-14195 Berlin, Germany.
   [Fox, Meredith A.] NIMH, NIH, Bethesda, MD 20892 USA.
RP Bert, B (reprint author), Free Univ Berlin, Sch Vet Med, Inst Pharmacol & Toxicol, Koserstr 20, D-14195 Berlin, Germany.
EM bettina.bert@fu-berlin.de
OI Bert, Bettina/0000-0002-8202-9290
FU Elsa-Neumann-Doctoral-Fellowship from the Land Berlin; NIMH Intramural
   Research Program
FX Robert Haberzettl received financial support from the
   Elsa-Neumann-Doctoral-Fellowship from the Land Berlin. This review was
   also supported by the NIMH Intramural Research Program (MAF).
NR 253
TC 23
Z9 26
U1 6
U2 16
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
EI 1872-7549
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD NOV 1
PY 2013
VL 256
BP 328
EP 345
DI 10.1016/j.bbr.2013.08.045
PG 18
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 267JO
UT WOS:000328094100041
PM 24004848
ER

PT J
AU Bat, T
   Steinberg, SM
   Childs, R
   Calvo, KR
   Barrett, AJ
   Battiwalla, M
   Baird, K
   Zhang, D
   Pulanic, D
   Dunbar, CE
   Pavletic, SZ
AF Bat, T.
   Steinberg, S. M.
   Childs, R.
   Calvo, K. R.
   Barrett, A. J.
   Battiwalla, M.
   Baird, K.
   Zhang, D.
   Pulanic, D.
   Dunbar, C. E.
   Pavletic, S. Z.
TI Active thrombopoiesis is associated with worse severity and activity of
   chronic GVHD
SO BONE MARROW TRANSPLANTATION
LA English
DT Article
DE Chronic GVHD; NIH score; platelets; AIPN
ID VERSUS-HOST-DISEASE; STEM-CELL TRANSPLANTATION; PROGNOSTIC-FACTORS;
   THROMBOCYTOPENIA; DESTRUCTION; CRITERIA
AB Chronic GVHD (cGVHD) is a major complication of allogeneic hematopoietic SCT. Post transplant thrombocytopenia in patients with cGVHD has been associated with poor outcome and its etiology is unclear. We investigated whether thrombopoiesis, assessed via measurement of the absolute immature platelet number (AIPN) in the blood, is impaired in cGVHD, and whether the level of thrombopoiesis correlates with the severity and activity of cGVHD as assessed via the National Institutes of Health (NIH) organ scoring system. We used a cohort of 110 well-characterized cGVHD patients, including 83 (75%) with severe cGVHD per NIH global score. Higher AIPN was associated with active therapeutic intent (P = 0.026), lower Karnofsky score (P = 0.0013), worse joint/fascia cGVHD (P = 0.0005) and worse skin cGVHD (P = 0.0044). AIPN correlated with platelet counts and was not correlated with ANC, WBC, C-reactive protein (CRP), absolute lymphocyte count (ALC), albumin, total and average NIH scores, or number of prior systemic therapies. AIPN values for cGVHD patients substantially overlapped those of the normal population. Higher AIPN, as marker of active thrombopoiesisis, was associated with worse severity and activity of cGVHD, especially skin and joints/fascia manifestations. Among patients with stable moderate or severe cGVHD, there was no evidence of hypoproduction of platelets. Future studies should further investigate the role of thrombopoiesis in cGVHD.
C1 [Bat, T.; Childs, R.; Barrett, A. J.; Battiwalla, M.; Dunbar, C. E.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Steinberg, S. M.] NCI, Biostat & Data Management Sect, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Calvo, K. R.] NIH, Hematol Sect, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Baird, K.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Zhang, D.; Pulanic, D.; Pavletic, S. Z.] NCI, Expt Immunol & Transplantat Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Pulanic, D.] Clin Hosp Ctr Zagreb, Dept Internal Med, Div Hematol, Zagreb, Croatia.
RP Dunbar, CE (reprint author), NHLBI, NIH, 9000 Rockville Pike,Bldg 10CRC,Room 4E-5132, Bethesda, MD 20892 USA.
EM dunbarc@nhlbi.nih.gov
OI Calvo, Katherine/0000-0002-0771-4191
FU Intramural NIH HHS [ZIA HL006063-04]
NR 22
TC 4
Z9 5
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
EI 1476-5365
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD NOV
PY 2013
VL 48
IS 12
BP 1569
EP 1573
DI 10.1038/bmt.2013.95
PG 5
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 266VC
UT WOS:000328051000015
PM 23832091
ER

EF