FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Papas, RK
Sidle, JE
Gakinya, BN
Baliddawa, JB
Martino, S
Mwaniki, MM
Songole, R
Omolo, OE
Kamanda, AM
Ayuku, DO
Ojwang, C
Owino-Ong'or, WD
Harrington, M
Bryant, KJ
Carroll, KM
Justice, AC
Hogan, JW
Maisto, SA
AF Papas, Rebecca K.
Sidle, John E.
Gakinya, Benson N.
Baliddawa, Joyce B.
Martino, Steve
Mwaniki, Michael M.
Songole, Rogers
Omolo, Otieno E.
Kamanda, Allan M.
Ayuku, David O.
Ojwang, Claris
Owino-Ong'or, Willis D.
Harrington, Magdalena
Bryant, Kendall J.
Carroll, Kathleen M.
Justice, Amy C.
Hogan, Joseph W.
Maisto, Stephen A.
TI Treatment outcomes of a stage 1 cognitive-behavioral trial to reduce
alcohol use among human immunodeficiency virus-infected out-patients in
western Kenya
SO ADDICTION
LA English
DT Article
DE Alcohol; cognitive-behavioral therapy; HIV; Kenya; randomized clinical
trial
ID COLLABORATIVE PROJECT; DRINKING BEHAVIOR; HIV-INFECTION; COPING SKILLS;
SELF-REPORTS; RISK; CONSUMPTION; CARE; PSYCHOTHERAPY; INTERVENTION
AB Aims Dual epidemics of human immunodeficiency virus (HIV) and alcohol use disorders, and a dearth of professional resources for behavioral treatment in sub-Saharan Africa, suggest the need for development of culturally relevant and feasible interventions. The purpose of this study was to test the preliminary efficacy of a culturally adapted six-session gender-stratified group cognitive-behavioral therapy (CBT) intervention delivered by paraprofessionals to reduce alcohol use among HIV-infected out-patients in Eldoret, Kenya. Design Randomized clinical trial comparing CBT against a usual care assessment-only control. Setting A large HIV out-patient clinic in Eldoret, Kenya, part of the Academic Model for Providing Access to Healthcare collaboration. Participants Seventy-five HIV-infected outpatients who were antiretroviral (ARV)-initiated or ARV-eligible and who reported hazardous or binge drinking. Measurements Percentage of drinking days (PDD) and mean drinks per drinking days (DDD) measured continuously using the Time line Follow back method. Findings There were 299 ineligible and 102 eligible out-patients with 12 refusals. Effect sizes of the change in alcohol use since baseline between the two conditions at the 30-day follow-up were large [d = 0.95, P = 0.0002, mean difference = 24.93, 95% confidence interval (CI): 12.43, 37.43 PDD; d = 0.76, P = 0.002, mean difference = 2.88, 95% CI: 1.05, 4.70 DDD]. Randomized participants attended 93% of the six CBT sessions offered. Reported alcohol abstinence at the 90-day follow-up was 69% (CBT) and 38% (usual care). Paraprofessional counselors achieved independent ratings of adherence and competence equivalent to college-educated therapists in the United States. Treatment effect sizes were comparable to alcohol intervention studies conducted in the United States. Conclusions Cognitive-behavioral therapy can be adapted successfully to group paraprofessional delivery in Kenya and may be effective in reducing alcohol use among HIV-infected Kenyan out-patients.
C1 [Papas, Rebecca K.] Brown Univ, Alpert Med Sch, Dept Psychiat & Human Behav, Providence, RI 02906 USA.
[Sidle, John E.; Gakinya, Benson N.; Baliddawa, Joyce B.; Songole, Rogers; Omolo, Otieno E.; Ayuku, David O.; Owino-Ong'or, Willis D.] Moi Univ, Sch Med, Eldoret, Kenya.
[Sidle, John E.] Indiana Univ Sch Med, Indianapolis, IN USA.
[Martino, Steve; Carroll, Kathleen M.; Justice, Amy C.] Yale Univ, Sch Med, New Haven, CT USA.
[Mwaniki, Michael M.; Kamanda, Allan M.] Kenya Hlth Behav Study, Eldoret, Kenya.
[Ojwang, Claris] USAID AMPATH Partnership, Eldoret, Kenya.
[Harrington, Magdalena] Rhode Isl Hosp, Providence, RI USA.
[Bryant, Kendall J.] NIAAA, Rockville, MD 20852 USA.
[Maisto, Stephen A.] Syracuse Univ, Syracuse, NY USA.
RP Papas, RK (reprint author), Brown Univ, Alpert Med Sch, Dept Psychiat & Human Behav, Providence, RI 02906 USA.
EM rebecca_papas@brown.edu
RI Hogan, Joseph/J-4579-2014;
OI Hogan, Joseph/0000-0001-7959-7361; Carroll, Kathleen/0000-0003-3263-3374
FU NIAAA [R21AA016884]; United States Agency for International Development;
[P50DA09241]
FX This research was sponsored by NIAAA-funded R21AA016884. It was also
supported in part by a grant to the USAID-AMPATH Partnership from the
United States Agency for International Development as part of the
President's Emergency Plan for AIDS Relief and by P50DA09241. We would
like to thank Joanne Corvino and Karen Hunkele for providing
consultation about treatment integrity, Traci Green, Charla Nich and
Jing Zhang for providing consultation about statistical analyses and
Tobista Nafula for her assistance with treatment delivery and data
quality monitoring. We also thank Robert Skipworth Comer from the
Indiana University School of Informatics for the contribution and
development of locally relevant CBT illustrations. We extend our
appreciation to Chematics, Inc. of North Webster, Indiana for the
generous donation of alcohol saliva tests for this project. We thank the
AMPATH clinic staff for facilitating this research. Finally, we thank
the participants in this project for providing contributions to the
development of this intervention.
NR 53
TC 28
Z9 28
U1 4
U2 7
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0965-2140
J9 ADDICTION
JI Addiction
PD DEC
PY 2011
VL 106
IS 12
BP 2156
EP 2166
DI 10.1111/j.1360-0443.2011.03518.x
PG 11
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 841SU
UT WOS:000296534200017
PM 21631622
ER
PT J
AU Leng, SX
Qu, T
Semba, RD
Li, HF
Yao, X
Nilles, T
Yang, X
Manwani, B
Walston, JD
Ferrucci, L
Fried, LP
Margolick, JB
Bream, JH
AF Leng, Sean X.
Qu, Tao
Semba, Richard D.
Li, Huifen
Yao, Xu
Nilles, Tricia
Yang, Xi
Manwani, Bhavish
Walston, Jeremy D.
Ferrucci, Luigi
Fried, Linda P.
Margolick, Joseph B.
Bream, Jay H.
TI Relationship between cytomegalovirus (CMV) IgG serology, detectable CMV
DNA in peripheral monocytes, and CMV pp65(495-503)-specific CD8(+) T
cells in older adults
SO AGE
LA English
DT Article
DE Monocytic CMV DNA; CMV pp65(495-503)-specific CD8+T cells; CMV IgG
serology; Older adults
ID SWEDISH NONA IMMUNE; LYMPHOCYTE SUBPOPULATIONS; MULTICENTER EVALUATION;
SINGLE-PLATFORM; INFECTION; REACTIVATION; REPERTOIRE; CD4(+); LATENT;
AGE
AB In immunocompetent individuals, cytomegalovirus (CMV) is thought to persist in a latent state in monocytes and myeloid progenitor cells, establishing a lifelong infection. In CMV-seropositive older adults, aging has been associated with both expansion of CMV pp65(495-503)-specific CD8(+) T cell clones and shrinkage of the T cell repertoire that characterize T cell immunosenescence. In fact it has been suggested that chronic CMV infection is a driving force in age-related T cell immunosenescence. In older adults, chronic CMV infection is conventionally diagnosed by positive IgG serology which does not distinguish between past and persistent infections. To better define the relationship between chronic CMV infection and expansion of CMV pp65(495-503)-specific CD8(+) T cells, we directly assessed CMV viral DNA in monocyte-enriched peripheral blood mononuclear cells in 16 HLA-A2-positive elderly volunteers (mean age = 83 years). While all participants had positive CMV IgG serology by enzyme-linked immunosorbent assays, only nine (56%) had detectable CMV DNA by nested polymerase chain reaction. These nine individuals had significantly higher percentages of CMV pp65(495-503) tetramer-positive CD8(+) T cells (median = 1.3%) than those without detectable CMV DNA (median = 0.1%; p < 0.001). Absolute CMV IgG antibody titers did not differ between these two groups (median = 54.6 vs 44.2 EU/ml, respectively, p = 0.4). CMV IgM titers were negative for all 16 participants, suggesting that recent primary CMV infection was unlikely. These results demonstrate a strong association between the presence of CMV DNA in peripheral monocytes and the expansion of CD8(+) T cells specific for the CMV immunodominant epitope pp65(495-503). Although the sample size in this study is relatively small, these findings provide initial evidence suggesting the heterogeneity of CMV IgG-seropositive older adult population and CMV viral DNA detection in peripheral monocytes as an informative tool to better understand the relationship between chronic CMV infection and T cell immunosenescence.
C1 [Leng, Sean X.; Qu, Tao; Li, Huifen; Yao, Xu; Yang, Xi; Manwani, Bhavish; Walston, Jeremy D.] Johns Hopkins Univ, Sch Med, Div Geriatr Med & Gerontol, Dept Med, Baltimore, MD 21224 USA.
[Semba, Richard D.] Johns Hopkins Univ, Sch Med, Dept Ophthalmol, Baltimore, MD 21224 USA.
[Nilles, Tricia; Margolick, Joseph B.; Bream, Jay H.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Mol Microbiol & Immunol, Baltimore, MD 21205 USA.
[Ferrucci, Luigi] NIA, Clin Res Branch, Longitudinal Studies Sect, Baltimore, MD 21224 USA.
[Fried, Linda P.] Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA.
RP Leng, SX (reprint author), Johns Hopkins Univ, Sch Med, Div Geriatr Med & Gerontol, Dept Med, 5505 Hopkins Bayview Circle, Baltimore, MD 21224 USA.
EM sleng1@jhmi.edu; jbream@jhsph.edu
FU Paul Beeson Career Development Award in Aging Research [K23 AG028963];
Johns Hopkins Older American Independence Center; National Institute on
Aging [P30 AG021334]
FX Dr. Sean Leng is a current recipient of the Paul Beeson Career
Development Award in Aging Research, K23 AG028963, support also from
Johns Hopkins Older American Independence Center funded by National
Institute on Aging, P30 AG021334 (PI: Jeremy Walston).
NR 35
TC 19
Z9 19
U1 2
U2 5
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0161-9152
J9 AGE
JI Age
PD DEC
PY 2011
VL 33
IS 4
BP 607
EP 614
DI 10.1007/s11357-011-9205-9
PG 8
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 841IR
UT WOS:000296506500009
PM 21274637
ER
PT J
AU Faupel-Badger, JM
Fichorova, RN
Allred, EN
Hecht, JL
Dammann, O
Leviton, A
McElrath, TF
AF Faupel-Badger, Jessica M.
Fichorova, Raina N.
Allred, Elizabeth N.
Hecht, Jonathan L.
Dammann, Olaf
Leviton, Alan
McElrath, Thomas F.
TI Cluster Analysis of Placental Inflammatory Proteins can Distinguish
Preeclampsia from Preterm Labor and Premature Membrane Rupture in
Singleton Deliveries Less Than 28 Weeks of Gestation
SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
LA English
DT Article
DE Inflammation; placenta; preterm delivery; preterm labor; preterm
premature membrane rupture
ID INTRAVENTRICULAR HEMORRHAGE; EXPRESSION; PATHOLOGY; INFANTS; LESIONS;
DAMAGE; BIRTH
AB Problem
Inflammation within the preterm placenta is common and leads to adverse outcomes for premature infants. The risks of complications are different between iatrogenic (e. g. PE) and spontaneous (e. g. PL and membrane rupture) causes of preterm delivery, suggesting different underlying biology contributes to these placental conditions.
Method of study
Thirty preterm singleton placentas from the following groups were analyzed: (i) severe PE, (ii) preterm premature membrane rupture (pPROM), and (iii) PL. Proinflammatory and anti-inflammatory cytokines, adhesion and angiogenic molecules were measured in placental lysates using a multiplex assay. K-means cluster analysis was used to generate patterns of protein level intensity.
Results
Three cluster patterns were apparent. Placentas from PE had high levels of vascular endothelial growth factor (VEGF) combined with low levels of acute inflammatory proteins (IL-1 beta, IL-18, IL-6, TNF-alpha), low IL-1 RA, and high transforming growth factor beta (TGF-beta). PL and pPROM had higher anti-inflammatory IL-1 RA and thrombomodulin combined with lower VEGF, regardless of proinflammatory cytokines and adhesion molecules. Half of the PL and pPROM cases had clusters of heightened inflammatory responses (lower TGF-beta clustered with higher intensity of inflammatory mediators).
Conclusion
Discriminating protein patterns were elucidated and may serve as a foundation from which to understand the biologic mechanisms underlying these pregnancy complications.
C1 [Faupel-Badger, Jessica M.] NCI, Canc Prevent Fellowship Program, Bethesda, MD 20892 USA.
[Fichorova, Raina N.; McElrath, Thomas F.] Brigham & Womens Hosp, Dept Obstet & Gynecol, Boston, MA 02115 USA.
[Allred, Elizabeth N.; Leviton, Alan] Childrens Hosp Boston, Neuroepidemiol Unit, Boston, MA USA.
[Hecht, Jonathan L.] Beth Israel Deaconess Med Ctr, Dept Pathol, Boston, MA USA.
[Dammann, Olaf] Tufts Med Ctr, Floating Hosp Children, Div Newborn Med, Boston, MA USA.
RP Faupel-Badger, JM (reprint author), NCI, Canc Prevent Fellowship Program, 6120 Execut Blvd EPS,Suite 150E,MSC 7105, Bethesda, MD 20892 USA.
EM badgerje@mail.nih.gov
RI Fichorova, Raina/G-9969-2014
FU National Institutes of Health - Institute of Neurological Disorders and
Stroke [U01 NS 40069-05]; NIH [K12 HD01255]
FX This work was supported by the National Institutes of Health - Institute
of Neurological Disorders and Stroke (U01 NS 40069-05). Dr McElrath
received support as a NICHD Women's Reproductive Health Research Scholar
(NIH K12 HD01255).
NR 28
TC 10
Z9 12
U1 0
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1046-7408
J9 AM J REPROD IMMUNOL
JI Am. J. Reprod. Immunol.
PD DEC
PY 2011
VL 66
IS 6
BP 488
EP 494
DI 10.1111/j.1600-0897.2011.01023.x
PG 7
WC Immunology; Reproductive Biology
SC Immunology; Reproductive Biology
GA 846KJ
UT WOS:000296896300006
PM 21623999
ER
PT J
AU Lee, J
Romero, R
Xu, Y
Kim, JS
Park, JY
Kusanovic, JP
Chaiworapongsa, T
Hassan, SS
Kim, CJ
AF Lee, JoonHo
Romero, Roberto
Xu, Yi
Kim, Jung-Sun
Park, Ji Young
Pedro Kusanovic, Juan
Chaiworapongsa, Tinnakorn
Hassan, Sonia S.
Kim, Chong Jai
TI Maternal HLA Panel-Reactive Antibodies in Early Gestation Positively
Correlate with Chronic Chorioamnionitis: Evidence in Support of the
Chronic Nature of Maternal Anti-fetal Rejection
SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
LA English
DT Article
DE Human leukocyte antigen; panel-reactive antibody; pregnancy; preterm
birth
ID NEONATAL ALLOIMMUNE THROMBOCYTOPENIA; REGULATORY T-CELLS; INFLAMMATORY
RESPONSE SYNDROME; IMMUNOGLOBULIN-G ANTIBODIES; UNKNOWN ETIOLOGY;
ALLOGRAFT-REJECTION; FETAL TOLERANCE; PRETERM BIRTH; TRANSPLANT
RECIPIENTS; HEART-TRANSPLANTATION
AB Problem
Maternal tolerance of the fetus is essential for viviparity, yet anti-fetal rejection occurs in several pregnancy complications. Chronic chorioamnionitis is a feature of anti-fetal cellular rejection. There is a robust association between chronic chorioamnionitis and maternal seropositivity for antihuman leukocyte antigen (HLA) panel-reactive antibodies (PRA) at the time of delivery. This longitudinal study was performed to assess maternal HLA PRA status in early gestation and the temporal evolution of maternal HLA PRA in the context of chronic chorioamnionitis and, thereby, to determine whether HLA PRA during the course of pregnancy is useful for the detection of anti-fetal rejection.
Method of study
Maternal sera obtained before 16 weeks of gestation and at delivery were analyzed for HLA PRA in cases with (N = 100) and without (N = 150) chronic chorioamnionitis.
Results
IgG (but not IgM) HLA class I and II PRA positivity at delivery was higher in cases with chronic chorioamnionitis than in those without chronic chorioamnionitis. IgG HLA class I PRA positivity before 16 weeks of gestation was higher in cases with chronic chorioamnionitis than in those without (30.3 versus 13.3%; P = 0.001). Positive conversion (negative HLA PRA before 16 weeks of gestation but positive at delivery) of IgG HLA class I and II PRA was significantly associated with chronic chorioamnionitis. Fetal HLA class I antigen-specific antibodies were confirmed in 12 of 16 mothers tested who were sensitized to HLA class I antigens before 16 weeks of gestation.
Conclusion
Positive maternal HLA PRA before 16 weeks of gestation and the temporal evolution of maternal HLA PRA are associated with the presence of chronic chorioamnionitis at the time of delivery. Maternal IgG HLA PRA has the potential to be a monitoring tool of anti-fetal rejection. Furthermore, the findings herein indicate that subsets of fetuses are exposed to alloimmune HLA antibodies for months, especially in cases with chronic chorioamnionitis.
C1 [Kim, Chong Jai] Wayne State Univ, Sch Med, Dept Pathol, Detroit, MI 48201 USA.
[Romero, Roberto] NICHD, Perinatol Res Branch, NIH, DHHS,Hutzel Womens Hosp, Detroit, MI 48201 USA.
[Lee, JoonHo; Romero, Roberto; Xu, Yi; Pedro Kusanovic, Juan; Chaiworapongsa, Tinnakorn; Hassan, Sonia S.; Kim, Chong Jai] NICHD, Perinatol Res Branch, NIH, DHHS, Bethesda, MD USA.
[Kim, Jung-Sun] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pathol, Seoul, South Korea.
[Park, Ji Young] Hallym Univ, Coll Med, Dept Lab Med, Seoul, South Korea.
[Pedro Kusanovic, Juan] Hosp Dr Sotero del Rio, Dept Obstet & Gynecol, Santiago, Chile.
[Pedro Kusanovic, Juan] Pontificia Univ Catolica Chile, Dept Obstet & Gynecol, Sch Med, Santiago, Chile.
[Chaiworapongsa, Tinnakorn; Hassan, Sonia S.] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA.
RP Kim, CJ (reprint author), Wayne State Univ, Sch Med, Dept Pathol, Hutzel Womens Hosp, 3990 John R St, Detroit, MI 48201 USA.
EM prbchiefstaff@med.wayne.edu; cjkim@med.wayne.edu
FU Perinatology Research Branch, Division of Intramural Research, Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health, U. S. Department of Health
and Human Services
FX This study was supported by the Perinatology Research Branch, Division
of Intramural Research, Eunice Kennedy Shriver National Institute of
Child Health and Human Development, National Institutes of Health, U. S.
Department of Health and Human Services.
NR 99
TC 21
Z9 22
U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1046-7408
J9 AM J REPROD IMMUNOL
JI Am. J. Reprod. Immunol.
PD DEC
PY 2011
VL 66
IS 6
BP 510
EP 526
DI 10.1111/j.1600-0897.2011.01066.x
PG 17
WC Immunology; Reproductive Biology
SC Immunology; Reproductive Biology
GA 846KJ
UT WOS:000296896300009
PM 21951517
ER
PT J
AU Park, SH
Kang, HJ
Kim, HS
Kim, MJ
Heo, JI
Kim, JH
Kho, YJ
Kim, SC
Kim, J
Park, JB
Lee, JY
AF Park, Seong-Hoon
Kang, Hong-Jun
Kim, Hyun-Seok
Kim, Min-Ju
Heo, Jee-In
Kim, Jeong-Hyeon
Kho, Yoon-Jung
Kim, Sung Chan
Kim, Jaebong
Park, Jae-Bong
Lee, Jae-Yong
TI Higher DNA repair activity is related with longer replicative life span
in mammalian embryonic fibroblast cells
SO BIOGERONTOLOGY
LA English
DT Article
DE DNA damage; DNA repair; DNA repair rate; Mammalian embryonic
fibroblasts; Replicative life span
ID HYDROGEN-PEROXIDE PRODUCTION; MITOCHONDRIAL SUPEROXIDE; TRANSCRIPTION
FACTORS; DERMAL FIBROBLASTS; HUMAN-LYMPHOCYTES; OXIDATIVE DAMAGE;
POLYMERASE-BETA; EXCISION-REPAIR; IN-VITRO; AGE
AB Since the detailed comparison of DNA repair activities among mammalian embryonic fibroblast cells with different replicative life spans has not been investigated, we tested DNA repair activities in embryonic fibroblast cells derived from mammals including human, dog, rat, and mouse. The cell viability after treatment of four DNA damage agents appeared to be decreased in the order of human embryonic fibroblasts (HEFs) > dog embryonic fibroblasts (DEFs) > rat embryonic fibroblasts (REFs) > mouse embryonic fibroblasts (MEFs) although statistical significance was lacking. The amounts of strand breaks and AP (apurinic/apyrimidinic) sites also appear to be decreased in the order of HEFs > DEFs > REFs a parts per thousand yen MEFs after treatment of DNA damage agents. The DNA repair activities and rates including base excision repair (BER), nucleotide excision repair (NER) and double-strand break repair (DSBR) including non-homologous end-joining (NHEJ) decreased again in the order of HEFs > DEFs > REFs a parts per thousand yen MEFs. BER and NHEJ activities in 3% O(2) also decreased in the order of HEFs > DEFs > REFs > MEFs. This order in DNA repair activity appears to be coincident with that of replicative life span of fibroblasts and that of life span of mammals. These results indicate that higher DNA repair activity is related with longer replicative life span in embryonic fibroblast cells.
C1 [Heo, Jee-In; Kho, Yoon-Jung; Lee, Jae-Yong] Hallym Univ, Coll Med, Inst Nat Med, Chunchon 200702, Gangwon Do, South Korea.
[Park, Seong-Hoon; Kim, Hyun-Seok] Vanderbilt Univ, Dept Radiat Oncol, Nashville, TN 37232 USA.
[Park, Seong-Hoon; Kim, Hyun-Seok] Vanderbilt Univ, Dept Pediat, Nashville, TN 37232 USA.
[Kang, Hong-Jun] NIDDK, Genet Dis Res Sect, NIH, Bethesda, MD 20892 USA.
[Kim, Min-Ju] Hallym Univ, Coll Med, Dept Anat & Neurobiol, Chunchon 200702, Gangwon Do, South Korea.
[Heo, Jee-In; Kim, Jeong-Hyeon; Kim, Sung Chan; Kim, Jaebong; Park, Jae-Bong; Lee, Jae-Yong] Hallym Univ, Coll Med, Dept Biochem, Chunchon 200702, Gangwon Do, South Korea.
RP Lee, JY (reprint author), Hallym Univ, Coll Med, Inst Nat Med, Chunchon 200702, Gangwon Do, South Korea.
EM jyolee@hallym.ac.kr
FU National Research Foundation of Korea (NRF); Ministry of Education,
Science and Technology [2010-0029642]; Priority Research Centers
FX This work was supported by Priority Research Centers Program through the
National Research Foundation of Korea (NRF) funded by the Ministry of
Education, Science and Technology (2010-0029642).
NR 41
TC 2
Z9 2
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1389-5729
J9 BIOGERONTOLOGY
JI Biogerontology
PD DEC
PY 2011
VL 12
IS 6
BP 565
EP 579
DI 10.1007/s10522-011-9355-2
PG 15
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 842WU
UT WOS:000296633300007
PM 21879286
ER
PT J
AU Britton, JC
Rauch, SL
AF Britton, Jennifer C.
Rauch, Scott L.
TI Attention Bias Modification and the Serotonin Transporter: Personalized
Treatment Implications of Gene Interactions with Learning
SO BIOLOGICAL PSYCHIATRY
LA English
DT Editorial Material
ID RANDOMIZED CONTROLLED-TRIAL; INDIVIDUALS; BEHAVIOR; DISORDER
C1 [Britton, Jennifer C.] NIMH, Sect Dev & Affect Neurosci, Bethesda, MD 20892 USA.
[Rauch, Scott L.] McLean Hosp, Belmont, MA 02178 USA.
RP Britton, JC (reprint author), NIMH, Sect Dev & Affect Neurosci, 9000 Rockville Pike,Bldg 15K, Bethesda, MD 20892 USA.
EM brittonjen@mail.nih.gov
RI Britton, Jennifer/J-4501-2013
FU NIMH NIH HHS [K99-MH091183-01]
NR 9
TC 2
Z9 2
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD DEC 1
PY 2011
VL 70
IS 11
BP 1004
EP 1005
DI 10.1016/j.biopsych.2011.09.028
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 842FL
UT WOS:000296578800002
PM 22045036
ER
PT J
AU Kumar, G
Tison, CK
Chatterjee, K
Pine, PS
McDaniel, JH
Salit, ML
Young, MF
Simon, CG
AF Kumar, Girish
Tison, Christopher K.
Chatterjee, Kaushik
Pine, P. Scott
McDaniel, Jennifer H.
Salit, Marc L.
Young, Marian F.
Simon, Carl G., Jr.
TI The determination of stem cell fate by 3D scaffold structures through
the control of cell shape
SO BIOMATERIALS
LA English
DT Article
DE Bone tissue engineering; Cell morphology; Nanotopography; Osteogenesis;
Scaffolds; Stem cell
ID OSTEOGENIC DIFFERENTIATION; STROMAL CELLS; MATRIX
AB Stem cell response to a library of scaffolds with varied 3D structures was investigated. Microarray screening revealed that each type of scaffold structure induced a unique gene expression signature in primary human bone marrow stromal cells (hBMSCs). Hierarchical cluster analysis showed that treatments sorted by scaffold structure and not by polymer chemistry suggesting that scaffold structure was more influential than scaffold composition. Further, the effects of scaffold structure on hBMSC function were mediated by cell shape. Of all the scaffolds tested, only scaffolds with a nanofibrous morphology were able to drive the hBMSCs down an osteogenic lineage in the absence of osteogenic supplements. Nanofiber scaffolds forced the hBMSCs to assume an elongated, highly branched morphology. This same morphology was seen in osteogenic controls where hBMSCs were cultured on flat polymer films in the presence of osteogenic supplements (OS). In contrast, hBMSCs cultured on flat polymer films in the absence of OS assumed a more rounded and less-branched morphology. These results indicate that cells are more sensitive to scaffold structure than previously appreciated and suggest that scaffold efficacy can be optimized by tailoring the scaffold structure to force cells into morphologies that direct them to differentiate down the desired lineage. Published by Elsevier Ltd.
C1 [Kumar, Girish; Tison, Christopher K.; Chatterjee, Kaushik; Simon, Carl G., Jr.] NIST, Div Polymers, Gaithersburg, MD 20899 USA.
[Kumar, Girish; Chatterjee, Kaushik; Young, Marian F.] Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD 20892 USA.
[Chatterjee, Kaushik] Indian Inst Sci, Dept Mat Engn, Bangalore 560012, Karnataka, India.
[Pine, P. Scott; McDaniel, Jennifer H.; Salit, Marc L.] NIST, Div Biochem Sci, Gaithersburg, MD 20899 USA.
RP Simon, CG (reprint author), NIST, Div Polymers, 100 Bur Dr, Gaithersburg, MD 20899 USA.
EM carl.simon@nist.gov
FU NIH-NIBIB/NIST NRC; NIST NRC; NIST; NIH/NIDCR (National Institute of
Dental and Craniofacial Research); NCRR of the NIH [P40RR017447]
FX G.K. and K.C. were supported by an NIH-NIBIB/NIST NRC Research
Associateship. C.K.T. was supported by a NIST NRC Research
Associateship. This work was supported by NIST and the Intramural
Program of the NIH/NIDCR (National Institute of Dental and Craniofacial
Research). Some of the materials employed in this work were provided by
the Tulane Center for Gene Therapy through a grant from NCRR of the NIH
P40RR017447. The "standard deviation" (S.D.) is the same as the
"combined standard uncertainty of the mean" for the purposes of this
work. The content is solely the responsibility of the authors and does
not necessarily represent the official views of NIH, NIBIB, NIDCR or
NIST. This article, a contribution of NIST, is not subject to US
copyright. Certain equipment and instruments or materials are identified
in the paper to adequately specify the experimental details. Such
identification does not imply recommendation by NIST, nor does it imply
the materials are necessarily the best available for the purpose.
NR 31
TC 107
Z9 108
U1 5
U2 55
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0142-9612
J9 BIOMATERIALS
JI Biomaterials
PD DEC
PY 2011
VL 32
IS 35
BP 9188
EP 9196
DI 10.1016/j.biomaterials.2011.08.054
PG 9
WC Engineering, Biomedical; Materials Science, Biomaterials
SC Engineering; Materials Science
GA 843PK
UT WOS:000296684200005
PM 21890197
ER
PT J
AU Buch, S
Yao, HH
Guo, ML
Mori, T
Su, TP
Wang, J
AF Buch, Shilpa
Yao, Honghong
Guo, Minglei
Mori, Tomohisa
Su, Tsung-Ping
Wang, John
TI Cocaine and HIV-1 Interplay: Molecular Mechanisms of Action and
Addiction
SO JOURNAL OF NEUROIMMUNE PHARMACOLOGY
LA English
DT Review
DE HIV; Cocaine; CNS
ID IMMUNODEFICIENCY-VIRUS TYPE-1; D-ASPARTATE RECEPTOR; CONDITIONED PLACE
PREFERENCE; MONONUCLEAR CELL COCULTURES; POLYAMINE-SENSITIVE-SITE;
MESSENGER-RNA EXPRESSION; CENTRAL-NERVOUS-SYSTEM; EARLY GENE-EXPRESSION;
D1 DOPAMINE-RECEPTOR; INJECTION-DRUG-USERS
AB Human immunodeficiency virus (HIV) infection is now being driven by drug-abusing populations. Epidemiological studies on drug abusers with AIDS link abuse of cocaine, even more than other drugs, to increased incidence of HIV seroprevalence and progression to AIDS. Both cell culture and animal studies demonstrate that cocaine can both potentiate HIV replication and can potentiate HIV proteins to cause enhanced glial cell activation, neurotoxicity, and breakdown of the blood-brain barrier. Based on the ability of both HIV proteins and cocaine to modulate NMDA receptor on neurons, NMDA receptors have been suggested as a common link underlying the crosstalk between drug addiction and HIV infection. While the role of dopamine system as a major target of cocaine cannot be overlooked, recent studies on the role of sigma receptors in mediating the effects of cocaine in both cell and organ systems warrants a deeper understanding of their functional role in the field. In this review, recent findings on the interplay of HIV infection and cocaine abuse and their possible implications in mode of action and/or addiction will be discussed.
C1 [Buch, Shilpa; Yao, Honghong] Univ Nebraska Med Ctr, Dept Pharmacol & Expt Neurosci, Omaha, NE 68198 USA.
[Guo, Minglei; Wang, John] Univ Missouri, Kansas City Sch Med, Dept Basic Med Sci, Kansas City, MO 64108 USA.
[Mori, Tomohisa; Su, Tsung-Ping] NIDA, Cellular Pathobiol Sect, Cellular Neurobiol Res Branch, IRP,NIH, Baltimore, MD 21224 USA.
RP Buch, S (reprint author), Univ Nebraska Med Ctr, Dept Pharmacol & Expt Neurosci, 985880 Nebraska Med Ctr,DRC 8011, Omaha, NE 68198 USA.
EM sbuch@unmc.edu
OI Guo, Ming-Lei/0000-0003-2969-0802; Buch, Shilpa/0000-0002-3103-6685
FU Intramural NIH HHS [ZIA DA000206-25]; NIDA NIH HHS [R01 DA010355]; NIMH
NIH HHS [R01 MH061469]
NR 128
TC 20
Z9 20
U1 2
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1557-1890
J9 J NEUROIMMUNE PHARM
JI J. Neuroimmune Pharm.
PD DEC
PY 2011
VL 6
IS 4
SI SI
BP 503
EP 515
DI 10.1007/s11481-011-9297-0
PG 13
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 843DC
UT WOS:000296651500007
PM 21766222
ER
PT J
AU Sinha, R
Sara, UVS
Khosa, RL
Stables, J
Jain, J
AF Sinha, Reema
Sara, U. V. Singh
Khosa, R. L.
Stables, James
Jain, Jainendra
TI Nicotinic acid hydrazones: a novel anticonvulsant pharmacophore
SO MEDICINAL CHEMISTRY RESEARCH
LA English
DT Article
DE Aryl acid hydrazones; Anticonvulsant activity; Antiepileptic drug
design; Maximal electroshock test; scPTZ; Docking; GABA-AT
ID ANTIEPILEPTIC DRUG DEVELOPMENT; AGENTS; SEMICARBAZONES; GENERATION;
DOCKING; DESIGN
AB A series of aryl acid hydrazones of substituted aromatic acid hydrazides (D (1) to D (20)) were synthesised and evaluated for anticonvulsant activity. Aryl acid hydrazones of Nicotinic acid hydrazide (D (8), D (9), and D (10)) have displayed excellent protection in maximal electroshock screen. These compounds have also exhibited excellent binding properties with Lys 329 residue of gamma amino butyrate amino transferase (GABA-AT) in Lamarckian genetic algorithm based flexible docking studies. Compound D (8), N (1)-(4-chlorobenzylidene) nicotinohydrazide was found to be the most potent analog with ED(50) value of 16.1 mg/kg and protective index (PI = TD(50)/ED(50)) value of > 20, which was much greater than that of the prototype drug phenytoin (PI = 6.9). It has shown free binding energy value of -10.20 kcal/mol and inhibition constant (Ki) value of 33.30 nM for GABA-AT, indicating that aryl acid hydrazones of nicotinic acid hydrazide could be considered as a new pharmacophore in the design of novel anticonvulsant drugs.
C1 [Sinha, Reema; Jain, Jainendra] RamEesh Inst Vocat & Tech Educ, Greater Noida 201308, Uttar Pradesh, India.
[Sara, U. V. Singh] DJ Coll Pharm, Ghaziabad 201202, Uttar Pradesh, India.
[Khosa, R. L.] Bharat Inst Technol, Dept Pharm, Meerut 250103, Uttar Pradesh, India.
[Stables, James] NINDS, NIH, Bethesda, MD 20892 USA.
RP Jain, J (reprint author), RamEesh Inst Vocat & Tech Educ, 3 Knowledge Pk 1, Greater Noida 201308, Uttar Pradesh, India.
EM jainendrem@yahoo.com
NR 19
TC 13
Z9 15
U1 0
U2 4
PU BIRKHAUSER BOSTON INC
PI CAMBRIDGE
PA 675 MASSACHUSETTS AVE, CAMBRIDGE, MA 02139 USA
SN 1054-2523
J9 MED CHEM RES
JI Med. Chem. Res.
PD DEC
PY 2011
VL 20
IS 9
SI SI
BP 1499
EP 1504
DI 10.1007/s00044-010-9396-0
PG 6
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 840YK
UT WOS:000296477900012
ER
PT J
AU Gupta, A
Kashaw, SK
Jain, N
Rajak, H
Soni, A
Stables, JP
AF Gupta, Anjali
Kashaw, Sushil K.
Jain, Neha
Rajak, Harish
Soni, Abhishek
Stables, J. P.
TI Design and synthesis of some novel 3-[5-(4-substituted)
phenyl-1,3,4-oxadiazole-2yl]-2-phenylquinazoline-4(3H)-ones as possible
anticonvulsant agent
SO MEDICINAL CHEMISTRY RESEARCH
LA English
DT Article
DE 1,3,4-Oxadiazole; Semicarbazone; Anticonvulsant
ID CNS-DEPRESSANT ACTIVITY; QUINAZOLINE-4(3H)-ONES
AB A novel series 7(a-f) 3-[5-(4-substituted) phenyl-1,3,4-oxadiazole-2yl]-2 phenylquinazoline-4(3H)-ones have been synthesized and screened for its anticonvulsant and neurotoxic activity. After i.p. injection to mice at doses of 30, 100, and 300 mg/kg body weight 2,3-disubstituted-quinazolin-4(3H)-ones were examined in the maximal electroshock induced seizures (MES) and subcutaneous pentylenetetrazole (scPTZ) induced seizure models in mice. Spectroscopic data were consistent with the structure of newly synthesized compounds. The neurotoxicity was assessed using the rotorod method. In the prepared series, 7a was found to be active in the MES screen at 0.5 h, whereas 7f showed anticonvulsant activity at both 0.5 and 4 h.
C1 [Gupta, Anjali; Kashaw, Sushil K.; Jain, Neha; Soni, Abhishek] Dr Hari Singh Gour Vishwavidyalaya, Pharmaceut Chem Div, Dept Pharmaceut Sci, Sagar 470003, MP, India.
[Rajak, Harish] Guru Ghasidas Univ, Inst Pharmaceut Sci, Bilaspur 495009, CG, India.
[Stables, J. P.] NIH, Preclin Pharmacol Sect, Epilepsy Branch, Bethesda, MD 20892 USA.
RP Kashaw, SK (reprint author), Dr Hari Singh Gour Vishwavidyalaya, Pharmaceut Chem Div, Dept Pharmaceut Sci, Sagar 470003, MP, India.
EM sushilkashaw@gmail.com
NR 18
TC 9
Z9 10
U1 0
U2 1
PU BIRKHAUSER BOSTON INC
PI CAMBRIDGE
PA 675 MASSACHUSETTS AVE, CAMBRIDGE, MA 02139 USA
SN 1054-2523
J9 MED CHEM RES
JI Med. Chem. Res.
PD DEC
PY 2011
VL 20
IS 9
SI SI
BP 1638
EP 1642
DI 10.1007/s00044-010-9475-2
PG 5
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 840YK
UT WOS:000296477900032
ER
PT J
AU Harlan, LC
Lynch, CF
Ballard-Barbash, R
Zeruto, C
AF Harlan, Linda C.
Lynch, Charles F.
Ballard-Barbash, Rachel
Zeruto, Christopher
TI Trends in the treatment and survival for local and regional cutaneous
melanoma in a US population-based study
SO MELANOMA RESEARCH
LA English
DT Article
DE sentinel lymph node biopsy; survival; surgery; treatment; tumor depth
ID HIGH-RISK MELANOMA; DOSE INTERFERON-ALPHA-2B; MALIGNANT-MELANOMA;
EXCISION MARGINS; ADJUVANT THERAPY; STAGE; METAANALYSIS
AB We examined trends in the treatment and survival in a population-based sample of white patients diagnosed with local-stage and regional-stage cutaneous melanoma in 1995, 1996, or 2001, treated in communities across the USA with vital status follow-up through 2007. White patients, aged 20 years or older with invasive cutaneous melanoma, were identified from the Surveillance, Epidemiology and End-Results population-based registries. Hospital and pathology records were reabstracted and physicians were asked to verify the provided therapy. The percentage of patients receiving lymph node biopsies increased over time. Sentinel lymph node biopsy increased between 1995 and 2001 from 5 to 32% for men and from 9 to 35% for women. The use of chemotherapy, hormonal therapy, and immunotherapy changed little. Facilities with approved residency training programs were more likely to perform lymph node dissections, to perform sentinel lymph node biopsy, and to treat patients more aggressively than were facilities without such programs. Men were significantly more likely than women to die of cutaneous melanoma. In multivariable survival analysis, after adjusting for age, Charlson score, and surgical margins, survival did not change significantly over this time. Deaths were associated with increasing tumor thickness for men and women. Surgical treatment of local or regional melanoma became more extensive over time with fewer local excisions and more lymph node dissections, but with little change in adjuvant therapy. Survival was associated with tumor thickness. Early detection when the tumor thickness is less may decrease mortality. Future research should especially target decreasing the disparity in survival between men and women. Melanoma Res 21:547-554 (C) 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins.
C1 [Harlan, Linda C.; Ballard-Barbash, Rachel] NCI, Appl Res Program, Bethesda, MD 20892 USA.
[Zeruto, Christopher] Informat Management Serv Inc, Silver Spring, MD USA.
[Lynch, Charles F.] Univ Iowa, Dept Epidemiol, Iowa City, IA USA.
RP Harlan, LC (reprint author), NCI, Appl Res Program, 6130 Execut Blvd,MSC 7344, Bethesda, MD 20892 USA.
EM lh50w@nih.gov
FU [N01-PC-35133]; [N01-PC-35135]; [N01-PC-35141]; [N01-PC-35136];
[N01-PC-35137]; [N01-PC-35138]; [N01-PC-35139]; [N01-PC-35142];
[N01-PC-35143]; [N01-PC-35145]; [N01-PC-54402]; [N01-PC-54404];
[N01-PC-54405]
FX N01-PC-35133, N01-PC-35135, N01-PC-35141, N01-PC-35136, N01-PC-35137,
N01-PC-35138, N01-PC-35139, N01-PC-35142, N01-PC-35143, N01-PC-35145,
N01-PC-54402, N01-PC-54404, N01-PC-54405.
NR 22
TC 3
Z9 3
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0960-8931
J9 MELANOMA RES
JI Melanoma Res.
PD DEC
PY 2011
VL 21
IS 6
BP 547
EP 554
DI 10.1097/CMR.0b013e32834b58e4
PG 8
WC Oncology; Dermatology; Medicine, Research & Experimental
SC Oncology; Dermatology; Research & Experimental Medicine
GA 844LX
UT WOS:000296749800011
PM 21897302
ER
PT J
AU Driscoll, I
Zhou, Y
An, Y
Sojkova, J
Davatzikos, C
Kraut, MA
Ye, WG
Ferrucci, L
Mathis, CA
Klunk, WE
Wong, DF
Resnick, SM
AF Driscoll, Ira
Zhou, Yun
An, Yang
Sojkova, Jitka
Davatzikos, Christos
Kraut, Michael A.
Ye, Weiguo
Ferrucci, Luigi
Mathis, Chester A.
Klunk, William E.
Wong, Dean F.
Resnick, Susan M.
TI Lack of association between C-11-PiB and longitudinal brain atrophy in
non-demented older individuals
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Alzheimer's disease; BLSA; Volumetric MRI; Normal aging: PET; C-11-PiB
ID MILD COGNITIVE IMPAIRMENT; PITTSBURGH COMPOUND-B; PRECLINICAL
ALZHEIMERS-DISEASE; CEREBROSPINAL-FLUID A-BETA(42); REFERENCE TISSUE
MODEL; SPATIAL CONSTRAINT; DEMENTIA; DIAGNOSIS; MRI; NEUROPATHOLOGY
AB Amyloid-beta plaques (A beta) are a hallmark of Alzheimer's disease (AD), begin deposition decades before the incipient disease, and are thought to be associated with neuronal loss, brain atrophy and cognitive impairment. We examine associations between C-11-PiB-PET measurement of A beta burden and brain volume changes in the preceding years in 57 non-demented individuals (age 64-86; M= 78.7). Participants were prospectively followed through the Baltimore Longitudinal Study of Aging, with up to 10 consecutive MRI scans (M = 8.1) and an C-11-PiB scan approximately 10 years after the initial MRI. Linear mixed effects models were used to determine whether mean cortical 11C-PiB distribution volume ratios, estimated by fitting a reference tissue model to the measured time activity curves, were associated with longitudinal regional brain volume changes of the whole brain, ventricular CSF, frontal, temporal, parietal, and occipital white and gray matter, the hippocampus, orbito-frontal cortex, and the precuneus. Despite significant longitudinal declines in the volumes of all investigated regions (p < 0.05), no associations were detected between current A beta burden and regional brain volume decline trajectories in the preceding years, nor did the regional volume trajectories differ between those with highest and lowest A beta burden. Consistent with a threshold model of disease, our findings suggest that A beta load does not seem to affect brain volume changes in individuals without dementia. Published by Elsevier Inc.
C1 [Driscoll, Ira] NIA, Biomed Res Ctr, IRP, NIH, Baltimore, MD 21224 USA.
[Zhou, Yun; Sojkova, Jitka; Kraut, Michael A.; Ye, Weiguo; Wong, Dean F.] Johns Hopkins Med Inst, Dept Radiol, Baltimore, MD USA.
[An, Yang] MedStar Res Inst, Baltimore, MD USA.
[Davatzikos, Christos] Univ Penn, Dept Radiol, Philadelphia, PA 19104 USA.
[Mathis, Chester A.] Univ Pittsburgh, Dept Radiol, Pittsburgh, PA 15260 USA.
[Klunk, William E.] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15260 USA.
RP Driscoll, I (reprint author), NIA, Biomed Res Ctr, IRP, NIH, 251 Bayview Blvd,Suite 100,Room 04B316, Baltimore, MD 21224 USA.
EM driscolli@mail.nih.gov; resnicks@mail.nih.gov
OI Klunk, William/0000-0001-5512-0251
FU NIH, National Institute on Aging (NIA) [N01-AG-3-2124, K24 DA00412]; NIA
[P01-AG025204, R37 AG025516, P50-AG005133]; MedStar Research Institute
FX We thank the staff of the PET facility at Johns Hopkins University and
the neuroimaging staff of the BLSA project National Institute on Aging
(NIA) for their assistance. Dr. Driscoll had full access to the data in
the study and takes responsibility for the integrity of the data and the
accuracy of the analysis. This research was supported in part by the
Intramural Research Program of the NIH, National Institute on Aging
(NIA), and N01-AG-3-2124 and K24 DA00412 (DFW). A portion of that
support was through an R&D contract with MedStar Research Institute. Dr.
Klunk and Dr. Mathis's contributions were supported by NIA grants
P01-AG025204, R37 AG025516 and P50-AG005133.
NR 40
TC 21
Z9 21
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD DEC
PY 2011
VL 32
IS 12
BP 2123
EP 2130
DI 10.1016/j.neurobiolaging.2009.12.008
PG 8
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA 839PJ
UT WOS:000296379900002
PM 20176414
ER
PT J
AU Kannangara, TS
Lucero, MJ
Gil-Mohapel, J
Drapala, RJ
Simpson, JM
Christie, BR
van Praag, H
AF Kannangara, Timal S.
Lucero, Melanie J.
Gil-Mohapel, Joana
Drapala, Robert J.
Simpson, Jessica M.
Christie, Brian R.
van Praag, Henriette
TI Running reduces stress and enhances cell genesis in aged mice
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Adult neurogenesis; Aging; Exercise; Hippocampus; Social environment;
Stress
ID LONG-TERM POTENTIATION; DENTATE GYRUS; VOLUNTARY EXERCISE; ENVIRONMENTAL
ENRICHMENT; HIPPOCAMPAL-NEURONS; PROGENITOR PROLIFERATION; SYNAPTIC
PLASTICITY; FREE CORTICOSTERONE; COGNITIVE DEFICITS; ALZHEIMERS-DISEASE
AB Cell proliferation and neurogenesis are diminished in the aging mouse dentate gyrus. However, it is not known whether isolated or social living affects cell genesis and stress levels in old animals To address this question, aged (17-18 months old) female C57B1/6 mice were single or group housed, under sedentary or running conditions. We demonstrate that both individual and socially housed aged C57B1/6 mice have comparable basal cell proliferation levels and demonstrate increased running-induced cell genesis. To assess stress levels in young and aged mice, corticosterone (CORT) was measured at the onset of the active/dark cycle and 4 h later. In young mice, no differences in CORT levels were observed as a result of physical activity or housing conditions. However, a significant increase in stress in socially housed, aged sedentary animals was observed at the onset of the dark cycle; CORT returned to basal levels 4 h later. Together, these results indicate that voluntary exercise reduces stress in group housed aged animals and enhances hippocampal cell proliferation. Published by Elsevier Inc.
C1 [van Praag, Henriette] NIA, Neuroplast & Behav Unit, Neurosci Lab, Biomed Res Ctr, Baltimore, MD 21224 USA.
[Kannangara, Timal S.; Gil-Mohapel, Joana; Simpson, Jessica M.; Christie, Brian R.] Univ Victoria, Div Med Sci, Victoria, BC, Canada.
[Kannangara, Timal S.; Christie, Brian R.] Univ British Columbia, Program Neurosci, Vancouver, BC V5Z 1M9, Canada.
[Kannangara, Timal S.; Drapala, Robert J.; Christie, Brian R.] Univ British Columbia, Dept Cellular & Physiol Sci, Vancouver, BC V5Z 1M9, Canada.
[Lucero, Melanie J.] Salk Inst Biol Studies, Genet Lab, La Jolla, CA 92037 USA.
RP van Praag, H (reprint author), NIA, Neuroplast & Behav Unit, Neurosci Lab, Biomed Res Ctr, Suite 100,251 Bayview Blvd, Baltimore, MD 21224 USA.
EM vanpraagh@mail.nih.gov
RI van Praag, Henriette/F-3939-2015;
OI van Praag, Henriette/0000-0002-5727-434X; Christie,
Brian/0000-0002-6830-0160
FU NSERC; CIHR; NIH, National Institute on Aging
FX The authors thank E. Wiebe, B.D. Eadie, A. Titterness, S. Howard, K.
Suter, N. Heivand, and S. See for advice and technical assistance. The
authors also thank Dr. Fred Gage for helpful discussions and for support
of initial experiments at the Salk Institute for Biological Studies, La
Jolla, CA. TSK holds a CGS scholarship from NSERC. JGM holds a
post-doctoral fellowship from NSERC. JMS holds a CGS scholarship from
NSERC. BRC is supported by grants from CIHR and NSERC and is a Michael
Smith Senior Scholar. HVP is supported by the Intramural Research
Program of the NIH, National Institute on Aging.
NR 40
TC 28
Z9 31
U1 1
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD DEC
PY 2011
VL 32
IS 12
BP 2279
EP 2286
DI 10.1016/j.neurobiolaging.2009.12.025
PG 8
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA 839PJ
UT WOS:000296379900017
PM 20106549
ER
PT J
AU Borghero, G
Floris, G
Cannas, A
Marrosu, MG
Murru, MR
Costantino, E
Parish, LD
Pugliatti, M
Ticca, A
Traynor, BJ
Calvo, A
Cammarosano, S
Moglia, C
Cistaro, A
Brunetti, M
Restagno, G
Chio, A
AF Borghero, Giuseppe
Floris, Gianluca
Cannas, Antonino
Marrosu, Maria G.
Murru, Maria R.
Costantino, Emanuela
Parish, Leslie D.
Pugliatti, Maura
Ticca, Anna
Traynor, Bryan J.
Calvo, Andrea
Cammarosano, Stefania
Moglia, Cristina
Cistaro, Angelina
Brunetti, Maura
Restagno, Gabriella
Chio, Adriano
TI A patient carrying a homozygous p.A382T TARDBP missense mutation shows a
syndrome including ALS, extrapyramidal symptoms, and FTD
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE amyotrophic lateral sclerosis; frontotemporal dementia; TARDBP;
homozygous mutation
ID AMYOTROPHIC-LATERAL-SCLEROSIS; TDP-43
AB We have recently published data showing that a founder mutation of the TARDBP gene (p.A382T) accounts for approximately one third of amyotrophic lateral sclerosis (ALS) cases on the Mediterranean island of Sardinia (Chi et al., 2011). In that report, we identified a 53-year-old man carrying a homozygous A382T missense mutation of the TARDBP gene with a complex neurological syndrome including amyotrophic lateral sclerosis, parkinsonian features, motor and vocal tics, and frontotemporal dementia (FTD). Due to the uniqueness of this case, here we provide a detailed clinical description, as well as neurophysiological, neuropsychological, and neuroimaging data for that case and his extended family. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Murru, Maria R.] Univ Cagliari, Multiple Sclerosis Ctr Lab, Cagliari, Italy.
[Borghero, Giuseppe; Floris, Gianluca; Cannas, Antonino; Marrosu, Maria G.; Costantino, Emanuela] Azienda Univ Osped Cagliari, Dept Neurol, Cagliari, Italy.
[Parish, Leslie D.; Pugliatti, Maura] Univ Sassari, Dept Neurosci, I-07100 Sassari, Italy.
[Ticca, Anna] Azienda Osped San Francesco, Dept Neurol, Nuoro, Italy.
[Traynor, Bryan J.] NIA, Neuromuscular Dis Res Grp, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Traynor, Bryan J.] Johns Hopkins Univ Hosp, Dept Neurol, Baltimore, MD 21287 USA.
[Calvo, Andrea; Cammarosano, Stefania; Moglia, Cristina; Chio, Adriano] Univ Turin, ALS Ctr, Dept Neurosci, San Giovanni Univ Hosp, I-10126 Turin, Italy.
[Calvo, Andrea; Cammarosano, Stefania; Moglia, Cristina; Chio, Adriano] NIT, Turin, Italy.
[Cistaro, Angelina] IRMET, Positron Emiss Tomog Ctr, Turin, Italy.
[Brunetti, Maura; Restagno, Gabriella] Osped Infantile Regina Margherita St Anna, Azienda Sanit Osped, Mol Genet Lab, Turin, Italy.
RP Chio, A (reprint author), Univ Turin, ALS Ctr, Dept Neurosci, Via Cherasco 15, I-10126 Turin, Italy.
EM achio@usa.net
RI Traynor, Bryan/G-5690-2010; Calvo, Andrea/K-4141-2016; Moglia,
Cristina/K-4142-2016;
OI Calvo, Andrea/0000-0002-5122-7243; Moglia, Cristina/0000-0001-7377-7222;
Chio, Adriano/0000-0001-9579-5341; Cammarosano,
Stefania/0000-0002-0981-5252; Marrosu, Maria
Giovanna/0000-0003-2334-2081
FU Regione Autonoma della Sardegna, RAS, Assessorato di Igiene e Sanita ed
Assistenza Sociale; Ministero della Salute, Progetti Finalizzati;
Compagnia di San Paolo; Regione Piemonte, Progetti Finalizzati; NIH,
National Institute on Aging [Z01-AG000949-02]
FX The work was supported by Regione Autonoma della Sardegna, RAS,
Assessorato di Igiene e Sanita ed Assistenza Sociale, 2007 (MP), by
Ministero della Salute, Progetti Finalizzati, 2007 (AC and GR), by
Compagnia di San Paolo, 2007 (AC) and by Regione Piemonte, Progetti
Finalizzati, 2008 (GR). This work was supported in part by the
Intramural Research Programs of the NIH, National Institute on Aging
(Z01-AG000949-02).
NR 10
TC 10
Z9 10
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD DEC
PY 2011
VL 32
IS 12
AR 2327.e1
DI 10.1016/j.neurobiolaging.2011.06.009
PG 5
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA 839PJ
UT WOS:000296379900051
PM 21803454
ER
PT J
AU Seneca, N
Finnema, SJ
Laszlovszky, I
Kiss, B
Horvath, A
Pasztor, G
Kapas, M
Gyertyan, I
Farkas, S
Innis, RB
Halldin, C
Gulyas, B
AF Seneca, Nicholas
Finnema, Sjoerd J.
Laszlovszky, Istvan
Kiss, Bela
Horvath, Attila
Pasztor, Gabriella
Kapas, Margo
Gyertyan, Istvan
Farkas, Sandor
Innis, Robert B.
Halldin, Christer
Gulyas, Balazs
TI Occupancy of dopamine D-2 and D-3 and serotonin 5-HT1A receptors by the
novel antipsychotic drug candidate, cariprazine (RGH-188), in monkey
brain measured using positron emission tomography
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE Cariprazine; Positron emission tomography (PET); Nonhuman primate brain;
Dopamine D-2; Dopamine D-3; Serotonin 5-HT1A; Receptor occupancy
ID AUTORADIOGRAPHIC LOCALIZATION; PRIMATE BRAIN; BINDING; PET;
NEUROLEPTICS; ANTAGONIST; KETAMINE; AGONIST; D3; D-1-DOPAMINE
AB Rationale Cariprazine is a novel antipsychotic drug candidate that exhibits high selectivity and affinity to dopamine D-3 and D-2 receptors and moderate affinity to serotonin 5-HT1A receptors. Targeting receptors other than D-2 may provide a therapeutic benefit for both positive and negative symptoms associated with schizophrenia. Positron emission tomography (PET) can be used as a tool in drug development to assess the in vivo distribution and pharmacological properties of a drug.
Objectives The objective of this study was to determine dopamine D-2/D-3 and serotonin 5-HT1A receptor occupancy in monkey brain after the administration of cariprazine.
Methods We examined three monkeys using the following PET radioligands: [C-11]MNPA (an agonist at D-2 and D-3 receptors), [C-11]raclopride (an antagonist at D-2 and D-3 receptors), and [C-11]WAY-100635 (an antagonist at 5-HT1A receptors). During each experimental day, the first PET measurement was a baseline study, the second after a low dose of cariprazine, and the third after the administration of a high dose.
Results We found that cariprazine occupied D-2/D-3 receptors in a dose-dependent and saturable manner, with the lowest dose occupying similar to 5% of receptors and the highest dose showing more than 90% occupancy. 5-HT1A receptor occupancy was considerably lower compared with D-2/D-3 occupancy at the same doses, with a maximal value of similar to 30% for the raphe nuclei.
Conclusions We conclude that cariprazine binds preferentially to dopamine D-2/D-3 rather than to serotonin 5-HT1A receptors in monkey brain. These findings can be used to guide the selection of cariprazine dosing in humans.
C1 [Seneca, Nicholas; Finnema, Sjoerd J.; Halldin, Christer; Gulyas, Balazs] Karolinska Inst, Dept Clin Neurosci, Psychiat Sect, S-17176 Stockholm, Sweden.
[Seneca, Nicholas; Innis, Robert B.] NIH, Mol Imaging Branch, NIMH, Bethesda, MD 20892 USA.
[Laszlovszky, Istvan; Kiss, Bela; Horvath, Attila; Pasztor, Gabriella; Kapas, Margo; Gyertyan, Istvan; Farkas, Sandor] Gedeon Richter Chem Works Ltd, H-1103 Budapest, Hungary.
RP Gulyas, B (reprint author), Karolinska Inst, Dept Clin Neurosci, Psychiat Sect, S-17176 Stockholm, Sweden.
EM balazs.gulyas@ki.se
RI Gulyas, Balazs/F-9508-2015
FU National Institute of Mental Health, Bethesda, Maryland, USA
FX We thank the members of the Karolinska PET group for their assistance.
This research was supported in part by the Intramural Program of the
National Institute of Mental Health, Bethesda, Maryland, USA.
NR 50
TC 19
Z9 19
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0033-3158
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD DEC
PY 2011
VL 218
IS 3
BP 579
EP 587
DI 10.1007/s00213-011-2343-z
PG 9
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 844EM
UT WOS:000296730500012
PM 21625907
ER
PT J
AU Patlolla, AK
Berry, A
Tchounwou, PB
AF Patlolla, Anita K.
Berry, Ashley
Tchounwou, Paul B.
TI Study of hepatotoxicity and oxidative stress in male Swiss-Webster mice
exposed to functionalized multi-walled carbon nanotubes
SO MOLECULAR AND CELLULAR BIOCHEMISTRY
LA English
DT Article
DE Multi-walled carbon nanotube; Serum amino-transferases; Alkaline
phosphatases; Reactive oxygen species (ROS); Hepatotoxicity;
Swiss-Webster mice
ID IN-VIVO; DRUG-DELIVERY; CYTOTOXICITY; TOXICITY; CELLS; BIODISTRIBUTION;
BIOAVAILABILITY; DEPENDENCE; HISTOLOGY; ANIMALS
AB Carbon nanotubes (CNTs), the most promising material with unique characteristics, find its application in different fields ranging from composite materials to medicine and from electronics to energy storage. However, little is known about the mechanisms behind the interaction of these particles with cells and their toxicity. The aim of this study was to assess the effects, after intraperitoneal (ip) injection, of functionalized multi-walled carbon nanotubes (MWCNT) (carboxyl groups) on various hepatotoxicity and oxidative stress biomarkers (ROS, LHP, ALT, AST, ALP, and morphology of liver) in the mouse model. The mice were dosed ip at 0.25, 0.5, and 0.75 mg/kg/day for 5 days of purified/functionalized MWCNTs and two controls (negative; saline and positive; carbon black 0.75 mg/kg) as appropriate. Samples were collected 24 h after the fifth day treatment following standard protocols. Exposure to carboxylated functionalized MWCNT; the body-weight gain of the mice decreased, induced reactive oxygen species (ROS), and enhanced the activities of serum amino-transferases (ALT/AST), alkaline phosphatases (ALP), and concentration of lipid hydro peroxide compared to control. Histopathology of exposed liver showed a statistically significant effect in the morphological alterations of the tissue compared to controls. The cellular findings reported here do suggest that purified carboxylated functionalized MWCNT has the potential to induce hepatotoxicity in Swiss-Webster mice through activation of the mechanisms of oxidative stress, which warrant in vivo animal exposure studies. However, more studies of functionalization in the in vivo toxicity of MWCNTs are required and parallel comparison is preferred.
C1 [Patlolla, Anita K.; Berry, Ashley; Tchounwou, Paul B.] Jackson State Univ, Mol Toxicol Res Lab, NIH, RCMI Ctr Environm Hlth,CSET, Jackson, MS 39217 USA.
[Berry, Ashley] Jackson State Univ, Dept Biol, CSET, Jackson, MS USA.
RP Patlolla, AK (reprint author), Jackson State Univ, Mol Toxicol Res Lab, NIH, RCMI Ctr Environm Hlth,CSET, Jackson, MS 39217 USA.
EM anita.k.patlolla@jsums.edu
FU Air Forces Research Laboratory/Wright Patterson AFB [FA8650-07-1-6851];
National Institutes of Health-RCMI Center for Environmental Health at
Jackson State University [2G12RR01349-12]
FX This research was supported in part by a grant from the Air Forces
Research Laboratory/Wright Patterson AFB (Grant No. FA8650-07-1-6851)
and in part by a grant from National Institutes of Health-RCMI Center
for Environmental Health (Grant No. 2G12RR01349-12) at Jackson State
University.
NR 56
TC 24
Z9 24
U1 2
U2 7
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0300-8177
J9 MOL CELL BIOCHEM
JI Mol. Cell. Biochem.
PD DEC
PY 2011
VL 358
IS 1-2
BP 189
EP 199
DI 10.1007/s11010-011-0934-y
PG 11
WC Cell Biology
SC Cell Biology
GA 838JZ
UT WOS:000296286700021
PM 21725842
ER
PT J
AU Buchsbaum, BR
Baldo, J
Okada, K
Berman, KF
Dronkers, N
D'Esposito, M
Hickok, G
AF Buchsbaum, Bradley R.
Baldo, Juliana
Okada, Kayoko
Berman, Karen F.
Dronkers, Nina
D'Esposito, Mark
Hickok, Gregory
TI Conduction aphasia, sensory-motor integration, and phonological
short-term memory - An aggregate analysis of lesion and fMRI data
SO BRAIN AND LANGUAGE
LA English
DT Article
DE Conduction aphasia; Working memory; Speech production; Planum temporale;
Brain lesion; Sensorimotor integration; Phonological short-term memory
ID SUPERIOR TEMPORAL GYRUS; DELAYED AUDITORY-FEEDBACK; WORKING-MEMORY;
FUNCTIONAL NEUROANATOMY; SPEECH-PERCEPTION; PLANUM TEMPORALE;
COMPREHENSION EVIDENCE; ARCUATE FASCICULUS; INFERIOR PARIETAL; SEMANTIC
FACTORS
AB Conduction aphasia is a language disorder characterized by frequent speech errors, impaired verbatim repetition, a deficit in phonological short-term memory, and naming difficulties in the presence of otherwise fluent and grammatical speech output. While traditional models of conduction aphasia have typically implicated white matter pathways, recent advances in lesions reconstruction methodology applied to groups of patients have implicated left temporoparietal zones. Parallel work using functional magnetic resonance imaging (fMRI) has pinpointed a region in the posterior most portion of the left planum temporale, area Spt, which is critical for phonological working memory. Here we show that the region of maximal lesion overlap in a sample of 14 patients with conduction aphasia perfectly circumscribes area Spt, as defined in an aggregate fMRI analysis of 105 subjects performing a phonological working memory task. We provide a review of the evidence supporting the idea that Spt is an interface site for the integration of sensory and vocal tract-related motor representations of complex sound sequences, such as speech and music and show how the symptoms of conduction aphasia can be explained by damage to this system. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Buchsbaum, Bradley R.] Baycrest Hosp, Rotman Res Inst, Toronto, ON M4Y1 M2, Canada.
[Baldo, Juliana; Dronkers, Nina] Ctr Aphasia & Related Disorders, VA No Calif Hlth Care Syst, Martinez, CA USA.
[D'Esposito, Mark] Univ Calif Berkeley, Dept Psychol, Berkeley, CA 94720 USA.
[Hickok, Gregory] Univ Calif Irvine, Dept Cognit Sci, Ctr Cognit Neurosci, Irvine, CA USA.
[Berman, Karen F.] NIMH, Sect Integrat Neuroimaging, Bethesda, MD 20892 USA.
RP Buchsbaum, BR (reprint author), Baycrest Hosp, Rotman Res Inst, 3560 Bathurst St, Toronto, ON M4Y1 M2, Canada.
EM Greg.Hickok@gmail.com
FU NIH [R01 DC03681]
FX Supported in part by NIH Grant R01 DC03681 (GH).
NR 88
TC 90
Z9 90
U1 4
U2 46
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0093-934X
J9 BRAIN LANG
JI Brain Lang.
PD DEC
PY 2011
VL 119
IS 3
BP 119
EP 128
DI 10.1016/j.bandl.2010.12.001
PG 10
WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences;
Psychology, Experimental
SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences &
Neurology; Psychology
GA 837RH
UT WOS:000296220400001
PM 21256582
ER
PT J
AU Shinagawa, A
Yoshida, Y
Kurokawa, T
Horiuchi, Y
Tsuyoshi, H
Orisaka, M
Sawamura, Y
Kleinman, HK
Kotsuji, F
AF Shinagawa, Akiko
Yoshida, Yoshio
Kurokawa, Tetsuji
Horiuchi, Yuko
Tsuyoshi, Hideaki
Orisaka, Makoto
Sawamura, Yoko
Kleinman, Hynda K.
Kotsuji, Fumikazu
TI The potent peptide antagonist to angiogenesis, C16Y, and cisplatin act
synergistically in the down-regulation of the Bcl-2/Bax ratio and the
induction of apoptosis in human ovarian cancer cells
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE anti-angiogenic peptide C16Y; Bcl-2/Bax ratio; synergy; cisplatin
ID INTEGRIN-ALPHA-V; EXTRACELLULAR-MATRIX; TUMOR-GROWTH; IDENTIFICATION;
METASTASIS
AB Cisplatin is one of the most potent antitumor agents for ovarian cancer, but has also been implicated in normal tissue cytotoxicity. We examined the effect of cisplatin alone and in combination with C16Y, a newly-identified anti-angiogenic peptide from the NH(2)-terminal domains of the gamma-chain of laminin-1, on the modulation of Bcl-2/Bax expression and induction of apoptosis in ovarian cancer cells (OVACAR3). C16Y did not elicit cell death of human umbilical vein endothelial cells (HUVECs). Cisplatin exerted a lethal effect with an EC(50) of 10 mu M in OVACAR3s. In the presence of 25 or 50 mu g/ml of C16Y (a range which has no effect against HUVECs), the EC(50) for cisplatin in OVACAR3s decreased to 3.5 and 2.0 mu M, respectively. Using fluorescence-activated cell sorting (FACS) analysis of DNA stained OVACAR3s and terminal deoxynucleotide tranferase-mediated dUTP nick end-labeling (TUNEL), we found that even at concentrations of 1 and 3 mu M cisplatin, C16Y at 10 and 25 mu g/ml increased the incidence of apoptosis in OVACAR3s by 3-5-fold. Each drug had some measurable effect on Bax protein expression. Furthermore, Bcl-2 protein expression levels were markedly reduced by C16Y alone and cisplatin alone in a dose-dependent manner. The combination of C16Y and cisplatin resulted in a further dramatic reduction in Bcl-2, underscoring the pronounced synergy produced by cisplatin and C16Y together. On the other hand, C16Y did not activate any other signal transduction pathways that usually culminate in the activation of apoptosis, such as the p53, p21(waf1), p73, ERK1/2 or PI3-AKT pathways. These observations suggest that the suppression of the Bcl-2/Bax ratio may play an important role in mediating the synergistic effect of cisplatin and C16Y on the induction of apoptosis in OVACAR3 cells.
C1 [Shinagawa, Akiko; Yoshida, Yoshio; Kurokawa, Tetsuji; Horiuchi, Yuko; Tsuyoshi, Hideaki; Orisaka, Makoto; Sawamura, Yoko; Kotsuji, Fumikazu] Univ Fukui, Fac Med Sci, Dept Gynecol, Eiheiji, Fukui 9101193, Japan.
[Kleinman, Hynda K.] Natl Inst Dent & Craniofacial Res, Craniofacial Dev Biol & Regenerat Branch, NIH, Bethesda, MD 20892 USA.
RP Yoshida, Y (reprint author), Univ Fukui, Fac Med Sci, Dept Gynecol, 23-3 Matsuoka Shimoaizuki, Eiheiji, Fukui 9101193, Japan.
EM yyoshida@u-fukui.ac.jp
FU Japan Society for the Promotion of Science [21592124]
FX This study was partly funded by a Grant-in-Aid for Scientific Research
from the Japan Society for the Promotion of Science (21592124).
NR 17
TC 8
Z9 10
U1 0
U2 3
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1019-6439
J9 INT J ONCOL
JI Int. J. Oncol.
PD DEC
PY 2011
VL 39
IS 6
BP 1359
EP 1364
DI 10.3892/ijo.2011.1134
PG 6
WC Oncology
SC Oncology
GA 838TP
UT WOS:000296315400002
PM 21935568
ER
PT J
AU Graham, BS
AF Graham, Barney S.
TI Future Opportunities for Passive Immunity Against Viral Diseases
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Editorial Material
ID RESPIRATORY SYNCYTIAL VIRUS; NEUTRALIZATION; GLYCOPROTEIN; MOTAVIZUMAB;
EPITOPES
C1 NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Graham, BS (reprint author), NIAID, Vaccine Res Ctr, NIH, 40 Convent Dr,Bldg 40,Room 2502, Bethesda, MD 20892 USA.
EM bgraham@nih.gov
NR 11
TC 0
Z9 0
U1 0
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD DEC 1
PY 2011
VL 204
IS 11
BP 1648
EP 1650
DI 10.1093/infdis/jir628
PG 3
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 838MZ
UT WOS:000296297900002
PM 21998473
ER
PT J
AU Meunier, JC
Bukh, J
Diaz, G
Tovo, PA
Casadei, AM
Quinti, I
Iorio, R
Emerson, S
Purcell, RH
Farci, P
AF Meunier, Jean-Christophe
Bukh, Jens
Diaz, Giacomo
Tovo, Pier-Angelo
Casadei, Anna Maria
Quinti, Isabella
Iorio, Raffaele
Emerson, Suzanne
Purcell, Robert H.
Farci, Patrizia
TI Neutralizing Antibodies to Hepatitis C Virus in Perinatally Infected
Children Followed Up Prospectively
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID PROGRESSION; EVOLUTION
AB Little is known about the presence and role of neutralizing antibodies (NtAbs) in perinatal hepatitis C virus (HCV) infection. Using HCV pseudoparticles, NtAbs were studied longitudinally in 12 HCV-infected children with or without evidence of acute hepatitis during the first year of life. Broadly reactive NtAbs of maternal origin did not prevent vertical HCV transmission or progression to chronicity. NtAbs against homologous genotype or subtype appeared during the chronic phase and were more abundant and sustained in children with acute hepatitis. Cross-reactive NtAbs were present in both groups of children, but their appearance did not correlate with better control of viremia or HCV clearance.
C1 [Meunier, Jean-Christophe; Bukh, Jens; Emerson, Suzanne; Purcell, Robert H.; Farci, Patrizia] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Bukh, Jens] Copenhagen Univ Hosp, Dept Infect Dis, Copenhagen Hepatitis Program CO HEP C, Hvidovre, Denmark.
[Bukh, Jens] Copenhagen Univ Hosp, Clin Res Ctr, Hvidovre, Denmark.
[Bukh, Jens] Univ Copenhagen, Fac Hlth Sci, Dept Int Hlth Immunol & Microbiol, DK-1168 Copenhagen, Denmark.
[Diaz, Giacomo] Univ Cagliari, Dept Biomed Sci & Technol, I-09124 Cagliari, Italy.
[Tovo, Pier-Angelo] Univ Turin, Dept Pediat, I-10124 Turin, Italy.
[Casadei, Anna Maria] Univ Roma La Sapienza, Dept Pediat, Rome, Italy.
[Quinti, Isabella] Univ Roma La Sapienza, Dept Clin Med, Rome, Italy.
[Iorio, Raffaele] Univ Naples Federico 2, Dept Pediat, Naples, Italy.
RP Farci, P (reprint author), NIAID, Infect Dis Lab, NIH, 50 South Dr,MSC 8009,Bldg 50,Rm 6529, Bethesda, MD 20892 USA.
EM pfarci@niaid.nih.gov
OI Tovo, Pier Angelo/0000-0002-0192-3240
FU National Institutes of Health, National Institute of Allergy and
Infectious Diseases
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Allergy and
Infectious Diseases.
NR 15
TC 6
Z9 7
U1 0
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD DEC 1
PY 2011
VL 204
IS 11
BP 1741
EP 1745
DI 10.1093/infdis/jir631
PG 5
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 838MZ
UT WOS:000296297900013
PM 22006993
ER
PT J
AU Tan, XL
Traore, B
Kayentao, K
Ongoiba, A
Doumbo, S
Waisberg, M
Doumbo, OK
Felgner, PL
Fairhurst, RM
Crompton, PD
AF Tan, Xiaolin
Traore, Boubacar
Kayentao, Kassoum
Ongoiba, Aissata
Doumbo, Safiatou
Waisberg, Michael
Doumbo, Ogobara K.
Felgner, Philip L.
Fairhurst, Rick M.
Crompton, Peter D.
TI Hemoglobin S and C Heterozygosity Enhances Neither the Magnitude nor
Breadth of Antibody Responses to a Diverse Array of Plasmodium
falciparum Antigens
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID SICKLE-CELL TRAIT; ERYTHROCYTE-MEMBRANE PROTEIN-1;
GLUTAMATE-RICH-PROTEIN; INFECTED ERYTHROCYTES; IMMUNE-RESPONSES; SEVERE
MALARIA; ACQUIRED-IMMUNITY; GAMMA-GLOBULIN; LIFE-CYCLE; PROTECTION
AB Background. Heterozygous states of hemoglobin (Hb) A and HbS (HbAS, sickle-cell trait) or HbC (HbAC) protect against Plasmodium falciparum malaria by unclear mechanisms. Several studies suggest that HbAS and HbAC accelerate the acquisition of immunity to malaria, possibly by enhancing P. falciparum-specific antibody responses.
Methods. We used a protein microarray representing 491 P. falciparum proteins expressed during exoerythrocytic and erythrocytic stages of the life cycle to test the hypothesis that HbAS and HbAC enhance the P. falciparum-specific IgG response compared with normal HbAA. Plasma samples were collected from Malian children aged 2-10 years before and after a 6-month malaria season and were probed against the microarray. Immunoglobulin G (IgG) profiles of children with HbAA (n = 106), HbAS (n = 15), and HbAC (n = 20) were compared.
Results. Although the magnitude and breadth of P. falciparum-specific IgG responses increased with age and from before to after the malaria season in each antigen category, Hb type did not independently predict significant differences in P. falciparum-specific IgG profiles.
Conclusions. These data do not support the hypothesis that HbAS and HbAC protect against malaria by enhancing P. falciparum-specific antibody responses. It remains possible that HbAS and HbAC protect against malaria by enhancing antibody responses to antigens not studied here or through other immune mechanisms.
C1 [Waisberg, Michael; Crompton, Peter D.] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
[Tan, Xiaolin; Felgner, Philip L.] Univ Calif Irvine, Div Infect Dis, Dept Med, Irvine, CA 92717 USA.
[Traore, Boubacar; Kayentao, Kassoum; Ongoiba, Aissata; Doumbo, Safiatou; Doumbo, Ogobara K.] Univ Bamako, Fac Med Pharm & Odontostomatol, Malaria Res & Training Ctr, Bamako, Mali.
[Felgner, Philip L.] Antigen Discovery, Irvine, CA USA.
[Fairhurst, Rick M.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
RP Crompton, PD (reprint author), NIAID, Immunogenet Lab, NIH, 12441 Parklawn Dr,Twinbrook 2 Bldg,Room 200F, Rockville, MD 20852 USA.
EM pcrompton@niaid.nih.gov
RI Crompton, Peter/N-1130-2016
FU Division of Intramural Research of the National Institute of Allergy and
Infectious Diseases, National Institutes of Health; National Institute
of Allergy and Infectious Diseases, National Institutes of Health
[1R43AI066791]
FX This work was supported by the Division of Intramural Research of the
National Institute of Allergy and Infectious Diseases, National
Institutes of Health; and by National Institute of Allergy and
Infectious Diseases, National Institutes of Health [1R43AI066791 to P.
L. F].
NR 43
TC 25
Z9 25
U1 0
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD DEC 1
PY 2011
VL 204
IS 11
BP 1750
EP 1761
DI 10.1093/infdis/jir638
PG 12
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 838MZ
UT WOS:000296297900015
PM 21998476
ER
PT J
AU Santos, LA
Monteiro-Cunha, JP
Araujo, AF
Brites, C
Galvao-Castro, B
Alcantara, LCJ
AF Santos, Luciane Amorim
Monteiro-Cunha, Joana Paixao
Araujo, Adriano Fernando
Brites, Carlos
Galvao-Castro, Bernardo
Junior Alcantara, Luiz Carlos
TI Detection of Distinct Human Immunodeficiency Virus Type 1 Circulating
Recombinant Forms in Northeast Brazil
SO JOURNAL OF MEDICAL VIROLOGY
LA English
DT Article
DE HIV-1; CRF; resistance
ID DYNAMICS IN-VIVO; HIV TYPE-1; ANTIRETROVIRAL THERAPY; DIVERSITY;
SUBTYPE; MUTATIONS; SEQUENCES
AB The extraordinary genetic diversity and immune evasion of human immunodeficiency virus (HIV) pose significant challenges for vaccine development and antiretroviral therapy efficacy. The objective of this study was to characterize the molecular profile of HIV-1 epidemic in Salvador, Bahia, Brazil, determining the genetic subtypes and the presence of antiretroviral resistance mutations. HIV-1 pol DNA sequences from 57 individuals infected with HIV were obtained by PCR, followed by sequencing. The subtypes were determined by phylogenetic analyses and the intersubtype recombination was investigated by bootscanning. The pol subtypes were compared with gag and env subtypes. Antiretroviral susceptibility was evaluated through the Stanford HIV resistance Database. The subtypes frequencies were: 77.2% of subtype B, 1.8% of subtype F1, and 21.0% of BF recombinant forms. Two intergenic and three intragenic BF recombinant patterns were observed. Six (10.5%) viruses were related to CRF28/CRF29, two were related to CRF12 (3.5%), and one (1.8%) was CRF39. Fourteen (24.6%) strains carried one or more mutations associated with at least intermediate resistance: 24.6% had resistance to nucleoside reverse transcriptase inhibitors, 21.0% to non-nucleoside reverse transcriptase inhibitors, and 7% to protease inhibitors. The substitutions I54V (7.0%), M184V (14.0%), and K103N (10.5%) were the most frequent within each class of drugs. The results show a high diversity of BF genotypes and a lower prevalence of major reverse transcriptase and protease drug resistance mutations in Salvador, compared with other regions of Brazil. These findings may contribute to improve treatment strategies of patients infected with HIV-1 from this Brazilian region. J. Med. Virol. 83: 2066-2072, 2011. (C) 2011 Wiley Periodicals, Inc.
C1 [Santos, Luciane Amorim; Monteiro-Cunha, Joana Paixao; Araujo, Adriano Fernando; Galvao-Castro, Bernardo; Junior Alcantara, Luiz Carlos] Fundacao Oswaldo Cruz, Ctr Pesquisa Goncalo Moniz, Lab Avancado Saude Publ, BR-40296610 Salvador, BA, Brazil.
[Brites, Carlos] Univ Fed Bahia, Salvador, BA, Brazil.
[Galvao-Castro, Bernardo; Junior Alcantara, Luiz Carlos] Bahia Fdn Sci Dev, Bahia Sch Med & Publ Hlth, HTLV Ctr, Salvador, BA, Brazil.
[Junior Alcantara, Luiz Carlos] NCI, NIH, Bethesda, MD 20892 USA.
RP Monteiro-Cunha, JP (reprint author), Fundacao Oswaldo Cruz, Ctr Pesquisa Goncalo Moniz, Lab Avancado Saude Publ, Rua Waldemar Falca,121 Candeal, BR-40296610 Salvador, BA, Brazil.
EM jmonteiro@bahia.fiocruz.br
OI Araujo, Fernando/0000-0001-6471-5564
FU FAPESB [303/03]; Brazilian Ministry of Health [306/04, 307/04]; CNPq
FX Grant sponsor: FAPESB; Grant number: 303/03; Grant sponsor: Brazilian
Ministry of Health; Grant numbers: 306/04; 307/04; Grant sponsor: CNPq.
NR 24
TC 5
Z9 5
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0146-6615
J9 J MED VIROL
JI J. Med. Virol.
PD DEC
PY 2011
VL 83
IS 12
BP 2066
EP 2072
DI 10.1002/jmv.22170
PG 7
WC Virology
SC Virology
GA 838AM
UT WOS:000296257900002
PM 22012712
ER
PT J
AU Oppenheim, IM
Canon, AM
Barcenas, W
Groden, C
Goker-Alpan, O
Resnik, CS
Sidransky, E
AF Oppenheim, Ian M.
Canon, Astrid Medina
Barcenas, William
Groden, Catherine
Goker-Alpan, Ozlem
Resnik, Charles S.
Sidransky, Ellen
TI Bilateral symmetrical cortical osteolytic lesions in two patients with
Gaucher disease
SO SKELETAL RADIOLOGY
LA English
DT Article
DE Type 3 Gaucher disease; Osteolytic; Genotype L444P/L444P;
Glucocerebrosidase; Gaucher cells
ID EXPRESSION; THERAPY
AB Gaucher disease (GD) is an autosomal recessive lysosomal storage disorder characterized by the reduced or absent activity of glucocerebrosidase. The disease is split into three types. Type 3, or chronic neuronopathic GD, manifests with heterogeneous clinical presentations. Skeletal manifestations of GD can include abnormal bone remodeling resulting in the characteristic Erlenmeyer flask deformities, painful bone crises, osteopenia, and an increased frequency of fractures. Osteolytic lesions can also occur but are rare and tend to be large, expanding intramedullary lesions with cortical thinning. We present two adolescent patients with type 3 GD who developed bilateral symmetrical cortical osteolytic lesions. The lesions in both cases demonstrate predominant cortical scalloping with fairly indolent growth. Neither patient manifests some of the more common bony manifestations of GD-bone crises or osteonecrosis. These atypical and unique skeletal findings in two unrelated probands with type 3 GD further expand the extent of phenotypic variation encountered in this single gene disorder.
C1 [Oppenheim, Ian M.; Groden, Catherine; Goker-Alpan, Ozlem; Sidransky, Ellen] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Canon, Astrid Medina] Hosp Infantil San Jose, Fdn Cardioinfantil, Bogota, Colombia.
[Barcenas, William] Barranquilla Seguro Social, Barranquilla, Colombia.
[Resnik, Charles S.] Univ Maryland, Sch Med, Dept Diagnost Radiol, Baltimore, MD 21201 USA.
RP Sidransky, E (reprint author), NHGRI, Med Genet Branch, NIH, Bldg 35,Room 1A213,35 Convent Dr,MSC 3708, Bethesda, MD 20892 USA.
EM sidranse@mail.nih.gov
FU Division of Intramural Research of the National Human Genome Research
Institute; National Institutes of Health
FX This research was supported by the Division of Intramural Research of
the National Human Genome Research Institute, and the National
Institutes of Health. The authors wish to thank Dr. Adriana Linares of
the Genzyme Corporation for putting the physicians of the two patients
in contact with each other, Dr. Grisel Lopez and Karla Garcia for help
with translation, Michael Melendez for help with image editing, and Drs.
Michael Collins, Les Folio, and Edward McCarthy for helpful discussions.
NR 9
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0364-2348
J9 SKELETAL RADIOL
JI Skeletal Radiol.
PD DEC
PY 2011
VL 40
IS 12
BP 1611
EP 1615
DI 10.1007/s00256-011-1260-x
PG 5
WC Orthopedics; Radiology, Nuclear Medicine & Medical Imaging
SC Orthopedics; Radiology, Nuclear Medicine & Medical Imaging
GA 835WI
UT WOS:000296067100016
PM 21935720
ER
PT J
AU Winder, D
Lovinger, DM
AF Winder, Danny
Lovinger, David M.
TI Introduction to the special issue on synaptic plasticity and addiction
SO NEUROPHARMACOLOGY
LA English
DT Editorial Material
C1 [Winder, Danny] Vanderbilt Univ, Dept Mol Physiol & Biophys, Sch Med, Nashville, TN 37232 USA.
[Lovinger, David M.] NIAAA, Lab Integrat Neurosci, Bethesda, MD 20892 USA.
RP Winder, D (reprint author), Vanderbilt Univ, Dept Mol Physiol & Biophys, Sch Med, 23rd & Pierce Ave S,Room 754, Nashville, TN 37232 USA.
EM danny.winder@vanderbilt.edu; lovindav@mail.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3908
J9 NEUROPHARMACOLOGY
JI Neuropharmacology
PD DEC
PY 2011
VL 61
IS 7
SI SI
BP 1051
EP 1051
DI 10.1016/j.neuropharm.2011.07.028
PG 1
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 834JX
UT WOS:000295956700001
ER
PT J
AU Daws, LC
Avison, MJ
Robertson, SD
Niswender, KD
Galli, A
Saunders, C
AF Daws, Lynette C.
Avison, Malcolm J.
Robertson, Sabrina D.
Niswender, Kevin D.
Galli, Aurelio
Saunders, Christine
TI Insulin signaling and addiction
SO NEUROPHARMACOLOGY
LA English
DT Review
DE Insulin; Dopamine; Dopamine transporter; Amphetamine; Obesity
ID DOPAMINE TRANSPORTER FUNCTION; HIGH-FAT DIET; MESSENGER-RNA; RAT-BRAIN;
NOREPINEPHRINE UPTAKE; HYPOINSULINEMIC RATS; NEURONAL CULTURES; FOOD
RESTRICTION; DORSAL STRIATUM; INDUCED OBESITY
AB Across species, the brain evolved to respond to natural rewards such as food and sex. These physiological responses are important for survival, reproduction and evolutionary processes. It is no surprise, therefore, that many of the neural circuits and signaling pathways supporting reward processes are conserved from Caenorhabditis elegans to Drosophilae, to rats, monkeys and humans. The central role of dopamine (DA) in encoding reward and in attaching salience to external environmental cues is well recognized. Less widely recognized is the role of reporters of the "internal environment", particularly insulin, in the modulation of reward. Insulin has traditionally been considered an important signaling molecule in regulating energy homeostasis and feeding behavior rather than a major component of neural reward circuits. However, research over recent decades has revealed that DA and insulin systems do not operate in isolation from each other, but instead, work together to orchestrate both the motivation to engage in consummatory behavior and to calibrate the associated level of reward. Insulin signaling has been found to regulate DA neurotransmission and to affect the ability of drugs that target the DA system to exert their neurochemical and behavioral effects. Given that many abused drugs target the DA system, the elucidation of how dopaminergic, as well as other brain reward systems, are regulated by insulin will create opportunities to develop therapies for drug and potentially food addiction. Moreover, a more complete understanding of the relationship between DA neurotransmission and insulin may help to uncover etiological bases for "food addiction" and the growing epidemic of obesity. This review focuses on the role of insulin signaling in regulating DA homeostasis and DA signaling, and the potential impact of impaired insulin signaling in obesity and psychostimulant abuse.
This article is part of a Special Issue entitled 'Synaptic Plasticity and Addiction'. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Galli, Aurelio] Vanderbilt Univ, Dept Mol Physiol & Biophys, Ctr Mol Neurosci, Sch Med, Nashville, TN 37232 USA.
[Daws, Lynette C.] Univ Texas Hlth Sci Ctr San Antonio, Dept Physiol, San Antonio, TX 78229 USA.
[Avison, Malcolm J.] Vanderbilt Univ, Sch Med, Inst Imaging Sci, Nashville, TN 37232 USA.
[Robertson, Sabrina D.] Natl Inst Environm Hlth, Dev Neurobiol Lab, Res Triangle Pk, NC USA.
[Niswender, Kevin D.] Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37232 USA.
[Niswender, Kevin D.] Tennessee Valley Healthcare Syst, Nashville, TN USA.
[Saunders, Christine] Vanderbilt Univ, Sch Med, Dept Pharmacol, Nashville, TN 37232 USA.
RP Galli, A (reprint author), Vanderbilt Univ, Dept Mol Physiol & Biophys, Ctr Mol Neurosci, Sch Med, 465 21st Ave S,Room 7124,Med Res Bldg 3, Nashville, TN 37232 USA.
EM aurelio.galli@vanderbilt.edu
OI Robertson, Sabrina/0000-0003-4598-6929
FU NIH [DA14684, DK085712]; Tennessee Valley Healthcare System
FX Work supported by NIH grants DA14684 (AG & LCD), DK085712 (KN & AG),
partially by resources of the Tennessee Valley Healthcare System.
NR 74
TC 36
Z9 36
U1 1
U2 16
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3908
J9 NEUROPHARMACOLOGY
JI Neuropharmacology
PD DEC
PY 2011
VL 61
IS 7
SI SI
BP 1123
EP 1128
DI 10.1016/j.neuropharm.2011.02.028
PG 6
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 834JX
UT WOS:000295956700008
PM 21420985
ER
PT J
AU Meadors, JL
Cui, YH
Chen, QR
Song, YK
Khan, J
Merlino, G
Tsokos, M
Orentas, RJ
Mackall, CL
AF Meadors, Joanna L.
Cui, Yonghzi
Chen, Qing-Rong
Song, Young K.
Khan, Javed
Merlino, Glenn
Tsokos, Maria
Orentas, Rimas J.
Mackall, Crystal L.
TI Murine Rhabdomyosarcoma Is Immunogenic and Responsive to T-Cell-Based
Immunotherapy
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE adoptive immunotherapy; embryonal rhabdomyosarcoma; immunotherapy;
regulatory T cells; rhabdomyosarcoma; tumor antigen; tumor vaccine
ID TUMOR-INFILTRATING LYMPHOCYTES; CHILDRENS ONCOLOGY GROUP; INTERGROUP
RHABDOMYOSARCOMA; METASTATIC RHABDOMYOSARCOMA; DENDRITIC CELLS; EWING
SARCOMA; MOUSE MODEL; CANCER; IMMUNITY; NEUROBLASTOMA
AB Background. Immunotherapies targeting cellular immunity are currently approved for treatment of melanoma, renal cell carcinoma, and prostate cancer. Studies on the immunogenicity and immune responsiveness of pediatric tumors are limited, therefore, it remains unclear to what extent T-cell-based immunotherapy holds promise for pediatric solid tumors. Procedure. A new rhabdomyosarcoma cell line (M3-9-M) was derived from an embryonal rhabdomyosarcoma (ERMS) occurring in a C57BL/6 mouse transgenic for hepatocyte growth factor and heterozygous for mutated p53. Primary tumors and metastases derived from M3-9-M were studied for similarities to human ERMS, and for immunogenicity and immune responsiveness. Results. Primary and metastatic tumors develop after orthotopic injection of M3-9-M into immunocompetent C57BL/6 mice, which mirror human ERMS with regard to histology, gene expression, and metastatic behavior. Whole cell vaccination using irradiated M3-9-M cells or M3-9-M-pulsed dendritic cells (DC)-induced tumor-specific T-cell responses that prevent tumor growth following low-dose tumor injection, and slow tumor growth following higher doses. Administration of anti-CD25 moAbs to deplete CD4(+)CD25(+)FOXP3(+) regulatory T cells prior to tumor vaccination enhanced the potency of the ERMS tumor vaccine. Adoptive immunotherapy with M3-9-M primed T cells plus DC-based vaccination resulted in complete eradication of day 10 M3-9-M derived tumors. Conclusions. M3-9-M derived murine ERMS is immunogenic and immunoresponsive; regulatory T cells contribute to immune evasion by murine rhabdomyosarcoma. Adoptive immunotherapy with DC vaccination can eradicate low tumor burdens. Future work will seek to identify the tumor-associated antigens that mediate protective and therapeutic immunity in this model. Pediatr Blood Cancer 2011; 57: 921-929. (C) 2011 Wiley-Liss, Inc.
C1 [Meadors, Joanna L.; Cui, Yonghzi; Orentas, Rimas J.; Mackall, Crystal L.] NCI, Immunol Sect, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Chen, Qing-Rong; Song, Young K.; Khan, Javed] NCI, Oncogen Sect, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Merlino, Glenn] NCI, Canc Modeling Sect, Lab Canc Biol & Genet, Ctr Canc Res, Bethesda, MD 20892 USA.
[Tsokos, Maria] NCI, Pathol Lab, Pediat Tumor Biol & Ultrastruct Pathol Sect, Bethesda, MD 20892 USA.
RP Mackall, CL (reprint author), 10-CRC 1W-3750,10 Ctr Dr,MSC 1104, Bethesda, MD 20892 USA.
EM cm35c@nih.gov
RI Khan, Javed/P-9157-2014
OI Khan, Javed/0000-0002-5858-0488
NR 46
TC 12
Z9 12
U1 0
U2 2
PU WILEY PERIODICALS, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN STREET, MALDEN, MA 02148-529 USA
SN 1545-5009
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD DEC
PY 2011
VL 57
IS 6
BP 921
EP 929
DI 10.1002/pbc.23048
PG 9
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA 825FX
UT WOS:000295257700007
PM 21462302
ER
PT J
AU Ware, RE
Schultz, WH
Yovetich, N
Mortier, NA
Alvarez, O
Hilliard, L
Iyer, RV
Miller, ST
Rogers, ZR
Scott, JP
Waclawiw, M
Helms, RW
AF Ware, Russell E.
Schultz, William H.
Yovetich, Nancy
Mortier, Nicole A.
Alvarez, Ofelia
Hilliard, Lee
Iyer, Rathi V.
Miller, Scott T.
Rogers, Zora R.
Scott, J. Paul
Waclawiw, Myron
Helms, Ronald W.
TI Stroke With Transfusions Changing to Hydroxyurea (SWiTCH): A Phase III
Randomized Clinical Trial for Treatment of Children With Sickle Cell
Anemia, Stroke, and Iron Overload
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE hydroxyurea; iron overload; stroke
ID RECURRENT STROKE; CEREBROVASCULAR ACCIDENTS; DISEASE; THERAPY; RISK;
ABNORMALITIES; PREVENTION; FREQUENCY; EFFICACY
AB Background. Stroke occurs in 5-10% of children with sickle cell anemia (SCA) and has a high (>50%) risk of recurrence without therapy. Chronic monthly erythrocyte transfusions effectively prevent recurrent stroke, but their long-term use is limited by serious side effects, including iron overload. An alternative to transfusion for secondary stroke prevention in SCA is needed, especially one that also improves the management of iron overload. Methods. Stroke With Transfusions Changing to Hydroxyurea (SWiTCH) is an NHLBI-sponsored Phase III multicenter randomized controlled clinical trial for children with SCA, stroke, and iron overload (NCT00122980). The primary goal of SWiTCH is to compare 30 months of alternative therapy (hydroxyurea and phlebotomy) with standard therapy (transfusions and chelation) for the prevention of secondary stroke and reduction of transfusional iron overload. Discussion. SWiTCH has several distinctive study features including novel methodological and design components: (1) composite primary endpoint including both stroke recurrence rate and iron burden; (2) non-inferiority design with an "acceptable" increased stroke risk; (3) transfusion goals based on current academic community practices; (4) special oversight for the enrollment and randomization process; (5) overlap treatment period within the alternative treatment arm; (6) masking of the overall trial Principal Investigator to treatment results; (7) inclusive independent stroke adjudication process for all suspected new neurological events; and (8) periodic therapeutic phlebotomy program to alleviate iron overload. Conclusion. Investigation of alternative treatments in SWiTCH could lead to changes in the management of cerebrovascular disease for selected patients with SCA, stroke, and iron overload. Pediatr Blood Cancer 2011; 57: 1011-1017. (C) 2011 Wiley-Liss, Inc.
C1 [Ware, Russell E.] Baylor Coll Med, St Jude Childrens Res Hosp, Int Hematol Ctr Excellence, Houston, TX 77030 USA.
[Yovetich, Nancy; Helms, Ronald W.] Rho Inc, Chapel Hill, NC USA.
[Alvarez, Ofelia] Univ Miami, Miami, FL USA.
[Hilliard, Lee] Univ Alabama Birmingham, Birmingham, AL USA.
[Iyer, Rathi V.] Univ Mississippi, Jackson, MS 39216 USA.
[Miller, Scott T.] SUNY Downstate, Brooklyn, NY USA.
[Rogers, Zora R.] Univ Texas SW, Dallas, TX USA.
[Scott, J. Paul] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Waclawiw, Myron] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Ware, RE (reprint author), Baylor Coll Med, St Jude Childrens Res Hosp, Int Hematol Ctr Excellence, Houston, TX 77030 USA.
EM reware@bcm.edu
FU NHLBI [U01 HL078787, U01 HL078987]
FX Grant sponsor: NHLBI; Grant numbers: U01 HL078787, U01 HL078987.
NR 27
TC 29
Z9 30
U1 0
U2 2
PU WILEY PERIODICALS, INC
PI SAN FRANCISCO
PA ONE MONTGOMERY ST, SUITE 1200, SAN FRANCISCO, CA 94104 USA
SN 1545-5009
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD DEC
PY 2011
VL 57
IS 6
BP 1011
EP 1017
DI 10.1002/pbc.23145
PG 7
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA 825FX
UT WOS:000295257700020
PM 21826782
ER
PT J
AU Bradley, DA
Daignault, S
Ryan, CJ
DiPaola, RS
Smith, DC
Small, E
Gross, ME
Stein, MN
Chen, A
Hussain, M
AF Bradley, Deborah A.
Daignault, Stephanie
Ryan, Charles J.
DiPaola, Robert S.
Smith, David C.
Small, Eric
Gross, Mitchell E.
Stein, Mark N.
Chen, Alice
Hussain, Maha
TI Cilengitide (EMD 121974, NSC 707544) in asymptomatic metastatic
castration resistant prostate cancer patients: a randomized phase II
trial by the prostate cancer clinical trials consortium
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE Prostate cancer; Metastatic disease; Integrins; Angiogenesis;
Cilengitide; Bone biomarkers
ID PLACEBO-CONTROLLED TRIAL; CELL-ADHESION MOLECULES; ADVANCED SOLID
TUMORS; BONE METASTASES; ZOLEDRONIC ACID; ALPHA(V)BETA(3) INTEGRIN;
EXTRACELLULAR-MATRIX; PREDICT SURVIVAL; WORKING GROUP; EXPRESSION
AB Background Integrins are involved in prostate cancer metastasis by regulating cell adhesion, migration, invasion, motility, angiogenesis and bone metabolism. We evaluated the efficacy of two dose levels of cilengitide in patients (pts) with castrate resistant prostate cancer (CRPC). Methods Chemotherapy-na < ve, asymptomatic metastatic CRPC pts were randomized to cilengitide 500 mg or 2,000 mg IV twice weekly using parallel 2-stage design. The primary endpoint was rate of objective clinical progression at 6-months. Secondary endpoints included clinical and PSA response rates, safety and effects of cilengitide treatment on circulating tumor cells (CTCs) and bone remodeling markers. Results Forty-four pts were accrued to first stage (22/arm). Median number of cycles was three in both arms (500 mg arm: 1-8; 2,000 mg arm: 1-15). At 6 months, two pts (9%) on the 500 mg arm and five pts (23%) on the 2,000 mg arm had not progressed. Best objective response was stable disease (SD) in seven pts for 9.9[8.1,20.9] months. There were three grade 3 and no grade 4 toxicities. At 12 weeks, analysis of bone markers did not reveal significant trends. At progression, bone specific alkaline phosphatase and N-telopeptide increased in all pts, less so in pts on the 2,000 mg arm and in pts on both arms who obtained SD at 6 months. CTCs increased over time in both arms. Conclusion Cilengitide was well tolerated with modest clinical effect in favor of the higher dose. The unique trial design including a shift from response rate to objective progression as the endpoint, and not acting on PSA increases was feasible.
C1 [Hussain, Maha] Univ Michigan, Med Ctr, Ann Arbor, MI 48109 USA.
[Bradley, Deborah A.] Duke Univ, Durham, NC USA.
[Ryan, Charles J.; Small, Eric] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[DiPaola, Robert S.; Stein, Mark N.] Canc Inst New Jersey, New Brunswick, NJ USA.
[Gross, Mitchell E.] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
[Chen, Alice] NCI, CTEP, Bethesda, MD 20892 USA.
RP Hussain, M (reprint author), Univ Michigan, Med Ctr, 7314 Canc Ctr,1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA.
EM mahahuss@umich.edu
FU CTEP; Prostate SPORE Grant [P50 CA069568-09]; Merck KGaA; Immunicon
Corporation; [PC051382]; [PC051375]; [PCF N008367]
FX CTEP, Prostate SPORE Grant P50 CA069568-09, Merck KGaA, PC051382,
PC051375, PCF N008367, Immunicon Corporation.
NR 50
TC 22
Z9 23
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-6997
EI 1573-0646
J9 INVEST NEW DRUG
JI Invest. New Drugs
PD DEC
PY 2011
VL 29
IS 6
BP 1432
EP 1440
DI 10.1007/s10637-010-9420-8
PG 9
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 819KQ
UT WOS:000294824200034
PM 20336348
ER
PT J
AU Shah, MA
Power, DG
Kindler, HL
Holen, KD
Kemeny, MM
Ilson, DH
Tang, L
Capanu, M
Wright, JJ
Kelsen, DP
AF Shah, Manish A.
Power, Derek G.
Kindler, Hedy L.
Holen, Kyle D.
Kemeny, Margaret M.
Ilson, David H.
Tang, Laura
Capanu, Marinela
Wright, John J.
Kelsen, David P.
TI A multicenter, phase II study of Bortezomib (PS-341) in patients with
unresectable or metastatic gastric and gastroesophageal junction
adenocarcinoma
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE Bortezomib; Proteasome; Gastric cancer; Nuclear factor k-B (NF-KB)
ID PROTEASOME INHIBITOR BORTEZOMIB; FACTOR-KAPPA-B; MULTIPLE-MYELOMA CELLS;
SOLID TUMORS; CHEMOTHERAPEUTIC-AGENTS; CANCER CELLS; TRIAL; ACTIVATION;
CARCINOMA; APOPTOSIS
AB Purpose The transcription factor nuclear factor-kB (NFkB) is implicated in gastric cancer carcinogenesis and survival, and its inhibition by proteosome inhibition is associated with preclinical gastric cancer anti-tumor activity. We examined the single agent efficacy of bortezomib, a selective proteasome inhibitor, in gastric adenocarcinoma. Experimental Design We performed a phase II trial of bortezomib in patients with advanced gastric adenocarcinoma. Bortezomib 1.3 mg/m(2) was administered on days 1, 4, 8, and 11 every 21 days. The primary endpoint was objective response rate(RR); the null hypothesis was RR < 1% versus the alternative a parts per thousand yen15%. One response in the first stage(15 patients) was required before proceeding with an additional 18 patients. If at least 2 or more responses out of 33 were observed, further study with bortezomib was warranted. Correlative studies evaluated pre-treatment tumor expression of NFkB, IkB, p53, p21, and cyclin D1. Results We enrolled 16 patients (15 evaluable for response) from four institutions. No patients demonstrated an objective response(95% CI, 0-22%); one patient achieved stable disease. Fourteen out of 16 patients experienced a parts per thousand yen grade 2 toxicity. The most common toxicity was fatigue in six patients (n = 4 grade 2, n = 2 grade 3). Seven patients experienced neuropathy (n = 5 grade 1, and 1 each grade 2 and 3). Seven (60%) had high cytoplasmic staining for NFkB. Conclusions Single agent bortezomib is inactive in metastatic gastric adenocarcinoma and should not be pursued. Future study of proteasome inhibition in gastric adenocarcinoma should be considered in combination with targeted inhibition of other non-overlapping oncogenic pathways as a potential rational approach.
C1 [Shah, Manish A.; Power, Derek G.; Ilson, David H.; Kelsen, David P.] Mem Sloan Kettering Canc Ctr, Dept Med, Gastrointestinal Oncol Serv, New York, NY 10021 USA.
[Shah, Manish A.; Power, Derek G.; Ilson, David H.; Kelsen, David P.] Cornell Univ, Weill Cornell Med Coll, Dept Med, New York, NY 10065 USA.
[Capanu, Marinela] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
[Kindler, Hedy L.] Univ Chicago, Med Ctr, Hematol Oncol Sect, Chicago, IL 60637 USA.
[Holen, Kyle D.] Univ Wisconsin, Paul P Carbone Comprehens Canc Ctr, Madison, WI USA.
[Kemeny, Margaret M.] Queens Hosp, Queens Canc Ctr, Dept Surg Oncol, Jamaica, NY USA.
[Tang, Laura] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA.
[Wright, John J.] NCI, Invest Drug Branch, Canc Therapy Evaluat Program, Rockville, MD USA.
RP Shah, MA (reprint author), Mem Sloan Kettering Canc Ctr, Dept Med, Gastrointestinal Oncol Serv, 1275 York Ave,H910, New York, NY 10021 USA.
EM shah1@mskcc.org
FU NCI [NO1-CM17105, 24XS072 NCI 6003]
FX Supported by the NCI Phase II Contract-NO1-CM17105 (PI David P. Kelsen,
MD), and NCI Translational Research Contract 24XS072 NCI 6003 (PI Manish
A. Shah, MD)
NR 38
TC 24
Z9 28
U1 2
U2 8
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-6997
J9 INVEST NEW DRUG
JI Invest. New Drugs
PD DEC
PY 2011
VL 29
IS 6
BP 1475
EP 1481
DI 10.1007/s10637-010-9474-7
PG 7
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 819KQ
UT WOS:000294824200039
PM 20574790
ER
PT J
AU Bradley, DA
Daignault, S
Ryan, CJ
DiPaola, RS
Cooney, KA
Smith, DC
Small, E
Mathew, P
Gross, ME
Stein, MN
Chen, A
Pienta, KJ
Escara-Wilke, J
Doyle, G
Al-Hawary, M
Keller, ET
Hussain, M
AF Bradley, Deborah A.
Daignault, Stephanie
Ryan, Charles J.
DiPaola, Robert S.
Cooney, Kathleen A.
Smith, David C.
Small, Eric
Mathew, Paul
Gross, Mitchell E.
Stein, Mark N.
Chen, Alice
Pienta, Kenneth J.
Escara-Wilke, June
Doyle, Gerald
Al-Hawary, Mahmoud
Keller, Evan T.
Hussain, Maha
TI Cilengitide (EMD 121974, NSC 707544) in asymptomatic metastatic
castration resistant prostate cancer patients: a randomized phase II
trial by the prostate cancer clinical trials consortium (vol 29, pg
1432, 2010)
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Correction
C1 [Hussain, Maha] Univ Michigan, Med Ctr, Ann Arbor, MI 48109 USA.
[Bradley, Deborah A.] Duke Univ, Durham, NC USA.
[Ryan, Charles J.; Small, Eric] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[DiPaola, Robert S.; Stein, Mark N.] Canc Inst New Jersey, New Brunswick, NJ USA.
[Mathew, Paul] Tufts Univ, Sch Med, Boston, MA 02111 USA.
[Gross, Mitchell E.] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
[Chen, Alice] NCI, CTEP, Bethesda, MD 20892 USA.
[Doyle, Gerald] Veridex LLC, Huntingdon Valley, PA USA.
RP Hussain, M (reprint author), Univ Michigan, Med Ctr, 7314 Canc Ctr,1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA.
EM deborah.bradley@duke.edu; sfaruzzi@umich.edu; ryanc@medicine.ucsf.edu;
dipaolrs@umdnj.edu; kcooney@umich.edu; dcsmith@umich.edu;
smalle@medicine.ucsf.edu; paul.mathew@tufts.edu; mitchell.gross@usc.edu;
steinm@umdnj.edu; chenali@mail.nih.gov; kpienta@umich.edu;
jfewilke@umich.edu; gdoyle1@its.jnj.com; alhawary@umich.edu;
etkeller@umich.edu; mahahuss@umich.edu
RI Keller, Evan/M-1446-2016
OI Keller, Evan/0000-0002-7592-7535
NR 1
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-6997
J9 INVEST NEW DRUG
JI Invest. New Drugs
PD DEC
PY 2011
VL 29
IS 6
BP 1517
EP 1518
DI 10.1007/s10637-010-9502-7
PG 2
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 819KQ
UT WOS:000294824200048
ER
PT J
AU Hu, CH
Zhang, LQ
Cannata, JM
Yen, J
Shung, KK
AF Hu, ChangHong
Zhang, Lequan
Cannata, Jonathan M.
Yen, Jesse
Shung, K. Kirk
TI Development of a 64 channel ultrasonic high frequency linear array
imaging system
SO ULTRASONICS
LA English
DT Article
DE High frequency ultrasound; Beamformer; FPGA; Linear array
ID TRANSDUCERS
AB In order to improve the lateral resolution and extend the field of view of a previously reported 48 element 30 MHz ultrasound linear array and 16-channel digital imaging system, the development of a 256 element 30 MHz linear array and an ultrasound imaging system with increased channel count has been undertaken. This paper reports the design and testing of a 64 channel digital imaging system which consists of an analog front-end pulser/receiver, 64 channels of Time-Gain Compensation (TGC), 64 channels of high-speed digitizer as well as a beamformer. A Personal Computer (PC) is used as the user interface to display real-time images. This system is designed as a platform for the purpose of testing the performance of high frequency linear arrays that have been developed in house. Therefore conventional approaches were taken it its implementation. Flexibility and ease of use are of primary concern whereas consideration of cost-effectiveness and novelty in design are only secondary. Even so, there are many issues at higher frequencies but do not exist at lower frequencies need to be solved. The system provides 64 channels of excitation pulsers while receiving simultaneously at a 20-120 MHz sampling rate to 12-bits. The digitized data from all channels are first fed through Field Programmable Gate Arrays (FPGAs), and then stored in memories. These raw data are accessed by the beamforming processor to re-build the image or to be downloaded to the PC for further processing. The beamformer that applies delays to the echoes of each channel is implemented with the strategy that combines coarse (8.3 ns) and fine delays (2 ns). The coarse delays are integer multiples of the sampling clock rate and are achieved by controlling the write enable pin of the First-In-First-Out (FIFO) memory to obtain valid beamforming data. The fine delays are accomplished with interpolation filters. This system is capable of achieving a maximum frame rate of 50 frames per second. Wire phantom images acquired with this system show a spatial resolution of 146 mu m (lateral) and 54 mu m (axial). Images with excised rabbit and pig eyeball as well as mouse embryo were also acquired to demonstrate its imaging capability. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Hu, ChangHong] Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA.
Univ So Calif, NIH Transducer Resource Ctr, Los Angeles, CA 90089 USA.
RP Hu, CH (reprint author), Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA.
EM changhoh@usc.edu
FU NIH [P41-EB2182]
FX This work has been supported by NIH Grant # P41-EB2182.
NR 13
TC 9
Z9 10
U1 1
U2 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0041-624X
J9 ULTRASONICS
JI Ultrasonics
PD DEC
PY 2011
VL 51
IS 8
BP 953
EP 959
DI 10.1016/j.ultras.2011.05.010
PG 7
WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
GA 795XK
UT WOS:000293011800013
PM 21684568
ER
PT J
AU Chambers, DA
AF Chambers, David A.
TI Advancing sustainability research: challenging existing paradigms
SO JOURNAL OF PUBLIC HEALTH DENTISTRY
LA English
DT Editorial Material
DE dissemination; implementation; interventions; sustainability; public
health
C1 NIMH, Div Serv & Intervent Res, Bethesda, MD 20892 USA.
RP Chambers, DA (reprint author), NIMH, Div Serv & Intervent Res, 6001 Execut Blvd,Room 7164, Bethesda, MD 20892 USA.
EM dchamber@mail.nih.gov
NR 3
TC 4
Z9 4
U1 0
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-4006
J9 J PUBLIC HEALTH DENT
JI J. Public Health Dent.
PD WIN
PY 2011
VL 71
SU 1
BP S99
EP S100
DI 10.1111/j.1752-7325.2011.00238.x
PG 2
WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
GA 737GV
UT WOS:000288558000025
PM 21656965
ER
PT J
AU Czajkowski, SM
AF Czajkowski, Susan M.
TI The importance of monitoring and maximizing treatment fidelity in public
health research
SO JOURNAL OF PUBLIC HEALTH DENTISTRY
LA English
DT Editorial Material
C1 NHLBI, Clin Applicat & Prevent Branch, Div Cardiovasc Sci, NIH, Bethesda, MD 20892 USA.
RP Czajkowski, SM (reprint author), NHLBI, Clin Applicat & Prevent Branch, Div Cardiovasc Sci, NIH, 6701 Rockledge Dr,Suite 10018, Bethesda, MD 20892 USA.
EM Czajkows@mail.nih.gov
NR 3
TC 2
Z9 2
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-4006
J9 J PUBLIC HEALTH DENT
JI J. Public Health Dent.
PD WIN
PY 2011
VL 71
SU 1
BP S67
EP S68
DI 10.1111/j.1752-7325.2011.00219.x
PG 2
WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
GA 737GV
UT WOS:000288558000017
PM 21656957
ER
PT J
AU Duffy, SQ
AF Duffy, Sarah Q.
TI Enhancing the usefulness of results from economic evaluations of
behavioral health interventions
SO JOURNAL OF PUBLIC HEALTH DENTISTRY
LA English
DT Editorial Material
DE cost-effectiveness; economic evaluations; behavioral interventions
C1 [Duffy, Sarah Q.] NIDA, Div Epidemiol Serv & Prevent Res, Bethesda, MD 20892 USA.
RP Duffy, SQ (reprint author), NIDA, Div Epidemiol Serv & Prevent Res, 6001 Execut Blvd,Rm 5195, Bethesda, MD 20892 USA.
EM duffys@nida.nih.gov
NR 3
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-4006
J9 J PUBLIC HEALTH DENT
JI J. Public Health Dent.
PD WIN
PY 2011
VL 71
SU 1
BP S121
EP S122
DI 10.1111/j.1752-7325.2011.00214.x
PG 2
WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
GA 737GV
UT WOS:000288558000028
PM 21656968
ER
PT J
AU Glasgow, RE
AF Glasgow, Russell E.
TI Planning models and theories: integrating components for addressing
complex challenges
SO JOURNAL OF PUBLIC HEALTH DENTISTRY
LA English
DT Editorial Material
DE oral health; intervention planning; PRECEDE-PROCEED
C1 NCI, Div Canc Control & Populat Sci, Rockville, MD 20852 USA.
RP Glasgow, RE (reprint author), NCI, Div Canc Control & Populat Sci, 6130 Execut Blvd,Room 6144, Rockville, MD 20852 USA.
EM glasgowre@mail.nih.gov
NR 3
TC 1
Z9 1
U1 1
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-4006
J9 J PUBLIC HEALTH DENT
JI J. Public Health Dent.
PD WIN
PY 2011
VL 71
SU 1
BP S17
EP S17
DI 10.1111/j.1752-7325.2011.00222.x
PG 1
WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
GA 737GV
UT WOS:000288558000004
PM 21656944
ER
PT J
AU Kobrin, S
AF Kobrin, Sarah
TI The charge to advance theory and improve health outcomes
SO JOURNAL OF PUBLIC HEALTH DENTISTRY
LA English
DT Editorial Material
DE theory; behavior; intervention
C1 NCI, Div Canc Control & Populat Sci, Bethesda, MD 20852 USA.
RP Kobrin, S (reprint author), NCI, Div Canc Control & Populat Sci, 6130 Execut Blvd,EPN 4096, Bethesda, MD 20852 USA.
EM kobrins@mail.nih.gov
NR 2
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-4006
J9 J PUBLIC HEALTH DENT
JI J. Public Health Dent.
PD WIN
PY 2011
VL 71
SU 1
BP S36
EP S36
DI 10.1111/j.1752-7325.2011.00229.x
PG 1
WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
GA 737GV
UT WOS:000288558000009
PM 21656949
ER
PT J
AU Meissner, HI
AF Meissner, Helen I.
TI Use of qualitative methods to ensure acceptability of interventions
SO JOURNAL OF PUBLIC HEALTH DENTISTRY
LA English
DT Editorial Material
DE qualitative methods; behavioral intervention; accepability
C1 NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
RP Meissner, HI (reprint author), NIH, Off Behav & Social Sci Res, 31 Ctr Dr,Bldg 31,Room B1C19, Bethesda, MD 20892 USA.
EM meissneh@od.nih.gov
NR 2
TC 5
Z9 5
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-4006
J9 J PUBLIC HEALTH DENT
JI J. Public Health Dent.
PD WIN
PY 2011
VL 71
SU 1
BP S83
EP S83
DI 10.1111/j.1752-7325.2011.00225.x
PG 1
WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
GA 737GV
UT WOS:000288558000021
PM 21656961
ER
PT J
AU Onken, L
AF Onken, Lisa
TI PRECEDE-PROCEED and the NIDA stage model: the value of a conceptual
framework for intervention research
SO JOURNAL OF PUBLIC HEALTH DENTISTRY
LA English
DT Editorial Material
DE behavioral treatment; intervention research; treatment development
C1 NIDA, Behav & Integrat Treatment Branch, Bethesda, MD 20892 USA.
RP Onken, L (reprint author), NIDA, Behav & Integrat Treatment Branch, 6001 Execut Blvd, Bethesda, MD 20892 USA.
EM lo10n@nih.gov
NR 3
TC 1
Z9 1
U1 3
U2 10
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-4006
J9 J PUBLIC HEALTH DENT
JI J. Public Health Dent.
PD WIN
PY 2011
VL 71
SU 1
BP S18
EP S19
DI 10.1111/j.1752-7325.2011.00221.x
PG 2
WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
GA 737GV
UT WOS:000288558000005
PM 21656945
ER
PT J
AU Gates, MA
Kannan, R
Giniger, E
AF Gates, Michael A.
Kannan, Ramakrishnan
Giniger, Edward
TI A genome-wide analysis reveals that the Drosophila transcription factor,
Lola, promotes axon growth in part by suppressing expression of the
actin nucleation factor, Spire
SO NEURAL DEVELOPMENT
LA English
DT Article
ID NERVOUS-SYSTEM; SYNAPSE FORMATION; TYROSINE KINASE; GUIDANCE; MIDLINE;
TARGET; MELANOGASTER; CAPPUCCINO; ENCODES; PROTEIN
AB Background: The phylogenetically conserved transcription factor Lola is essential for many aspects of axon growth and guidance, synapse formation and neural circuit development in Drosophila. To date it has been difficult, however, to obtain an overall view of Lola functions and mechanisms.
Results: We use expression microarrays to identify the lola-dependent transcriptome in the Drosophila embryo. We find that lola regulates the expression of a large selection of genes that are known to affect each of several lola-dependent developmental processes. Among other loci, we find lola to be a negative regulator of spire, an actin nucleation factor that has been studied for its essential role in oogenesis. We show that spire is expressed in the nervous system and is required for a known lola-dependent axon guidance decision, growth of ISNb motor axons. We further show that reducing spire gene dosage suppresses this aspect of the lola phenotype, verifying that derepression of spire is an important contributor to the axon stalling phenotype of embryonic motor axons in lola mutants.
Conclusions: These data shed new light on the molecular mechanisms of many lola-dependent processes, and also identify several developmental processes not previously linked to lola that are apt to be regulated by this transcription factor. These data further demonstrate that excessive expression of the actin nucleation factor Spire is as deleterious for axon growth in vivo as is the loss of Spire, thus highlighting the need for a balance in the elementary steps of actin dynamics to achieve effective neuronal morphogenesis.
C1 [Gates, Michael A.; Kannan, Ramakrishnan; Giniger, Edward] Natl Inst Neurol Disorders & Stroke, Basic Neurosci Program, NIH, Bethesda, MD 20892 USA.
[Gates, Michael A.; Kannan, Ramakrishnan; Giniger, Edward] NHGRI, NIH, Bethesda, MD 20892 USA.
[Gates, Michael A.; Giniger, Edward] Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA.
[Gates, Michael A.; Giniger, Edward] Univ Washington, Grad Program Mol & Cellular Biol, Seattle, WA 98109 USA.
RP Giniger, E (reprint author), Natl Inst Neurol Disorders & Stroke, Basic Neurosci Program, NIH, Bethesda, MD 20892 USA.
EM ginigere@ninds.nih.gov
RI Giniger, Edward/C-1764-2015
OI Giniger, Edward/0000-0002-8340-6158
FU NSF [IBN-9904519]; NINDS, NIH [Z01 NS003013]
FX We thank all the members of our lab for their advice and assistance with
these experiments. For much helpful advice we also thank Celeste Berg,
Cecilia Moens, Tom Reh, Kathleen Kerr, Ben Feldman, Chi-Hon Lee and Ward
Odenwald, and for comments on the manuscript we thank Katie Kerr, Don
van Meyel, Akinao Nose and Brian Oliver. We thank the Berkeley
Drosophila Genome Project for the gift of the Drosophila Gene
Collection. We are particularly grateful to Jeff Delrow and the
Microarray Facility of the FHCRC for their assistance in designing,
performing and analyzing the microarray experiments. These experiments
were supported in part by NSF grant IBN-9904519 to EG, and by funds from
the Basic Neuroscience Program of the Intramural Research Program NINDS,
NIH (Z01 NS003013).
NR 55
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Z9 10
U1 0
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1749-8104
J9 NEURAL DEV
JI Neural Dev.
PD NOV 30
PY 2011
VL 6
AR 37
DI 10.1186/1749-8104-6-37
PG 14
WC Developmental Biology; Neurosciences
SC Developmental Biology; Neurosciences & Neurology
GA 893OO
UT WOS:000300365400001
PM 22129300
ER
PT J
AU Lopez-Barragan, MJ
Lemieux, J
Quinones, M
Williamson, KC
Molina-Cruz, A
Cui, KR
Barillas-Mury, C
Zhao, KJ
Su, XZ
AF Lopez-Barragan, Maria J.
Lemieux, Jacob
Quinones, Mariam
Williamson, Kim C.
Molina-Cruz, Alvaro
Cui, Kairong
Barillas-Mury, Carolina
Zhao, Keji
Su, Xin-zhuan
TI Directional gene expression and antisense transcripts in sexual and
asexual stages of Plasmodium falciparum
SO BMC GENOMICS
LA English
DT Article
ID HUMAN MALARIA PARASITE; MESSENGER-RNA; COMPARATIVE GENOMICS; SPLICE
JUNCTIONS; SEQUENCE; SEQ; IDENTIFICATION; GAMETOCYTES; INHIBITION;
DISCOVERY
AB Background: It has been shown that nearly a quarter of the initial predicted gene models in the Plasmodium falciparum genome contain errors. Although there have been efforts to obtain complete cDNA sequences to correct the errors, the coverage of cDNA sequences on the predicted genes is still incomplete, and many gene models for those expressed in sexual or mosquito stages have not been validated. Antisense transcripts have widely been reported in P. falciparum; however, the extent and pattern of antisense transcripts in different developmental stages remain largely unknown.
Results: We have sequenced seven bidirectional libraries from ring, early and late trophozoite, schizont, gametocyte II, gametocyte V, and ookinete, and four strand-specific libraries from late trophozoite, schizont, gametocyte II, and gametocyte V of the 3D7 parasites. Alignment of the cDNA sequences to the 3D7 reference genome revealed stage-specific antisense transcripts and novel intron-exon splicing junctions. Sequencing of strand-specific cDNA libraries suggested that more genes are expressed in one direction in gametocyte than in schizont. Alternatively spliced genes, antisense transcripts, and stage-specific expressed genes were also characterized.
Conclusions: It is necessary to continue to sequence cDNA from different developmental stages, particularly those of non-erythrocytic stages. The presence of antisense transcripts in some gametocyte and ookinete genes suggests that these antisense RNA may play an important role in gene expression regulation and parasite development. Future gene expression studies should make use of directional cDNA libraries. Antisense transcripts may partly explain the observed discrepancy between levels of mRNA and protein expression.
C1 [Lopez-Barragan, Maria J.; Lemieux, Jacob; Williamson, Kim C.; Molina-Cruz, Alvaro; Barillas-Mury, Carolina; Su, Xin-zhuan] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
[Quinones, Mariam] NIAID, Bioinformat & Computat Biosci Branch, NIH, Bethesda, MD 20892 USA.
[Williamson, Kim C.] Loyola Univ, Dept Biol, Chicago, IL 60660 USA.
[Cui, Kairong; Zhao, Keji] NHLBI, Syst Biol Ctr, NIH, Bethesda, MD 20892 USA.
RP Su, XZ (reprint author), NIAID, Lab Malaria & Vector Res, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM xsu@niaid.nih.gov
OI Su, Xinzhuan/0000-0003-3246-3248
FU Divisions of Intramural Research at the National Institute of Allergy
and Infectious Diseases; National Heart, Lung and Blood Institute,
National Institutes of Health; Public Health Service from National
Institute of Allergy and Infectious Disease, National Institutes of
Health [AI069314]
FX This work was supported by the Divisions of Intramural Research at the
National Institute of Allergy and Infectious Diseases and the National
Heart, Lung and Blood Institute, National Institutes of Health, and by
Public Health Service grant AI069314 from the National Institute of
Allergy and Infectious Disease, National Institutes of Health. We thank
Qingsong Tang, Louri Chepelev, Yan Luo, and Jun Zhu for assistance with
Illumina sequencing, and NIAID intramural editor Brenda Rae Marshall.
NR 48
TC 69
Z9 70
U1 1
U2 5
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 30
PY 2011
VL 12
AR 587
DI 10.1186/1471-2164-12-587
PG 13
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 887AR
UT WOS:000299898000001
PM 22129310
ER
PT J
AU Dennison, SM
Sutherland, LL
Jaeger, FH
Anasti, KM
Parks, R
Stewart, S
Bowman, C
Xia, SM
Zhang, RJ
Shen, XY
Scearce, RM
Ofek, G
Yang, YP
Kwong, PD
Santra, S
Liao, HX
Tomaras, G
Letvin, NL
Chen, B
Alam, SM
Haynes, BF
AF Dennison, S. Moses
Sutherland, Laura L.
Jaeger, Frederick H.
Anasti, Kara M.
Parks, Robert
Stewart, Shelley
Bowman, Cindy
Xia, Shi-Mao
Zhang, Ruijun
Shen, Xiaoying
Scearce, Richard M.
Ofek, Gilad
Yang, Yongping
Kwong, Peter D.
Santra, Sampa
Liao, Hua-Xin
Tomaras, Georgia
Letvin, Norman L.
Chen, Bing
Alam, S. Munir
Haynes, Barton F.
TI Induction of Antibodies in Rhesus Macaques That Recognize a
Fusion-Intermediate Conformation of HIV-1 gp41
SO PLOS ONE
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; PROXIMAL EXTERNAL REGION; BROADLY
NEUTRALIZING ANTIBODIES; HUMAN MONOCLONAL-ANTIBODIES; AUTOREACTIVE
B-CELLS; SURFACE-ANTIGEN; VACCINE DESIGN; 2F5 EPITOPE; MEMBRANE;
ENVELOPE
AB A component to the problem of inducing broad neutralizing HIV-1 gp41 membrane proximal external region (MPER) antibodies is the need to focus the antibody response to the transiently exposed MPER pre-hairpin intermediate neutralization epitope. Here we describe a HIV-1 envelope (Env) gp140 oligomer prime followed by MPER peptide-liposomes boost strategy for eliciting serum antibody responses in rhesus macaques that bind to a gp41 fusion intermediate protein. This Env-liposome immunization strategy induced antibodies to the 2F5 neutralizing epitope (664)DKW residues, and these antibodies preferentially bound to a gp41 fusion intermediate construct as well as to MPER scaffolds stabilized in the 2F5-bound conformation. However, no serum lipid binding activity was observed nor was serum neutralizing activity for HIV-1 pseudoviruses present. Nonetheless, the Env-liposome prime-boost immunization strategy induced antibodies that recognized a gp41 fusion intermediate protein and was successful in focusing the antibody response to the desired epitope.
C1 [Dennison, S. Moses; Sutherland, Laura L.; Jaeger, Frederick H.; Anasti, Kara M.; Parks, Robert; Stewart, Shelley; Bowman, Cindy; Xia, Shi-Mao; Zhang, Ruijun; Shen, Xiaoying; Scearce, Richard M.; Liao, Hua-Xin; Tomaras, Georgia; Alam, S. Munir; Haynes, Barton F.] Duke Univ, Sch Med, Human Vaccine Inst, Durham, NC 27710 USA.
[Santra, Sampa; Letvin, Norman L.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Childrens Hosp,Dept Med, Boston, MA 02215 USA.
[Chen, Bing] Harvard Univ, Childrens Hosp, Sch Med, Div Mol Med, Boston, MA 02115 USA.
[Ofek, Gilad; Yang, Yongping; Kwong, Peter D.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Dennison, SM (reprint author), Duke Univ, Sch Med, Human Vaccine Inst, Durham, NC 27710 USA.
EM alam0004@mc.duke.edu; hayne002@mc.duke.edu
RI Tomaras, Georgia/J-5041-2016
FU Bill & Melinda Gates Foundation [38643]; Center for HIV/AIDS Vaccine
Immunology (CHAVI) from the NIH, NIAID [AI067854]
FX This research was conducted as part of the Collaboration for AIDS
Vaccine Discovery (CAVD) with support from the Bill & Melinda Gates
Foundation to BFH (38643) and from the Center for HIV/AIDS Vaccine
Immunology (CHAVI) AI067854 from the NIH, NIAID. The funders had no role
in study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 53
TC 31
Z9 31
U1 0
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 30
PY 2011
VL 6
IS 11
AR e27824
DI 10.1371/journal.pone.0027824
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 863MI
UT WOS:000298168100019
PM 22140469
ER
PT J
AU Algin, O
Turkbey, B
Ozmen, E
Algin, E
AF Algin, Oktay
Turkbey, Baris
Ozmen, Evrim
Algin, Efnan
TI Magnetic resonance enterography findings of chronic radiation enteritis
SO CANCER IMAGING
LA English
DT Article
DE Chronic radiation enteritis; enterography; radiotherapy; small bowel
imaging; MRI; oral contrast
ID CT ENTEROGRAPHY
AB The diagnosis of chronic radiation enteritis (CRE) is considerably challenging both for clinicians and radiologists. The aim of this study was to evaluate the role of magnetic resonance enterography (MRE) in the diagnosis of CRE. To the best of our knowledge, there are no reports on the role of MRE in the diagnosis of CRE specifically. In this report, we present MRE findings of 4 patients with CRE. The most important factors in CRE diagnosis are the clinical findings and medical history, but focal abnormal bowel loop in the region of a known radiation field is the most important information. This abnormal loop is generally located in the distal ileum as present in our patients. Other associated findings helpful for the diagnosis are small bowel thickening, contrast material enhancement in a long segment, mesenteric stranding and luminal narrowing. MRE can be sufficient and useful in the diagnosis of CRE and for treatment planning, especially in patients with significant comorbidities who have had radiotherapy in the past. Adding MRE into the diagnostic algorithm can be helpful in post-radiotherapy patients with acute/subacute gastrointestinal symptoms.
C1 [Algin, Oktay; Ozmen, Evrim] Ataturk Training & Res Hosp, Dept Radiol, Bilkent, Turkey.
[Turkbey, Baris] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Algin, Efnan] Gazi Univ, Fac Med, Dept Med Oncol, Ankara, Turkey.
RP Algin, O (reprint author), Ataturk Training & Res Hosp, Dept Radiol, Bilkent, Turkey.
EM droktayalgin@gmail.com
NR 10
TC 6
Z9 6
U1 1
U2 5
PU E-MED
PI LONDON
PA PO BOX 29761, LONDON, NW3 7ZS, ENGLAND
SN 1470-7330
J9 CANCER IMAGING
JI Cancer Imaging
PD NOV 30
PY 2011
VL 11
IS 1
BP 189
EP 194
DI 10.1102/1470-7330.2011.0026
PG 6
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 864IL
UT WOS:000298232800002
PM 22138564
ER
PT J
AU Kaila, VRI
Hummer, G
AF Kaila, Ville R. I.
Hummer, Gerhard
TI Energetics of Direct and Water-Mediated Proton-Coupled Electron Transfer
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID HYDROGEN-ATOM TRANSFER; DENSITY-FUNCTIONAL THEORY; SELF-EXCHANGE
REACTIONS; RIBONUCLEOTIDE REDUCTASE; BASIS-SETS; PHENOXYL/PHENOL;
BENZYL/TOLUENE; OXIDATION; DYNAMICS; BIOLOGY
AB Proton-coupled electron transfer (PCET) is an elementary chemical reaction crucial for biological oxidoreduction. We perform quantum chemical calculations to study the direct and water-mediated PCET between two stacked tyrosines, TyrO(center dot) + TyrOH -> TyrOH + TyrO(center dot), to mimic a key step in the catalytic reaction of class Ia ribonucleotide reductase (RNR). The energy surfaces of electronic ground and excited states are separated by a large gap of similar to 20 kcal mol(-1), indicative of an electronically adiabatic transfer mechanism. In response to chemical substitutions of the proton donor, the energy of the transition state for direct PCET shifts by exactly half of the change in energetic driving force, resulting in a linear free energy relation with a Bronsted slope of 1/2. In contrast, for water-mediated PCET, we observe integer Bronsted slopes of 1 and 0 for proton acceptor and donor modifications, respectively. Our calculations suggest that the pi-stacking of the tyrosine dimer in RNR results in strong electronic coupling and adiabatic PCET. Water participation in the PCET can be identified perturbatively in a Bronsted analysis.
C1 [Kaila, Ville R. I.; Hummer, Gerhard] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Kaila, VRI (reprint author), NIDDK, Chem Phys Lab, NIH, Bldg 5, Bethesda, MD 20892 USA.
EM ville.kaila@nih.gov; gerhard.hummer@nih.gov
RI Hummer, Gerhard/A-2546-2013
OI Hummer, Gerhard/0000-0001-7768-746X
FU National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health; European Molecular Biology Organization
(EMBO)
FX V.R.I.K acknowledges Prof. Marten Wikstrom and Prof. Dage Sundholm for
insightful discussions. This research was supported by the Intramural
Research Program of the National Institute of Diabetes and Digestive and
Kidney Diseases, National Institutes of Health. V.R.I.K. acknowledges
the European Molecular Biology Organization (EMBO) for a Long-Term
Fellowship. The Biowulf cluster at NIH (http://biowulf.nih.gov/) is
acknowledged for computer time.
NR 40
TC 19
Z9 19
U1 2
U2 41
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD NOV 30
PY 2011
VL 133
IS 47
BP 19040
EP 19043
DI 10.1021/ja2082262
PG 4
WC Chemistry, Multidisciplinary
SC Chemistry
GA 856SD
UT WOS:000297662800007
PM 21988482
ER
PT J
AU Amarnath, S
Mangus, CW
Wang, JCM
Wei, F
He, A
Kapoor, V
Foley, JE
Massey, PR
Felizardo, TC
Riley, JL
Levine, BL
June, CH
Medin, JA
Fowler, DH
AF Amarnath, Shoba
Mangus, Courtney W.
Wang, James C. M.
Wei, Fang
He, Alice
Kapoor, Veena
Foley, Jason E.
Massey, Paul R.
Felizardo, Tania C.
Riley, James L.
Levine, Bruce L.
June, Carl H.
Medin, Jeffrey A.
Fowler, Daniel H.
TI The PDL1-PD1 Axis Converts Human T(H)1 Cells into Regulatory T Cells
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Article
ID VERSUS-HOST-DISEASE; PROGRAMMED DEATH-1; INTERFERON-GAMMA; TH17 CELLS;
PLASTICITY; RESPONSES; PATHWAY; INTERLEUKIN-12; ACTIVATION; EXPRESSION
AB Immune surveillance by T helper type 1 (T(H)1) cells is not only critical for the host response to tumors and infection, but also contributes to autoimmunity and graft-versus-host disease (GVHD) after transplantation. The inhibitory molecule programmed death ligand 1 (PDL1) has been shown to anergize human T(H)1 cells, but other mechanisms of PDL1-mediated T(H)1 inhibition such as the conversion of T(H)1 cells to a regulatory phenotype have not been well characterized. We hypothesized that PDL1 may cause T(H)1 cells to manifest differentiation plasticity. Conventional T cells or irradiated K562 myeloid tumor cells overexpressing PDL1 converted TBET+ T(H)1 cells into FOXP3(+) regulatory T (T-reg) cells in vivo, thereby preventing human-into-mouse xenogeneic GVHD (xGVHD). Either blocking PD1 expression on T(H)1 cells by small interfering RNA targeting or abrogation of PD1 signaling by SHP1/2 pharmacologic inhibition stabilized T(H)1 cell differentiation during PDL1 challenge and restored the capacity of T(H)1 cells to mediate lethal xGVHD. PD1 signaling therefore induces human T(H)1 cells to manifest in vivo plasticity, resulting in a T-reg phenotype that severely impairs cell-mediated immunity. Converting human T(H)1 cells to a regulatory phenotype with PD1 signaling provides a potential way to block GVHD after transplantation. Moreover, because this conversion can be prevented by blocking PD1 expression or pharmacologically inhibiting SHP1/2, this pathway provides a new therapeutic direction for enhancing T cell immunity to cancer and infection.
C1 [Amarnath, Shoba; Mangus, Courtney W.; He, Alice; Kapoor, Veena; Foley, Jason E.; Massey, Paul R.; Felizardo, Tania C.; Fowler, Daniel H.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Mangus, Courtney W.] Natl Inst Hlth Res Scholars Program, Howard Hughes Med Inst, Chevy Chase, MD 20815 USA.
[Wang, James C. M.; Medin, Jeffrey A.] Univ Hlth Network, Inst Med Sci, Toronto, ON M5G 2M1, Canada.
[Wei, Fang; Riley, James L.; Levine, Bruce L.; June, Carl H.] Univ Penn, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA.
[Medin, Jeffrey A.] Univ Hlth Network, Ontario Canc Inst, Toronto, ON M5G 2M1, Canada.
RP Amarnath, S (reprint author), NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
EM samarnath@mail.nih.gov
RI Levine, Bruce/D-1688-2009;
OI Riley, James/0000-0002-1057-576X
FU Centre for Cancer Research, National Cancer Institute; Juvenile Diabetes
Research Foundation Collaborative Centre for Cell Therapy;
[P01AI080192]
FX We thank H. Kong for her technical expertise. Funding: Supported by the
Centre for Cancer Research, National Cancer Institute, Intramural
Research Program, and by P01AI080192 and Juvenile Diabetes Research
Foundation Collaborative Centre for Cell Therapy. Author contributions:
S. A. designed and performed the research, performed the analysis, and
wrote the manuscript. C. W. M., J.C.M.W., F. W., A. H., V. K., J.E.F.,
P. R. M., and T. C. F. performed the research. J.L.R., B. L. L., C.H.J.,
J.A.M., and D. H. F. designed the research and wrote the manuscript.
Competing interests: J.L.R. has an advisory relationship with
Bristol-Myers Squibb. The other authors declare that they have no
competing interests. D. H. F. and J.A.M. are authors on a patent
relating to TMPK cell fate (thymidylate kinase fusions and uses thereof,
patent number: US12/933,460). J.L.R. is an author on a patent related to
the use of PDL1 expressing aAPCs to treat autoimmune disease.
NR 50
TC 54
Z9 56
U1 3
U2 13
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1946-6234
J9 SCI TRANSL MED
JI Sci. Transl. Med.
PD NOV 30
PY 2011
VL 3
IS 111
AR 111ra120
DI 10.1126/scitranslmed.3003130
PG 13
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 862GX
UT WOS:000298079000003
PM 22133721
ER
PT J
AU Yu, S
Yang, HD
Nakahara, H
Santos, GS
Nikolic, D
Plenz, D
AF Yu, Shan
Yang, Hongdian
Nakahara, Hiroyuki
Santos, Gustavo S.
Nikolic, Danko
Plenz, Dietmar
TI Higher-Order Interactions Characterized in Cortical Activity
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID INFORMATION-GEOMETRIC MEASURE; NEURONAL AVALANCHES; FIRING PATTERNS;
NEOCORTICAL CIRCUITS; NEURAL POPULATION; CELL ASSEMBLIES; PRIMATE
RETINA; IN-VITRO; NETWORKS; CORTEX
AB In the cortex, the interactions among neurons give rise to transient coherent activity patterns that underlie perception, cognition, and action. Recently, it was actively debated whether the most basic interactions, i.e., the pairwise correlations between neurons or groups of neurons, suffice to explain those observed activity patterns. So far, the evidence reported is controversial. Importantly, the overall organization of neuronal interactions and the mechanisms underlying their generation, especially those of high-order interactions, have remained elusive. Here we show that higher-order interactions are required to properly account for cortical dynamics such as ongoing neuronal avalanches in the alert monkey and evoked visual responses in the anesthetized cat. A Gaussian interaction model that utilizes the observed pairwise correlations and event rates and that applies intrinsic thresholding identifies those higher-order interactions correctly, both in cortical local field potentials and spiking activities. This allows for accurate prediction of large neuronal population activities as required, e. g., in brain-machine interface paradigms. Our results demonstrate that higher-order interactions are inherent properties of cortical dynamics and suggest a simple solution to overcome the apparent formidable complexity previously thought to be intrinsic to those interactions.
C1 [Yu, Shan; Yang, Hongdian; Plenz, Dietmar] NIMH, Sect Crit Brain Dynam, Lab Syst Neurosci, Bethesda, MD 20892 USA.
[Yang, Hongdian] Univ Maryland, Inst Phys Sci & Technol, Biophys Program, College Pk, MD 20742 USA.
[Nakahara, Hiroyuki; Santos, Gustavo S.] RIKEN Brain Sci Inst, Lab Integrated Theoret Neurosci, Wako, Saitama 3510198, Japan.
[Nakahara, Hiroyuki] Tokyo Inst Technol, Dept Computat Intelligence & Syst Sci, Midori Ku, Yokohama, Kanagawa 2268503, Japan.
[Nikolic, Danko] Max Planck Inst Brain Res, Dept Neurophysiol, D-60528 Frankfurt, Germany.
[Nikolic, Danko] Goethe Univ Frankfurt, Frankfurt Inst Adv Studies, D-60325 Frankfurt, Germany.
RP Plenz, D (reprint author), NIMH, Sect Crit Brain Dynam, Lab Syst Neurosci, 6001 Execut Blvd, Bethesda, MD 20892 USA.
EM plenzd@mail.nih.gov
RI Yang, Hongdian/D-1450-2015; Nakahara, Hiroyuki/N-5411-2015
OI Nakahara, Hiroyuki/0000-0001-6891-1175
FU National Institute of Mental Health; Deutsche Forschungsgemeinschaft [NI
708/2-1]; Hertie Stiftung; Max-Planck Society; Frankfurt Institute for
Advanced Studies
FX This study was supported by the Intramural Research Program of the
National Institute of Mental Health. Experiments with cat recordings
were supported by a Deutsche Forschungsgemeinschaft Grant NI 708/2-1,
Hertie Stiftung, Max-Planck Society, and the Frankfurt Institute for
Advanced Studies. We thank Andrew Mitz and Richard Saunders for help in
data collection and Steven Wise for his support during the initial phase
of the project.
NR 51
TC 58
Z9 58
U1 1
U2 12
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 30
PY 2011
VL 31
IS 48
BP 17514
EP 17526
DI 10.1523/JNEUROSCI.3127-11.2011
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA 860FY
UT WOS:000297935400019
PM 22131413
ER
PT J
AU Furl, N
Averbeck, BB
AF Furl, Nicholas
Averbeck, Bruno B.
TI Parietal Cortex and Insula Relate to Evidence Seeking Relevant to
Reward-Related Decisions
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID PERCEPTUAL DECISION; HUMAN BRAIN; RISK; UNCERTAINTY; NEURONS; SIGNALS;
MODEL; FMRI
AB Decisions are most effective after collecting sufficient evidence to accurately predict rewarding outcomes. We investigated whether human participants optimally seek evidence and we characterized the brain areas associated with their evidence seeking. Participants viewed sequences of bead colors drawn from hidden urns and attempted to infer the majority bead color in each urn. When viewing each bead color, participants chose either to seek more evidence about the urn by drawing another bead (draw choices) or to infer the urn contents (urn choices). We then compared their evidence seeking against that predicted by a Bayesian ideal observer model. By this standard, participants sampled less evidence than optimal. Also, when faced with urns that had bead color splits closer to chance (60/40 versus 80/20) or potential monetary losses, participants increased their evidence seeking, but they showed less increase than predicted by the ideal observer model. Functional magnetic resonance imaging showed that urn choices evoked larger hemodynamic responses than draw choices in the insula, striatum, anterior cingulate, and parietal cortex. These parietal responses were greater for participants who sought more evidence on average and for participants who increased more their evidence seeking when draws came from 60/40 urns. The parietal cortex and insula were associated with potential monetary loss. Insula responses also showed modulation with estimates of the expected gains of urn choices. Our findings show that participants sought less evidence than predicted by an ideal observer model and their evidence-seeking behavior may relate to responses in the insula and parietal cortex.
C1 [Furl, Nicholas; Averbeck, Bruno B.] NIMH, Unit Learning & Decis Making, Neuropsychol Lab, Bethesda, MD 20892 USA.
RP Furl, N (reprint author), MRC, Cognit & Brain Sci Unit, 15 Chaucer Rd, Cambridge CB2 7EF, England.
EM nick.furl@mrc-cbu.cam.ac.uk
OI furl, nicholas/0000-0003-2488-1343
FU NIH, National Institute of Mental Health
FX This work was supported by the Intramural Research Program of the NIH,
National Institute of Mental Health. Editorial assistance for the
article was provided by the National Institutes of Health Fellows
Editorial Board. We thank Peter Dayan and Michael Moutoussis for sharing
their ideal observer model, which inspired this experiment, Maria Barsky
for her assistance with data analysis, and Barry Richmond and Chris
Baker for their comments.
NR 32
TC 39
Z9 40
U1 0
U2 8
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 30
PY 2011
VL 31
IS 48
BP 17572
EP 17582
DI 10.1523/JNEUROSCI.4236-11.2011
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 860FY
UT WOS:000297935400024
PM 22131418
ER
PT J
AU Buch, ER
Johnen, VM
Nelissen, N
O'Shea, J
Rushworth, MFS
AF Buch, Ethan R.
Johnen, Vanessa M.
Nelissen, Natalie
O'Shea, Jacinta
Rushworth, Matthew F. S.
TI Noninvasive Associative Plasticity Induction in a Corticocortical
Pathway of the Human Brain
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID TRANSCRANIAL MAGNETIC STIMULATION; PRIMARY MOTOR CORTEX; MEDIAL
FRONTAL-CORTEX; VENTRAL PREMOTOR CORTEX; FUNCTIONAL CONNECTIVITY;
CORTICAL INTERACTIONS; SUBTHALAMIC NUCLEUS; INHIBITORY CONTROL; ACTION
SELECTION; MACAQUE MONKEY
AB Coincident pairing of presynaptic and postsynaptic activity selectively strengthens synaptic connections, a key mechanism underlying cortical plasticity. Using paired associative transcranial magnetic stimulation (TMS), we demonstrate selective potentiation of physiological connectivity between two human brain regions, ventral premotor cortex (PMv) and primary motor cortex (M1) after repeated paired-pulse TMS of PMv and M1. The effect was anatomically specific: paired stimulation of the presupplementary motor area and M1 did not induce changes in PMv-M1 pathway connectivity. The effect was dependent on stimulation order: repeated stimulation of PMv before M1 led to strengthening of the PMv-M1 pathway, while repeated stimulation of M1 before PMv diminished the strength of the PMv-M1 pathway. The expression of the change in the pathway depended on the cognitive state of the subject at the time of testing: when the subject was tested at rest, paired PMv-M1 stimulation led to an increased inhibitory influence of PMv over M1, but when the subject was tested while engaged in a visuomotor task, PMv-M1 stimulation led to an increased facilitatory influence of PMv over M1. Plasticity evolved rapidly, lasted for at least 1 h, and began to reverse 3 h after intervention.
C1 [Buch, Ethan R.; Johnen, Vanessa M.; Nelissen, Natalie; O'Shea, Jacinta; Rushworth, Matthew F. S.] Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England.
[Buch, Ethan R.; Johnen, Vanessa M.; O'Shea, Jacinta; Rushworth, Matthew F. S.] Univ Oxford, John Radcliffe Hosp, Ctr Funct Magnet Resonance Imaging Brain, Oxford OX3 9DU, England.
[Buch, Ethan R.] Natl Inst Neurol Disorders & Stroke, Human Cort Physiol & Stroke Neurorehabil Sect, NIH, Bethesda, MD 20814 USA.
RP Buch, ER (reprint author), Bldg 10,Room 7D52,MSC 1428,10 Ctr Dr, Bethesda, MD 20892 USA.
EM buche@ninds.nih.gov; vanessa.johnen@psy.ox.ac.uk
RI Buch, Ethan/G-1981-2011;
OI O'Shea, Jacinta/0000-0002-6007-0698
FU Medical Research Council; NINDS; Henry F. Jackson Foundation Center for
Neuroscience and Regenerative Medicine; Research Foundation Flanders;
Royal Society
FX This work was supported by the Medical Research Council (V.M.J.,
M.F.S.R.), the NINDS intramural program (E.R.B.), the Henry F. Jackson
Foundation Center for Neuroscience and Regenerative Medicine (E.R.B.),
the Research Foundation Flanders (N.N.), and the Royal Society (J.O.).
NR 42
TC 33
Z9 33
U1 1
U2 10
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 30
PY 2011
VL 31
IS 48
BP 17669
EP 17679
DI 10.1523/JNEUROSCI.1513-11.2011
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 860FY
UT WOS:000297935400033
PM 22131427
ER
PT J
AU Lee, M
Fine, JP
AF Lee, Minjung
Fine, Jason P.
TI Inference for cumulative incidence quantiles via parametric and
nonparametric approaches
SO STATISTICS IN MEDICINE
LA English
DT Article
DE breast cancer; competing risks; confidence interval; cumulative
incidence function; quantile
ID MEDIAN SURVIVAL-TIME; COMPETING RISKS; CONFIDENCE-INTERVALS; MULTISTATE
MODELS; PROGRESSION
AB In survival analysis, a point estimate and confidence interval for median survival time have been frequently used to summarize the survival curve. However, such quantile analyses on competing risks data have not been widely investigated. In this paper, we propose parametric inferences for quantiles from the cumulative incidence function and develop parametric confidence intervals for quantiles. In addition, we study a simplified method of inference for the nonparametric approach. We compare the parametric and nonparametric inferences in empirical studies. Simulation studies show that the procedures perform well, with parametric analyses yielding smaller mean square error when the model is not too badly misspecified. We illustrate the methods with data from a breast cancer clinical trial. Copyright (C) 2011 John Wiley & Sons, Ltd.
C1 [Lee, Minjung] Univ Wisconsin, Dept Stat, Madison, WI 53706 USA.
[Fine, Jason P.] Univ N Carolina, Dept Biostat, Chapel Hill, NC 27599 USA.
RP Lee, M (reprint author), NCI, Data Anal & Interpretat Branch, Div Canc Control & Populat Sci, Bethesda, MD 20852 USA.
EM leem5@mail.nih.gov
NR 28
TC 3
Z9 3
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD NOV 30
PY 2011
VL 30
IS 27
BP 3221
EP 3235
DI 10.1002/sim.4349
PG 15
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 860UK
UT WOS:000297973100005
PM 21898525
ER
PT J
AU Tang, LY
Yamashita, M
Coussens, NP
Tang, Y
Wang, XC
Li, CL
Deng, CX
Cheng, SY
Zhang, YE
AF Tang, Liu-Ya
Yamashita, Motozo
Coussens, Nathan P.
Tang, Yi
Wang, Xiangchun
Li, Cuiling
Deng, Chu-Xia
Cheng, Steven Y.
Zhang, Ying E.
TI Ablation of Smurf2 reveals an inhibition in TGF-beta signalling through
multiple mono-ubiquitination of Smad3
SO EMBO JOURNAL
LA English
DT Article
DE Smad3; Smurf2; TGF-beta; ubiquitination
ID GROWTH-FACTOR-BETA; TUMOR-SUPPRESSOR SMAD4/DPC4; DEPENDENT DEGRADATION;
TRANSCRIPTIONAL ACTIVATION; I RECEPTOR; LIGASE; PHOSPHORYLATION;
TARGETS; SPECIFICITY; GENE
AB TGF-beta signalling is regulated by post-translational modifications of Smad proteins to translate quantitative difference in ligand concentration into proportional transcriptional output. Previous studies in cell culture systems suggested that Smad ubiquitination regulatory factors (Smurfs) act in this regulation by targeting Smads for proteasomal degradation, but whether this mechanism operates under physiological conditions is not clear. Here, we generated mice harbouring a target-disrupted Smurf2 allele. Using primary mouse embryonic fibroblasts and dermal fibroblasts, we show that TGF-beta-mediated, Smad-dependent transcriptional responses are elevated in the absence of Smurf2. Instead of promoting poly-ubiquitination and degradation, we show that Smurf2 actually induces multiple mono-ubiquitination of Smad3 in vivo. Phosphorylation of T179, immediately upstream of the Smad3 PY motif, enhances Smurf2 and Smad3 interaction and Smad3 ubiquitination. We have mapped Smurf2-induced Smad3 ubiquitination sites to lysine residues at the MH2 domain, and demonstrate that Smad3 ubiquitination inhibits the formation of Smad3 complexes. Thus, our data support a model in which Smurf2 negatively regulates TGF-beta signalling by attenuating the activity of Smad3 rather than promoting its degradation. The EMBO Journal (2011) 30, 4777-4789. doi:10.1038/emboj.2011.393; Published online 1 November 2011
C1 [Zhang, Ying E.] NCI, Lab Cellular & Mol Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Li, Cuiling; Deng, Chu-Xia] NIDDK, Mammalian Genet Sect, Genet Dev & Dis Branch, NIH, Bethesda, MD USA.
[Cheng, Steven Y.] Nanjing Med Univ, Ctr Regenerat Med, Dept Dev Genet, Nanjing, Jiangsu, Peoples R China.
RP Zhang, YE (reprint author), NCI, Lab Cellular & Mol Biol, Ctr Canc Res, NIH, Bldg 37,RM 2056B, Bethesda, MD 20892 USA.
EM zhangyin@mail.nih.gov
RI Zhang, Ying/G-3657-2015; deng, chuxia/N-6713-2016
OI Zhang, Ying/0000-0003-2753-7601;
FU NIH, National Cancer Institute, Center for Cancer Research; JSPS
[21689053]
FX We thank Drs F Liu, P ten Dijke, and Z Xiao for various plasmid and
antibody reagents, Dr V Barr for assistance with microscope and computer
software, N Morris for animal service, and Dr P Randazzo's lab for
assistance with protein purification. This research was supported by the
intramural research program of the NIH, National Cancer Institute,
Center for Cancer Research. MY was partially supported by JSPS Grant
#21689053.
NR 54
TC 51
Z9 51
U1 4
U2 13
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0261-4189
J9 EMBO J
JI Embo J.
PD NOV 30
PY 2011
VL 30
IS 23
BP 4777
EP 4789
DI 10.1038/emboj.2011.393
PG 13
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 857CO
UT WOS:000297692100010
PM 22045334
ER
PT J
AU Elking, DM
Perera, L
Duke, R
Darden, T
Pedersen, LG
AF Elking, Dennis M.
Perera, Lalith
Duke, Robert
Darden, Thomas
Pedersen, Lee G.
TI A Finite Field Method for Calculating Molecular Polarizability Tensors
for Arbitrary Multipole Rank
SO JOURNAL OF COMPUTATIONAL CHEMISTRY
LA English
DT Article
DE multipole; quadrupole; octupole; polarizability; finite field
ID HARTREE-FOCK THEORY; DIPOLE-OCTOPOLE POLARIZABILITY; GAUSSIAN-BASIS
SETS; CHARGE FORCE-FIELD; FLUCTUATING CHARGE; DISTRIBUTED
POLARIZABILITIES; AB-INITIO; GRADIENT POLARIZABILITIES; ELECTRON
CORRELATION; WATER MOLECULE
AB A finite field method for calculating spherical tensor molecular polarizability tensors alpha(lm;l'm') = partial derivative Delta(lm)/partial derivative phi(l'm')* by numerical derivatives of induced molecular multipole Delta(lm) with respect to gradients of electrostatic potential phi(l'm')* is described for arbitrary multipole ranks l and l'. Interconversion formulae for transforming multipole moments and polarizability tensors between spherical and traceless Cartesian tensor conventions are derived. As an example, molecular polarizability tensors up to the hexadecapole-hexadecapole level are calculated for water using the following ab initio methods: Hartree-Fock (HF), Becke three-parameter Lee-Yang-Parr exchange-correlation functional (B3LYP), Moller-Plesset perturbation theory up to second order (MP2), and Coupled Cluster theory with single and double excitations (CCSD). In addition, intermolecular electrostatic and polarization energies calculated by molecular multipoles and polarizability tensors are compared with ab initio reference values calculated by the Reduced Variation Space method for several randomly oriented small molecule dimers separated by a large distance. It is discussed how higher order molecular polarizability tensors can be used as a tool for testing and developing new polarization models for future force fields. (C) 2011 Wiley Periodicals, Inc. J Comput Chem 32:3283-3295, 2011
C1 [Elking, Dennis M.; Duke, Robert; Pedersen, Lee G.] Univ N Carolina, Dept Chem, Chapel Hill, NC 27599 USA.
[Perera, Lalith; Pedersen, Lee G.] NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA.
[Darden, Thomas] OpenEye Sci Software, Santa Fe, NM 87508 USA.
RP Elking, DM (reprint author), Univ N Carolina, Dept Chem, CB 3290, Chapel Hill, NC 27599 USA.
EM lee_pedersen@unc.edu
RI perera, Lalith/B-6879-2012; Pedersen, Lee/E-3405-2013
OI perera, Lalith/0000-0003-0823-1631; Pedersen, Lee/0000-0003-1262-9861
FU National Institute of Health [HL-06350]; National Science Foundation
[FRG DMR 084549]; NIH-National Institute of Environmental Health
Sciences [Z01 ES125392]
FX Contract/grant sponsor: HL-06350/National Institute of Health;
Contract/grant number: FRG DMR 084549/National Science Foundation;
Contract/grant number: Z01 ES125392/NIH-National Institute of
Environmental Health Sciences (Intramural Research Program).
NR 91
TC 10
Z9 10
U1 1
U2 20
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0192-8651
EI 1096-987X
J9 J COMPUT CHEM
JI J. Comput. Chem.
PD NOV 30
PY 2011
VL 32
IS 15
BP 3283
EP 3295
DI 10.1002/jcc.21914
PG 13
WC Chemistry, Multidisciplinary
SC Chemistry
GA 823LM
UT WOS:000295123800016
PM 21915883
ER
PT J
AU Sahoo, SS
Nguyen, V
Bodenreider, O
Parikh, P
Minning, T
Sheth, AP
AF Sahoo, Satya S.
Vinh Nguyen
Bodenreider, Olivier
Parikh, Priti
Minning, Todd
Sheth, Amit P.
TI A unified framework for managing provenance information in translational
research
SO BMC BIOINFORMATICS
LA English
DT Article
ID SEMANTIC PROVENANCE
AB Background: A critical aspect of the NIH Translational Research roadmap, which seeks to accelerate the delivery of "bench-side" discoveries to patient's "bedside," is the management of the provenance metadata that keeps track of the origin and history of data resources as they traverse the path from the bench to the bedside and back. A comprehensive provenance framework is essential for researchers to verify the quality of data, reproduce scientific results published in peer-reviewed literature, validate scientific process, and associate trust value with data and results. Traditional approaches to provenance management have focused on only partial sections of the translational research life cycle and they do not incorporate "domain semantics", which is essential to support domain-specific querying and analysis by scientists.
Results: We identify a common set of challenges in managing provenance information across the pre-publication and post-publication phases of data in the translational research lifecycle. We define the semantic provenance framework (SPF), underpinned by the Provenir upper-level provenance ontology, to address these challenges in the four stages of provenance metadata:
(a) Provenance collection - during data generation
(b) Provenance representation - to support interoperability, reasoning, and incorporate domain semantics
(c) Provenance storage and propagation - to allow efficient storage and seamless propagation of provenance as the data is transferred across applications
(d) Provenance query - to support queries with increasing complexity over large data size and also support knowledge discovery applications
We apply the SPF to two exemplar translational research projects, namely the Semantic Problem Solving Environment for Trypanosoma cruzi (T. cruzi SPSE) and the Biomedical Knowledge Repository (BKR) project, to demonstrate its effectiveness.
Conclusions: The SPF provides a unified framework to effectively manage provenance of translational research data during pre and post-publication phases. This framework is underpinned by an upper-level provenance ontology called Provenir that is extended to create domain-specific provenance ontologies to facilitate provenance interoperability, seamless propagation of provenance, automated querying, and analysis.
C1 [Sahoo, Satya S.; Vinh Nguyen; Parikh, Priti; Sheth, Amit P.] Wright State Univ, Dept Comp Sci & Engn, Knoesis Ctr, Dayton, OH 45435 USA.
[Minning, Todd] Univ Georgia, Ctr Trop & Emerging Global Dis, Athens, GA 30602 USA.
[Bodenreider, Olivier] NIH, Lister Hill Natl Ctr Biomed Commun, Natl Lib Med, Bethesda, MD 20892 USA.
[Sahoo, Satya S.] Case Western Reserve Univ, Sch Med, Div Med Informat, Cleveland, OH USA.
RP Sahoo, SS (reprint author), Wright State Univ, Dept Comp Sci & Engn, Knoesis Ctr, Dayton, OH 45435 USA.
EM satyasahoo@gmail.com
FU NIH [1R01HL087795-01A1]; National Institutes of Health (NIH), National
Library of Medicine (NLM)
FX This research was supported in part by the NIH RO1 Grant#
1R01HL087795-01A1 and the Intramural Research Program of the National
Institutes of Health (NIH), National Library of Medicine (NLM).
NR 53
TC 1
Z9 1
U1 0
U2 5
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 29
PY 2011
VL 12
AR 461
DI 10.1186/1471-2105-12-461
PG 18
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Mathematical & Computational Biology
GA 906XE
UT WOS:000301381600001
PM 22126369
ER
PT J
AU Li, CC
Kuo, JC
Waterman, CM
Kiyama, R
Moss, J
Vaughan, M
AF Li, Chun-Chun
Kuo, Jean-Cheng
Waterman, Clare M.
Kiyama, Ryoiti
Moss, Joel
Vaughan, Martha
TI Effects of brefeldin A-inhibited guanine nucleotide-exchange (BIG) 1 and
KANK1 proteins on cell polarity and directed migration during wound
healing
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID ADP-RIBOSYLATION FACTORS; RECYCLING ENDOSOMES; ARP2/3 COMPLEX; SEC7
DOMAIN; MYOSIN IXB; KINASE-A; GOLGI; LOCALIZATION; ACTIN; ARF
AB Brefeldin A-inhibited guanine nucleotide-exchange protein (BIG) 1 activates class I ADP ribosylation factors (ARFs) by accelerating the replacement of bound GDP with GTP to initiate recruitment of coat proteins for membrane vesicle formation. Among proteins that interact with BIG1, kinesin family member 21A (KIF21A), a plus-end-directed motor protein, moves cargo away from the microtubule-organizing center (MTOC) on microtubules. Because KANK1, a protein containing N-terminal KN, C-terminal ankyrin-repeat, and intervening coiled-coil domains, has multiple actions in cells and also interacts with KIF21A, we explored a possible interaction between it and BIG1. We obtained evidence for a functional and physical association between these proteins, and found that the effects of BIG1 and KANK1 depletion on cell migration in wound-healing assays were remarkably similar. Treatment of cells with BIG1- or KANK1-specific siRNA interfered significantly with directed cell migration and initial orientation of Golgi/MTOC toward the leading edge, which was not mimicked by KIF21A depletion. Although colocalization of overexpressed KANK1 and endogenous BIG1 in HeLa cells was not clear microscopically, their reciprocal immunoprecipitation (IP) is compatible with the presence of small percentages of each protein in the same complexes. Depletion or overexpression of BIG1 protein appeared not to affect KANK1 distribution. Our data identify actions of both BIG1 and KANK1 in regulating cell polarity during directed migration; these actions are consistent with the presence of both BIG1 and KANK1 in dynamic multimolecular complexes that maintain Golgi/MTOC orientation, differ from those that might contain all three proteins (BIG1, KIF21A, and KANK1), and function in directed transport along microtubules.
C1 [Li, Chun-Chun; Moss, Joel; Vaughan, Martha] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Kuo, Jean-Cheng; Waterman, Clare M.] NHLBI, Cell Biol & Physiol Ctr, NIH, Bethesda, MD 20892 USA.
[Kiyama, Ryoiti] Natl Inst Adv Ind Sci & Technol, Signaling Mol Res Grp, Biomed Res Inst, Tsukuba, Ibaraki 3058566, Japan.
RP Vaughan, M (reprint author), NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
EM vaughanm@nhlbi.nih.gov
OI Waterman, Clare/0000-0001-6142-6775
FU NIH, NHLBI
FX We are grateful to members of the Cell Biology and Physiology Center,
National Heart, Lung and Blood Institute (NHLBI), National Institutes of
Health (NIH) for invaluable help in time-lapse imaging and to Drs.
Daniela Malide and Christian Combs (Light Microscopy Core Facility,
NHLBI) for their much appreciated assistance in confocal microscopy.
This research was supported by the Intramural Research Program of the
NIH, NHLBI.
NR 54
TC 6
Z9 7
U1 1
U2 6
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 29
PY 2011
VL 108
IS 48
BP 19228
EP 19233
DI 10.1073/pnas.1117011108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 853ZB
UT WOS:000297463100032
PM 22084092
ER
PT J
AU Kobayashi, M
Sabouri, Z
Sabouri, S
Kitawaki, Y
Pommier, Y
Abe, T
Kiyonari, H
Honjo, T
AF Kobayashi, Maki
Sabouri, Zahra
Sabouri, Somayeh
Kitawaki, Yoko
Pommier, Yves
Abe, Takaya
Kiyonari, Hiroshi
Honjo, Tasuku
TI Decrease in topoisomerase I is responsible for activation-induced
cytidine deaminase (AID)-dependent somatic hypermutation
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE DNA cleavage; non-B DNA structure
ID CLASS-SWITCH RECOMBINATION; B DNA CONFORMATIONS; CELL-LINE; MEIOTIC
RECOMBINATION; IMMUNOGLOBULIN GENES; GENOMIC INSTABILITY; MU REGION;
TRANSCRIPTION; AID; EXPRESSION
AB Somatic hypermutation (SHM) and class-switch recombination (CSR) of the Ig gene require both the transcription of the locus and the expression of activation-induced cytidine deaminase (AID). During CSR, AID decreases the amount of topoisomerase I (Top1); this decrease alters the DNA structure and induces cleavage in the S region. Similarly, Top1 is involved in transcription-associated mutation at dinucleotide repeats in yeast and in triplet-repeat contraction in mammals. Here, we report that the AID-induced decrease in Top1 is critical for SHM. Top1 knockdown or haploinsufficiency enhanced SHM, whereas Top1 overexpression down-regulated it. A specific Top1 inhibitor, camptothecin, suppressed SHM, indicating that Top1's activity is required for DNA cleavage. Nonetheless, suppression of transcription abolished SHM, even in cells with Top1 knockdown, suggesting that transcription is critical. These results are consistent with a model proposed for CSR and triplet instability, in which transcription-induced non-B structure formation is enhanced by Top1 reduction and provides the target for irreversible cleavage by Top1. We speculate that the mechanismfor transcription-coupled genome instability was adopted to generate immune diversity when AID evolved.
C1 [Kobayashi, Maki; Sabouri, Zahra; Sabouri, Somayeh; Kitawaki, Yoko; Honjo, Tasuku] Kyoto Univ, Dept Immunol & Genom Med, Grad Sch Med, Kyoto 6068501, Japan.
[Pommier, Yves] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Abe, Takaya; Kiyonari, Hiroshi] RIKEN Ctr Dev Biol, Lab Anim Resources & Genet Engn, Kobe, Hyogo 6500047, Japan.
RP Honjo, T (reprint author), Kyoto Univ, Dept Immunol & Genom Med, Grad Sch Med, Kyoto 6068501, Japan.
EM honjo@mfour.med.kyoto-u.ac.jp
RI Kiyonari, Hiroshi/N-7936-2015; Honjo, Tasuku/N-4470-2016
FU Ministry of Education, Culture, Sports, Science and Technology of Japan
[17002015]
FX The authors are grateful to Dr. Kei-ichiro Suzuki for the method of the
germinal center B-cell isolation and to Ms. Y. Shiraki for preparation
of the manuscript. This research was supported by a Grant-in-Aid for
Specially Promoted Research (17002015) of the Ministry of Education,
Culture, Sports, Science and Technology of Japan.
NR 55
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Z9 16
U1 0
U2 2
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 29
PY 2011
VL 108
IS 48
BP 19305
EP 19310
DI 10.1073/pnas.1114522108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 853ZB
UT WOS:000297463100045
PM 22080610
ER
PT J
AU Pitzer, VE
Patel, MM
Lopman, BA
Viboud, C
Parashar, UD
Grenfell, BT
AF Pitzer, Virginia E.
Patel, Manish M.
Lopman, Ben A.
Viboud, Cecile
Parashar, Umesh D.
Grenfell, Bryan T.
TI Modeling rotavirus strain dynamics in developed countries to understand
the potential impact of vaccination on genotype distributions
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE mathematical modeling; transmission dynamics; strain replacement
ID TRANSMISSION DYNAMICS; UNITED-STATES; IMMUNOLOGICAL DETERMINANTS;
MOLECULAR EPIDEMIOLOGY; DEPENDENT ENHANCEMENT; CROSS-IMMUNITY; GROUP-A;
INFLUENZA; INFECTION; EVOLUTION
AB Understanding how immunity shapes the dynamics of multistrain pathogens is essential in determining the selective pressures imposed by vaccines. There is currently much interest in elucidating the strain dynamics of rotavirus to determine whether vaccination may lead to the replacement of vaccine-type strains. In developed countries, G1P[8] strains constitute the majority of rotavirus infections most years, but occasionally other genotypes dominate for reasons that are not well understood. We developed a mathematical model to examine the interaction of five common rotavirus genotypes. We explored a range of estimates for the relative strength of homotypic vs. heterotypic immunity and compared model predictions against observed genotype patterns from six countries. We then incorporated vaccination in the model to examine its impact on rotavirus incidence and the distribution of strains. Our model can explain the coexistence and cyclical pattern in the distribution of genotypes observed in most developed countries. The predicted frequency of cycling depends on the relative strength of homotypic vs. heterotypic immunity. Vaccination that provides strong protection against G1 and weaker protection against other strains will likely lead to an increase in the relative prevalence of non-G1 strains, whereas a vaccine that provides equally strong immunity against all strains may promote the continued predominance of G1. Overall, however, disease incidence is expected to be substantially reduced under both scenarios and remain below prevaccination levels despite the possible emergence of new strains. Better understanding of homotypic vs. heterotypic immunity, both natural and vaccine-induced, will be critical in predicting the impact of vaccination.
C1 [Pitzer, Virginia E.; Grenfell, Bryan T.] Princeton Univ, Dept Ecol & Evolutionary Biol, Princeton, NJ 08544 USA.
[Grenfell, Bryan T.] Princeton Univ, Woodrow Wilson Sch Publ & Int Affairs, Princeton, NJ 08544 USA.
[Pitzer, Virginia E.; Viboud, Cecile; Grenfell, Bryan T.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Patel, Manish M.; Lopman, Ben A.; Parashar, Umesh D.] Ctr Dis Control & Prevent, Epidemiol Branch, Div Viral Dis, Natl Ctr Immunizat & Resp Dis, Atlanta, GA 30333 USA.
RP Pitzer, VE (reprint author), Princeton Univ, Dept Ecol & Evolutionary Biol, Princeton, NJ 08544 USA.
EM vepitzer@princeton.edu
OI Pitzer, Virginia/0000-0003-1015-2289
FU National Institutes of Health [R01 GM083983-01]; Bill and Melinda Gates
Foundation; Research and Policy for Infectious Disease Dynamics (RAPIDD)
of the Science and Technology Directorate, Department of Homeland
Security; Fogarty International Center, National Institutes of Health
FX This work was supported by National Institutes of Health Grant R01
GM083983-01, the Bill and Melinda Gates Foundation, and 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 (V. E. P and
B. G.). The findings and conclusions in this report are those of the
authors and do not necessarily represent the views of the Centers for
Disease Control and Prevention (CDC).
NR 57
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U1 3
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 29
PY 2011
VL 108
IS 48
BP 19353
EP 19358
DI 10.1073/pnas.1110507108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 853ZB
UT WOS:000297463100053
PM 22084114
ER
PT J
AU Bahl, J
Nelson, MI
Chan, KH
Chen, RB
Vijaykrishna, D
Halpin, RA
Stockwell, TB
Lin, XD
Wentworth, DE
Ghedin, E
Guan, Y
Peiris, JSM
Riley, S
Rambaut, A
Holmes, EC
Smith, GJD
AF Bahl, Justin
Nelson, Martha I.
Chan, Kwok H.
Chen, Rubing
Vijaykrishna, Dhanasekaran
Halpin, Rebecca A.
Stockwell, Timothy B.
Lin, Xudong
Wentworth, David E.
Ghedin, Elodie
Guan, Yi
Peiris, J. S. Malik
Riley, Steven
Rambaut, Andrew
Holmes, Edward C.
Smith, Gavin J. D.
TI Temporally structured metapopulation dynamics and persistence of
influenza A H3N2 virus in humans
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE evolution; molecular epidemiology; source-sink; phylogeography
ID PHYLOGENETIC ANALYSIS; SEASONALITY; EVOLUTION; EPIDEMIC; CITY
AB Populations of seasonal influenza virus experience strong annual bottlenecks that pose a considerable extinction risk. It has been suggested that an influenza source population located in tropical Southeast or East Asia seeds annual temperate epidemics. Here we investigate the seasonal dynamics and migration patterns of influenza A H3N2 virus by analysis of virus samples obtained from 2003 to 2006 from Australia, Europe, Japan, New York, New Zealand, Southeast Asia, and newly sequenced viruses from Hong Kong. In contrast to annual temperate epidemics, relatively low levels of relative genetic diversity and no seasonal fluctuations characterized virus populations in tropical Southeast Asia and Hong Kong. Bayesian phylogeographic analysis using discrete temporal and spatial characters reveal high rates of viral migration between urban centers tested. Although the virus population that migrated between Southeast Asia and Hong Kong persisted through time, this was dependent on virus input from temperate regions and these tropical regions did not maintain a source for annual H3N2 influenza epidemics. We further show that multiple lineages may seed annual influenza epidemics, and that each region may function as a potential source population. We therefore propose that the global persistence of H3N2 influenza A virus is the result of a migrating metapopulation in which multiple different localities may seed seasonal epidemics in temperate regions in a given year. Such complex global migration dynamics may confound control efforts and contribute to the emergence and spread of antigenic variants and drug-resistant viruses.
C1 [Bahl, Justin; Chan, Kwok H.; Vijaykrishna, Dhanasekaran; Halpin, Rebecca A.; Guan, Yi; Peiris, J. S. Malik; Smith, Gavin J. D.] Univ Hong Kong, State Key Lab Emerging Infect Dis, Dept Microbiol, Pokfulam, Hong Kong, Peoples R China.
[Riley, Steven] Univ Hong Kong, Li Ka Shing Fac Med, Dept Community Med, Pokfulam, Hong Kong, Peoples R China.
[Riley, Steven] Univ Hong Kong, Li Ka Shing Fac Med, Sch Publ Hlth, Pokfulam, Hong Kong, Peoples R China.
[Peiris, J. S. Malik] Univ Hong Kong, Hong Kong Univ Pasteur Res Ctr, Pokfulam, Hong Kong, Peoples R China.
[Bahl, Justin; Vijaykrishna, Dhanasekaran; Smith, Gavin J. D.] Duke Natl Univ Singapore, Grad Sch Med, Program Emerging Infect Dis, Lab Virus Evolut, Singapore 169857, Singapore.
[Nelson, Martha I.; Rambaut, Andrew; Holmes, Edward C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Chen, Rubing] Univ Texas Med Branch, Galveston, TX 77555 USA.
[Halpin, Rebecca A.; Stockwell, Timothy B.; Lin, Xudong; Wentworth, David E.; Ghedin, Elodie] J Craig Venter Inst, Rockville, MD 20850 USA.
[Ghedin, Elodie] Univ Pittsburgh, Sch Med, Dept Computat & Syst Biol, Ctr Vaccine Res, Pittsburgh, PA 15261 USA.
[Riley, Steven] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, Dept Infect Dis Epidemiol, Med Res Council,Ctr Outbreak Anal & Modelling, London W2 1PG, England.
[Rambaut, Andrew] Univ Edinburgh, Inst Evolutionary Biol, Edinburgh EH9 3JT, Midlothian, Scotland.
[Holmes, Edward C.] Penn State Univ, Dept Biol, Ctr Infect Dis Dynam, University Pk, PA 16802 USA.
RP Bahl, J (reprint author), Univ Hong Kong, State Key Lab Emerging Infect Dis, Dept Microbiol, Pokfulam, Hong Kong, Peoples R China.
EM justin.bahl@duke-nus.edu.sg; gavin.smith@duke-nus.edu.sg
RI Bahl, Justin/A-4728-2011; Vijaykrishna, Dhanasekaran/D-1011-2010; Chen,
Rubing/A-2276-2010;
OI Bahl, Justin/0000-0001-7572-4300; Vijaykrishna,
Dhanasekaran/0000-0003-3293-6279; Wentworth, David/0000-0002-5190-980X;
Rambaut, Andrew/0000-0003-4337-3707; Holmes, Edward/0000-0001-9596-3552;
Smith, Gavin JD/0000-0001-5031-468X
FU National Institute of Allergy and Infectious Disease, National
Institutes of Health, Department of Health and Human Services
[HHSN266200700005C, HHSN272200900007]; Area of Excellence Scheme of the
University Grants Committee of the Hong Kong Special Administrative
Region Government; RAPIDD of the Science and Technology Directorate, US
Department of Homeland Security; Fogarty International Center, National
Institutes of Health under National Institute of Allergy and Infectious
Diseases [HHSN266200700005C]; Duke-National University of Singapore;
Agency for Science, Technology and Research, Singapore; Ministry of
Health, Singapore
FX This study was supported by Contracts HHSN266200700005C and
HHSN272200900007 for the Influenza Genome Sequencing Project of the
National Institute of Allergy and Infectious Disease, National
Institutes of Health, Department of Health and Human Services; the Area
of Excellence Scheme of the University Grants Committee (Grant
AoE/M-12/06) of the Hong Kong Special Administrative Region Government;
the RAPIDD program of the Science and Technology Directorate, US
Department of Homeland Security and the Fogarty International Center,
National Institutes of Health (S. R.), a career development award under
National Institute of Allergy and Infectious Diseases Contract
HHSN266200700005C (to G.J.D.S.); and the Duke-National University of
Singapore Signature Research Program funded by the Agency for Science,
Technology and Research, Singapore, and the Ministry of Health,
Singapore (J.B., D.V., and G.J.D.S.).
NR 27
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U1 3
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 29
PY 2011
VL 108
IS 48
BP 19359
EP 19364
DI 10.1073/pnas.1109314108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 853ZB
UT WOS:000297463100054
PM 22084096
ER
PT J
AU Guderian, S
Brigham, D
Mishkin, M
AF Guderian, Sebastian
Brigham, Danielle
Mishkin, Mortimer
TI Two processes support visual recognition memory in rhesus monkeys
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID RECEIVER-OPERATING CHARACTERISTICS; CHARACTERISTICS ROCS; RECOLLECTION;
RATS; FAMILIARITY; HIPPOCAMPUS; PICTURES; CURVES; MODELS; ITEM
AB A large body of evidence in humans suggests that recognition memory can be supported by both recollection and familiarity. Recollection-based recognition is characterized by the retrieval of contextual information about the episode in which an item was previously encountered, whereas familiarity-based recognition is characterized instead by knowledge only that the item had been encountered previously in the absence of any context. To date, it is unknown whether monkeys rely on similar mnemonic processes to perform recognition memory tasks. Here, we present evidence from the analysis of receiver operating characteristics, suggesting that visual recognition memory in rhesus monkeys also can be supported by two separate processes and that these processes have features considered to be characteristic of recollection and familiarity. Thus, the present study provides converging evidence across species for a dual process model of recognition memory and opens up the possibility of studying the neural mechanisms of recognition memory in nonhuman primates on tasks that are highly similar to the ones used in humans.
C1 [Guderian, Sebastian; Brigham, Danielle; Mishkin, Mortimer] NIMH, Neuropsychol Lab, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Guderian, S (reprint author), NIMH, Neuropsychol Lab, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
EM guderians@mail.nih.gov; brighad@gmail.com; mishkinm@mail.nih.gov
FU National Institute of Mental Health/National Institutes of
Health/Department of Health and Human Services
FX We thank Bruno B. Averbeck for advice on data analysis, and Howard
Eichenbaum, Robert R. Hampton, Barry J. Richmond, Richard C. Saunders,
and Andrew P. Yonelinas for their many valuable comments on the
manuscript. This work was supported by the Intramural Research Program
of the National Institute of Mental Health/National Institutes of
Health/Department of Health and Human Services.
NR 25
TC 12
Z9 12
U1 0
U2 1
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 29
PY 2011
VL 108
IS 48
BP 19425
EP 19430
DI 10.1073/pnas.1117078108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 853ZB
UT WOS:000297463100065
PM 22084079
ER
PT J
AU Klingeborn, M
Race, B
Meade-White, KD
Chesebro, B
AF Klingeborn, Mikael
Race, Brent
Meade-White, Kimberly D.
Chesebro, Bruce
TI Lower specific infectivity of protease-resistant prion protein generated
in cell-free reactions
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE Creutzfeldt-Jakob disease; amyloid; neurodegeneration; protein
polymerization; protein aggregation
ID CHRONIC WASTING DISEASE; IN-VITRO; SPONGIFORM ENCEPHALOPATHIES; SCRAPIE
AGENT; CYCLIC AMPLIFICATION; INCUBATION PERIOD; TRANSGENIC MICE; BRAIN;
ASSAY; REPLICATION
AB Prions are unconventional infectious agents that cause transmissible spongiform encephalopathy (TSE) diseases, or prion diseases. The biochemical nature of the prion infectious agent remains unclear. Previously, using a protein misfolding cyclic amplification (PMCA) reaction, infectivity and disease-associated protease-resistant prion protein (PrPres) were both generated under cell-free conditions, which supported a nonviral hypothesis for the agent. However, these studies lacked comparative quantitation of both infectivity titers and PrPres, which is important both for biological comparison with in vivo-derived infectivity and for excluding contamination to explain the results. Here during four to eight rounds of PMCA, end-point dilution titrations detected a > 320-fold increase in infectivity versus that in controls. These results provide strong support for the hypothesis that the agent of prion infectivity is not a virus. PMCA-generated samples caused the same clinical disease and neuropathology with the same rapid incubation period as the input brain-derived scrapie samples, providing no evidence for generation of a new strain in PMCA. However, the ratio of the infectivity titer to the amount of PrPres (specific infectivity) was much lower in PMCA versus brain-derived samples, suggesting the possibility that a substantial portion of PrPres generated in PMCA might be noninfectious.
C1 [Klingeborn, Mikael; Race, Brent; Meade-White, Kimberly D.; Chesebro, Bruce] NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, Hamilton, MT 59840 USA.
RP Chesebro, B (reprint author), NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, Hamilton, MT 59840 USA.
EM bchesebro@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases, Division of
Intramural Research
FX The authors thank Rebecca Rosenke, Lori Lubke, Nancy Kurtz, Dan Long,
and Katie Phillips for technical support. The authors also thank Byron
Caughey, Suzette Priola, Andrew Timmes, James Carroll, and James
Striebel for critical suggestions about the manuscript and Jeffrey
Severson for animal husbandry. This work was supported by the National
Institute of Allergy and Infectious Diseases, Division of Intramural
Research.
NR 49
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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 29
PY 2011
VL 108
IS 48
BP E1244
EP E1253
DI 10.1073/pnas.1111255108
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 853ZB
UT WOS:000297463100005
PM 22065744
ER
PT J
AU Lo, B
Swafford, ADE
Shafer-Weaver, KA
Jerome, LF
Rakhlin, L
Mathern, DR
Callahan, CA
Jiang, P
Davison, LJ
Stevens, HE
Lucas, CL
White, J
von Borstel, R
Todd, JA
Lenardo, MJ
AF Lo, Bernice
Swafford, Austin D. E.
Shafer-Weaver, Kimberly A.
Jerome, Lawrence F.
Rakhlin, Luba
Mathern, Douglas R.
Callahan, Conor A.
Jiang, Ping
Davison, Lucy J.
Stevens, Helen E.
Lucas, Carrie L.
White, Jill
von Borstel, Reid
Todd, John A.
Lenardo, Michael J.
TI Antibodies against insulin measured by electrochemiluminescence predicts
insulitis severity and disease onset in non-obese diabetic mice and can
distinguish human type 1 diabetes status
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE NOD mice; diabetes; human autoantibodies; insulin;
electrochemiluminescence; IAA; IA; ECL
ID LINKED-IMMUNOSORBENT-ASSAY; NOD MICE; 1ST-DEGREE RELATIVES;
GENERAL-POPULATION; IMMUNE DYSREGULATION; CELL AUTOIMMUNITY; AFFECTED
CHILDREN; AUTOANTIBODIES; GAD; IMMUNOASSAYS
AB Background: The detection of insulin autoantibodies (IAA) aids in the prediction of autoimmune diabetes development. However, the long-standing, gold standard I-125-insulin radiobinding assay (RBA) has low reproducibility between laboratories, long sample processing times and requires the use of newly synthesized radiolabeled insulin for each set of assays. Therefore, a rapid, non-radioactive, and reproducible assay is highly desirable.
Methods: We have developed electrochemiluminescence (ECL)-based assays that fulfill these criteria in the measurement of IAA and anti-insulin antibodies (IA) in non-obese diabetic (NOD) mice and in type 1 diabetic individuals, respectively. Using the murine IAA ECL assay, we examined the correlation between IAA, histopathological insulitis, and blood glucose in a cohort of female NOD mice from 4 up to 36 weeks of age. We developed a human IA ECL assay that we compared to conventional RBA and validated using samples from 34 diabetic and 59 non-diabetic individuals in three independent laboratories.
Results: Our ECL assays were rapid and sensitive with a broad dynamic range and low background. In the NOD mouse model, IAA levels measured by ECL were positively correlated with insulitis severity, and the values measured at 8-10 weeks of age were predictive of diabetes onset. Using human serum and plasma samples, our IA ECL assay yielded reproducible and accurate results with an average sensitivity of 84% at 95% specificity with no statistically significant difference between laboratories.
Conclusions: These novel, non-radioactive ECL-based assays should facilitate reliable and fast detection of antibodies to insulin and its precursors sera and plasma in a standardized manner between laboratories in both research and clinical settings. Our next step is to evaluate the human IA assay in the detection of IAA in prediabetic subjects or those at risk of type 1 diabetes and to develop similar assays for other autoantibodies that together are predictive for the diagnosis of this common disorder, in order to improve prediction and facilitate future therapeutic trials.
C1 [Lo, Bernice; Swafford, Austin D. E.; Shafer-Weaver, Kimberly A.; Rakhlin, Luba; Mathern, Douglas R.; Callahan, Conor A.; Jiang, Ping; Lucas, Carrie L.; Lenardo, Michael J.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Swafford, Austin D. E.; Davison, Lucy J.; Stevens, Helen E.; Todd, John A.] Univ Cambridge, Addenbrookes Hosp, NIHR Biomed Res Ctr,Juvenile Diabet Res Fdn, Cambridge Inst Med Res,Dept Med Genet,Wellcome Tr, Cambridge CB2 0XY, England.
[Jerome, Lawrence F.; White, Jill] Wellstat Diagnost LLC, Gaithersburg, MD 20878 USA.
[von Borstel, Reid] Wellstat Therapeutics Corp, Gaithersburg, MD 20878 USA.
RP Lenardo, MJ (reprint author), NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
EM lenardo@nih.gov
OI Lo, Bernice/0000-0002-1087-6845
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases (NIAID), NIH; Wellstat Diagnostics, LLC through
NIAID; Juvenile Diabetes Research Foundation (JDRF) International;
Wellcome Trust (WT) [WT061858/091157, 079895]; National Institute for
Health Research Cambridge Biomedical Research Centre (CBRC); Medical
Research Council (MRC); National Science Foundation; Wellstat
Diagnostics, LLC; United States government
FX This work was supported by the Division of Intramural Research, National
Institute of Allergy and Infectious Diseases (NIAID), NIH and Wellstat
Diagnostics, LLC through a cooperative research and development
agreement with NIAID. Additional support was provided by the Juvenile
Diabetes Research Foundation (JDRF) International, the Wellcome Trust
(WT; WT061858/091157), the National Institute for Health Research
Cambridge Biomedical Research Centre (CBRC) and the Medical Research
Council (MRC) Cusrow Wadia Fund, and the National Science Foundation.
ADES is an NIH-Cambridge Health Science Research Scholar and a National
Science Foundation Graduate Research Fellow. LJD was supported by a
Wellcome Trust Intermediate Clinical Fellowship (082549/Z/07/Z). The
Cambridge Institute for Medical Research (CIMR) is in receipt of a
Wellcome Trust Strategic Award (079895). We kindly thank Dr. Monica
Skarulis, NIDDK for providing the serum samples through NIDDK study
NCT00896610 and Michelle Ashmus, NIDDK for coordinating their delivery.
We thank all study participants and family members. We thank David
Dunger and Barry Widmer of the University of Cambridge, and the British
Society for Paediatric Endocrinology and Diabetes for the TID case
collection. We gratefully acknowledge the participation of the Cambridge
BioResource (CBR) donors. We thank members of the CBR recruitment team,
Management Committee and Scientific Advisory Board. We thank K. Beer, J.
Rice, P. Tagart and M. Wiesner for donor coordination and blood sample
collection and M. Woodburn, and T. Attwood for their contribution to
sample management and P.M. Clarke for sample provision. We also thank
Alan Remaley (Laboratory of Lipoprotein Metabolism, NHLBI, NIH) for
providing normal control human serum samples. The authors thank Dr.
Monika Hermankova Jung (Laboratory of Immunology, NIAID, NIH) for
technical expertise and assistance in experimental design. The authors
also thank Jing Qin (Biostatistics Research Branch, NIAID, NIH) for
statistical support and Kristin Tarbell (Immune Tolerance Section,
NIDDK, NIH) for critical review of the manuscript.; Dr. Lenardo, Dr. Lo,
Dr. Shafer-Weaver, Austin Swafford, and Lawrence Jerome may be entitled
to future patent royalties from technology described in this manuscript.
Lawrence Jerome and Jill White are employees of Wellstat Diagnostics,
LLC. Reid von Borstel is employed by Wellstat Therapeutics Corporation.
Dr. Lenardo has funding from Wellstat Diagnostics, LLC through a
Cooperative Research and Development Agreement between the United States
government and Wellstat Diagnostics, LLC.
NR 56
TC 11
Z9 11
U1 1
U2 6
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD NOV 28
PY 2011
VL 9
AR 203
DI 10.1186/1479-5876-9-203
PG 16
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 901HR
UT WOS:000300955800001
PM 22123298
ER
PT J
AU Lee, JJ
Liu, ST
Nacif, MS
Ugander, M
Han, J
Kawel, N
Sibley, CT
Kellman, P
Arai, AE
Bluemke, DA
AF Lee, Jason J.
Liu, Songtao
Nacif, Marcelo S.
Ugander, Martin
Han, Jing
Kawel, Nadine
Sibley, Christopher T.
Kellman, Peter
Arai, Andrew E.
Bluemke, David A.
TI Myocardial T1 and Extracellular Volume Fraction Mapping at 3 Tesla
SO JOURNAL OF CARDIOVASCULAR MAGNETIC RESONANCE
LA English
DT Article
ID CARDIOVASCULAR MAGNETIC-RESONANCE; INVERSION-RECOVERY; FIBROSIS; HUMANS;
HEART; QUANTIFICATION; RELAXATION; VALIDATION; INFARCTION; FREQUENCY
AB Background: To compare 11 heartbeat (HB) and 17 HB modified lock locker inversion recovery (MOLLI) pulse sequence at 3T and to establish preliminary reference values for myocardial T1 and the extracellular volume fraction (ECV).
Methods: Both phantoms and normal volunteers were scanned at 3T using 11 HB and 17 HB MOLLI sequence with the following parameters: spatial resolution = 1.75 x 1.75 x 10 mm on a 256 x 180 matrix, TI initial = 110 ms, TI increment = 80 ms, flip angle = 35 degrees, TR/TE = 1.9/1.0 ms. All volunteers were administered Gadolinium-DTPA (Magnevist, 0.15 mmol/kg), and multiple post-contrast MOLLI scans were performed at the same pre-contrast position from 3.5-23.5 minutes after a bolus contrast injection. Late gadolinium enhancement (LGE) images were also acquired 12-30 minutes after the gadolinium bolus.
Results: T1 values of 11 HB and 17 HB MOLLI displayed good agreement in both phantom and volunteers. The average pre-contrast myocardial and blood T1 was 1315 +/- 39 ms and 2020 +/- 129 ms, respectively. ECV was stable between 8.5 to 23.5 minutes post contrast with an average of 26.7 +/- 1.0%.
Conclusion: The 11 HB MOLLI is a faster method for high-resolution myocardial T1 mapping at 3T. ECV fractions are stable over a wide time range after contrast administration.
C1 [Lee, Jason J.; Liu, Songtao; Nacif, Marcelo S.; Kawel, Nadine; Sibley, Christopher T.; Bluemke, David A.] Natl Inst Hlth Clin Ctr, Bethesda, MD 20814 USA.
[Liu, Songtao; Sibley, Christopher T.; Bluemke, David A.] Natl Inst Biomed Imaging & Bioengn, Mol Biomed Imaging Lab, Bethesda, MD USA.
[Ugander, Martin; Kellman, Peter; Arai, Andrew E.] NHLBI, Cardiac Energet Lab, Bethesda, MD 20892 USA.
[Han, Jing] US FDA, Rockville, MD 20857 USA.
RP Bluemke, DA (reprint author), Natl Inst Hlth Clin Ctr, Bethesda, MD 20814 USA.
EM bluemked@nih.gov
RI Sibley, Christopher/C-9900-2013;
OI Bluemke, David/0000-0002-8323-8086; Ugander, Martin/0000-0003-3665-2038
FU NIH
FX Research funding was provided by the NIH intramural research program. We
thank Jacquin L. Jones, RN for recruiting the volunteers.
NR 24
TC 50
Z9 56
U1 0
U2 8
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1097-6647
J9 J CARDIOVASC MAGN R
JI J. Cardiov. Magn. Reson.
PD NOV 28
PY 2011
VL 13
AR 75
DI 10.1186/1532-429X-13-75
PG 10
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA 892XC
UT WOS:000300317900001
PM 22123333
ER
PT J
AU Azare, J
Doane, A
Leslie, K
Chang, Q
Berishaj, M
Nnoli, J
Mark, K
Al-Ahmadie, H
Gerald, W
Hassimi, M
Viale, A
Stracke, M
Lyden, D
Bromberg, J
AF Azare, Janeen
Doane, Ashley
Leslie, Kenneth
Chang, Qing
Berishaj, Marjan
Nnoli, Jennifer
Mark, Kevin
Al-Ahmadie, Hikmat
Gerald, William
Hassimi, Maryam
Viale, Agnes
Stracke, Mary
Lyden, David
Bromberg, Jacqueline
TI Stat3 Mediates Expression of Autotaxin in Breast Cancer
SO PLOS ONE
LA English
DT Article
ID EPITHELIAL-MESENCHYMAL TRANSITION; MOTILITY-STIMULATING PROTEIN;
ACTIVATED SIGNAL TRANSDUCER; CIRCULATING TUMOR-CELLS; HUMAN-MELANOMA
CELLS; NF-KAPPA-B; LYSOPHOSPHATIDIC ACID; CARCINOMA CELLS;
GENE-EXPRESSION; CONSTITUTIVE ACTIVATION
AB We determined that signal transducer and activator of transcription 3 (Stat3) is tyrosine phosphorylated in 37% of primary breast tumors and 63% of paired metastatic axillary lymph nodes. Examination of the distribution of tyrosine phosphorylated (pStat3) in primary tumors revealed heterogenous expression within the tumor with the highest levels found in cells on the edge of tumors with relatively lower levels in the central portion of tumors. In order to determine Stat3 target genes that may be involved in migration and metastasis, we identified those genes that were differentially expressed in primary breast cancer samples as a function of pStat3 levels. In addition to known Stat3 transcriptional targets (Twist, Snail, Tenascin-C and IL-8), we identified ENPP2 as a novel Stat3 regulated gene, which encodes autotaxin (ATX), a secreted lysophospholipase which mediates mammary tumorigenesis and cancer cell migration. A positive correlation between nuclear pStat3 and ATX was determined by immunohistochemical analysis of primary breast cancer samples and matched axillary lymph nodes and in several breast cancer derived cell lines. Inhibition of pStat3 or reducing Stat3 expression led to a decrease in ATX levels and cell migration. An association between Stat3 and the ATX promoter, which contains a number of putative Stat3 binding sites, was determined by chromatin immunoprecipitation. These observations suggest that activated Stat3 may regulate the migration of breast cancer cells through the regulation of ATX.
C1 [Azare, Janeen; Leslie, Kenneth; Chang, Qing; Berishaj, Marjan; Nnoli, Jennifer; Mark, Kevin; Bromberg, Jacqueline] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA.
[Doane, Ashley; Al-Ahmadie, Hikmat; Gerald, William] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA.
[Hassimi, Maryam; Viale, Agnes] Mem Sloan Kettering Canc Ctr, Genom Core Lab, New York, NY 10021 USA.
[Lyden, David] Mem Sloan Kettering Canc Ctr, Dept Pediat, New York, NY 10021 USA.
[Stracke, Mary] NCI, Pathol Lab, Div Clin Sci, NIH, Bethesda, MD 20892 USA.
[Lyden, David] Weill Cornell Med Coll, Dept Pediat, New York, NY USA.
RP Azare, J (reprint author), Mem Sloan Kettering Canc Ctr, Dept Med, 1275 York Ave, New York, NY 10021 USA.
EM dcl2001@med.cornell.edu; bromberj@mskcc.org
RI Doane, Ashley Stephen/B-7027-2008; Doane, Ashley/R-4263-2016;
OI Doane, Ashley Stephen/0000-0002-1489-1786; Doane,
Ashley/0000-0002-1489-1786; Al-Ahmadie, Hikmat/0000-0002-2938-6627
FU National Institutes of Health [R01 CA87637]; Marjorie and Charles
Holloway Foundation; Breast Cancer Alliance Award; Sussman Family Fund;
Lerner Awards; Cancer Research and Prevention Foundation; Intercultural
Cancer Council; National Cancer Institute, CMBB (Comprehensive Minority
Biomedical Branch)
FX This project was supported by grants from the National Institutes of
Health (R01 CA87637), Marjorie and Charles Holloway Foundation, Breast
Cancer Alliance Award, Sussman Family Fund and Lerner Awards to JB and a
Cancer Research and Prevention Foundation and Intercultural Cancer
Council Fellowship and a National Cancer Institute, CMBB (Comprehensive
Minority Biomedical Branch) Training Award to JA. The funders had no
role in study design, data collection and analysis, decision to publish,
or preparation of the manuscript.
NR 89
TC 20
Z9 22
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 28
PY 2011
VL 6
IS 11
AR e27851
DI 10.1371/journal.pone.0027851
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 863KW
UT WOS:000298163400019
PM 22140473
ER
PT J
AU Lockwood, S
Voth, DE
Brayton, KA
Beare, PA
Brown, WC
Heinzen, RA
Broschat, SL
AF Lockwood, Svetlana
Voth, Daniel E.
Brayton, Kelly A.
Beare, Paul A.
Brown, Wendy C.
Heinzen, Robert A.
Broschat, Shira L.
TI Identification of Anaplasma marginale Type IV Secretion System Effector
Proteins
SO PLOS ONE
LA English
DT Article
ID LEGIONELLA-PNEUMOPHILA; ANKYRIN REPEAT; COXIELLA-BURNETII; HUMAN
MACROPHAGES; MEMBRANE VACCINE; DIVERSITY; TRANSLOCATION; INFECTION;
GENOME; MECHANISMS
AB Background: Anaplasma marginale, an obligate intracellular alphaproteobacterium in the order Rickettsiales, is a tick-borne pathogen and the leading cause of anaplasmosis in cattle worldwide. Complete genome sequencing of A. marginale revealed that it has a type IV secretion system (T4SS). The T4SS is one of seven known types of secretion systems utilized by bacteria, with the type III and IV secretion systems particularly prevalent among pathogenic Gram-negative bacteria. The T4SS is predicted to play an important role in the invasion and pathogenesis of A. marginale by translocating effector proteins across its membrane into eukaryotic target cells. However, T4SS effector proteins have not been identified and tested in the laboratory until now.
Results: By combining computational methods with phylogenetic analysis and sequence identity searches, we identified a subset of potential T4SS effectors in A. marginale strain St. Maries and chose six for laboratory testing. Four (AM185, AM470, AM705 [AnkA], and AM1141) of these six proteins were translocated in a T4SS-dependent manner using Legionella pneumophila as a reporter system.
Conclusions: The algorithm employed to find T4SS effector proteins in A. marginale identified four such proteins that were verified by laboratory testing. L. pneumophila was shown to work as a model system for A. marginale and thus can be used as a screening tool for A. marginale effector proteins. The first T4SS effector proteins for A. marginale have been identified in this work.
C1 [Lockwood, Svetlana; Broschat, Shira L.] Washington State Univ, Sch Elect Engn & Comp Sci, Pullman, WA 99164 USA.
[Voth, Daniel E.] Univ Arkansas Med Sci, Dept Microbiol & Immunol, Little Rock, AR 72205 USA.
[Brayton, Kelly A.; Brown, Wendy C.; Broschat, Shira L.] Washington State Univ, Dept Vet Microbiol & Pathol, Pullman, WA 99164 USA.
[Brayton, Kelly A.; Brown, Wendy C.; Broschat, Shira L.] Washington State Univ, Paul G Allen Sch Global Anim Hlth, Pullman, WA 99164 USA.
[Beare, Paul A.; Heinzen, Robert A.] NIAID, Coxiella Pathogenesis Sect, Intracellular Parasites Lab, Rocky Mt Labs,NIH, Hamilton, MT USA.
RP Lockwood, S (reprint author), Washington State Univ, Sch Elect Engn & Comp Sci, Pullman, WA 99164 USA.
EM shira@eecs.wsu.edu
OI Lockwood, Svetlana/0000-0002-9401-239X
FU National Institutes of Health (NIH) National Institutes of Allergy and
Infectious Diseases (NIAID) [AI44005, AI053692, R01AI087669]; Carl M.
Hansen Foundation
FX This study was supported by National Institutes of Health (NIH) National
Institutes of Allergy and Infectious Diseases (NIAID) grants AI44005 and
AI053692 (to KAB and WCB) and R01AI087669 (DEV) and by the Intramural
Research Program of the NIH, NIAID (to RAH and PAB). SL was supported in
part by the Carl M. Hansen Foundation. The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 51
TC 18
Z9 18
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 28
PY 2011
VL 6
IS 11
AR e27724
DI 10.1371/journal.pone.0027724
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 863KW
UT WOS:000298163400015
PM 22140462
ER
PT J
AU Wu, XW
Brooks, BR
AF Wu, Xiongwu
Brooks, Bernard R.
TI Force-momentum-based self-guided Langevin dynamics: A rapid sampling
method that approaches the canonical ensemble
SO JOURNAL OF CHEMICAL PHYSICS
LA English
DT Article
ID HYDROPHOBIC GRAPHITE SURFACE; PROTEIN-FOLDING SIMULATIONS; IONIC
COMPLEMENTARY PEPTIDE; MOLECULAR-DYNAMICS; EXPLICIT WATER;
AQUEOUS-SOLUTION; COMPLEX; BINDING; SYSTEM; MOTION
AB The self-guided Langevin dynamics (SGLD) is a method to accelerate conformational searching. This method is unique in the way that it selectively enhances and suppresses molecular motions based on their frequency to accelerate conformational searching without modifying energy surfaces or raising temperatures. It has been applied to studies of many long time scale events, such as protein folding. Recent progress in the understanding of the conformational distribution in SGLD simulations makes SGLD also an accurate method for quantitative studies. The SGLD partition function provides a way to convert the SGLD conformational distribution to the canonical ensemble distribution and to calculate ensemble average properties through reweighting. Based on the SGLD partition function, this work presents a force-momentum-based self-guided Langevin dynamics (SGLDfp) simulation method to directly sample the canonical ensemble. This method includes interaction forces in its guiding force to compensate the perturbation caused by the momentum-based guiding force so that it can approximately sample the canonical ensemble. Using several example systems, we demonstrate that SGLDfp simulations can approximately maintain the canonical ensemble distribution and significantly accelerate conformational searching. With optimal parameters, SGLDfp and SGLD simulations can cross energy barriers of more than 15 kT and 20 kT, respectively, at similar rates for LD simulations to cross energy barriers of 10 kT. The SGLDfp method is size extensive and works well for large systems. For studies where preserving accessible conformational space is critical, such as free energy calculations and protein folding studies, SGLDfp is an efficient approach to search and sample the conformational space. [doi:10.1063/1.3662489]
C1 [Wu, Xiongwu; Brooks, Bernard R.] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
RP Wu, XW (reprint author), NHLBI, Lab Computat Biol, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM wuxw@nhlbi.nih.gov
FU NIH, NHLBI
FX This research was supported by the Intramural Research Program of the
NIH, NHLBI. We thank the reviewers for their valuable comments and
suggestions that lead to a significant improvement of the manuscript. We
thank Terry Brooks for proof reading the manuscript.
NR 34
TC 7
Z9 7
U1 0
U2 12
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
J9 J CHEM PHYS
JI J. Chem. Phys.
PD NOV 28
PY 2011
VL 135
IS 20
AR 204101
DI 10.1063/1.3662489
PG 15
WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical
SC Chemistry; Physics
GA 860JM
UT WOS:000297944600005
PM 22128922
ER
PT J
AU Regairaz, M
Zhang, YW
Fu, HQ
Agama, KK
Tata, N
Agrawal, S
Aladjem, MI
Pommier, Y
AF Regairaz, Marie
Zhang, Yong-Wei
Fu, Haiqing
Agama, Keli K.
Tata, Nalini
Agrawal, Surbhi
Aladjem, Mirit I.
Pommier, Yves
TI Mus81-mediated DNA cleavage resolves replication forks stalled by
topoisomerase I-DNA complexes
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID DOUBLE-STRAND BREAKS; SACCHAROMYCES-CEREVISIAE MUS81-MMS4;
INTRA-S-PHASE; HOMOLOGOUS RECOMBINATION; MAMMALIAN-CELLS; COVALENT
COMPLEXES; VERTEBRATE CELLS; ANTITUMOR DRUGS; HISTONE H2AX; CROSS-LINKS
AB Deoxyribonucleic acid (DNA) topoisomerases are essential for removing the supercoiling that normally builds up ahead of replication forks. The camptothecin (CPT) Top1 (topoisomerase I) inhibitors exert their anticancer activity by reversibly trapping Top1-DNA cleavage complexes (Top1cc's) and inducing replication-associated DNA double-strand breaks (DSBs). In this paper, we propose a new mechanism by which cells avoid Top1-induced replication-dependent DNA damage. We show that the structure-specific endonuclease Mus81-Eme1 is responsible for generating DSBs in response to Top1 inhibition and for allowing cell survival. We provide evidence that Mus81 cleaves replication forks rather than excises Top1cc's. DNA combing demonstrated that Mus81 also allows efficient replication fork progression after CPT treatment. We propose that Mus81 cleaves stalled replication forks, which allows dissipation of the excessive supercoiling resulting from Top1 inhibition, spontaneous reversal of Top1cc, and replication fork progression.
C1 [Regairaz, Marie; Zhang, Yong-Wei; Fu, Haiqing; Agama, Keli K.; Tata, Nalini; Agrawal, Surbhi; Aladjem, Mirit I.; Pommier, Yves] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Pommier, Y (reprint author), NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM pommier@nih.gov
RI ZHANG, YONGWEI/E-6252-2012; Aladjem, Mirit/G-2169-2010
OI Aladjem, Mirit/0000-0002-1875-3110
FU Center for Cancer Research (National Cancer Institute, National
Institutes of Health)
FX This work was supported by the Center for Cancer Research (National
Cancer Institute Intramural Research Program, National Institutes of
Health).
NR 63
TC 53
Z9 53
U1 1
U2 4
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0021-9525
J9 J CELL BIOL
JI J. Cell Biol.
PD NOV 28
PY 2011
VL 195
IS 5
BP 739
EP 749
DI 10.1083/jcb.201104003
PG 11
WC Cell Biology
SC Cell Biology
GA 858RJ
UT WOS:000297819900006
PM 22123861
ER
PT J
AU Magalhaes, MAO
Larson, DR
Mader, CC
Bravo-Cordero, JJ
Gil-Henn, H
Oser, M
Chen, XM
Koleske, AJ
Condeelis, J
AF Magalhaes, Marco A. O.
Larson, Daniel R.
Mader, Christopher C.
Bravo-Cordero, Jose Javier
Gil-Henn, Hava
Oser, Matthew
Chen, Xiaoming
Koleske, Anthony J.
Condeelis, John
TI Cortactin phosphorylation regulates cell invasion through a pH-dependent
pathway
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID EXTRACELLULAR-MATRIX DEGRADATION; BREAST-TUMOR CELLS; H EXCHANGER NHE1;
NA-H; ACTIN POLYMERIZATION; ARP2/3 COMPLEX; NA+/H+ EXCHANGE;
CANCER-CELLS; INTRACELLULAR PH; CARCINOMA-CELLS
AB Invadopodia are invasive protrusions with proteolytic activity uniquely found in tumor cells. Cortactin phosphorylation is a key step during invadopodia maturation, regulating Nck1 binding and cofilin activity. The precise mechanism of cortactin-dependent cofilin regulation and the roles of this pathway in invadopodia maturation and cell invasion are not fully understood. We provide evidence that cortactin-cofilin binding is regulated by local pH changes at invadopodia that are mediated by the sodium-hydrogen exchanger NHE1. Furthermore, cortactin tyrosine phosphorylation mediates the recruitment of NHE1 to the invadopodium compartment, where it locally increases the pH to cause the release of cofilin from cortactin. We show that this mechanism involving cortactin phosphorylation, local pH increase, and cofilin activation regulates the dynamic cycles of invadopodium protrusion and retraction and is essential for cell invasion in 3D. Together, these findings identify a novel pH-dependent regulation of cell invasion.
C1 [Magalhaes, Marco A. O.; Bravo-Cordero, Jose Javier; Oser, Matthew; Chen, Xiaoming; Condeelis, John] Yeshiva Univ, Albert Einstein Coll Med, Dept Anat & Struct Biol, Bronx, NY 10461 USA.
[Magalhaes, Marco A. O.; Bravo-Cordero, Jose Javier; Condeelis, John] Yeshiva Univ, Albert Einstein Coll Med, Gruss Lipper Biophoton Ctr, Bronx, NY 10461 USA.
[Larson, Daniel R.] NCI, NIH, Bethesda, MD 20892 USA.
[Mader, Christopher C.] Yale Univ, Dept Cell Biol, New Haven, CT 06520 USA.
[Gil-Henn, Hava; Koleske, Anthony J.] Yale Univ, Dept Mol Biophys & Biochem, New Haven, CT 06520 USA.
RP Condeelis, J (reprint author), Yeshiva Univ, Albert Einstein Coll Med, Dept Anat & Struct Biol, Bronx, NY 10461 USA.
EM john.condeelis@einstein.yu.edu
RI Larson, Daniel/B-9829-2008
OI Larson, Daniel/0000-0001-9253-3055
FU Breast Cancer Alliance; National Science Foundation; [CA150344];
[CA100324]; [NIHCA133346]; [NIHNS39475]
FX This work was funded by CA150344, CA100324 (to M. Oser, M.A.O.
Magalhaes, and J. Condeelis), NIHCA133346, NIHNS39475; an Exceptional
Project Grant from the Breast Cancer Alliance (to A. J. Koleske); and a
National Science Foundation Graduate Research Fellowship (to C. C.
Mader).
NR 87
TC 87
Z9 87
U1 0
U2 15
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0021-9525
J9 J CELL BIOL
JI J. Cell Biol.
PD NOV 28
PY 2011
VL 195
IS 5
BP 903
EP 920
DI 10.1083/jcb.201103045
PG 18
WC Cell Biology
SC Cell Biology
GA 858RJ
UT WOS:000297819900017
PM 22105349
ER
PT J
AU Haubrich, RH
Riddler, SA
Ribaudo, H
DiRenzo, G
Klingman, KL
Garren, KW
Butcher, DL
Rooney, JF
Havlir, DV
Mellors, JW
AF Haubrich, Richard H.
Riddler, Sharon A.
Ribaudo, Heather
DiRenzo, Gregory
Klingman, Karin L.
Garren, Kevin W.
Butcher, David L.
Rooney, James F.
Havlir, Diane V.
Mellors, John W.
CA AIDS Clinical Trials Grp ACTG
AIDS Clinical Trials Grp ACTG
TI Initial viral decay to assess the relative antiretroviral potency of
protease inhibitor-sparing, nonnucleoside reverse transcriptase
inhibitor-sparing, and nucleoside reverse transcriptase
inhibitor-sparing regimens for first-line therapy of HIV infection
SO AIDS
LA English
DT Article
DE antiretroviral therapy; nonnucleoside reverse transcriptase inhibitor;
protease inhibitor; treatment outcome; viral dynamics
ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS CLINICAL-TRIALS; BASE-LINE FACTORS;
VIROLOGICAL RESPONSES; NAIVE SUBJECTS; RNA DYNAMICS; COMBINATION;
MODELS; PROGRESSION; EFAVIRENZ
AB Objectives: To evaluate the effects of sex and initial antiretroviral regimen on decay of HIV-RNA and virologic outcome.
Methods: We conducted a viral dynamics substudy of A5142, a trial comparing lopinavir (LPV)/ritonavir with efavirenz (LPV/EFV) versus LPV and two nucleoside reverse transcriptase inhibitor (NRTI) (LPV) versus EFV and two NRTI (EFV) in antiretroviral (ARV)-naive individuals. HIV-RNA was measured at days 2, 10, and 14 in the substudy and at weeks 1, 4, and 8 in A5142 participants. Two-phase viral decay was estimated in the substudy with biexponential mixed-effects modeling and compared using Wilcoxon tests. Week 1 HIV-RNA change was assessed as a predictor of virologic failure (HIV-RNA above 50 or 200 copies/ml) at weeks 24-96 using logistic regression.
Results: Sixty-eight individuals were enrolled in the substudy (median HIV-RNA 4.9 log(10) copies/ml). Median rates of phase 1 viral decay by treatment were 0.61(EFV/LPV), 0.53(LPV), and 0.63(EFV) per day. Phase 1 decay was significantly faster for EFV than LPV (P = 0.023); other comparisons were not significant (P > 0.11). Viral decay did not differ by sex (P = 0.10). Week 1 HIV-RNA change, calculated in 571 participants of A5142, was greater for the EFV (median -1.47 log10 copies/ml) than either the LPV/EFV or LPV groups (-1.21 and -1.16 log(10) copies/ml, respectively; P < 0.001). Week 1 HIV-RNA change was associated with virologic failure above 50 copies/ml at weeks 24 and 48 (P < 0.018), but not above 200 copies/ml at these time points or for any value at week 96.
Conclusion: Phase 1 decay was faster for EFV than LPV or LPV/EFV. Week 1 HIV-RNA change predicted virologic outcome up to week 48, but not at week 96. (C) 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins
C1 [Haubrich, Richard H.] Univ Calif San Diego, Antiviral Res Ctr, San Diego, CA 92103 USA.
[Riddler, Sharon A.; Mellors, John W.] Univ Pittsburgh, Pittsburgh, PA USA.
[Ribaudo, Heather; DiRenzo, Gregory] Harvard Univ, Sch Publ Hlth, Stat & Data Anal Ctr, Boston, MA 02115 USA.
[DiRenzo, Gregory] SUNY Albany, Albany, NY 12222 USA.
[Klingman, Karin L.] NIAID, Div Aids, Bethesda, MD 20892 USA.
[Garren, Kevin W.] Abbott Labs, Abbott Pk, IL 60064 USA.
[Butcher, David L.] Bristol Myers Squibb Co, Virol Med Affairs, Plainsboro, NJ USA.
[Rooney, James F.] Gilead Sci Inc, Foster City, CA 94404 USA.
[Havlir, Diane V.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP Haubrich, RH (reprint author), Univ Calif San Diego, Antiviral Res Ctr, 200 W Arbor Dr,Mail Code 8208, San Diego, CA 92103 USA.
EM rhaubrich@ucsd.edu
FU National Institute of Allergy and Infectious Disease, National
Institutes of Health [DA 12121]; Abbott; Bristol-Myers Squibb; Gilead
Sciences; GSK; Merck; Monogram; Pfizer; Roche; Tibotec; ViiV;
GlaxoSmithKline; NIH; [AI 068636]; [AI 068634]; [AI 069471]; [AI
27661]; [AI 069439]; [AI 25859]; [AI 069477]; [AI 06951]; [AI
069452]; [AI 27673]; [AI 069470]; [AI 069474]; [AI 069411]; [AI
069423]; [AI 069494]
FX This work was supported by grants AI 068636 (AIDS Clinical Trials Group
Central Grant), AI 068634, AI 069471, AI 27661, AI 069439, AI 25859, AI
069477, AI 06951, AI 069452, AI 27673, AI 069470, AI 069474, AI 069411,
AI 069423, AI 069494, AI 069484, AI 069472, AI 38858, AI 069501, AI
32783, AI 069450, AI 32782, AI 069465, AI 069424, AI 38858, AI 069447,
AI 069495, AI 069502, AI 069556, AI 069432, AI 46370, AI 069532, AI
46381, AI 46376, AI 34853, AI 069434, AI 060354, AI 064086, AI 36214, AI
069419, AI 069418, AI 50410, AI 45008, RR 00075, RR 00032, RR 00044, RR
00046, RR 02635, RR 00051, RR 00052, RR 00096, RR 00047, RR 00039, and
DA 12121 from the National Institute of Allergy and Infectious Disease,
National Institutes of Health. The collaborating pharmaceutical
companies provided lopinavir-ritonavir (Abbott), efavirenz and stavudine
XR (Bristol-Myers Squibb), and tenofovir DF (Gilead).; R.H.H. reports
having received honoraria or consultant fees from Abbott, Bristol-Myers
Squibb, Gilead Sciences, GSK, Merck, Monogram, Pfizer, Roche, Tibotec,
and ViiV, and research support (to UCSD) from Abbott, GlaxoSmithKline,
Merck, Pfizer, and ViiV.; D.V.H. is the principal investigator of a
NIH-sponsored study in which Abbott pharmaceuticals provides study drug.
NR 25
TC 15
Z9 15
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0269-9370
J9 AIDS
JI Aids
PD NOV 28
PY 2011
VL 25
IS 18
BP 2269
EP 2278
DI 10.1097/QAD.0b013e32834d0c20
PG 10
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 844XC
UT WOS:000296784300009
PM 21941167
ER
PT J
AU Ford, N
Calmy, A
Mofenson, L
AF Ford, Nathan
Calmy, Alexandra
Mofenson, Lynne
TI Safety of efavirenz in the first trimester of pregnancy: an updated
systematic review and meta-analysis
SO AIDS
LA English
DT Article
ID ACTIVE ANTIRETROVIRAL THERAPY; HIV-INFECTED WOMEN;
CONGENITAL-ABNORMALITIES; EXPOSURE; OUTCOMES
AB Evidence of the risk of birth defects with efavirenz use is limited. We updated a meta-analysis of birth defects in infants with first trimester efavirenz exposure up to July 2011. In 21 studies, there were 39 defects among live births in 1437 women receiving first trimester efavirenz [2.0%, 95% confidence interval (CI) 0.82-3.18]. The relative risk of defects comparing women on efavirenz-based (1290 live births) and nonefavirenz-based regimens (8122 live births) was 0.85 (95% CI 0.61-1.20). One neural tube defect was observed (myelomeningocele), giving an incidence of 0.07% (95% CI 0.002-0.39).
C1 [Ford, Nathan] Univ Cape Town, Ctr Infect Dis Epidemiol & Res, ZA-7925 Cape Town, South Africa.
[Ford, Nathan] Med Sans Frontieres, Geneva, Switzerland.
[Calmy, Alexandra] Univ Hosp Geneva, HIV Unit, Infect Dis Serv, Geneva, Switzerland.
[Mofenson, Lynne] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pediat Adolescent & Maternal AIDS Branch, Ctr Res Mothers & Children, NIH, Bethesda, MD USA.
RP Ford, N (reprint author), Univ Cape Town, Ctr Infect Dis Epidemiol & Res, Anzio Rd, ZA-7925 Cape Town, South Africa.
EM nathan.ford@msf.org
OI Mofenson, Lynne/0000-0002-2818-9808
NR 25
TC 62
Z9 62
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0269-9370
J9 AIDS
JI Aids
PD NOV 28
PY 2011
VL 25
IS 18
BP 2301
EP 2304
DI 10.1097/QAD.0b013e32834cdb71
PG 4
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 844XC
UT WOS:000296784300013
PM 21918421
ER
PT J
AU Hurst, FP
Altieri, M
Patel, PP
Jindal, TR
Guy, SR
Sidawy, AN
Agodoa, LY
Abbott, KC
Jindal, RM
AF Hurst, Frank P.
Altieri, Maria
Patel, Purav P.
Jindal, Tarun R.
Guy, Stephen R.
Sidawy, Anton N.
Agodoa, Lawrence Y.
Abbott, Kevin C.
Jindal, Rahul M.
TI Effect of Smoking on Kidney Transplant Outcomes: Analysis of the United
States Renal Data System
SO TRANSPLANTATION
LA English
DT Article
DE Smoking; Smoking cessation; USRDS; Graft survival; Patient survival
ID CIGARETTE-SMOKING; PATIENT SURVIVAL; HUMAN COSTS; TOBACCO USE;
RECIPIENTS; NEPHROPATHY; PROGRESSION; FAILURE; RISK
AB Background. Weinvestigated the effect of smoking on postkidney transplant outcomes in the United States Renal Data System.
Methods. In a retrospective cohort of 41,705 adult Medicare primary renal transplant recipients in the United States Renal Data System database transplanted from January 1, 2000, to June 30, 2006, and followed through October 31, 2006, we assessed Medicare claims for smoking. The association between renal allograft loss and death and smoking as a time-dependent variable was assessed with Cox nonproportional hazards regression.
Results. Of 41,705 Medicare primary adult renal transplant patients, there were 9.9% patients who had evidence of prior smoking and 4.6% patients with new claims for smoking after transplant. Incident smoking (new onset smokers) occurred at a mean of 1.29 +/- 0.88 years after transplant. In the adjusted analysis, factors associated with new smoking included male gender, history of drug or alcohol use, history of chronic obstructive pulmonary disease, and later year of transplant. Compared with never smokers, incident smoking after transplant was associated with increased risk of death-censored allograft loss (adjusted hazard ratio [AHR] 1.46 [95% confidence interval {CI}: 1.19-1.79]; P<0.001) and death (AHR 2.32 [95% CI: 1.98-2.72]; P<0.001). In a sensitivity analysis excluding patients with history of chronic obstructive pulmonary disease, similar results were obtained with increased risk of death-censored allograft loss (AHR 1.43 [95% CI: 1.16-1.76]; P=0.001) and death (AHR 2.26 [95% CI: 1.91-2.66]; P<0.001).
Discussion. Incident smoking was detrimental to graft and patient survival. Transplant programs should screen those at risk during transplant follow-up and have smoking cessation programs.
C1 [Altieri, Maria; Sidawy, Anton N.; Jindal, Rahul M.] Walter Reed Army Med Ctr, Dept Surg, Washington, DC 20307 USA.
[Altieri, Maria; Sidawy, Anton N.; Jindal, Rahul M.] George Washington Univ, Washington, DC USA.
[Patel, Purav P.] Med Univ Lublin, Lublin, Poland.
[Jindal, Tarun R.] Indiana Univ, Sch Med, Indianapolis, IN USA.
[Guy, Stephen R.] Drexel Univ, Dept Surg, Div Organ Transplant, Philadelphia, PA 19104 USA.
[Agodoa, Lawrence Y.] NIDDK, NIH, Bethesda, MD USA.
RP Jindal, RM (reprint author), Walter Reed AMC, Dept Transplantat, Georgia Av, Washington, DC USA.
EM jindalr@msn.com
OI Abbott, Kevin/0000-0003-2111-7112
NR 28
TC 16
Z9 18
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0041-1337
J9 TRANSPLANTATION
JI Transplantation
PD NOV 27
PY 2011
VL 92
IS 10
BP 1101
EP 1107
DI 10.1097/TP.0b013e3182336095
PG 7
WC Immunology; Surgery; Transplantation
SC Immunology; Surgery; Transplantation
GA 845BP
UT WOS:000296798100012
PM 21956202
ER
PT J
AU Galvan, SC
Martinez-Salazar, M
Galvan, VM
Mendez, R
Diaz-Contreras, GT
Alvarado-Hermida, M
Alcantara-Silva, R
Garcia-Carranca, A
AF Galvan, Silvia C.
Martinez-Salazar, Martha
Galvan, Victor M.
Mendez, Rocio
Diaz-Contreras, Gibran T.
Alvarado-Hermida, Moises
Alcantara-Silva, Rogelio
Garcia-Carranca, Alejandro
TI Analysis of CpG methylation sites and CGI among human papillomavirus DNA
genomes
SO BMC GENOMICS
LA English
DT Article
ID E1-BOOLEAN-AND-E4 PROTEIN; LIFE-CYCLE; CERVICAL NEOPLASIA; TYPE-16 DNA;
CODON USAGE; CELL-LINES; ISLANDS; SEQUENCES; VIRUSES; BINDING
AB Background: The Human Papillomavirus (HPV) genome is divided into early and late coding sequences, including 8 open reading frames (ORFs) and a regulatory region (LCR). Viral gene expression may be regulated through epigenetic mechanisms, including cytosine methylation at CpG dinucleotides. We have analyzed the distribution of CpG sites and CpG islands/clusters (CGI) among 92 different HPV genomes grouped in function of their preferential tropism: cutaneous or mucosal. We calculated the proportion of CpG sites (PCS) for each ORF and calculated the expected CpG values for each viral type.
Results: CpGs are underrepresented in viral genomes. We found a positive correlation between CpG observed and expected values, with mucosal high-risk (HR) virus types showing the smallest O/E ratios. The ranges of the PCS were similar for most genomic regions except E4, where the majority of CpGs are found within islands/clusters. At least one CGI belongs to each E2/E4 region. We found positive correlations between PCS for each viral ORF when compared with the others, except for the LCR against four ORFs and E6 against three other ORFs. The distribution of CpG islands/clusters among HPV groups is heterogeneous and mucosal HR-HPV types exhibit both lower number and shorter island sizes compared to cutaneous and mucosal Low-risk (LR) HPVs (all of them significantly different).
Conclusions: There is a difference between viral and cellular CpG underrepresentation. There are significant correlations between complete genome PCS and a lack of correlations between several genomic region pairs, especially those involving LCR and E6. L2 and L1 ORF behavior is opposite to that of oncogenes E6 and E7. The first pair possesses relatively low numbers of CpG sites clustered in CGIs while the oncogenes possess a relatively high number of CpG sites not associated to CGIs. In all HPVs, E2/E4 is the only region with at least one CGI and shows a higher content of CpG sites in every HPV type with an identified E4. The mucosal HR-HPVs show either the shortest CGI size, followed by the mucosal LR-HPVs and lastly by the cutaneous viral subgroup, and a trend to the lowest CGI number, followed by the cutaneous viral subgroup and lastly by the mucosal LR-HPVs.
C1 [Galvan, Silvia C.; Martinez-Salazar, Martha; Garcia-Carranca, Alejandro] Univ Nacl Autonoma Mexico, Inst Invest Biomed, Mexico City 04510, DF, Mexico.
[Galvan, Victor M.] Univ Autonoma Metropolitana Xochimilco, Dept Hombre & Ambiente, Mexico City, DF, Mexico.
[Diaz-Contreras, Gibran T.; Alvarado-Hermida, Moises; Alcantara-Silva, Rogelio] Univ Nacl Autonoma Mexico, Fac Ingn, Mexico City 04510, DF, Mexico.
[Galvan, Silvia C.; Alcantara-Silva, Rogelio; Garcia-Carranca, Alejandro] Univ Nacl Autonoma Mexico, Mexico City, DF, Mexico.
[Mendez, Rocio; Garcia-Carranca, Alejandro] NCI, Bethesda, MD 20892 USA.
[Galvan, Victor M.] Metropolitan Univ, Mexico City, DF, Mexico.
RP Galvan, SC (reprint author), Univ Nacl Autonoma Mexico, Inst Invest Biomed, Mexico City 04510, DF, Mexico.
EM sgalvan@unam.mx
FU PAPIIT-UNAM [IN215411-3, IN226408]
FX We want to acknowledge support from PAPIIT-UNAM IN215411-3 (to SCG) and
IN226408 (to AGC). This work was performed at Unidad de Investigacion
Biomedica en Cancer, Instituto de Investigaciones Biomedicas,
Universidad Nacional Autonoma de Mexico and Instituto Nacional de
Cancerologia, SSA, in collaboration with researchers from Facultad de
Ingenieria, Universidad Nacional Autonoma de Mexico and from Instituto
Nacional de Cancerologia, SSA. We thank Prof. Luis Bojorquez-Castro for
helpful discussions and statistical advice, and Dr. Elizabeth Langley
and QFB Martha D. Sanchez-Barrios for critical review of the manuscript.
We are also grateful to two anonymous reviewers for excellent
constructive criticism.
NR 49
TC 3
Z9 3
U1 1
U2 4
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 25
PY 2011
VL 12
AR 580
DI 10.1186/1471-2164-12-580
PG 10
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 907RU
UT WOS:000301436100001
PM 22118413
ER
PT J
AU Nemecek, D
Cheng, NQ
Qiao, J
Mindich, L
Steven, AC
Heymann, JB
AF Nemecek, Daniel
Cheng, Naiqian
Qiao, Jian
Mindich, Leonard
Steven, Alasdair C.
Heymann, J. Bernard
TI Stepwise Expansion of the Bacteriophage phi 6 Procapsid: Possible
Packaging Intermediates
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Article
DE cryo-electron microscopy; Cystoviridae; virus; capsid; segmented genome
ID STRANDED-RNA BACTERIOPHAGE-PHI-6; 3 GENOMIC SEGMENTS; DSRNA
BACTERIOPHAGE-PHI-6; CRYOELECTRON MICROSCOPY; POLYMERASE COMPLEX;
PROTEIN; TOMOGRAPHY; BINDING; MECHANISM; DYNAMICS
AB The initial assembly product of bacteriophage 416, the procapsid, undergoes major structural transformation during the sequential packaging of its three segments of single-stranded RNA. The procapsid, a compact icosahedrally symmetric particle with deeply recessed vertices, expands to the spherical mature capsid, increasing the volume available to accommodate the genome by 2.5-fold. It has been proposed that expansion and packaging are linked, with each stage in expansion presenting a binding site for a particular RNA segment. To investigate procapsid transformability, we induced expansion by acidification, heating, and elevated salt concentration. Cryo-electron microscopy reconstructions after all three treatments yielded the same partially expanded particle. Analysis by cryo-electron tomography showed that all vertices of a given capsid were either in a compact or an expanded state, indicating a highly cooperative transition. To benchmark the mature capsid, we analyzed filled (in vivo packaged) capsids. When these particles were induced to release their RNA, they reverted to the same intermediate state as expanded procapsids (intermediate 1) or to a second, further expanded state (intermediate 2). This partial reversibility of expansion suggests that the mature spherical capsid conformation is obtained only when sufficient outward pressure is exerted by packaged RNA. The observation of two intermediates is consistent with the proposed three-step packaging process. The model is further supported by the observation that a mutant capable of packaging the second RNA segment without previously packaging the first segment has enhanced susceptibility for switching spontaneously from the procapsid to the first intermediate state. Published by Elsevier Ltd.
C1 [Nemecek, Daniel; Cheng, Naiqian; Steven, Alasdair C.; Heymann, J. Bernard] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Qiao, Jian; Mindich, Leonard] Univ Med & Dent New Jersey, Dept Microbiol, Publ Hlth Res Inst Ctr, Newark, NJ 07103 USA.
RP Steven, AC (reprint author), NIAMSD, NIH, 50 South Dr, Bethesda, MD 20892 USA.
EM stevena@mail.nih.gov
FU National Institute of Arthritis and Musculoskeletal and Skin; National
Institutes of Health [GM34352]
FX We thank Austin Luskin, a summer student at the National Institutes of
Health, for initial DSC measurements. This work was supported by the
Intramural Research Program of National Institute of Arthritis and
Musculoskeletal and Skin and by grant GM34352 to L.M. from the National
Institutes of Health.
NR 38
TC 14
Z9 14
U1 0
U2 9
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0022-2836
J9 J MOL BIOL
JI J. Mol. Biol.
PD NOV 25
PY 2011
VL 414
IS 2
BP 260
EP 271
DI 10.1016/j.jmb.2011.10.004
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 862XN
UT WOS:000298127500008
PM 22019738
ER
PT J
AU Moss, ML
Powell, G
Miller, MA
Edwards, L
Qi, B
Sang, QXA
De Strooper, B
Tesseur, I
Lichtenthaler, SF
Taverna, M
Zhong, JL
Dingwall, C
Ferdous, T
Schlomann, U
Zhou, P
Griffith, LG
Lauffenburger, DA
Petrovich, R
Bartsch, JW
AF Moss, Marcia L.
Powell, Gary
Miller, Miles A.
Edwards, Lori
Qi, Bin
Sang, Qing-Xiang Amy
De Strooper, Bart
Tesseur, Ina
Lichtenthaler, Stefan F.
Taverna, Mara
Zhong, Julia Li
Dingwall, Colin
Ferdous, Taheera
Schlomann, Uwe
Zhou, Pei
Griffith, Linda G.
Lauffenburger, Douglas A.
Petrovich, Robert
Bartsch, Joerg W.
TI ADAM9 Inhibition Increases Membrane Activity of ADAM10 and Controls
alpha-Secretase Processing of Amyloid Precursor Protein
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID NECROSIS-FACTOR-ALPHA; CONVERTING-ENZYME TACE;
DISINTEGRIN-METALLOPROTEINASE; RHEUMATOID-ARTHRITIS;
SELECTIVE-INHIBITION; SOLUBLE NEUROPILIN-2; THERAPEUTIC TARGET; TISSUE
INHIBITOR; RECEPTOR CD23; CANCER
AB Prodomains of A disintegrin and metalloproteinase (ADAM) metallopeptidases can act as highly specific intra- and intermolecular inhibitors of ADAM catalytic activity. The mouse ADAM9 prodomain (proA9; amino acids 24-204), expressed and characterized from Escherichia coli, is a competitive inhibitor of human ADAM9 catalyticidisintegrin domain with an overall inhibition constant of 280 +/- 34 nM and high specificity toward ADAM9. In SY5Y neuroblastoma cells overexpressing amyloid precursor protein, proA9 treatment reduces the amount of endogenous ADAM 10 enzyme in the medium while increasing membrane-bound ADAM10, as shown both by Western and activity assays with selective fluorescent peptide substrates using proteolytic activity matrix analysis. An increase in membrane-bound ADAM 10 generates higher levels of soluble amyloid precursor protein alpha in the medium, whereas soluble amyloid precursor protein beta levels are decreased, demonstrating that inhibition of ADAM9 increases alpha-secretase activity on the cell membrane. Quantification of physiological ADAM10 substrates by a proteomic approach revealed that substrates, such as epidermal growth factor (EGF), HER2, osteoactivin, and CD40-ligand, are increased in the medium of BT474 breast tumor cells that were incubated with proA9, demonstrating that the regulation of ADAM10 by ADAM9 applies for many ADAM10 substrates. Taken together, our results demonstrate that ADAM 10 activity is regulated by inhibition of ADAM9, and this regulation may be used to control shedding of amyloid precursor protein by enhancing alpha-secretase activity, a key regulatory step in the etiology of Alzheimer disease.
C1 [Moss, Marcia L.] BioZyme Inc, Apex, NC 27523 USA.
[Powell, Gary; Edwards, Lori; Petrovich, Robert] NIEHS, NIH, Durham, NC 27709 USA.
[Miller, Miles A.; Griffith, Linda G.; Lauffenburger, Douglas A.] MIT, Dept Biol Engn, Cambridge, MA 02139 USA.
[Qi, Bin; Sang, Qing-Xiang Amy] Florida State Univ, Dept Chem & Biochem, Tallahassee, FL 32306 USA.
[De Strooper, Bart; Tesseur, Ina] Catholic Univ Louvain, Ctr Human Genet, B-3000 Louvain, Belgium.
[Lichtenthaler, Stefan F.; Taverna, Mara] DZNE German Ctr Neurodegenerat Dis, D-80336 Munich, Germany.
[Dingwall, Colin; Ferdous, Taheera; Schlomann, Uwe; Bartsch, Joerg W.] Kings Coll London, Inst Pharm, London SE1 9NH, England.
[Zhong, Julia Li] Chongqing Univ, Coll Bioengn, Chongqing 400044, Peoples R China.
[Zhou, Pei] Duke Univ, Med Ctr, Dept Biochem, Durham, NC 27710 USA.
[Bartsch, Joerg W.] Univ Marburg, Univ Hosp, Dept Neurosurg, D-35053 Marburg, Germany.
RP Bartsch, JW (reprint author), Univ Hosp, Dept Neurosurg, Baldingerstr, D-35033 Marburg, Germany.
EM jbartsch@med.uni-marburg.de
RI Schlomann, Uwe/F-6419-2012; De Strooper, Bart/F-6507-2012;
Lichtenthaler, Stefan/B-6587-2016
OI De Strooper, Bart/0000-0001-5455-5819; Lichtenthaler,
Stefan/0000-0003-2211-2575
FU National Institutes of Health [R01EB010246, R01GM081336]; Heptagon Fund
London; Cancer Research Technology UK; Whitehead Foundation; Duke Bridge
Fund for Research Resources; Bundesministerium fur Bildung und
Forschung: Krankheitsbezogene Kompetenznetz Degenerative Demenzen;
Chinese Scholarship Council, People's Republic of China; Florida State
University
FX This work was supported, in whole or in part, by National Institutes of
Health Grants R01EB010246 (to L. G. G.) and R01GM081336 (to D. A. L.).
This work was also supported by the Heptagon Fund London and Cancer
Research Technology UK (to J. W. B.), the Whitehead Foundation and the
Duke Bridge Fund for Research Resources (to P. Z.), the
Bundesministerium fur Bildung und Forschung: Krankheitsbezogene
Kompetenznetz Degenerative Demenzen (to S. F. L.), a National Fellowship
from the Chinese Scholarship Council, People's Republic of China (to B.
Q.), and grants from Florida State University (to Q. X. A. S.).
NR 52
TC 22
Z9 22
U1 4
U2 9
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 25
PY 2011
VL 286
IS 47
BP 40443
EP 40451
DI 10.1074/jbc.M111.280495
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 852AN
UT WOS:000297315400004
PM 21956108
ER
PT J
AU Zhao, YG
Thornton, AM
Kinney, MC
Ma, CA
Spinner, JJ
Fuss, IJ
Shevach, EM
Jain, A
AF Zhao, Yongge
Thornton, Angela M.
Kinney, Matthew C.
Ma, Chi A.
Spinner, Jacob J.
Fuss, Ivan J.
Shevach, Ethan M.
Jain, Ashish
TI The Deubiquitinase CYLD Targets Smad7 Protein to Regulate Transforming
Growth Factor beta (TGF-beta) Signaling and the Development of
Regulatory T Cells
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID TRANSCRIPTION FACTOR FOXP3; TUMOR-SUPPRESSOR CYLD; KINASE TAK1;
UBIQUITIN LIGASE; INDUCTION; RECEPTOR; ACTIVATION; ENZYME; RESPONSES;
BINDS
AB CYLD is a lysine 63-deubiquitinating enzyme that inhibits NF-kappa B and JNK signaling. Here, we show that CYLD knock-out mice have markedly increased numbers of regulatory T cells (Tregs) in peripheral lymphoid organs but not in the thymus. In vitro stimulation of CYLD-deficient naive T cells with anti-CD3/28 in the presence of TGF-beta led to a marked increase in the number of Foxp3-expressing T cells when compared with stimulated naive control CD4(+) cells. Under endogenous conditions, CYLD formed a complex with Smad7 that facilitated CYLD deubiquitination of Smad7 at lysine 360 and 374 residues. Moreover, this site-specific ubiquitination of Smad7 was required for activation of TAK1 and p38 kinases. Finally, knockdown of Smad7 or inhibition of p38 activity in primary T cells impaired Treg differentiation. Together, our results show that CYLD regulates TGF-beta signaling function in T cells and the development of Tregs through deubiquitination of Smad7.
C1 [Zhao, Yongge; Kinney, Matthew C.; Ma, Chi A.; Spinner, Jacob J.; Fuss, Ivan J.; Jain, Ashish] NIAID, Lab Host Def, NIH, Bethesda, MD 20892 USA.
[Thornton, Angela M.; Shevach, Ethan M.] NIAID, Lab Immunol, NIH, Bethesda, MD 20892 USA.
RP Jain, A (reprint author), Clin Res Ctr, Rm 5-W-3950,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM ajain@niaid.nih.gov
FU National Institutes of Health through the NIAID
FX This work was supported by the Intramural Research Program of the
National Institutes of Health through the NIAID.
NR 34
TC 27
Z9 29
U1 1
U2 2
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 25
PY 2011
VL 286
IS 47
BP 40520
EP 40530
DI 10.1074/jbc.M111.292961
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 852AN
UT WOS:000297315400011
PM 21931165
ER
PT J
AU Lu, JH
Ellsworth, JL
Hamacher, N
Oak, SW
Sun, PD
AF Lu, Jinghua
Ellsworth, Jeff L.
Hamacher, Nels
Oak, Si Won
Sun, Peter D.
TI Crystal Structure of Fc gamma Receptor I and Its Implication in High
Affinity gamma-Immunoglobulin Binding
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID COLLAGEN-INDUCED ARTHRITIS; HUMAN-IGG; AUTOIMMUNE-DISEASE;
MOLECULAR-BASIS; EPSILON-RI; COMPLEX; FRAGMENT; GLYCOSYLATION;
RECOGNITION; DOMAINS
AB Fc gamma receptors (Fc gamma Rs) play critical roles in humoral and cellular immune responses through interactions with the Fc region of immunoglobulin G (IgG). Among them, Fc gamma RI is the only high affinity receptor for IgG and thus is a potential target for immunotherapy. Here we report the first crystal structure of an Fc gamma RI with all three extracellular Ig-like domains (designated as D1, D2, and D3). The structure shows that, first, Fc gamma RI has an acute D1-D2 hinge angle similar to that of Fc epsilon RI but much smaller than those observed in the low affinity Fc gamma receptors. Second, the D3 domain of Fc gamma RI is positioned away from the putative IgG binding site on the receptor and is thus unlikely to make direct contacts with Fc. Third, the replacement of Fc gamma RIII FG-loop ((171)LVGSKNV(177)) with that of Fc gamma RI ((171)MGKHRY(176)) resulted in a 15-fold increase in IgG, binding affinity, whereas a valine insertion in the Fc gamma RI FG-loop ((171)MVGKHRY(177)) abolished the affinity enhancement. Thus, the Fc gamma RI FG-loop with its conserved one-residue deletion is critical to the high affinity IgG binding. The structural results support Fc gamma RI binding to IgG in a similar mode as its low affinity counterparts. Taken together, our study suggests a molecular mechanism for the high affinity IgG recognition by Fc gamma RI and provides a structural basis for understanding its physiological function and its therapeutic implication in treating autoimmune diseases.
C1 [Lu, Jinghua; Oak, Si Won; Sun, Peter D.] NIAID, Struct Immunol Sect, Lab Immunogenet, NIH, Rockville, MD USA.
[Hamacher, Nels] ZymoGenetics, Dept BioProc Dev, Seattle, WA 98102 USA.
[Ellsworth, Jeff L.] ZymoGenetics, Dept Immunol, Seattle, WA 98102 USA.
RP Sun, PD (reprint author), 12441 Parklawn Dr, Rockville, MD 20852 USA.
EM psun@niaid.nih.gov
RI lu, jinghua/G-5872-2012
FU National Institutes of Health (NIAID)
FX This work was supported, in whole or in part, by National Institutes of
Health intramural research funding (NIAID).
NR 45
TC 43
Z9 44
U1 1
U2 10
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 25
PY 2011
VL 286
IS 47
BP 40608
EP 40613
DI 10.1074/jbc.M111.257550
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 852AN
UT WOS:000297315400021
PM 21965667
ER
PT J
AU Kaiser, HJ
Surma, MA
Mayer, F
Levental, I
Grzybek, M
Klemm, RW
Da Cruz, S
Meisinger, C
Muller, V
Simons, K
Lingwood, D
AF Kaiser, Hermann-Josef
Surma, Michal A.
Mayer, Florian
Levental, Ilya
Grzybek, Michal
Klemm, Robin W.
Da Cruz, Sandrine
Meisinger, Chris
Mueller, Volker
Simons, Kai
Lingwood, Daniel
TI Molecular Convergence of Bacterial and Eukaryotic Surface Order
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID SHOTGUN MASS-SPECTROMETRY; ALPHA-HELICAL PEPTIDES; MODEL MEMBRANES;
LIPID RAFTS; HOMEOVISCOUS ADAPTATION; BIOLOGICAL-MEMBRANES; SECRETORY
VESICLES; BILAYER THICKNESS; PLASMA-MEMBRANES; PHASE-DIAGRAMS
AB The conservation of fluidity is a theme common to all cell membranes. In this study, an analysis of lipid packing was conducted via C-laurdan spectroscopy of cell surface membranes prepared from representative species of Bacteria and Eukarya. We found that despite their radical differences in composition (namely the presence and absence of membrane-rigidifying sterol) the membrane order of all taxa converges on a remarkably similar level, To understand how this similarity is constructed, we reconstituted membranes with either bacterial or eukaryotic components. We found that transmembrane segments of proteins have an important role in buffering lipid-mediated packing. This buffering ensures that sterol-free and sterol-containing membranes exhibit similar barrier properties.
C1 [Kaiser, Hermann-Josef; Surma, Michal A.; Levental, Ilya; Grzybek, Michal; Simons, Kai; Lingwood, Daniel] Max Planck Inst Mol Cell Biol & Genet, D-01307 Dresden, Germany.
[Mayer, Florian; Mueller, Volker] Goethe Univ Frankfurt, Inst Mol Biosci, Dept Mol Microbiol & Bioenerget, D-60438 Frankfurt, Germany.
[Klemm, Robin W.] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
[Da Cruz, Sandrine] Univ Calif San Diego, Dept Cellular & Mol Med, La Jolla, CA 92093 USA.
[Da Cruz, Sandrine] Univ Calif San Diego, Ludwig Inst, La Jolla, CA 92093 USA.
[Meisinger, Chris] Univ Freiburg, ZBMZ, Inst Biochem & Mol Biol, D-79104 Freiburg, Germany.
[Meisinger, Chris] Univ Freiburg, Ctr Biol Signaling Studies BIOSS, D-79104 Freiburg, Germany.
RP Lingwood, D (reprint author), NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM daniel.lingwood@nih.gov
RI Klemm, Robin/C-5463-2014; Meisinger, Chris/J-1110-2014; Surma,
Michal/B-1955-2016; Grzybek, Michal/D-3802-2017
OI Klemm, Robin/0000-0003-2313-8240; Surma, Michal/0000-0001-7833-2214;
Grzybek, Michal/0000-0003-2083-0506
FU Max Planck Institute for Molecular Cell Biology and Genetics; Deutsche
Forschungsgemeinschaft (DFG) Sonderforschungsbereiche [807]; DFG
Schwerpunktprogramm1175 [SI459/2-1]; DFG Transregio [TRR83 TP02];
European Science Foundation LIPIDPROD [SI459/3-1]; Bundesministerium fur
Bildung und Forschung ForMaT [03FO1212]; Klaus Tschira Foundation
FX This work was supported by a Max Planck Institute for Molecular Cell
Biology and Genetics stipend (to D. L.), by Deutsche
Forschungsgemeinschaft (DFG) Sonderforschungsbereiche Grant 807 (to V.
M.), and by DFG Schwerpunktprogramm1175 Grant SI459/2-1, DFG Transregio
83 Grant TRR83 TP02; European Science Foundation LIPIDPROD Grant
SI459/3-1; Bundesministerium fur Bildung und Forschung ForMaT Grant
03FO1212, and The Klaus Tschira Foundation (to K. S.).
NR 51
TC 20
Z9 20
U1 2
U2 5
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 25
PY 2011
VL 286
IS 47
BP 40631
EP 40637
DI 10.1074/jbc.M111.276444
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 852AN
UT WOS:000297315400024
PM 21965671
ER
PT J
AU Ueyama, T
Nakakita, J
Nakamura, T
Kobayashi, T
Kobayashi, T
Son, J
Sakuma, M
Sakaguchi, H
Leto, TL
Saito, N
AF Ueyama, Takehiko
Nakakita, Junya
Nakamura, Takashi
Kobayashi, Takeshi
Kobayashi, Toshihiro
Son, Jeonghyun
Sakuma, Megumi
Sakaguchi, Hirofumi
Leto, Thomas L.
Saito, Naoaki
TI Cooperation of p40(phox) with p47(phox) for Nox2-based NADPH Oxidase
Activation during Fc gamma Receptor (Fc gamma R)-mediated Phagocytosis
MECHANISM FOR ACQUISITION OF p40(phox) PHOSPHATIDYLINOSITOL 3-PHOSPHATE
(PI(3)P) BINDING
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID CHRONIC GRANULOMATOUS-DISEASE; R-MEDIATED PHAGOCYTOSIS;
PROTEIN-KINASE-C; SRC HOMOLOGY-3 DOMAINS; PX DOMAIN; SH3 DOMAIN;
SUBCELLULAR-LOCALIZATION; HUMAN-NEUTROPHILS; INTRAMOLECULAR INTERACTION;
SUPEROXIDE-PRODUCTION
AB During activation of the phagocyte (Nox2-based) NADPH oxidase, the cytoplasmic Phox complex (p47(phox)-p67(phox) p40(phox) translocates and associates with the membrane-spanning flavocytochrome b(558). It is unclear where (in cytoplasm or on membranes), when (before or after assembly), and how p40(phox) acquires its PI(3)P-binding capabilities. We demonstrated that in addition to conformational changes induced by H2O2 in the cytoplasm, p40(phox) acquires PI(3)P-binding through direct or indirect membrane targeting. We also found that p40(phox) is essential when p47(phox) is partially phosphorylated during Fc gamma R-mediated oxidase activation; however, p40(phox) is less critical when p47(phox) is adequately phosphorylated, using phosphorylation-mimicking mutants in HEK293(Nox2/Fc gamma RIIa) and RAW264.7(P40/P47KD) cells. Moreover, PI binding to p47(phox) is less important when the autoinhibitory PX-PB1 domain interaction in p40(phox) is disrupted or when p40(phox) is targeted to membranes. Furthermore, we suggest that high affinity PI(3)P binding of the p40(phox) PX domain is critical during its accumulation on phagosomes, even when masked by the PB1 domain in the resting state. Thus, in addition to mechanisms for directly acquiring P I(3)P binding in the cytoplasm by H2O2, p40(phox) can acquire PI(3)P binding on targeted membranes in a p47(phox)-dependent manner and functions both as a "carrier" of the cytoplasmic Phox complex to phagosomes and an "adaptor" of oxidase assembly on phagosomes in cooperation with p47(phox), using positive feedback mechanisms.
C1 [Ueyama, Takehiko; Nakakita, Junya; Nakamura, Takashi; Son, Jeonghyun; Sakuma, Megumi; Saito, Naoaki] Kobe Univ, Mol Pharmacol Lab, Biosignal Res Ctr, Kobe, Hyogo 6578501, Japan.
[Kobayashi, Takeshi] Nagoya Univ, Grad Sch Med, Dept Physiol, Nagoya, Aichi 4668550, Japan.
[Kobayashi, Toshihiro] Kobe Int Univ, Dept Phys Therapy, Kobe, Hyogo 6580032, Japan.
[Sakaguchi, Hirofumi] Kyoto Prefectural Univ Med, Dept Otolaryng Head & Neck Surg, Kyoto 6028566, Japan.
[Leto, Thomas L.] NIAID, Mol Def Sect, Lab Host Def, NIH, Rockville, MD 20852 USA.
RP Ueyama, T (reprint author), Kobe Univ, Mol Pharmacol Lab, Biosignal Res Ctr, Kobe, Hyogo 6578501, Japan.
EM tueyama@kobe-u.ac.jp; naosaito@kobe-u.ac.jp
FU National Institutes of Health, NIAID; Ministry of Education, Culture,
Sports, Science and Technology, Japan; Japan Society for the Promotion
of Science and Hungarian Academy of Sciences; Naito Foundation; Suzuken
Memorial Foundation; Takeda Science Foundation
FX This work was supported in part by the National Institutes of Health,
NIAID, Intramural Research Program. This work was also supported in part
by Grants-in-aid for scientific research; on the Global Center of
Excellence Program, on Priority Areas "Transportsome," on Innovative
Areas 'Fluorescence Live Imaging" and (C), from the Ministry of
Education, Culture, Sports, Science and Technology, Japan. This work was
also supported by the "Japan-Hungary Research Cooperative Program" grant
from the Japan Society for the Promotion of Science and Hungarian
Academy of Sciences, by a grant from the Naito Foundation, by a grant
from the Suzuken Memorial Foundation, and by a grant from the Takeda
Science Foundation.
NR 73
TC 17
Z9 17
U1 2
U2 5
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 25
PY 2011
VL 286
IS 47
BP 40693
EP 40705
DI 10.1074/jbc.M111.237289
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 852AN
UT WOS:000297315400030
PM 21956105
ER
PT J
AU Liu, J
Nussinov, R
AF Liu, Jin
Nussinov, Ruth
TI Flexible Cullins in Cullin-RING E3 Ligases Allosterically Regulate
Ubiquitination
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID SOCS-BOX; CUL5-RBX2 MODULES; STRUCTURAL BASIS; COMPLEX REVEALS; PROTEIN;
RECOGNITION; SPECIFICITY; MACHINERY; CUL2-RBX1; INSIGHTS
AB How do the cullins, with conserved structures, accommodate substrate-binding proteins with distinct shapes and sizes? Cullin-RING E3 ubiquitin ligases facilitate ubiquitin transfer from E2 to the substrate, tagging the substrate for degradation. They contain substrate-binding, adaptor, cullin, and Rbx proteins. Previously, we showed that substrate-binding and Rbx proteins are flexible. This allows shortening of the E2-substrate distance for initiation of ubiquitination or increasing the distance to accommodate the polyubiquitin chain. However, the role of the cullin remained unclear. Is cullin a rigid scaffold, or is it flexible and actively assists in the ubiquitin transfer reaction? Why are there different cullins, and how do these cullins specifically facilitate ubiquitination for different substrates? To answer these questions, we performed structural analysis and molecular dynamics simulations based on Cull, Cul4A, and Cu15 crystal structures. Our results show that these three cullins are not rigid scaffolds but are flexible with conserved hinges in the N-terminal domain. However, the degrees of flexibilities are distinct among the different cullins. Of interest, Cull flexibility can also be changed by deletion of the long loop (which is absent in Cul4A) in the N-terminal domain, suggesting that the loop may have an allosteric functional role. In all three cases, these conformational changes increase the E2-substrate distance to a specific range to facilitate polyubiquitination, suggesting that rather than being inert scaffold proteins, cullins allosterically regulate ubiquitination.
C1 [Liu, Jin; Nussinov, Ruth] NCI, Basic Sci Program, SAIC Frederick Inc, Ctr Canc Res Nanobiol Program,NIH, Frederick, MD 21702 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Sch Med, Sackler Inst Mol Med, Dept Human Genet & Mol Med, IL-69978 Tel Aviv, Israel.
RP Nussinov, R (reprint author), NCI, Basic Sci Program, SAIC Frederick Inc, Ctr Canc Res Nanobiol Program,NIH, Frederick, MD 21702 USA.
EM ruthnu@helix.nih.gov
FU National Institutes of Health from NCI [HHSN261200800001E]; National
Cancer Institute Center for Cancer Research of the National Institutes
of Health
FX This work was supported, in whole or in part, by National Institutes of
Health Contract HHSN261200800001E from NCI and the National Cancer
Institute Center for Cancer Research Intramural Research Program of the
National Institutes of Health.
NR 41
TC 31
Z9 31
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
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 25
PY 2011
VL 286
IS 47
BP 40934
EP 40942
DI 10.1074/jbc.M111.277236
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 852AN
UT WOS:000297315400053
PM 21937436
ER
PT J
AU Deshmukh, L
Meller, N
Alder, N
Byzova, T
Vinogradova, O
AF Deshmukh, Lalit
Meller, Nahum
Alder, Nathan
Byzova, Tatiana
Vinogradova, Olga
TI Tyrosine Phosphorylation as a Conformational Switch A CASE STUDY OF
INTEGRIN beta(3) CYTOPLASMIC TAIL
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID NMR-SPECTROSCOPY; STRUCTURAL BASIS; ALPHA-IIB-BETA-3; TRANSMEMBRANE;
ACTIVATION; COMPLEX; SYSTEM; ALPHA(IIB)BETA(3); MECHANISM; DYNAMICS
AB Reversible protein phosphorylation is vital for many fundamental cellular processes. The actual impact of adding and removing phosphate group(s) is 3-fold: changes in the local/global geometry, alterations in the electrostatic potential and, as the result of both, modified protein-target interactions. Here we present a comprehensive structural investigation of the effects of phosphorylation on the conformational as well as functional states of a crucial cell surface receptor, alpha(IIb)beta(3) integrin. We have analyzed phosphorylated (Tyr(747) and Tyr(759)) beta(3) integrin cytoplasmic tail (CT) primarily by NMR, and our data demonstrate that under both aqueous and membrane-mimetic conditions, phosphorylation causes substantial conformational rearrangements. These changes originate from novel ionic interactions and revised phospholipid binding. Under aqueous conditions, the critical Tyr(747) phosphorylation prevents beta 3CT from binding to its heterodimer partner alpha IIbCT, thus likely maintaining an activated state of the receptor. This conclusion was tested in vivo and confirmed by integrin-dependent endothelial cells adhesion assay. Under membrane-mimetic conditions, phosphorylation results in a modified membrane embedding characterized by significant changes in the secondary structure pattern and the overall fold of beta 3CT. Collectively these data provide unique molecular insights into multiple regulatory roles of phosphorylation.
C1 [Deshmukh, Lalit; Vinogradova, Olga] Univ Connecticut, Dept Pharmaceut Sci, Sch Pharm, Storrs, CT 06269 USA.
[Alder, Nathan] Univ Connecticut, Dept Mol & Cell Biol, Storrs, CT 06269 USA.
[Meller, Nahum; Byzova, Tatiana] Cleveland Clin Fdn, Dept Mol Cardiol, Lerner Res Inst, Cleveland, OH 44195 USA.
[Deshmukh, Lalit] NIDDK, Phys Chem Lab, NIH, Bethesda, MD 20892 USA.
RP Vinogradova, O (reprint author), Univ Connecticut, Dept Pharmaceut Sci, Sch Pharm, 69 N Eagleville Rd,Unit 3092, Storrs, CT 06269 USA.
EM olga.vinogradova@uconn.edu
RI Deshmukh, Lalit/C-5073-2015;
OI Vinogradova, Olga/0000-0001-5101-7361
FU American Heart Association; National Institutes of Health (NIH)
FX This work was supported in part by American Heart Association and
National Institutes of Health (NIH) Grants (to O. V.) and NIH grants (to
T. B.).
NR 32
TC 14
Z9 14
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
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 25
PY 2011
VL 286
IS 47
BP 40943
EP 40953
DI 10.1074/jbc.M111.231951
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 852AN
UT WOS:000297315400054
PM 21956114
ER
PT J
AU Pejchal, R
Doores, KJ
Walker, LM
Khayat, R
Huang, PS
Wang, SK
Stanfield, RL
Julien, JP
Ramos, A
Crispin, M
Depetris, R
Katpally, U
Marozsan, A
Cupo, A
Maloveste, S
Liu, Y
McBride, R
Ito, Y
Sanders, RW
Ogohara, C
Paulson, JC
Feizi, T
Scanlan, CN
Wong, CH
Moore, JP
Olson, WC
Ward, AB
Poignard, P
Schief, WR
Burton, DR
Wilson, IA
AF Pejchal, Robert
Doores, Katie J.
Walker, Laura M.
Khayat, Reza
Huang, Po-Ssu
Wang, Sheng-Kai
Stanfield, Robyn L.
Julien, Jean-Philippe
Ramos, Alejandra
Crispin, Max
Depetris, Rafael
Katpally, Umesh
Marozsan, Andre
Cupo, Albert
Maloveste, Sebastien
Liu, Yan
McBride, Ryan
Ito, Yukishige
Sanders, Rogier W.
Ogohara, Cassandra
Paulson, James C.
Feizi, Ten
Scanlan, Christopher N.
Wong, Chi-Huey
Moore, John P.
Olson, William C.
Ward, Andrew B.
Poignard, Pascal
Schief, William R.
Burton, Dennis R.
Wilson, Ian A.
TI A Potent and Broad Neutralizing Antibody Recognizes and Penetrates the
HIV Glycan Shield
SO SCIENCE
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; ENVELOPE GLYCOPROTEIN COMPLEX;
MONOCLONAL-ANTIBODIES; TYPE-1; GP120; IMMUNOGENS; TRIMERS; PANEL
AB The HIV envelope (Env) protein gp120 is protected from antibody recognition by a dense glycan shield. However, several of the recently identified PGT broadly neutralizing antibodies appear to interact directly with the HIV glycan coat. Crystal structures of antigen-binding fragments (Fabs) PGT 127 and 128 with Man(9) at 1.65 and 1.29 angstrom resolution, respectively, and glycan binding data delineate a specific high mannose-binding site. Fab PGT 128 complexed with a fully glycosylated gp120 outer domain at 3.25 angstroms reveals that the antibody penetrates the glycan shield and recognizes two conserved glycans as well as a short beta-strand segment of the gp120 V3 loop, accounting for its high binding affinity and broad specificify. Furthermore, our data suggest that the high neutralization potency of PGT 127 and 128 immunoglobulin Gs may be mediated by cross-linking Env trimers on the viral surface.
C1 [Doores, Katie J.; Walker, Laura M.; Ramos, Alejandra; Poignard, Pascal; Schief, William R.; Burton, Dennis R.] Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
[Pejchal, Robert; Doores, Katie J.; Walker, Laura M.; Khayat, Reza; Stanfield, Robyn L.; Julien, Jean-Philippe; Ramos, Alejandra; Ward, Andrew B.; Poignard, Pascal; Schief, William R.; Burton, Dennis R.; Wilson, Ian A.] Scripps Res Inst, IAVI Neutralizing Antibody Ctr, La Jolla, CA 92037 USA.
[Pejchal, Robert; Khayat, Reza; Stanfield, Robyn L.; Julien, Jean-Philippe; Ward, Andrew B.; Wilson, Ian A.] Scripps Res Inst, Dept Mol Biol, Skaggs Inst Chem Biol, La Jolla, CA 92037 USA.
[Doores, Katie J.; Burton, Dennis R.] Ragon Inst MGH MIT & Harvard, Cambridge, MA 02129 USA.
[Huang, Po-Ssu; Ogohara, Cassandra; Schief, William R.] Univ Washington, Dept Biochem, Seattle, WA 98195 USA.
[Wang, Sheng-Kai; Wong, Chi-Huey] Scripps Res Inst, Dept Chem, La Jolla, CA 92037 USA.
[Crispin, Max; Scanlan, Christopher N.] Univ Oxford, Dept Biochem, Oxford Glycobiol Inst, Oxford OX1 3QU, England.
[Depetris, Rafael; Sanders, Rogier W.; Moore, John P.] Cornell Univ, Weill Med Coll, New York, NY 10021 USA.
[Katpally, Umesh; Marozsan, Andre; Cupo, Albert; Olson, William C.] Progen Pharmaceut, Tarrytown, NY 10591 USA.
[Maloveste, Sebastien] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Liu, Yan; Feizi, Ten] Univ London Imperial Coll Sci Technol & Med, Dept Med, Glycosci Lab, London W12 0NN, England.
[McBride, Ryan; Paulson, James C.] Scripps Res Inst, Dept Physiol Chem, La Jolla, CA 92037 USA.
[Ito, Yukishige] RIKEN Adv Sci Inst, Wako, Saitama 3510198, Japan.
[Ito, Yukishige] Japan Sci & Technol Agcy, Exploratory Res Adv Technol, Wako, Saitama 3510198, Japan.
[Sanders, Rogier W.] Univ Amsterdam, Acad Med Ctr, Dept Med Microbiol, NL-1105 AZ Amsterdam, Netherlands.
[Poignard, Pascal] Int AIDS Vaccine Initiat, New York, NY 10038 USA.
RP Burton, DR (reprint author), Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
EM burton@scripps.edu; wilson@scripps.edu
RI McBride, Ryan/E-6812-2011; poignard, pascal/N-6678-2013; Ward,
Andrew/F-9203-2014; Ito, Yukishige/M-5119-2014; Liu, Yan/D-9117-2013;
OI Ward, Andrew/0000-0001-7153-3769; Ito, Yukishige/0000-0001-6251-7249;
Feizi, Ten/0000-0001-6495-0329; Doores, Katie/0000-0002-5507-1725
FU International AIDS Vaccine Initiative Neutralizing Antibody Center; NIH
[AI84817, AI74372]; National Institute of Allergy and Infectious
Diseases [AI33292]; Canadian Institutes of Health Research [FRN
HFE-224662]; HIV Vaccine Research and Design grant [AI082362]; UK
Research Councils' Basic Technology Initiative [GRS/79268]; Engineering
and Physical Sciences Research Council [EP/G037604/1]; National Cancer
Institute (NCI) [U01 CA128416, Y1-CO-1020]; Ragon Institute; NIH through
the National Center for Research Resources' [RR017573]; DOE Office of
Biological and Environmental Research; NIH's National Center for
Research Resources [P41RR001209]; National Institute of General Medical
Sciences (NIGMS) [Y1-GM-1104]; DOE, Basic Energy Sciences, Office of
Science [DE-AC02-06CH11357]
FX We thank Y. Hua, K. Le, and V. Thaney for technical assistance; D.
Ekiert for help with initial cloning of PGTs 125 and 126; X. Dai and X.
Zhu for help with x-ray data collection and analysis; C. Corbaci and C.
Williams for help with figure preparation; B. Walker for helpful
comments on the manuscript; and members of The Glycosciences Laboratory
for their collaboration in the establishment of the neoglycolipid-based
microarray system. This work was supported by the International AIDS
Vaccine Initiative Neutralizing Antibody Center, NIH grant AI84817 (I.
A. W.), National Institute of Allergy and Infectious Diseases grant
AI33292 (D. R. B.), NIH/National Research Service Award fellowship
AI74372 (R. P.), Canadian Institutes of Health Research fellowship FRN
HFE-224662 (J.-P.J.), HIV Vaccine Research and Design grant AI082362
(W.C.O., J.P.M., and I. A. W.), UK Research Councils' Basic Technology
Initiative "Glycoarrays" grant GRS/79268, Engineering and Physical
Sciences Research Council Translational Grant EP/G037604/1, National
Cancer Institute (NCI) Alliance of Glycobiologists for Detection of
Cancer and Cancer Risk grant U01 CA128416, and the Ragon Institute. The
three-dimensional reconstructions were conducted at the National
Resource for Automated Molecular Microscopy, which is supported by NIH
through the National Center for Research Resources' P41 program
(RR017573). Portions of this research were carried out at the Stanford
Synchrotron Radiation Lightsource (SSRL), a Directorate of the SLAC
National Accelerator Laboratory and an Office of Science User Facility
operated for the U. S. Department of Energy (DOE) Office of Science by
Stanford University. The SSRL Structural Molecular Biology Program is
supported by the DOE Office of Biological and Environmental Research;
NIH's National Center for Research Resources, Biomedical Technology
Program (P41RR001209); and the National Institute of General Medical
Sciences (NIGMS). Use of the Advanced Photon Source was supported by the
DOE, Basic Energy Sciences, Office of Science, under contract no.
DE-AC02-06CH11357. GM/CA CAT has been funded in whole or in part with
federal funds from NCI (grant Y1-CO-1020) and NIGMS (grant Y1-GM-1104).
Coordinates and structure factors for the Fab PGT 128/Man9,
Fab PGT 127/Man9, and Fab PGT 128/eODmV3 structures have been
deposited with the Protein Data Bank under accession codes 3TV3, 3TWC,
and 3TYG. The Fab PGT 128/d664G trimer EM reconstruction density has
been deposited with the Electron Microscopy Data Bank under accession
code EMD-1970. Progenics Pharmaceuticals and the Cornell Research
Foundation, on behalf of Cornell University, are the joint owners of U.
S. Patent 7,939,083 and have additional patent applications on the
stabilized Env trimer used in this manuscript. The IAVI and Theraclone
hold U. S. patent 61/515,528 on the PGT antibodies. The Scripps Research
Institute and IAVI have applied for a patent relating to the eODmV3
construct. Materials will be made available for noncommercial use under
material transfer agreements with Progenics or Cornell (stabilized Env
664G trimer), IAVI (PGT antibodies), and TSRI (eODmV3). This is
manuscript 21407-MB from The Scripps Research Institute.
NR 38
TC 350
Z9 351
U1 3
U2 68
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD NOV 25
PY 2011
VL 334
IS 6059
BP 1097
EP 1103
DI 10.1126/science.1213256
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 852AF
UT WOS:000297313900041
PM 21998254
ER
PT J
AU Rao, VK
Oliveira, JB
AF Rao, V. Koneti
Oliveira, Joao Bosco
TI How I treat autoimmune lymphoproliferative syndrome
SO BLOOD
LA English
DT Article
ID BONE-MARROW-TRANSPLANTATION; SOMATIC FAS MUTATIONS; SYNDROME ALPS;
LYMPHOCYTE APOPTOSIS; DOMINANT INHIBITION; GENE-MUTATIONS; CD95 GENE;
T-CELLS; DISEASE; CYTOPENIAS
AB Autoimmune lymphoproliferative syndrome (ALPS) represents a failure of apoptotic mechanisms to maintain lymphocyte homeostasis, permitting accumulation of lymphoid mass and persistence of autoreactive cells that often manifest in childhood with chronic nonmalignant lymphadenopathy, hepatosplenomegaly, and recurring multilineage cytopenias. Cytopenias in these patients can be the result of splenic sequestration as well as autoimmune complications manifesting as autoimmune hemolytic anemia, immune-mediated thrombocytopenia, and autoimmune neutropenia. More than 300 families with hereditary ALPS have now been described; nearly 500 patients from these families have been studied and followed worldwide over the last 20 years by our colleagues and ourselves. Some of these patients with FAS mutations affecting the intracellular portion of the FAS protein also have an increased risk of B-cell lymphoma. The best approaches to diagnosis, follow-up, and management of ALPS, its associated cytopenias, and other complications resulting from infiltrative lymphoproliferation and autoimmunity are presented. This trial was registered at www.clinicaltrial.gov as #NCT00001350. (Blood. 2011;118(22):5741-5751)
C1 [Rao, V. Koneti] NIAID, ALPS Unit, Lab Clin & Infect Dis, NIH, Bethesda, MD 20892 USA.
[Oliveira, Joao Bosco] NIH, Human Disorders Lymphocyte Homeostasis Unit, Serv Immunol, Dept Lab Med,Clin Ctr, Bethesda, MD 20892 USA.
RP Rao, VK (reprint author), NIAID, ALPS Unit, Lab Clin Infect Dis, NIH, 10 Ctr Dr,Rm 11N 230, Bethesda, MD 20892 USA.
EM korao@niaid.nih.gov
OI Oliveira, Joao/0000-0001-9388-8173
FU (Division of Intramural Research) of the National Institute of Allergy
and Infectious Diseases, National Institutes of Health
FX This work was supported by the Intramural Research Program (Division of
Intramural Research) of the National Institute of Allergy and Infectious
Diseases, National Institutes of Health.
NR 79
TC 37
Z9 40
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 24
PY 2011
VL 118
IS 22
BP 5741
EP 5751
DI 10.1182/blood-2011-07-325217
PG 11
WC Hematology
SC Hematology
GA 855PL
UT WOS:000297576600012
PM 21885601
ER
PT J
AU Klatt, NR
Vinton, CL
Lynch, RM
Canary, LA
Ho, J
Darrah, PA
Estes, JD
Seder, RA
Moir, SL
Brenchley, JM
AF Klatt, Nichole R.
Vinton, Carol L.
Lynch, Rebecca M.
Canary, Lauren A.
Ho, Jason
Darrah, Patricia A.
Estes, Jacob D.
Seder, Robert A.
Moir, Susan L.
Brenchley, Jason M.
TI SIV infection of rhesus macaques results in dysfunctional T- and B-cell
responses to neo and recall Leishmania major vaccination
SO BLOOD
LA English
DT Article
ID ACTIVE-ANTIRETROVIRAL-THERAPY; IMMUNODEFICIENCY-VIRUS-INFECTION;
FOLLICULAR DENDRITIC CELLS; INFLUENZA VACCINATION; HIV-1 INFECTION;
MEMORY CD4(+); IN-VIVO; INDIVIDUALS; ACTIVATION; DISEASE
AB HIV infection is characterized by immune system dysregulation, including depletion of CD4(+) T cells, immune activation, and abnormal B-and T-cell responses. However, the immunologic mechanisms underlying lymphocytic dysfunctionality and whether it is restricted to immune responses against neo antigens, recall antigens, or both is unclear. Here, we immunized SIV-infected and uninfected rhesus macaques to induce immune responses against neo and recall antigens using a Leishmania major polyprotein (MML) vaccine given with poly-ICLC adjuvant. We found that vaccinated SIV-uninfected animals induced high frequencies of polyfunctional MML-specific CD4(+) T cells. However, in SIV-infected animals, CD4(+) T-cell functionality decreased after both neo (P = .0025) and recall (P = .0080) MML vaccination. Furthermore, after SIV infection, the frequency of MML-specific antibody-secreting classic memory B cells was decreased compared with vaccinated, SIV-uninfected animals. Specifically, antibody-secreting classic memory B cells that produced IgA in response to either neo (P = .0221) or recall (P = .0356) MML vaccinations were decreased. Furthermore, we found that T-follicular helper cells, which are essential for priming B cells, are preferentially infected with SIV. These data indicate that SIV infection results in dysfunctional T-cell responses to neo and recall vaccinations, and direct SIV infection of T-follicular helper cells, both of which probably contribute to deficient B-cell responses and, presumably, susceptibility to certain opportunistic infections. (Blood. 2011;118(22):5803-5812)
C1 [Klatt, Nichole R.; Vinton, Carol L.; Canary, Lauren A.; Brenchley, Jason M.] NIAID, Program Barrier Immun & Repair, NIH, Bethesda, MD 20892 USA.
[Klatt, Nichole R.; Vinton, Carol L.; Canary, Lauren A.; Brenchley, Jason M.] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Lynch, Rebecca M.] NIAID, VRC, NIH, Bethesda, MD 20892 USA.
[Ho, Jason; Moir, Susan L.] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Darrah, Patricia A.; Seder, Robert A.] NIAID, Cellular Immunol Sect, VRC, NIH, Bethesda, MD 20892 USA.
[Estes, Jacob D.] NCI, AIDS & Canc Virus Program, SAIC, NIH, Frederick, MD 21701 USA.
RP Brenchley, JM (reprint author), NIAID, Program Barrier Immun & Repair, NIH, 9000 Rockville Pike,Bldg 4,Rm 301, Bethesda, MD 20892 USA.
EM jbrenchl@mail.nih.gov
FU Intramural National Institute of Allergy and Infectious Diseases,
National Institutes of Health
FX This study was supported by the Intramural National Institute of Allergy
and Infectious Diseases, National Institutes of Health program.
NR 56
TC 29
Z9 29
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 24
PY 2011
VL 118
IS 22
BP 5803
EP 5812
DI 10.1182/blood-2011-07-365874
PG 10
WC Hematology
SC Hematology
GA 855PL
UT WOS:000297576600020
PM 21960586
ER
PT J
AU Bushar, ND
Snyder, JT
Chakrabarty, S
Shen, JJ
Chen, Q
Ragheb, JA
AF Bushar, Nicholas D.
Snyder, James T.
Chakrabarty, Sagarika
Shen, Jijia
Chen, Qian
Ragheb, Jack A.
TI Peripheral blood monocytes, but not resting, activated, or transformed B
cells, costimulate early CD40L expression Response
SO BLOOD
LA English
DT Letter
ID DIFFERENTIATION
C1 [Ragheb, Jack A.] NIAID, Immunol Lab, Div Therapeut Prot, Off Biol Prod,Ctr Drug Evaluat & Res,US FDA,NIH, Bethesda, MD 20892 USA.
[Chakrabarty, Sagarika] Scripps Res Inst, La Jolla, CA 92037 USA.
[Shen, Jijia] Anhui Med Univ, Hefei, Anhui, Peoples R China.
[Chen, Qian] Harvard Univ, Ragon Inst, Boston, MA 02115 USA.
RP Ragheb, JA (reprint author), NIAID, Immunol Lab, Div Therapeut Prot, Off Biol Prod,Ctr Drug Evaluat & Res,US FDA,NIH, Bldg 10, Bethesda, MD 20892 USA.
EM jr50b@nih.gov
NR 5
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 24
PY 2011
VL 118
IS 22
BP 5980
EP 5981
DI 10.1182/blood-2011-09-372235
PG 4
WC Hematology
SC Hematology
GA 855PL
UT WOS:000297576600041
ER
PT J
AU Yanovski, SZ
AF Yanovski, Susan Z.
TI Obesity Treatment in Primary Care - Are We There Yet?
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
C1 NIDDK, Off Obes Res, NIH, Bethesda, MD 20892 USA.
RP Yanovski, SZ (reprint author), NIDDK, Off Obes Res, NIH, Bethesda, MD 20892 USA.
NR 5
TC 11
Z9 11
U1 0
U2 0
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 24
PY 2011
VL 365
IS 21
BP 2030
EP 2031
DI 10.1056/NEJMe1111487
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 851PF
UT WOS:000297282600014
PM 22085319
ER
PT J
AU Berg, CD
Aberle, DR
AF Berg, Christine D.
Aberle, Denise R.
CA Natl Lung Screening Trial Res Team
TI Reduced Lung-Cancer Mortality with CT Screening REPLY
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
C1 [Berg, Christine D.] NCI, Bethesda, MD 20892 USA.
[Aberle, Denise R.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
RP Berg, CD (reprint author), NCI, Bethesda, MD 20892 USA.
EM bergc@mail.nih.gov
RI Berg , Christine/K-1047-2014
NR 2
TC 0
Z9 0
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
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 24
PY 2011
VL 365
IS 21
BP 2037
EP 2038
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 851PF
UT WOS:000297282600026
ER
PT J
AU Maciag, AE
Nandurdikar, RS
Hong, SY
Chakrapan, H
Diwan, B
Morris, NL
Shami, PJ
Shiao, YH
Anderson, LM
Keefer, LK
Saavedra, JE
AF Maciag, Anna E.
Nandurdikar, Rahul S.
Hong, Sam Y.
Chakrapan, Harinath
Diwan, Bhalchandra
Morris, Nicole L.
Shami, Paul J.
Shiao, Yih-Horng
Anderson, Lucy M.
Keefer, Larry K.
Saavedra, Joseph E.
TI Activation of the c-Jun N-terminal Kinase/Activating Transcription
Factor 3 (ATF3) Pathway Characterizes Effective Arylated
Diazeniumdiolate-Based Nitric Oxide-Releasing Anticancer Prodrugs
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID CELL LUNG-CANCER; JS-K; IN-VITRO; ENDOTHELIAL-CELLS; INDUCED APOPTOSIS;
DEATH PATHWAY; DNA-DAMAGE; KINASE; GENE; VIVO
AB Improved therapies are needed for nonsmall cell lung cancer. Diazeniumdiolate-based nitric oxide (NO)-releasing prodrugs are a growing class of promising NO-based therapeutics. Recently, we have shown that O-2-(2,4-dinitrophenyl) 1-[(4-ethoxycarbonyl)piperazin-1-yl]diazen-1-ium-1,2-diolate (JS-K, 1) is effective against nonsmall cell lung cancer (NSCLC) cells in culture and in vivo. Here we report mechanistic studies with compound 1 and its homopiperazine analogue and structural modification of these into more stable prodrugs. Compound 1 and its., homopiperazine analogue were potent cytotoxic agents against NSCLC cells in vitro and in vivo, concomitant with activation of the SAPK/JNK stress pathway and upregulation of its downstream effector ATF3. Apoptosis followed these events. An aryl-substituted analogue, despite extended half-life in the presence of glutathione, did not activate JNK or have antitumor activity. The data suggest that rate of reactivity with glutathione and activation of JNK/ATF3 are determinants of cancer cell killing by these prodrugs.
C1 [Maciag, Anna E.; Diwan, Bhalchandra; Saavedra, Joseph E.] SAIC Frederick Inc, Basic Sci Program, NCI, Frederick, MD 21702 USA.
[Nandurdikar, Rahul S.; Hong, Sam Y.; Shiao, Yih-Horng; Anderson, Lucy M.; Keefer, Larry K.] NCI, Biol Chem Lab, Frederick, MD 21702 USA.
[Chakrapan, Harinath] Indian Inst Sci Educ & Res, Dept Chem, Pune 411008, Maharashtra, India.
[Morris, Nicole L.] SAIC Frederick Inc, Lab Anim Sci Program, NCI, Frederick, MD 21702 USA.
[Shami, Paul J.] Univ Utah, Div Hematol & Hematol Malignancies, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
RP Maciag, AE (reprint author), SAIC Frederick Inc, Basic Sci Program, NCI, Frederick, MD 21702 USA.
EM maciaga@mail.nih.gov
RI Keefer, Larry/N-3247-2014
OI Keefer, Larry/0000-0001-7489-9555
FU National Institutes of Health; National Cancer Institute
[HHSN261200800001E]
FX We thank Ken Kosak (University of Utah) for providing the Pluronics P123
formulation, Donna Butcher (PHL, SAIC-Frederick, Inc., NCI-Frederick)
for immunohistochemical analysis, Kathleen Noer and Guity Mohammadi
(Frederick-CCR Flow Cytometry Core, SAIC-Frederick, Inc., NCI-Frederick)
for FACS analysis, and Dr. Debanjan Biswas for critical comments on the
manuscript. This research was supported by the Intramural Research
Program of National Institutes of Health, National Cancer Institute, and
with federal funds from the National Cancer Institute under contract
HHSN261200800001E.
NR 22
TC 12
Z9 12
U1 0
U2 10
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
J9 J MED CHEM
JI J. Med. Chem.
PD NOV 24
PY 2011
VL 54
IS 22
BP 7751
EP 7758
DI 10.1021/jm2004128
PG 8
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 847VW
UT WOS:000297001600002
PM 22003962
ER
PT J
AU Skirzewski, M
Lopez, W
Mosquera, E
Betancourt, L
Catlow, B
Chiurillo, M
Loureiro, N
Hernandez, L
Rada, P
AF Skirzewski, M.
Lopez, W.
Mosquera, E.
Betancourt, L.
Catlow, B.
Chiurillo, M.
Loureiro, N.
Hernandez, L.
Rada, P.
TI ENHANCED GABAERGIC TONE IN THE VENTRAL PALLIDUM: MEMORY OF UNPLEASANT
EXPERIENCES?
SO NEUROSCIENCE
LA English
DT Article
DE GABA; vigabatrin; GABA-A receptor; ventral pallidum; forced swim test;
sucrose preference test
ID GAMMA-AMINOBUTYRIC-ACID; INDUCED FLUORESCENCE DETECTION; CEREBELLAR
GRANULE CELLS; ELEMENT-BINDING PROTEIN; SUBUNIT MESSENGER-RNAS;
EXTRACELLULAR GABA CONCENTRATION; CONDITIONED TASTE-AVERSION; CODES
HEDONIC REWARD; FREELY MOVING RATS; PORSOLT SWIM TEST
AB The nucleus accumbens (NAc) has emerged as an important part of the neural circuitry regulating depressive-like behaviors. Given that the NAc GABAergic medium spiny neurons project to the ventral pallidum (VP), it is reasonable to suggest that the VP may also be involved in these behaviors. Consequently, we explored the role of the VP GABAergic terminals during depressive-like behaviors in rats using the forced swim test (FST) and the sucrose preference test (SPT). Microdialysis coupled with micellar electrokinetic chromatography was used to monitor in vivo changes of GABA in the VP during the FST. GABA levels significantly increased during day-1 and day-2 during swimming, returning to the pre-swimming levels after the test. Basal concentrations of GABA on day-2 of the FST significantly increased with respect to day-1. In another set of experiments, intra-VP injections of vigabatrin (a GABA transaminase inhibitor) increased extracellular GABA and immobility behaviors in the FST while the direct GABAA receptor antagonist bicuculline reduced immobility behaviors. In the SPT, intra-VP vigabatrin injection significantly reduced preference for sucrose while bicuculline did not produce any change. At the postsynaptic side, we used semiquantitative RT-PCR to measure mRNA expression of 17 GABAA receptor subunits (alpha 1-alpha 6, beta 1-beta 3, gamma 2, delta, epsilon, 0, pi, and rho 1-rho 3) in rats subjected to the FST. We found a significant reduction of alpha 3 and gamma 2 subunit expression and an increase of 8 subunit expression after day-2 in rats
C1 [Skirzewski, M.; Lopez, W.; Mosquera, E.; Loureiro, N.] Univ Ctr Occidental Lisandro Alvarado, Lab Fisiol Celular, Barquisimeto 3001, Venezuela.
[Skirzewski, M.; Betancourt, L.; Hernandez, L.; Rada, P.] Univ Los Andes, Lab Fisiol Conducta, Fac Med, Merida 5101A, Venezuela.
[Betancourt, L.] Univ Los Andes, Histol Lab, Fac Med, Merida 5101A, Venezuela.
[Catlow, B.] NINDS, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Chiurillo, M.] Univ Ctr Occidental Lisandro Alvarado, Lab Genet Mol Dr Jorge Yunis Turbay, Barquisimeto 3001A, Venezuela.
RP Skirzewski, M (reprint author), Univ Ctr Occidental Lisandro Alvarado, Lab Fisiol Celular, Av Libertador Con Av Andres Bello, Barquisimeto 3001, Venezuela.
EM miguelsk@ucla.edu.ve
OI Skirzewski, Miguel/0000-0002-0980-0878
FU Consejo de Desarrollo Cientifico, Humanistico y Tecnologico (CDCHT-UCLA)
[014-ME-2007, 022-ME-2007]
FX This work was supported by Consejo de Desarrollo Cientifico, Humanistico
y Tecnologico (CDCHT-UCLA) grant numbers 014-ME-2007 and 022-ME-2007.
NR 133
TC 9
Z9 9
U1 0
U2 6
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4522
J9 NEUROSCIENCE
JI Neuroscience
PD NOV 24
PY 2011
VL 196
BP 131
EP 146
DI 10.1016/j.neuroscience.2011.08.058
PG 16
WC Neurosciences
SC Neurosciences & Neurology
GA 837OO
UT WOS:000296213300012
PM 21914462
ER
PT J
AU Wendte, JM
Gibson, AK
Grigg, ME
AF Wendte, Jered M.
Gibson, Amanda K.
Grigg, Michael E.
TI Population genetics of Toxoplasma gondii: New perspectives from parasite
genotypes in wildlife
SO VETERINARY PARASITOLOGY
LA English
DT Article
DE Toxoplasma gondii; Population genetics; Genotype; Wildlife
ID RACCOONS PROCYON-LOTOR; ENHYDRA-LUTRIS-NEREIS; WALLABIES
MACROPUS-RUFOGRISEUS; OPOSSUMS DIDELPHIS-VIRGINIANA; SARCOCYSTIS-NEURONA
STRAINS; DOLPHINS TURSIOPS-TRUNCATUS; SKUNK MEPHITIS-MEPHITIS;
MULTILOCUS PCR-RFLP; FREE-RANGE CHICKENS; ATYPICAL GENOTYPES
AB Toxoplasma gondii, a zoonotic protozoal parasite, is well-known for its global distribution and its ability to infect virtually all warm-blooded vertebrates. Nonetheless, attempts to describe the population structure of T. gondii have been primarily limited to samples isolated from humans and domesticated animals. More recent studies, however, have made efforts to characterize T. gondii isolates from a wider range of host species and geographic locales. These findings have dramatically changed our perception of the extent of genetic diversity in T. gondii and the relative roles of sexual recombination and clonal propagation in the parasite's lifecycle. In particular, identification of novel, disease-causing T. gondii strains in wildlife has raised concerns from both a conservation and public health perspective as to whether distinct domestic and sylvatic parasite gene pools exist. If so, overlap of these cycles may represent regions of high probability of disease emergence. Here, we attempt to answer these key questions by reviewing recent studies of T. gondii infections in wildlife, highlighting those which have advanced our understanding of the genetic diversity and population biology of this important zoonotic pathogen. Published by Elsevier B.V.
C1 [Wendte, Jered M.; Gibson, Amanda K.; Grigg, Michael E.] NIAID, Mol Parasitol Unit, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Wendte, Jered M.; Grigg, Michael E.] Oklahoma State Univ, Ctr Vet Hlth Sci, Dept Vet Pathobiol, Stillwater, OK 74074 USA.
RP Grigg, ME (reprint author), NIAID, Mol Parasitol Unit, Parasit Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM griggm@niaid.nih.gov
FU NIH; NIAID; Morris Animal Foundation [D10ZO-416]; [AI001018]
FX Thanks to all members of the Grigg lab for helpful discussions. This
work was supported by the Intramural Research program of the NIH and
NIAID, grant # AI001018 and The Morris Animal Foundation wildlife
training fellowship grant # D10ZO-416 (JMW). MEG is a scholar of the
Canadian Institute for Advanced Research (CIFAR) Program for Integrated
Microbial Biodiversity.
NR 158
TC 36
Z9 40
U1 5
U2 43
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-4017
J9 VET PARASITOL
JI Vet. Parasitol.
PD NOV 24
PY 2011
VL 182
IS 1
SI SI
BP 96
EP 111
DI 10.1016/j.vetpar.2011.07.018
PG 16
WC Parasitology; Veterinary Sciences
SC Parasitology; Veterinary Sciences
GA 834YY
UT WOS:000296001600009
PM 21824730
ER
PT J
AU Klase, Z
Houzet, L
Jeang, KT
AF Klase, Zachary
Houzet, Laurent
Jeang, Kuan-Teh
TI Replication competent HIV-1 viruses that express intragenomic microRNA
reveal discrete RNA-interference mechanisms that affect viral
replication
SO CELL AND BIOSCIENCE
LA English
DT Article
DE miRNA; HIV-1; RNA interference; viral replication; miR326; miR211
ID VECTORS ENCODING SHRNAS; CELLULAR MICRORNA; LENTIVIRAL VECTORS;
MESSENGER-RNAS; TAR ELEMENT; PROTEIN; DICER; INFECTION; SITES;
IDENTIFICATION
AB Background: It remains unclear whether retroviruses can encode and express an intragenomic microRNA (miRNA). Some have suggested that processing by the Drosha and Dicer enzymes might preclude the viability of a replicating retroviral RNA genome that contains a cis-embedded miRNA. To date, while many studies have shown that lentiviral vectors containing miRNAs can transduce mammalian cells and express the inserted miRNA efficiently, no study has examined the impact on the replication of a lentivirus such as HIV-1 after the deliberate intragenomic insertion of a bona fide miRNA.
Results: We have constructed several HIV-1 molecular clones, each containing a discrete cellular miRNA positioned in Nef. These retroviral genomes express the inserted miRNA and are generally replication competent in T-cells. The inserted intragenomic miRNA was observed to elicit two different consequences for HIV-1 replication. First, the expression of miRNAs with predicted target sequences in the HIV-1 genome was found to reduce viral replication. Second, in one case, where an inserted miRNA was unusually well-processed by Drosha, this processing event inhibited viral replication.
Conclusion: This is the first study to examine in detail the replication competence of HIV-1 genomes that express cis-embedded miRNAs. The results indicate that a replication competent retroviral genome is not precluded from encoding and expressing a viral miRNA.
C1 [Klase, Zachary; Houzet, Laurent; Jeang, Kuan-Teh] NIAID, Mol Virol Sect, Mol Microbiol Lab, Bethesda, MD 20892 USA.
RP Jeang, KT (reprint author), NIAID, Mol Virol Sect, Mol Microbiol Lab, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM kjeang@niaid.nih.gov
FU NIAID
FX ZK conceived of the study, participated in its design, performed the
molecular analyses and wrote the manuscript. LH participated in the
study design and assisted with the qPCR analysis. KTJ oversaw the work,
the design, and the conception of the experiments and wrote the
manuscript. All authors read and approved the final manuscript, and
support was from NIAID intramural funding.
NR 74
TC 9
Z9 9
U1 0
U2 2
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 23
PY 2011
VL 1
AR 38
DI 10.1186/2045-3701-1-38
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 982QN
UT WOS:000307060600001
PM 22112720
ER
PT J
AU Urano, Y
Sakabe, M
Kosaka, N
Ogawa, M
Mitsunaga, M
Asanuma, D
Kamiya, M
Young, MR
Nagano, T
Choyke, PL
Kobayashi, H
AF Urano, Yasuteru
Sakabe, Masayo
Kosaka, Nobuyuki
Ogawa, Mikako
Mitsunaga, Makoto
Asanuma, Daisuke
Kamiya, Mako
Young, Matthew R.
Nagano, Tetsuo
Choyke, Peter L.
Kobayashi, Hisataka
TI Rapid Cancer Detection by Topically Spraying a
gamma-Glutamyltranspeptidase-Activated Fluorescent Probe
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Article
ID GLUTAMYL-TRANSFERASE; OVARIAN-CANCER; PROTEASE ACTIVITY; MOUSE MODEL;
EXPRESSION; TUMORS; SERUM; GLUTAMYLTRANSFERASE; TRANSPEPTIDASE;
LAPAROSCOPY
AB The ability of the unaided human eye to detect small cancer foci or accurate borders between cancer and normal tissue during surgery or endoscopy is limited. Fluorescent probes are useful for enhancing visualization of small tumors but are typically limited by either high background signal or the requirement for administration hours to days before use. We synthesized a rapidly activatable, cancer-selective fluorescence imaging probe, gamma-glutamyl hydroxymethyl rhodamine green (gGlu-HMRG), with intramolecular spirocyclic caging for complete quenching. Activation occurs by rapid one-step cleavage of glutamate with gamma-glutamyltranspeptidase (GGT), which is not expressed in normal tissue, but is overexpressed on the cell membrane of various cancer cells, thus leading to complete uncaging and dequenching of the fluorescence probe. In vitro activation of gGlu-HMRG was evident in 11 human ovarian cancer cell lines tested. In vivo in mouse models of disseminated human peritoneal ovarian cancer, activation of gGlu-HMRG occurred within 1 min of topically spraying the tumor, creating high signal contrast between the tumor and the background. The gGlu-HMRG probe is practical for clinical application during surgical or endoscopic procedures because of its rapid and strong activation upon contact with GGT on the surface of cancer cells.
C1 [Urano, Yasuteru; Asanuma, Daisuke; Kamiya, Mako] Univ Tokyo, Grad Sch Med, Tokyo 1130033, Japan.
[Urano, Yasuteru] Japan Sci & Technol Agcy, Basic Res Program, Tokyo 1020075, Japan.
[Sakabe, Masayo; Nagano, Tetsuo] Univ Tokyo, Grad Sch Pharmaceut Sci, Tokyo 1130033, Japan.
[Kosaka, Nobuyuki; Ogawa, Mikako; Mitsunaga, Makoto; Choyke, Peter L.; Kobayashi, Hisataka] NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Young, Matthew R.] NCI, Lab Can Prevent, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
RP Urano, Y (reprint author), Univ Tokyo, Grad Sch Med, Tokyo 1130033, Japan.
EM uranokun@m.u-tokyo.ac.jp; kobayash@mail.nih.gov
RI Urano, Yasuteru/H-1380-2012
FU U.S. NIH, National Cancer Institute, Center for Cancer Research;
Ministry of Education, Culture, Sports, Science and Technology of Japan
[23249004, 20117003, 19205021]
FX This research was supported by the Intramural Research Program of the
U.S. NIH, National Cancer Institute, Center for Cancer Research. This
work was also financially supported by the Ministry of Education,
Culture, Sports, Science and Technology of Japan (grants 23249004,
20117003, and 19205021 to Y.U.).
NR 33
TC 116
Z9 117
U1 19
U2 94
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1946-6234
J9 SCI TRANSL MED
JI Sci. Transl. Med.
PD NOV 23
PY 2011
VL 3
IS 110
AR 110ra119
DI 10.1126/scitranslmed.3002823
PG 11
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 853EA
UT WOS:000297407800006
PM 22116934
ER
PT J
AU Kim, CH
Kim, HK
Rettig, RL
Kim, J
Lee, ET
Aprelikova, O
Choi, IJ
Munroe, DJ
Green, JE
AF Kim, Chang Hee
Kim, Hark K.
Rettig, R. Luke
Kim, Joseph
Lee, Eunbyul T.
Aprelikova, Olga
Choi, Il J.
Munroe, David J.
Green, Jeffrey E.
TI miRNA signature associated with outcome of gastric cancer patients
following chemotherapy
SO BMC MEDICAL GENOMICS
LA English
DT Article
ID COLORECTAL-CANCER; EXPRESSION; MICRORNAS; CELLS; RESISTANCE;
HSA-MIR-181B; PROGRESSION; SURVIVAL
AB Background: Identification of patients who likely will or will not benefit from cytotoxic chemotherapy through the use of biomarkers could greatly improve clinical management by better defining appropriate treatment options for patients. microRNAs may be potentially useful biomarkers that help guide individualized therapy for cancer because microRNA expression is dysregulated in cancer. In order to identify miRNA signatures for gastric cancer and for predicting clinical resistance to cisplatin/ fluorouracil (CF) chemotherapy, a comprehensive miRNA microarray analysis was performed using endoscopic biopsy samples.
Methods: Biopsy samples were collected prior to chemotherapy from 90 gastric cancer patients treated with CF and from 34 healthy volunteers. At the time of disease progression, post-treatment samples were additionally collected from 8 clinical responders. miRNA expression was determined using a custom-designed Agilent microarray. In order to identify a miRNA signature for chemotherapy resistance, we correlated miRNA expression levels with the time to progression (TTP) of disease after CF therapy.
Results: A miRNA signature distinguishing gastric cancer from normal stomach epithelium was identified. 30 miRNAs were significantly inversely correlated with TTP whereas 28 miRNAs were significantly positively correlated with TTP of 82 cancer patients (P<0.05). Prominent among the upregulated miRNAs associated with chemosensitivity were miRNAs known to regulate apoptosis, including let-7g, miR-342, miR-16, miR-181, miR-1, and miR-34. When this 58-miRNA predictor was applied to a separate set of pre-and post-treatment tumor samples from the 8 clinical responders, all of the 8 pre-treatment samples were correctly predicted as low-risk, whereas samples from the post-treatment tumors that developed chemoresistance were predicted to be in the high-risk category by the 58 miRNA signature, suggesting that selection for the expression of these miRNAs occurred as chemoresistance arose.
Conclusions: We have identified 1) a miRNA expression signature that distinguishes gastric cancer from normal stomach epithelium from healthy volunteers, and 2) a chemoreresistance miRNA expression signature that is correlated with TTP after CF therapy. The chemoresistance miRNA expression signature includes several miRNAs previously shown to regulate apoptosis in vitro, and warrants further validation.
C1 [Kim, Hark K.; Kim, Joseph; Lee, Eunbyul T.; Aprelikova, Olga; Green, Jeffrey E.] NCI, Lab Canc Biol & Genet, Bethesda, MD 20892 USA.
[Kim, Chang Hee; Rettig, R. Luke; Munroe, David J.] NCI, Adv Technol Program, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Kim, Hark K.; Choi, Il J.] Natl Canc Ctr, Goyang 410769, Gyeonggi, South Korea.
RP Green, JE (reprint author), NCI, Lab Canc Biol & Genet, Bethesda, MD 20892 USA.
EM jegreen@nih.gov
FU National Institute of Health; Center for Cancer Research; National
Cancer Institute; Ministry of Education, Science and Technology of Korea
[2010K001121, 2011K000888]; Korean National Cancer Center [0910570];
National Cancer Institute, National Institutes of Health
[HHSN261200800001E]
FX The work was supported in part by National Institute of Health
Intramural Program, Center for Cancer Research, National Cancer
Institute; by the Converging Research Center Program through the
Ministry of Education, Science and Technology of Korea (2010K001121 ->
2011K000888); by the Korean National Cancer Center Grant 0910570; and in
part with federal funds from the National Cancer Institute, National
Institutes of Health, under contract HHSN261200800001E.
NR 25
TC 63
Z9 70
U1 0
U2 13
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 23
PY 2011
VL 4
AR 79
DI 10.1186/1755-8794-4-79
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 898VZ
UT WOS:000300771800001
PM 22112324
ER
PT J
AU Correa-Cerro, LS
Piao, YL
Sharov, AA
Nishiyama, A
Cadet, JS
Yu, H
Sharova, LV
Xin, L
Hoang, HG
Thomas, M
Qian, Y
Dudekula, DB
Meyers, E
Binder, BY
Mowrer, G
Bassey, U
Longo, DL
Schlessinger, D
Ko, MSH
AF Correa-Cerro, Lina S.
Piao, Yulan
Sharov, Alexei A.
Nishiyama, Akira
Cadet, Jean S.
Yu, Hong
Sharova, Lioudmila V.
Xin, Li
Hoang, Hien G.
Thomas, Marshall
Qian, Yong
Dudekula, Dawood B.
Meyers, Emily
Binder, Bernard Y.
Mowrer, Gregory
Bassey, Uwem
Longo, Dan L.
Schlessinger, David
Ko, Minoru S. H.
TI Generation of mouse ES cell lines engineered for the forced induction of
transcription factors
SO SCIENTIFIC REPORTS
LA English
DT Article
ID GENE SET ENRICHMENT; MICROARRAY DATA; GENOME-WIDE; EXPRESSION; NETWORKS;
SYSTEM
AB Here we report the generation and characterization of 84 mouse ES cell lines with doxycycline-controllable transcription factors (TFs) which, together with the previous 53 lines, cover 7-10% of all TFs encoded in the mouse genome. Global gene expression profiles of all 137 lines after the induction of TFs for 48 hrs can associate each TF with the direction of ES cell differentiation, regulatory pathways, and mouse phenotypes. These cell lines and microarray data provide building blocks for a variety of future biomedical research applications as a community resource.
C1 [Correa-Cerro, Lina S.; Piao, Yulan; Sharov, Alexei A.; Nishiyama, Akira; Cadet, Jean S.; Yu, Hong; Sharova, Lioudmila V.; Xin, Li; Hoang, Hien G.; Thomas, Marshall; Qian, Yong; Dudekula, Dawood B.; Meyers, Emily; Binder, Bernard Y.; Mowrer, Gregory; Bassey, Uwem; Longo, Dan L.; Schlessinger, David; Ko, Minoru S. H.] NIA, NIH, Baltimore, MD 21224 USA.
RP Ko, MSH (reprint author), NIA, NIH, Baltimore, MD 21224 USA.
EM kom@mail.nih.gov
RI Ko, Minoru/B-7969-2009;
OI Ko, Minoru/0000-0002-3530-3015; Dudekula, Dawood/0000-0002-4054-1827
FU NIH, National Institute on Aging
FX This research was supported entirely by the Intramural Research Program
of the NIH, National Institute on Aging.
NR 22
TC 17
Z9 17
U1 0
U2 2
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 23
PY 2011
VL 1
AR 167
DI 10.1038/srep00167
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 896IX
UT WOS:000300560100002
PM 22355682
ER
PT J
AU Sherman, E
Barr, V
Manley, S
Patterson, G
Balagopalan, L
Akpan, I
Regan, CK
Merrill, RK
Sommers, CL
Lippincott-Schwartz, J
Samelson, LE
AF Sherman, Eilon
Barr, Valerie
Manley, Suliana
Patterson, George
Balagopalan, Lakshmi
Akpan, Itoro
Regan, Carole K.
Merrill, Robert K.
Sommers, Connie L.
Lippincott-Schwartz, Jennifer
Samelson, Lawrence E.
TI Functional Nanoscale Organization of Signaling Molecules Downstream of
the T Cell Antigen Receptor
SO IMMUNITY
LA English
DT Article
ID IMMUNOLOGICAL SYNAPSE; PROTEIN NETWORKS; ACTIVATION; ACTIN; DOMAINS;
COMPLEX; LAT; MICROCLUSTERS; MICROSCOPY; CLUSTERS
AB Receptor-regulated cellular signaling often is mediated by formation of transient, heterogeneous protein complexes of undefined structure. We used single and two-color photoactivated localization microscopy to study complexes downstream of the T cell antigen receptor (TCR) in single-molecule detail at the plasma membrane of intact T cells. The kinase ZAP-70 distributed completely with the TCR zeta chain and both partially mixed with the adaptor LAT in activated cells, thus showing localized activation of LAT by TCR-coupled ZAP-70. In resting and activated cells, LAT primarily resided in nanoscale clusters as small as dimers whose formation depended on protein-protein and protein-lipid interactions. Surprisingly, the adaptor SLP-76 localized to the periphery of LAT clusters. This nanoscale structure depended on polymerized actin and its disruption affected TCR-dependent cell function. These results extend our understanding of the mechanism of T cell activation and the formation and organization of TCR-mediated signaling complexes, findings also relevant to other receptor systems.
C1 [Sherman, Eilon; Barr, Valerie; Balagopalan, Lakshmi; Akpan, Itoro; Regan, Carole K.; Merrill, Robert K.; Sommers, Connie L.; Samelson, Lawrence E.] NCI, Lab Cellular & Mol Biol, NIH, Bethesda, MD 20892 USA.
[Manley, Suliana; Patterson, George; Lippincott-Schwartz, Jennifer] NICHD, Cell Biol & Metab Program, NIH, Bethesda, MD 20892 USA.
RP Samelson, LE (reprint author), NCI, Lab Cellular & Mol Biol, NIH, Bethesda, MD 20892 USA.
EM samelson@helix.nih.gov
RI Manley, Suliana/D-3818-2012; Sherman, Eilon /B-3688-2014
OI Manley, Suliana/0000-0002-4755-4778; Sherman, Eilon /0000-0002-7403-6036
FU National Cancer Institute (The Center for Cancer Research); Eunice
Kennedy Shriver National Institute of Child Health and Human Development
FX The authors would like to thank B.J. Taylor at the NCI Flow Cytometry
Core Facility, Zeiss, H. Hess (HHMI, Janelia Farm) for providing the
PALM software, W. Lased (University of Maryland) for multiple
discussions on data analyses, and T. Wiegand (Helmholtz Centre for
Environmental Research - UFZ) for providing us his point-pattern
analyses software. We thank P. Sengupta, M. Renz, and T.
Jovanovic-Talisman (NIH/NICHD) for reading the manuscript. This research
was supported by the Intramural Research Programs of the National Cancer
Institute (The Center for Cancer Research) and of the Eunice Kennedy
Shriver National Institute of Child Health and Human Development.
NR 39
TC 125
Z9 127
U1 6
U2 22
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD NOV 23
PY 2011
VL 35
IS 5
BP 705
EP 720
DI 10.1016/j.immuni.2011.10.004
PG 16
WC Immunology
SC Immunology
GA 852XM
UT WOS:000297390800011
PM 22055681
ER
PT J
AU Siegel, AM
Heimall, J
Freeman, AF
Hsu, AP
Brittain, E
Brenchley, JM
Douek, DC
Fahle, GH
Cohen, JI
Holland, SM
Milner, JD
AF Siegel, Andrea M.
Heimall, Jennifer
Freeman, Alexandra F.
Hsu, Amy P.
Brittain, Erica
Brenchley, Jason M.
Douek, Daniel C.
Fahle, Gary H.
Cohen, Jeffrey I.
Holland, Steven M.
Milner, Joshua D.
TI A Critical Role for STAT3 Transcription Factor Signaling in the
Development and Maintenance of Human T Cell Memory
SO IMMUNITY
LA English
DT Article
ID HYPER-IGE SYNDROME; CHRONIC VIRAL-INFECTION; X-LINKED
AGAMMAGLOBULINEMIA; FOLLICULAR-HELPER-CELLS; EPSTEIN-BARR-VIRUS; TH17
CELLS; FUNGAL-INFECTIONS; HERPES-ZOSTER; GENERATION; RECEPTOR
AB STAT3 transcription factor signaling in specific T helper cell differentiation has been well described, although the broader roles for STAT3 in lymphocyte memory are less clear. Patients with autosomal-dominant hyper-IgE syndrome (AD-HIES) carry dominant-negative STAT3 mutations and are susceptible to a variety of bacterial and fungal infections. We found that AD-HIES patients have a cell-intrinsic defect in the number of central memory CD4(+) and CD8(+) T cells compared to healthy controls. Naive T cells from AD-HIES patients had lower expression of memory-related transcription factors BCL6 and SOCS3, a primary proliferation defect, and they failed to acquire central memory-like surface phenotypes in vitro. AD-HIES patients showed a decreased ability to control varicella zoster virus (VZV) and Epstein-Barr virus (EBV) latency, and T cell memory to both of these viruses was compromised. These data point to a specific role for STAT3 in human central memory T cell formation and in control of certain chronic viruses.
C1 [Siegel, Andrea M.; Milner, Joshua D.] NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA.
[Heimall, Jennifer; Freeman, Alexandra F.; Hsu, Amy P.; Holland, Steven M.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Brittain, Erica] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
[Brenchley, Jason M.] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Douek, Daniel C.] NIAID, Human Immunol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Cohen, Jeffrey I.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Fahle, Gary H.] NIH, Microbiol Serv, Div Lab Med, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA.
RP Milner, JD (reprint author), NIAID, Lab Allerg Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM jdmilner@niaid.nih.gov
FU NIAID
FX The authors would like to thank all of the members of the J.D.M.
laboratory for their helpful discussions. We would like to thank the
Flow Cytometry Core for all of their sorting assistance. We thank all of
the patients and clinical staff whose dedication to human research was
invaluable. This work was supported by the intramural research program
of the NIAID. A.M.S., J.H., A.P.H., J.M.B., G.H.F., and J.D.M. performed
experiments and analyzed data. J.H., A.F.F., S.M.H., and J.D.M.
evaluated patients and obtained samples. E.B. performed statistical
analysis. J.I.C. and D.C.D. provided sample material and analysis.
A.M.S., J.H., and J.D.M. conceived the study, designed experiments, and
interpreted data. A.M.S. and J.D.M. wrote the manuscript.
NR 63
TC 92
Z9 95
U1 1
U2 15
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD NOV 23
PY 2011
VL 35
IS 5
BP 806
EP 818
DI 10.1016/j.immuni.2011.09.016
PG 13
WC Immunology
SC Immunology
GA 852XM
UT WOS:000297390800019
PM 22118528
ER
PT J
AU Chen, JJ
Dexheimer, TS
Ai, YX
Liang, Q
Villamil, MA
Inglese, J
Maloney, DJ
Jadhav, A
Simeonov, A
Zhuang, ZH
AF Chen, Junjun
Dexheimer, Thomas S.
Ai, Yongxing
Liang, Qin
Villamil, Mark A.
Inglese, James
Maloney, David J.
Jadhav, Ajit
Simeonov, Anton
Zhuang, Zhihao
TI Selective and Cell-Active Inhibitors of the USP1/UAF1 Deubiquitinase
Complex Reverse Cisplatin Resistance in Non-small Cell Lung Cancer Cells
SO CHEMISTRY & BIOLOGY
LA English
DT Article
ID SMALL-MOLECULE INHIBITOR; FANCONI-ANEMIA PATHWAY; MONOUBIQUITINATED
PCNA; POLYUBIQUITIN CHAINS; SCREENING ASSAYS; POLYMERASE-ETA;
DNA-DAMAGE; UBIQUITIN; PROTEASOME; ENZYME
AB Ubiquitin-specific proteases (USPs) have in recent years emerged as a promising therapeutic target class. We identified selective small-molecule inhibitors against a deubiquitinase complex, the human USP1/UAF1, through quantitative high throughput screening (qHTS) of a collection of bioactive molecules. The top inhibitors, pimozide and GW7647, inhibited USP1/UAF1 noncompetitively with a K(i) of 0.5 and 0.7 mu M, respectively, and displayed selectivity against a number of deubiquitinases, deSUMOylase, and cysteine proteases. The USP1/UAF1 inhibitors act synergistically with cisplatin in inhibiting cisplatin-resistant non-small cell lung cancer (NSCLC) cell proliferation. USP1/UAF1 represents a promising target for drug intervention because of its involvement in translesion synthesis and Fanconi anemia pathway important for normal DNA damage response. Our results support USP1/UAF1 as a potential therapeutic target and provide an example of targeting the USP/WD40 repeat protein complex for inhibitor discovery.
C1 [Dexheimer, Thomas S.; Inglese, James; Maloney, David J.; Jadhav, Ajit; Simeonov, Anton] NHGRI, NIH Chem Genom Ctr, NIH, Bethesda, MD 20892 USA.
[Chen, Junjun; Ai, Yongxing; Liang, Qin; Villamil, Mark A.; Zhuang, Zhihao] Univ Delaware, Dept Chem & Biochem, Newark, DE 19716 USA.
RP Simeonov, A (reprint author), NHGRI, NIH Chem Genom Ctr, NIH, 9800 Med Ctr Dr,MSC 3370, Bethesda, MD 20892 USA.
EM asimeono@mail.nih.gov; zzhuang@udel.edu
RI liang, qin/C-8284-2016
FU US National Institute of Health [R03 DA030552]; Molecular Libraries
Program; National Human Genome Research Institute, National Institutes
of Health
FX This work was supported in part by a grant from the US National
Institute of Health to Z.Z. (Grant R03 DA030552), the Molecular
Libraries Program, and the Intramural Research Program of the National
Human Genome Research Institute, National Institutes of Health. We thank
Zhijiang Van and Weidong Wang at National Institute on Aging for the
protocol of FANCD2 western blot analysis. We also thank Douglas A. Gray
and Jan Brun in Ottawa Health Research Institute for the protocol of
PCNA western blot analysis.
NR 56
TC 67
Z9 71
U1 1
U2 11
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-5521
J9 CHEM BIOL
JI Chem. Biol.
PD NOV 23
PY 2011
VL 18
IS 11
BP 1390
EP 1400
DI 10.1016/j.chembiol.2011.08.014
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 855ZA
UT WOS:000297603600011
PM 22118673
ER
PT J
AU Duckworth, BP
Geders, TW
Tiwari, D
Boshoff, HI
Sibbald, PA
Barry, CE
Schnappinger, D
Finzel, BC
Aldrich, CC
AF Duckworth, Benjamin P.
Geders, Todd W.
Tiwari, Divya
Boshoff, Helena I.
Sibbald, Paul A.
Barry, Clifton E., III
Schnappinger, Dirk
Finzel, Barry C.
Aldrich, Courtney C.
TI Bisubstrate Adenylation Inhibitors of Biotin Protein Ligase from
Mycobacterium tuberculosis
SO CHEMISTRY & BIOLOGY
LA English
DT Article
ID ISOTHERMAL TITRATION CALORIMETRY; SIDEROPHORE BIOSYNTHESIS; BINDING
ENERGETICS; ESCHERICHIA-COLI; COA CARBOXYLASE; GENE-EXPRESSION;
FATTY-ACID; AMP LIGASE; SPECIFICITY; SYNTHETASE
AB The mycobacterial biotin protein ligase (MtBPL) globally regulates lipid metabolism in Mtb through the posttranslational biotinylation of acyl coenzyme A carboxylases involved in lipid biosynthesis that catalyze the first step in fatty acid biosynthesis and pyruvate coenzyme A carboxylase, a gluconeogenic enzyme vital for lipid catabolism. Here we describe the design, development, and evaluation of a rationally designed bisubstrate inhibitor of MtBPL. This inhibitor displays potent subnanomolar enzyme inhibition and antitubercular activity against multidrug resistant and extensively drug resistant Mtb strains. We show that the inhibitor decreases in vivo protein biotinylation of key enzymes involved in fatty acid biosynthesis and that the antibacterial activity is MtBPL dependent. Additionally, the gene encoding BPL was found to be essential in M. smegmatis. Finally, the X-ray cocrystal structure of inhibitor bound MtBPL was solved providing detailed insight for further structure-activity analysis. Collectively, these data suggest that MtBPL is a promising target for further antitubercular therapeutic development.
C1 [Duckworth, Benjamin P.; Sibbald, Paul A.; Aldrich, Courtney C.] Univ Minnesota, Ctr Drug Design, Minneapolis, MN 55455 USA.
[Geders, Todd W.; Finzel, Barry C.] Univ Minnesota, Dept Med Chem, Minneapolis, MN 55455 USA.
[Tiwari, Divya; Schnappinger, Dirk] Weill Cornell Med Coll, Dept Microbiol & Immunol, New York, NY 10065 USA.
[Boshoff, Helena I.; Barry, Clifton E., III] NIAID, TB Res Sect, Bethesda, MD 20892 USA.
RP Aldrich, CC (reprint author), Univ Minnesota, Ctr Drug Design, Minneapolis, MN 55455 USA.
EM aldri015@umn.edu
RI Barry, III, Clifton/H-3839-2012;
OI Finzel, Barry/0000-0001-8761-3384
FU National Institutes of Health [AI-091790]; Bill and Melinda Gates
Foundation; Wellcome Trust through the Grand Challenges in Global Health
Initiative; National Institutes of Health National Institute of Allergy
and Infectious Disease
FX This research was supported by the National Institutes of Health (Grant
AI-091790 to D.S. and C.C.A.), the Bill and Melinda Gates Foundation and
the Wellcome Trust through the Grand Challenges in Global Health
Initiative (support to Douglas Young, Imperial College), and the
Intramural Research Program of the National Institutes of Health
National Institute of Allergy and Infectious Disease (support to
C.E.B.). We thank Dr. Sabine Ehrt for enolase specific antiserum, Dr.
Christine Salomon and Mr. Michael Donald for antimicrobial specificity
testing, and Dr. David Ferguson and Mr. Adam Benoit for DU145 cell
testing.
NR 52
TC 28
Z9 28
U1 1
U2 11
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-5521
J9 CHEM BIOL
JI Chem. Biol.
PD NOV 23
PY 2011
VL 18
IS 11
BP 1432
EP 1441
DI 10.1016/j.chembiol.2011.08.013
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 855ZA
UT WOS:000297603600015
PM 22118677
ER
PT J
AU Cruz, PG
Auld, DS
Schultz, PJ
Lovell, S
Battaile, KP
MacArthur, R
Shen, M
Tamayo-Castillo, G
Inglese, J
Sherman, DH
AF Cruz, Patricia G.
Auld, Douglas S.
Schultz, Pamela J.
Lovell, Scott
Battaile, Kevin P.
MacArthur, Ryan
Shen, Min
Tamayo-Castillo, Giselle
Inglese, James
Sherman, David H.
TI Titration-Based Screening for Evaluation of Natural Product Extracts:
Identification of an Aspulvinone Family of Luciferase Inhibitors
SO CHEMISTRY & BIOLOGY
LA English
DT Article
ID ASPERGILLUS-TERREUS; FIREFLY LUCIFERASE; CHEMICAL LIBRARIES; DRUG
DISCOVERY; MOLECULAR-GRAPHICS; MECHANISM; ASSAYS; STABILIZATION;
DIFFRACTION; DERIVATIVES
AB The chemical diversity of nature has tremendous potential for the discovery of molecular probes and medicinal agents. However, sensitivity of HTS assays to interfering components of crude extracts derived from plants, and macro- and microorganisms has curtailed their use in lead discovery. Here, we describe a process for leveraging the concentration-response curves obtained from quantitative HTS to improve the initial selection of "actives" from a library of partially fractionated natural product extracts derived from marine actinomycetes and fungi. By using pharmacological activity, the first-pass CRC paradigm improves the probability that labor-intensive subsequent steps of reculturing, extraction, and bioassay-guided isolation of active component(s) target the most promising strains and growth conditions. We illustrate how this process identified a family of fungal metabolites as potent inhibitors of firefly luciferase, subsequently resolved in molecular detail by X-ray crystallography.
C1 [Auld, Douglas S.; MacArthur, Ryan; Shen, Min; Inglese, James] NHGRI, NIH Chem Genom Ctr, NIH, Bethesda, MD 20892 USA.
[Cruz, Patricia G.; Schultz, Pamela J.; Sherman, David H.] Univ Michigan, Inst Life Sci, Ann Arbor, MI 48109 USA.
[Sherman, David H.] Univ Michigan, Dept Med Chem, Ann Arbor, MI 48109 USA.
[Sherman, David H.] Univ Michigan, Dept Chem, Ann Arbor, MI 48109 USA.
[Sherman, David H.] Univ Michigan, Dept Microbiol & Immunol, Ann Arbor, MI 48109 USA.
[Lovell, Scott] Univ Kansas, Del Shankel Struct Biol Ctr, Prot Struct Lab, Lawrence, KS 66047 USA.
[Battaile, Kevin P.] Argonne Natl Lab, Hauptman Woodward Med Res Inst, IMCA CAT, Argonne, IL 60439 USA.
[Tamayo-Castillo, Giselle] Univ Costa Rica, Escuela Quim, San Pedro 2060, Costa Rica.
[Tamayo-Castillo, Giselle] Inst Nacl Biodiversidad INBio, Unidad Estrateg Bioprospecc, Santo Domingo De Heredia, Costa Rica.
RP Inglese, J (reprint author), NHGRI, NIH Chem Genom Ctr, NIH, Bethesda, MD 20892 USA.
EM jinglese@mail.nih.gov; davidhs@umich.edu
RI Tamayo, Giselle/J-3609-2015;
OI Tamayo, Giselle/0000-0002-4912-8895; Battaile, Kevin/0000-0003-0833-3259
FU Industrial Macromolecular Crystallography Association; Hauptman-Woodward
Medical Research Institute; U.S. Department of Energy, Office of
Science, Office of Basic Energy Sciences [DE-AC02-06CH11357]; NIH from
the National Center for Research Resources [P20 RR-17708]; NIH Roadmap
for Medical Research; NIH as part of the International Cooperative
Biodiversity Group initiative at the Fogarty International Center [U01
TW007404]; Spanish Foundation of Science and Technology (FECYT)
FX The authors gratefully acknowledge Shao-Liang Zheng for the aspulvinone
F X-ray diffraction studies and Christopher Rath for assistance with
mass spectra interpretation (University of Michigan). At the NCGC, we
acknowledge Sam Michael and Paul Shinn for automation and sample
management support, and Adam Yasgar, Anton Simeonov, Ron Johnson, and
Wei Zheng for examining NPEs in several MLPCN assays. Use of the
IMCA-CAT beamline 17-ID at the Advanced Photon Source was supported by
the companies of the Industrial Macromolecular Crystallography
Association through a contract with Hauptman-Woodward Medical Research
Institute. Use of the Advanced Photon Source was supported by the U.S.
Department of Energy, Office of Science, Office of Basic Energy
Sciences, under Contract No. DE-AC02-06CH11357. Use of the University of
Kansas COBRE Protein Structure Laboratory was supported by NIH Grant
Number P20 RR-17708 from the National Center for Research Resources.
This work was supported by the NIH Roadmap for Medical Research (to J.I.
and D.S.A.), NIH Grant U01 TW007404 as part of the International
Cooperative Biodiversity Group initiative at the Fogarty International
Center, and the Hans W. Vahlteich Professorship (to OHS.). P.G.C.
gratefully acknowledges the Spanish Foundation of Science and Technology
(FECYT) for a postdoctoral fellowship. We thank the Technical Office,
CONAGEBIO, Ministry of the Environment and Telecommunications, Costa
Rica for providing sample collection permits.
NR 46
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Z9 18
U1 1
U2 19
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-5521
J9 CHEM BIOL
JI Chem. Biol.
PD NOV 23
PY 2011
VL 18
IS 11
BP 1442
EP 1452
DI 10.1016/j.chembiol.2011.08.011
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 855ZA
UT WOS:000297603600016
PM 22118678
ER
PT J
AU Anthis, NJ
Doucleff, M
Clore, GM
AF Anthis, Nicholas J.
Doucleff, Michaeleen
Clore, G. Marius
TI Transient, Sparsely Populated Compact States of Apo and Calcium-Loaded
Calmodulin Probed by Paramagnetic Relaxation Enhancement: Interplay of
Conformational Selection and Induced Fit
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID MOLECULAR-STRUCTURE DETERMINATION; PROTEIN-PROTEIN ASSOCIATION;
LIGHT-CHAIN KINASE; BIOLOGICAL MACROMOLECULES; ENCOUNTER COMPLEXES;
TARGET RECOGNITION; PEPTIDE COMPLEX; NMR RELAXATION; XPLOR-NIH; BINDING
AB Calmodulin (CaM) is the universal calcium sensor in eukaryotes, regulating the function of numerous proteins. Crystallography and NMR show that free CaM-4Ca(2+) exists in an extended conformation with significant interdomain separation, but clamps down upon target peptides to form a highly compact structure. NMR has revealed substantial interdomain motions in CaM-4Ca(2+), enabled by a flexible linker. In one instance, CaM-4Ca(2+) has been crystallized in a compact configuration; however, no direct evidence for transient interdomain contacts has been observed in solution, and little is known about how large-scale interdomain motions contribute to biological function. Here, we use paramagnetic relaxation enhancement (PRE) to characterize transient compact states of free CaM that are too sparsely populated to observe by traditional NMR methods. We show that unbound CaM samples a range of compact structures, populated at 5-10%, and that Ca(2+) dramatically alters the distribution of these configurations in favor of states resembling the peptide-bound structure. In the absence of Ca(2+), the target peptide binds only to the C-terminal domain, and the distribution of compact states is similar with and without peptide. These data suggest an alternative pathway of CaM action in which CaM remains associated with its kinase targets even in the resting state. Only CaM-4Ca(2+), however, shows an innate propensity to form the physiologically active compact structures, suggesting that Ca(2+) activates CaM not only through local structural changes within each domain but also through more global remodeling of interdomain interactions. Thus, these findings illustrate the subtle interplay between conformational selection and induced fit.
C1 [Anthis, Nicholas J.; Doucleff, Michaeleen; Clore, G. Marius] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Clore, GM (reprint author), NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
EM mariusc@mail.nih.gov
RI Clore, G. Marius/A-3511-2008
OI Clore, G. Marius/0000-0003-3809-1027
FU NIH, NIDDK; Office of the Director of the NIH
FX We thank Ad Bax, Dusty Baber, Dan Garrett, Charles Schwieters, Nico
Tjandra, and Jinfa Ying for useful discussions, and Max Valenstein for
technical support. This work was supported by the Intramural Program of
the NIH, NIDDK, and the Intramural AIDS Targeted Antiviral Program of
the Office of the Director of the NIH (to G.M.C.)
NR 52
TC 54
Z9 54
U1 3
U2 26
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD NOV 23
PY 2011
VL 133
IS 46
BP 18966
EP 18974
DI 10.1021/ja2082813
PG 9
WC Chemistry, Multidisciplinary
SC Chemistry
GA 853AP
UT WOS:000297398900068
PM 21999431
ER
PT J
AU Brooks, MJ
Rajasimha, HK
Roger, JE
Swaroop, A
AF Brooks, Matthew J.
Rajasimha, Harsha K.
Roger, Jerome E.
Swaroop, Anand
TI Next-generation sequencing facilitates quantitative analysis of
wild-type and Nrl(-/-) retinal transcriptomes
SO MOLECULAR VISION
LA English
DT Article
ID GENE-EXPRESSION ANALYSIS; RNA-SEQ; MOUSE RETINA; COMPREHENSIVE ANALYSIS;
COMPLETE GENOME; MICROARRAY; NRL; PHOTORECEPTORS; IDENTIFICATION;
PSEUDOGENES
AB Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived retinal transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT-PCR) methods and to evaluate protocols for optimal high-throughput data analysis.
Methods: Retinal mRNA profiles of 21-day-old wild-type (WT) and neural retina leucine zipper knockout (Nrl(-/-)) mice were generated by deep sequencing, in triplicate, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows-Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT-PCR validation was performed using TaqMan and SYBR Green assays.
Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (build mm9) and identified 16,014 transcripts in the retinas of WT and Nrl(-/-)mice with BWA workflow and 34,115 transcripts with TopHat workflow. RNA-seq data confirmed stable expression of 25 known housekeeping genes, and 12 of these were validated with qRT-PCR. RNA-seq data had a linear relationship with qRT-PCR for more than four orders of magnitude and a goodness of fit (R-2) of 0.8798. Approximately 10% of the transcripts showed differential expression between the WT and Nrl(-/-)retina, with a fold change >= 1.5 and p value < 0.05. Altered expression of 25 genes was confirmed with qRT-PCR, demonstrating the high degree of sensitivity of the RNA-seq method. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to retinal function. Data analysis with BWA and TopHat workflows revealed a significant overlap yet provided complementary insights in transcriptome profiling.
Conclusions: Our study represents the first detailed analysis of retinal transcriptomes, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.
C1 [Brooks, Matthew J.; Rajasimha, Harsha K.; Roger, Jerome E.; Swaroop, Anand] NEI, Neurobiol Neurodegenerat & Repair Lab, NIH, Bethesda, MD 20892 USA.
RP Swaroop, A (reprint author), NEI, Neurobiol Neurodegenerat & Repair Lab, NIH, MSC0610,6 Ctr Dr, Bethesda, MD 20892 USA.
EM swaroopa@nei.nih.gov
OI Swaroop, Anand/0000-0002-1975-1141
FU National Eye Institute, National Institutes of Health, Bethesda, MD
FX This research was supported by Intramural Research Program of the
National Eye Institute, National Institutes of Health, Bethesda, MD.
NR 72
TC 46
Z9 46
U1 1
U2 9
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 23
PY 2011
VL 17
IS 327-30
BP 3034
EP 3054
PG 21
WC Biochemistry & Molecular Biology; Ophthalmology
SC Biochemistry & Molecular Biology; Ophthalmology
GA 852DM
UT WOS:000297328400001
PM 22162623
ER
PT J
AU Freedman, ND
Silverman, DT
Abnet, CC
AF Freedman, Neal D.
Silverman, Debra T.
Abnet, Christian C.
TI Tobacco Smoking and Bladder Cancer Reply
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Letter
C1 [Freedman, Neal D.; Silverman, Debra T.; Abnet, Christian C.] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
RP Freedman, ND (reprint author), NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
EM freedmanne@mail.nih.gov
RI Abnet, Christian/C-4111-2015; Freedman, Neal/B-9741-2015
OI Abnet, Christian/0000-0002-3008-7843; Freedman, Neal/0000-0003-0074-1098
NR 3
TC 0
Z9 0
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 23
PY 2011
VL 306
IS 20
BP 2217
EP 2217
DI 10.1001/jama.2011.1718
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 851GD
UT WOS:000297255500016
ER
PT J
AU Walkey, AJ
Wiener, RS
Ghobrial, JM
Curtis, LH
Benjamin, EJ
AF Walkey, Allan J.
Wiener, Renda Soylemez
Ghobrial, Joanna M.
Curtis, Lesley H.
Benjamin, Emelia J.
TI Incident Stroke and Mortality Associated With New-Onset Atrial
Fibrillation in Patients Hospitalized With Severe Sepsis
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID CRITICALLY-ILL PATIENTS; ACUTE ISCHEMIC-STROKE; INTENSIVE-CARE-UNIT;
ADMINISTRATIVE DATA; RISK-FACTORS; MYOCARDIAL-INFARCTION;
PULMONARY-ARTERY; ICD-9-CM CODES; INFECTION; ACCURACY
AB Context New-onset atrial fibrillation (AF) has been reported in 6% to 20% of patients with severe sepsis. Chronic AF is a known risk factor for stroke and death, but the clinical significance of new-onset AF in the setting of severe sepsis is uncertain.
Objective To determine the in-hospital stroke and in-hospital mortality risks associated with new-onset AF in patients with severe sepsis.
Design and Setting Retrospective population-based cohort of California State Inpatient Database administrative claims data from nonfederal acute care hospitals for January 1 through December 31, 2007.
Patients Data were available for 3 144 787 hospitalized adults. Severe sepsis (n=49 082 [1.56%]) was defined by validated International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) code 995.92. New-onset AF was defined as AF that occurred during the hospital stay, after excluding AF cases present at admission.
Main Outcome Measures A priori outcome measures were in-hospital ischemic stroke (ICD-9-CM codes 433, 434, or 436) and mortality.
Results Patients with severe sepsis were a mean age of 69 (SD, 16) years and 48% were women. New-onset AF occurred in 5.9% of patients with severe sepsis vs 0.65% of patients without severe sepsis (multivariable-adjusted odds ratio [OR], 6.82; 95% CI, 6.54-7.11; P < .001). Severe sepsis was present in 14% of all new-onset AF in hospitalized adults. Compared with severe sepsis patients without new-onset AF, patients with new-onset AF during severe sepsis had greater risks of in-hospital stroke (75/2896 [2.6%] vs 306/46 186 [0.6%] strokes; adjusted OR, 2.70; 95% CI, 2.05-3.57; P < .001) and in-hospital mortality (1629 [56%] vs 18 027 [39%] deaths; adjusted relative risk, 1.07; 95% CI, 1.04-1.11; P < .001). Findings were robust across 2 definitions of severe sepsis, multiple methods of addressing confounding, and multiple sensitivity analyses.
Conclusion Among patients with severe sepsis, patients with new-onset AF were at increased risk of in-hospital stroke and death compared with patients with no AF and patients with preexisting AF. JAMA. 2011;306(20):2248-2255 Published online November 13, 2011. doi:10.1001/jama.2011.1615
C1 [Walkey, Allan J.; Wiener, Renda Soylemez] Boston Univ, Sch Med, Ctr Pulm, Div Pulm & Crit Care Med, Boston, MA 02118 USA.
[Walkey, Allan J.; Wiener, Renda Soylemez; Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Med, Whitaker Cardiovasc Inst, Boston, MA 02118 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02118 USA.
[Wiener, Renda Soylemez] Edith Nourse Rogers Mem Vet Adm Hosp, Ctr Hlth Qual Outcomes & Econ Res, Bedford, MA 01730 USA.
[Wiener, Renda Soylemez] Dartmouth Coll, Hitchcock Med Ctr, Dartmouth Med Sch, Dartmouth Inst Hlth Policy & Clin Practice, Hanover, NH 03756 USA.
[Ghobrial, Joanna M.] Univ Washington, Sch Med, Dept Med, Div Cardiol, Seattle, WA 98195 USA.
[Curtis, Lesley H.] Duke Univ, Sch Med, Duke Clin Res Inst, Durham, NC USA.
[Curtis, Lesley H.] Duke Univ, Sch Med, Dept Med, Durham, NC 27706 USA.
[Benjamin, Emelia J.] NHLBI, Framingham, MA USA.
[Benjamin, Emelia J.] Boston Univ, Framingham Heart Study, Framingham, MA USA.
RP Walkey, AJ (reprint author), Boston Univ, Sch Med, Ctr Pulm, Div Pulm & Crit Care Med, R-304, Boston, MA 02118 USA.
EM alwalkey@bu.edu
OI Walkey, Allan/0000-0003-4685-6894; Benjamin, Emelia/0000-0003-4076-2336;
Wiener, Renda/0000-0001-7712-2135
FU Boston University Clinical Translational Research Institute
[UL1RR025771]; Evans Center for Interdisciplinary Biomedical Research
ARC on Atrial Fibrillation at Boston University; National Heart, Lung,
and Blood Institute [1R01HL092577, 1RC1HL101056, 1R01 HL102214];
National Cancer Institute [K07 CA138772]; Department of Veterans Affairs
FX This study was funded by grant UL1RR025771 from the Boston University
Clinical Translational Research Institute (Dr Walkey); by the Evans
Center for Interdisciplinary Biomedical Research ARC on Atrial
Fibrillation at Boston University
(http://www.bumc.bu.edu/evanscenteribr/) (Drs Walkey, Curtis, and
Benjamin); by National Heart, Lung, and Blood Institute grants
1R01HL092577 and 1RC1HL101056 (Dr Benjamin) and 1R01 HL102214 (Drs
Curtis and Benjamin); by National Cancer Institute grant K07 CA138772
(Dr Wiener); and by the Department of Veterans Affairs (Dr Wiener).
NR 46
TC 100
Z9 103
U1 1
U2 8
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 23
PY 2011
VL 306
IS 20
BP 2248
EP 2255
DI 10.1001/jama.2011.1615
PG 8
WC Medicine, General & Internal
SC General & Internal Medicine
GA 851GD
UT WOS:000297255500024
PM 22081378
ER
PT J
AU Mukhamedyarov, D
Makarova, KS
Severinov, K
Kuznedelov, K
AF Mukhamedyarov, Damir
Makarova, Kira S.
Severinov, Konstantin
Kuznedelov, Konstantin
TI Francisella RNA polymerase contains a heterodimer of non-identical alpha
subunits
SO BMC MOLECULAR BIOLOGY
LA English
DT Article
ID TERMINAL ASSEMBLY DOMAIN; FUNCTIONAL MAP; TRANSCRIPTION ACTIVATION;
PROTEIN EVOLUTION; DNA-BINDING; GENE; IDENTIFICATION; RECONSTITUTION;
HELICOBACTERS; PURIFICATION
AB Background: All sequenced genomes of representatives of the Francisella genus contain two rpoA genes, which encode non-identical RNA polymerase (RNAP) subunits, alpha 1 and alpha 2. In all other bacteria studied to date, a dimer of identical alpha subunits initiates the assembly of the catalytically proficient RNAP core (subunit composition alpha(2)beta beta'). Based on an observation that both alpha 1 and alpha 2 are incorporated into Francisella RNAP, Charity et al. (2007) previously suggested that up to four different species of RNAP core enzyme might form in the same Francisella cell.
Results: By in vitro assembly from fully denatured state, we determined that both Francisella a subunits are required for efficient dimerization; no homodimer formation was detected. Bacterial two-hybrid system analysis likewise indicated strong interactions between the alpha 1 and alpha 2 N-terminal domains (NTDs, responsible for dimerization). NTDs of alpha 2 did not interact detectably, while weak interaction between a1 NTDs was observed. This weak homotypic interaction may explain low-level transcription activity observed in in vitro RNAP reconstitution reactions containing Francisella large subunits (beta', beta) and alpha 1. No activity was observed with RNAP reconstitution reactions containing alpha 2, while robust transcription activity was detected in reactions containing alpha 1 and alpha 2. Phylogenetic analysis based on RpoA resulted in a tree compatible with standard bacterial taxonomy with both Francisella RpoA branches positioned within g-proteobacteria. The observed phylogeny and analysis of constrained trees are compatible with Francisella lineage-specific rpoA duplication followed by acceleration of evolutionary rate and subfunctionalization.
Conclusions: The results strongly suggest that most Francisella RNAP contains alpha heterodimer with a minor subfraction possibly containing alpha 1 homodimer. Comparative sequence analysis suggests that this heterodimer is oriented, in a sense that only one monomer, alpha 1, interacts with the beta subunit during the alpha(2)beta RNAP subassembly formation. Most likely the two rpoA copies in Francisella have emerged through a lineage-specific duplication followed by subfunctionalization of interacting paralogs.
C1 [Mukhamedyarov, Damir; Severinov, Konstantin; Kuznedelov, Konstantin] Rutgers State Univ, Dept Biochem & Mol Biol, Piscataway, NJ 08854 USA.
[Mukhamedyarov, Damir; Severinov, Konstantin; Kuznedelov, Konstantin] Rutgers State Univ, Waksman Inst Microbiol, Piscataway, NJ 08854 USA.
[Makarova, Kira S.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
[Severinov, Konstantin] Russian Acad Sci, Inst Gene Biol, Moscow, Russia.
[Severinov, Konstantin] Russian Acad Sci, Inst Mol Genet, Moscow, Russia.
RP Kuznedelov, K (reprint author), Rutgers State Univ, Dept Biochem & Mol Biol, Piscataway, NJ 08854 USA.
EM kuznedelo@waksman.rutgers.edu
RI Severinov, Konstantin/C-8545-2016
FU NIAID [AI090558]; US Department of Health and Human Services (National
Library of Medicine); NIH [GM59295]; Russian Academy of Sciences
FX The authors thank Y. Wolf and S. Nechaev for critical reading of the
manuscript and useful discussions. The project was supported by NIAID
Award AI090558 to KK. KSM is supported by the intramural funds of the US
Department of Health and Human Services (National Library of Medicine).
This work was partially supported by an NIH GM59295 grant and Russian
Academy of Sciences Presidium program grant in Molecular and Cellular
Biology to KS.
NR 48
TC 4
Z9 4
U1 0
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2199
J9 BMC MOL BIOL
JI BMC Mol. Biol.
PD NOV 22
PY 2011
VL 12
AR 50
DI 10.1186/1471-2199-12-50
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 903RZ
UT WOS:000301138400001
PM 22108176
ER
PT J
AU Acker, MA
Argenziano, M
Puskas, JD
Ferguson, TB
Gelijns, AC
Horvath, K
Miller, MA
Welsh, S
Moquete, E
Su, KN
Weinberg, A
Moskowitz, AJ
O'Gara, PT
Blackstone, EH
AF Acker, Michael A.
Argenziano, Michael
Puskas, John D.
Ferguson, T. B.
Gelijns, Annetine C.
Horvath, Keith
Miller, Marissa A.
Welsh, Stacey
Moquete, Ellen
Su, Kevin N.
Weinberg, Alan
Moskowitz, Alan J.
O'Gara, Patrick T.
Blackstone, Eugene H.
TI Infections After Cardiac Surgery: Initial Experience from the
Cardiothoracic Surgical Trials Network
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiovascular disease; Surgery; Health policy; Quality of medical care
C1 [Acker, Michael A.] Hosp Univ Penn, Philadelphia, PA 19104 USA.
[Argenziano, Michael] Columbia Univ, Med Cntr, New York, NY USA.
[Puskas, John D.] Emory Univ, Atlanta, GA 30322 USA.
[Ferguson, T. B.] E Carolina Heart Inst, Greenville, NC USA.
[Gelijns, Annetine C.; Moquete, Ellen; Su, Kevin N.; Weinberg, Alan; Moskowitz, Alan J.] Mt Sinai Sch Med, New York, NY USA.
[Horvath, Keith] Suburban Hosp, NIH, Heart Cntr, Bethesda, MD USA.
[Miller, Marissa A.] NHLBI, Bethesda, MD 20892 USA.
[Welsh, Stacey] Duke Univ, Durham, NC USA.
[O'Gara, Patrick T.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Blackstone, Eugene H.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
NR 0
TC 2
Z9 2
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A12247
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738704152
ER
PT J
AU Bidulescu, A
Liu, JK
Hickson, DA
Coverson, DL
Taylor, HA
Gibbons, GH
Sumner, AE
AF Bidulescu, Aurelian
Liu, Jiankang
Hickson, DeMarc A.
Coverson, Dorothy L.
Taylor, Herman A.
Gibbons, Gary H.
Sumner, Anne E.
TI Sex-Differences in the Association of Abdominal Visceral Adipose Tissue
with Adiponectin and Leptin in African Americans: The Jackson Heart
Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Adipokine; Disparities; Biomarkers; Ultrasound; Obesity
C1 [Bidulescu, Aurelian; Coverson, Dorothy L.; Gibbons, Gary H.] Morehouse Sch Med, Cardiovasc Rsch Inst, Atlanta, GA 30310 USA.
[Liu, Jiankang; Hickson, DeMarc A.; Taylor, Herman A.] Univ Mississippi, Med Ctr, Jackson, MS 39216 USA.
[Sumner, Anne E.] NIDDK, Clin Endocrinol Branch, NIH, Bethesda, MD USA.
RI Bidulescu, Aurelian/N-2617-2014
OI Bidulescu, Aurelian/0000-0001-8211-8309
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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A10028
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738702203
ER
PT J
AU Blaha, MJ
McEvoy, B
Blankstein, R
Budoff, MJ
Sibley, C
Gregory, B
Szklo, M
Blumenthal, RS
Kronmal, R
Nasir, K
AF Blaha, Michael J.
McEvoy, Bill
Blankstein, Ron
Budoff, Matthew J.
Sibley, Christopher
Gregory, Burke
Szklo, Moyses
Blumenthal, Roger S.
Kronmal, Richard
Nasir, Khurram
TI Comparing Zero Coronary Artery Calcium With Other Negative Risk Factors
for Coronary Heart Disease - Multi-Ethnic Study of Atherosclerosis
(MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
DE Risk factors; Coronary artery disease; Cardiac CT; Epidemiologic methods
C1 [Blaha, Michael J.; McEvoy, Bill; Blumenthal, Roger S.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[Blankstein, Ron] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Budoff, Matthew J.] Harbor UCLA Med Cntr, Los Angeles Biomed Rsch Inst, Torrance, CA USA.
[Sibley, Christopher] Johns Hopkins Univ Hosp, NIH, Bethesda, MD USA.
[Gregory, Burke] Wake Forest Univ Hlth Sci, Dept Publ Hlth Sci, Winston Salem, NC USA.
[Szklo, Moyses] Johns Hopkins Univ, Baltimore, MD USA.
[Kronmal, Richard] Univ Washington, Seattle, WA 98195 USA.
[Nasir, Khurram] Yale Med Cntr, New Haven, CT USA.
RI Sibley, Christopher/C-9900-2013
NR 0
TC 1
Z9 1
U1 1
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A14321
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738706081
ER
PT J
AU Britton, K
Pedley, A
Massaro, J
Corsini, E
Murabito, JM
Hoffmann, U
Ingram, C
Keaney, J
Vasan, R
Fox, C
AF Britton, Kathryn
Pedley, Alison
Massaro, Joseph
Corsini, Erin
Murabito, Joanne M.
Hoffmann, Udo
Ingram, Cheryl
Keaney, John
Vasan, Ramachandran
Fox, Caroline
TI Adipose Tissue Depots and Their Cross-Sectional Association With
Circulating Biomarkers of Metabolic Regulation
SO CIRCULATION
LA English
DT Meeting Abstract
DE Obesity; Biomarkers; Adipokine; Epidemiology
C1 [Britton, Kathryn] Brigham & Womens Hosp, Dept Med, Div Cardiovasc, Boston, MA 02115 USA.
[Pedley, Alison; Murabito, Joanne M.; Vasan, Ramachandran; Fox, Caroline] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Massaro, Joseph] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
[Corsini, Erin; Hoffmann, Udo] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Ingram, Cheryl; Keaney, John] Univ Massachusetts, Sch Med, Div Cardiovasc Med, Worcester, MA USA.
[Vasan, Ramachandran] Boston Univ, Dept Med, Cardiol Sect, Framingham, MA USA.
[Vasan, Ramachandran] Boston Univ, Dept Med, Sect Prevent Med, Framingham, MA USA.
[Fox, Caroline] NHLBI, Div Endocrinol Metab & Hypertens, Framingham, MA USA.
[Fox, Caroline] Cntr Populat Studies, Framingham, 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A12918
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738704362
ER
PT J
AU Brown, TM
Bittner, V
Loria, C
Safford, MM
Lewis, CE
AF Brown, Todd M.
Bittner, Vera
Loria, Catherine
Safford, Monika M.
Lewis, Cora E.
TI The Association of Multiple Phenotypic Presentations of Metabolic
Syndrome with Subclinical Atherosclerosis in the Coronary Artery Risk
Development in Young Adults (CARDIA) Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Metabolic syndrome; Subclinical atherosclerosis; Prevention; Obesity
C1 [Brown, Todd M.; Bittner, Vera] UAB Div Cardiol, Birmingham, AL USA.
[Loria, Catherine] NHLBI, Div Prevent & Populat Sci, Bethesda, MD 20892 USA.
[Safford, Monika M.; Lewis, Cora E.] UAB Div Prevent Med, Birmingham, AL 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A14214
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738706049
ER
PT J
AU Budoff, MJ
Lopez, VA
Nasir, K
Blumenthal, RS
Detrano, RC
Kronmal, R
Bild, D
Guerci, A
Liu, K
Shea, S
Szlko, M
Post, W
Lima, JA
Bertoni, A
Wong, ND
AF Budoff, Matthew J.
Lopez, Victor A.
Nasir, Khurram
Blumenthal, Roger S.
Detrano, Robert C.
Kronmal, Richard
Bild, Diane
Guerci, Alan
Liu, Kiang
Shea, Steven
Szlko, Moyses
Post, Wendy
Lima, Joao A.
Bertoni, Alain
Wong, Nathan D.
TI Progression of Coronary Calcium and Incident Coronary Heart Disease
Events: The Multi-Ethnic Study of Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
DE Calcification; Epidemiology; Outcomes
C1 [Budoff, Matthew J.; Lopez, Victor A.; Nasir, Khurram; Detrano, Robert C.] Los Angeles Biomed Rsch Inst, Torrance, CA USA.
[Blumenthal, Roger S.] Johns Hopkins, Torrance, CA USA.
[Kronmal, Richard] Univ Washington, Torrance, CA USA.
[Bild, Diane] NIH, Torrance, CA USA.
[Guerci, Alan] St Francis Hosp, Torrance, CA USA.
[Liu, Kiang] Northwestern, Chicago, IL USA.
[Shea, Steven] Columbia Univ, New York, NY USA.
[Bertoni, Alain] Wake Forest, Wake Forest, NC USA.
[Szlko, Moyses; Post, Wendy; Lima, Joao A.] Johns Hopkins, Baltimore, MD USA.
[Wong, Nathan D.] UC Irvine, Irvine, 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 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A10053
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738702216
ER
PT J
AU Chen, MY
Bandettini, WP
Shanbhag, SM
Vasu, S
Booker, OJ
Leung, SW
Wilson, JR
Kellman, P
Hsu, LY
Arai, AE
AF Chen, Marcus Y.
Bandettini, W. P.
Shanbhag, Sujata M.
Vasu, Sujethra
Booker, Oscar J.
Leung, Steve W.
Wilson, Joel R.
Kellman, Peter
Hsu, Li-Yueh
Arai, Andrew E.
TI Prognostic Value and Accuracy of Vasodilator Stress Cardiac MRI and
320-Row Coronary CTA
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac imaging; Cardiac MRI; Cardiac CT; Coronary artery disease;
Prognosis
C1 [Chen, Marcus Y.; Bandettini, W. P.; Shanbhag, Sujata M.; Vasu, Sujethra; Booker, Oscar J.; Leung, Steve W.; Wilson, Joel R.; Kellman, Peter; Hsu, Li-Yueh; Arai, Andrew E.] NHLBI, NIH, Bethesda, MD 20892 USA.
RI Leung, Steve/E-5624-2011
OI Leung, Steve/0000-0003-2832-2258
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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A15490
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738707092
ER
PT J
AU Chirinos, JA
Kips, J
Jacobs, DR
Brumback, L
Kronmal, R
Duprez, DA
Bluemke, DA
Townsend, RR
Vermeersch, S
Segers, P
AF Chirinos, Julio A.
Kips, Jan
Jacobs, David R., Jr.
Brumback, Lyndia
Kronmal, Richard
Duprez, Daniel A.
Bluemke, David A.
Townsend, Raymond R.
Vermeersch, Sebastian
Segers, Patrick
TI Central Pressure Profiles as Predictors of Incident Cardiovascular
Events and Heart Failure: The Multiethnic Study of Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Heart failure; Hemodynamics; Blood pressure; Blood pressure
C1 [Chirinos, Julio A.] Uivers Pennsylvania, Philadelphia, PA USA.
[Kips, Jan; Vermeersch, Sebastian; Segers, Patrick] Univ Ghent, IBiTech, B-9000 Ghent, Belgium.
[Jacobs, David R., Jr.; Duprez, Daniel A.] Univ Minnesota, Minneapolis, MN USA.
[Jacobs, David R., Jr.] Univ Oslo, Minneapolis, MN USA.
[Brumback, Lyndia; Kronmal, Richard] Univ Washington, Seattle, WA 98195 USA.
[Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
[Townsend, Raymond R.] Univ Penn, Philadelphia, PA 19104 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A8395
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738701091
ER
PT J
AU Chotenimitkhun, R
Hamilton, CA
Jeffries, N
Harman, JL
Taylor, H
Carr, JJ
Hundley, WG
AF Chotenimitkhun, Runyawan
Hamilton, Craig A.
Jeffries, Neal
Harman, Jane L.
Taylor, Herman, Jr.
Carr, J. J.
Hundley, W. G.
TI Age Related Change in Aortic Stiffness in the Thoracic and Abdominal
Aorta Among African Americans: The Jackson Heart Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Aorta; Hypertension; Blood flow; Cardiac MRI
C1 [Chotenimitkhun, Runyawan] Wake Forest Sch Med, Cardiol Sect, Winston Salem, NC USA.
[Harman, Jane L.] NHLBI, Program Prevent & Populat Sci, Div Cardiovasc Sci, NIH, Bethesda, MD 20892 USA.
[Taylor, Herman, Jr.] Univ Mississippi, Internal Med Cardiol Sect, Med Cntr, Jackson, MS 39216 USA.
[Carr, J. J.] Wake Forest Sch Med, Radiol & Translat Sci Inst TSI, Winston Salem, NC USA.
[Hundley, W. G.] Wake Forest Sch Med, Internal Med Cardiol Sect, Winston Salem, NC USA.
RI Carr, John/A-1938-2012
OI Carr, John/0000-0002-4398-8237
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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A8579
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738701139
ER
PT J
AU Colangelo, L
Whooley, MA
Vu, THT
Siddique, J
Reis, JP
Liu, K
AF Colangelo, Laura
Whooley, Mary A.
Thanh-Huyen T Vu
Siddique, Juned
Reis, Jared P.
Liu, Kiang
TI Ideal Cardiovascular Health and Development of Depressive Symptoms: The
CARDIA Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Depression
C1 [Colangelo, Laura; Thanh-Huyen T Vu; Siddique, Juned; Liu, Kiang] Northwestern Univ, Chicago, IL 60611 USA.
[Whooley, Mary A.] Univ Calif San Francisco, Dept Vet Affairs, Med Cntr, San Francisco, CA 94143 USA.
[Reis, Jared P.] NHLBI, Div Cardiovasc Sci, 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 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A10761
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738703038
ER
PT J
AU Cook, NR
Paynter, NP
Eaton, CB
Manson, JE
Martin, LW
Robinson, JG
Rossouw, J
Wassertheil-Smoller, S
Ridker, PM
AF Cook, Nancy R.
Paynter, Nina P.
Eaton, Charles B.
Manson, JoAnn E.
Martin, Lisa W.
Robinson, Jennifer G.
Rossouw, Jacques
Wassertheil-Smoller, Sylvia
Ridker, Paul M.
TI Validation of Framingham and Reynolds Cardiovascular Risk Prediction
Models in the Women's Health Initiative
SO CIRCULATION
LA English
DT Meeting Abstract
DE Prevention; Risk factors; Epidemiology; Cardiovascular disease
prevention
C1 [Cook, Nancy R.; Paynter, Nina P.; Manson, JoAnn E.; Ridker, Paul M.] Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA.
[Eaton, Charles B.] Brown Univ, Mem Hosp Rhode Isl, Cntr Primary Care & Prevent, Pawtucket, RI 02860 USA.
[Martin, Lisa W.] George Washington Univ, Sch Med, Washington, DC USA.
[Robinson, Jennifer G.] Univ Iowa, Dept Epidemiol, Iowa City, IA USA.
[Robinson, Jennifer G.] Univ Iowa, Dept Med, Iowa City, IA 52242 USA.
[Rossouw, Jacques] NHLBI, NIH, Bethesda, MD 20892 USA.
[Wassertheil-Smoller, Sylvia] Albert Einstein Coll Med, Bronx, NY 10467 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A10030
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738702205
ER
PT J
AU Das, S
Ferlito, M
Wang, R
Liu, DL
Raghavachari, N
Wheelan, S
Murphy, E
Steenbergen, C
AF Das, Samarjit
Ferlito, Marcella
Wang, Richard
Liu, Delong
Raghavachari, Nalini
Wheelan, Sarah
Murphy, Elizabeth
Steenbergen, Charles
TI Mitochondrial Import of miRNA as a Mechanism of Mitochondrial Gene
Regulation
SO CIRCULATION
LA English
DT Meeting Abstract
DE Mitochondria; Microrna; Cardioprotection; Ischemia reperfusion;
Molecular biology
C1 [Wheelan, Sarah] Johns Hopkins Univ, Biostat & Bioinformat Cntr Computat Genom, Baltimore, MD USA.
[Wang, Richard; Raghavachari, Nalini] NHLBI, Genom Core Facil, NIH, Bethesda, MD 20892 USA.
[Liu, Delong] NHLBI, Math & Stat Comp Lab, Cntr Informat Technol, NIH, Bethesda, MD 20892 USA.
[Murphy, Elizabeth] NHLBI, Cardiac Physiol Sect, Vasc Med Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A17072
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738708253
ER
PT J
AU Desai, CS
Ning, HY
Kang, J
Polak, JF
Folsom, AR
Sibley, CT
Tracey, R
Lloyd-Jones, DM
AF Desai, Chintan S.
Ning, Hongyan
Kang, Joseph
Polak, Joseph F.
Folsom, Aaron R.
Sibley, Christopher T.
Tracey, Russell
Lloyd-Jones, Donald M.
TI Competing Cardiovascular Outcomes Associated with Presence of
Subclinical Atherosclerosis: The Multi-Ethnic Study of Atherosclerosis
(mesa)
SO CIRCULATION
LA English
DT Meeting Abstract
DE Subclinical atherosclerosis; Outcomes
C1 [Desai, Chintan S.; Ning, Hongyan; Kang, Joseph; Lloyd-Jones, Donald M.] Northwestern Univ, Sch Med, Chicago, IL USA.
[Polak, Joseph F.] Tufts Univ, Sch Med, Boston, MA 02111 USA.
[Folsom, Aaron R.] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Sibley, Christopher T.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Tracey, Russell] Univ Vermont, Burlington, VT USA.
RI Lloyd-Jones, Donald/C-5899-2009; Sibley, Christopher/C-9900-2013
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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A12300
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738704174
ER
PT J
AU Donaldson, C
Palmer, B
Zile, M
Ashikaga, T
Meyer, M
VanBuren, P
Spinale, F
Maughan, D
Redfield, M
Bull, D
LeWinter, M
AF Donaldson, Cameron
Palmer, Bradley
Zile, Michael
Ashikaga, Takamaru
Meyer, Markus
VanBuren, Peter
Spinale, Francis
Maughan, David
Redfield, Margaret
Bull, David
LeWinter, Martin
CA NHLBI Heart Failure Rsch Network
TI Passive Myocardial Tension in Patients With Hypertension, Type 2
Diabetes Mellitus and Coronary Artery Disease
SO CIRCULATION
LA English
DT Meeting Abstract
DE Diastolic function; Hypertension; Ventricular function; Myocardium
C1 [Donaldson, Cameron; Palmer, Bradley; Ashikaga, Takamaru; Meyer, Markus; VanBuren, Peter; Maughan, David; LeWinter, Martin] Univ Vermont, Burlington, VT USA.
[Zile, Michael; Spinale, Francis] Med Univ S Carolina, Charleston, SC 29425 USA.
[Redfield, Margaret] Mayo Clin, Rochester, MN USA.
[Bull, David] Univ Utah, Salt Lake City, UT USA.
[NHLBI Heart Failure Rsch Network] 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A13461
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738705166
ER
PT J
AU Fernandez, AB
Wong, TY
Klein, R
Collins, D
Burke, G
Cotch, MF
Klein, B
Sadeghi, MM
Chen, J
AF Fernandez, Antonio B.
Wong, Tien Y.
Klein, Ronald
Collins, Dorothea
Burke, Gregory
Cotch, Mary Frances
Klein, Barbara
Sadeghi, Mehran M.
Chen, Jersey
TI Age-Related Macular Degeneration and Incident Cardiovascular Disease:
The Multi-Ethnic Study of Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Coronary artery disease; Aging; Prevention
C1 [Fernandez, Antonio B.] Brown Univ, Alpert Med Sch, Div Cardiol, Providence, RI 02912 USA.
[Wong, Tien Y.] Natl Univ Singapore, Yong Loo Lin Sch Med, Singapore Eye Rsch Inst, Singapore 117595, Singapore.
[Klein, Ronald; Klein, Barbara] Univ Wisconsin, Sch Med & Publ Hlth, Dept Ophthalmol & Visual Sci, Madison, WI USA.
[Collins, Dorothea] Yale Univ, Sch Med, VA Connecticut Healthcare Syst, Div Cardiol, West Haven, CT 06516 USA.
[Burke, Gregory] Wake Forest Univ, Bowman Gray Sch Med, Div Publ Hlth Sci, Winston Salem, NC USA.
[Cotch, Mary Frances] NEI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA.
[Sadeghi, Mehran M.] Yale Univ, Sch Med, Sect Cardiovasc Med, New Haven, CT USA.
[Chen, Jersey] Yale Univ, Sch Med, Sect Cardiovasc Dis, New Haven, CT 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A8656
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738701157
ER
PT J
AU Fiuzat, M
Wojdyla, D
Whellan, D
Chiswell, K
Kitzman, D
Kraus, W
Keteyian, S
Patterson, H
Adams, K
Fleg, J
Pina, I
O'Connor, CM
AF Fiuzat, Mona
Wojdyla, Daniel
Whellan, David
Chiswell, Karen
Kitzman, Dalane
Kraus, William
Keteyian, Steven
Patterson, Herb
Adams, Kirkwood
Fleg, Jerome
Pina, Ileana
O'Connor, Christopher M.
TI Relationship of Beta-Blocker (BB) Dose with Outcomes in Ambulatory Heart
Failure (HF) Patients with Systolic Dysfunction: Results from the
HF-ACTION Trial
SO CIRCULATION
LA English
DT Meeting Abstract
DE Beta blocker Dose response relation drug Heart failure
C1 [Fiuzat, Mona; Kraus, William; O'Connor, Christopher M.] Duke Univ, Med Cntr, Durham, NC USA.
[Wojdyla, Daniel; Chiswell, Karen] Duke Clin Rsch Inst, Durham, NC USA.
[Whellan, David] Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
[Kitzman, Dalane] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Keteyian, Steven] Henry Ford Hosp, Detroit, MI 48202 USA.
[Patterson, Herb; Adams, Kirkwood] Univ N Carolina, Chapel Hill, NC USA.
[Fleg, Jerome] NHLBI, NIH, Bethesda, MD 20892 USA.
[Pina, Ileana] Case Western Reserve Univ, Cleveland, OH 44106 USA.
NR 0
TC 0
Z9 0
U1 3
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A12023
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738704080
ER
PT J
AU Forman, DE
Fleg, J
Kitzman, D
Brawner, C
Swank, A
McKelvie, R
Clare, R
Ellis, S
Dunlap, M
Bittner, V
AF Forman, Daniel E.
Fleg, Jerome
Kitzman, Dalane
Brawner, Clinton
Swank, Ann
McKelvie, Robert
Clare, Robert
Ellis, Stephen
Dunlap, Mark
Bittner, Vera
TI Does the 6 Minute Walk Test Provide Useful Prognostic Information in
Systolic Heart Failure Patients?
SO CIRCULATION
LA English
DT Meeting Abstract
C1 [Forman, Daniel E.] Brigham & Womens Hosp, Div Cardiovasc Med, Boston, MA 02115 USA.
[Fleg, Jerome] NHLBI, Clin Trials Rsch Grp, Bethesda, MD 20892 USA.
[Kitzman, Dalane] Wake Forest Univ Hlth Sci, Div Cardiovasc Med, Winston Salem, NC USA.
[Brawner, Clinton] Henry Ford Hosp, Div Cardiovasc Med, Detroit, MI 48202 USA.
[Swank, Ann] Univ Louisville, Dept Hlth & Sports Sci, Louisville, KY 40292 USA.
[McKelvie, Robert] Hamilton Hlth Sci, Div Cardiovasc Med, Hamilton, ON, Canada.
[Clare, Robert; Ellis, Stephen] Duke Clin Rsch Inst, Durham, NC USA.
[Dunlap, Mark] MetraHlth Med Cntr, Div Cardiovasc Med, Cleveland, OH USA.
[Bittner, Vera] Univ Alabama, Div Cardiovasc Med, Birmingham, AL 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A16348
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738708006
ER
PT J
AU Frommelt, PC
Guey, LT
Bhat, M
Bradley, T
Colan, SD
Ensing, G
Gorentz, J
Heydarian, H
John, JB
Lai, WW
Levine, J
Mahle, WT
Miller, S
Minich, L
Ohye, RG
Pearson, GD
Shirali, GS
Wong, P
Cohen, MS
AF Frommelt, Peter C.
Guey, Lin T.
Bhat, Majeed
Bradley, Tim
Colan, Steve D.
Ensing, Greg
Gorentz, Jessica
Heydarian, Haleh
John, J. B.
Lai, Wyman W.
Levine, Jami
Mahle, William T.
Miller, Stephen
Minich, LuAnn
Ohye, Richard G.
Pearson, Gail D.
Shirali, Girish S.
Wong, Pierre
Cohen, Meryl S.
CA Pediat Heart Network Investigators
TI Does Initial Shunt Type for the Norwood Procedure Impact
Echocardiographic Measures of Cardiac Size and Function During Infancy?
The Single Ventricle Reconstruction Trial
SO CIRCULATION
LA English
DT Meeting Abstract
DE Hypoplastic left heart; Echocardiography; Congenital heart surgery;
Congenital heart disease
C1 [Frommelt, Peter C.; Gorentz, Jessica] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Guey, Lin T.] New England Rsch Inst, Watertown, MA USA.
[Bhat, Majeed] Nemours Cardiac Cntr, Wilmington, DE USA.
[Bradley, Tim] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Colan, Steve D.; Levine, Jami] Childrens Hosp Boston, Boston, MA USA.
[Ensing, Greg; Ohye, Richard G.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Heydarian, Haleh] Cincinnati Childrens Hosp, Cincinnati, OH USA.
[John, J. B.] Pediat Cardiol Associates, Tampa, FL USA.
[Lai, Wyman W.] Columbia Univ, New York, NY USA.
[Mahle, William T.] Emory Univ, Atlanta, GA 30322 USA.
[Miller, Stephen] Duke Univ, Durham, NC USA.
[Minich, LuAnn] Primary Childrens Med Cntr, Salt Lake City, UT USA.
[Pearson, Gail D.] NHLBI, Bethesda, MD 20892 USA.
[Shirali, Girish S.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Wong, Pierre] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Cohen, Meryl S.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A13454
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738705162
ER
PT J
AU Gardin, JM
Kitzman, DW
Leifer, ES
Cohen, G
Landzberg, JS
Cotts, WG
Wolfel, EE
Safford, RE
Bess, RL
Fleg, JL
AF Gardin, Julius M.
Kitzman, Dalane W.
Leifer, Eric S.
Cohen, Gerald
Landzberg, Joel S.
Cotts, William G.
Wolfel, Eugene E.
Safford, Robert E.
Bess, Renee L.
Fleg, Jerome L.
TI Left Ventricular Diastolic Function and Peak Exercise Oxygen Consumption
Contribute Independently to Predicting Clinical Outcomes in Patients
With Systolic Heart Failure in Heart Failure: A Controlled Trial
Investigating Outcomes of Exercise TraiNing (HF-ACTION)
SO CIRCULATION
LA English
DT Meeting Abstract
DE Heart failure; Echocardiography; Exercise tests; Outcomes
C1 [Gardin, Julius M.; Landzberg, Joel S.] Hackensack Univ, Med Ctr, Dept Med, Hackensack, NJ USA.
[Kitzman, Dalane W.] Wake Forest Baptist Hlth, Dept Internal Med, Winston Salem, NC USA.
[Leifer, Eric S.] Natl Heart Lung & Blood Inst, Off Biostat Rsch, Bethesda, MD USA.
[Cohen, Gerald] St Johns Hosp, Dept Med, Detroit, MI USA.
[Cohen, Gerald] Med Ctr, Detroit, MI USA.
[Cotts, William G.] Northwestern Univ, Dept Med, Feinberg Sch Med, Chicago, IL 60611 USA.
[Wolfel, Eugene E.] Univ Colorado, Dept Med, Ctr Hlth Sci, Aurora, CO USA.
[Safford, Robert E.] Mayo Clin, Dept Cardiovasc Dis, Jacksonville, FL 32224 USA.
[Fleg, Jerome L.] Natl Heart Lung & Blood Inst, Div Cardiovasc Sci, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A16091
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738707297
ER
PT J
AU Georgiopoulou, VV
Kalogeropoulos, AP
Marti, CN
Laskar, SR
Smith, AL
Bibbins-Domingo, K
Newman, AB
Harris, T
Kritchevsky, SB
Butler, J
AF Georgiopoulou, Vasiliki V.
Kalogeropoulos, Andreas P.
Marti, Catherine N.
Laskar, Sonjoy R.
Smith, Andrew L.
Bibbins-Domingo, Kirsten
Newman, Anne B.
Harris, Tamara
Kritchevsky, Stephen B.
Butler, Javed
TI Exercise Capacity and Risk for Heart Failure in Older Adults. The
Health, Aging, and Body Composition Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Heart failure; Elderly; Exercise tests; Epidemiology; Risk factors
C1 [Georgiopoulou, Vasiliki V.; Kalogeropoulos, Andreas P.; Marti, Catherine N.; Laskar, Sonjoy R.; Smith, Andrew L.; Butler, Javed] Emory Univ, Atlanta, GA 30322 USA.
[Bibbins-Domingo, Kirsten] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Newman, Anne B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Harris, Tamara] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
[Kritchevsky, Stephen B.] Wake Forest Univ, Winston Salem, NC 27109 USA.
RI Newman, Anne/C-6408-2013
OI Newman, Anne/0000-0002-0106-1150
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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A13480
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738705174
ER
PT J
AU Goldberg, CS
Allen, K
Tabbutt, S
Atz, AM
Bhatt, M
Clabby, M
Cooper, DS
Eghtesady, P
Frommelt, PC
Gruber, PJ
Hill, KD
Kaltman, JR
Laussen, PC
Lewis, AB
Lurito, KJ
Minich, LL
Ohye, RG
Schonbeck, J
Schwartz, SM
Singh, RK
Ghanayem, NS
AF Goldberg, Caren S.
Allen, Kerstin
Tabbutt, Sarah
Atz, Andrew M.
Bhatt, Majeed
Clabby, Martha
Cooper, David S.
Eghtesady, Pirooz
Frommelt, Peter C.
Gruber, Peter J.
Hill, Kevin D.
Kaltman, Jonathan R.
Laussen, Peter C.
Lewis, Alan B.
Lurito, Karen J.
Minich, L. LuAnn
Ohye, Richard G.
Schonbeck, Julie
Schwartz, Steven M.
Singh, Rakesh K.
Ghanayem, Nancy S.
CA Pediat Heart Network Investigators
TI Interstage Mortality after the Norwood Procedure: Results of the
Multi-Center Single Ventricle Reconstruction Trial
SO CIRCULATION
LA English
DT Meeting Abstract
DE Congenital heart disease; Congenital heart surgery; Hypoplastic left
heart
C1 [Goldberg, Caren S.; Ohye, Richard G.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Allen, Kerstin; Schonbeck, Julie] New England Rsch Inst, Watertown, MA USA.
[Tabbutt, Sarah] Univ San Francisco, Pediat Cardiac Intens Care Unit, San Francisco, CA 94117 USA.
[Atz, Andrew M.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Bhatt, Majeed] Nemours Cardiac Cntr, Wilmington, DE USA.
[Clabby, Martha] Childrens Healthcare Atlanta, Cardiol, Atlanta, GA USA.
[Cooper, David S.] Congenital Heart Inst Florida, St Petersburg, FL USA.
[Eghtesady, Pirooz] St Louis Childrens Hosp, St Louis, MO 63178 USA.
[Frommelt, Peter C.; Ghanayem, Nancy S.] Childrens Hosp Wisconsin, Milwaukee, WI 53201 USA.
[Gruber, Peter J.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Hill, Kevin D.] Duke Childrens Cardiol Fayet, Pediat Cardiol, Fayetteville, NC USA.
[Kaltman, Jonathan R.] NHLBI, Branch Div Cardiovasc Dis, Bethesda, MD 20892 USA.
[Laussen, Peter C.] Childrens Hosp, Boston, MA 02115 USA.
[Lewis, Alan B.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Lurito, Karen J.] ECU Brody Sch Med, Greenville, NC USA.
[Minich, L. LuAnn] Primary Childrens Med Cntr, Salt Lake City, UT USA.
[Schwartz, Steven M.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Singh, Rakesh K.] Columbia Univ, New York, NY 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A12185
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738704133
ER
PT J
AU Gopal, DM
Georgiopoulou, VV
Kalogeropoulos, AP
Smith, AL
Bauer, DC
Newman, AB
Bibbins-Domingo, K
Tindle, H
Harris, TB
Kritchevsky, SB
Tang, WHW
Butler, J
AF Gopal, Deepa M.
Georgiopoulou, Vasiliki V.
Kalogeropoulos, Andreas P.
Smith, Andrew L.
Bauer, Douglas C.
Newman, Anne B.
Bibbins-Domingo, Kirsten
Tindle, Hillary
Harris, Tamara B.
Kritchevsky, Stephen B.
Tang, W. H. Wilson
Butler, Javed
TI Cumulative Cigarette Smoking Exposure and Heart Failure Risk in Older
Adults the Health, Aging, and Body Composition (Health ABC) Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Smoking; Heart failure; Risk factors; Epidemiology; Elderly
C1 [Gopal, Deepa M.] Boston Univ, Div Cardiol, Boston, MA 02215 USA.
[Georgiopoulou, Vasiliki V.; Kalogeropoulos, Andreas P.; Smith, Andrew L.; Butler, Javed] Emory Univ, Div Cardiol, Atlanta, GA 30322 USA.
[Bauer, Douglas C.; Bibbins-Domingo, Kirsten] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Newman, Anne B.; Tindle, Hillary] Univ Pittsburgh, Pittsburgh, PA USA.
[Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
[Kritchevsky, Stephen B.] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Tang, W. H. Wilson] Cleveland Clin Fdn, Div Cardiol, Cleveland, OH 44195 USA.
RI Tang, Wai Hong/I-1238-2013; Newman, Anne/C-6408-2013
OI Newman, Anne/0000-0002-0106-1150
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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A14029
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738705381
ER
PT J
AU Gulati, A
Davendralingam, N
Ferreira, P
Hsu, LY
Goncalves, C
Ismail, N
Wage, R
Ismail, T
Ali, A
Khawaja, J
Banya, W
Gatehouse, P
Pennell, D
Firmin, D
Arai, A
Prasad, S
AF Gulati, Ankur
Davendralingam, Natasha
Ferreira, Pedro
Hsu, Li-Yueh
Goncalves, Carla
Ismail, Nizar
Wage, Ricardo
Ismail, Tevfik
Ali, Aamir
Khawaja, Jahanzaib
Banya, Winston
Gatehouse, Peter
Pennell, Dudley
Firmin, David
Arai, Andrew
Prasad, Sanjay
TI Microvascular Dysfunction Exists in Dilated Cardiomyopathy and
Correlates with Disease Severity
SO CIRCULATION
LA English
DT Meeting Abstract
DE Perfusion imaging; Magnetic resonance imaging; Cardiomyopathy;
Ventricular remodeling
C1 [Gulati, Ankur; Davendralingam, Natasha; Ferreira, Pedro; Goncalves, Carla; Ismail, Nizar; Wage, Ricardo; Ismail, Tevfik; Ali, Aamir; Khawaja, Jahanzaib; Banya, Winston; Gatehouse, Peter; Pennell, Dudley; Firmin, David; Prasad, Sanjay] Royal Brompton Hosp, CMR Dept, London SW3 6LY, England.
[Hsu, Li-Yueh; Arai, Andrew] NHLBI, NIH, Bethesda, WA USA.
OI Ferreira, Pedro/0000-0002-0436-3496
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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A11921
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738704044
ER
PT J
AU Jain, A
Liu, K
Ferrucci, L
Criqui, MH
Tian, L
Guralnik, JM
Tao, HM
McDermott, MM
AF Jain, Atul
Liu, Kiang
Ferrucci, Luigi
Criqui, Michael H.
Tian, Lu
Guralnik, Jack M.
Tao, Huimin
McDermott, Mary M.
TI Associations of the Ankle Brachial Index With Functional Performance
Varies Between Participants With Vs. Without Diabetes Mellitus
SO CIRCULATION
LA English
DT Meeting Abstract
DE Peripheral arterial disease; Cardiovascular disease; Epidemiology; Type
2 Diabetes; Vascular disease
C1 [Jain, Atul; McDermott, Mary M.] Northwestern Univ, Div Gen Internal Med, Chicago, IL 60611 USA.
[Ferrucci, Luigi] NIA, Clin Rsch Branch, Baltimore, MD 21224 USA.
[Criqui, Michael H.] Univ Calif San Diego, Sch Med, La Jolla, CA 92093 USA.
[Tian, Lu] Stanford Univ, Sch Med, Palo Alto, CA 94304 USA.
[Guralnik, Jack M.] Univ Maryland, Sch Med, Baltimore, MD 21201 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A13207
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738705081
ER
PT J
AU Kallianos, KG
Engel, LC
Szymonifka, J
Maurovich-Horvat, P
Schlett, CL
Fox, CS
Nagurney, JT
Hoffmann, U
Truong, QA
AF Kallianos, Kimberly G.
Engel, Leif-Christopher
Szymonifka, Jackie
Maurovich-Horvat, Pal
Schlett, Christopher L.
Fox, Caroline S.
Nagurney, John T.
Hoffmann, Udo
Truong, Quynh A.
TI Pericoronary Fat is Independently Associated to the Presence and Extent
of Coronary Artery Disease as Compared to Other Thoracic Fat Depots
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac CT; Adipose; Coronary artery disease
C1 [Kallianos, Kimberly G.; Engel, Leif-Christopher; Maurovich-Horvat, Pal; Schlett, Christopher L.; Hoffmann, Udo; Truong, Quynh A.] Massachusetts Gen Hosp, Cardiac MR PET CT Program, Boston, MA 02114 USA.
[Fox, Caroline S.] NHLBI, Framingham Heart Study, Boston, MA 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A13661
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738705246
ER
PT J
AU Kizer, JR
Arnold, AM
Benkeser, D
Mukamal, KJ
Djousse, L
Zieman, SJ
Siscovick, DS
Tracy, RP
Mantzoros, CS
Gottdiener, JS
Ix, JH
AF Kizer, Jorge R.
Arnold, Alice M.
Benkeser, David
Mukamal, Kenneth J.
Djousse, Luc
Zieman, Susan J.
Siscovick, David S.
Tracy, Russell P.
Mantzoros, Christos S.
Gottdiener, John S.
Ix, Joachim H.
TI Total and High Molecular Weight Adiponectin and Future Risk of Ischemic
Stroke and Coronary Heart Disease in Older Adults
SO CIRCULATION
LA English
DT Meeting Abstract
DE Aging; Adiponectin; Cardiovascular disease
C1 [Kizer, Jorge R.] Cornell Univ, Weill Med Coll, New York, NY 10021 USA.
[Arnold, Alice M.; Benkeser, David; Siscovick, David S.] Univ Washington, Seattle, WA 98195 USA.
[Mukamal, Kenneth J.; Mantzoros, Christos S.] Beth Israel Deaconess Med Cntr, Boston, MA USA.
[Djousse, Luc] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Zieman, Susan J.] NIA, Bethesda, MD 20892 USA.
[Tracy, Russell P.] Univ Vermont, Colchester, VT USA.
[Gottdiener, John S.] Univ Maryland, Baltimore, MD 21201 USA.
[Ix, Joachim H.] Univ Calif San Diego, La Jolla, CA 92093 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A10013
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738702200
ER
PT J
AU Kohr, MJ
Sun, JH
Aponte, A
Wang, GH
Gucek, M
Steenbergen, C
Murphy, E
AF Kohr, Mark J.
Sun, Junhui
Aponte, Angel
Wang, Guanghui
Gucek, Marjan
Steenbergen, Charles
Murphy, Elizabeth
TI S-Nitrosylation Occupancy is Increased With Ischemic Preconditioning
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardioprotection; Preconditioning; Nitric oxide; Nitric oxide synthase
C1 [Kohr, Mark J.; Steenbergen, Charles] Johns Hopkins Med Insts, Baltimore, MD USA.
[Sun, Junhui; Murphy, Elizabeth] NHLBI, Syst Biol Cntr, NIH, Bethesda, MD 20892 USA.
[Aponte, Angel; Wang, Guanghui; Gucek, Marjan] NHLBI, Prote Core Facil, NIH, Bethesda, MD 20892 USA.
RI Sun, Junhui/C-3499-2011
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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A13440
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738705157
ER
PT J
AU Leung, SW
Hsu, LY
Berry, C
Wilson, JR
Kellman, P
Arai, AE
AF Leung, Steve W.
Hsu, Li-Yueh
Berry, Colin
Wilson, Joel R.
Kellman, Peter
Arai, Andrew E.
TI Early Gadolinium Enhancement Represents Area at Risk Not Infarct Size:
Timing and Kinetics Are Critical in Interpreting MRI of Acute Myocardial
Infarction
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac MRI; Myocardial infarction; Infarct size
C1 [Leung, Steve W.; Hsu, Li-Yueh; Wilson, Joel R.; Kellman, Peter; Arai, Andrew E.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Berry, Colin] Univ Glasgow, BHF Glasgow Cardiovasc Rsch Cntr, Glasgow, Lanark, Scotland.
RI Leung, Steve/E-5624-2011
OI Leung, Steve/0000-0003-2832-2258
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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A16686
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738708122
ER
PT J
AU Lubitz, S
Moser, C
Sullivan, L
Rienstra, M
Fontes, J
Villalon, M
Pai, MJ
Magnani, J
Yin, XY
Levy, D
Pencina, M
Larson, M
Ellinor, P
Benjamin, E
AF Lubitz, Steven
Moser, Carlee
Sullivan, Lisa
Rienstra, Michiel
Fontes, Joao
Villalon, Mark
Pai, Manju
Magnani, Jared
Yin, Xiaoyan
Levy, Daniel
Pencina, Michael
Larson, Martin
Ellinor, Patrick
Benjamin, Emelia
TI Atrial Fibrillation Patterns in the Community and Risks of Stroke, Heart
Failure, or Death
SO CIRCULATION
LA English
DT Meeting Abstract
DE Atrial fibrillation; Epidemiology; Prognosis; Longitudinal studies; Risk
factors
C1 [Lubitz, Steven; Ellinor, Patrick] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
[Moser, Carlee; Sullivan, Lisa; Pencina, Michael; Larson, Martin] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Rienstra, Michiel] Massachusetts Gen Hosp, Cardiovasc Rsch Cntr, Charlestown, MA USA.
[Fontes, Joao; Magnani, Jared] Boston Univ, Sch Med, Dept Cardiol, Boston, MA 02118 USA.
[Villalon, Mark; Pai, Manju] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Yin, Xiaoyan; Benjamin, Emelia] Boston Univ, Framingham Heart Study, Framingham, MA USA.
[Levy, Daniel] NHLBI, Framingham Heart Study, Framingham, MA 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A13665
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738705247
ER
PT J
AU McDermott, M
Liu, K
Ferrucci, L
Tian, L
Guralnik, J
Kopp, P
Tao, HM
Van Horn, L
Green, D
Criqui, MH
AF McDermott, Mary
Liu, Kiang
Ferrucci, Luigi
Tian, Lu
Guralnik, Jack
Kopp, Peter
Tao, Huimin
Van Horn, Linda
Green, David
Criqui, Michael H.
TI Vitamin D Levels in People with Peripheral Arterial Disease and
Associations with Functional, Muscle, and Nerve Outcomes
SO CIRCULATION
LA English
DT Meeting Abstract
DE Peripheral arterial disease; Vascular disease; Vitamins
C1 [McDermott, Mary; Liu, Kiang; Kopp, Peter; Tao, Huimin; Van Horn, Linda; Green, David] Northwestern Univ, Chicago, IL 60611 USA.
[Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Bethesda, MD 20892 USA.
[Tian, Lu] Stanford Univ, Stanford, CA 94305 USA.
[Guralnik, Jack] Univ Maryland, Baltimore, MD 21201 USA.
[Criqui, Michael H.] Univ Calif San Diego, La Jolla, CA 92093 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A13137
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738705054
ER
PT J
AU Mcevoy, JW
Blaha, MJ
Lima, JA
Bluemke, DA
Hundley, G
Min, JK
Shaw, LJ
Lloyd-Jones, DM
Barr, G
Budoff, MJ
Blumenthal, RS
Nasir, K
AF Mcevoy, John W.
Blaha, Michael J.
Lima, Joao A.
Bluemke, David A.
Hundley, Gregory
Min, James K.
Shaw, Leslee J.
Lloyd-Jones, Donald M.
Barr, Graham
Budoff, Matthew J.
Blumenthal, Roger S.
Nasir, Khurram
TI Cigarette Smoking: Relationship with Inflammation, Arterial Stiffness,
and Subclinical Atherosclerosis. The Multi-Ethnic Study of
Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
CT Scientific Sessions of the American-Heart-Association/Resuscitation
Science Symposium
CY NOV 12-16, 2011
CL Orlando, FL
SP Amer Heart Assoc
DE Smoking; Inflammation; Coronary artery disease; Calcification; Aortic
diseases
C1 [Mcevoy, John W.; Blaha, Michael J.; Blumenthal, Roger S.; Nasir, Khurram] Johns Hopkins Univ, Johns Hopkins Hosp, Ciccarone Prevent Cardiol Cntr, Baltimore, MD USA.
[Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
[Hundley, Gregory] Wake Forest Baptist Med Cntr, Winston Salem, NC USA.
[Min, James K.] Weill Cornell Med Coll, New York, NY USA.
[Shaw, Leslee J.] Emory Univ, Sch Med, Atlanta, GA USA.
[Lloyd-Jones, Donald M.] Northwestern Univ, Dept Prevent Med, Feinberg Sch Med, Chicago, IL 60611 USA.
[Barr, Graham] Columbia Univ, Div Pulm Allergy & Crit Care Med, New York, NY USA.
[Budoff, Matthew J.] Univ Calif Los Angeles, Harbor UCLA, Los Angeles Biomed Rsch Inst, Los Angeles, CA USA.
RI Lloyd-Jones, Donald/C-5899-2009
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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A9713
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738702106
ER
PT J
AU Mcevoy, JW
Blaha, MJ
Lima, JA
Bluemke, DA
Hundley, G
Min, JK
Shaw, LJ
Lloyd-Jones, DM
Barr, G
Budoff, MJ
Blumenthal, RS
Nasir, K
AF Mcevoy, John W.
Blaha, Michael J.
Lima, Joao A.
Bluemke, David A.
Hundley, Gregory
Min, James K.
Shaw, Leslee J.
Lloyd-Jones, Donald M.
Barr, Graham
Budoff, Matthew J.
Blumenthal, Roger S.
Nasir, Khurram
TI Cigarette Smoking: Association Between Inflammation, Subclinical
Atherosclerosis and Cardiovascular Events. The Multi-Ethnic Study of
Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
DE Smoking; Inflammation; Cardiac CT; Calcification; Outcomes
C1 [Mcevoy, John W.; Blaha, Michael J.; Lima, Joao A.; Blumenthal, Roger S.; Nasir, Khurram] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
[Hundley, Gregory] Wake Forest Univ, Ctr Hlth, Winston Salem, NC 27109 USA.
[Min, James K.] Weill Cornell Med Coll, New York, NY USA.
[Shaw, Leslee J.] Emory Univ, Sch Med, Atlanta, GA USA.
[Lloyd-Jones, Donald M.] Northwestern Univ, Feinverg Sch Med, Chicago, IL 60611 USA.
[Barr, Graham] Columbia Univ, Div Pulm Allergy & Crit Care Med, New York, NY USA.
[Budoff, Matthew J.] Univ Calif Los Angeles, Los Angeles Biomed Rsch Inst Harbor, Los Angeles, CA USA.
RI Lloyd-Jones, Donald/C-5899-2009
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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA 9726
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738702110
ER
PT J
AU Michler, RE
Gillinov, AM
Perrault, LP
Ascheim, DD
Ailawadi, G
Smith, PK
Parides, MK
Voisine, P
Page, P
Taddei-Peters, WC
Mayer, ML
Gardner, TJ
Kron, IL
AF Michler, Robert E.
Gillinov, A. M.
Perrault, Louis P.
Ascheim, Deborah D.
Ailawadi, Gorav
Smith, Peter K.
Parides, Michael K.
Voisine, Pierre
Page, Pierre
Taddei-Peters, Wendy C.
Mayer, Mary Lou
Gardner, Timothy J.
Kron, Irving L.
TI Enrollment Challenges in Cardiovascular Surgical Trials: Experience of
the Cardiothoracic Surgical Trials Network
SO CIRCULATION
LA English
DT Meeting Abstract
DE Mitral valve disease; Healthcare innovation; Outcomes; Health policy;
Quality of medical care
C1 [Michler, Robert E.] Montefiore Einstein Heart Cntr, Bronx, NY USA.
[Gillinov, A. M.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Perrault, Louis P.] Montreal Heart Inst, Montreal, PQ H1T 1C8, Canada.
[Ascheim, Deborah D.; Parides, Michael K.] Mt Sinai Sch Med, New York, NY USA.
[Ailawadi, Gorav; Kron, Irving L.] Univ Virginia Hlth Syst, Charlottesville, VA USA.
[Smith, Peter K.] Duke Univ, Durham, NC USA.
[Voisine, Pierre] Inst Univ Cardiol Quebec, Hop Laval, Quebec City, PQ, Canada.
[Page, Pierre] Hop Sacre Coeur, Montreal, PQ H4J 1C5, Canada.
[Taddei-Peters, Wendy C.] NHLBI, Bethesda, MD 20892 USA.
[Mayer, Mary Lou] Hosp Univ Penn, Philadelphia, PA 19104 USA.
[Gardner, Timothy J.] Christiana Care Hlth Syst, Heart & Vasc Surg, Newark, DE 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A12251
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738704156
ER
PT J
AU Moser, DK
Pelter, MM
Nesbitt, T
Robinson, S
Biddle, MJ
Cooper, L
Dracup, K
AF Moser, Debra K.
Pelter, Michele M.
Nesbitt, Thomas
Robinson, Susan
Biddle, Martha J.
Cooper, Lawton
Dracup, Kathleen
TI Which Patients with Heart Failure Have the Poorest Health Literacy?
SO CIRCULATION
LA English
DT Meeting Abstract
DE Heart failure; Health education
C1 [Moser, Debra K.; Biddle, Martha J.] Univ Kentucky, Coll Nursing, Lexington, KY USA.
[Pelter, Michele M.] Univ Reno, Coll Nursing, Reno, NV USA.
[Nesbitt, Thomas] Univ Calif Davis, Davis, CA 95616 USA.
[Robinson, Susan] Univ Calif San Francisco, Coll Nursing, San Francisco, CA 94143 USA.
[Cooper, Lawton] NHLBI, NIH, Bethesda, MD 20892 USA.
[Dracup, Kathleen] Univ Calif San Francisco, Sch Nursing, San Francisco, CA 94143 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A9157
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738701280
ER
PT J
AU Murabito, JM
Pedley, A
Massaro, JM
Vasan, RS
Glazer, NL
Hoffman, U
Fox, CS
AF Murabito, Joanne M.
Pedley, Alison
Massaro, Joseph M.
Vasan, Ramachandran S.
Glazer, Nicole L.
Hoffman, Udo
Fox, Caroline S.
TI The Relation of Physical Activity With Accelerometry and Adipose Tissue
Depots in a Community-Based Sample of Adults: The Framingham Third
Generation Cohort
SO CIRCULATION
LA English
DT Meeting Abstract
DE Physical activity; Adipose; Obesity
C1 [Murabito, Joanne M.] Boston Univ, Sch Med, Gen Internal Med Sect, Framingham, MA USA.
[Fox, Caroline S.] NHLBI, Framingham Heart Study, Div Endocrinol, Framingham, MA USA.
[Massaro, Joseph M.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
[Hoffman, Udo] Massachusetts Gen Hosp, Dept Cardiac MR PET CT, Boston, MA 02114 USA.
[Hoffman, Udo; Fox, Caroline S.] Harvard Univ, Sch Med, Boston, 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A13457
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738705164
ER
PT J
AU Newburger, JW
Sleeper, LA
Bellinger, DC
Goldberg, CS
Tabbutt, S
Lu, MM
Mussatto, KA
Williams, IA
Gustafson, KE
Mital, S
Pike, N
Sood, E
Mahle, WT
Cooper, DS
Dunbar-Masterson, C
Krawczeski, CD
Lewis, A
Menon, S
Pemberton, VL
Ravishankar, C
Atz, TW
Ohye, RG
Gaynor, JW
AF Newburger, Jane W.
Sleeper, Lynn A.
Bellinger, David C.
Goldberg, Caren S.
Tabbutt, Sarah
Lu, Minmin
Mussatto, Kathleen A.
Williams, Ismee A.
Gustafson, Kathryn E.
Mital, Seema
Pike, Nancy
Sood, Erica
Mahle, William T.
Cooper, David S.
Dunbar-Masterson, Carolyn
Krawczeski, Catherine Dent
Lewis, Allan
Menon, Shaji
Pemberton, Victoria L.
Ravishankar, Chitra
Atz, Theresa W.
Ohye, Richard G.
Gaynor, J. W.
TI Early Neurodevelopmental Outcome in Hypoplastic Left Heart Syndrome and
Related Anomalies: The Single Ventricle Reconstruction Trial
SO CIRCULATION
LA English
DT Meeting Abstract
DE Congenital heart disease; Congenital heart surgery; Brain; Cognitive
function; Pediatric cardiology
C1 [Newburger, Jane W.; Bellinger, David C.; Dunbar-Masterson, Carolyn] Childrens Hosp, Boston, MA 02115 USA.
[Sleeper, Lynn A.] New England Rsch Inst, Pediat Heart Network, Watertown, MA USA.
[Goldberg, Caren S.] Univ Michigan Hlth Syst, Ann Arbor, MI USA.
[Tabbutt, Sarah] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Lu, Minmin] New England Rsch Inst, Pediat Heart Assoc, Watertown, MA USA.
[Mussatto, Kathleen A.] Childrens Hosp Wisconsin, Wauwatosa, WI USA.
[Williams, Ismee A.] Columbia Univ, Med Ctr, New York, NY USA.
[Gustafson, Kathryn E.] Duke Univ, Med Ctr, Durham, NC USA.
[Mital, Seema] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Pike, Nancy] Univ Calif Los Angeles, Sch Nursing, Los Angeles, CA 90024 USA.
[Sood, Erica] Alfred I duPont Hosp Children, Nemours Cardiac Cntr, Wilmington, DE USA.
[Mahle, William T.] Sibley Heart Cntr, Atlanta, GA USA.
[Cooper, David S.] Univ S Florida, All Childrens Hosp, St Petersburg, FL 33701 USA.
[Krawczeski, Catherine Dent] Cincinnati Childrens Hosp, Cardiol CICU, Med Ctr, Cincinnati, OH USA.
[Lewis, Allan] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Menon, Shaji] Primary Childrens Med Ctr, Salt Lake City, UT 84103 USA.
[Pemberton, Victoria L.] NIH, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
[Ravishankar, Chitra] Childrens Hosp Philadelphia, Cardiac Cntr, Philadelphia, PA 19104 USA.
[Atz, Theresa W.] Med Univ S Carolina, Coll Nursing, Charleston, SC USA.
[Ohye, Richard G.] Univ Michigan, Congenital Heart Cntr, Ann Arbor, MI 48109 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A8457
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738701109
ER
PT J
AU Nguyen, TT
Wong, RP
Chen, Y
Gucek, M
Li, JH
Sack, MN
Murphy, E
AF Nguyen, Tiffany T.
Wong, Renee P.
Chen, Yong
Gucek, Marjan
Li, Jianhua
Sack, Michael N.
Murphy, Elizabeth
TI Cyclosporine a Attenuates Acetylation of Mitochondrial Proteins:
Implications for Cardioprotection Against Ischemia/Reperfusion Injury
SO CIRCULATION
LA English
DT Meeting Abstract
DE Ischemia reperfusion; Mitochondria; Cardioprotective drugs; Proteomics;
Myocardial infarction
C1 [Nguyen, Tiffany T.; Wong, Renee P.] NHLBI, Syst Biol Ctr, NIH, Bethesda, MD 20892 USA.
[Chen, Yong; Gucek, Marjan] NHLBI, Prote Core Facil, NIH, Bethesda, MD 20892 USA.
[Li, Jianhua; Sack, Michael N.] NHLBI, Ctr Mol Med, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A10909
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738703084
ER
PT J
AU Noseworthy, PA
Peloso, GM
Hwang, SJ
Larson, MG
Levy, D
O'Donnell, CJ
Newton-Cheh, C
AF Noseworthy, Peter A.
Peloso, Gina M.
Hwang, Shih-Jen
Larson, Martin G.
Levy, Daniel
O'Donnell, Christopher J.
Newton-Cheh, Christopher
TI QT Interval Duration and Incident Mortality in the Framingham Heart
Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Qt interval; Sudden cardiac death; Heart rate/Heart rate variability
C1 [Noseworthy, Peter A.; Newton-Cheh, Christopher] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Peloso, Gina M.; Hwang, Shih-Jen; Larson, Martin G.; Levy, Daniel; O'Donnell, Christopher J.] NHLBI, Framingham Heart Study, Framingham, 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A9138
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738701272
ER
PT J
AU Ohye, RG
Schonbeck, JV
Eghtesady, P
Laussen, PC
Pizarro, C
Shrader, P
Frank, DU
Graham, EM
Hill, KD
Jacobs, JP
Kanter, KR
Kirsh, JA
Lambert, LM
Lewis, AB
Ravishankar, C
Tweddell, JS
Williams, IA
Pearson, GD
AF Ohye, Richard G.
Schonbeck, Julie V.
Eghtesady, Pirooz
Laussen, Peter C.
Pizarro, Christian
Shrader, Peter
Frank, Deborah U.
Graham, Eric M.
Hill, Kevin D.
Jacobs, Jeffrey P.
Kanter, Kirk R.
Kirsh, Joel A.
Lambert, Linda M.
Lewis, Alan B.
Ravishankar, Chitra
Tweddell, James S.
Williams, Ismee A.
Pearson, Gail D.
CA Pediat Heart Network Investigators
TI Cause, Timing and Location of Death in the Single Ventricle
Reconstruction Trial
SO CIRCULATION
LA English
DT Meeting Abstract
DE Congenital heart disease; Congenital heart surgery; Single ventricle
C1 [Ohye, Richard G.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Schonbeck, Julie V.; Shrader, Peter] NERI, Watertown, MA USA.
[Eghtesady, Pirooz] St Louis Childrens Hosp, St Louis, MO 63178 USA.
[Laussen, Peter C.] Childrens Hosp Boston, Boston, MA USA.
[Pizarro, Christian] Alfred I duPont Hosp Children, Wilmington, DE USA.
[Frank, Deborah U.; Lambert, Linda M.] Univ Utah, Sch Med, Salt Lake City, UT USA.
[Graham, Eric M.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Hill, Kevin D.] Duke Univ, Med Cntr, Durham, NC USA.
[Jacobs, Jeffrey P.] Congenital Heart Inst Florida, Cardiac Surg Associates, St Petersburg, FL USA.
[Kanter, Kirk R.] Emory Univ, Sch Med, Atlanta, GA USA.
[Kirsh, Joel A.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Lewis, Alan B.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Ravishankar, Chitra] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Tweddell, James S.] Childrens Hosp Wisconsin, Wauwatosa, WI USA.
[Williams, Ismee A.] Columbia Univ, Coll Phys & Surg, New York, NY USA.
[Pearson, Gail D.] NHLBI, Adult & Pediat Cardiac Rsch Program, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A10098
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738702232
ER
PT J
AU Ravishankar, C
Tabbutt, S
Allen, K
Cooper, DS
Frank, DU
Frommelt, PC
Ghanayem, NS
Goldberg, CS
Graham, EM
Kirsh, JA
Krawczeski, CD
Lai, WW
Lewis, A
Lodge, AJ
Mahony, L
Simsic, J
Sleeper, LA
Stylianou, M
Wang, YL
Laussen, P
AF Ravishankar, Chitra
Tabbutt, Sarah
Allen, Kerstin
Cooper, David S.
Frank, Deborah U.
Frommelt, Peter C.
Ghanayem, Nancy S.
Goldberg, Caren S.
Graham, Eric M.
Kirsh, Joel A.
Krawczeski, Catherine Dent
Lai, Wyman W.
Lewis, Alan
Lodge, Andrew J.
Mahony, Lynn
Simsic, Janet
Sleeper, Lynn A.
Stylianou, Mario
Wang, Yanli
Laussen, Peter
CA Pediat Heart Network Investigators
TI Impact of Extracorporeal Membrane Oxygenation and Cardiopulmonary
Resuscitation on Norwood Procedure Outcomes: Data from the Single
Ventricle Reconstruction Trail
SO CIRCULATION
LA English
DT Meeting Abstract
DE Congenital heart surgery; Extracorporeal circulation; Cardiopulmonary
resuscitation
C1 [Ravishankar, Chitra] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Tabbutt, Sarah] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Allen, Kerstin; Sleeper, Lynn A.; Wang, Yanli] New England Rsch Inst, Cntr Stat Anal & Rsch, Watertown, MA USA.
[Cooper, David S.] Congenital Heart Inst Florida, St Petersburg, FL USA.
[Frank, Deborah U.] Primary Childrens Med Ctr, Salt Lake City, UT 84103 USA.
[Frank, Deborah U.] Univ Utah, Salt Lake City, UT USA.
[Frommelt, Peter C.; Ghanayem, Nancy S.] Childrens Hosp Wisconsin, Milwaukee, WI 53201 USA.
[Frommelt, Peter C.; Ghanayem, Nancy S.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Goldberg, Caren S.] Univ Michigan, Sch Med, Ann Arbor, MI USA.
[Graham, Eric M.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Kirsh, Joel A.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Krawczeski, Catherine Dent] Cincinnati Childrens Med Cntr, Cincinnati, OH USA.
[Lai, Wyman W.] Childrens Hosp New York, New York, NY USA.
[Lewis, Alan] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Lodge, Andrew J.] Duke Univ, Med Ctr, Durham, NC USA.
[Mahony, Lynn] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Simsic, Janet] Emory Univ, Atlanta, GA 30322 USA.
[Stylianou, Mario] NHLBI, Bethesda, MD 20892 USA.
[Laussen, Peter] Childrens Hosp, Boston, MA 02115 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A9897
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738702156
ER
PT J
AU Rodriguez, CJ
Moran, A
Chen, HY
Bertoni, A
Bluemke, D
Seeman, T
Darwin, C
Watson, K
Diez-Roux, A
AF Rodriguez, Carlos J.
Moran, Andrew
Chen, Haiying
Bertoni, Alain
Bluemke, David
Seeman, Teresa
Darwin, Christine
Watson, Karol
Diez-Roux, Ana
TI Acculturation is Associated with Left Ventricular Mass in a Multiethnic
Sample: The Multi-ethnic Study of Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Hypertrophy; Behavioral aspects; Epidemiology
C1 [Rodriguez, Carlos J.; Chen, Haiying; Bertoni, Alain] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Moran, Andrew] Columbia Univ, New York, NY USA.
[Bluemke, David] NIH, Bethesda, MD 20892 USA.
[Seeman, Teresa; Darwin, Christine; Watson, Karol] Univ Calif Los Angeles, Los Angeles, CA USA.
[Diez-Roux, Ana] Univ Michigan, Ann Arbor, MI 48109 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A10477
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738702327
ER
PT J
AU Sasaki, T
Miller, CF
Hansford, R
Zviman, MM
Henrikson, CA
Marine, JE
Spragg, D
Cheng, AA
Tandri, H
Sinha, S
Kolandaivelu, A
Tomaselli, GF
Berger, RD
Calkins, H
Bluemke, DA
Nazarian, S
AF Sasaki, Takeshi
Miller, Christopher F.
Hansford, Rozann
Zviman, Menekhem M.
Henrikson, Charles A.
Marine, Joseph E.
Spragg, David
Cheng, Alan
Tandri, Harikrishna
Sinha, Sunil
Kolandaivelu, Aravindan
Tomaselli, Gordon F.
Berger, Ronald D.
Calkins, Hugh
Bluemke, David A.
Nazarian, Saman
TI Non-Invasive Magnetic Resonance Based Three-Dimensional Voltage Maps for
Electrophysiology Procedure Guidance
SO CIRCULATION
LA English
DT Meeting Abstract
DE Noninvasive cardiac imaging; Cardiac MRI; Ventricular tachycardia;
Myocardial infarction; Electrophysiology
C1 [Sasaki, Takeshi; Miller, Christopher F.; Hansford, Rozann; Zviman, Menekhem M.; Henrikson, Charles A.; Marine, Joseph E.; Spragg, David; Cheng, Alan; Tandri, Harikrishna; Sinha, Sunil; Kolandaivelu, Aravindan; Tomaselli, Gordon F.; Berger, Ronald D.; Calkins, Hugh; Nazarian, Saman] Johns Hopkins Univ, Baltimore, MD USA.
[Bluemke, David A.] NIH, Bethesda, MD 20892 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A9642
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738702082
ER
PT J
AU Schelbert, EB
Ceyrolles, WJ
Testa, SM
Meier, CG
Ludwig, DR
Blair, AJ
Kellman, P
Schwartzman, D
Shroff, SG
Wong, TC
AF Schelbert, Erik B.
Ceyrolles, William J.
Testa, Stephen M.
Meier, Christopher G.
Ludwig, Daniel R.
Blair, Alexander J.
Kellman, Peter
Schwartzman, David
Shroff, Sanjeev G.
Wong, Timothy C.
TI Diffuse Myocardial Fibrosis Quantification by Cardiac MR is Strongly
Associated with B-type Natriuretic Peptide (BNP) and Low Ejection
Fraction: Implications for Paradigms of Myocardial Dysfunction
SO CIRCULATION
LA English
DT Meeting Abstract
DE Fibrosis; Cardiac MRI; Cardiomyopathy; Heart failure; Natriuretic
peptide
C1 [Schelbert, Erik B.; Testa, Stephen M.; Meier, Christopher G.; Ludwig, Daniel R.; Blair, Alexander J.; Schwartzman, David; Wong, Timothy C.] Univ Pittsburgh, Cardiovasc Inst, Pittsburgh, PA USA.
[Ceyrolles, William J.] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA.
[Kellman, Peter] NHLBI, Cardiac Energet Lab, Bethesda, MD 20892 USA.
[Shroff, Sanjeev G.] Univ Pittsburgh, Dept Bioengn, Pittsburgh, PA 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A18396
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738709155
ER
PT J
AU Schelbert, EB
Cao, JJ
Sigurdsson, S
Aspelund, T
Kellman, P
Aletras, AH
Dyke, C
Thorgeirsson, G
Eiriksdottir, G
Launer, LJ
Gudnason, V
Harris, TB
Arai, AE
AF Schelbert, Erik B.
Cao, Jie J.
Sigurdsson, Sigurdur
Aspelund, Thor
Kellman, Peter
Aletras, Anthony H.
Dyke, Christopher
Thorgeirsson, Gudmundur
Eiriksdottir, Gudny
Launer, Lenore J.
Gudnason, Vilmundur
Harris, Tamara B.
Arai, Andrew E.
TI Prevalence and Prognosis of Unrecognized Myocardial Infarction by
Cardiac Magnetic Resonance versus ECG in the ICELANDMI Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Magnetic resonance imaging; Electrocardiography; Myocardial infarction;
Prognosis; Population science
C1 [Schelbert, Erik B.; Cao, Jie J.; Kellman, Peter; Aletras, Anthony H.; Arai, Andrew E.] NHLBI, Cardiac Energet Lab, Bethesda, MD 20892 USA.
[Sigurdsson, Sigurdur; Aspelund, Thor; Eiriksdottir, Gudny] Iceland Heart Assoc, Kopavogur, Iceland.
[Dyke, Christopher] Alaska Heart Inst, Anchorage, AK USA.
[Thorgeirsson, Gudmundur] Univ Iceland, Reykjavik, Iceland.
[Launer, Lenore J.; Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
[Gudnason, Vilmundur] Iceland Heart Assoc, Rsch Inst, Kopavogur, MD USA.
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 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A16205
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738707335
ER
PT J
AU Shanmugam, P
Valente, AJ
Delafontaine, L
Gardner, JD
Siebenlist, U
Chandrasekar, B
AF Shanmugam, Prakashsrinivas
Valente, Anthony J.
Delafontaine, Laurent
Gardner, Jason D.
Siebenlist, Ulrich
Chandrasekar, Bysani
TI Deletion of CIKS (Act1 or traf3ip2) Abrogates Angiotensin-II-induced
Cardiac Hypertrophy in vitro and in vivo
SO CIRCULATION
LA English
DT Meeting Abstract
DE Angiotensin II; Hypertrophy; Signal transduction; Blood pressure;
Extracellular matrix
C1 [Shanmugam, Prakashsrinivas] SLVHCS, Res Serv, New Orleans, LA USA.
[Valente, Anthony J.] Univ Texas Hlth Sci Cntr, San Antonio, TX USA.
[Delafontaine, Laurent; Chandrasekar, Bysani] Tulane Univ, Sch Med, Inst Heart & Vasc, New Orleans, LA 70112 USA.
[Gardner, Jason D.] Louisiana State Univ, Hlth Sci Cntr, New Orleans, LA USA.
[Siebenlist, Ulrich] NIAID, Immunoregulat Lab, 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A8742
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738701185
ER
PT J
AU Shufelt, CL
Johnson, DB
Mehta, PK
Anderson, RD
Thomson, L
Berman, DS
Petersen, JW
Handberg, E
Kar, S
Samuels, B
Azarbal, B
Kothawade, K
Kelsey, SF
Sharaf, BL
Sopko, G
Shaw, L
Pepine, CJ
Merz, CNB
AF Shufelt, Chrisandra L.
Johnson, Delia B.
Mehta, Puja K.
Anderson, R. David
Thomson, Louise
Berman, Daniel S.
Petersen, John W.
Handberg, Eileen
Kar, Saibal
Samuels, Bruce
Azarbal, Babak
Kothawade, Kamlesh
Kelsey, Sheryl F.
Sharaf, Barry L.
Sopko, George
Shaw, Leslee
Pepine, Carl J.
Merz, C. Noel Bairey
TI Noninvasive Detection of Microvascular Coronary Dysfunction Using
Cardiac Magnetic Resonance Imaging: The NHLBI-Sponsored Women's Ischemia
Syndrome Evaluation (WISE) Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Acetylcholine; Ischemic heart disease; Cardiac MRI; Endothelial
function; Coronary microcirculation
C1 [Shufelt, Chrisandra L.; Mehta, Puja K.; Kothawade, Kamlesh; Merz, C. Noel Bairey] Cedars Sinai Med Cntr, Womens Heart Cntr, Los Angeles, CA USA.
[Johnson, Delia B.] Univ Pittsburgh, Sch Publ Hlth, Pittsburgh, PA 15260 USA.
[Handberg, Eileen; Pepine, Carl J.] Univ Florida, Div Cardiovasc Med, Gainesville, FL USA.
[Kar, Saibal] Cedars Sinai Med Cntr, Cedars Sinai Heart Inst, Los Angeles, CA USA.
[Samuels, Bruce] Cedars Sinai Med Cntr, Cardiovasc Med Grp So Calif, Los Angeles, CA USA.
[Azarbal, Babak] Cedars Sinai Med Cntr, Calif Heart Cntr, Los Angeles, CA USA.
[Sharaf, Barry L.] Rhode Isl Hosp, Div Cardiol, Providence, RI USA.
[Sopko, George] NHLBI, Div Cardiovasc Dis, Bethesda, MD 20892 USA.
[Shaw, Leslee] Emory Univ, Sch Med, Atlanta, GA 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A10364
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738702305
ER
PT J
AU Shukla, P
Singh, K
Quan, A
Al-Omran, M
Teoh, H
Lovren, F
Liu, C
Rovira, I
Pan, Y
Brezden-Masley, C
Deng, CX
Leong-Poi, H
Stanford, W
Parker, T
Schneider, M
Finkel, T
Verma, S
AF Shukla, Praphulla
Singh, Krishna
Quan, Adrian
Al-Omran, Mohammed
Teoh, Hwee
Lovren, Fina
Liu, Cao
Rovira, Ilsa
Pan, Yi
Brezden-Masley, Christine
Deng, Chu-Xia
Leong-Poi, Howard
Stanford, William
Parker, Thomas
Schneider, Michael
Finkel, Toren
Verma, Subodh
TI BRCA1 Induces Cardiac Protection Through a P53-Dependent Pathway
SO CIRCULATION
LA English
DT Meeting Abstract
DE Apoptosis; Myocardial infarction
C1 [Shukla, Praphulla; Singh, Krishna; Quan, Adrian; Teoh, Hwee; Lovren, Fina; Pan, Yi; Brezden-Masley, Christine; Deng, Chu-Xia; Verma, Subodh] St Michaels Hosp, Toronto, ON M5B 1W8, Canada.
[Al-Omran, Mohammed] King Saud Univ, Riyadh, Saudi Arabia.
[Liu, Cao; Rovira, Ilsa; Finkel, Toren] NHLBI, Translat Med Branch, Bethesda, MD 20892 USA.
[Leong-Poi, Howard; Parker, Thomas] NIDDK, Mammalian Genet Sect, Bethesda, MD USA.
[Stanford, William] Univ Toronto, Inst Biomat & Biomed Engn, Toronto, ON, Canada.
[Schneider, Michael] Univ London Imperial Coll Sci Technol & Med, London, England.
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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A11516
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738703264
ER
PT J
AU Silverman, MG
Blaha, MJ
Budoff, MJ
Blankstein, R
Sibley, CT
Blumenthal, RS
Nasir, K
AF Silverman, Michael G.
Blaha, Michael J.
Budoff, Matthew J.
Blankstein, Ron
Sibley, Christopher T.
Blumenthal, Roger S.
Nasir, Khurram
TI Impact of Coronary Artery Calcium on Coronary Heart Disease Events In
Individuals at the Extremes of Traditional Risk Factor Burden: The
Multi-Ethnic Study of Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac CT; Risk factors; Epidemiology
C1 [Silverman, Michael G.; Blaha, Michael J.; Blumenthal, Roger S.; Nasir, Khurram] Johns Hopkins Ciccarone Prevent Cardiol Cntr, Baltimore, MD USA.
[Budoff, Matthew J.] Los Angeles Biomed Rsch Inst, Torrance, CA USA.
[Blankstein, Ron] Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA.
[Sibley, Christopher T.] NIH, Bethesda, MD 20892 USA.
RI Sibley, Christopher/C-9900-2013
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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A14517
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738706137
ER
PT J
AU Sinner, M
Greiner, MA
Mi, XJ
Hernandez, AF
Jensen, PN
Piccini, JP
Setoguchi, S
Walkey, AJ
Heckbert, SR
Benjamin, EJ
Curtis, LH
AF Sinner, Moritz
Greiner, Melissa A.
Mi, Xioajuan
Hernandez, Adrian F.
Jensen, Paul N.
Piccini, Jonathan P.
Setoguchi, Soko
Walkey, Allan J.
Heckbert, Susan R.
Benjamin, Emelia J.
Curtis, Lesley H.
TI Guideline Recommended Evaluation in Patients with a First Episode of
Atrial Fibrillation
SO CIRCULATION
LA English
DT Meeting Abstract
DE Atrial fibrillation; Guidelines; Quality of medical care; Epidemiologic
methods
C1 [Sinner, Moritz] Massachusetts Gen Hosp, Cardiovasc Rsch Cntr, Charlestown, MA USA.
[Greiner, Melissa A.; Mi, Xioajuan; Hernandez, Adrian F.; Piccini, Jonathan P.; Setoguchi, Soko; Curtis, Lesley H.] Duke Univ, Sch Med, Duke Clin Rsch Inst, Durham, NC USA.
[Jensen, Paul N.; Heckbert, Susan R.] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA.
[Walkey, Allan J.] Boston Univ, Sch Med, Ctr Pulm, Boston, MA 02118 USA.
[Benjamin, Emelia J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Benjamin, Emelia J.] Boston Univ, Framingham Heart Study, Framingham, MA 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A8440
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738701105
ER
PT J
AU Tabbutt, S
Ghanayem, N
Cooper, DS
Frank, DU
Lu, MM
Frommelt, P
Lai, WW
Goldberg, CS
Graham, EM
Krawczeski, CD
Mahony, L
Ravishankar, C
Sleeper, LA
Kirsh, JA
Lewis, A
Lodge, A
Ohye, R
Pizarro, C
Simsic, J
Spurrier, E
Stylianou, M
Laussen, P
AF Tabbutt, Sarah
Ghanayem, Nancy
Cooper, David S.
Frank, Deborah U.
Lu, Minmin
Frommelt, Peter
Lai, Wyman W.
Goldberg, Caren S.
Graham, Eric M.
Krawczeski, Catherine Dent
Mahony, Lynn
Ravishankar, Chitra
Sleeper, Lynn A.
Kirsh, Joel A.
Lewis, Alan
Lodge, Andrew
Ohye, Rick
Pizarro, Christian
Simsic, Janet
Spurrier, Ellen
Stylianou, Mario
Laussen, Peter
CA Pediat Heart Network Investigators
TI Risk Factors For Hospital Mortality And Morbidity Following The Norwood
Procedure: Results From The Multicenter Single Ventricle Reconstruction
Trial
SO CIRCULATION
LA English
DT Meeting Abstract
DE Congenital heart surgery
C1 [Tabbutt, Sarah; Ravishankar, Chitra] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Ghanayem, Nancy; Frommelt, Peter] Childrens Hosp Wisconsin, Milwaukee, WI 53201 USA.
[Ghanayem, Nancy; Frommelt, Peter] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Cooper, David S.] Congenital Heart Inst Florida, St Petersburg, FL USA.
[Frank, Deborah U.] Univ Utah, Salt Lake City, UT USA.
[Frank, Deborah U.] Primary Childrens Med Ctr, Salt Lake City, UT 84103 USA.
[Lu, Minmin; Sleeper, Lynn A.] New England Res Inst, Cntr Stat Anal & Rsch, Watertown, MA 02172 USA.
[Lai, Wyman W.] Childrens Hosp New York, New York, NY USA.
[Goldberg, Caren S.; Ohye, Rick] Univ Michigan, Sch Med, Ann Arbor, MI USA.
[Graham, Eric M.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Krawczeski, Catherine Dent] Cincinnati Childrens Med Cntr, Cincinnati, OH USA.
[Mahony, Lynn] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Kirsh, Joel A.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Lewis, Alan] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Lodge, Andrew] Duke Univ, Med Ctr, Durham, NC USA.
[Pizarro, Christian; Spurrier, Ellen] Alfred I duPont Hosp Children, Nemours Cardiac Cntr, Wilmington, DE USA.
[Simsic, Janet] Emory Univ, Atlanta, GA 30322 USA.
[Stylianou, Mario] NHLBI, Bethesda, MD 20892 USA.
[Laussen, Peter] Childrens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A8160
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738701059
ER
PT J
AU Turkbey, EB
Jorgensen, NW
Bertoni, AG
Johnson, WC
Roux, AD
Polak, JF
Tracy, R
Ainsworth, B
Jacobs, D
Shea, S
Lima, JA
Bluemke, DA
AF Turkbey, Evrim B.
Jorgensen, Neal W.
Bertoni, Alain G.
Johnson, W. Craig
Roux, Ana Diez
Polak, Joseph F.
Tracy, Russell
Ainsworth, Barbara
Jacobs, David
Shea, Steven
Lima, Joao A.
Bluemke, David A.
TI Physical Activity and Cardiovascular Events in the Multi-Ethnic Study of
Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
DE Physical activity; Cardiovascular disease
C1 [Turkbey, Evrim B.; Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
[Jorgensen, Neal W.; Johnson, W. Craig] Univ Washington, Collaborat Hlth Studies Coordinating Ctr, Seattle, WA 98195 USA.
[Bertoni, Alain G.] Wake Forest Univ Hlth Sci, Dept Publ Hlth Sci, Winston Salem, NC USA.
[Roux, Ana Diez] Univ Michigan, Dept Epidemiol, Ann Arbor, MI 48109 USA.
[Polak, Joseph F.] Tufts Med Ctr, Ultrasound Reading Ctr, Boston, MA USA.
[Tracy, Russell] Univ Vermont, Dept Pathol, Colchester, VT USA.
[Ainsworth, Barbara] Arizona State Univ, Dept Exercise & Wellness, Mesa, AZ USA.
[Jacobs, David] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Shea, Steven] Columbia Univ, New York, NY USA.
[Lima, Joao A.] Johns Hopkins Sch Med, Dept Cardiol, Baltimore, MD 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A13126
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738705083
ER
PT J
AU Turkbey, EB
Gai, N
Lima, JA
van der Geest, RJ
Wagner, KR
Tomaselli, GF
Bluemke, DA
Nazarian, S
AF Turkbey, Evrim B.
Gai, Neville
Lima, Joao A.
van der Geest, Rob J.
Wagner, Kathryn R.
Tomaselli, Gordon F.
Bluemke, David A.
Nazarian, Saman
TI Assessment of Cardiac Involvement in Myotonic Muscular Dystrophy
Patients Using T1 Mapping MRI
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac MRI; Fibrosis
C1 [Turkbey, Evrim B.; Gai, Neville; Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
[Lima, Joao A.] Johns Hopkins Univ, Dept Caridol, Baltimore, MD USA.
[van der Geest, Rob J.] Leiden Univ, Dept Radiol, Leiden, Netherlands.
[Wagner, Kathryn R.] Kennedy Krieger Inst, Baltimore, MD USA.
[Tomaselli, Gordon F.; Nazarian, Saman] Johns Hopkins Univ, Dept Cardiol, Baltimore, MD USA.
RI van der Geest, Rob/J-8193-2015
OI van der Geest, Rob/0000-0002-9084-5597
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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A13041
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738705019
ER
PT J
AU Turkbey, EB
Backlund, JYC
Small, A
Redheuil, A
Cleary, PA
Lachin, JM
Lima, J
Bluemke, DA
AF Turkbey, Evrim B.
Backlund, Jye-Yu C.
Small, Alex
Redheuil, Alban
Cleary, Patricia A.
Lachin, John M.
Lima, Joao
Bluemke, David A.
CA DCCT EDIC Res Grp
TI Relationship of Aortic Distensibility to Cardiovascular Disease Risk
Factors in Type 1 Diabetes Mellitus: the Diabetes Control and
Complications Trial (DCCT)/Epidemiology of Diabetes Interventions and
Complications (EDIC) Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Aorta; Magnetic resonance imaging; Type 1 Diabetes
C1 [Turkbey, Evrim B.; Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
[Backlund, Jye-Yu C.; Cleary, Patricia A.; Lachin, John M.] George Washington Univ, Biostat Cntr, Rockville, MD USA.
[Small, Alex] Mt Sinai Sch Med, Sch Med, New York, NY USA.
[Redheuil, Alban; Lima, Joao] Johns Hopkins Univ, Dept Cardiol, Baltimore, MD 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A12919
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738704363
ER
PT J
AU Tweddell, JS
Sleeper, LA
McCrindle, BW
Williams, IA
Mahony, L
Pizarro, C
Ravishankar, C
Cnota, J
Frommelt, PC
Pemberton, V
Bradley, S
Li, JS
Puchalski, M
Laussen, PC
Jacobs, JP
Pike, N
Paul, K
Hirsch, JC
Ohye, RG
AF Tweddell, James S.
Sleeper, Lynn A.
McCrindle, Brian W.
Williams, Ismee A.
Mahony, Lynn
Pizarro, Christian
Ravishankar, Chitra
Cnota, James
Frommelt, Peter C.
Pemberton, Victoria
Bradley, Scott
Li, Jennifer S.
Puchalski, Michael
Laussen, Peter C.
Jacobs, Jeffrey P.
Pike, Nancy
Paul, Kirshbom
Hirsch, Jennifer C.
Ohye, Richard G.
CA Pediat Heart Network Investigators
TI Risk Factors for Mortality in the Single Ventricle Reconstruction Trial:
Beyond Shunt Type
SO CIRCULATION
LA English
DT Meeting Abstract
DE Hypoplastic left heart; Congenital heart surgery; Congenital heart
disease; Outcomes
C1 [Tweddell, James S.; Frommelt, Peter C.] Med Coll Wisconsin, Childrens Hosp Wisconsin, Milwaukee, WI 53226 USA.
[Sleeper, Lynn A.] New England Rsch Inst, Cntr Stat Anal & Rsch, Watertown, MA USA.
[McCrindle, Brian W.] Hosp Sick Children, Cardiovasc Clin Rsch Unit, Toronto, ON M5G 1X8, Canada.
[Williams, Ismee A.] Columbia Univ, New York, NY USA.
[Mahony, Lynn] Univ Texas Dallas, SW MC, Dallas, TX 75230 USA.
[Pizarro, Christian] Nemours Cardiac Cntr, Wilmington, DE USA.
[Ravishankar, Chitra] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Cnota, James] Cincinnati Childrens Hosp, Med Ctr, Cincinnati, OH USA.
[Pemberton, Victoria] NHLBI, NIH, Bethesda, MD 20892 USA.
[Bradley, Scott] Med Univ S Carolina, Charleston, SC 29425 USA.
[Li, Jennifer S.] Duke Univ, Med Ctr, Durham, NC USA.
[Puchalski, Michael] Primary Childrens Med Ctr, Salt Lake City, UT 84103 USA.
[Laussen, Peter C.] Childrens Hosp, Boston, MA 02115 USA.
[Jacobs, Jeffrey P.] Congenital Heart Inst Florid, St Petersburg, FL USA.
[Pike, Nancy] Univ Calif Los Angeles, Sch Nursing, Los Angeles, CA 90024 USA.
[Paul, Kirshbom] Emory Univ, Atlanta, GA 30322 USA.
[Hirsch, Jennifer C.; Ohye, Richard G.] Univ Michigan, Ann Arbor, MI 48109 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A11634
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738703299
ER
PT J
AU Ugander, M
Chen, MY
Chen, B
Bagi, PS
Hsu, LY
Kellman, P
Arai, AE
AF Ugander, Martin
Chen, Marcus Y.
Chen, Billy
Bagi, Paul S.
Hsu, Li-Yueh
Kellman, Peter
Arai, Andrew E.
TI Contrast Enhanced CT and MRI Measures of Extracellular Volume Fraction
Confirm Presence of Peri-Infarct Edema in Acute Myocardial Infarction
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac CT; Cardiac MRI; Myocardial infarction; Magnetic resonance
imaging; Cardiac imaging
C1 [Ugander, Martin; Chen, Marcus Y.; Chen, Billy; Bagi, Paul S.; Hsu, Li-Yueh; Kellman, Peter; Arai, Andrew E.] NHLBI, NIH, 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 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A16534
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738708072
ER
PT J
AU Valente, AJ
Prabhu, SD
Siebenlist, U
Chandrasekar, B
AF Valente, Anthony J.
Prabhu, Sumanth D.
Siebenlist, Ulrich
Chandrasekar, Bysani
TI Critical Role of CIKS/Act1 In Lipopolysaccharide (LPS)-Induced Cardiac
Dysfunction in vivo And Cardiomyocyte Contractility in vitro
SO CIRCULATION
LA English
DT Meeting Abstract
DE Heart failure; Ischemic heart disease; Contractility; Inflammation;
Signal transduction
C1 [Valente, Anthony J.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
[Prabhu, Sumanth D.] Univ Louisville, Louisville, KY 40292 USA.
[Siebenlist, Ulrich] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Chandrasekar, Bysani] Tulane Univ, Sch Med, Inst Heart & Vasc, New Orleans, LA 70112 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A8420
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738701099
ER
PT J
AU Yang, XP
Becker, LC
Amar, M
Remaley, AT
AF Yang, Xiaoping
Becker, Lewis C.
Amar, Marcelo
Remaley, Alan T.
TI Lp(a) is a Novel Ligand for Scavenger Receptor-B1
SO CIRCULATION
LA English
DT Meeting Abstract
DE Lipoproteins; Receptors
C1 [Yang, Xiaoping; Becker, Lewis C.] Johns Hopkins Univ, Dept Med, Div Cardiol, Baltimore, MD USA.
[Amar, Marcelo; Remaley, Alan T.] NIH, Pulm & Vasc Med Branch, 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 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A13434
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738705155
ER
PT J
AU Yoneyama, K
Gjesdal, O
Choi, EY
Wu, CO
Hundley, GW
Gomes, AS
Liu, CY
McClelland, RL
Bluemke, DA
Lima, JA
AF Yoneyama, Kihei
Gjesdal, Ola
Choi, Eui-Young
Wu, Colin O.
Hundley, Gregory W.
Gomes, Antoinette S.
Liu, Chia -Ying
McClelland, Robyn L.
Bluemke, David A.
Lima, Joao A.
TI Age and Gender-Related Remodeling Influences Left Ventricular Torsion
Assessed by Tagged Cardiac Magnetic Resonance in Asymptomatic
Individuals: the Multi-Ethnic Study of Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Myocardial torsion and recoil; Cardiovascular imaging; Statins; Cardiac
MRI
C1 [Yoneyama, Kihei; Gjesdal, Ola; Choi, Eui-Young; Liu, Chia -Ying; Lima, Joao A.] Johns Hopkins Univ, Baltimore, MD USA.
[Wu, Colin O.] NHLBI, Off Biostat Rsch, Bethesda, MD 20892 USA.
[Hundley, Gregory W.] Wake Forest Univ Hlth Sci, Dept Internal Med Cardiol, Winston Salem, NC USA.
[Gomes, Antoinette S.] Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA.
[McClelland, Robyn L.] Univ Washington, Collaborat Hlth Studies Coordinating Ctr, Seattle, WA 98195 USA.
[Bluemke, David A.] Natl Inst Biomed Imaging & Bioengn, NIH, Ctr Clin, Bethesda, 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A15304
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738707020
ER
PT J
AU Zavodni, AE
Wasserman, BA
McClelland, RL
Gomes, AS
Folsom, AR
Polak, JF
Lima, JA
Bluemke, DA
AF Zavodni, Anna E.
Wasserman, Bruce A.
McClelland, Robyn L.
Gomes, Antoinette S.
Folsom, Aaron R.
Polak, Joseph F.
Lima, Joao A.
Bluemke, David A.
TI Carotid Magnetic Resonance Imaging and Ultrasound Intima-Media Thickness
for the Prediction of Cardiovascular Events: the Multi-Ethnic Study of
Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Biomarkers; Carotid arteries; Subclinical atherosclerosis; Outcomes;
Magnetic resonance imaging
C1 [Zavodni, Anna E.; Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
[Wasserman, Bruce A.; Lima, Joao A.] Johns Hopkins Univ, Baltimore, MD USA.
[McClelland, Robyn L.] Univ Washington, Collaborat Hlth Studies Coordinating Cntr, Seattle, WA 98195 USA.
[Gomes, Antoinette S.] Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA.
[Folsom, Aaron R.] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Polak, Joseph F.] Tufts Med Cntr, Ultrasound Reading Cntr, Boston, MA USA.
NR 0
TC 1
Z9 1
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
SU S
MA A15452
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 884WE
UT WOS:000299738707075
ER
PT J
AU Zhang, JD
Geer, LY
Bolton, EE
Bryant, SH
AF Zhang, Jun D.
Geer, Lewis Y.
Bolton, Evan E.
Bryant, Stephen H.
TI Automated annotation of chemical names in the literature with tunable
accuracy
SO JOURNAL OF CHEMINFORMATICS
LA English
DT Article
ID PATENT ABSTRACTS; TEXT; DICTIONARY
AB Background: A significant portion of the biomedical and chemical literature refers to small molecules. The accurate identification and annotation of compound name that are relevant to the topic of the given literature can establish links between scientific publications and various chemical and life science databases. Manual annotation is the preferred method for these works because well-trained indexers can understand the paper topics as well as recognize key terms. However, considering the hundreds of thousands of new papers published annually, an automatic annotation system with high precision and relevance can be a useful complement to manual annotation.
Results: An automated chemical name annotation system, MeSH Automated Annotations (MAA), was developed to annotate small molecule names in scientific abstracts with tunable accuracy. This system aims to reproduce the MeSH term annotations on biomedical and chemical literature that would be created by indexers. When comparing automated free text matching to those indexed manually of 26 thousand MEDLINE abstracts, more than 40% of the annotations were false-positive (FP) cases. To reduce the FP rate, MAA incorporated several filters to remove "incorrect" annotations caused by nonspecific, partial, and low relevance chemical names. In part, relevance was measured by the position of the chemical name in the text. Tunable accuracy was obtained by adding or restricting the sections of the text scanned for chemical names. The best precision obtained was 96% with a 28% recall rate. The best performance of MAA, as measured with the F statistic was 66%, which favorably compares to other chemical name annotation systems.
Conclusions: Accurate chemical name annotation can help researchers not only identify important chemical names in abstracts, but also match unindexed and unstructured abstracts to chemical records. The current work is tested against MEDLINE, but the algorithm is not specific to this corpus and it is possible that the algorithm can be applied to papers from chemical physics, material, polymer and environmental science, as well as patents, biological assay descriptions and other textual data.
C1 [Zhang, Jun D.; Geer, Lewis Y.; Bolton, Evan E.; Bryant, Stephen H.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Dept Hlth & Human Serv, Bethesda, MD 20894 USA.
RP Geer, LY (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Dept Hlth & Human Serv, 8600 Rockville Pike, Bethesda, MD 20894 USA.
EM lewis.geer@nih.gov
RI Geer, Lewis/H-2714-2014
NR 25
TC 2
Z9 2
U1 0
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1758-2946
J9 J CHEMINFORMATICS
JI J. Cheminformatics
PD NOV 22
PY 2011
VL 3
AR 52
DI 10.1186/1758-2946-3-52
PG 10
WC Chemistry, Multidisciplinary; Computer Science, Information Systems;
Computer Science, Interdisciplinary Applications
SC Chemistry; Computer Science
GA 894SV
UT WOS:000300448100001
PM 22107874
ER
PT J
AU Nishioka, N
Matsuoka, T
Yashiro, M
Hirakawa, K
Olden, K
Roberts, JD
AF Nishioka, N.
Matsuoka, T.
Yashiro, M.
Hirakawa, K.
Olden, K.
Roberts, J. D.
TI Linoleic acid enhances angiogenesis through suppression of angiostatin
induced by plasminogen activator inhibitor 1
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE gastric carcinoma; linoleic acid; plasminogen activator inhibitor 1;
angiostatin; invasion
ID ENDOTHELIAL-CELL MIGRATION; GASTRIC-CARCINOMA; CANCER-CELLS; IN-VITRO;
TGF-BETA; GROWTH; INVASION; METASTASIS; PROTEIN; EXPRESSION
AB BACKGROUND: The intake of dietary fatty acids is highly correlated with the risk of various cancers. Linoleic acid (LA) is the most abundant polyunsaturated fat in the western diet, but the mechanism(s) by fatty acids such as LA modulate cancer cells is unclear. In this study, we examined the role of LA in various steps in gastric cancer progression.
METHODS: The difference in gene expression between LA-treated and untreated OCUM-2MD3 gastric carcinoma cells was examined by mRNA differential display. The involvement of candidate genes was examined by oligo-and plasmid-mediated RNA interference. Biological functions of several of these genes were examined using in vitro assays for invasion, angiogenesis, apoptosis, cell viability, and matrix digestion. Angiogenesis in vivo was measured by CD-31 immunohistochemistry and microvessel density scoring.
RESULTS: LA enhanced the plasminogen activator inhibitor 1 (PAI-1) mRNA and protein expression, which are controlled by PAI-1 mRNA-binding protein. LA-stimulated invasion depended on PAI-1. LA also enhanced angiogenesis by suppression of angiostatin, also through PAI-1. LA did not alter cell growth in culture, but increased dietary LA-enhanced tumour growth in an animal model.
CONCLUSION: Our findings suggest that dietary LA impacts multiple steps in cancer invasion and angiogenesis, and that reducing LA in the diet may help slow cancer progression. British Journal of Cancer (2011) 105, 1750-1758. doi:10.1038/bjc.2011.434 www.bjcancer.com
C1 [Nishioka, N.; Matsuoka, T.; Olden, K.; Roberts, J. D.] NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Yashiro, M.; Hirakawa, K.] Osaka City Univ, Dept Surg Oncol, Grad Sch Med, Osaka 5458585, Japan.
RP Matsuoka, T (reprint author), NIEHS, Mol Carcinogenesis Lab, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM matsuoka@med.osaka-cu.ac.jp
FU NIH; NIEHS
FX This study was supported by the Intramural Research Programme of the NIH
and NIEHS.
NR 33
TC 4
Z9 4
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
J9 BRIT J CANCER
JI Br. J. Cancer
PD NOV 22
PY 2011
VL 105
IS 11
BP 1750
EP 1758
DI 10.1038/bjc.2011.434
PG 9
WC Oncology
SC Oncology
GA 857BA
UT WOS:000297687600019
PM 22015554
ER
PT J
AU Benavente, Y
Mbisa, G
Labo, N
Casabonne, D
Becker, N
Maynadie, M
Foretova, L
Cocco, PL
Nieters, A
Staines, A
Bofetta, P
Brennan, P
Whitby, D
de Sanjose, S
AF Benavente, Y.
Mbisa, G.
Labo, N.
Casabonne, D.
Becker, N.
Maynadie, M.
Foretova, L.
Cocco, P. L.
Nieters, A.
Staines, A.
Bofetta, P.
Brennan, P.
Whitby, D.
de Sanjose, S.
TI Antibodies against lytic and latent Kaposi's sarcoma-associated herpes
virus antigens and lymphoma in the European EpiLymph case-control study
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE epidemiology; Kaposi's sarcoma-associated herpes virus; human herpes
virus 8; serology; lymphoma
ID EPSTEIN-BARR-VIRUS; HUMAN-HERPESVIRUS-8 SEROPREVALENCE; BLOOD-DONORS;
INFECTION; CELLS; RISK
AB BACKGROUND: Kaposi's sarcoma-associated herpes virus is associated with primary effusion lymphoma and multicentric Castleman's disease.
METHODS: Seropositivity to lytic and latent Kaposi's sarcoma herpes virus (KSHV) antigens were examined in 2083 lymphomas and 2013 controls from six European countries.
RESULTS: Antibodies against KSHV latent and lytic antigens were detectable in 4.5% and 3.4% of controls, respectively, and 3.6% of cases (P>0.05). The KSHV seropositivity was associated with splenic marginal zone lymphoma (SMZL) (odds ratio (OR) = 4.11, 95% confidence interval (CI) 1.57-10.83) and multiple myeloma (OR = 0.31, 95% CI = 0.11-0.85).
CONCLUSION: The KSHV is unlikely to contribute importantly to lymphomagenesis among immunocompetent subjects. However, the observed association with SMZL may underline a chronic antigen mechanism in its aetiology. British Journal of Cancer (2011) 105, 1768-1771. doi:10.1038/bjc.2011.392 www.bjcancer.com
C1 [Benavente, Y.; Casabonne, D.; de Sanjose, S.] IDIBELL, Unit Infect & Canc UNIC, Canc Epidemiol Res Programme, Inst Catala Oncol, Barcelona 08908, Spain.
[Benavente, Y.; Casabonne, D.; de Sanjose, S.] CIBERESP, Sao Paulo, Brazil.
[Mbisa, G.] NCI, Viral Technol Lab, Adv Technol Program, SAIC Frederick Inc, Ft Detrick, MD 21702 USA.
[Labo, N.; Whitby, D.] NCI, Viral Oncol Sect, AIDS & Canc Virus Program, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Becker, N.] German Canc Res Ctr, Div Canc Epidemiol, D-69120 Heidelberg, Germany.
[Maynadie, M.] Univ Burgundy, Registre Hemopathies Malignes Cote Or, EA 4184, Dijon, France.
[Foretova, L.] Masaryk Mem Canc Inst, Brno, Czech Republic.
[Cocco, P. L.] Univ Cagliari, Dept Publ Hlth, Occupat Hlth Sect, Cagliari, Italy.
[Nieters, A.] Univ Med Ctr Freiburg, Dept Mol Epidemiol, Ctr Chron Immunodeficiency, Freiburg, Germany.
[Nieters, A.] German Canc Res Ctr, Dept Mol Tumour Epidemiol, D-69120 Heidelberg, Germany.
[Staines, A.] Publ Hlth Univ Coll, Dublin, Ireland.
[Bofetta, P.] Mt Sinai Sch Med, Tisch Canc Inst, New York, NY USA.
[Bofetta, P.] Int Prevent Res Inst, Lyon, France.
[Brennan, P.] Int Prevent Res Inst, IARC, F-69006 Lyon, France.
[Maynadie, M.] Biol Hematol Unit, Dijon, France.
[Maynadie, M.] Univ Hosp Dijon, CRB Ferdinand Cabanne, Dijon, France.
RP de Sanjose, S (reprint author), IDIBELL, Unit Infect & Canc UNIC, Canc Epidemiol Res Programme, Inst Catala Oncol, Gran Via Km 199-203, Barcelona 08908, Spain.
EM s.sanjose@iconcologia.net
RI Labo, Nazzarena/H-8655-2012; Casabonne, Delphine/H-6425-2014; de Sanjose
Llongueras, Silvia/H-6339-2014; Benavente, Yolanda/H-9810-2014;
OI Labo, Nazzarena/0000-0001-5953-4064; Staines,
Anthony/0000-0001-9161-1357
FU European Commission [QLK4-CT-2000-00422]; Association pour la Recherche
contre le Cancer (ARC) [5111]; Fondation de France (EpiLymph France)
[1999 008471]; Compagnia di San Paolo di Torino (EpiLymph-Italy);
Italian Ministry of Education, University and Research [2007WEJLZB];
Spanish Ministry of Health (EpiLymph-Spain) [C03/09, C03/10,
RD06/0020/0095, 06/02/0073, FIS 08-1555]; Agencia de Gestio d'Ajuts
Universitaris i de Recerca - Generalitat de Catalunya [AGAUR 2005SGR
00695, AGAUR 2009SGR1465, AGAUR 2009SGR126]; German Federal Ofce for
Radiation Protection (EpiLymp-Germany) [StSch4261, StSch4420]
FX We would like to thank all those who took part in this study, providing
questionnaire data and blood samples. This work was supported by a
European Commission Grant no. QLK4-CT-2000-00422 (EpiLymph studies);
Association pour la Recherche contre le Cancer (ARC no. 5111); the
Fondation de France (1999 008471; EpiLymph France); Compagnia di San
Paolo di Torino, Programma Oncologia 2001 (EpiLymph-Italy); Italian
Ministry of Education, University and Research (PRIN 2007, 2007WEJLZB);
Spanish Ministry of Health grants RCESP (C03/09), RTICESP (C03/10), RTIC
(RD06/0020/0095), CIBERESP (06/02/0073), FIS 08-1555 (EpiLymph-Spain)
and from the Agencia de Gestio d'Ajuts Universitaris i de Recerca -
Generalitat de Catalunya (AGAUR 2005SGR 00695, AGAUR 2009SGR1465 and
AGAUR 2009SGR126) who had no role in the data collection, analysis or
interpretation of the results; the German Federal Ofce for Radiation
Protection (StSch4261 and StSch4420; EpiLymp-Germany).
NR 12
TC 7
Z9 7
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
J9 BRIT J CANCER
JI Br. J. Cancer
PD NOV 22
PY 2011
VL 105
IS 11
BP 1768
EP 1771
DI 10.1038/bjc.2011.392
PG 4
WC Oncology
SC Oncology
GA 857BA
UT WOS:000297687600021
PM 21952625
ER
PT J
AU Hofmann, JN
Baccarelli, A
Schwartz, K
Davis, FG
Ruterbusch, JJ
Hoxha, M
McCarthy, BJ
Savage, SA
Wacholder, S
Rothman, N
Graubard, BI
Colt, JS
Chow, WH
Purdue, MP
AF Hofmann, J. N.
Baccarelli, A.
Schwartz, K.
Davis, F. G.
Ruterbusch, J. J.
Hoxha, M.
McCarthy, B. J.
Savage, S. A.
Wacholder, S.
Rothman, N.
Graubard, B. I.
Colt, J. S.
Chow, W-H
Purdue, M. P.
TI Risk of renal cell carcinoma in relation to blood telomere length in a
population-based case-control study
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE telomere; renal cell carcinoma; kidney cancer
ID PREDISPOSITION FACTOR; CIGARETTE-SMOKING; AFRICAN-AMERICANS;
QUANTITATIVE PCR; CANCER; ASSOCIATION; OBESITY; HYPERTENSION;
DYSFUNCTION
AB BACKGROUND: There are few known risk factors for renal cell carcinoma (RCC). Two small hospital-based case-control studies suggested an association between short blood telomere length (TL) and increased RCC risk.
METHODS: We conducted a large population-based case-control study in two metropolitan regions of the United States comparing relative TL in DNA derived from peripheral blood samples from 891 RCC cases and 894 controls. Odds ratios and 95% confidence intervals were estimated using unconditional logistic regression in both unadjusted and adjusted models.
RESULTS: Median TL was 0.85 for both cases and controls (P = 0.40), and no differences in RCC risk by quartiles of TL were observed. Results of analyses stratified by age, sex, race, tumour stage, and time from RCC diagnosis to blood collection were similarly null. In multivariate analyses among controls, increasing age and history of hypertension were associated with shorter TL (P<0.001 and P = 0.07, respectively), and African Americans had longer TL than Caucasians (P<0.001).
CONCLUSION: These data do not support the hypothesis that blood TL is associated with RCC. This population-based case-control study is, to our knowledge, the largest investigation to date of TL and RCC. British Journal of Cancer (2011) 105, 1772-1775. doi:10.1038/bjc.2011.444 www.bjcancer.com
C1 [Hofmann, J. N.; Savage, S. A.; Wacholder, S.; Rothman, N.; Graubard, B. I.; Colt, J. S.; Chow, W-H; Purdue, M. P.] NCI, Div Canc Epidemiol & Genet, Occupat & Environm Epidemiol Branch, Bethesda, MD 20892 USA.
[Baccarelli, A.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Schwartz, K.; Ruterbusch, J. J.] Wayne State Univ, Dept Family Med & Publ Hlth Sci, Karmanos Canc Inst, Detroit, MI USA.
[Davis, F. G.; McCarthy, B. J.] Univ Illinois, Sch Publ Hlth, Div Epidemiol & Biostat, Chicago, IL USA.
[Hoxha, M.] Univ Milan, Dept Occupat & Environm Hlth, Milan, Italy.
[Hoxha, M.] Ca Granda Osped Maggiore Policlin Hosp IRCCS Fdn, Milan, Italy.
RP Hofmann, JN (reprint author), NCI, Div Canc Epidemiol & Genet, Occupat & Environm Epidemiol Branch, 6120 Execut Blvd,EPS 8109, Bethesda, MD 20892 USA.
EM hofmannjn@mail.nih.gov
RI Purdue, Mark/C-9228-2016; Savage, Sharon/B-9747-2015;
OI Purdue, Mark/0000-0003-1177-3108; Savage, Sharon/0000-0001-6006-0740;
Baccarelli, Andrea/0000-0002-3436-0640
FU National Institutes of Health, National Cancer Institute, Division of
Cancer Epidemiology and Genetics; HSPH-NIEHS Center for Environmental
Health [ES000002]
FX This research was supported in part by the Intramural Research Program
of the National Institutes of Health, National Cancer Institute,
Division of Cancer Epidemiology and Genetics. We thank Kate Torres,
Marsha Dunn, and other staff at Westat, Inc. and Stella Munuo and other
staff at Information Management Services, Inc. for their efforts on this
project. Finally, we express our gratitude to the participants in this
study for their involvement.; Dr Baccarelli receives salary support from
New Investigator funding from the HSPH-NIEHS Center for Environmental
Health (ES000002). The other authors declare no conflict of interest.
NR 19
TC 8
Z9 8
U1 1
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
J9 BRIT J CANCER
JI Br. J. Cancer
PD NOV 22
PY 2011
VL 105
IS 11
BP 1772
EP 1775
DI 10.1038/bjc.2011.444
PG 4
WC Oncology
SC Oncology
GA 857BA
UT WOS:000297687600022
PM 22033273
ER
PT J
AU Hochman, JS
Reynolds, HR
Dzavik, V
Buller, CE
Ruzyllo, W
Sadowski, ZP
Maggioni, AP
Carvalho, AC
Rankin, JM
White, HD
Goldberg, S
Forman, SA
Mark, DB
Lamas, GA
AF Hochman, Judith S.
Reynolds, Harmony R.
Dzavik, Vladimir
Buller, Christopher E.
Ruzyllo, Witold
Sadowski, Zygmunt P.
Maggioni, Aldo P.
Carvalho, Antonio C.
Rankin, James M.
White, Harvey D.
Goldberg, Suzanne
Forman, Sandra A.
Mark, Daniel B.
Lamas, Gervasio A.
CA Occluded Artery Trial
TI Long-Term Effects of Percutaneous Coronary Intervention of the Totally
Occluded Infarct-Related Artery in the Subacute Phase After Myocardial
Infarction
SO CIRCULATION
LA English
DT Article
DE myocardial infarction; stents; trials
ID LEFT-VENTRICULAR DYSFUNCTION; TRIAL OAT; VIABILITY; REVASCULARIZATION;
CLOPIDOGREL; THERAPY; ASSOCIATION; ELEVATION; OCCLUSION; ASPIRIN
AB Background-Despite observations suggesting a benefit for late opening of totally occluded infarct-related arteries after myocardial infarction, the Occluded Artery Trial (OAT) demonstrated no reduction in the composite of death, reinfarction, and class IV heart failure over a 2.9-year mean follow-up. Follow-up was extended to determine whether late trends would favor either treatment group.
Methods and Results-OAT randomized 2201 stable patients with infarct-related artery total occlusion >24 hours (calendar days 3-28) after myocardial infarction. Patients with severe inducible ischemia, rest angina, class III-IV heart failure, and 3-vessel/left main disease were excluded. We conducted extended follow-up of enrolled patients for an additional 3 years for the primary end point and angina (6-year median survivor follow-up; longest, 9 years; 12 234 patient-years). Rates of the primary end point (hazard ratio, 1.06; 95% confidence interval, 0.88-1.28), fatal and nonfatal myocardial infarction (hazard ratio, 1.25; 95% confidence interval, 0.89-1.75), death, and class IV heart failure were similar for the percutaneous coronary intervention (PCI) and medical therapy alone groups. No interactions between baseline characteristics and treatment group on outcomes were observed. The vast majority of patients at each follow-up visit did not report angina. There was less angina in the PCI group through early in follow-up; by 3 years, the between group difference was consistently <4 patients per 100 treated and not significantly different, although there was a trend toward less angina in the PCI group at 3 and 5 years. The 7-year rate of PCI of the infarct-related artery during follow-up was 11.1% for the PCI group compared with 14.7% for the medical therapy alone group (hazard ratio, 0.79; 95% confidence interval, 0.61-1.01; P = 0.06).
Conclusions-Extended follow-up of the OAT cohort provides robust evidence for no reduction of long-term rates of clinical events after routine PCI in stable patients with a totally occluded infarct-related artery and without severe inducible ischemia in the subacute phase after myocardial infarction.
C1 [Hochman, Judith S.] NYU, Sch Med, Cardiovasc Clin Res Ctr, Leon Charney Div Cardiol, New York, NY 10016 USA.
[Dzavik, Vladimir] Univ Hlth Network, Peter Munk Cardiac Ctr, Toronto, ON, Canada.
[Buller, Christopher E.] Univ Toronto, St Michaels Hosp, Div Cardiol, Toronto, ON M5B 1W8, Canada.
[Buller, Christopher E.] Univ Toronto, Dept Med, Toronto, ON, Canada.
[Ruzyllo, Witold; Sadowski, Zygmunt P.] Natl Inst Cardiol, Warsaw, Poland.
[Maggioni, Aldo P.] Italian Assoc Hosp Cardiologist ANMCO, Res Ctr, Florence, Italy.
[Carvalho, Antonio C.] Hosp Sao Paulo, Sao Paulo, Brazil.
[Rankin, James M.] Royal Perth Hosp, Dept Cardiovasc Med, Perth, WA, Australia.
[White, Harvey D.] Auckland City Hosp, Green Lane Cardiovasc Serv, Auckland, New Zealand.
[Goldberg, Suzanne] NHLBI, NIH, Bethesda, MD 20892 USA.
[Forman, Sandra A.] Clin Trials & Surveys Corp, Owings Mills, MD USA.
[Mark, Daniel B.] Duke Univ, Duke Clin Res Inst, Durham, NC USA.
[Lamas, Gervasio A.] Mt Sinai Med Ctr, Miami Beach, FL 33140 USA.
RP Hochman, JS (reprint author), NYU, Sch Med, Cardiovasc Clin Res Ctr, Leon Charney Div Cardiol, 530 1st Ave,SKI 9R, New York, NY 10016 USA.
EM Judith.Hochman@nyumc.org
RI Reynolds, Harmony/M-4818-2013;
OI Reynolds, Harmony/0000-0003-0284-0655; Mark, Daniel/0000-0001-6340-8087;
Hochman, Judith/0000-0002-5889-5981; Maggioni, Aldo
Pietro/0000-0003-2764-6779
FU NHLBI [U01HL062509, U01HL062511]
FX The NHLBI funded and oversaw the conduct of this trial. The project
described was supported by awards U01HL062509 and U01HL062511 from the
NHLBI. The content is solely the responsibility of the authors and does
not necessarily represent the official views of the NHLBI or the
National Institutes of Health.
NR 28
TC 21
Z9 25
U1 0
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
BP 2320
EP 2328
DI 10.1161/CIRCULATIONAHA.111.041749
PG 9
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 852BR
UT WOS:000297320900016
PM 22025606
ER
PT J
AU Murphy, TP
Cutlip, D
Regensteiner, J
Mohler, E
Goldberg, S
Massaro, J
Cohen, D
Reynolds, M
Lewis, B
Cerezo, J
Oldenburg, N
Thum, C
Hirsch, A
AF Murphy, Timothy P.
Cutlip, Donald
Regensteiner, Judith
Mohler, Emile
Goldberg, Suzanne
Massaro, Joseph
Cohen, David
Reynolds, Matthew
Lewis, Beth
Cerezo, Joselyn
Oldenburg, Niki
Thum, Claudia
Hirsch, Alan
TI Claudication Treatment Comparative Effectiveness: 6 Month Outcomes From
the CLEVER Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT American-Heart-Association Scientific Sessions on Resuscitation Science
Symposium
CY NOV 12-15, 2011
CL Orlando, FL
SP Amer Heart Assoc
C1 [Murphy, Timothy P.; Cerezo, Joselyn] Rhode Isl Hosp, Providence, RI USA.
[Cutlip, Donald; Reynolds, Matthew] Beth Israel Deaconess Med Ctr, Boston, MA USA.
[Regensteiner, Judith] Univ Colorado Hlth Sci Cntr, Denver, CO USA.
[Mohler, Emile] Univ Penn, Philadelphia, PA 19104 USA.
[Goldberg, Suzanne] NHLBI, Bethesda, MD 20892 USA.
[Massaro, Joseph] Boston Univ, Boston, MA 02215 USA.
[Cohen, David] St Lukes Hosp, Kansas City, MO USA.
[Lewis, Beth] Hlth Partners, Minneapolis, MN USA.
[Oldenburg, Niki; Hirsch, Alan] Univ Minnesota, Minneapolis, MN USA.
[Thum, Claudia] Harvard Clin Rsch Inst, Boston, MA 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
BP 2371
EP 2371
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 852BR
UT WOS:000297320900041
ER
PT J
AU Traverse, JH
Henry, TD
Ellis, SG
Pepine, CJ
Willerson, JT
Zhao, DX
Simpson, LM
Perin, EC
Penn, MS
Baran, KW
Chambers, J
Lambert, C
Raveendran, G
Simon, DI
Gee, AP
Forder, JR
Taylor, DA
Cogle, CR
Olson, RE
Jorgenson, BC
Smith, DX
Geither, C
Skarlatos, SI
Moye, LA
Simari, RD
AF Traverse, Jay H.
Henry, Timothy D.
Ellis, Stephen G.
Pepine, Carl J.
Willerson, James T.
Zhao, David X.
Simpson, Lara M.
Perin, Emerson C.
Penn, Marc S.
Baran, Kenneth W.
Chambers, Jeffrey
Lambert, Charles
Raveendran, Ganesh
Simon, Daniel I.
Gee, Adrian P.
Forder, John R.
Taylor, Doris A.
Cogle, Christopher R.
Olson, Rachel E.
Jorgenson, Beth C.
Smith, Deirdre X.
Geither, Carrie
Skarlatos, Sonia I.
Moye, Lemuel A.
Simari, Robert D.
TI Results From LateTIME: A Randomized, Placebo Controlled Trial of
Intracoronary Stem Cell Delivery Two to Three Weeks Following Acute
Myocardial Infarction
SO CIRCULATION
LA English
DT Meeting Abstract
CT American-Heart-Association Scientific Sessions on Resuscitation Science
Symposium
CY NOV 12-15, 2011
CL Orlando, FL
SP Amer Heart Assoc
C1 [Traverse, Jay H.; Henry, Timothy D.; Olson, Rachel E.; Jorgenson, Beth C.] Abbott NW Hosp, Minneapolis Heart Inst, Minneapolis, MN 55407 USA.
[Ellis, Stephen G.; Penn, Marc S.; Geither, Carrie] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Pepine, Carl J.; Cogle, Christopher R.] Univ Florida Sch Med, Gainesville, FL USA.
[Willerson, James T.; Perin, Emerson C.; Smith, Deirdre X.] Texas Heart Inst, Houston, TX 77025 USA.
[Zhao, David X.] Vanderbilt Univ Sch Med, Nashville, TN USA.
[Simpson, Lara M.; Moye, Lemuel A.] Univ Texas Sch Publ Hlth, Houston, TX USA.
[Baran, Kenneth W.] St Paul Heart Clin United Hosp, St Paul, MN USA.
[Chambers, Jeffrey] Metro Cardiol Mercy Hosp, Coon Rapids, MN USA.
[Lambert, Charles] Pepin Heart Hosp, Tampa, FL USA.
[Lambert, Charles] Patel Res Inst, Tampa, FL USA.
[Raveendran, Ganesh; Simari, Robert D.] Univ Minnesota, Minneapolis, MN USA.
[Simon, Daniel I.] Univ Hosp Case Med Cntr, Cleveland, OH USA.
[Gee, Adrian P.] Baylor Univ Sch Med, Houston, TX USA.
[Forder, John R.] Univ Florida Sch Med, Gainesville, FL USA.
[Taylor, Doris A.] Univ Minnesota Sch Med, Minneapolis, MN USA.
[Skarlatos, Sonia I.] NHLBI, Bethesda, MD 20892 USA.
[Simari, Robert D.] Mayo Clin, Rochester, MN 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
J9 CIRCULATION
JI Circulation
PD NOV 22
PY 2011
VL 124
IS 21
BP 2372
EP 2372
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 852BR
UT WOS:000297320900044
ER
PT J
AU Sadeh, B
Pitcher, D
Brandman, T
Eisen, A
Thaler, A
Yovel, G
AF Sadeh, Boaz
Pitcher, David
Brandman, Talia
Eisen, Ami
Thaler, Avner
Yovel, Galit
TI Stimulation of Category-Selective Brain Areas Modulates ERP to Their
Preferred Categories
SO CURRENT BIOLOGY
LA English
DT Article
ID TRANSCRANIAL MAGNETIC STIMULATION; FACE-SENSITIVE N170; POTENTIAL
COMPONENT; EVOKED-POTENTIALS; BODY PERCEPTION; PARIETAL CORTEX; INVERTED
FACES; OBJECTS; FMRI; RECOGNITION
AB Neural selectivity to specific object categories has been demonstrated in extrastriate cortex with both functional MRI [1-3] and event-related potential (ERP) [4, 5]. Here we tested for a causal relationship between the activation of category-selective areas and ERP to their preferred categories. Electroencephalogram (EEG) was recorded while participants observed faces and headless bodies. Concurrently with EEG recording, we delivered two pulses of transcranial magnetic stimulation (TMS) over the right occipital face area (OFA) or extrastriate body area (EBA) at 60 and 100 ms after stimulus onset. Results showed a clear dissociation between the stimulated site and the stimulus category on ERP modulation: stimulation of the OFA significantly increased the N1 amplitude to faces but not to bodies, whereas stimulation of the EBA significantly increased the N1 amplitude to bodies but not to faces. These findings provide the first evidence for a specific and causal link between activity in category-selective networks and scalp-recorded ERP to their preferred categories. This result also demonstrates that the face and body N1 reflects several nonoverlapping neural sources, rather than changes in face-selective mechanisms alone. Lastly, because early stimulation (60-100 ms) affected selectivity of a later ERP component (150-200 ms), the results could imply a feed-forward connection between occipital and temporal category-selective areas.
C1 [Sadeh, Boaz; Brandman, Talia; Eisen, Ami; Yovel, Galit] Tel Aviv Univ, Dept Psychol, IL-69978 Tel Aviv, Israel.
[Pitcher, David] NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA.
[Thaler, Avner] Tel Aviv Sourasky Med Ctr, Wohl Inst Adv Imaging, Funct Brain Ctr, IL-46239 Tel Aviv, Israel.
RP Sadeh, B (reprint author), Tel Aviv Univ, Dept Psychol, IL-69978 Tel Aviv, Israel.
EM boazsadeh@gmail.com; galit@freud.tau.ac.il
RI sadeh, boaz/B-2726-2012
FU Levie-Edersheim-Gitter Institute for Brain Mapping; Israeli Science
Foundation [65/08, 1657/08]; British Council
FX We thank M. Medvedovsky, S. Ghalchi, M. Livne, and J. Walerstein for
assistance in data collection. We also thank V. Axelrod, G. Fuggetta, R.
Stormer, and Z. Peremen for useful advice. This research was funded by a
fellowship from the Levie-Edersheim-Gitter Institute for Brain Mapping
to B.S, grants 65/08 and 1657/08 from the Israeli Science Foundation to
G.Y, and a travel grant from the British Council Researcher Exchange
Programme to G.Y and D.P.
NR 43
TC 26
Z9 26
U1 1
U2 8
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0960-9822
J9 CURR BIOL
JI Curr. Biol.
PD NOV 22
PY 2011
VL 21
IS 22
BP 1894
EP 1899
DI 10.1016/j.cub.2011.09.030
PG 6
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 852XY
UT WOS:000297392000019
PM 22036183
ER
PT J
AU Panda, D
Das, A
Dinh, PX
Subramaniam, S
Nayak, D
Barrows, NJ
Pearson, JL
Thompson, J
Kelly, DL
Ladunga, I
Pattnaik, AK
AF Panda, Debasis
Das, Anshuman
Dinh, Phat X.
Subramaniam, Sakthivel
Nayak, Debasis
Barrows, Nicholas J.
Pearson, James L.
Thompson, Jesse
Kelly, David L.
Ladunga, Istvan
Pattnaik, Asit K.
TI RNAi screening reveals requirement for host cell secretory pathway in
infection by diverse families of negative-strand RNA viruses
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE RNA interference; transcription and replication; host cell factors for
virus infection
ID VESICULAR STOMATITIS-VIRUS; FUNCTIONAL GENOMIC SCREEN; EXCHANGE FACTOR
GBF1; WEST-NILE-VIRUS; DENGUE VIRUS; REPLICATION; GOLGI; PROTEINS;
GENES; TRANSLATION
AB Negative-strand (NS) RNA viruses comprise many pathogens that cause serious diseases in humans and animals. Despite their clinical importance, little is known about the host factors required for their infection. Using vesicular stomatitis virus (VSV), a prototypic NS RNA virus in the family Rhabdoviridae, we conducted a human genome-wide siRNA screen and identified 72 host genes required for viral infection. Many of these identified genes were also required for infection by two other NS RNA viruses, the lymphocytic choriomeningitis virus of the Arenaviridae family and human parainfluenza virus type 3 of the Paramyxoviridae family. Genes affecting different stages of VSV infection, such as entry/uncoating, gene expression, and assembly/release, were identified. Depletion of the proteins of the coatomer complex I or its upstream effectors ARF1 or GBF1 led to detection of reduced levels of VSV RNA. Coatomer complex I was also required for infection of lymphocytic choriomeningitis virus and human parainfluenza virus type 3. These results highlight the evolutionarily conserved requirements for gene expression of diverse families of NS RNA viruses and demonstrate the involvement of host cell secretory pathway in the process.
C1 [Panda, Debasis; Das, Anshuman; Dinh, Phat X.; Subramaniam, Sakthivel; Pattnaik, Asit K.] Univ Nebraska, Sch Vet Med & Biomed Sci, Lincoln, NE 68583 USA.
[Panda, Debasis; Das, Anshuman; Dinh, Phat X.; Subramaniam, Sakthivel; Thompson, Jesse; Pattnaik, Asit K.] Univ Nebraska, Nebraska Ctr Virol, Lincoln, NE 68583 USA.
[Nayak, Debasis] Natl Inst Neurol Disorders & Stroke, NIH, Bethesda, MD 20892 USA.
[Barrows, Nicholas J.; Pearson, James L.] Duke Univ, Duke RNAi Screening Facil, Med Ctr, Durham, NC 27710 USA.
[Kelly, David L.] Univ Nebraska Med Ctr, Omaha, NE 68198 USA.
[Ladunga, Istvan] Univ Nebraska, Dept Stat, Lincoln, NE 68588 USA.
RP Pattnaik, AK (reprint author), Univ Nebraska, Sch Vet Med & Biomed Sci, Lincoln, NE 68583 USA.
EM apattnaik2@unl.edu
RI Subramaniam, Sakthivel/L-2265-2016;
OI Subramaniam, Sakthivel/0000-0001-6299-3835; Panda,
Debasis/0000-0003-3806-6665
FU National Institutes of Health [R01AI34956]
FX We thank G. Belov, P. Collins, J. Donaldson, D. Lyles, D. McGavern, and
E. Sztul for reagents and Z. H. Gill for excellent assistance in the
laboratory. The work was supported in part by National Institutes of
Health Grant R01AI34956.
NR 50
TC 39
Z9 39
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 22
PY 2011
VL 108
IS 47
BP 19036
EP 19041
DI 10.1073/pnas.1113643108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 851DY
UT WOS:000297249800040
PM 22065774
ER
PT J
AU Arana, ME
Potapova, O
Kunkel, TA
Joyce, CM
AF Arana, Mercedes E.
Potapova, Olga
Kunkel, Thomas A.
Joyce, Catherine M.
TI Kinetic Analysis of the Unique Error Signature of Human DNA Polymerase
nu
SO BIOCHEMISTRY
LA English
DT Article
ID I KLENOW FRAGMENT; CROSS-LINK REPAIR; ESCHERICHIA-COLI;
SACCHAROMYCES-CEREVISIAE; LOW-FIDELITY; CRYSTAL-STRUCTURE; REPLICATION;
BASE; PROCESSIVITY; EXONUCLEASE
AB The fidelity of DNA synthesis by A-family DNA polymerases ranges from very accurate for bacterial, bacteriophage, and mitochondrial family members to very low for certain eukaryotic homologues. The latter include DNA polymerase nu (Pol nu) which, among all A-family polymerases, is uniquely prone to misincorporating dTTP opposite template G in a highly sequence-dependent manner. Here we present a kinetic analysis of this unusual error specificity, in four different sequence contexts and in comparison to Pol nu's more accurate A-family homologue, the Klenow fragment of Escherichia coli DNA polymerase I. The kinetic data strongly correlate with rates of stable misincorporation during gap-filling DNA synthesis. The lower fidelity of Pol nu compared to that of Klenow fragment can be attributed primarily to a much lower catalytic efficiency for correct dNTP incorporation, whereas both enzymes have similar kinetic parameters for G-dTTP misinsertion. The major contributor to sequence-dependent differences in Pol nu error rates is the reaction rate, k(pol). In the sequence context where fidelity is highest, k(pol) for correct G-dCTP incorporation by Pol nu is similar to 15-fold faster than k(pol) for G-dTTP misinsertion. However, in sequence contexts where the error rate is higher, k(pol) is the same for both correct and mismatched dNTPs, implying that the transition state does not provide additional discrimination against misinsertion. The results suggest that Pol nu may be fine-tuned to function when high enzyme activity is not a priority and may even be disadvantageous and that the relaxed active-site specificity toward the G-dTTP mispair may be associated with its cellular function(s).
C1 [Joyce, Catherine M.] Yale Univ, Dept Mol Biophys & Biochem, Bass Ctr Mol & Struct Biol, New Haven, CT 06520 USA.
[Arana, Mercedes E.; Kunkel, Thomas A.] NIEHS, Mol Genet Lab, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
[Arana, Mercedes E.; Kunkel, Thomas A.] NIEHS, Struct Biol Lab, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
RP Joyce, CM (reprint author), Yale Univ, Dept Mol Biophys & Biochem, Bass Ctr Mol & Struct Biol, 266 Whitney Ave,POB 208114, New Haven, CT 06520 USA.
EM catherine.joyce@yale.edu
FU Division of Intramural Research of the National Institute of
Environmental Health Sciences [Z01 ES065070]; National Institutes of
Health [GM28550]
FX This work was supported by Project Z01 ES065070 (to T.A.K.) from the
Division of Intramural Research of the National Institute of
Environmental Health Sciences, and National Institutes of Health Grant
GM28550 (to C.M.J.).
NR 56
TC 7
Z9 7
U1 1
U2 3
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD NOV 22
PY 2011
VL 50
IS 46
BP 10126
EP 10135
DI 10.1021/bi201197p
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 846JO
UT WOS:000296893700018
PM 22008035
ER
PT J
AU Roy, CJ
Ault, A
Sivasubramani, SK
Gorres, JP
Wei, CJ
Andersen, H
Gall, J
Roederer, M
Rao, SS
AF Roy, Chad J.
Ault, Alida
Sivasubramani, Satheesh K.
Gorres, J. Patrick
Wei, Chih-Jen
Andersen, Hanne
Gall, Jason
Roederer, Mario
Rao, Srinivas S.
TI Aerosolized adenovirus-vectored vaccine as an alternative vaccine
delivery method
SO RESPIRATORY RESEARCH
LA English
DT Article
ID A VIRUS-INFECTION; HETEROSUBTYPIC IMMUNITY; INFLUENZA-VIRUS;
RESPIRATORY-TRACT; CROSS-PROTECTION; IN-VITRO; IMMUNIZATION; RESPONSES;
MICE; H5N1
AB Conventional parenteral injection of vaccines is limited in its ability to induce locally-produced immune responses in the respiratory tract, and has logistical disadvantages in widespread vaccine administration. Recent studies suggest that intranasal delivery or vaccination in the respiratory tract with recombinant viral vectors can enhance immunogenicity and protection against respiratory diseases such as influenza and tuberculosis, and can offer more broad-based generalized protection by eliciting durable mucosal immune responses. Controlled aerosolization is a method to minimize vaccine particle size and ensure delivery to the lower respiratory tract. Here, we characterize the dynamics of aerosolization and show the effects of vaccine concentration on particle size, vector viability, and the actual delivered dose of an aerosolized adenoviral vector. In addition, we demonstrate that aerosol delivery of a recombinant adenoviral vaccine encoding H1N1 hemagglutinin is immunogenic and protects ferrets against homologous viral challenge. Overall, aerosol delivery offers comparable protection to intramuscular injection, and represents an attractive vaccine delivery method for broad-based immunization campaigns.
C1 [Ault, Alida; Gorres, J. Patrick; Rao, Srinivas S.] NIH, Lab Anim Med, Vaccine Res Ctr, Bethesda, MD 20895 USA.
[Roy, Chad J.; Sivasubramani, Satheesh K.] Tulane Natl Primate Res Ctr, Div Microbiol, Covington, LA 70447 USA.
[Wei, Chih-Jen] NIH, Vector Core Sect, Vaccine Res Ctr, Bethesda, MD 20895 USA.
[Andersen, Hanne] BIOQUAL Inc, Rockville, MD 20850 USA.
[Gall, Jason] GenVec Inc, Gaithersburg, MD 20878 USA.
[Roederer, Mario] NIH, ImmunoTechnol Sect, Vaccine Res Ctr, Bethesda, MD 20895 USA.
RP Rao, SS (reprint author), NIH, Lab Anim Med, Vaccine Res Ctr, Bethesda, MD 20895 USA.
EM srao1@mail.nih.gov
NR 38
TC 10
Z9 10
U1 0
U2 4
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1465-993X
J9 RESP RES
JI Respir. Res.
PD NOV 21
PY 2011
VL 12
AR 153
DI 10.1186/1465-9921-12-153
PG 7
WC Respiratory System
SC Respiratory System
GA 911KE
UT WOS:000301714900001
PM 22103776
ER
PT J
AU Machado, JP
Johnson, WE
O'Brien, SJ
Vasconcelos, V
Antunes, A
AF Machado, Joao Paulo
Johnson, Warren E.
O'Brien, Stephen J.
Vasconcelos, Vitor
Antunes, Agostinho
TI Adaptive evolution of the matrix extracellular phosphoglycoprotein in
mammals
SO BMC EVOLUTIONARY BIOLOGY
LA English
DT Article
ID AMINO-ACID SITES; DETECTING POSITIVE SELECTION; MEPE-ASARM-PEPTIDE;
MAXIMUM-LIKELIHOOD; NUCLEOTIDE SUBSTITUTION; PHYLOGENETIC ANALYSIS;
MOLECULAR EVOLUTION; PURIFYING SELECTION; SEQUENCE ALIGNMENT;
BAYESIAN-INFERENCE
AB Background: Matrix extracellular phosphoglycoprotein (MEPE) belongs to a family of small integrin-binding ligand N-linked glycoproteins (SIBLINGs) that play a key role in skeleton development, particularly in mineralization, phosphate regulation and osteogenesis. MEPE associated disorders cause various physiological effects, such as loss of bone mass, tumors and disruption of renal function (hypophosphatemia). The study of this developmental gene from an evolutionary perspective could provide valuable insights on the adaptive diversification of morphological phenotypes in vertebrates.
Results: Here we studied the adaptive evolution of the MEPE gene in 26 Eutherian mammals and three birds. The comparative genomic analyses revealed a high degree of evolutionary conservation of some coding and non coding regions of the MEPE gene across mammals indicating a possible regulatory or functional role likely related with mineralization and/or phosphate regulation. However, the majority of the coding region had a fast evolutionary rate, particularly within the largest exon (1467 bp). Rodentia and Scandentia had distinct substitution rates with an increased accumulation of both synonymous and non-synonymous mutations compared with other mammalian lineages. Characteristics of the gene (e. g. biochemical, evolutionary rate, and intronic conservation) differed greatly among lineages of the eight mammalian orders. We identified 20 sites with significant positive selection signatures (codon and protein level) outside the main regulatory motifs (dentonin and ASARM) suggestive of an adaptive role. Conversely, we find three sites under selection in the signal peptide and one in the ASARM motif that were supported by at least one selection model. The MEPE protein tends to accumulate amino acids promoting disorder and potential phosphorylation targets.
Conclusion: MEPE shows a high number of selection signatures, revealing the crucial role of positive selection in the evolution of this SIBLING member. The selection signatures were found mainly outside the functional motifs, reinforcing the idea that other regions outside the dentonin and the ASARM might be crucial for the function of the protein and future studies should be undertaken to understand its importance.
C1 [Machado, Joao Paulo; Vasconcelos, Vitor; Antunes, Agostinho] Univ Porto, CIMAR CIIMAR, Ctr Interdisciplinar Invest Marinha & Ambiental, P-4050123 Oporto, Portugal.
[Machado, Joao Paulo] Univ Porto, Inst Ciencias Biomed Abel Salazar ICBAS, Oporto, Portugal.
[Johnson, Warren E.; O'Brien, Stephen J.; Antunes, Agostinho] NCI, Lab Genom Divers, Frederick, MD 21702 USA.
[Vasconcelos, Vitor; Antunes, Agostinho] Univ Porto, Dept Biol, Fac Ciencias, P-4169007 Oporto, Portugal.
RP Antunes, A (reprint author), Univ Porto, CIMAR CIIMAR, Ctr Interdisciplinar Invest Marinha & Ambiental, Rua Bragas 177, P-4050123 Oporto, Portugal.
EM aantunes@ciimar.up.pt
RI Vasconcelos, Vitor/A-8933-2008; Scientific output, CIIMAR/E-5122-2012;
Johnson, Warren/D-4149-2016;
OI Vasconcelos, Vitor/0000-0003-3585-2417; Scientific output,
CIIMAR/0000-0001-6270-2153; Johnson, Warren/0000-0002-5954-186X;
O'Brien, Stephen J./0000-0001-7353-8301; Antunes,
Agostinho/0000-0002-1328-1732
FU Portuguese Fundacao para a Ciencia e a Tecnologia (FCT)
[SFRH/BD/65245/2009]; Iceland through the EEA Financial Mechanism;
Liechtenstein through the EEA Financial Mechanism; Norway through the
EEA Financial Mechanism; Norwegian Financial Mechanism;
[PTDC/BIA-BDE/69144/2006 (FCOMP-01-0124-FEDER-007065];
[PTDC/AAC-AMB/104983/2008 (FCOMP-01-0124-FEDER-008610)]
FX The authors acknowledge the Portuguese Fundacao para a Ciencia e a
Tecnologia (FCT) for financial support to JPM (SFRH/BD/65245/2009) and
the project PTDC/BIA-BDE/69144/2006 (FCOMP-01-0124-FEDER-007065) and
PTDC/AAC-AMB/104983/2008 (FCOMP-01-0124-FEDER-008610). This work was
further supported by a grant from Iceland, Liechtenstein and Norway
through the EEA Financial Mechanism and the Norwegian Financial
Mechanism. We thank Siby Philip from LEGE/CIIMAR for discussion and
helpful suggestions. Comments made by the anonymous reviewers improved a
previous version of this manuscript.
NR 104
TC 11
Z9 11
U1 1
U2 12
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2148
J9 BMC EVOL BIOL
JI BMC Evol. Biol.
PD NOV 21
PY 2011
VL 11
AR 342
DI 10.1186/1471-2148-11-342
PG 23
WC Evolutionary Biology; Genetics & Heredity
SC Evolutionary Biology; Genetics & Heredity
GA 873NH
UT WOS:000298889500001
PM 22103247
ER
PT J
AU Hickman, HD
Li, L
Reynoso, GV
Rubin, EJ
Skon, CN
Mays, JW
Gibbs, J
Schwartz, O
Bennink, JR
Yewdell, JW
AF Hickman, Heather D.
Li, Lily
Reynoso, Glennys V.
Rubin, Erica J.
Skon, Cara N.
Mays, Jacqueline W.
Gibbs, James
Schwartz, Owen
Bennink, Jack R.
Yewdell, Jonathan W.
TI Chemokines control naive CD8(+) T cell selection of optimal lymph node
antigen presenting cells
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID SUBCAPSULAR SINUS MACROPHAGES; CD8-ALPHA(+) DENDRITIC CELLS; IN-VIVO
DEPLETION; B-CELLS; ANTIVIRAL IMMUNITY; CYTOSOLIC PEPTIDES; VIRAL
CLEARANCE; INFECTION; VIRUS; RESPONSES
AB Naive antiviral CD8(+) T cells are activated in the draining LN (DLN) by dendritic cells (DCs) presenting viral antigens. However, many viruses infect LN macrophages, which participate in initiation of innate immunity and B cell activation. To better understand how and why T cells select infected DCs rather than macrophages, we performed intravital microscopy and ex vivo analyses after infecting mice with vaccinia virus (V V), a large DNA virus that infects both LN macrophages and DCs. Although CD8(+) T cells interact with both infected macrophages and DCs in the LN peripheral interfollicular region (PIR), DCs generate more frequent and stable interactions with T cells. V V infection induces rapid release of CCR5-binding chemokines in the LN, and administration of chemokine-neutralizing antibodies diminishes T cell activation by increasing T cell localization to macrophages in the macrophage-rich region (MRR) at the expense of PIR DCs. Similarly, DC ablation increases both T cell localization to the MRR and the duration of T cell-macrophage contacts, resulting in suboptimal T cell activation. Thus, virusinduced chemokines in DLNs enable antiviral CD8(+) T cells to distinguish DCs from macrophages to optimize T cell priming.
C1 [Hickman, Heather D.; Li, Lily; Reynoso, Glennys V.; Rubin, Erica J.; Skon, Cara N.; Mays, Jacqueline W.; Gibbs, James; Bennink, Jack R.; Yewdell, Jonathan W.] NIAID, Cell Biol Sect, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
[Hickman, Heather D.; Li, Lily; Reynoso, Glennys V.; Rubin, Erica J.; Skon, Cara N.; Mays, Jacqueline W.; Gibbs, James; Bennink, Jack R.; Yewdell, Jonathan W.] NIAID, Viral Immunol Sect, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
[Schwartz, Owen] NIAID, Biol Imaging Facil, Res Technol Branch, NIH, Bethesda, MD 20892 USA.
RP Yewdell, JW (reprint author), NIAID, Cell Biol Sect, Viral Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM jyewdell@mail.nih.gov
RI yewdell, jyewdell@nih.gov/A-1702-2012
FU Division of Intramural Research, NIAID, National Institutes of Health
FX This work was funded by the Division of Intramural Research, NIAID,
National Institutes of Health
NR 52
TC 45
Z9 46
U1 1
U2 6
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0022-1007
J9 J EXP MED
JI J. Exp. Med.
PD NOV 21
PY 2011
VL 208
IS 12
BP 2511
EP 2524
DI 10.1084/jem.20102545
PG 14
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 859IS
UT WOS:000297870700018
PM 22042976
ER
PT J
AU Fatakia, SN
Costanzi, S
Chow, CC
AF Fatakia, Sarosh N.
Costanzi, Stefano
Chow, Carson C.
TI Molecular Evolution of the Transmembrane Domains of G Protein-Coupled
Receptors
SO PLOS ONE
LA English
DT Article
ID ADAPTIVE EVOLUTION; PHYLOGENETIC ANALYSIS; FUNCTIONAL EVOLUTION; GENES;
GENOME; RHODOPSIN; SEQUENCE; CRYSTAL; MODELS; YEAST
AB G protein-coupled receptors (GPCRs) are a superfamily of integral membrane proteins vital for signaling and are important targets for pharmaceutical intervention in humans. Previously, we identified a group of ten amino acid positions (called key positions), within the seven transmembrane domain (7TM) interhelical region, which had high mutual information with each other and many other positions in the 7TM. Here, we estimated the evolutionary selection pressure at those key positions. We found that the key positions of receptors for small molecule natural ligands were under strong negative selection. Receptors naturally activated by lipids had weaker negative selection in general when compared to small molecule-activated receptors. Selection pressure varied widely in peptide-activated receptors. We used this observation to predict that a subgroup of orphan GPCRs not under strong selection may not possess a natural small-molecule ligand. In the subgroup of MRGX1-type GPCRs, we identified a key position, along with two non-key positions, under statistically significant positive selection.
C1 [Fatakia, Sarosh N.; Costanzi, Stefano; Chow, Carson C.] NIDDK, Lab Biol Modeling, NIH, Bethesda, MD USA.
RP Fatakia, SN (reprint author), NIDDK, Lab Biol Modeling, NIH, Bethesda, MD USA.
EM carsonc@mail.nih.gov
RI Chow, Carson/A-7970-2009; Costanzi, Stefano/G-8990-2013;
OI Costanzi, Stefano/0000-0003-3183-7332; Fatakia,
Sarosh/0000-0003-0430-3191
FU National Institutes of Health (NIH)/National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK)
FX This research was supported by the Intramural Research Program of the
National Institutes of Health (NIH)/National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK). The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 70
TC 8
Z9 8
U1 1
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 21
PY 2011
VL 6
IS 11
AR e27813
DI 10.1371/journal.pone.0027813
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 858IO
UT WOS:000297789900024
PM 22132149
ER
PT J
AU Cattoli, G
Fusaro, A
Monne, I
Coven, F
Joannis, T
El-Hamid, HSA
Hussein, AA
Cornelius, C
Amarin, NM
Mancin, M
Holmes, EC
Capua, I
AF Cattoli, Giovanni
Fusaro, Alice
Monne, Isabella
Coven, Fethiye
Joannis, Tony
El-Hamid, Hatem S. Abd
Hussein, Aly Ahmed
Cornelius, Claire
Amarin, Nadim Mukhles
Mancin, Marzia
Holmes, Edward C.
Capua, Ilaria
TI Evidence for differing evolutionary dynamics of A/H5N1 viruses among
countries applying or not applying avian influenza vaccination in
poultry
SO VACCINE
LA English
DT Article
DE Avian influenza; H5N1; Egypt; Virus evolution
ID ANTIGENIC SITES; HEMAGGLUTININ MOLECULE; PHYLOGENETIC ANALYSIS; MULTIPLE
SUBLINEAGES; NEURAMINIDASE GENES; H5N1; SUBSTITUTION; SEQUENCES;
VACCINES; NIGERIA
AB Highly pathogenic avian influenza (HPAI) H5N1 (clade 2.2) was introduced into Egypt in early 2006. Despite the control measures taken, including mass vaccination of poultry, the virus rapidly spread among commercial and backyard flocks. Since the initial outbreaks, the virus in Egypt has evolved into a third order clade (clade 2.2.1) and diverged into antigenically and genetically distinct subclades. To better understand the dynamics of HPAI H5N1 evolution in countries that differ in vaccination policy, we undertook an in-depth analysis of those virus strains circulating in Egypt between 2006 and 2010, and compared countries where vaccination was adopted (Egypt and Indonesia) to those where it was not (Nigeria, Turkey and Thailand). This study incorporated 751 sequences (Egypt n = 309, Indonesia n = 149. Nigeria n = 106, Turkey n = 87, Thailand n = 100) of the complete haemagglutinin (HA) open reading frame, the major antigenic determinant of influenza A virus. Our analysis revealed that two main Egyptian subclades (termed A and B) have co-circulated in domestic poultry since late 2007 and exhibit different profiles of positively selected codons and rates of nucleotide substitution. The mean evolutionary rate of subclade A H5N1 viruses was 4.07 x 10(-3) nucleotide substitutions per site, per year (HPD 95%, 3.23-4.91), whereas subclade B possessed a markedly higher substitution rate (8.87 x 10(-3); 95% HPD 7.0-10.72 x 10(-3)) and a stronger signature of positive selection. Although the direct association between H5N1 vaccination and virus evolution is difficult to establish, we found evidence for a difference in the evolutionary dynamics of H5N1 viruses among countries where vaccination was or was not adopted. In particular, both evolutionary rates and the number of positively selected sites were higher in virus populations circulating in countries applying avian influenza vaccination for H5N1, compared to viruses circulating in countries which had never used vaccination. We therefore urge a greater consideration of the potential consequences of inadequate vaccination on viral evolution. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Cattoli, Giovanni; Fusaro, Alice; Monne, Isabella; Mancin, Marzia; Capua, Ilaria] OIE Collaborating Ctr Dis Human Anim Interface, Ist Zooprofilatt Sperimentale Venezie, Dept Res & Dev, OIE FAO, I-35020 Padua, Italy.
[Cattoli, Giovanni; Fusaro, Alice; Monne, Isabella; Mancin, Marzia; Capua, Ilaria] OIE Collaborating Ctr Dis Human Anim Interface, Natl Reference Lab Newcastle Dis & Avian Influenz, I-35020 Padua, Italy.
[Coven, Fethiye] Bornova Vet Control & Res Inst, Izmir, Turkey.
[Hussein, Aly Ahmed] Cairo Univ, Fac Vet Med, Giza, Egypt.
[Cornelius, Claire] USN, Med Res Unit 3, Cairo, Egypt.
[Amarin, Nadim Mukhles] Boehringer Ingelheim GmbH & Co KG, Dubai, U Arab Emirates.
[Holmes, Edward C.] Penn State Univ, Dept Biol, Ctr Infect Dis Dynam, Mueller Lab, University Pk, PA 16802 USA.
[Holmes, Edward C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Cattoli, G (reprint author), OIE Collaborating Ctr Dis Human Anim Interface, Ist Zooprofilatt Sperimentale Venezie, Dept Res & Dev, OIE FAO, Viale Univ 10, I-35020 Padua, Italy.
EM gcattoli@izsvenezie.it
RI Valle, Ruben/A-7512-2013;
OI Fusaro, Alice/0000-0002-8213-5472; Holmes, Edward/0000-0001-9596-3552
FU Italian Ministry of Health [RC IZS VE 14/09]
FX We acknowledge the Ministry of Agriculture of Egypt for its continuous
support and for assistance with the avian influenza control program in
the country. The laboratories that have shared and deposited the genetic
sequences included in the present study in public database (GenBank) are
gratefully acknowledged. In particular, National Laboratory for
Veterinary Quality Control on Poultry Production, Animal Health Research
Institute (Dokki, Giza, Egypt); Chulalongkorn University (Pathumwan,
Bangkok, Thailand); Yuko Uchida National Institute of Animal Health
(Tsukuba, Japan); Molecular Biology and Virology Unit, Faculty of
Veterinary Science, Mahidol University (Phuttamonthon District,
Nakornpathom, Thailand); Division of Virology, Institute of Medical
Science, University of Tokyo (Shirokanedai, Minato-ku, Tokyo; Japan),
Southeast Poultry Research Laboratory, Athens, GA 30605, USA; WHO
Collaborating Center for Surveillance, Epidemiology and Control of
Influenza, Influenza Branch, Centers for Disease Control and Prevention
(Atlanta,GA 30333, USA), Department of Microbiology, The University of
Hong Kong (Hong Kong SAR, China); WHO Collaborating Centre for Reference
and Research on Influenza Centre (Parkville, Australia). Ms Francesca
Ellero is gratefully acknowledged for the proof reading of the article.
Part of this work was financially supported by the Italian Ministry of
Health through the RC IZS VE 14/09.
NR 52
TC 64
Z9 64
U1 0
U2 11
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
J9 VACCINE
JI Vaccine
PD NOV 21
PY 2011
VL 29
IS 50
BP 9368
EP 9375
DI 10.1016/j.vaccine.2011.09.127
PG 8
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 858ED
UT WOS:000297777800016
PM 22001877
ER
PT J
AU Lamart, S
Bouville, A
Simon, SL
Eckerman, KF
Melo, D
Lee, C
AF Lamart, Stephanie
Bouville, Andre
Simon, Steven L.
Eckerman, Keith F.
Melo, Dunstana
Lee, Choonsik
TI Comparison of internal dosimetry factors for three classes of adult
computational phantoms with emphasis on I-131 in the thyroid
SO PHYSICS IN MEDICINE AND BIOLOGY
LA English
DT Article
ID RADIATION-DOSIMETRY; ANTHROPOMORPHIC MODELS; ABSORBED FRACTIONS;
ELECTRON SOURCES; VOXEL PHANTOM; FEMALE; HYPERTHYROIDISM; EMITTERS;
ANATOMY; VALUES
AB The S values for 11 major target organs for I-131 in the thyroid were compared for three classes of adult computational human phantoms: stylized, voxel and hybrid phantoms. In addition, we compared specific absorbed fractions (SAFs) with the thyroid as a source region over a broader photon energy range than the x-and gamma-rays of I-131. The S and SAF values were calculated for the International Commission on Radiological Protection (ICRP) reference voxel phantoms and the University of Florida (UF) hybrid phantoms by using the Monte Carlo transport method, while the S and SAF values for the Oak Ridge National Laboratory (ORNL) stylized phantoms were obtained from earlier publications. Phantoms in our calculations were for adults of both genders. The 11 target organs and tissues that were selected for the comparison of S values are brain, breast, stomach wall, small intestine wall, colon wall, heart wall, pancreas, salivary glands, thyroid, lungs and active marrow for I-131 and thyroid as a source region. The comparisons showed, in general, an underestimation of S values reported for the stylized phantoms compared to the values based on the ICRP voxel and UF hybrid phantoms and relatively good agreement between the S values obtained for the ICRP and UF phantoms. Substantial differences were observed for some organs between the three types of phantoms. For example, the small intestine wall of ICRP male phantom and heart wall of ICRP female phantom showed up to eightfold and fourfold greater S values, respectively, compared to the reported values for the ORNL phantoms. UF male and female phantoms also showed significant differences compared to the ORNL phantom, 4.0-fold greater for the small intestine wall and 3.3-fold greater for the heart wall. In our method, we directly calculated the S values without using the SAFs as commonly done. Hence, we sought to confirm the differences observed in our S values by comparing the SAFs among the phantoms with the thyroid as a source region for selected target organs-small intestine wall, lungs, pancreas and breast-as well as illustrate differences in energy deposition across the energy range (12 photon energies from 0.01 to 4 MeV). Differences were found in the SAFs between phantoms in a similar manner as the differences observed in S values but with larger differences at lower photon energies. To investigate the differences observed in the S and SAF values, the chord length distributions (CLDs) were computed for the selected source-target pairs and compared across the phantoms. As demonstrated by the CLDs, we found that the differences between phantoms in those factors used in internal dosimetry were governed to a significant degree by inter-organ distances which are a function of organ shape as well as organ location.
C1 [Lamart, Stephanie; Simon, Steven L.; Lee, Choonsik] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Eckerman, Keith F.] Oak Ridge Natl Lab, Div Environm Sci, Oak Ridge, TN 37831 USA.
[Melo, Dunstana] Inst Radioprotecao & Dosimetria, Rio De Janeiro, Brazil.
RP Lee, C (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
EM leechoonsik@mail.nih.gov
RI Lee, Choonsik/C-9023-2015
OI Lee, Choonsik/0000-0003-4289-9870
FU Intra-Agency agreement between the National Institute of Allergy and
Infectious Diseases; National Cancer Institute; NIAID [Y2-AI-5077]; NCI
[Y3-CO-5117]
FX The authors would like to express their appreciation for valuable
comments from Dr Wesley Bolch at the University of Florida and for
technical assistance from Mr Brian Moroz at the Radiation Epidemiology
Branch at the National Cancer Institute. This work was supported by the
Intra-Agency agreement between the National Institute of Allergy and
Infectious Diseases and the National Cancer Institute, NIAID agreement
#Y2-AI-5077 and NCI agreement #Y3-CO-5117.
NR 37
TC 9
Z9 10
U1 1
U2 3
PU IOP PUBLISHING LTD
PI BRISTOL
PA TEMPLE CIRCUS, TEMPLE WAY, BRISTOL BS1 6BE, ENGLAND
SN 0031-9155
J9 PHYS MED BIOL
JI Phys. Med. Biol.
PD NOV 21
PY 2011
VL 56
IS 22
BP 7317
EP 7335
DI 10.1088/0031-9155/56/22/020
PG 19
WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging
SC Engineering; Radiology, Nuclear Medicine & Medical Imaging
GA 844SX
UT WOS:000296768700024
PM 22040775
ER
PT J
AU Jatoi, I
Anderson, WF
Jeong, JH
Redmond, CK
AF Jatoi, Ismail
Anderson, William F.
Jeong, Jong-Hyeon
Redmond, Carol K.
TI Some Additional Thoughts on Time-Varying Treatment Effects in Breast
Cancer Reply
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Letter
C1 [Jatoi, Ismail] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
[Anderson, William F.] NCI, NIH, Bethesda, MD 20892 USA.
[Jeong, Jong-Hyeon] Univ Pittsburgh, Natl Surg Adjuvant Breast Canc Project Biostat Ct, Pittsburgh, PA USA.
RP Jatoi, I (reprint author), Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
NR 3
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 20
PY 2011
VL 29
IS 33
BP 4470
EP 4470
DI 10.1200/JCO.2011.38.2218
PG 1
WC Oncology
SC Oncology
GA 851GW
UT WOS:000297257400032
ER
PT J
AU Furukawa-Hibi, Y
Alkam, T
Nitta, A
Matsuyama, A
Mizoguchi, H
Suzuki, K
Moussaoui, S
Yu, QS
Greig, NH
Nagai, T
Yamada, K
AF Furukawa-Hibi, Yoko
Alkam, Tursun
Nitta, Atsumi
Matsuyama, Akihiro
Mizoguchi, Hiroyuki
Suzuki, Kazuhiko
Moussaoui, Saliha
Yu, Qian-Sheng
Greig, Nigel H.
Nagai, Taku
Yamada, Kiyofumi
TI Butyrylcholinesterase inhibitors ameliorate cognitive dysfunction
induced by amyloid-beta peptide in mice
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article
DE Acetylcholinesterase; Butyrylcholinesterase; Amyloid-beta
ID NITRIC-OXIDE SYNTHASE; NECROSIS-FACTOR-ALPHA; ALZHEIMERS-DISEASE;
CHOLINERGIC DYSFUNCTION; OXIDATIVE DAMAGE; RAT-BRAIN; RECOGNITION
MEMORY; PROTEIN-PRECURSOR; REGULATED KINASE; IN-VIVO
AB The cholinesterase inhibitor, rivastigmine, ameliorates cognitive dysfunction and is approved for the treatment of Alzheimer's disease (AD). Rivastigmine is a dual inhibitor of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE); however, the impact of BuChE inhibition on cognitive dysfunction remains to be determined. We compared the effects of a selective BuChE inhibitor, N1-phenethylnorcymserine (PEC), rivastigmine and donepezil (an AChE-selective inhibitor) on cognitive dysfunction induced by amyloid-beta peptide (A beta(1-40)) in mice. Five-week-old imprinting control region (ICR) mice were injected intracerebroventricularly (i.c.v.) with either A beta(1-40) or the control peptide A beta(40-1) on Day 0, and their recognition memory was analyzed by a novel object recognition test. Treatment with donepezil (1.0 mg/kg), rivastigmine (0.03, 0.1, 0.3 mg/kg) or PEC (1.0, 3.0 mg/kg) 20 min prior to, or immediately after the acquisition session (Day 4) ameliorated the A beta(1-40) induced memory impairment, indicating a beneficial effect on memory acquisition and consolidation. In contrast, none of the investigated drugs proved effective when administrated before the retention session (Day 5). Repeated daily administration of donepezil, rivastigmine or PEC, on Days 0-3 inclusively, ameliorated the cognitive dysfunction in A beta(1-40) challenged mice. Consistent with the reversal of memory impairments, donepezil, rivastigmine or PEC treatment significantly reduced A beta(1-40) induced tyrosine nitration of hippocampal proteins, a marker of oxidative damage. These results indicate that BuChE inhibition, as well as AChE inhibition, is a viable therapeutic strategy for cognitive dysfunction in AD. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Furukawa-Hibi, Yoko; Alkam, Tursun; Nitta, Atsumi; Matsuyama, Akihiro; Nagai, Taku; Yamada, Kiyofumi] Nagoya Univ, Dept Neuropsychopharmacol & Hosp Pharm, Grad Sch Med, Showa Ku, Nagoya, Aichi 4668560, Japan.
[Mizoguchi, Hiroyuki] Nagoya Univ, Environm Med Res Inst, Futurist Environm Simulat Ctr, Nagoya, Aichi 4648601, Japan.
[Suzuki, Kazuhiko] Novartis Pharma KK, Translat Sci, Tokyo 1068618, Japan.
[Moussaoui, Saliha] Novartis Pharma AG, Neurosci Res, Novartis Inst BioMed Res, CH-4002 Basel, Switzerland.
[Yu, Qian-Sheng; Greig, Nigel H.] NIA, Drug Design & Dev Sect, Neurosci Lab, NIH, Baltimore, MD 21224 USA.
RP Yamada, K (reprint author), Nagoya Univ, Dept Neuropsychopharmacol & Hosp Pharm, Grad Sch Med, Showa Ku, 65 Tsuruma Cho, Nagoya, Aichi 4668560, Japan.
EM kyamada@med.nagoya-u.ac.jp
RI Nagai, Taku/I-7507-2014; Yamada, Kiyofumi/I-7487-2014
OI Yamada, Kiyofumi/0000-0002-5280-5180
FU Japan Society for the Promotion of Science [22390046, 23659135];
Ministry of Education, Culture, Sports, Science and Technology of Japan;
Ministry of Education, Culture, Sports, Science and Technology (MEXT);
Novartis Pharma KK; ONO Pharmaceutical Co., Ltd.; National Institutes of
Health
FX This study was supported in part by the following funding sources: (i)
grants-in-aid for Scientific Research (No. 22390046, 23659135) from the
Japan Society for the Promotion of Science; (ii) a grant from the global
COE program from the Ministry of Education, Culture, Sports, Science and
Technology of Japan; (iii) a grant from the Academic Frontier Project
for Private Universities, matching fund subsidy from MEXT, 2007-2011;
(iv) a grant from the Regional Joint Research Program supported by
grants to Private Universities to Cover Current Expenses from the
Ministry of Education, Culture, Sports, Science and Technology (MEXT);
(v) a grant from Novartis Pharma KK and ONO Pharmaceutical Co., Ltd.
(vi) The Intramural Research Program of the National Institute on Aging,
National Institutes of Health.
NR 53
TC 38
Z9 42
U1 3
U2 21
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD NOV 20
PY 2011
VL 225
IS 1
BP 222
EP 229
DI 10.1016/j.bbr.2011.07.035
PG 8
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 831YL
UT WOS:000295766900030
PM 21820013
ER
PT J
AU Collins, FS
Tabak, LA
AF Collins, Francis S.
Tabak, Lawrence A.
TI Race Disparity in Grants: Oversight at Home - Response
SO SCIENCE
LA English
DT Letter
C1 [Collins, Francis S.; Tabak, Lawrence A.] NIH, Bethesda, MD 20892 USA.
RP Tabak, LA (reprint author), NIH, 1 Ctr Dr, Bethesda, MD 20892 USA.
EM lawrence.tabak@nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD NOV 18
PY 2011
VL 334
IS 6058
BP 903
EP 903
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 849CA
UT WOS:000297101800020
ER
PT J
AU Anasetti, C
Logan, BR
Lee, SJ
Waller, EK
Weisdorf, DJ
Wingard, JR
Cutler, CS
Westervelt, P
Woolfrey, A
Couban, S
Johnston, L
Maziarz, RT
Pulsipher, M
Anderlini, P
Bensinger, WI
Leitman, SF
Rowley, SD
Carter, SL
Horowitz, MM
Confer, DL
AF Anasetti, Claudio
Logan, Brent R.
Lee, Stephanie J.
Waller, Edmund K.
Weisdorf, Daniel J.
Wingard, John R.
Cutler, Corey S.
Westervelt, Peter
Woolfrey, Ann
Couban, Stephen
Johnston, Laura
Maziarz, Richard T.
Pulsipher, Michael
Anderlini, Paolo
Bensinger, William I.
Leitman, Susan F.
Rowley, Scott D.
Carter, Shelly L.
Horowitz, Mary M.
Confer, Dennis L.
TI Increased Incidence of Chronic Graft-Versus-Host Disease (GVHD) and No
Survival Advantage with Filgrastim-Mobilized Peripheral Blood Stem Cells
(PBSC) Compared to Bone Marrow (BM) Transplants From Unrelated Donors:
Results of Blood and Marrow Transplant Clinical Trials Network (BMT CTN)
Protocol 0201, a Phase III, Prospective, Randomized Trial
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Anasetti, Claudio] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
[Bensinger, William I.] Fred Hutchinson Canc Res Ctr, Clin Div, Seattle, WA 98104 USA.
[Waller, Edmund K.] Emory Univ, Winship Canc Inst, Dept Heamtol Med Oncol, Atlanta, GA 30322 USA.
[Weisdorf, Daniel J.] Univ Minnesota, Med Ctr, Blood & Marrow Transplant Program, Minneapolis, MN 55455 USA.
[Wingard, John R.] Univ Florida, Shands Canc Ctr, Gainesville, FL USA.
[Cutler, Corey S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Westervelt, Peter] Washington Univ, Sch Med, Dept Med, Siteman Canc Ctr, St Louis, MO 63110 USA.
[Couban, Stephen] Dalhousie Univ, Halifax, NS, Canada.
[Johnston, Laura] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
[Maziarz, Richard T.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Pulsipher, Michael] Univ Utah, Med Ctr, Salt Lake City, UT USA.
[Anderlini, Paolo] Univ Texas MD Anderson Canc Ctr, Dept Stem Cell Transplantat & Cellular Therapy, Houston, TX 77030 USA.
[Leitman, Susan F.] NIH, Dept Transfus Med, Bethesda, MD 20892 USA.
[Rowley, Scott D.] Hackensack Univ, John Theurer Canc Ctr, Med Ctr, Hackensack, NJ USA.
[Carter, Shelly L.] EMMES Corp, Rockville, MD USA.
[Horowitz, Mary M.] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
[Confer, Dennis L.] Natl Marrow Donor Program, Minneapolis, MN USA.
NR 0
TC 2
Z9 2
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 3
EP 3
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100002
ER
PT J
AU Rogers, ZR
Fish, B
Luo, ZY
Iyer, RV
Thornburg, CD
Sarnaik, SA
Rana, SR
Luchtman-Jones, L
Jackson, SM
Howard, TH
Casella, JF
Brown, RC
Alvarez, OA
Goldsmith, JC
Miller, ST
Wang, WC
AF Rogers, Zora R.
Fish, Billie
Luo, Zhaoyu
Iyer, Rathi V.
Thornburg, Courtney D.
Sarnaik, Sharada A.
Rana, Sohail R.
Luchtman-Jones, Lori
Jackson, Sherron M.
Howard, Thomas H.
Casella, James F.
Brown, R. Clark
Alvarez, Ofelia A.
Goldsmith, Jonathan C.
Miller, Scott T.
Wang, Winfred C.
TI Hydroxyurea Treatment of Young Children with Sickle Cell Anemia: Safety
and Efficacy of Continued Treatment - the BABY HUG Follow-up Study
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Rogers, Zora R.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Fish, Billie; Luo, Zhaoyu] Clin Trials & Surveys Corp, Owings Mills, MD USA.
[Iyer, Rathi V.] Univ Mississippi, Jackson, MS 39216 USA.
[Thornburg, Courtney D.] Duke Univ, Med Ctr, Durham, NC USA.
[Sarnaik, Sharada A.] Childrens Hosp Michigan, Detroit, MI 48201 USA.
[Rana, Sohail R.] Howard Univ, Washington, DC 20059 USA.
[Luchtman-Jones, Lori] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Jackson, Sherron M.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Howard, Thomas H.] Univ Alabama, Birmingham, AL USA.
[Casella, James F.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Brown, R. Clark] Emory Univ Childrens Healthcare Atlanta, Atlanta, GA USA.
[Alvarez, Ofelia A.] Univ Miami, Sch Med, Miami, FL USA.
[Goldsmith, Jonathan C.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Miller, Scott T.] SUNY Brooklyn, Brooklyn, NY USA.
[Wang, Winfred C.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 9
EP 9
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100008
ER
PT J
AU Hsieh, MM
Fitzhugh, CD
Weitzel, RP
Coles, W
Link, MB
Tisdale, JF
AF Hsieh, Matthew M.
Fitzhugh, Courtney D.
Weitzel, R. Patrick
Coles, Wynona
Link, M. Beth
Tisdale, John F.
TI Non-Myeloablative Allogeneic Hematopoietic Stem Cell Transplantation
(allo-HSCT) for Patients with Severe Sickle Cell Disease (SCD)
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Hsieh, Matthew M.; Fitzhugh, Courtney D.; Weitzel, R. Patrick; Coles, Wynona; Link, M. Beth; Tisdale, John F.] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 10
EP 10
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100011
ER
PT J
AU Winkler, T
Decker, JE
Hong, SG
Wu, CF
Morgan, MJ
Dunbar, CE
Young, NS
Calado, RT
AF Winkler, Thomas
Decker, Jake E.
Hong, So Gun
Wu, Chuanfeng
Morgan, Mary J.
Dunbar, Cynthia E.
Young, Neal S.
Calado, Rodrigo T.
TI Telomere Dynamics in Pluripotent Stem Cells Derived From Patients with
Telomere Diseases
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Winkler, Thomas; Hong, So Gun; Wu, Chuanfeng; Morgan, Mary J.; Dunbar, Cynthia E.; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Decker, Jake E.] Cleveland Clin, Lerner Coll Med, Cleveland, OH 44106 USA.
[Calado, Rodrigo T.] Univ Sao Paulo, BR-14049 Ribeirao Preto, SP, Brazil.
RI Calado, Rodrigo/G-2619-2011
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 25
EP 26
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100052
ER
PT J
AU Olnes, MJ
Scheinberg, P
Calvo, K
Tang, Y
Soto, S
Feng, XM
Desmond, RG
Lozier, JN
Young, NS
Dunbar, CE
AF Olnes, Matthew J.
Scheinberg, Phillip
Calvo, Katherine
Tang, Yong
Soto, Susan
Feng, Xingmin
Desmond, Ronan G.
Lozier, Jay N.
Young, Neal S.
Dunbar, Cynthia E.
TI Eltrombopag Can Stimulate Trilineage Hematopoiesis with Transfusion
Independence in Patients with Refractory Severe Aplastic Anemia: Results
From a Phase II Trial
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Olnes, Matthew J.; Soto, Susan; Young, Neal S.] NHLBI, NIH, Hematol Branch, Bethesda, MD 20892 USA.
[Scheinberg, Phillip] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Calvo, Katherine] Hematol Sect, Dept Lab Med, Bethesda, MD USA.
[Lozier, Jay N.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
RI Scheinberg, Phillip/H-5251-2012
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 27
EP 27
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100055
ER
PT J
AU Roberts, KG
Morin, RD
Zhang, JH
Hirst, M
Harvey, RC
Kasap, C
Chen, X
Edmonson, M
Chen, IM
Shah, N
Devidas, M
Reaman, GH
Smith, MA
Pui, CH
Downing, JR
Gerhard, DS
Willman, CL
Loh, ML
Hunger, SP
Marra, MA
Mullighan, CG
AF Roberts, Kathryn G.
Morin, Ryan D.
Zhang, Jinghui
Hirst, Martin
Harvey, Richard C.
Kasap, Corynn
Chen, Xiang
Edmonson, Michael
Chen, I-Ming
Shah, Neil
Devidas, Meenakshi
Reaman, Gregory H.
Smith, Malcolm A.
Pui, Ching-Hon
Downing, James R.
Gerhard, Daniela S.
Willman, Cheryl L.
Loh, Mignon L.
Hunger, Stephen P.
Marra, Marco A.
Mullighan, Charles' G.
TI Novel Chromosomal Rearrangements and Sequence Mutations in High-Risk
Ph-Like Acute Lymphoblastic Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Roberts, Kathryn G.; Zhang, Jinghui; Chen, Xiang; Pui, Ching-Hon; Downing, James R.; Mullighan, Charles' G.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
[Morin, Ryan D.; Hirst, Martin; Marra, Marco A.] British Columbia Canc Agcy, Genome Sci Ctr, Vancouver, BC V5Z 4E6, Canada.
[Willman, Cheryl L.] Univ New Mexico, Ctr Canc, UNM Canc Res Facil, Albuquerque, NM 87131 USA.
[Loh, Mignon L.] Univ Calif San Francisco, Div Pediat Hematol Oncol, San Francisco, CA 94143 USA.
[Edmonson, Michael] NCI, Lab Populat Genet, Bethesda, MD 20892 USA.
[Devidas, Meenakshi] Univ Florida, Coll Med, Dept Biostat, Gainesville, FL USA.
[Reaman, Gregory H.] George Washington Univ, Childrens Natl Med Ctr, Washington, DC USA.
[Smith, Malcolm A.] NCI Ctep Cib, NIH, Bethesda, MD USA.
[Gerhard, Daniela S.] NCI, Off Canc Genom, Bethesda, MD 20892 USA.
[Loh, Mignon L.] Univ Calif San Francisco, Helen Diller Comprehens Canc Ctr, San Francisco, CA 94143 USA.
[Kasap, Corynn; Shah, Neil] Univ Calif San Francisco, Dept Med, Div Hematol Oncol, San Francisco, CA 94143 USA.
[Hunger, Stephen P.] Univ Colorado, Coll Med, Pediat Hematol Oncol BMT, Aurora, CO USA.
RI Hirst, Martin/B-7684-2016
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 32
EP 32
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100068
ER
PT J
AU Lucas, D
Scheiermann, C
Chow, A
Kunisaki, Y
Barrick, C
Tessarollo, L
Frenette, PS
AF Lucas, Daniel
Scheiermann, Christoph
Chow, Andrew
Kunisaki, Yuya
Barrick, Colleen
Tessarollo, Lino
Frenette, Paul S.
TI Bone Marrow Neuropathy Prevents Hematopoietic Regeneration
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Lucas, Daniel; Scheiermann, Christoph; Kunisaki, Yuya; Frenette, Paul S.] Albert Einstein Coll Med, Ruth L & David S Gottesman Inst Stem Cell & Regen, New York, NY USA.
[Chow, Andrew] Mt Sinai Sch Med, Dept Gene & Cell Med, New York, NY USA.
[Barrick, Colleen; Tessarollo, Lino] NCI, Neural Dev Sect, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21701 USA.
RI Frenette, Paul/J-8272-2012; Scheiermann, Christoph/B-8261-2014
OI Scheiermann, Christoph/0000-0002-9212-0995
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 67
EP 67
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100140
ER
PT J
AU Jacobsohn, D
Lee, SJ
Kurland, B
Cutler, CS
Pidala, J
Carpenter, PA
Chai, S
Arai, S
Arora, M
Palmer, J
Martin, PJ
Pavletic, SZ
Flowers, MED
AF Jacobsohn, David
Lee, Stephanie J.
Kurland, Brenda
Cutler, Corey S.
Pidala, Joseph
Carpenter, Paul A.
Chai, Shawn
Arai, Sally
Arora, Mukta
Palmer, Jeanne
Martin, Paul J.
Pavletic, Steven Z.
Flowers, Mary E. D.
TI Change in NIH Skin Score 0-3 Correlates with Provider- and
Patient-Reported Skin Changes and Overall Survival: Results From the
Chronic Gvhd Consortium
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Jacobsohn, David] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Lee, Stephanie J.; Kurland, Brenda; Carpenter, Paul A.; Chai, Shawn; Martin, Paul J.; Flowers, Mary E. D.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Cutler, Corey S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Pidala, Joseph] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Arai, Sally] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
[Arora, Mukta] Univ Minnesota, Minneapolis, MN USA.
[Palmer, Jeanne] MCW & Froedtert Clin Canc Ctr, Milwaukee, WI USA.
[Pavletic, Steven Z.] NCI, Expt Transplantat & hnmunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 73
EP 74
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100152
ER
PT J
AU Kochenderfer, JN
Dudley, ME
Feldman, S
Wilson, WH
Spaner, D
Devillier, L
Carpenter, R
Nathan, DAN
Maric, I
Morgan, RA
Rosenberg, SA
AF Kochenderfer, James N.
Dudley, Mark E.
Feldman, Steven
Wilson, Wyndham H.
Spaner, David
Devillier, Laura
Carpenter, Robert
Nathan, Debbie-Ann N.
Maric, Irina
Morgan, Richard A.
Rosenberg, Steven A.
TI B-Cell Depletion, Remissions of Malignancy, and Cytokine-Associated
Toxicity in a Clinical Trial of T Cells Genetically-Engineered to
Express An Anti-CD19 Chimeric Antigen Receptor
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Kochenderfer, James N.; Carpenter, Robert] NCI, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA.
[Dudley, Mark E.; Feldman, Steven; Devillier, Laura; Nathan, Debbie-Ann N.; Morgan, Richard A.; Rosenberg, Steven A.] NCI, Surg Branch, Bethesda, MD 20892 USA.
[Wilson, Wyndham H.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
[Spaner, David] Sunybrook Odette Canc Ctr, Toronto, ON, Canada.
[Maric, Irina] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 5
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 82
EP 82
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100168
ER
PT J
AU Hogart, A
Lichtenberg, J
Ajay, S
Margulies, E
Bodine, DM
AF Hogart, Amber
Lichtenberg, Jens
Ajay, Subramanian
Margulies, Elliott
Bodine, David M.
TI Genome-Wide DNA Methylation Profiling of Hematopoietic Stem and
Progenitor Cells Reveals Over-Representation of ETS Transcrition Factor
Binding Sites
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Hogart, Amber; Lichtenberg, Jens; Bodine, David M.] NHGRI, Genet & Mol Biol Branch, Bethesda, MD 20892 USA.
[Ajay, Subramanian; Margulies, Elliott] NHGRI, Genome Technol Branch, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 98
EP 99
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100212
ER
PT J
AU Deng, CW
Li, Y
Liang, S
Salz, T
Qiu, Y
Roeder, R
Zhao, K
Bungert, J
Huang, SM
AF Deng, Changwang
Li, Ying
Liang, Shermi
Salz, Tal
Qiu, Yi
Roeder, Robert
Zhao, Keji
Bungert, Jorg
Huang, Suming
TI Role of hSET1 Complex in Epigenetic Controls of HoxB4 Expression and
Development of Hematopoietic Stem Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Huang, Suming] Univ Florida, Coll Med, Shands Canc Ctr Biochem & Mol Biol, Gainesville, FL USA.
[Roeder, Robert] Rockefeller Univ, Biochem & Mol Biol Lab, New York, NY 10021 USA.
[Zhao, Keji] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 99
EP 99
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100213
ER
PT J
AU Krause, DS
Fulzele, K
Barry, K
Lotinun, S
Baron, R
Bonewald, L
Feng, JQ
Chen, M
Weinstein, LS
Bouxsein, M
Scadden, DT
Divieti-Pajevic, P
AF Krause, Daniela S.
Fulzele, Keertik
Barry, Kevin
Lotinun, Sutada
Baron, Roland
Bonewald, Lynda
Feng, Jian Q.
Chen, Min
Weinstein, Lee S.
Bouxsein, Mary
Scadden, David T.
Divieti-Pajevic, Paola
TI Osteocytes Support Hematopoiesis by Altering the Bone Marrow
Microenvironment Through Gs alpha Signaling
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Krause, Daniela S.] Massachusetts Gen Hosp, Ctr Regenerat Med, Boston, MA 02114 USA.
[Fulzele, Keertik; Barry, Kevin; Divieti-Pajevic, Paola] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
[Lotinun, Sutada; Baron, Roland] Harvard Univ, Sch Dent Med, Boston, MA 02115 USA.
[Bonewald, Lynda] Univ Missouri, Dept Oral Biol, Kansas City, MO 64110 USA.
[Feng, Jian Q.] Baylor Coll Dent, Texas A&M Hlth Sci Ctr, Dept Biomed Sci, Dallas, TX 75246 USA.
[Chen, Min; Weinstein, Lee S.] NIDDK, Metab Dis Branch, NIH, Bethesda, MD USA.
[Bouxsein, Mary] Beth Israel Deaconess Med Ctr, Ctr Adv Orthoped Studies, Boston, MA 02215 USA.
[Bouxsein, Mary] Harvard Univ, Sch Med, Boston, MA USA.
[Scadden, David T.] Harvard Univ, Ctr Stem Cell & Regenerat Biol, Cambridge, MA 02138 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 101
EP 101
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100220
ER
PT J
AU Li, ZJ
Huang, H
Li, YY
Jiang, X
Chen, P
Arnovitz, S
Radmacher, MD
Maharry, K
Elkahloun, A
Yang, XN
He, CJ
Price, CO
Dohner, K
Zhang, ZY
Shen, C
Neilly, MB
Lussier, YA
Zhang, YM
Larson, RA
Le Beau, MM
Caligiuri, MA
Bullinger, L
Valk, P
Delwel, R
Lowenberg, B
Liu, PP
Marcucci, G
Bloomfield, CD
Rowley, JD
Chen, JJ
AF Li, Zejuan
Huang, Hao
Li, Yuanyuan
Jiang, Xi
Chen, Ping
Arnovitz, Stephen
Radmacher, Michael D.
Maharry, Kati
Elkahloun, Abdel
Yang, Xinan
He, Chunjiang
Price, Colles O.
Dohner, Konstanze
Zhang, Zhiyu
Shen, Chen
Neilly, Mary Beth
Lussier, Yves A.
Zhang, Yanming
Larson, Richard A.
Le Beau, Michelle M.
Caligiuri, Michael A.
Bullinger, Lars
Valk, Peter
Delwel, Ruud
Lowenberg, Bob
Liu, Paul P.
Marcucci, Guido
Bloomfield, Clara D.
Rowley, Janet D.
Chen, Jianjun
TI Activation of a Mir-181-Targeting HOXA-PBX3 Homeobox Gene Signature Is
Associated with Adverse Prognosis of Cytogenetically Abnormal Acute
Myeloid Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Li, Zejuan; Huang, Hao; Li, Yuanyuan; Jiang, Xi; Chen, Ping; Arnovitz, Stephen; He, Chunjiang; Neilly, Mary Beth; Larson, Richard A.; Le Beau, Michelle M.; Rowley, Janet D.; Chen, Jianjun] Univ Chicago, Dept Med, Hematol Oncol Sect, Chicago, IL 60637 USA.
[Radmacher, Michael D.; Maharry, Kati; Caligiuri, Michael A.; Marcucci, Guido; Bloomfield, Clara D.] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
[Elkahloun, Abdel; Liu, Paul P.] NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
[Yang, Xinan] Univ Chicago, Med Genet Sect, Chicago, IL 60637 USA.
[Yang, Xinan] Univ Chicago, DOM Ctr Biomed Informat, Chicago, IL 60637 USA.
[Bullinger, Lars] Univ Ulm, Dept Internal Med 3, D-7900 Ulm, Germany.
[Shen, Chen] IIT, Chicago, IL 60616 USA.
[Zhang, Yanming] Northwestern Univ, Chicago, IL 60611 USA.
[Caligiuri, Michael A.] Ohio State Univ, James Canc Hosp, Columbus, OH 43210 USA.
[Valk, Peter] Erasmus MC, Dept Hematol, Rotterdam, Netherlands.
[Delwel, Ruud] Erasmus MC, Univ Med Ctr Rotterdam, Dept Hem, Rotterdam, Netherlands.
[Lowenberg, Bob] Erasmus MC, Dept Hematol, Rotterdam, Netherlands.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 108
EP 108
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100237
ER
PT J
AU Wayne, AS
Bhojwani, D
Silverman, LB
Richards, K
Stetler-Stevenson, M
Shah, NN
Jeha, S
Pui, CH
Buzoianu, M
FitzGerald, DJ
Kreitman, RJ
Ibrahim, R
Pastan, I
AF Wayne, Alan S.
Bhojwani, Deepa
Silverman, Lewis B.
Richards, Kelly
Stetler-Stevenson, Maryalice
Shah, Nirali N.
Jeha, Sima
Pui, Ching-Hon
Buzoianu, Manuela
FitzGerald, David J.
Kreitman, Robert J.
Ibrahim, Ramy
Pastan, Ira
TI A Novel Anti-CD22 Immunotoxin, Moxetumomab Pasudotox: Phase I Study in
Pediatric Acute Lymphoblastic Leukemia (ALL)
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Wayne, Alan S.; Richards, Kelly; Shah, Nirali N.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Bhojwani, Deepa; Jeha, Sima; Pui, Ching-Hon] St Jude Childrens Hosp, Memphis, TN 38105 USA.
[Silverman, Lewis B.] Childrens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Stetler-Stevenson, Maryalice] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Buzoianu, Manuela; Ibrahim, Ramy] MedImmune LLC, Gaithersburg, MD USA.
[Pastan, Ira] NCI, Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 10
Z9 9
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 113
EP 113
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100249
ER
PT J
AU Zingone, A
Korde, N
Chen, JQ
Xi, LQ
Raffeld, M
Holkova, B
Kmieciak, M
Sullivan, D
Doyle, A
Maric, I
Calvo, K
Yancey, MA
Mulquin, M
Annunziata, C
Grant, S
Landgren, O
AF Zingone, Adriana
Korde, Neha
Chen, Jinqiu
Xi, Liqiang
Raffeld, Mark
Holkova, Beata
Kmieciak, Maciej
Sullivan, Daniel
Doyle, Austin
Maric, Irina
Calvo, Katherine
Yancey, Mary Ann
Mulquin, Marcia
Annunziata, Christina
Grant, Steven
Landgren, Ola
TI Molecular Characterization and Clinical Correlations of MEK1/2
Inhibition (AZD6244) in Relapse or Refractory Multiple Myeloma: Analysis
From a Phase II Study
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Zingone, Adriana] NCI, Multiple Myeloma Sect, NIH, Bethesda, MD 20892 USA.
[Raffeld, Mark] NCI, Lab Pathol, NIH, Bethesda, MD 20892 USA.
[Holkova, Beata; Kmieciak, Maciej; Grant, Steven] Virginia Commonwealth Univ, Massey Canc Ctr, Richmond, VA USA.
[Sullivan, Daniel] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
[Maric, Irina] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Calvo, Katherine] Dept Lab Med, Hematol Sect, Bethesda, MD USA.
[Yancey, Mary Ann; Mulquin, Marcia] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RI Annunziata, Christina/L-3219-2016
OI Annunziata, Christina/0000-0003-2033-6532
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 143
EP 143
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100307
ER
PT J
AU McIver, ZA
Melenhorst, JJ
Zheng, HY
Wu, CO
Grim, A
Ito, S
Cho, I
Hensel, NF
Barrett, AJ
AF McIver, Zachariah A.
Melenhorst, J. Joseph
Zheng, Haiyun
Wu, Colin O.
Grim, Andrew
Ito, Sawa
Cho, Irene
Hensel, Nancy F.
Barrett, A. John
TI Low Thymic Natural Regulatory T Cell Output in the Donor Is Associated
with An Increased Incidence of Extensive Chronic GvHD After T Cell
Depleted Matched Sibling Stem Cell Transplantation (SCT)
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [McIver, Zachariah A.] NHLBI, NIH, Rockville, MD USA.
[Zheng, Haiyun; Wu, Colin O.] NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA.
[Ito, Sawa; Hensel, Nancy F.; Barrett, A. John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 154
EP 154
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100329
ER
PT J
AU Ranuncolo, SM
Xiao, WM
Wright, G
Abu-Asab, MS
Pittaluga, S
Jaffe, ES
Lewis, BA
AF Ranuncolo, Stella M.
Xiao, Wenming
Wright, George
Abu-Asab, Mones S.
Pittaluga, Stefania
Jaffe, Elaine S.
Lewis, Brian A.
TI A Constitutivly Active NFkB Non Canonical Pathway Is Maintained by RelB
Repression of TRAF2 to Prevent Autophagy-Mediated Cell Death in Hodgkin
Lymphomas
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Ranuncolo, Stella M.; Lewis, Brian A.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Xiao, Wenming] NIH, Bioinformat & Mol Anal Sect, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
[Wright, George] NCI, Biometr Res Branch, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
[Abu-Asab, Mones S.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 197
EP 198
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100429
ER
PT J
AU Schmitz, R
Jhavar, S
Xiao, WM
Liu, XL
Powell, J
Wright, GW
Chan, WC
Jaffe, ES
Gascoyne, RD
Campo, E
Rosenwald, A
Ott, G
Delabie, J
Rimsza, LM
Staudt, LM
AF Schmitz, Roland
Jhavar, Sameer
Xiao, Wenming
Liu, Xuelu
Powell, John
Wright, George W.
Chan, Wing C.
Jaffe, Elaine S.
Gascoyne, Randy D.
Campo, Elias
Rosenwald, Andreas
Ott, German
Delabie, Jan
Rimsza, Lisa M.
Staudt, Louis M.
TI Recurrent Oncogenic Mutations in CCND3 in Aggressive Lymphomas
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Schmitz, Roland; Jhavar, Sameer; Staudt, Louis M.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
[Xiao, Wenming; Liu, Xuelu; Powell, John] NIH, Bioinformat & Mol Anal Sect, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
[Wright, George W.] NCI, Biometr Res Branch, DCTD, Bethesda, MD 20892 USA.
[Chan, Wing C.] Univ Nebraska, Med Ctr, Omaha, NE USA.
[Jaffe, Elaine S.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Gascoyne, Randy D.] British Columbia Canc Agcy, Ctr Lymphoid Canc, Vancouver, BC V5Z 4E6, Canada.
[Campo, Elias] Hosp Clin Barcelona, Hematopathol Unit, Barcelona, Spain.
[Rosenwald, Andreas] Univ Wurzburg, Dept Pathol, Stuttgart, Germany.
[Ott, German] Robert Bosch Krankenhaus, Dept Clin Pathol, Stuttgart, Germany.
[Ott, German] Dr Margarete Fischer Bosch Inst Clin Pharmacol, D-7000 Stuttgart, Germany.
[Delabie, Jan] Oslo Univ Hosp, Dept Pathol, Oslo, Norway.
[Rimsza, Lisa M.] Univ Arizona, Dept Pathol, Tucson, AZ USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 200
EP 201
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100436
ER
PT J
AU Min, DJ
Kim, M
Ezponda, T
Will, C
Martinez-Garcia, E
Popovic, R
Elenitoba-Johnson, KSJ
Venkatesha, B
Licht, JD
AF Min, Dong-Joon
Kim, Marianne
Ezponda, Teresa
Will, Christine
Martinez-Garcia, Eva
Popovic, Relja
Elenitoba-Johnson, Kojo S. J.
Venkatesha, Basrur
Licht, Jonathan D.
TI MMSET Stimulates Myeloma Cell Growth Through MicroRNA-Mediated
Modulation of c-MYC
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Min, Dong-Joon; Martinez-Garcia, Eva] Northwestern Univ, Feinberg Sch Med, Robert H Lurie Comprehens Canc Ctr, Div Hematol Oncol, Chicago, IL 60611 USA.
[Kim, Marianne] NCI, Med Oncol Branch, Bethesda, MD 20892 USA.
[Elenitoba-Johnson, Kojo S. J.] Univ Michigan, Sch Med, Dept Pathol, Ann Arbor, MI USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 217
EP 217
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100470
ER
PT J
AU de Latour, RP
Calado, RT
Busson, M
Abrams, J
Robin, M
Larghero, J
Dhedin, N
Clave, E
Toubert, A
Loiseau, P
Socie, G
Young, NS
AF de Latour, Regis Peffault
Calado, Rodrigo T.
Busson, Marc
Abrams, Jeffrey
Robin, Marie
Larghero, Jerome
Dhedin, Nathalie
Clave, Emmanuel
Toubert, Antoine
Loiseau, Pascale
Socie, Gerard
Young, Neal S.
TI Age-Adjusted Recipient Pre-Transplant Telomere Length and Treatment
Related Mortality After Hematopoietic Stem Cell Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [de Latour, Regis Peffault; Loiseau, Pascale] Hop St Louis, Paris, France.
[Calado, Rodrigo T.; Young, Neal S.] NHLBI, NIH, Hematol Branch, Bethesda, MD 20892 USA.
[Busson, Marc; Clave, Emmanuel; Toubert, Antoine] Univ Paris Diderot, AP HP, INSERM, Dept Immunol,UMRS 940, Paris, France.
[Larghero, Jerome] St Louis Hosp, Cell Biol Unit, Paris, France.
[Socie, Gerard] INSERM, U728, Paris, France.
RI Calado, Rodrigo/G-2619-2011
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 228
EP 228
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100491
ER
PT J
AU Desai, AA
Ahmad, H
Zhou, T
Zhang, W
Trevino, S
Wade, M
Raghavachari, N
Kato, GJ
Thiruvoipati, T
Turner, K
Artz, N
Patel, AR
Yuan, JX
Gordeuk, VR
Lang, RM
Garcia, JGN
Machado, RF
AF Desai, Ankit A.
Ahmad, Homaa
Zhou, Tong
Zhang, Wei
Trevino, Sharon
Wade, Michael
Raghavachari, Nalini
Kato, Gregory J.
Thiruvoipati, Tejasi
Turner, Kristin
Artz, Nicole
Patel, Amit R.
Yuan, Jason X.
Gordeuk, Victor R.
Lang, Roberto M.
Garcia, Joe G. N.
Machado, Roberto F.
TI Integration of Genomic and Genetic Approaches Highlight a Novel
Validated Gene Signature for Pulmonary Hypertension Associated with
Sickle Cell Disease
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Zhou, Tong; Trevino, Sharon; Wade, Michael; Yuan, Jason X.; Garcia, Joe G. N.; Machado, Roberto F.] Univ Illinois, Inst Personalized Resp Med, Chicago, IL USA.
[Zhang, Wei] Univ Illinois, Dept Pediat, Chicago, IL USA.
[Raghavachari, Nalini] NHLBI, Genet & Dev Biol Ctr, NIH, Bethesda, MD 20892 USA.
[Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Thiruvoipati, Tejasi; Patel, Amit R.; Lang, Roberto M.] Univ Chicago, Chicago, IL 60637 USA.
[Turner, Kristin; Artz, Nicole] Loyola Univ, Maywood, IL 60153 USA.
[Gordeuk, Victor R.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 0
U2 5
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 238
EP 239
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100512
ER
PT J
AU Bae, HT
Baldwin, CT
Gladwin, MT
Ashley-Koch, AE
Garrett, M
Soldano, K
Taylor, JG
Kato, GJ
Telen, MJ
Sebastiani, P
Steinberg, MH
Klings, ES
AF Bae, Harold T.
Baldwin, Clinton T.
Gladwin, Mark. T.
Ashley-Koch, Allison E.
Garrett, Melanie
Soldano, Karen
Taylor, James G.
Kato, Gregory J.
Telen, Marilyn J.
Sebastiani, Paola
Steinberg, Martin H.
Klings, Elizabeth S.
TI An Elevated Tricuspid Regurgitant Jet Velocity in Sickle Cell Disease Is
Associated with Polymorphisms in Genes Impacting Innate Immunity
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Bae, Harold T.; Sebastiani, Paola] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Baldwin, Clinton T.] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Gladwin, Mark. T.] Univ Pittsburgh, Inst Pulm, Pittsburgh, PA USA.
[Ashley-Koch, Allison E.; Garrett, Melanie; Soldano, Karen] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
[Taylor, James G.; Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Telen, Marilyn J.] Duke Univ, Dept Med, Div Hematol, Durham, NC USA.
[Steinberg, Martin H.] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Klings, Elizabeth S.] Boston Univ, Sch Med, Ctr Pulm, Boston, MA 02118 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 240
EP 240
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100515
ER
PT J
AU Nouraie, M
Rana, SR
Castro, OL
Luchtman-Jones, L
Sable, C
Dham, N
Minniti, C
Kato, GJ
Gladwin, MT
Ensing, G
Arteta, M
Campbell, A
Gordeuk, VR
AF Nouraie, Mehdi
Rana, Sohail R.
Castro, Oswaldo L.
Luchtman-Jones, Lori
Sable, Craig
Dham, Niti
Minniti, Caterina
Kato, Gregory J.
Gladwin, Mark T.
Ensing, Gregory
Arteta, Manuel
Campbell, Andrew
Gordeuk, Victor R.
TI Predictors of Mortality in Children and Adolescents with Sickle Cell
Disease: The PUSH Study
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Nouraie, Mehdi; Castro, Oswaldo L.; Gordeuk, Victor R.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
[Dham, Niti] Childrens Natl Med Ctr, Dept Cardiol, Washington, DC 20010 USA.
[Minniti, Caterina; Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Gladwin, Mark T.] Univ Pittsburgh, Inst Pulm, Pittsburgh, PA USA.
[Arteta, Manuel; Campbell, Andrew] Univ Michigan, Med Ctr, Ann Arbor, MI USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 240
EP 241
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100516
ER
PT J
AU Unnisa, Z
Clark, JP
Wojtowicz, E
Tessarollo, L
Copeland, NG
Jenkins, NA
Kumar, A
AF Unnisa, Zeenath
Clark, Jason P.
Wojtowicz, Elizabeth
Tessarollo, Lino
Copeland, Neal G.
Jenkins, Nancy A.
Kumar, Ashish
TI MEIS1 Is Required for the Maintenance of Long Term Hematopoietic Stem
Cells Wherein It Regulates Quiescence
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Unnisa, Zeenath; Clark, Jason P.; Wojtowicz, Elizabeth] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH USA.
[Tessarollo, Lino] NCI, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21701 USA.
[Copeland, Neal G.; Jenkins, Nancy A.] Cincinnati Childrens Hosp Med Ctr, Inst Mol & Cell Biol, Cincinnati, OH USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 254
EP 254
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100552
ER
PT J
AU Leshchenko, VV
Kuo, PY
Ulahannan, N
Braunschweig, E
Yu, YT
Suh, KS
Weniger, MA
Goy, A
Wilson, WH
Wiestner, A
Verma, A
Parekh, S
AF Leshchenko, Violetta V.
Kuo, Pei-Yu
Ulahannan, Netha
Braunschweig, Elana
Yu, Yiting
Suh, K. Stephen
Weniger, Marc A.
Goy, Andre
Wilson, Wyndham H.
Wiestner, Adrian
Verma, Amit
Parekh, Samir
TI High-Resolution Sequencing Identifies NOXA1 De-Methylation As a Novel
Strategy to Overcome Bortezomib Resistance in Mantle Cell Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Leshchenko, Violetta V.; Kuo, Pei-Yu; Ulahannan, Netha; Braunschweig, Elana; Yu, Yiting; Verma, Amit; Parekh, Samir] Albert Einstein Coll Med, Albert Einstein Canc Ctr, Bronx, NY 10467 USA.
[Suh, K. Stephen; Goy, Andre] Hackensack Univ, Med Ctr, John Theurer Canc Ctr, Hackensack, NJ USA.
[Weniger, Marc A.; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Wilson, Wyndham H.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 256
EP 257
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100558
ER
PT J
AU Khandanpour, C
Phelan, JD
Chen, RY
Horman, S
Vassen, L
Gaudreau, MC
Krongold, J
Zhu, JF
Paul, WE
Schutte, J
Goettgens, B
Duehrsen, U
Grimes, HL
Moroy, T
AF Khandanpour, Cyrus
Phelan, James D.
Chen, Riyan
Horman, Shane
Vassen, Lothar
Gaudreau, Marie-Claude
Krongold, Joseph
Zhu, Jinfang
Paul, William E.
Schuette, Judith
Goettgens, Berthold
Duehrsen, Ulrich
Grimes, H. Leighton
Moroy, Tarik
TI Growth Factor Independent-1 (Gfi1) As a New Target for Human Leukemia
Therapy
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Khandanpour, Cyrus; Duehrsen, Ulrich] Univ Hosp Essen, W German Canc Ctr, Dept Hematol, Essen, Germany.
[Phelan, James D.; Grimes, H. Leighton] Cincinnati Childrens Hosp, Div Immunobiol, Med Ctr, Cincinnati, OH USA.
[Chen, Riyan; Vassen, Lothar; Gaudreau, Marie-Claude; Krongold, Joseph; Moroy, Tarik] IRCM, Inst Rech Clin Montreal, Montreal, PQ, Canada.
[Zhu, Jinfang; Paul, William E.] NIAID, NIH, Bethesda, MD 20892 USA.
[Schuette, Judith; Goettgens, Berthold] Univ Cambridge, Cambridge Inst Med Res, Dept Haematol, Cambridge, England.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 258
EP 258
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100561
ER
PT J
AU Lee, DW
Kochenderfer, JN
Orentas, RJ
Gardner, EG
Mackall, CL
AF Lee, Daniel W., III
Kochenderfer, James N.
Orentas, Rimas J.
Gardner, Elizabeth G.
Mackall, Crystal L.
TI ALL Xenografts Reveal the Importance of Anti-CD19-Chimeric Antigen
Receptor Cell Dose, Cell Persistence and Surprising Antitumor Activity
of CD4+Anti-CD19-CAR T Cells in Eradicating Pediatric Acute Lymphocytic
Leukemia In Vivo
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Orentas, Rimas J.; Mackall, Crystal L.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Kochenderfer, James N.] NCI, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 264
EP 265
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100575
ER
PT J
AU Kuo, PY
Leshchenko, VV
Gellen, TA
Ulahannan, N
Zumbo, P
Mason, CE
Wilson, WH
Wiestner, A
Suh, KS
Goy, A
Yang, DT
Kahl, BS
Gascoyne, RD
Melnick, A
Parekh, S
AF Kuo, Pei-Yu
Leshchenko, Violetta V.
Gellen, Tobias A.
Ulahannan, Netha
Zumbo, Paul
Mason, Christopher E.
Wilson, Wyndham H.
Wiestner, Adrian
Suh, K. Stephen
Goy, Andre
Yang, David T.
Kahl, Brad S.
Gascoyne, Randy D.
Melnick, Ari
Parekh, Samir
TI High-Resolution Chromatin Immunoprecipitation (ChIP) Sequencing
Identifies Novel Binding Targets and Prognostic Role for SOX11 in Mantle
Cell Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Kuo, Pei-Yu; Leshchenko, Violetta V.; Gellen, Tobias A.; Ulahannan, Netha; Parekh, Samir] Albert Einstein Coll Med, Albert Einstein Canc Ctr, Bronx, NY 10467 USA.
[Zumbo, Paul; Mason, Christopher E.] Weill Cornell Med Coll, Dept Physiol & Biophys, New York, NY USA.
[Zumbo, Paul; Mason, Christopher E.] Weill Cornell Med Coll, Inst Computat Biomed, New York, NY USA.
[Wilson, Wyndham H.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
[Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Suh, K. Stephen; Goy, Andre] Hackensack Univ Med Ctr, John Theurer Canc Ctr, Hackensack, NJ USA.
[Kahl, Brad S.] Univ Wisconsin, Dept Med Hematol Oncol, Madison, WI USA.
[Gascoyne, Randy D.] British Columbia Canc Agcy, Ctr Lymphoid Canc, Vancouver, BC V5Z 4E6, Canada.
[Melnick, Ari] Weill Cornell Med Coll, Dept Med, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 269
EP 270
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100586
ER
PT J
AU Herman, SEM
Sun, XM
Buggy, JJ
Aue, G
Perez-Galan, P
Wiestner, A
AF Herman, Sarah E. M.
Sun, Xiameng
Buggy, Joseph J.
Aue, Georg
Perez-Galan, Patricia
Wiestner, Adrian
TI The Bruton Tyrosine Kinase Inhibitor, PCI-32765, Inhibits Activation and
Proliferation of Human Chronic Lymphocytic Leukemia Cells in the NSG
Xenograph Mouse Model of the Tissue Microenvironment
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Herman, Sarah E. M.; Sun, Xiameng; Aue, Georg; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Buggy, Joseph J.] Pharmacyclics Inc, Sunnyvale, CA USA.
[Perez-Galan, Patricia] IDIAPS, Dept Hematooncol, Barcelona, Spain.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 274
EP 274
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100597
ER
PT J
AU Hudecek, M
Lupo-Stanghellini, MT
Kosasih, P
Bet, J
Paszkiewicz, P
Maloney, DG
Jensen, MC
Rader, C
Riddell, SR
AF Hudecek, Michael
Lupo-Stanghellini, Maria-Teresa
Kosasih, Paula
Bet, Jeannette
Paszkiewicz, Paulina
Maloney, David G.
Jensen, Michael C.
Rader, Christoph
Riddell, Stanley R.
TI Naive CD4+T Cells Modified to Express a ROR1-Specific CAR Mediate
Anti-Tumor Activity and Provide Superior Help to CD8+ROR1-CAR T Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Hudecek, Michael; Lupo-Stanghellini, Maria-Teresa; Kosasih, Paula; Bet, Jeannette; Paszkiewicz, Paulina; Maloney, David G.; Riddell, Stanley R.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
[Jensen, Michael C.] Seattle Childrens Res Inst, Ctr Childhood Canc Res, Seattle, WA USA.
[Rader, Christoph] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 294
EP 294
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100644
ER
PT J
AU Gormley, NJ
Wilder, J
Khuu, H
Pantin, J
Donohue, T
Kurlander, R
Ito, S
Battiwalla, M
Barrett, AJ
Grasmeder, S
Cook, L
Ramos, C
Prince, P
Stroncek, D
Flegel, WA
Berg, M
Reger, R
Bolan, CD
Adams, S
Childs, R
AF Gormley, Nicole J.
Wilder, Jennifer
Khuu, Hahn
Pantin, Jeremy
Donohue, Theresa
Kurlander, Roger
Ito, Sawa
Battiwalla, Minoo
Barrett, A. John
Grasmeder, Sophie
Cook, Lisa
Ramos, Catalina
Prince, Patricia
Stroncek, David
Flegel, Willy A.
Berg, Maria
Reger, Robert
Bolan, Charles D., Jr.
Adams, Sharon
Childs, Richard
TI Co-Infusion of Allogeneic Cord Blood with Haploidentical CD34+Cells
Improved Transplant Outcome for Patients with Severe Aplastic Anemia
Undergoing Cord Blood Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Gormley, Nicole J.] Fed Drug Adm, Off Oncol Drug Prod, Silver Spring, MD USA.
[Wilder, Jennifer] SAIC, Clin Res Directorate CMRP, Frederick, MD USA.
[Khuu, Hahn; Stroncek, David; Flegel, Willy A.; Adams, Sharon] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Pantin, Jeremy; Donohue, Theresa; Ito, Sawa; Battiwalla, Minoo; Barrett, A. John; Grasmeder, Sophie; Cook, Lisa; Ramos, Catalina; Berg, Maria; Reger, Robert; Bolan, Charles D., Jr.; Childs, Richard] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Kurlander, Roger] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 299
EP 299
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100655
ER
PT J
AU Noh, SJ
Lee, YT
Byrnes, C
Rabel, A
Miller, JL
AF Noh, Seung-Jae
Lee, Y. Terry
Byrnes, Colleen
Rabel, Antoinette
Miller, Jeffery L.
TI Trafficking Kinesin Binding Protein Is Essential for Human
Erythropoiesis
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Noh, Seung-Jae; Lee, Y. Terry; Byrnes, Colleen; Rabel, Antoinette; Miller, Jeffery L.] NIDDK, Mol Genom & Therapeut Sect, Mol Med Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 313
EP 313
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100684
ER
PT J
AU Abdollahpour, H
Appaswamy, G
Beier, R
Schaffer, AA
Gertz, EM
Kreipe, HH
Pfeifer, D
Grimbacher, B
Lohrmann, S
Sherkat, R
Klein, C
AF Abdollahpour, Hengameh
Appaswamy, Giridharan
Beier, Rita
Schaeffer, Alejandro A.
Gertz, E. Michael
Kreipe, Hans H.
Pfeifer, Dietmar
Grimbacher, Bodo
Lohrmann, Sabine
Sherkat, Roya
Klein, Christoph
TI The Phenotype of Human STK4 Deficiency
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Appaswamy, Giridharan; Beier, Rita] Hannover Med Sch, Dept Pediat Hematol Oncol, D-3000 Hannover, Germany.
[Schaeffer, Alejandro A.; Gertz, E. Michael] NCBI, Natl Lib Med, NIH, Computat Biol Branch, Bethesda, MD 20892 USA.
[Kreipe, Hans H.] Hannover Med Sch, Inst Pathol, D-3000 Hannover, Germany.
[Pfeifer, Dietmar] Univ Freiburg, Med Ctr, Freiburg, Germany.
[Grimbacher, Bodo] Royal Free Hosp, Dept Immunol, London NW3 2QG, England.
[Grimbacher, Bodo] UCL, London, England.
[Klein, Christoph] Dr von Haunersches Kinderspital, Univ Childrens Hosp, Munich, Germany.
RI Schaffer, Alejandro/F-2902-2012
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 316
EP 317
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100693
ER
PT J
AU Dowdell, KC
Lu, LH
Rao, VK
Fleisher, TA
Oliveira, JB
AF Dowdell, Kennichi C.
Lu Lianghao
Rao, V. Koneti
Fleisher, Thomas A.
Oliveira, Joao Bosco
TI The BH3 Mimetic, Small Molecule, ABT-737, Was Effective As Lympholytic
Therapy in the MRL/lpr(-/-) Mouse Model of Autoimmune
Lymphoproliferative Syndrome (ALPS)
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Dowdell, Kennichi C.; Rao, V. Koneti] NIAID, ALPS Unit, LCID, NIH, Bethesda, MD 20892 USA.
[Lu Lianghao; Fleisher, Thomas A.; Oliveira, Joao Bosco] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 317
EP 318
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100696
ER
PT J
AU Moetter, J
Kartal, M
Meerpohl, J
Fischer, A
Simon, T
Urbaniak, S
Hirabayashi, S
Kapp, F
Noellke, P
Kratz, C
Niemeyer, CM
Wlodarski, MW
AF Moetter, Jessica
Kartal, Mutlu
Meerpohl, Joerg
Fischer, Alexandra
Simon, Thorsten
Urbaniaek, Sandra
Hirabayashi, Shinsuke
Kapp, Friedrich
Noellke, Peter
Kratz, Christian
Niemeyer, Charlotte M.
Wlodarski, Marcin W.
TI Analysis of Ribosomal Protein Genes Associated with Diamond Blackfan
Anemia (DBA) In German DBA Patients and Their Relatives
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Moetter, Jessica; Kartal, Mutlu; Meerpohl, Joerg; Fischer, Alexandra; Urbaniaek, Sandra; Hirabayashi, Shinsuke; Kapp, Friedrich; Noellke, Peter; Niemeyer, Charlotte M.; Wlodarski, Marcin W.] Univ Freiburg, Div Pediat Hematol & Oncol, D-79106 Freiburg, Germany.
[Simon, Thorsten] Univ Cologne, D-50931 Cologne, Germany.
[Kratz, Christian] NCI, Bethesda, MD 20892 USA.
RI Meerpohl, Joerg/J-4224-2013
OI Meerpohl, Joerg/0000-0002-1333-5403
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 330
EP 330
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597100730
ER
PT J
AU Vire, B
David, A
Thomas, JD
Burke, TR
Rader, C
Wiestner, A
AF Vire, Berengere
David, Alexandre
Thomas, Joshua D.
Burke, Terrence R., Jr.
Rader, Christoph
Wiestner, Adrian
TI Fc mu-Receptor (Fc mu R; TOSO/FAIM3) Mediated Internalization of
Antibody-Drug Conjugates: A Novel Approach to Selectively Target Chronic
Lymphocytic Leukemia Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Vire, Berengere; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[David, Alexandre] NIAID, NIH, Bethesda, MD 20892 USA.
[Thomas, Joshua D.; Burke, Terrence R., Jr.] NCI, NIH, Frederick, MD 21701 USA.
[Rader, Christoph] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RI David, Alexandre/B-2447-2013; Burke, Terrence/N-2601-2014
OI David, Alexandre/0000-0003-3365-1339;
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 332
EP 333
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101005
ER
PT J
AU Zamarin, D
Bhutani, M
Chimento, D
Giralt, S
Lendvai, N
Landau, H
Lesokhin, A
Chung, D
Babu, D
Hassoun, H
AF Zamarin, Dmitriy
Bhutani, Manisha
Chimento, Danielle
Giralt, Sergio
Lendvai, Nikoletta
Landau, Heather
Lesokhin, Alex
Chung, David
Babu, Dilip
Hassoun, Hani
TI Patterns of Disease Relapse and Progression in Patients with Multiple
Myeloma After First Line Therapy With Autologous Stem Cell
Transplantation: Implications for Patient Monitoring After
Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Giralt, Sergio; Landau, Heather; Chung, David] Mem Sloan Kettering Canc Ctr, Adult BMT Serv, New York, NY 10021 USA.
[Bhutani, Manisha] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Lendvai, Nikoletta; Lesokhin, Alex; Hassoun, Hani] Mem Sloan Kettering Canc Ctr, Myeloma Lymphoma Serv, New York, NY 10021 USA.
[Babu, Dilip] St Lukes Roosevelt Hosp, New York, NY 10025 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 376
EP 376
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101096
ER
PT J
AU Ayas, M
Le-Rademacher, J
Deeg, HJ
Gale, RP
Davies, SM
Bajwa, RPS
Battiwalla, M
Slavin, S
Camitta, B
Bierings, MB
Harris, RE
Olsson, R
Wirk, B
George, B
Bonfim, C
Saber, W
AF Ayas, Mouhab
Le-Rademacher, Jennifer
Deeg, H. Joachim
Gale, Robert Peter
Davies, Stella M.
Bajwa, Rajinder P. S.
Battiwalla, Minoo
Slavin, Shimon
Camitta, Bruce
Bierings, Marc B.
Harris, Richard E.
Olsson, Richard
Wirk, Baldeep
George, Biju
Bonfim, Carmem
Saber, Wael
TI Results of Allogeneic Hematopoietic Cell Transplantation in Persons with
Fanconi Anemia and Pretransplant Cytogenetic Abnormalities,
Myelodysplastic Syndrome, or Acute Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Ayas, Mouhab] King Faisal Specialist Hosp & Res Ctr, Riyadh 11211, Saudi Arabia.
[Le-Rademacher, Jennifer] Med Coll Wisconsin CIBMTR, Milwaukee, WI USA.
[Deeg, H. Joachim] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Gale, Robert Peter] Celgene Corp, Summit, NJ USA.
[Davies, Stella M.; Harris, Richard E.] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH USA.
[Bajwa, Rajinder P. S.] Nationwide Childrens Hosp, Dept Hematol Oncol & BMT, Columbus, OH USA.
[Battiwalla, Minoo] NHLBI, NIH, Bethesda, MD 20892 USA.
[Slavin, Shimon] Int Ctr Cell Therapy & Canc Immunotheraphy, Tel Aviv, Israel.
[Camitta, Bruce] Med Coll Wisconsin, Wauwatosa, WI USA.
[Bierings, Marc B.] Univ Med Ctr Utrecht, Dept Pediat Hematol Oncol, Utrecht, Netherlands.
[Olsson, Richard] Karolinska Univ Hosp, Ctr Allogene Stem Cell Transplantat, Stockholm, Sweden.
[Wirk, Baldeep] Univ Florida, Bone Marrow Transplant Program, Gainesville, FL USA.
[George, Biju] Christian Med Coll & Hosp, Dept Haematol, Vellore, Tamil Nadu, India.
[Bonfim, Carmem] Univ Fed Parana, Hosp Clin, Bone Marrow Transplantat Ctr, BR-80060000 Curitiba, Parana, Brazil.
[Saber, Wael] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
RI Bajwa, Rajinder/J-4304-2014
NR 0
TC 0
Z9 0
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 382
EP 383
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101109
ER
PT J
AU Li, PL
Pugach, EK
Riley, EB
Panigrahy, D
Heffner, GC
Bowman, TV
Tamplin, OJ
McKinney-Freeman, S
Schlaeger, TM
Daley, GQ
Zeldin, DC
Zon, LI
AF Li, Pulin
Pugach, Emily K.
Riley, Elizabeth B.
Panigrahy, Dipak
Heffner, Garrett C.
Bowman, Teresa V.
Tamplin, Owen J.
McKinney-Freeman, Shannon
Schlaeger, Thprsten M.
Daley, George Q.
Zeldin, Darryl C.
Zon, Leonard I.
TI Epoxyeicosatrienoic Acids Regulate Hematopoietic Stem/Progenitor Cell
Fate Decision During Stress Response and Embryonic Hematopoiesis
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Daley, George Q.; Zon, Leonard I.] Childrens Hosp Boston, Stem Cell Program, Howard Hughes Med Inst, Boston, MA USA.
[Daley, George Q.; Zon, Leonard I.] Childrens Hosp Boston, Div Hematol Oncol, Howard Hughes Med Inst, Boston, MA USA.
[McKinney-Freeman, Shannon] St Jude Childrens Hosp, Memphis, TN 38105 USA.
[Zeldin, Darryl C.] Natl Inst Environm Hlth Sci, Div Intramural Res, NIH, Res Triangle Pk, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 392
EP 393
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101131
ER
PT J
AU Greenblatt, SM
Li, L
Slape, C
Novak, RL
Duffield, AS
Nguyen, B
Huso, D
Borowitz, MJ
Aplan, P
Small, D
AF Greenblatt, Sarah M.
Li, Li
Slape, Christopher
Novak, Rachel L.
Duffield, Amy S.
Bao Nguyen
Huso, David
Borowitz, Michael J.
Aplan, Peter
Small, Donald
TI Knock-in of a FLT3 Internal Tandem Duplication Mutation Cooperates with
a NUP98-HOXD13 Fusion to Generate Acute Myeloid Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Borowitz, Michael J.] Johns Hopkins Univ, Dept Pathol, Baltimore, MD USA.
[Slape, Christopher] Monash Univ, Cent Clin Sch, Melbourne, Vic, Australia.
[Novak, Rachel L.; Aplan, Peter] NCI, Genet Branch, NIH, Bethesda, MD 20892 USA.
[Duffield, Amy S.] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Small, Donald] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
RI Slape, Christopher/H-8586-2016; Aplan, Peter/K-9064-2016
OI Slape, Christopher/0000-0002-8407-3092;
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 394
EP 395
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101136
ER
PT J
AU Zhao, L
Melenhorst, JJ
Alemu, L
Anderson, S
Kirby, M
Hoogstraten-Miller, S
Brinster, L
Kench, M
Kamikubo, Y
Gilliland, DG
Liu, PP
AF Zhao, Ling
Melenhorst, J. Joseph
Alemu, Lemlem
Anderson, Stacie
Kirby, Martha
Hoogstraten-Miller, Shelley
Brinster, Lauren
Kench, Maggie
Kamikubo, Yasuhiko
Gilliland, D. Gary
Liu, Pu Paul
TI KIT with D816 Mutations Cooperates with CBFB-MYH11 for Leukemogenesis in
Mice
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Zhao, Ling; Alemu, Lemlem; Liu, Pu Paul] NHGRI, GMBB, ODS, NIH, Bethesda, MD 20892 USA.
[Melenhorst, J. Joseph] NHLBI, NIH, Bethesda, MD 20892 USA.
[Brinster, Lauren] NIH, OD, Bethesda, MD 20892 USA.
[Kench, Maggie] Flow Cytometry Core, Bethesda, MD USA.
[Kamikubo, Yasuhiko] Univ Tokyo, Grad Sch Med, Dept Hematol & Oncol, Tokyo, Japan.
[Gilliland, D. Gary] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Div Hematol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 395
EP 396
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101138
ER
PT J
AU Wang, XD
Kato, GJ
Mendelsohn, L
AF Wang, Xunde
Kato, Gregory J.
Mendelsohn, Laurel
TI Iron Containing Compound Stimulates Expression of Pulmonary Hypertension
Promoting Factor PlGF
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 411
EP 412
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101171
ER
PT J
AU Kreitman, RJ
Xi, LQ
Navarro, W
Stetler-Stevenson, M
Arons, E
Raffeld, M
AF Kreitman, Robert J.
Xi, Liqiang
Navarro, Winnifred
Stetler-Stevenson, Maryalice
Arons, Evgeny
Raffeld, Mark
TI Presence and Absence of the BRAF V600E Mutation in Hairy Cell Leukemia
and Its Variants
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Kreitman, Robert J.; Arons, Evgeny] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Xi, Liqiang; Navarro, Winnifred; Stetler-Stevenson, Maryalice; Raffeld, Mark] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 423
EP 424
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101202
ER
PT J
AU Sun, XM
Herman, SEM
Hsieh, MM
Tisdale, JF
Chen, JC
Aue, G
Perez-Galan, P
Wiestner, A
AF Sun, Xiameng
Herman, Sarah E. M.
Hsieh, Matthew M.
Tisdale, John F.
Chen, Jichun
Aue, Georg
Perez-Galan, Patricia
Wiestner, Adrian
TI The NSG - Human CLL Xenograft Model Recapitulates the Human Lymph Node
Microenvironment in Regards to B-Cell Activation and Tumor Proliferation
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Sun, Xiameng; Herman, Sarah E. M.; Chen, Jichun; Aue, Georg; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Hsieh, Matthew M.; Tisdale, John F.] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
[Perez-Galan, Patricia] IDIAPS, Barcelona, Spain.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 445
EP 445
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101244
ER
PT J
AU Aue, G
Pittaluga, S
Liu, DL
Stennett, L
Soto, S
Valdez, J
Biancotto, A
McCoy, JP
Wiestner, A
AF Aue, Georg
Pittaluga, Stefania
Liu, Delong
Stennett, Larry
Soto, Susan
Valdez, Janet
Biancotto, Angelique
McCoy, J. Philip, Jr.
Wiestner, Adrian
TI Correlates of Lenalidomide Induced Immune Stimulation and Response in
CLL: Analysis in Patients on Treatment
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Aue, Georg; Liu, Delong; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Pittaluga, Stefania] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 447
EP 448
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101250
ER
PT J
AU Reger, RN
Berg, M
Lundqvist, A
Donohue, T
Carlsten, M
Betters, DM
Cook, L
Ramos, C
Grasmeder, S
Su, S
Stroncek, D
Pantin, J
Keyvanfar, K
Carvallo, CA
Khuu, H
Childs, R
AF Reger, Robert N.
Berg, Maria
Lundqvist, Andreas
Donohue, Theresa
Carlsten, Mattias
Betters, Dawn M.
Cook, Lisa
Ramos, Catalina
Grasmeder, Sophia
Su, Su
Stroncek, David
Pantin, Jeremy
Keyvanfar, Keyvan
Carvallo, Cristian A.
Khuu, Hahn
Childs, Richard
TI A Phase I Trial of Adoptively Transferred Ex-Vivo Expanded Autologous
Natural Killer (NK) Cells Following Treatment with Bortezomib to
Sensitize Tumors to NK Cell Cytotoxicity
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Reger, Robert N.; Berg, Maria; Donohue, Theresa; Carlsten, Mattias; Betters, Dawn M.; Cook, Lisa; Ramos, Catalina; Grasmeder, Sophia; Su, Su; Pantin, Jeremy; Keyvanfar, Keyvan; Childs, Richard] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Lundqvist, Andreas] Karolinska Inst, Canc Ctr Karolinska, Dept Pathol & Oncol, Stockholm, Sweden.
[Stroncek, David; Khuu, Hahn] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Carvallo, Cristian A.] Univ Los Andes, Clin Santa Maria, Santiago, Chile.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 457
EP 458
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101272
ER
PT J
AU Uchida, N
Tian, Y
Jin, P
Bonifacino, AC
Metzger, ME
Stroncek, D
Tisdale, JF
Donahue, RE
AF Uchida, Naoya
Tian, Yu
Jin, Ping
Bonifacino, Aylin C.
Metzger, Mark E.
Stroncek, David
Tisdale, John F.
Donahue, Robert E.
TI Evaluation of Human and Rhesus CD34+CXCR4+and CD34+CXCR4-Subpopulations
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Uchida, Naoya; Tisdale, John F.; Donahue, Robert E.] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
[Tian, Yu; Bonifacino, Aylin C.; Metzger, Mark E.] NHLBI, Hematol Branch, NIH, Rockville, MD USA.
[Jin, Ping; Stroncek, David] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 461
EP 461
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101278
ER
PT J
AU Byrnes, C
Lee, YT
Meier, ER
Rabel, A
Miller, JL
AF Byrnes, Colleen
Lee, Y. Terry
Meier, Emily Riehm
Rabel, Antoinette
Miller, Jeffery L.
TI Dosed Deficiency of Iron Restricts Terminal Maturation and Enucleation
of Cultured Human Erythroblasts
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Byrnes, Colleen; Lee, Y. Terry; Meier, Emily Riehm; Rabel, Antoinette; Miller, Jeffery L.] NIDDKD, Mol Genom & Therapeut Sect, Mol Med Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 480
EP 481
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101312
ER
PT J
AU Goel, R
Hassell, KL
Machado, RF
Barst, RJ
Yovetich, N
Kato, GJ
Gordeuk, VR
Little, JA
Gibbs, JSR
Schraufnagel, DE
Girgis, RE
Rosenzweig, EB
Morris, CR
Badesch, DB
Lanzkron, S
Onyekwere, O
Nouraie, M
Castro, OL
Sachdev, V
Waclawiw, M
Woolson, R
Goldsmith, JC
Gladwin, MT
Krishnamurti, L
AF Goel, Ruchika
Hassell, Kathryn L.
Machado, Roberto F.
Barst, Robyn J.
Yovetich, Nancy
Kato, Gregory J.
Gordeuk, Victor R.
Little, Jane A.
Gibbs, J. Simon R.
Schraufnagel, Dean E.
Girgis, Reda E.
Rosenzweig, Erika Berman
Morris, Claudia R.
Badesch, David B.
Lanzkron, Sophie
Onyekwere, Onyinye
Nouraie, Mehdi
Castro, Oswaldo L.
Sachdev, Vandana
Waclawiw, Myron
Woolson, Robert
Goldsmith, Jonathan C.
Gladwin, Mark T.
Krishnamurti, Lakshmanan
TI Non-Cardiopulmonary Factors Affecting the Six-Minute Walk Distance in
Patients with Sickle Cell Disease: Results From the Walk-PHaSST Study
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Goel, Ruchika; Krishnamurti, Lakshmanan] UPMC, Childrens Hosp Pittsburgh, BMT, Div Hematol Oncol, Pittsburgh, PA USA.
[Hassell, Kathryn L.] Univ Colorado Denver, Hlth Sci Ctr, Denver, CO USA.
[Machado, Roberto F.] Univ Illinois, Sect Pulm Crit Care Med Sleep & Allergy, Chicago, IL USA.
[Barst, Robyn J.] Columbia Univ, Scarsdale, NY USA.
[Yovetich, Nancy; Woolson, Robert] Rho World, Chapel Hill, NC USA.
[Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Gordeuk, Victor R.; Onyekwere, Onyinye; Nouraie, Mehdi; Castro, Oswaldo L.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
[Little, Jane A.] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Gibbs, J. Simon R.] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW7 2AZ, England.
[Girgis, Reda E.] Johns Hopkins Univ, Baltimore, MD USA.
[Rosenzweig, Erika Berman] Columbia Univ, New York, NY USA.
[Morris, Claudia R.] Childrens Hosp & Res Ctr Oakland, Oakland, CA USA.
[Lanzkron, Sophie] Johns Hopkins Sch Med, Dept Med, Baltimore, MD USA.
NHLBI, Translat Med Branch, NIH, Bethesda, MD 20892 USA.
[Gladwin, Mark T.] Univ Pittsburgh, Vasc Med Inst Pulm Allergy Crit Care Med, Pittsburgh, PA USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 493
EP 494
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101344
ER
PT J
AU Zhang, YZ
Zeng, QL
Belfer, I
Goel, R
Porter, M
Chu, YX
Barst, RJ
Hassell, KL
Machado, RF
Goldsmith, JC
Gladwin, MT
Krishnamurti, L
AF Zhang, Yingze
Zeng, Qilu
Belfer, Inna
Goel, Ruchika
Porter, Martha
Chu, Yanxia
Barst, Robyn J.
Hassell, Kathryn L.
Machado, Roberto F.
Goldsmith, Jonathan C.
Gladwin, Mark T.
Krishnamurti, Lakshmanan
TI Association of Genetic Variation in the Catechol-O-Methyl Transferase
Gene with Pain and Six Minute Walk Distance in Sickle Cell Anemia
Patients From the Walk-PHaSST Study
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Zhang, Yingze; Zeng, Qilu; Porter, Martha; Chu, Yanxia] Univ Pittsburgh, Div Pulm Allergy & Crit Care Med, Pittsburgh, PA USA.
[Belfer, Inna] Univ Pittsburgh, Dept Anesthesiol, Pittsburgh, PA USA.
[Belfer, Inna] Univ Pittsburgh, Dept Human Genet, Pittsburgh, PA USA.
[Goel, Ruchika; Krishnamurti, Lakshmanan] UPMC, Childrens Hosp Pittsburgh, BMT, Div Hematol Oncol, Pittsburgh, PA USA.
[Barst, Robyn J.] Columbia Univ, Scarsdale, NY USA.
[Hassell, Kathryn L.] Univ Colorado Denver, Hlth Sci Ctr, Denver, CO USA.
[Machado, Roberto F.] Univ Illinois, Sect Pulm Crit Care Med Sleep & Allergy, Chicago, IL USA.
[Goldsmith, Jonathan C.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Gladwin, Mark T.] Univ Pittsburgh, Vasc Med Inst, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 494
EP 494
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101345
ER
PT J
AU Milton, JN
Sebastiani, P
Zhang, YZ
Nouraie, M
Lee, J
Baldwin, CT
Zhao, XJ
Xiong, ZY
Zeng, QL
Kato, GJ
Goldsmith, JC
Taylor, JG
Onyekwere, O
Gordeuk, VR
Machado, RF
Steinberg, MH
Gladwn, MT
AF Milton, Jacqueline N.
Sebastiani, Paola
Zhang, Yingze
Nouraie, Mehdi
Lee, Janet
Baldwin, Clinton T.
Zhao, Xuejun
Xiong, Zeyu
Zeng, Qilu
Kato, Gregory J.
Goldsmith, Jonathan C.
Taylor, James G.
Onyekwere, Onyinye
Gordeuk, Victor R.
Machado, Roberto F.
Steinberg, Martin H.
Gladwn, Mark T.
TI Clinical and Genetic Variability of Red Blood Cell Hemolysis in Sickle
Cell Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Milton, Jacqueline N.; Sebastiani, Paola] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Zhang, Yingze; Xiong, Zeyu; Zeng, Qilu] Univ Pittsburgh, Div Pulm Allergy & Crit Care Med, Pittsburgh, PA USA.
[Nouraie, Mehdi; Onyekwere, Onyinye; Gordeuk, Victor R.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
[Lee, Janet] Univ Pittsburgh, Div Pulm Allergy & Crit Care Med, Pittsburgh, PA USA.
[Baldwin, Clinton T.] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Zhao, Xuejun; Gladwn, Mark T.] Univ Pittsburgh, Vasc Med Inst, Pittsburgh, PA USA.
[Kato, Gregory J.; Taylor, James G.] NHLBI, Sickle Cell Vasc Dis Sect, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Machado, Roberto F.] Univ Illinois, Sect Pulm Crit Care Med Sleep & Allergy, Chicago, IL USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 1
U2 9
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 495
EP 495
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101347
ER
PT J
AU Lee, YT
Byrnes, C
Meier, ER
Rabel, A
Miller, JL
AF Lee, Y. Terry
Byrnes, Colleen
Meier, Emily Riehm
Rabel, Antoinette
Miller, Jeffery L.
TI Ineffective Erythropoiesis and Production of Normoblasts with a Beta
Thalassemia Major Phenotype Using CD34+Cells From Healthy Donors
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Lee, Y. Terry; Byrnes, Colleen; Meier, Emily Riehm; Rabel, Antoinette; Miller, Jeffery L.] NIDDK, Mol Genom & Therapeut Sect, Mol Med Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 498
EP 498
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101355
ER
PT J
AU Aerbajinai, W
Chin, K
Zhu, JQ
Rodgers, GP
AF Aerbajinai, Wulin
Chin, Kyung
Zhu, Jianqiong
Rodgers, Griffin P.
TI Glia Maturation Factor-Gamma Negatively Modulates Fatty Acid-Induced
Inflammation in Macrophages Via PI3K/AKT Pathway
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Aerbajinai, Wulin; Chin, Kyung; Zhu, Jianqiong; Rodgers, Griffin P.] NHLBI NIH, Mol & Clin Hematol Branch, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 503
EP 504
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101366
ER
PT J
AU Longo, D
Louie, B
Mathi, K
Pos, Z
Wang, E
Hawtin, RE
Marincola, F
Cesano, A
AF Longo, Diane
Louie, Brent
Mathi, Kavita
Pos, Zoltan
Wang, Ena
Hawtin, Rachael E.
Marincola, Francesco
Cesano, Alessandra
TI Single Cell Network Profiling (SCNP) Reveals Race-Associated Differences
in B Cell Receptor Signaling Pathway Activation
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Longo, Diane; Louie, Brent; Mathi, Kavita; Hawtin, Rachael E.; Cesano, Alessandra] Nodality Inc, San Francisco, CA USA.
[Pos, Zoltan] Semmelweis Univ, Dept Genet Cell & Immunobiol, Budapest, Hungary.
[Wang, Ena; Marincola, Francesco] NIH, Infect Dis & Immunogenet Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Wang, Ena; Marincola, Francesco] NIH, Ctr Human Immunol, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 513
EP 513
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101394
ER
PT J
AU Pandey, GS
Garfield, S
Curran, JE
Moses, EK
Kimchi-Sarfaty, C
Yanover, C
Howard, TE
Sauna, ZE
AF Pandey, Gouri Shankar
Garfield, Susan
Curran, Joanne E.
Moses, Eric K.
Kimchi-Sarfaty, Chava
Yanover, Chen
Howard, Tom E.
Sauna, Zuben E.
TI The Entire Primary Sequence of Factor VIII Is Synthesized As Two
Polypeptide Chains in Hemophilia A Patients with the Intron-22-Inversion
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Pandey, Gouri Shankar] US FDA, Lab Hemostasis, DH CBER, Bethesda, MD 20014 USA.
[Garfield, Susan] NCI, NIH, Bethesda, MD 20892 USA.
[Curran, Joanne E.] SW Fdn Biomed Res, Dept Genet, San Antonio, TX USA.
[Kimchi-Sarfaty, Chava; Sauna, Zuben E.] US FDA, Ctr Biol Evaluat & Res, Div Hematol, Bethesda, MD 20892 USA.
[Yanover, Chen] Fred Hutchinson Canc Res Ctr, Program Computat Biol, Seattle, WA 98104 USA.
[Howard, Tom E.] Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 531
EP 532
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101445
ER
PT J
AU Donahue, RE
Jin, P
Klinman, JI
Bonifacino, AC
Metzger, ME
Stroncek, D
AF Donahue, Robert E.
Jin, Ping
Klinman, Johanna I.
Bonifacino, Aylin C.
Metzger, Mark E.
Stroncek, David
TI The Microarray Signature of Rhesus Macaque CD34+CD123 (IL-3 Receptor)+
Hematopoietic Stem/Progenitor Cells Isolated Following Mobilization with
Plerixafor Alone or in Combination with Granulocyte Colony-Stimulating
Factor (G-CSF)
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Donahue, Robert E.; Klinman, Johanna I.; Bonifacino, Aylin C.; Metzger, Mark E.] NHLBI, Hematol Branch, NIH, Rockville, MD USA.
[Jin, Ping; Stroncek, David] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 576
EP 577
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101570
ER
PT J
AU Zhu, JQ
Chin, K
Aerbajinai, W
Kumkhaek, C
Liu, WL
Rodgers, GP
AF Zhu, Jianqiong
Chin, Kyung
Aerbajinai, Wulin
Kumkhaek, Chutima
Liu, Wenli
Rodgers, Griffin P.
TI SAR1 Is Critical to the HbF-Inducing Effect of HU and Other Therapeutic
Cytotoxic Agents
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Zhu, Jianqiong] NHLBI, MCHB, NIH, Bethesa, MD USA.
[Chin, Kyung; Aerbajinai, Wulin; Kumkhaek, Chutima; Liu, Wenli; Rodgers, Griffin P.] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 578
EP 578
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101575
ER
PT J
AU Hyde, RK
Zhao, L
Alemu, L
Liu, PP
AF Hyde, R. Katherine
Zhao, Ling
Alemu, Lemlem
Liu, Pu Paul
TI Runx1 Is Required for Cbfb-MYH11 Activity During Primitive Hematopoiesis
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Hyde, R. Katherine; Zhao, Ling; Alemu, Lemlem; Liu, Pu Paul] NHGRI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 596
EP 596
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101626
ER
PT J
AU Shojaee, S
Buchner, M
Geng, HM
Silvia, B
Koeffler, P
Muschen, M
AF Shojaee, Seyedmehdi
Buchner, Maike
Geng, Huimin
Silvia, Bolland
Koeffler, Phillip
Muschen, Markus
TI Targeting Inhibitory Phosphatases in Tyrosine Kinase-Driven Leukemias
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Shojaee, Seyedmehdi; Muschen, Markus] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA.
[Buchner, Maike] Univ Hosp Freiburg, Freiburg, Germany.
[Geng, Huimin] Weill Cornell Med Coll, Inst Computat Biomed, New York, NY USA.
[Silvia, Bolland] NIAID, Bethesda, MD 20892 USA.
[Koeffler, Phillip] UCLA Sch Med, Cedars Sinai Med Ctr, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 605
EP 605
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101651
ER
PT J
AU Beachy, SH
Onozawa, M
Chung, YJ
Slape, C
Bilke, S
Francis, P
Pineda, M
Walker, RL
Meltzer, PS
Aplan, P
AF Beachy, Sarah H.
Onozawa, Masahiro
Chung, Yang Jo
Slape, Christopher
Bilke, Sven
Francis, Princy
Pineda, Marbin
Walker, Robert L.
Meltzer, Paul S.
Aplan, Peter
TI Enforced Expression of Lin28b Drives Development of Peripheral T Cell
Lymphoma In Vivo
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Beachy, Sarah H.; Onozawa, Masahiro; Chung, Yang Jo; Bilke, Sven; Francis, Princy; Pineda, Marbin; Walker, Robert L.; Meltzer, Paul S.; Aplan, Peter] NCI, Genet Branch, NIH, Bethesda, MD 20892 USA.
[Slape, Christopher] Monash Univ, Cent Clin Sch, Melbourne, Vic, Australia.
RI Slape, Christopher/H-8586-2016; Aplan, Peter/K-9064-2016
OI Slape, Christopher/0000-0002-8407-3092;
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 608
EP 608
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101661
ER
PT J
AU Kentsis, A
Sanda, T
Reed, C
Rodig, SJ
Tholouli, E
Ngo, V
Kutok, JL
Dahlberg, SE
Moreau, LA
Woude, GV
Christensen, J
Byers, R
Kung, AL
Staudt, LM
Look, T
AF Kentsis, Alex
Sanda, Takaomi
Reed, Casie
Rodig, Scott J.
Tholouli, Eleni
Vu Ngo
Kutok, Jeffery Lorne
Dahlberg, Suzanne E.
Moreau, Lisa A.
Woude, George Vande
Christensen, James
Byers, Richard
Kung, Andrew L.
Staudt, Louis M.
Look, Thomas
TI Combined Targeting of the MET and FGF Receptor Tyrosine Kinases Induces
Sustained AML Cell Death by Preventing Compensatory Upregulation of HGF
in Response to MET Kinase Inhibition
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Kentsis, Alex; Sanda, Takaomi] Harvard Univ, Sch Med, Dana Farber Canc Inst, Childrens Hosp Boston, Boston, MA 02115 USA.
[Kutok, Jeffery Lorne] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Tholouli, Eleni; Byers, Richard] Cent Manchester Univ Hosp NHS Fdn Trust, Manchester, Lancs, England.
[Dahlberg, Suzanne E.] Dana Farber Canc Inst, Dept Biostat Sci, Boston, MA 02115 USA.
[Woude, George Vande] Van Andel Res Inst, Grand Rapids, MI USA.
[Christensen, James] Pfizer, San Diego, CA USA.
[Kung, Andrew L.] Dana Farber Canc Inst, Lurie Family Imaging Ctr, Boston, MA 02115 USA.
[Kung, Andrew L.] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Staudt, Louis M.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 612
EP 612
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597101673
ER
PT J
AU Polizzotto, MN
Uldrick, TS
Wang, V
Aleman, K
Wyvill, KM
Marshall, V
Pittaluga, S
O'Mahony, D
Whitby, D
Tosato, G
Steinberg, SM
Little, RF
Yarchoan, R
AF Polizzotto, Mark N.
Uldrick, Thomas S.
Wang, Victoria
Aleman, Karen
Wyvill, Kathleen M.
Marshall, Vickie
Pittaluga, Stefania
O'Mahony, Deirdre
Whitby, Denise
Tosato, Giovanna
Steinberg, Seth M.
Little, Richard F.
Yarchoan, Robert
TI Distinct Human and Viral Interleukin-6 Profiles and Other Viral and
Immunologic Abnormalities In KSHV-Associated Multicentric Castleman
Disease: Relationship with Disease Activity and Individual Disease
Manifestations
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Polizzotto, Mark N.; Uldrick, Thomas S.; Wang, Victoria; Aleman, Karen; Wyvill, Kathleen M.; O'Mahony, Deirdre; Little, Richard F.; Yarchoan, Robert] NCI, HIV AIDS Malignancy Bratzch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Marshall, Vickie; Whitby, Denise] NCI, Viral Oncol Sect, AIDS & Canc Virus Program, SAIC Frederick, Frederick, MD 21701 USA.
[Pittaluga, Stefania] NCI, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Tosato, Giovanna] NCI, Cellular Oncol Lab, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 683
EP 684
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102168
ER
PT J
AU Dunleavy, K
Shovlin, M
Pittaluga, S
Grant, C
Steinberg, SM
Jaffe, ES
Wilson, WH
AF Dunleavy, Kieron
Shovlin, Margaret
Pittaluga, Stefania
Grant, Cliona
Steinberg, Seth M.
Jaffe, Elaine S.
Wilson, Wyndham H.
TI DA-EPOCH Chemotherapy Is Highly Effective in ALK-Positive and
ALK-Negative ALCL: Results of a Prospective Study of PTCL Subtypes in
Adults
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Dunleavy, Kieron; Shovlin, Margaret; Pittaluga, Stefania; Grant, Cliona; Steinberg, Seth M.; Jaffe, Elaine S.; Wilson, Wyndham H.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 704
EP 704
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102213
ER
PT J
AU Chung, YJ
Robert, C
Gough, SM
Rassool, F
Aplan, P
AF Chung, Yang Jo
Robert, Carine
Gough, Sheryl M.
Rassool, Feyruz
Aplan, Peter
TI Increased Mutation Frequency Induced by Oxidative Stress in the
NUP98-HOXD13 MDS Mouse Model
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Chung, Yang Jo; Gough, Sheryl M.; Aplan, Peter] NCI, Genet Branch, NIH, Bethesda, MD 20892 USA.
[Robert, Carine; Rassool, Feyruz] Univ Maryland, Sch Med, Dept Radiat Oncol, Baltimore, MD 21201 USA.
RI Aplan, Peter/K-9064-2016
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 743
EP 743
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102300
ER
PT J
AU Parikh, AR
Yang, Y
Wu, CO
Poon, A
Smith, KG
Young, NS
Barrett, AJ
Olnes, MJ
AF Parikh, Ankur R.
Yang, Yang
Wu, Colin O.
Poon, Andrea
Smith, Karen G.
Young, Neal S.
Barrett, A. John
Olnes, Matthew J.
TI Immunosuppressive Treatment for Patients with Myelodysplastic Syndromes:
A Review of 358 Patients
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Young, Neal S.; Olnes, Matthew J.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Wu, Colin O.] NHLBI, Off Biostat Res, NIH, Bethesda, MD USA.
[Smith, Karen G.] NIH Lib, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 748
EP 748
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102312
ER
PT J
AU Bandara, G
Bai, Y
Chan, EC
Maric, I
Simakova, O
Wise, SC
Flynn, D
Metcalfe, DD
Gilfillan, AM
Wilson, TM
AF Bandara, Geethani
Bai, Yun
Chan, Eunice Ching
Maric, Irina
Simakova, Olga
Wise, Scott C.
Flynn, Daniel
Metcalfe, Dean D.
Gilfillan, Alasdair M.
Wilson, Todd M.
TI Targeting the KIT Activating Switch Control Pocket: A Novel Mechanism to
Inhibit Mast Cell Activation and KIT D816V Neoplastic Mast Cell
Proliferation
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Bandara, Geethani; Bai, Yun; Chan, Eunice Ching; Wilson, Todd M.] NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA.
[Maric, Irina] DLM CC NIH, Bethesda, MD USA.
[Simakova, Olga] NIH, Dept Lab Med, Lawrence, KS USA.
[Wise, Scott C.; Flynn, Daniel] Deciphera Pharmaceut LLC, Lawrence, KS USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 759
EP 759
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102335
ER
PT J
AU Mc-Devitt, MA
Dilley, RL
Pratz, KW
Smith, BD
Moliterno, AR
Yen, Y
Malick, L
Gore, SD
Jones, RJ
Maciejewski, JP
Espinoza-Delgado, I
Karp, JE
AF Mc-Devitt, Michael A.
Dilley, Robert L.
Pratz, Keith W.
Smith, B. Douglas
Moliterno, Alison R.
Yen, Yun
Malick, Lisa
Gore, Steven D.
Jones, Richard J.
Maciejewski, Jaroslaw P.
Espinoza-Delgado, Igor
Karp, Judith E.
TI Final Results From a Phase II Trial of Triapine (R) Plus Fludarabine for
Adults with Aggressive Myeloproliferative Disorders
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Mc-Devitt, Michael A.; Moliterno, Alison R.] Johns Hopkins Univ, Sch Med, Div Hematol, Baltimore, MD USA.
[Pratz, Keith W.; Smith, B. Douglas; Malick, Lisa; Gore, Steven D.; Jones, Richard J.; Karp, Judith E.] Sidney Kimmel Comprehens Canc Ctr, Div Hematol Malignancies, Baltimore, MD USA.
[Yen, Yun] City Hope Natl Med Ctr, Duarte, CA USA.
[Maciejewski, Jaroslaw P.] Cleveland Clin, Tazissig Canc Inst, Cleveland, OH 44106 USA.
[Espinoza-Delgado, Igor] CTEP NIH, Bethesda, MD USA.
RI Dilley, Robert/C-7842-2012
NR 0
TC 0
Z9 0
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 765
EP 766
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102350
ER
PT J
AU Sivina, M
Kreitman, RJ
Peled, A
Ravandi, F
Burger, JA
AF Sivina, Mariela
Kreitman, Robert J.
Peled, Amnon
Ravandi, Farhad
Burger, Jan A.
TI Adhesion of Hairy Cells Leukemia (HCL) Cells to Stromal Cells Can Be
Inhibited by Blocking VLA-4 Integrins and CXCR4 Chemokine Receptors
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Sivina, Mariela; Burger, Jan A.] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Houston, TX 77030 USA.
[Kreitman, Robert J.] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Peled, Amnon] Goldyne Savad Inst Gene Therapy, Jerusalem, Israel.
NR 0
TC 1
Z9 1
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 768
EP 768
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102355
ER
PT J
AU Weiss, BM
Hurst, F
Agodoa, L
Abbott, KC
AF Weiss, Brendan M.
Hurst, Frank
Agodoa, Lawrence
Abbott, Kevin C.
TI Outcomes of Myeloma Patients on Hemodialysis in the Era of Novel
Therapies: An Analysis of the US Renal Data System
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Weiss, Brendan M.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Hurst, Frank; Abbott, Kevin C.] Walter Reed Army Med Ctr, Serv Nephrol, Washington, DC 20307 USA.
[Agodoa, Lawrence] NIDDK, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 787
EP 788
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102398
ER
PT J
AU Salit, RB
Bishop, MR
Pavletic, SZ
Hakim, FT
Steinberg, SM
Odom, J
Bryant, K
Wilder, J
Avila, DN
Blacklock-Schuver, B
Gress, RE
Fowler, DH
AF Salit, Rachel B.
Bishop, Michael R.
Pavletic, Steven Z.
Hakim, Frances T.
Steinberg, Seth M.
Odom, Jeanne
Bryant, Kelly
Wilder, Jennifer
Avila, Daniele N.
Blacklock-Schuver, Bazetta
Gress, Ronald E.
Fowler, Daniel H.
TI Concurrent Fludarabine and Cyclophosphamide As a Reduced Intensity
Conditioning Regimen Prior to Allogeneic Hematopoietic Stem Cell
Transplantation Ablates Host T-Cells and Results in Rapid Full Donor
Chimerism
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Salit, Rachel B.; Pavletic, Steven Z.; Gress, Ronald E.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Bishop, Michael R.] Med Coll Wisconsin, Clin Canc Ctr, Milwaukee, WI 53226 USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, NIH, Rockville, MD USA.
[Wilder, Jennifer] SAIC, Clin Res Directorate, CMRP, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 844
EP 844
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102532
ER
PT J
AU Palmer, J
Lee, SJ
Chai, XY
Storer, B
Pidala, J
Cutler, CS
Arora, M
Flowers, MED
Pavletic, SZ
Vogelsang, GB
Inamoto, Y
Jagasia, M
George, C
Martin, PJ
AF Palmer, Jeanne
Lee, Stephanie J.
Chai, Xiaoyu
Storer, Barry
Pidala, Joseph
Cutler, Corey S.
Arora, Mukta
Flowers, Mary E. D.
Pavletic, Steven Z.
Vogelsang, Georgia B.
Inamoto, Yoshihiro
Jagasia, Madan
George, Chen
Martin, Paul J.
TI Comparison of Proposed NIH Response Criteria with Clinician-Reported
Changes in Organ-Specific and Overall Response
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Palmer, Jeanne] MCW & Froedtert Clin Canc Ctr, Milwaukee, WI USA.
[Storer, Barry] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
[Pidala, Joseph] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Cutler, Corey S.] Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
[Arora, Mukta] Univ Minnesota, Med Blood & Marrow Transplant Program, Minneapolis, MN USA.
[Pavletic, Steven Z.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Vogelsang, Georgia B.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[Jagasia, Madan] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
[George, Chen] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 863
EP 863
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102573
ER
PT J
AU Inamoto, Y
Cutler, CS
Chai, XY
Arora, M
Martin, PJ
Pidala, J
Palmer, J
Pavletic, SZ
Jagasia, MH
Jacobsohn, D
Carpenter, PA
Flowers, MED
Khera, N
Vogelsang, GB
Weisdorf, DJ
Storer, B
Lee, SJ
AF Inamoto, Yoshihiro
Cutler, Corey S.
Chai, Xiaoyu
Arora, Mukta
Martin, Paul J.
Pidala, Joseph
Palmer, Jeanne
Pavletic, Steven Z.
Jagasia, Madan H.
Jacobsohn, David
Carpenter, Paul A.
Flowers, Mary E. D.
Khera, Nandita
Vogelsang, Georgia B.
Weisdorf, Daniel J.
Storer, Barry
Lee, Stephanie J.
TI Calculated NIH Response Correlates with Changes in Patient-Reported
Symptoms but Not with Quality of Life: Results From the Chronic Gvhd
Consortium
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Inamoto, Yoshihiro; Chai, Xiaoyu; Martin, Paul J.; Carpenter, Paul A.; Flowers, Mary E. D.; Khera, Nandita; Storer, Barry; Lee, Stephanie J.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Cutler, Corey S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Arora, Mukta; Weisdorf, Daniel J.] Univ Minnesota, Minneapolis, MN USA.
[Pidala, Joseph] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Palmer, Jeanne] MCW, Milwaukee, WI USA.
[Palmer, Jeanne] Froedtert Clin Canc Ctr, Milwaukee, WI USA.
[Pavletic, Steven Z.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Jagasia, Madan H.] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
[Jacobsohn, David] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Vogelsang, Georgia B.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 868
EP 868
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102583
ER
PT J
AU McIver, ZA
Hughes, T
Ito, S
Battiwalla, M
Koklanaris, EK
Haggerty, J
Hensel, NF
Barrett, AJ
AF McIver, Zachariah A.
Hughes, Thomas
Ito, Sawa
Battiwalla, Minoo
Koklanaris, Eleftheria K.
Haggerty, Janice
Hensel, Nancy F.
Barrett, A. John
TI Second Stem Cell Transplantation (SCT) for Relapsed Leukemia Provides
Only Modest Prolongation of Survival
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [McIver, Zachariah A.; Ito, Sawa; Battiwalla, Minoo; Koklanaris, Eleftheria K.; Haggerty, Janice; Hensel, Nancy F.; Barrett, A. John] NHLBI, NIH, Bethesda, MD 20892 USA.
[Hughes, Thomas] NIH, CC, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 873
EP 873
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102596
ER
PT J
AU Uchida, N
Hsieh, MM
Bonifacino, AC
Price, SD
Krouse, AE
Metzger, ME
Donahue, RE
Tisdale, JF
AF Uchida, Naoya
Hsieh, Matthew M.
Bonifacino, Aylin C.
Price, Sandra D.
Krouse, Allen E.
Metzger, Mark E.
Donahue, Robert E.
Tisdale, John F.
TI TRIM5 alpha Variation Affects Lentiviral Transduction Efficiency for
Long-Term Hematopoietic Repopulating Cells in a Rhesus Stem Cell
Transplantation Model
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Uchida, Naoya; Hsieh, Matthew M.; Tisdale, John F.] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
[Bonifacino, Aylin C.; Price, Sandra D.; Krouse, Allen E.; Metzger, Mark E.; Donahue, Robert E.] NHLBI, Hematol Branch, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 902
EP 903
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102651
ER
PT J
AU Cui, YZ
Garber, H
Onozawa, M
Qin, HY
Fry, TJ
Aplan, P
Mackall, CL
AF Cui, Yongzhi
Garber, Haven
Onozawa, Masahiro
Qin, Haiying
Fry, Terry J.
Aplan, Peter
Mackall, Crystal L.
TI T Cell Lymphoblastic Lymphoma Resulting From Expression of Self-Reactive
TCRs During Early Thymopoiesis
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Cui, Yongzhi; Garber, Haven; Qin, Haiying; Fry, Terry J.; Mackall, Crystal L.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Onozawa, Masahiro; Aplan, Peter] NCI, Genet Branch, NIH, Bethesda, MD 20892 USA.
RI Aplan, Peter/K-9064-2016
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 903
EP 903
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102652
ER
PT J
AU Darbari, DS
Hildeshem, M
Minniti, C
Kato, GJ
Taylor, JG
AF Darbari, Deepika S.
Hildeshem, Mariana
Minniti, Caterina
Kato, Gregory J.
Taylor, James G.
TI Health Care Utilization for Painful Events Is Associated with Early
Mortality in a Contemporary Population of Adults with Sickle Cell Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Darbari, Deepika S.] NHLBI, Pediat Hematol & Oncol NHLBI Pulm and Vasc Med, Childrens Natl Med Ctr, Washington, DC USA.
[Minniti, Caterina; Kato, Gregory J.; Taylor, James G.] NHLBI, Sickle Cell Vasc Dis Sect, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 926
EP 926
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102710
ER
PT J
AU Ask, A
Mendelsohn, LG
Alam, S
Mehari, A
Minniti, C
Taylor, JG
Kato, GJ
AF Ask, Antje
Mendelsohn, Laurel G.
Alam, Shoaib
Mehari, Alem
Minniti, Caterina
Taylor, James G.
Kato, Gregory J.
TI A Cell-Based Adhesion Molecule Bioassay Detects Unexpected Properties of
Plasma From Patients with Sickle Cell Disease with Documented Pulmonary
Hypertension
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Ask, Antje; Mendelsohn, Laurel G.; Alam, Shoaib; Mehari, Alem; Minniti, Caterina; Taylor, James G.; Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 928
EP 928
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102715
ER
PT J
AU Pakbaz, Z
Hildesheim, ME
Alam, S
Allen, D
Minniti, C
Taylor, JG
Kato, GJ
AF Pakbaz, Zahra
Hildesheim, Mariana E.
Alam, Shoaib
Allen, Darlene
Minniti, Caterina
Taylor, James G.
Kato, Gregory J.
TI Serum Transferrin: An Independent Predictor of Mortality in Sickle Cell
Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Hildesheim, Mariana E.] NIH, Dept Crit Care Med, Bethesda, MD 20892 USA.
[Alam, Shoaib; Allen, Darlene; Minniti, Caterina; Taylor, James G.; Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 931
EP 931
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102721
ER
PT J
AU Meier, ER
Byrnes, C
Lee, YT
Weissman, M
Noel, P
Schechter, AN
Luban, NLC
Miller, JL
AF Meier, Emily R.
Byrnes, Colleen
Lee, Y. Terry
Weissman, Maxine
Noel, Pierre
Schechter, Alan N.
Luban, Naomi L. C.
Miller, Jeffery L.
TI Increased Reticulocytosis in Infants with Sickle Cell Disease May Be a
Marker for Future Disease Severity
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Meier, Emily R.] Childrens Natl Med Ctr, Div Hematol, Washington, DC 20010 USA.
[Meier, Emily R.] NIDDK, Mol Med Branch, NIH, Washington, DC USA.
[Byrnes, Colleen; Lee, Y. Terry; Miller, Jeffery L.] NIDDK, Mol Genom & Therapeut Sect, Mol Med Branch, NIH, Bethesda, MD USA.
[Weissman, Maxine; Noel, Pierre] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 932
EP 932
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597102723
ER
PT J
AU Donahue, RE
Tuschong, L
Bauer, TR
Hickstein, DD
Yau, YY
Leitman, SF
AF Donahue, Robert E.
Tuschong, Laura
Bauer, Thomas R.
Hickstein, Dennis D.
Yau, Yu Ying
Leitman, Susan F.
TI Leukocyte Integrin Activation and Alterations in Parathyroid Hormone
Levels Following G-CSF Administration
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Donahue, Robert E.] NHLBI, Hematol Branch, NIH, Rockville, MD USA.
[Tuschong, Laura; Bauer, Thomas R.; Hickstein, Dennis D.] NCI, Expt Transplantat & Immunol Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Yau, Yu Ying; Leitman, Susan F.] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 947
EP 947
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103032
ER
PT J
AU Diestelhorst, J
Kotlarz, D
Appaswamy, G
Beier, R
Krawitz, PM
Robinson, PN
Hecht, J
Puchalka, J
Schaffer, AA
Pfeifer, D
Baumann, U
Pfister, ED
Brandes, G
Palla, G
Jacobs, R
Kreipe, HH
Mundlos, S
Klein, C
AF Diestelhorst, Jana
Kotlarz, Daniel
Appaswamy, Giridharan
Beier, Rita
Krawitz, Peter M.
Robinson, Peter N.
Hecht, Jochen
Puchalka, Jacek
Schaeffer, Alejandro A.
Pfeifer, Dietmar
Baumann, Ulrich
Pfister, Eva-Doreen
Brandes, Gudrun
Palla, Gabriella
Jacobs, Roland
Kreipe, Hans H.
Mundlos, Stefan
Klein, Christoph
TI G6PC3 Deficiency Associated with Congenital Neutropenia and
Enterocolitis
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Diestelhorst, Jana; Appaswamy, Giridharan; Beier, Rita] Hannover Med Sch, Dept Pediat Hematol Oncol, D-3000 Hannover, Germany.
[Kotlarz, Daniel; Puchalka, Jacek; Kreipe, Hans H.; Klein, Christoph] Univ Munich, Dr von Hauner Kinderspital, Dept Pediat, Munich, Germany.
[Krawitz, Peter M.] Charite, Inst Med Genet & Humangenet, D-13353 Berlin, Germany.
[Robinson, Peter N.] Max Planck Inst Mol Genet, D-14195 Berlin, Germany.
[Hecht, Jochen] Charite, Berlin Brandenburg Ctr Regenerat Therapies, D-13353 Berlin, Germany.
[Schaeffer, Alejandro A.] NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA.
[Pfeifer, Dietmar] Univ Freiburg, Med Ctr, Dept Hematol & Oncol, Genom Core Lab, Freiburg, Germany.
[Baumann, Ulrich; Pfister, Eva-Doreen] Hannover Med Sch, Dept Pediat Kidney Liver & Metab Dis, D-3000 Hannover, Germany.
[Brandes, Gudrun] Hannover Med Sch, Ctr Anat, Inst Cellular Biol, D-3000 Hannover, Germany.
[Palla, Gabriella] Univ Pisa, Dept Gastroenterol & Hepatol, Pisa, Italy.
[Jacobs, Roland] Hannover Med Sch, Dept Clin Immunol & Rheumatol, D-3000 Hannover, Germany.
[Kreipe, Hans H.] Hannover Med Sch, Inst Pathol, D-3000 Hannover, Germany.
RI Schaffer, Alejandro/F-2902-2012
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 948
EP 949
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103038
ER
PT J
AU Olnes, MJ
Biancotto, A
Wang, E
Reger, R
Perl, S
Dickler, H
Mccoy, JP
Marincola, F
Childs, R
Young, NS
AF Olnes, Matthew J.
Biancotto, Angelique
Wang, Ena
Reger, Robert
Perl, Shira
Dickler, Howard
McCoy, J. Philip
Marincola, Francesco
Childs, Richard
Young, Neal S.
TI Systemically Administered Hydrocortisone Exerts Differential Effects on
B and T Lymphocytes and Natural Killer Cells in Healthy Donors
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Olnes, Matthew J.; Reger, Robert; Childs, Richard; Young, Neal S.] NHLBI, NIH, Hematol Branch, Bethesda, MD 20892 USA.
[Biancotto, Angelique] NHLBI, Flow Cytometry Core, NIH, Bethesda, MD 20892 USA.
[Wang, Ena; Marincola, Francesco] NIH, Infect Dis & Immunogenet Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Wang, Ena; Marincola, Francesco] NIH, Ctr Human Immunol, Bethesda, MD 20892 USA.
[Perl, Shira; Dickler, Howard; McCoy, J. Philip] NIH, Trans NIH Ctr Human Immunol Autoimmun & Inflammat, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 952
EP 953
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103046
ER
PT J
AU Rissone, AF
Jagadeesh, GJ
Simon, K
Bishop, K
English, M
Blake, T
Nissen, RM
Sood, RB
Candotti, F
AF Rissone, Alberto F.
Jagadeesh, Guridevi Jayashree
Simon, Karen
Bishop, Kevin
English, Milton
Blake, Trevor
Nissen, Robert M.
Sood, Raman B.
Candotti, Fabio
TI Characterization of AK2 Gene Function in Zebrafish Hematopoiesis
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Jagadeesh, Guridevi Jayashree] NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
[Bishop, Kevin; English, Milton; Sood, Raman B.] NHGRI, Oncogenesis & Dev Sect, Bethesda, MD 20892 USA.
[Nissen, Robert M.] Calif State Univ Los Angeles, Dept Biol Sci, Los Angeles, CA 90032 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 954
EP 955
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103052
ER
PT J
AU Chang, L
Price, S
Perkins, K
Davis, J
Aldridge, P
Recht, M
Kelleher, J
Rao, VK
AF Chang, Leejah
Price, Susan
Perkins, Katie
Davis, Joie
Aldridge, Patricia
Recht, Michael
Kelleher, John
Rao, V. Koneti
TI Mycophenolate Mofetil and Thrombopoietin Receptor Agonists in the
Treatment of Refractory Thrombocytopenia in Patients with Autoimmune
Lymphoproliferative Syndrome
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Chang, Leejah; Price, Susan; Perkins, Katie; Davis, Joie; Aldridge, Patricia; Rao, V. Koneti] NIAID, ALPS Unit, LCID, NIH, Bethesda, MD 20892 USA.
[Recht, Michael] Oregon Hlth & Sci Univ, Hemophilia Ctr, Portland, OR 97201 USA.
[Kelleher, John] W Virginia Univ, Morgantown, WV 26506 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 965
EP 966
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103085
ER
PT J
AU Strom, T
Zeng, XY
Candotti, F
Conley, ME
Anur, P
Prislovsky, A
AF Strom, Ted
Zeng, Xueying
Candotti, Fabio
Conley, Mary Ellen
Anur, Praveen
Prislovsky, Amanda
TI Platelets From WAS Patients Are More Susceptible Than Controls to
Phagocytosis by Activated THP-1 Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Strom, Ted; Prislovsky, Amanda] Memphis VA Med Ctr, Pathol & Lab Med, Memphis, TN USA.
[Zeng, Xueying] Univ Tennessee, Ctr Hlth Sci, Pathol & Lab Med, Memphis, TN 38163 USA.
[Candotti, Fabio] NHGRI, NIH, Bethesda, MD 20892 USA.
[Conley, Mary Ellen] St Jude Childrens Hosp, Memphis, TN 38105 USA.
[Anur, Praveen] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 967
EP 968
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103089
ER
PT J
AU Follit, CA
Brunker, PAR
Flegel, WA
AF Follit, Courtney A.
Brunker, Patricia A. R.
Flegel, Willy A.
TI SNP Genotyping and LD Testing in ERMAP: Revealing Scianna Blood Group
Diversity in NIH Blood Donors
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Follit, Courtney A.; Brunker, Patricia A. R.] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1006
EP 1007
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103189
ER
PT J
AU Keller, JR
Ji, M
Li, HJ
Kozlov, SV
Tessarollo, L
Klarmann, KD
AF Keller, Jonathan R.
Ji, Ming
Li, Huajie
Kozlov, Serguei V.
Tessarollo, Lino
Klarmann, Kimberly D.
TI Dynamic Expression of Id2 Determines Cell Fate Decisions in Multipotent
Hematopoietic Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Keller, Jonathan R.; Ji, Ming; Li, Huajie; Klarmann, Kimberly D.] NCI, Lab Canc Prevent, BSP SAIC Frederick, Ctr Canc Res, Frederick, MD 21701 USA.
[Kozlov, Serguei V.] NCI, Ctr Adv Preclin Res, LASP, SAIC Frederick,Ctr Canc Res, Frederick, MD 21701 USA.
[Tessarollo, Lino] NCI, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1021
EP 1021
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103235
ER
PT J
AU Meyer, SE
Rogers, AM
Lal, A
Lieberman, J
Aronow, BJ
Komurov, K
Grimes, HL
AF Meyer, Sara E.
Rogers, Andrew M.
Lal, Ashish
Lieberman, Judy
Aronow, Bruce J.
Komurov, Kakajan
Grimes, H. Leighton
TI Unbiased Analyses of Signaling Through Leukemia Associated MicroRNA
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Meyer, Sara E.; Rogers, Andrew M.; Grimes, H. Leighton] Cincinnati Childrens Hosp, Med Ctr, Div Immunobiol, Cincinnati, OH USA.
[Lal, Ashish] NCI, Genet Branch, Regulatory RNAs & Canc Sect, Bethesda, MD 20892 USA.
[Lieberman, Judy] Harvard Univ, Childrens Hosp, Immune Dis Inst, Program Cellular & Mol Med,Sch Med, Boston, MA 02115 USA.
[Aronow, Bruce J.] Cincinnati Childrens Hosp, Med Ctr, Div Biomed Informat, Cincinnati, OH USA.
RI Aronow, Bruce/F-8438-2012;
OI Meyer, Sara/0000-0003-2930-748X
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1022
EP 1023
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103239
ER
PT J
AU Feng, XM
Scheinberg, P
Biancotto, A
Rios, O
Donaldson, S
Wu, CO
Zheng, HY
Sato, K
McCoy, JP
Young, NS
AF Feng, Xingmin
Scheinberg, Phillip
Biancotto, Angelique
Rios, Olga
Donaldson, Sarah
Wu, Colin O.
Zheng, Haiyun
Sato, Kazuya
McCoy, J. Philip, Jr.
Young, Neal S.
TI Different In Vivo Effects of Horse and Rabbit Antithymocyte Globulin in
Patients with Severe Aplastic Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Feng, Xingmin; Scheinberg, Phillip; Rios, Olga; Sato, Kazuya; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Biancotto, Angelique; McCoy, J. Philip, Jr.] NHLBI, Flow Cytometry Core, NIH, Bethesda, MD 20892 USA.
[Donaldson, Sarah] Washington Univ, Sch Med, St Louis, MO USA.
[Wu, Colin O.] NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA.
[Zheng, Haiyun] George Washington Univ, Dept Stat, Washington, DC 20052 USA.
RI Scheinberg, Phillip/H-5251-2012
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1032
EP 1032
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103265
ER
PT J
AU Alter, BP
Rosenberg, PS
Day, T
Menzel, S
Giri, N
Savage, SA
Thein, SL
AF Alter, Blanche P.
Rosenberg, Philip S.
Day, Thomas
Menzel, Stephan
Giri, Neelam
Savage, Sharon A.
Thein, Swee Lay
TI Stress Erythropoiesis and Genetic Regulation of Fetal Hemoglobin in
Inherited Bone Marrow Failure Syndromes
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Alter, Blanche P.; Giri, Neelam; Savage, Sharon A.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Rosenberg, Philip S.] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD USA.
[Thein, Swee Lay] Kings Coll London, Sch Med, Kings Coll Hosp Haematol Med, London WC2R 2LS, England.
RI Savage, Sharon/B-9747-2015
OI Savage, Sharon/0000-0001-6006-0740
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1033
EP 1033
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103267
ER
PT J
AU Aalbers, AM
Kajigaya, S
van der Velden, VHJ
van den Heuvel-Eibrink, MM
Calado, RT
Young, NS
AF Aalbers, Anna M.
Kajigaya, Sachiko
van der Velden, Vincent H. J.
van den Heuvel-Eibrink, Marry M.
Calado, Rodrigo T.
Young, Neal S.
TI Human Telomere Disease Due to Disruption of the CCAAT Box of the TERC
Promoter
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Aalbers, Anna M.; van den Heuvel-Eibrink, Marry M.] Erasmus MC, Dept Pediat Oncol Hematol, Rotterdam, Netherlands.
[Kajigaya, Sachiko; Calado, Rodrigo T.; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[van der Velden, Vincent H. J.] Erasmus MC, Dept Immunol, Rotterdam, Netherlands.
RI Calado, Rodrigo/G-2619-2011
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1034
EP 1034
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103271
ER
PT J
AU Scheinberg, P
Nunez, O
Scheinberg, P
Weinstein, B
Wu, CO
Young, NS
AF Scheinberg, Phillip
Nunez, Olga
Scheinberg, Priscila
Weinstein, Barbara
Wu, Colin O.
Young, Neal S.
TI Cyclosporine Taper Does Not Prevent Relapse in Severe Aplastic Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Scheinberg, Phillip; Nunez, Olga; Scheinberg, Priscila; Weinstein, Barbara; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Wu, Colin O.] NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA.
RI Scheinberg, Phillip/H-5251-2012
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1035
EP 1035
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103272
ER
PT J
AU Fares, J
Wolff, L
Bies, J
AF Fares, Joanna
Wolff, Linda
Bies, Juraj
TI Modulation of Myeloid-Derived Dendritic Cell Maturity: Unmasking a Novel
Role for the Tumor Suppressor p15Ink4b in Immunity
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Fares, Joanna; Wolff, Linda; Bies, Juraj] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1058
EP 1058
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103335
ER
PT J
AU Gough, SM
Lee, F
Chung, YJ
Walker, RL
Yang, F
Zhu, YL
Ning, Y
Meltzer, PS
Aplan, P
AF Gough, Sheryl M.
Lee, Fan
Chung, Yang Jo
Walker, Robert L.
Yang, Fan
Zhu, Yuelin (Jack)
Ning, Yi
Meltzer, Paul S.
Aplan, Peter
TI A NUP98-PHF23 Transgenic Mouse Model Develops AML and T-ALL
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Gough, Sheryl M.; Lee, Fan; Chung, Yang Jo; Walker, Robert L.; Yang, Fan; Zhu, Yuelin (Jack); Meltzer, Paul S.; Aplan, Peter] NCI, Genet Branch, NIH, CCR, Bethesda, MD 20892 USA.
[Ning, Yi] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
RI Aplan, Peter/K-9064-2016
NR 0
TC 1
Z9 1
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1058
EP 1058
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103333
ER
PT J
AU Hyde, RK
Kamikubo, Y
Zhao, L
Alemu, L
Garrett, L
Liu, PP
AF Hyde, R. Katherine
Kamikubo, Yasuhiko
Zhao, Ling
Alemu, Lemlem
Garrett, Lisa
Liu, Pu Paul
TI The C-Terminal of MYH11 Is Required for Cbfb-MYH11 Activity During
Embryonic Hematopoiesis and Leukemogenesis
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Hyde, R. Katherine; Zhao, Ling; Alemu, Lemlem; Liu, Pu Paul] NHGRI, GMBB ODS, NIH, Bethesda, MD 20892 USA.
[Kamikubo, Yasuhiko] Univ Tokyo, Grad Sch Med, Dept Hematol & Oncol, Tokyo, Japan.
[Garrett, Lisa] NHGRI, GDRB Transgen Mouse Core, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1059
EP 1060
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103338
ER
PT J
AU Morton, LM
Clarke, CA
Chang, ET
Hall, EC
Lynch, CF
Pfieffer, R
Weisenburger, DD
Engels, EA
AF Morton, Lindsay M.
Clarke, Christina A.
Chang, Ellen T.
Hall, Erin C.
Lynch, Charles F.
Pfieffer, Ruth
Weisenburger, Dennis D.
Engels, Eric A.
TI Risk of Acute Myeloid Leukemia Among Solid Organ Transplant Recipients
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Morton, Lindsay M.; Pfieffer, Ruth; Engels, Eric A.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Rockville, MD USA.
[Clarke, Christina A.; Chang, Ellen T.] Canc Prevent Inst Calif, Fremont, CA USA.
[Hall, Erin C.] Johns Hopkins Sch Med, Dept Surg, Baltimore, MD USA.
[Lynch, Charles F.] Univ Iowa, Dept Epidemiol, Iowa City, IA USA.
[Weisenburger, Dennis D.] Univ Nebraska Med Ctr, Dept Pathol, Omaha, NE USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1097
EP 1098
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103425
ER
PT J
AU Kreitman, RJ
Singh, R
Stetler-Stevenson, M
Waldmann, TA
Pastan, I
AF Kreitman, Robert J.
Singh, Rajat
Stetler-Stevenson, Maryalice
Waldmann, Thomas A.
Pastan, Ira
TI Regression of Adult T-Cell Leukemia with Anti-CD25 Recombinant
Immunotoxin LMB-2 Preceded by Chemotherapy
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Kreitman, Robert J.; Singh, Rajat; Pastan, Ira] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Stetler-Stevenson, Maryalice] NCI, Lab Pathol, NIH, Bethesda, MD 20892 USA.
[Waldmann, Thomas A.] NCI, Metabolism Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1105
EP 1105
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103441
ER
PT J
AU Burk, CR
Fix, W
Qin, HY
Fry, TJ
AF Burk, Chad R.
Fix, William
Qin, Haiying
Fry, Terry J.
TI ALL Progression Induces PD1 on T Cells and Blockade of PD1 Enhances
Adoptive Immunotherapy
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Burk, Chad R.] Howard Hughes Med Inst, Bethesda, MD 20817 USA.
[Fix, William; Qin, Haiying; Fry, Terry J.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1110
EP 1111
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103453
ER
PT J
AU Cozen, W
Hwang, A
Marshall, V
Mack, TM
Whitby, D
AF Cozen, Wendy
Hwang, Amie
Marshall, Vickie
Mack, Thomas M.
Whitby, Denise
TI EBV Copy Number Variation in Twins Discordant for Young Adult Hodgkin
Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Hwang, Amie; Mack, Thomas M.] Univ So Calif, Norris Canc Ctr, Los Angeles, CA USA.
[Marshall, Vickie] Natinoal Canc Inst, AIDS & Canc Virus Program, Viral Oncol Sect, Ferderick, MD USA.
[Whitby, Denise] NCI, Viral Oncol Sect, AIDS & Canc Virus Program, SAIC Frederick, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1130
EP 1130
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597103497
ER
PT J
AU Grant, C
Neelapu, SS
Kwak, LW
Dunleavy, K
White, T
Miller, BW
Jaffe, ES
Steinberg, SM
Bird, BH
Wilson, WH
AF Grant, Cliona
Neelapu, Sattva S.
Kwak, Larry W.
Dunleavy, Kieron
White, Therese
Miller, Barry W.
Jaffe, Elaine S.
Steinberg, Seth M.
Bird, Brian Healey
Wilson, Wyndham H.
TI Eleven-Year Follow-up of Idiotype Vaccine and DA-EPOCH-Rituximab in
Untreated Mantle Cell Lymphoma: Correlation of Survival with Idiotype
Immune Response
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Jaffe, Elaine S.] NCI, Ctr Canc Res, Pathol Lab, Bethesda, MD 20892 USA.
[Neelapu, Sattva S.] UT MD Anderson Canc Ctr, Div Canc Med, Houston, TX USA.
[Neelapu, Sattva S.] UT MD Anderson Canc Ctr, Ctr Canc Immunol Res, Houston, TX USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, NIH, Rockville, MD USA.
[Bird, Brian Healey] Bons Secours Hosptial, Cork, Ireland.
[Wilson, Wyndham H.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1164
EP 1165
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104058
ER
PT J
AU Staudt, LM
Dunleavy, K
Buggy, JJ
Hedrick, E
Lucas, N
Pittaluga, S
Jhavar, S
Schmitz, R
Williams, M
Lih, J
Jaffe, ES
Wilson, WH
AF Staudt, Louis M.
Dunleavy, Kieron
Buggy, Joseph J.
Hedrick, Eric
Lucas, Nicole
Pittaluga, Stefania
Jhavar, Sameer
Schmitz, Roland
Williams, Mickey
Lih, Jason
Jaffe, Elaine S.
Wilson, Wyndham H.
TI The Bruton's Tyrosine Kinase (Btk) Inhibitor PCI-32765 Modulates Chronic
Active BCR Signaling and Induces Tumor Regression in Relapsed/Refractory
ABC DLBCL
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Staudt, Louis M.; Schmitz, Roland; Wilson, Wyndham H.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
[Lucas, Nicole] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Buggy, Joseph J.] Pharmacyclics Inc, Res, Sunnyvale, CA USA.
[Williams, Mickey] NCI, Frederick, MD 21701 USA.
[Lih, Jason] NCI, SAIC, NIH, Bethesda, MD 20892 USA.
NR 0
TC 2
Z9 2
U1 0
U2 5
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1168
EP 1169
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104067
ER
PT J
AU Ito, S
Battiwalla, M
Koklanaris, EK
Superata, J
Childs, R
Barrett, J
AF Ito, Sawa
Battiwalla, Minoo
Koklanaris, Eleftheria K.
Superata, Jeanine
Childs, Richard
Barrett, John
TI Impact of Tyrosine Kinase Inhibitor (TKI) in Chronic Myeloid Leukemia
(CML) Relapsing After T Cell Depleted Allogeneic Stem Cell
Transplantation (SCT)
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Ito, Sawa; Battiwalla, Minoo; Koklanaris, Eleftheria K.; Superata, Jeanine; Childs, Richard; Barrett, John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1188
EP 1189
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104113
ER
PT J
AU Xu, HM
Menendez, S
Deblasio, TR
Aplan, P
Nimer, S
AF Xu, Haiming
Menendez, Silvia
Deblasio, Tony R.
Aplan, Peter
Nimer, Stephen
TI Loss of p53 Accelerates the Complications of Myelodysplastic Syndromes
(MDS) In the NUP98-HOXD13 Transgenic Mouse Model
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Xu, Haiming; Menendez, Silvia; Deblasio, Tony R.; Nimer, Stephen] Mem Sloan Kettering Canc Ctr, Mol Pharmacol & Chem Program, New York, NY 10021 USA.
[Aplan, Peter] NCI, Genet Branch, NIH, Bethesda, MD 20892 USA.
RI Aplan, Peter/K-9064-2016
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1209
EP 1210
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104155
ER
PT J
AU Vire, B
David, A
Wiestner, A
AF Vire, Berengere
David, Alexandre
Wiestner, Adrian
TI Fc mu R (TOSO/FAIM3) Is An O-Glycosylated Endocytic Receptor That
Shuttles IgM From the Cell Surface to the Lysosome and Whose Expression
Is Regulated by TLR Signaling
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Vire, Berengere; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[David, Alexandre] NIAID, NIH, Bethesda, MD 20892 USA.
RI David, Alexandre/B-2447-2013
OI David, Alexandre/0000-0003-3365-1339
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1218
EP 1219
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104179
ER
PT J
AU Kreitman, RJ
Wilson, WH
Zhou, H
Raffeld, M
Stetler-Stevenson, M
Arons, E
AF Kreitman, Robert J.
Wilson, Wyndham H.
Zhou, Hong
Raffeld, Mark
Stetler-Stevenson, Maryalice
Arons, Evgeny
TI Interim Results of Secondary Endpoints From a Randomized Trial of
Cladribine with Early Vs Delayed Rituximab for Treatment of Early Hairy
Cell Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Kreitman, Robert J.; Zhou, Hong; Arons, Evgeny] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Wilson, Wyndham H.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
[Raffeld, Mark; Stetler-Stevenson, Maryalice] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1232
EP 1232
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104207
ER
PT J
AU Brown, JR
Tesar, B
Werner, L
Mikler, E
Reynolds, H
Thompson, C
Fisher, DC
Takebe, N
Neuberg, D
Freedman, AS
AF Brown, Jennifer R.
Tesar, Bethany
Werner, Lillian
Mikler, Evgeny
Reynolds, Hazel
Thompson, Christina
Fisher, David C.
Takebe, Naoko
Neuberg, Donna
Freedman, Arnold S.
TI Obatoclax in Combination with Fludarabine and Rituximab (FR) Is
Well-Tolerated and Shows Promising Clinical Activity in Relapsed CLL/SLL
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Brown, Jennifer R.; Fisher, David C.; Freedman, Arnold S.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med, Boston, MA 02115 USA.
[Mikler, Evgeny; Reynolds, Hazel; Thompson, Christina] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Takebe, Naoko] NCI, Canc Therapy Evaluat Program NCI CTEP, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1236
EP 1236
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104216
ER
PT J
AU Tembhare, PR
Yuan, C
Korde, N
Maric, I
Calvo, K
Yancey, MA
Mulquin, M
Landgren, O
Stetler-Stevenson, M
AF Tembhare, Prashant Ramesh
Yuan, Constance
Korde, Neha
Maric, Irina
Calvo, Katherine
Yancey, Mary Ann
Mulquin, Marcia
Landgren, Ola
Stetler-Stevenson, Maryalice
TI CD81: A Novel, Specific and Highly Sensitive Marker in Flow Cytometric
Diagnosis of Plasma Cell Dyscrasia
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Tembhare, Prashant Ramesh; Yuan, Constance; Stetler-Stevenson, Maryalice] NCI, Flow Cytometry Unit, Pathol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Korde, Neha; Yancey, Mary Ann; Mulquin, Marcia] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Maric, Irina] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Calvo, Katherine] Dept Lab Med, Hematol Sect, Bethesda, MD USA.
[Landgren, Ola] NCI, Multiple Myeloma Sect, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1243
EP 1243
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104231
ER
PT J
AU Tan, E
Lindenberg, L
Korde, N
Berg, A
Mena, E
Turkbey, B
Aras, O
Steinberg, SM
Weiss, B
Minter, A
Yancey, MA
Mulquin, M
Choyke, P
Kurdziel, K
Landgren, O
AF Tan, Esther
Lindenberg, Liza
Korde, Neha
Berg, Alexandra
Mena, Esther
Turkbey, Bans
Aras, Omer
Steinberg, Seth M.
Weiss, Brendan
Minter, Alex
Yancey, Mary Ann
Mulquin, Marcia
Choyke, Peter
Kurdziel, Karen
Landgren, Ola
TI Novel Molecular Imaging Detects Evidence of Altered Bone Marrow Biology
in Myeloma Precursor Disease (MGUS and smoldering myeloma): A
Prospective Clinical Study
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Tan, Esther; Korde, Neha; Berg, Alexandra; Weiss, Brendan; Minter, Alex; Yancey, Mary Ann; Mulquin, Marcia; Landgren, Ola] NCI, Multiple Myeloma Sect, NIH, Bethesda, MD 20892 USA.
[Lindenberg, Liza; Mena, Esther; Turkbey, Bans; Aras, Omer; Choyke, Peter; Kurdziel, Karen] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 5
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1246
EP 1246
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104239
ER
PT J
AU Holkova, B
Badros, AZ
Geller, R
Voorhees, PM
Zingone, A
Korde, N
Lin, HY
Tombes, MB
Shrader, E
Sankala, H
Kmieciak, M
Roberts, JD
Sullivan, D
Landgren, O
Grant, S
AF Holkova, Beata
Badros, Ashraf Z.
Geller, Robert
Voorhees, Peter M.
Zingone, Adriana
Korde, Neha
Lin, Hui-Yi
Tombes, Mary Beth
Shrader, Ellen
Sankala, Heidi
Kmieciak, Maciej
Roberts, John D.
Sullivan, Daniel
Landgren, Ola
Grant, Steven
TI A Phase II Study of the MEK 1/2 Inhibitor AZD6244 (Selumetinib,
ARRY-142866) in Relapsed or Refractory Multiple Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Holkova, Beata; Tombes, Mary Beth; Shrader, Ellen; Sankala, Heidi; Kmieciak, Maciej; Roberts, John D.; Grant, Steven] Virginia Commonwealth Univ, Massey Canc Ctr, Richmond, VA USA.
[Badros, Ashraf Z.] Univ Maryland, Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
[Geller, Robert] Billings Clin, Billings, MT USA.
[Voorhees, Peter M.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Zingone, Adriana; Korde, Neha; Landgren, Ola] NCI, Multiple Myeloma Sect, NIH, Bethesda, MD 20892 USA.
[Lin, Hui-Yi; Sullivan, Daniel] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1264
EP 1264
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104282
ER
PT J
AU Korde, N
Trepel, J
Carlsten, M
Zingone, A
Costello, R
Yancey, MA
Mulquin, M
Maric, I
Calvo, K
Tembhare, PR
Yuan, C
Stetler-Stevenson, M
Lee, MJ
Alarcon, S
Carter, G
Childs, R
Landgren, O
AF Korde, Neha
Trepel, Jane
Carlsten, Mattias
Zingone, Adriana
Costello, Rene
Yancey, Mary Ann
Mulquin, Marcia
Maric, Irina
Calvo, Katherine
Tembhare, Prashant Ramesh
Yuan, Constance
Stetler-Stevenson, Maryalice
Lee, Min-Jung
Alarcon, Sylvia
Carter, George
Childs, Richard
Landgren, Ola
TI A Phase II Trial of IPH2101 (anti-KIR mAb) in Smoldering Multiple
Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Korde, Neha; Zingone, Adriana; Costello, Rene; Yancey, Mary Ann; Mulquin, Marcia; Landgren, Ola] NCI, Multiple Myeloma Sect, NIH, Bethesda, MD 20892 USA.
[Trepel, Jane; Lee, Min-Jung; Alarcon, Sylvia; Carter, George] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Childs, Richard] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Maric, Irina] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Calvo, Katherine] Dept Lab Med, Hematol Sect, Bethesda, MD USA.
[Tembhare, Prashant Ramesh; Yuan, Constance; Stetler-Stevenson, Maryalice] NCI, Flow Cytometry Unit, Pathol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1270
EP 1270
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104295
ER
PT J
AU Shand, JC
Capitini, CM
Qin, HY
Nasholm, N
Duncan, BB
Fry, TJ
AF Shand, Jessica C.
Capitini, Christian M.
Qin, Haiying
Nasholm, Nicole
Duncan, Brynn B.
Fry, Terry J.
TI Alloreactivity Directed Against the Widely Distributed HY Antigen
Impairs Antitumor Immunity and Results in T-Cell Dysfunction
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Capitini, Christian M.; Qin, Haiying; Fry, Terry J.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1279
EP 1279
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104315
ER
PT J
AU Weber, G
Gerdemann, U
Hensel, NF
Leen, AM
Bollard, CM
Barrett, AJ
AF Weber, Gerrit
Gerdemann, Ulrike
Hensel, Nancy F.
Leen, Ann M.
Bollard, Catherine M.
Barrett, A. John
TI Generation of Multi-Antigen Specific T Cells for Adoptive Immunotherapy
of Myeloid Leukemia and Identification of MHC Class I and II-Restricted
Peptides for WT1, Proteinase 3 and Human Neutrophil Elastase
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Weber, Gerrit; Hensel, Nancy F.; Barrett, A. John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Bollard, Catherine M.] Texas Childrens Hosp, Baylor Coll Med, Methodist Hosp, Ctr Cell & Gene Therapy, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1286
EP 1286
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104336
ER
PT J
AU Hanley, PJ
Melenhorst, JJ
Scheinberg, P
Demmler-Harrison, GJ
Lilleri, D
Gerna, G
Heslop, HE
Rooney, CM
Barrett, AJ
Shpall, EJ
Bollard, CM
AF Hanley, Patrick J.
Melenhorst, J. Joseph
Scheinberg, Phillip
Demmler-Harrison, Gail J.
Lilleri, Daniele
Gerna, Giuseppe
Heslop, Helen E.
Rooney, Cliona M.
Barrett, A. John
Shpall, Elizabeth J.
Bollard, Catherine M.
TI Naive T Cell-Derived CTL Recognize Atypical Epitopes of CMVpp65 with
Higher Avidity Than CMV-Seropositive Donor-Derived CTL a Basis for
Treatment of Post-Transplant Viral Infection by Adoptive Transfer of T
Cells From Virus-naive Donors
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Hanley, Patrick J.] Baylor Coll Med, Ctr Cell & Gene Therapy, Houston, TX 77030 USA.
[Scheinberg, Phillip] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Lilleri, Daniele] Inst Biomed Res, Bellinzona, Switzerland.
[Gerna, Giuseppe] Fdn IRCCS Policlin San, Serv Virol, Pavia, Italy.
[Heslop, Helen E.; Bollard, Catherine M.] Texas Childrens Hosp, Methodist Hosp, Baylor Coll Med, Ctr Cell & Gene Therapy, Houston, TX 77030 USA.
[Shpall, Elizabeth J.] Univ Texas MD Anderson Canc Ctr, Dept Stem Cell Transplantat & Cellular Theraphy, Houston, TX 77030 USA.
RI Scheinberg, Phillip/H-5251-2012; Lilleri, Daniele/K-7776-2016
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1293
EP 1293
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104353
ER
PT J
AU Tolar, J
Deeg, HJ
Arai, S
Horwitz, M
Antin, JH
McCarty, JM
Adams, RH
Eapen, M
Ewell, M
Leifer, E
Gersten, I
Carter, SL
Horowitz, MM
Confer, DL
Nakamura, R
Pulsipher, M
DiFronzo, NL
Anderlini, P
AF Tolar, Jakub
Deeg, H. Joachim
Arai, Sally
Horwitz, Mitchell
Antin, Joseph H.
McCarty, John M.
Adams, Roberta H.
Eapen, Mary
Ewell, Marian
Leifer, Eric
Gersten, Iris
Carter, Shelly L.
Horowitz, Mary M.
Confer, Dennis L.
Nakamura, Ryotaro
Pulsipher, Michael
DiFronzo, Nancy L.
Anderlini, Paolo
TI Fludarabine-Based Conditioning for Allogeneic Marrow Transplantation
From Unrelated Donors in Severe Aplastic Anemia (SAA): Serious and
Unexpected Adverse Events in Pre-Defined Cyclophosphamide (CY) Dose
Levels
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Tolar, Jakub] Univ Minnesota, Dept Pediat, Div Blood & Marrow Transplantat, Mason Canc Ctr, Minneapolis, MN 55455 USA.
[Deeg, H. Joachim] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Arai, Sally] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
[Horwitz, Mitchell] Duke Univ, Med Ctr, Durham, NC USA.
[Antin, Joseph H.] Brigham & Womens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
[McCarty, John M.] Virginia Commonwealth Univ, Med Coll Virginia, VCU Hlth Syst, Richmond, VA 23298 USA.
[Adams, Roberta H.] Mayo Clin Arizona, Div Hematol & Med Oncol, Scottsdale, AZ USA.
[Horowitz, Mary M.] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
[Ewell, Marian; Gersten, Iris; Carter, Shelly L.] EMMES Corp, Rockville, MD USA.
[DiFronzo, Nancy L.] NHLBI, Blood Div, Bethesda, MD 20892 USA.
[Confer, Dennis L.] Natl Marrow Donor Program, Minneapolis, MN USA.
[Nakamura, Ryotaro] City Hope Natl Med Ctr, Dept Hematol HCT, Duarte, CA USA.
[Pulsipher, Michael] Univ Utah, Med Ctr, Salt Lake City, UT USA.
[Anderlini, Paolo] Univ Texas MD Anderson Canc Ctr, Dept Stem Cell Transplantat & Cellular Therapy, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1296
EP 1296
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104360
ER
PT J
AU Roy, DC
Guerin, M
Boumedine, RS
Lachance, S
Cohen, S
Sauvageau, G
Kiss, T
Busque, L
Morin, J
Guertin, MC
Velardi, A
Rezvani, K
Mielke, S
Egeler, M
Barrett, AJ
Perreault, C
Roy, J
AF Roy, Denis-Claude
Guerin, Mireille
Boumedine, Radia Sidi
Lachance, Silvy
Cohen, Sandra
Sauvageau, Guy
Kiss, Thomas
Busque, Lambert
Morin, Jean
Guertin, Marie-Claude
Velardi, Andrea
Rezvani, Katayoun
Mielke, Stephan
Egeler, Maarten
Barrett, A. John
Perreault, Claude
Roy, Jean
TI Reduction in Incidence of Severe Infections by Transplantation of High
Doses of Haploidentical T Cells Selectively Depleted of Alloreactive
Units
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Roy, Denis-Claude] Univ Montreal, Dept Med, Montreal, PQ H3C 3J7, Canada.
[Guerin, Mireille; Boumedine, Radia Sidi; Lachance, Silvy; Cohen, Sandra; Sauvageau, Guy; Kiss, Thomas; Busque, Lambert; Morin, Jean; Perreault, Claude; Roy, Jean] Hop Maison Neuve Rosemont, Res Ctr, Montreal, PQ H1T 2M4, Canada.
[Guertin, Marie-Claude] Montreal Heart Inst Coordinating Ctr, Montreal, PQ, Canada.
[Velardi, Andrea] Univ Perugia, Div Hematol & Clin Immunol, I-06100 Perugia, Italy.
[Rezvani, Katayoun] Hammersmith Hosp, Blood & Marrow Transplant Program, London, England.
[Mielke, Stephan] Univ Wurzburg, Div Hematol Oncol, Wurzburg, Germany.
[Egeler, Maarten] Kiadis Pharma, Ped Imm Hem Onc BMT, Amsterdam, Netherlands.
[Barrett, A. John] NIH, Bethesda, MD 20892 USA.
NR 0
TC 2
Z9 2
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1301
EP 1301
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104371
ER
PT J
AU Shah, NN
Loeb, D
Khuu, H
Stroncek, D
Raffeld, M
Delbrook, C
Richards, K
Baird, K
Levine, J
Leitman, SF
Mackall, CL
Fry, TJ
Wayne, AS
AF Shah, Nirali N.
Loeb, David
Khuu, Hahn
Stroncek, David
Raffeld, Mark
Delbrook, Cindy
Richards, Kelly
Baird, Kristin
Levine, Jason
Leitman, Susan F.
Mackall, Crystal L.
Fry, Terry J.
Wayne, Alan S.
TI A Pilot Trial of WT1 Peptide-Loaded Allogeneic Dendritic Cell Vaccine
and Donor Lymphocyte Infusion for WT1-Expressing Hematologic
Malignancies and Post-Transplant Relapse
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Shah, Nirali N.; Delbrook, Cindy; Richards, Kelly; Baird, Kristin; Levine, Jason; Mackall, Crystal L.; Fry, Terry J.; Wayne, Alan S.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Loeb, David] Johns Hopkins Univ, Baltimore, MD USA.
[Stroncek, David; Leitman, Susan F.] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Raffeld, Mark] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1317
EP 1318
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104406
ER
PT J
AU Hale, GA
Grupp, SA
Kasow, KA
Bishop, MR
Bitan, M
Childs, R
Copelan, EA
Cairo, MS
Camitta, B
Chan, KW
Davies, SM
Diaz, MA
Doyle, JJ
Gale, RP
Gonzalez, VM
Horn, BN
Jodele, S
Kamani, NR
Lazarus, HM
Lewis, VA
Myers, KC
Pulsipher, MA
Qayed, M
Sanders, J
Shaw, PJ
Soni, S
Stadtmauer, EA
Stiff, P
Wall, DA
Arora, M
AF Hale, Gregory A.
Grupp, Stephan A.
Kasow, Kimberly A.
Bishop, Michael R.
Bitan, Menachem
Childs, Richard
Copelan, Edward A.
Cairo, Mitchell S.
Camitta, Bruce
Chan, Ka Wah
Davies, Stella M.
Diaz, Miguel A.
Doyle, John J.
Gale, Robert Peter
Gonzalez, Vicent M.
Horn, Biljana N.
Jodele, Sonata
Kamani, Naynesh R.
Lazarus, Hillard M.
Lewis, Victor A.
Myers, Kasiani C.
Pulsipher, Michael A.
Qayed, Muna
Sanders, Jean
Shaw, Peter J.
Soni, Sandeep
Stadtmauer, Edward A.
Stiff, Patrick
Wall, Donna A.
Arora, Mukta
TI Allogeneic Hematopoietic Cell Transplantation (HCT) for Neuroblastoma
(NB): The CIBMTR Experience
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Hale, Gregory A.] Univ S Florida, All Childrens Hosp, St Petersburg, FL 33701 USA.
[Grupp, Stephan A.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Kasow, Kimberly A.] Univ N Carolina, Chapel Hill, NC USA.
[Bishop, Michael R.] NCI, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA.
[Bitan, Menachem] Tel Aviv Univ, Tel Aviv Sourasky Med Ctr, IL-69978 Tel Aviv, Israel.
[Childs, Richard] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Copelan, Edward A.] Cleveland Clin, Taussig Canc Inst, Cleveland, OH 44106 USA.
[Cairo, Mitchell S.] New York Med Coll, Valhalla, NY 10595 USA.
[Camitta, Bruce] Med Coll Wisconsin, Pediat Hematol Oncol BMT, Wauwatosa, WI USA.
[Chan, Ka Wah] Texas Transplant Inst, San Antonio, TX USA.
[Davies, Stella M.; Myers, Kasiani C.] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH USA.
[Diaz, Miguel A.] Hosp Infantil Univ Nino Jesus, Div Hematopoiet Stem Cell Transplantat, Madrid, Spain.
[Diaz, Miguel A.] Hosp Infantil Univ Nino Jesus, Cell Therapy Unit, Madrid, Spain.
[Doyle, John J.] Univ Toronto, Hosp Sick Children, Dept Hem Onc BMT, Toronto, ON M5G 1X8, Canada.
[Gale, Robert Peter] Ctr Adv Studies Leukemia, Los Angeles, CA USA.
[Gonzalez, Vicent M.] Hosp Nino Jesus, Madrid, Spain.
[Horn, Biljana N.] UCSF Childrens Hosp, Blood & Marrow Transplant Program, San Francisco, CA USA.
[Jodele, Sonata] Cincinnati Childrens Med Ctr, Cincinnati, OH USA.
[Kamani, Naynesh R.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Lazarus, Hillard M.] Univ Hosp Case Med Ctr, Cleveland, OH USA.
[Lewis, Victor A.] Alberta Childrens Prov Gen Hosp, Calgary, AB, Canada.
[Pulsipher, Michael A.] Univ Utah, Salt Lake City, UT USA.
[Qayed, Muna] Emory Univ, Sch Med, Atlanta, GA USA.
[Sanders, Jean] Seattle Canc Alliance, Seattle, WA USA.
[Shaw, Peter J.] Childrens Hosp Westmead, Dept Oncol, Sydney, NSW, Australia.
[Soni, Sandeep] Nationwide Childrens Hosp, Dept Hematol Oncol & BMT, Columbus, OH USA.
[Stadtmauer, Edward A.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Stiff, Patrick] Loyola Univ, Maywood, IL 60153 USA.
[Wall, Donna A.] Univ Manitoba, Winnipeg, MB, Canada.
[Arora, Mukta] Univ Minnesota, Med Blood & Marrow Transplant Program, Minneapolis, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1326
EP 1326
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104425
ER
PT J
AU Nash, RA
Hutton, GJ
Racke, MK
Popat, UR
Devine, SM
Griffith, LM
Muraro, PA
Openshaw, H
Sayre, PH
Stuve, O
Arnold, DL
Wruck, L
Wundes, A
Kraft, GH
Bowen, JD
AF Nash, Richard A.
Hutton, George J.
Racke, Michael K.
Popat, Uday R.
Devine, Steven M.
Griffith, Linda M.
Muraro, Paolo A.
Openshaw, Harry
Sayre, Peter H.
Stuve, Olaf
Arnold, Douglas L.
Wruck, Lisa
Wundes, Annette
Kraft, George H.
Bowen, James D.
TI Treatment of Severe Relapsing-Remitting Multiple Sclerosis with
High-Dose Immunosuppressive Therapy and Autologous Hematopoietic Cell
Transplantation: Early Results of the HALT MS Clinical Trial (Immune
Tolerance Network: ITN033AI)
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Nash, Richard A.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
[Nash, Richard A.; Wundes, Annette; Kraft, George H.] Univ Washington, Seattle, WA 98195 USA.
[Hutton, George J.] Baylor Coll Med, Houston, TX 77030 USA.
[Devine, Steven M.] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
[Popat, Uday R.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Griffith, Linda M.] NIAID, Div Allergy Immunol & Transplantat, NIH, Bethesda, MD 20892 USA.
[Muraro, Paolo A.] Imperial Coll, Div Neurosci & Mental Hlth, London, England.
[Openshaw, Harry] City Hope Natl Med Ctr, Dept Neurol, Duarte, CA USA.
[Stuve, Olaf] Univ Texas SW Med Sch, Dallas, TX USA.
[Arnold, Douglas L.] McGill Univ, Montreal, PQ H3A 2T5, Canada.
[Wruck, Lisa] Rho Inc, Chapel Hill, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1326
EP 1327
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104426
ER
PT J
AU Battiwalla, M
Ellis, K
Pavletic, SZ
Akpek, G
Hematti, P
Klumpp, TR
Maziarz, RT
Savani, BN
Aljurf, M
Cairo, MS
Drobyski, WR
George, B
Hahn, T
Khera, N
Litzow, MR
Loren, AW
Saber, W
Arora, M
Urbano-Ispizua, A
Cutler, CS
Flowers, MED
Spellman, S
AF Battiwalla, Minoo
Ellis, Kristin
Pavletic, Steven Z.
Akpek, Gorgun
Hematti, Peiman
Klumpp, Thomas R.
Maziarz, Richard T.
Savani, Bipin N.
Aljurf, Mahmoud
Cairo, Mitchell S.
Drobyski, William R.
George, Biju
Hahn, Theresa
Khera, Nandita
Litzow, Mark R.
Loren, Alison W.
Saber, Wael
Arora, Mukta
Urbano-Ispizua, Alvaro
Cutler, Corey S.
Flowers, Mary E. D.
Spellman, Stephen
TI HLA DR15 Antigen Status Does Not Impact Graft-Versus-Host Disease or
Disease-Free Survival in HLA-Matched Sibling Transplantation for
Hematologic Malignancies
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Battiwalla, Minoo] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Ellis, Kristin; Saber, Wael] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
[Pavletic, Steven Z.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Akpek, Gorgun] Univ Maryland, Marlene & Stewart Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
[Hematti, Peiman] Univ Wisconsin, Sch Med & Publ Hlth, Clin Sci Ctr H4 534, Madison, WI USA.
[Maziarz, Richard T.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Savani, Bipin N.] Vanderbilt Univ, Med Ctr, Dept Med, Hematol & Stem Cell Transplantat Sect,Div Hematol, Nashville, TN USA.
[Aljurf, Mahmoud] King Faisal Specialist Hosp & Res Ctr, Ctr Oncol, Riyadh 11211, Saudi Arabia.
[Cairo, Mitchell S.] New York Med Coll, Valhalla, NY 10595 USA.
[George, Biju] Christian Med Coll & Hosp, Dept Haematol, Vellore, Tamil Nadu, India.
[Hahn, Theresa] Roswell Pk Canc Inst, Dept Med, Buffalo, NY 14263 USA.
[Khera, Nandita; Flowers, Mary E. D.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Litzow, Mark R.] Mayo Clin, Dept Internal Med, Div Hematol, Rochester, MN USA.
[Loren, Alison W.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Arora, Mukta] Univ Minnesota, Minneapolis, MN USA.
[Urbano-Ispizua, Alvaro] Hosp Clin Barcelona, Barcelona, Spain.
[Cutler, Corey S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Spellman, Stephen] Ctr Int Blood & Marrow Transplant Res, Minneapolis, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1337
EP 1337
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104445
ER
PT J
AU Ikawa, Y
Uchiyama, T
Jagadeesh, GJ
Candotti, F
AF Ikawa, Yasuhiro
Uchiyama, Toru
Jagadeesh, Guridevi Jayashree
Candotti, Fabio
TI Comparison of Immortalization Potential of Gamma-Retroviral, Lentiviral
and Foamy Virus Gene Transfer Vectors
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Ikawa, Yasuhiro; Uchiyama, Toru; Jagadeesh, Guridevi Jayashree; Candotti, Fabio] NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1347
EP 1347
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104466
ER
PT J
AU Uchida, N
Hargrove, PW
Lap, CJ
Phang, O
Bonifacino, AC
Krouse, AE
Metzger, ME
Nguyen, AD
Hsieh, MM
Wolfsberg, TG
Donahue, RE
Persons, DA
Tisdale, JF
AF Uchida, Naoya
Hargrove, Phillip W.
Lap, Coen J.
Phang, Oswald, Jr.
Bonifacino, Aylin C.
Krouse, Allen E.
Metzger, Mark E.
Anh-Dao Nguyen
Hsieh, Matthew M.
Wolfsberg, Tyra G.
Donahue, Robert E.
Persons, Derek A.
Tisdale, John F.
TI High Transgene Expression Rates After Extended Follow up Among Rhesus
Macaque Recipients of Autologous Hematopoietic Stem Cells Transduced
with a Modified HIV1-Based Lentiviral Vector
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Uchida, Naoya; Lap, Coen J.; Phang, Oswald, Jr.; Hsieh, Matthew M.; Tisdale, John F.] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
[Hargrove, Phillip W.; Persons, Derek A.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
[Bonifacino, Aylin C.; Krouse, Allen E.; Metzger, Mark E.; Donahue, Robert E.] NHLBI, Hematol Branch, NIH, Rockville, MD USA.
[Anh-Dao Nguyen; Wolfsberg, Tyra G.] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1347
EP 1348
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104468
ER
PT J
AU Zhu, JQ
Choi, WS
McCoy, JG
Negri, A
Zhu, JH
Naini, S
Li, JH
Shen, M
Huang, WW
Thomas, CJ
Filizola, M
Springer, T
Coller, BS
AF Zhu, Jieqing
Choi, Won-Seok
McCoy, Joshua G.
Negri, Ana
Zhu, Jianghai
Naini, Sarasija
Li, Jihong
Shen, Min
Huang, Wenwei
Thomas, Craig J.
Filizola, Marta
Springer, Timothy
Coller, Barry S.
TI Structure-Guided Design of A Novel High Affinity Integrin alpha IIb beta
3 Receptor Antagonist (RUC-2) That Displaces Mg2+ From the beta 3 MIDAS
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Zhu, Jieqing; Zhu, Jianghai; Springer, Timothy] Harvard Univ, Sch Med, Immune Dis Inst, Boston, MA USA.
[Zhu, Jieqing; Zhu, Jianghai; Springer, Timothy] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Choi, Won-Seok; Naini, Sarasija; Li, Jihong; Coller, Barry S.] Rockefeller Univ, Lab Blood & Vasc Biol, New York, NY 10021 USA.
[McCoy, Joshua G.; Shen, Min; Huang, Wenwei; Thomas, Craig J.] NIH Chem Genom Ctr, Bethesda, MD USA.
[Negri, Ana; Filizola, Marta] Mt Sinai Sch Med, New York, NY USA.
RI Zhu, Jianghai/B-7339-2014
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1401
EP 1402
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597104605
ER
PT J
AU Steiner, LA
Schulz, V
Maksimova, Y
Seidel, NE
Bodine, DM
Gallagher, PG
AF Steiner, Laurie A.
Schulz, Vincent
Maksimova, Yelena
Seidel, Nancy E.
Bodine, David M.
Gallagher, Patrick G.
TI Unbiased Identification of Functional Barrier Insulators in Primary
Human Erythroid Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Steiner, Laurie A.] Univ Rochester, Rochester, NY USA.
[Gallagher, Patrick G.] Yale Univ, Sch Med, New Haven, CT USA.
[Seidel, Nancy E.; Bodine, David M.] NHGRI, Genet & Mol Biol Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1451
EP 1451
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597105115
ER
PT J
AU Du, HY
Elghetany, MT
Alter, BP
Shimamura, A
AF Du, Hong-Yan
Elghetany, M. Tarek
Alter, Blanche P.
Shimamura, Akiko
TI P53 is Activated without RPL11 Upregulation in Diamond-Blackfan Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Du, Hong-Yan; Shimamura, Akiko] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Elghetany, M. Tarek] Baylor Coll Med, Houston, TX 77030 USA.
[Elghetany, M. Tarek] Texas Childrens Hosp, Houston, TX 77030 USA.
[Alter, Blanche P.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1467
EP 1468
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597105161
ER
PT J
AU Giri, N
Alter, BP
Peredo-Pinto, H
Elghetany, MT
Maric, I
Savage, SA
Arthur, DC
AF Giri, Neelam
Alter, Blanche P.
Peredo-Pinto, Helkha
Elghetany, M. Tarek
Maric, Irina
Savage, Sharon A.
Arthur, Diane C.
TI Significance of Bone Marrow Karyotype and Morphology in Patients with
Inherited Bone Marrow Failure Syndromes
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Giri, Neelam; Alter, Blanche P.; Savage, Sharon A.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Peredo-Pinto, Helkha] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Elghetany, M. Tarek] Baylor Coll Med, Houston, TX 77030 USA.
[Elghetany, M. Tarek] Texas Childrens Hosp, Houston, TX 77030 USA.
[Maric, Irina] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Arthur, Diane C.] NCI, NIH, Bethesda, MD 20892 USA.
RI Savage, Sharon/B-9747-2015
OI Savage, Sharon/0000-0001-6006-0740
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1467
EP 1467
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597105160
ER
PT J
AU Sandoval, S
Cho, M
Kraus, C
Cho, EC
Wolff, L
Sakamoto, KM
AF Sandoval, Salemiz
Cho, Michelle
Kraus, Christina
Cho, Er-Chieh
Wolff, Linda
Sakamoto, Kathleen M.
TI Sox4 and CREB Cooperate in Myeloid Transformation
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Sandoval, Salemiz; Cho, Michelle; Kraus, Christina; Cho, Er-Chieh; Sakamoto, Kathleen M.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Wolff, Linda] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1476
EP 1476
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597105181
ER
PT J
AU Weniger, MA
Liu, DL
Ni, T
Zhu, J
Wiestner, A
AF Weniger, Marc A.
Liu, Delong
Ni, Ting
Zhu, Jun
Wiestner, Adrian
TI Transcriptome-Wide Analysis of Polyadenylation Sites in Mantle Cell
Lymphoma Using Polyadenylation Signal Sequencing
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Weniger, Marc A.; Liu, Delong; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Ni, Ting; Zhu, Jun] NHLBI, DNA Sequencing & Computat Biol Core, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1484
EP 1485
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597105207
ER
PT J
AU Orgel, E
Sposto, R
Malvar, J
Seibel, NL
Ladas, EJ
Gaynon, P
Freyer, DR
AF Orgel, Etan
Sposto, Richard
Malvar, Jemily
Seibel, Nita L.
Ladas, Elena J.
Gaynon, Paul
Freyer, David R.
TI Extremes of Weight Are Associated with Increased Treatment-Related
Toxicity in High-Risk Acute Lymphoblastic Leukemia: A Report From the
Children's Oncology Group
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Orgel, Etan; Sposto, Richard; Malvar, Jemily; Gaynon, Paul; Freyer, David R.] Childrens Hosp Los Angeles, Childrens Ctr Canc & Blood Dis, Los Angeles, CA 90027 USA.
[Seibel, Nita L.] NCI, Bethesda, MD 20892 USA.
[Ladas, Elena J.] Columbia Univ, Med Ctr, Childrens Hosp New York, New York, NY USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1525
EP 1526
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597105303
ER
PT J
AU Thein, MS
Jemal, A
Baer, MR
Ershler, WB
Yates, JW
AF Thein, Mya S.
Jemal, Ahmedin
Baer, Maria R.
Ershler, William B.
Yates, Jerome W.
TI Improved Survival Rates Among Acute Myeloid Leukemia (AML) Patients 65
to 74 Years: Population-Based Estimates Over Three Decades
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Thein, Mya S.; Ershler, William B.; Yates, Jerome W.] Univ MD, NIA, Baltimore, MD USA.
[Jemal, Ahmedin] Amer Canc Soc, Atlanta, GA 30329 USA.
[Baer, Maria R.] Univ Maryland, Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1533
EP 1533
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597105320
ER
PT J
AU Pratz, KW
Kaufmann, SH
Litzow, MR
Ji, JP
Chen, A
Rudek, MA
Karp, JE
AF Pratz, Keith W.
Kaufmann, Scott H.
Litzow, Mark R.
Ji, Jiuping
Chen, Alice
Rudek, Michelle A.
Karp, Judith E.
TI Phase I Trial of the Oral Poly (ADP-ribose) Polymerase (PARP) Inhibitor
Veliparib (ABT-888, V) Combined Wtih Topoecan (T) and Carboplatin (C)
for Adults with Relapsed and Refractory Acute Leukemias
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Karp, Judith E.] Johns Hopkins, Sidney Kimmel Comprehens Canc Ctr, Div Hematol Malignancies, Dept Oncol, Baltimore, MD USA.
[Kaufmann, Scott H.] Mayo Clin, Dept Oncol, Rochester, MN USA.
[Ji, Jiuping] NCI, Invest Drug Branch, Bethesda, MD 20892 USA.
[Chen, Alice] NCI, IDB, CTEP, Rockville, MD USA.
[Rudek, Michelle A.] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1552
EP 1552
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597105363
ER
PT J
AU Roschewski, M
Weniger, MA
Liu, DL
Lindenberg, M
Pittaluga, S
Kurdziel, K
Dunleavy, K
Wilson, WH
Wiestner, A
AF Roschewski, Mark
Weniger, Marc A.
Liu, Delong
Lindenberg, Maria
Pittaluga, Stefania
Kurdziel, Karen
Dunleavy, Kieron
Wilson, Wyndham H.
Wiestner, Adrian
TI FDG-PET SUV Correlates with Expression of Genes Reflecting
Proliferation, Metabolism, and Oncogene Activity in Mantle Cell Lymphoma
(MCL)
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Roschewski, Mark] Walter Reed Army Med Ctr, Dept Hematol Oncol, Washington, DC 20307 USA.
[Liu, Delong; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Pittaluga, Stefania] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Wilson, Wyndham H.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1569
EP 1569
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597105398
ER
PT J
AU Waldmann, TA
Janik, J
Morris, JC
Conlon, K
O'Mahony, D
Pittaluga, S
Jaffe, ES
Brechbiel, M
Paik, CH
Chen, C
Whatley, M
Fleisher, TA
White, J
Stewart, D
Fioravanti, S
Goldman, C
Bryant, B
Decker, J
Junghans, R
Carrasquillo, JA
AF Waldmann, Thomas A.
Janik, John
Morris, John C.
Conlon, Kevin
O'Mahony, Deirdre
Pittaluga, Stefania
Jaffe, Elaine S.
Brechbiel, Martin
Paik, Chang H.
Chen, Clara
Whatley, Millie
Fleisher, Thomas A.
White, Jeffrey
Stewart, Donn
Fioravanti, Suzanne
Goldman, Carolyn
Bryant, Bonita
Decker, Jean
Junghans, Richard
Carrasquillo, Jorge A.
TI Yttrium-90 Radiolabeled Daclizumab, An Anti-CD25 Monoclonal Antibody,
Provides Effective Therapy for Refractory and Relapsed Hodgkin's
Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Waldmann, Thomas A.; Janik, John; Morris, John C.; O'Mahony, Deirdre; Goldman, Carolyn; Decker, Jean; Junghans, Richard] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
[Pittaluga, Stefania; Jaffe, Elaine S.] NCI, Ctr Canc Res, Pathol Lab, Bethesda, MD 20892 USA.
[Brechbiel, Martin] NCI, Ctr Canc Res, Radiat Oncol Branch, Bethesda, MD 20892 USA.
[Paik, Chang H.; Chen, Clara] NIH, Magnunson Clin Ctr, Bethesda, MD 20892 USA.
[Whatley, Millie] NIH, Positron Emiss Tomog Dept, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA.
[Fleisher, Thomas A.] NIH, Clin Ctr Lab, Magnuson Clin Ctr, Bethesda, MD 20892 USA.
[Carrasquillo, Jorge A.] NIH, Magnuson Clin Ctr, Dept Nucl Med, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1583
EP 1584
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597105434
ER
PT J
AU Buglio, D
Lemoine, M
Estrella, J
Neelapu, SS
Davis, RE
Doyle, L
Little, RF
Berry, D
Younes, A
AF Buglio, Daniela
Lemoine, Manuela
Estrella, Jaymie
Neelapu, Sattva S.
Davis, Richard Eric
Doyle, Laurence
Little, Richard F.
Berry, Donald
Younes, Anas
TI The Allosteric AKT Inhibitor MK-2206 Demonstrates Potent
Antiproliferative Activity in Lymphoma Cells and Synergizes with the
HDAC Inhibitor Vorinostat
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Neelapu, Sattva S.] UT MD Anderson Canc Ctr, Div Canc Med, Houston, TX USA.
[Neelapu, Sattva S.] UT MD Anderson Canc Ctr, Ctr Canc Immunol Res, Houston, TX USA.
[Davis, Richard Eric] Univ Texas MD Anderson Canc Ctr, Dept Lymphoma & Myeloma, Houston, TX 77030 USA.
[Little, Richard F.] NIH NCI, CTEP Clin Invest Branch, Bethesda, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1592
EP 1593
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597105457
ER
PT J
AU Raza, A
Greenberg, PL
Olnes, MJ
Silverman, LR
Wilhelm, F
AF Raza, Azra
Greenberg, Peter L.
Olnes, Matthew J.
Silverman, Lewis R.
Wilhelm, Francois
TI Final Phase I/II Results of Rigosertib (ON 01910.Na) Hematological
Effects in Patients with Myelodysplastic Syndrome and Correlation with
Overall Survival
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Raza, Azra] Columbia Univ, Med Ctr, New York, NY USA.
[Greenberg, Peter L.] Stanford Univ, Div Hematol, Stanford Canc Ctr, Stanford, CA 94305 USA.
[Olnes, Matthew J.] NHLBI, NIH, Hematol Branch, Bethesda, MD 20892 USA.
[Silverman, Lewis R.] Mt Sinai Sch Med, Div Hematol, New York, NY USA.
[Wilhelm, Francois] Onconova Therapeut Inc, Newtown, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1633
EP 1633
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597105550
ER
PT J
AU Cokic, VP
Markovic, D
Mitrovic, O
Vignjevic, S
Djikic, D
Beleslin-Cokic, BB
Perunicic, M
Ilic, B
Jovcic, G
Gotic, M
Noguchi, CT
Schechter, AN
AF Cokic, Vladan P.
Markovic, Dragana
Mitrovic, Olivera
Vignjevic, Sanja
Djikic, Dragoslava
Beleslin-Cokic, Bojana B.
Perunicic, Maja
Ilic, Bojana
Jovcic, Gordana
Gotic, Mirjana
Noguchi, Constance Tom
Schechter, Alan N.
TI Angiogenic Factors eNOS and VEGF Have Increased Expression in
Granulocytes of JAK2V617F Homozygous Forms of Polycythemia Vera
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Cokic, Vladan P.; Jovcic, Gordana] Univ Belgrade, Lab Expt Hematol, Inst Med Res, Belgrade, Serbia.
[Markovic, Dragana] Univ Belgrade, Inst Med Res, Immunol Lab, Belgrade, Serbia.
[Mitrovic, Olivera; Vignjevic, Sanja; Djikic, Dragoslava] Univ Belgrade, Inst Med Res, Lab Pathol & Cytol, Belgrade, Serbia.
[Beleslin-Cokic, Bojana B.; Ilic, Bojana] Univ Belgrade, Clin Ctr Serbia, Clin Endocrinol Diabet & Dis Metab, Belgrade, Serbia.
[Perunicic, Maja; Gotic, Mirjana] Univ Belgrade, Clin Ctr Serbia, Clin Hematol, Belgrade, Serbia.
[Noguchi, Constance Tom; Schechter, Alan N.] NIDDK, Mol Med Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1645
EP 1645
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597106017
ER
PT J
AU Hultcrantz, ML
Hinchliffe, SR
Kristinsson, SY
Andersson, TML
Eloranta, S
Derolf, AR
Samuelsson, J
Landgren, O
Dickman, PW
Lambert, P
Bjorkholm, M
AF Hultcrantz, Malin L.
Hinchliffe, Sally R.
Kristinsson, Sigurdur Y.
Andersson, Therese M-L
Eloranta, Sandra
Derolf, Asa Rangert
Samuelsson, Jan
Landgren, Ola
Dickman, Paul W.
Lambert, Paul
Bjorkholm, Magnus
TI Risk and Cause of Death in 9,563 Patients Diagnosed with
Myeloproliferative Neoplasms in Sweden Between 1973 and 2005
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Hultcrantz, Malin L.; Kristinsson, Sigurdur Y.; Derolf, Asa Rangert; Bjorkholm, Magnus] Karolinska Univ Hosp, Dept Med, Div Hematol, Stockholm, Sweden.
[Hinchliffe, Sally R.; Lambert, Paul] Univ Leicester, Dept Hlth Sci, Ctr Biostat & Genet Epidemiol, Leicester, Leics, England.
[Andersson, Therese M-L; Eloranta, Sandra; Dickman, Paul W.] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Samuelsson, Jan] Stockholm S Hosp, Dept Internal Med, Stockholm, Sweden.
[Landgren, Ola] NCI, Multiple Myeloma Sect, NIH, Bethesda, MD 20892 USA.
RI Dickman, Paul/B-4572-2013; Kristinsson, Sigurdur /M-2910-2015
OI Dickman, Paul/0000-0002-5788-3380; Kristinsson, Sigurdur
/0000-0002-4964-7476
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1648
EP 1649
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597106025
ER
PT J
AU Cokic, VP
Mossuz, P
Han, J
Diklic, M
Budec, M
Sefer, D
Lekovic, D
Antic, D
Brekovic, T
Mojsilovic, S
Puri, RK
Noguchi, CT
Schechter, AN
AF Cokic, Vladan P.
Mossuz, Pascal
Han, Jing
Diklic, Milos
Budec, Mirela
Sefer, Dijana
Lekovic, Danijela
Antic, Darko
Brekovic, Tijana
Mojsilovic, Sonja
Puri, Raj K.
Noguchi, Constance Tom
Schechter, Alan N.
TI Microarray and Proteomic Analysis of Myeloproliferative Neoplasms
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Cokic, Vladan P.; Diklic, Milos] Univ Belgrade, Inst Med Res, Lab Expt Hematol, Belgrade, Serbia.
[Mossuz, Pascal] CHU Grenoble, Inst Biol & Pathol, Lab Hematol Cellulaire & Mol, F-38043 Grenoble, France.
[Han, Jing; Puri, Raj K.] US FDA, Tumor Vaccines & Biotechnol Branch, Div Cellular & Gene Therapies, Ctr Biol Evaluat & Res, Bethesda, MD 20014 USA.
[Budec, Mirela; Brekovic, Tijana] Univ Belgrade, Inst Med Res, Lab Pathol & Cytol, Belgrade, Serbia.
[Sefer, Dijana; Lekovic, Danijela; Antic, Darko] Univ Belgrade, Clin Ctr Serbia, Clin Hematol, Belgrade, Serbia.
[Mojsilovic, Sonja] Univ Belgrade, Inst Med Res, Immunol Lab, Belgrade, Serbia.
[Noguchi, Constance Tom; Schechter, Alan N.] NIDDK, Mol Med Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1649
EP 1649
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597106026
ER
PT J
AU Slager, SL
Lanasa, MC
Allgood, SD
Achenbach, SJ
Norman, A
Vachon, CM
Goldin, L
Leis, JF
Kay, N
Weinberg, JB
Rabe, K
Call, TG
Cerhan, JR
Shanafelt, TD
Caporaso, NE
Marti, GE
Hanson, CA
AF Slager, Susan L.
Lanasa, Mark C.
Allgood, Sallie D.
Achenbach, Sara J.
Norman, Aaron
Vachon, Celine M.
Goldin, Lynn
Leis, Jose F.
Kay, Neil
Weinberg, J. Brice
Rabe, Kari
Call, Timothy G.
Cerhan, James R.
Shanafelt, Tait D.
Caporaso, Neil E.
Marti, Gerald E.
Hanson, Curtis A.
TI Prevalence of MBL Increases Over Time In Relatives of CLL Families
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Kay, Neil; Call, Timothy G.; Shanafelt, Tait D.] Mayo Clin, Div Hematol, Rochester, MN USA.
[Lanasa, Mark C.] Duke Univ, Med Ctr, Durham, NC USA.
[Allgood, Sallie D.; Weinberg, J. Brice] Durham VA Med Ctr, Durham, NC USA.
[Goldin, Lynn] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Leis, Jose F.] Mayo Clin Arizona, Div Hematol & Med Oncol, Scottsdale, AZ USA.
[Rabe, Kari; Cerhan, James R.] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
[Hanson, Curtis A.] Mayo Clin, Dept Lab Med, Div Hematopathol, Rochester, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1659
EP 1659
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597106051
ER
PT J
AU Kreitman, RJ
Stetler-Stevenson, M
Wilson, WH
Jeffrey, S
Roth, L
Arons, E
AF Kreitman, Robert J.
Stetler-Stevenson, Maryalice
Wilson, Wyndham H.
Jeffrey, Sapolsky
Roth, Laura
Arons, Evgeny
TI Bendamustine and Rituximab for the Treatment of Multiply Relapsed Hairy
Cell Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Kreitman, Robert J.; Jeffrey, Sapolsky; Roth, Laura; Arons, Evgeny] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Stetler-Stevenson, Maryalice] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Wilson, Wyndham H.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1672
EP 1672
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597106079
ER
PT J
AU Kristinsson, SY
Goldin, L
Turesson, I
Bjorkholm, M
Landgren, O
AF Kristinsson, Sigurdur Y.
Goldin, Lynn
Turesson, Ingemar
Bjorkholm, Magnus
Landgren, Ola
TI Family History of Venous Thromboembolism As a Risk Factor for Thrombosis
in Multiple Myeloma Patients: A Population-Based Study
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Kristinsson, Sigurdur Y.; Bjorkholm, Magnus] Karolinska Univ Hosp, Div Hematol, Dept Med, Stockholm, Sweden.
[Kristinsson, Sigurdur Y.] Karolinska Inst, Stockholm, Sweden.
[Goldin, Lynn] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Turesson, Ingemar] Skane Univ Hosp Malmo, Malmo, Sweden.
[Landgren, Ola] NCI, Multiple Myeloma Sect, NIH, Bethesda, MD 20892 USA.
RI Kristinsson, Sigurdur /M-2910-2015
OI Kristinsson, Sigurdur /0000-0002-4964-7476
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1706
EP 1706
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597106156
ER
PT J
AU Grkovic, L
Mitchell, SA
Baird, K
Steinberg, SM
Cowen, EW
Williams, KM
Datiles, MB
Aria, D
Bassim, C
Joe, G
Comis, L
Pulanic, D
Baruffaldi, J
Zhang, D
Sportes, C
Salit, RB
Fowler, DH
Hakim, FT
Gress, RE
Pavletic, SZ
AF Grkovic, Lana
Mitchell, Sandra A.
Baird, Kristin
Steinberg, Seth M.
Cowen, Edward W.
Williams, Kirsten M.
Datiles, Manuel B., III
Aria, Dean
Bassim, Carol
Joe, Galen
Comis, Leora
Pulanic, Drazen
Baruffaldi, Judy
Zhang, Dan
Sportes, Claude
Salit, Rachel B.
Fowler, Dan H.
Hakim, Frances T.
Gress, Ronald E.
Pavletic, Steven Z.
TI Assessing the Validity of the NIH Response Criteria for Chronic
Graft-Versus-Host Disease (cGVHD): Consensus Measures Correlate with
Clinical Outcomes
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Grkovic, Lana; Williams, Kirsten M.; Baruffaldi, Judy; Sportes, Claude; Salit, Rachel B.; Fowler, Dan H.; Hakim, Frances T.; Gress, Ronald E.; Pavletic, Steven Z.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Mitchell, Sandra A.] NCI, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Baird, Kristin] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Steinberg, Seth M.; Zhang, Dan] NCI, Biostat & Data Management Sect, NIH, Bethesda, MD 20892 USA.
[Cowen, Edward W.] NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA.
[Datiles, Manuel B., III] NEI, NIH, Bethesda, MD 20892 USA.
[Aria, Dean; Bassim, Carol] Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD USA.
[Joe, Galen; Comis, Leora] NIH, Dept Rehabil Med, Ctr Clin, Bethesda, MD 20892 USA.
[Pulanic, Drazen] Clin Hosp Ctr Zagreb, Dept Hematol, Zagreb, Croatia.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1739
EP 1740
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597106243
ER
PT J
AU Cruz, CRY
Micklethwaite, KP
Savoldo, B
Ku, S
Krance, RA
Diouf, O
Kamble, R
Barrett, AJ
Shpall, EJ
Heslop, HE
Rooney, CM
Brenner, MK
Bollard, CM
Dotti, G
AF Cruz, Conrad Russell Y.
Micklethwaite, Kenneth P.
Savoldo, Barbara
Ku, Stephanie
Krance, Robert A.
Diouf, Oumar
Kamble, Rammurti
Barrett, A. John
Shpall, Elizabeth J.
Heslop, Helen E.
Rooney, Cliona M.
Brenner, Malcolm K.
Bollard, Catherine M.
Dotti, Gianpietro
TI Infusion of CD19-Directed and Multivirus Specific Cytotoxic T
Lymphocytes After Allogeneic Hematopoietic Stem Cell Transplantation for
B Cell Malignancies
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Cruz, Conrad Russell Y.; Micklethwaite, Kenneth P.; Savoldo, Barbara; Ku, Stephanie; Krance, Robert A.; Diouf, Oumar; Kamble, Rammurti; Heslop, Helen E.; Rooney, Cliona M.; Brenner, Malcolm K.; Bollard, Catherine M.; Dotti, Gianpietro] Texas Childrens Hosp, Baylor Coll Med, Methodist Hosp, Ctr Cell & Gene Therapy, Houston, TX 77030 USA.
[Barrett, A. John] NHLBI, Stem Cell Allogene Transplant Sect, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Shpall, Elizabeth J.] Univ Texas MD Anderson Canc Ctr, Dept Stem Cell Transplantat & Cellular Therapy, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1743
EP 1744
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597106252
ER
PT J
AU Pophali, PA
Chawla, K
Koklanaris, EK
Antia, A
Chawla, S
Ito, S
Klotz, JK
Le, RQ
Barrett, AJ
Battiwalla, M
AF Pophali, Priyanka A.
Chawla, Kamna
Koklanaris, Eleftheria K.
Antia, Avan
Chawla, Simar
Ito, Sawa
Klotz, Jeffrey K.
Le, Robert Q.
Barrett, A. John
Battiwalla, Minoo
TI Chronic Graft Versus Host Disease (GVHD) Does Not Impact Cardiovascular
Risk Factors in Survivors of Allogeneic Hematopoietic Stem Cell
Transplantation (SCT) up to the Second Decade Post-Transplant
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Chawla, Kamna; Koklanaris, Eleftheria K.; Ito, Sawa; Le, Robert Q.; Battiwalla, Minoo] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RI Pophali, Priyanka/P-8646-2016
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1750
EP 1750
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597106267
ER
PT J
AU Green, RM
Tisdale, JF
Uchida, N
AF Green, Rashidah M.
Tisdale, John F.
Uchida, Naoya
TI Determining Limitations in Human CD34(+) Cell Transduction with An
HIV1-Based Lentiviral Vector
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Green, Rashidah M.; Tisdale, John F.; Uchida, Naoya] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1785
EP 1786
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597106338
ER
PT J
AU Rosenberg, PS
Anderson, WF
AF Rosenberg, Philip S.
Anderson, William F.
TI Incidence Rates of the Leukemias in the United States Are Significantly
Associated with Birth Cohort
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Rosenberg, Philip S.; Anderson, William F.] NCI, Biostat Branch, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1798
EP 1798
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597106369
ER
PT J
AU Leonard, WJ
AF Leonard, Warren J.
TI The Yin and Yang of Interleukin-21 in Allergy, Autoimmunity and Cancer
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Leonard, Warren J.] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1809
EP 1810
PG 2
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597106396
ER
PT J
AU Holland, SM
AF Holland, Steven M.
TI Novel Defects in Host Defense Evinced As Nontuberculous Mycobacterial
and Dimorphic Mold Infections: GATA2 Deficiency, STAT1 Mutations,
Anticytokine Autoantibodies
SO BLOOD
LA English
DT Meeting Abstract
CT 53rd Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis
CY DEC 10-13, 2011
CL San Diego, CA
SP Amer Soc Hematol (ASH)
C1 [Holland, Steven M.] NIAID, Lab Clin Infect Dis, Immunopathogenesis Sect, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2011
VL 118
IS 21
BP 1813
EP 1813
PG 1
WC Hematology
SC Hematology
GA 882XL
UT WOS:000299597106410
ER
PT J
AU Lee, JM
Han, JJ
Altwerger, G
Kohn, EC
AF Lee, Jung-min
Han, Jasmine J.
Altwerger, Gary
Kohn, Elise C.
TI Proteomics and biomarkers in clinical trials for drug development
SO JOURNAL OF PROTEOMICS
LA English
DT Review
DE Proteomics; Biomarkers; Clinical trial; Drug development; Cancer;
Targeted therapy
ID CELL LUNG-CANCER; EPIDERMAL-GROWTH-FACTOR; PHASE PROTEIN MICROARRAYS;
EPITHELIAL OVARIAN-CANCER; CHRONIC MYELOID-LEUKEMIA; SURROGATE
END-POINTS; ABL TYROSINE KINASE; BREAST-CANCER; FACTOR RECEPTOR;
ADJUVANT CHEMOTHERAPY
AB Proteomics allows characterization of protein structure and function, protein-protein interactions, and peptide modifications. It has given us insight into the perturbations of signaling pathways within tumor cells and has improved the discovery of new therapeutic targets and possible indicators of response to and duration of therapy. The discovery, verification, and validation of novel biomarkers are critical in streamlining clinical development of targeted compounds, and directing rational treatments for patients whose tumors are dependent upon select signaling pathways. Studies are now underway in many diseases to examine the immune or inflammatory proteome, vascular proteome, cancer or disease proteome, and other subsets of the specific pathology microenvironment. Successful assay verification and biological validation of such biomarkers will speed development of potential agents to targetable dominant pathways and lead to selection of individuals most likely to benefit. Reconsideration of analytical and clinical trials methods for acquisition, examination, and translation of proteomics data must occur before we march further into future of drug development. Published by Elsevier B.V.
C1 [Lee, Jung-min; Han, Jasmine J.; Altwerger, Gary; Kohn, Elise C.] NCI, Mol Signaling Sect, Med Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Lee, JM (reprint author), 10 Ctr Dr MSC1906,Bldg 10,Room 12N-226, Bethesda, MD 20892 USA.
EM leej6@mail.nih.gov
FU Center for Cancer Research, National Cancer Institute, USA
FX This work was supported by the Intramural Program of the Center for
Cancer Research, National Cancer Institute, USA.
NR 70
TC 31
Z9 32
U1 0
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1874-3919
J9 J PROTEOMICS
JI J. Proteomics
PD NOV 18
PY 2011
VL 74
IS 12
BP 2632
EP 2641
DI 10.1016/j.jprot.2011.04.023
PG 10
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 865IZ
UT WOS:000298305900006
PM 21570499
ER
PT J
AU Meng, ZJ
Veenstra, TD
AF Meng, Zhaojing
Veenstra, Timothy D.
TI Targeted mass spectrometry approaches for protein biomarker verification
SO JOURNAL OF PROTEOMICS
LA English
DT Review
DE Mass spectrometry; Biomarkers; MRM-MS; Quantitation; Verification
ID MULTIPLEXED ABSOLUTE QUANTIFICATION; PERFORMANCE LIQUID-CHROMATOGRAPHY;
CONCATENATED SIGNATURE PEPTIDES; PROSTATE-SPECIFIC ANTIGEN;
ISOTOPE-DILUTION; PLASMA-PROTEINS; PROTEOMICS; SERUM; QUANTITATION;
ASSAYS
AB The search for protein biomarkers has been a highly pursued topic in the proteomics community in the last decade. This relentless search is due to the constant need for validated biomarkers that could facilitate disease risk stratification, disease diagnosis, prognosis, monitoring as well as drug development, which ultimately would improve our quality of life. The recent development of proteomic technologies including the advancement of mass spectrometers with high sensitivity and speed has greatly advanced the discovery of potential biomarkers. One of the bottlenecks lies in the development of well-established verification assays to screen the biomarker candidates identified in the discovery stage. Recently, absolute quantitation using multiple-reaction monitoring mass spectrometry (MRM-MS) in combination with isotope-labeled internal standards has been extensively investigated as a tool for high-throughput protein biomarker verification. In this review, we describe and discuss recent developments and applications of MRM-MS methods for biomarker verification. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Meng, Zhaojing; Veenstra, Timothy D.] NCI, Lab Prote & Analyt Technol, Adv Technol Program, SAIC Frederick Inc, Frederick, MD 21702 USA.
RP Veenstra, TD (reprint author), NCI, Lab Prote & Analyt Technol, Adv Technol Program, SAIC Frederick Inc, Frederick, MD 21702 USA.
EM veenstra@ncifcrf.gov
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 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 United States
Government.
NR 40
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U1 4
U2 34
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1874-3919
J9 J PROTEOMICS
JI J. Proteomics
PD NOV 18
PY 2011
VL 74
IS 12
BP 2650
EP 2659
DI 10.1016/j.jprot.2011.04.011
PG 10
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 865IZ
UT WOS:000298305900008
PM 21540133
ER
PT J
AU Song, BJ
Abdelmegeed, MA
Yoo, SH
Kim, BJ
Jo, SA
Jo, I
Moon, KH
AF Song, Byoung-Joon
Abdelmegeed, Mohamed A.
Yoo, Seong-Ho
Kim, Bong-Jo
Jo, Sangmee A.
Jo, Inho
Moon, Kwan-Hoon
TI Post-translational modifications of mitochondrial aldehyde dehydrogenase
and biomedical implications
SO JOURNAL OF PROTEOMICS
LA English
DT Review
DE Aldehyde dehydrogenases; Post-translational modifications; Cellular
defense; Drug toxicity; Disease states; Translational research
ID ALCOHOLIC FATTY LIVER; GLUTATHIONE-S-TRANSFERASE; OXIDATIVE STRESS;
RAT-LIVER; NITRIC-OXIDE; HEPATOMA-CELLS; PROTEIN-KINASE;
HEPATOCELLULAR-CARCINOMA; ACETALDEHYDE METABOLISM; CARBON-TETRACHLORIDE
AB Aldehyde dehydrogenases (ALDHs) represent large family members of NAD(P)(+)-dependent dehydrogenases responsible for the irreversible metabolism of many endogenous and exogenous aldehydes to the corresponding acids. Among 19 ALDH isozymes, mitochondrial ALDH2 is a low K(m) enzyme responsible for the metabolism of acetaldehyde and lipid peroxides such as malondialdehyde and 4-hydroxynonenal, both of which are highly reactive and toxic. Consequently, inhibition of ALDH2 would lead to elevated levels of acetaldehyde and other reactive lipid peroxides following ethanol intake and/or exposure to toxic chemicals. In addition, many East Asian people with a dominant negative mutation in ALDH2 gene possess a decreased ALDH2 activity with increased risks for various types of cancer, myocardial infarct, alcoholic liver disease, and other pathological conditions. The aim of this review is to briefly describe the multiple post-translational modifications of mitochondrial ALDH2, as an example, after exposure to toxic chemicals or under different disease states and their pathophysiological roles in promoting alcohol/drug-mediated tissue damage. We also briefly mention exciting preclinical translational research opportunities to identify small molecule activators of ALDH2 and its isozymes as potentially therapeutic/preventive agents against various disease states where the expression or activity of ALDH enzymes is altered or inactivated. Published by Elsevier B.V.
C1 [Song, Byoung-Joon; Abdelmegeed, Mohamed A.; Yoo, Seong-Ho; Kim, Bong-Jo; Moon, Kwan-Hoon] NIAAA, Sect Mol Pharmacol & Toxicol, Lab Membrane Biochem & Biophys, Bethesda, MD 20892 USA.
[Yoo, Seong-Ho] Seoul Natl Univ, Coll Med, Dept Forens Med, Seoul, South Korea.
[Kim, Bong-Jo] KCDC, Korean Natl Inst Hlth, Div Struct & Funct Genom, Ctr Genom Sci, Osong, South Korea.
[Jo, Sangmee A.] Dankook Univ, Sch Pharm, Dept Pharm, Cheonan, South Korea.
[Jo, Inho] Ewha Womans Univ, Sch Med, Dept Mol Med, Seoul, South Korea.
RP Song, BJ (reprint author), NIAAA, Sect Mol Pharmacol & Toxicol, Lab Membrane Biochem & Biophys, Bethesda, MD 20892 USA.
EM bj.song@nih.gov
RI Yoo, Sung Ho/J-5549-2012
FU National Institute on Alcohol Abuse and Alcoholism; Center for
Biological Modulators in South Korea
FX This research was supported by the Intramural Program Fund at the
National Institute on Alcohol Abuse and Alcoholism. Part of this
research was also supported by a grant for the Chronic Liver Disease
Project (to B.J. Song) from the Center for Biological Modulators in
South Korea. We are grateful to Drs. Timothy D. Veenstra, Brian L. Hood,
Thomas P. Conrads, Li-Rong Yu, and Xiaoying Ye at the Laboratory of
Proteomics and Analytical Technologies, Advanced Technology Program,
SAIC-Frederick Inc, Frederick, Maryland for the mass-spectral analysis
to determine the identities of the oxidatively-modified proteins in our
experimental models. We also thank Dr. Klaus Gawrisch for his support.
The authors do not have any conflict of interest.
NR 136
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U1 2
U2 10
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1874-3919
J9 J PROTEOMICS
JI J. Proteomics
PD NOV 18
PY 2011
VL 74
IS 12
BP 2691
EP 2702
DI 10.1016/j.jprot.2011.05.013
PG 12
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 865IZ
UT WOS:000298305900011
PM 21609791
ER
PT J
AU Francischetti, IMB
Anderson, JM
Manoukis, N
Pham, VM
Ribeiro, JMC
AF Francischetti, Ivo M. B.
Anderson, Jennifer M.
Manoukis, Nicholas
Pham, Van M.
Ribeiro, Jose M. C.
TI An insight into the sialotranscriptome and proteome of the coarse
bontlegged tick, Hyalomma marginatum rufipes
SO JOURNAL OF PROTEOMICS
LA English
DT Article
DE Tick; Hematophagy; Salivary glands; Sialome
ID CONGO HEMORRHAGIC-FEVER; RHIPICEPHALUS-APPENDICULATUS TICKS;
PLATELET-AGGREGATION INHIBITORS; PANCREATIC TRYPSIN-INHIBITOR; MULTIPLE
SEQUENCE ALIGNMENT; SALIVARY-GLAND TRANSCRIPTS; HEPARIN-BINDING EXOSITE;
IXODES-SCAPULARIS; HAEMAPHYSALIS-LONGICORNIS; SOFT TICK
AB Ticks are mites specialized in acquiring blood from vertebrates as their sole source of food and are important disease vectors to humans and animals. Among the specializations required for this peculiar diet, ticks evolved a sophisticated salivary potion that can disarm their host's hemostasis, inflammation, and immune reactions. Previous transcriptome analysis of tick salivary proteins has revealed many new protein families indicative of fast evolution, possibly due to host immune pressure. The hard ticks (family Ixodidae) are further divided into two basal groups, of which the Metastriata have 11 genera. While salivary transcriptomes and proteomes have been described for some of these genera, no tick of the genus Hyalomma has been studied so far. The analysis of 2084 expressed sequence tags (EST) from a salivary gland cDNA library allowed an exploration of the proteome of this tick species by matching peptide ions derived from MS/MS experiments to this data set. We additionally compared these MS/MS derived peptide sequences against the proteins from the bovine host, finding many host proteins in the salivary glands of this tick. This annotated data set can assist the discovery of new targets for anti-tick vaccines as well as help to identify pharmacologically active proteins.
C1 [Francischetti, Ivo M. B.; Anderson, Jennifer M.; Manoukis, Nicholas; Pham, Van M.; Ribeiro, Jose M. C.] NIAID, NIH, Sect Vector Biol, Lab Malaria & Vector Res, Rockville, MD 20852 USA.
RP Ribeiro, JMC (reprint author), NIAID, NIH, Sect Vector Biol, Lab Malaria & Vector Res, Rockville, MD 20852 USA.
EM jribeiro@niaid.nih.gov
RI Ribeiro, Jose/J-7011-2015;
OI Manoukis, Nicholas/0000-0001-5062-7256; Ribeiro,
Jose/0000-0002-9107-0818
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health
FX This work was supported by the Intramural Research Program of the
Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health. We thank NIAID
intramural editor Brenda Rae Marshall for assistance. We are grateful
for the support of the Research Technologies Section, Rocky Mountain
Laboratories, National Institute of Allergy and Infectious Diseases,
National Institutes of Health, Hamilton, MT 59840, USA, for DNA
sequencing.
NR 82
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U1 5
U2 17
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1874-3919
J9 J PROTEOMICS
JI J. Proteomics
PD NOV 18
PY 2011
VL 74
IS 12
BP 2892
EP 2908
DI 10.1016/j.jprot.2011.07.015
PG 17
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 865IZ
UT WOS:000298305900028
PM 21851864
ER
PT J
AU Srinivasula, SM
Ashwell, JD
AF Srinivasula, Srinivasa M.
Ashwell, Jonathan D.
TI A20: More Than One Way to Skin a Cat
SO MOLECULAR CELL
LA English
DT Editorial Material
ID NF-KAPPA-B; ACTIVATION; UBIQUITINATION; NEMO; IKK
C1 [Srinivasula, Srinivasa M.; Ashwell, Jonathan D.] NCI, Lab Immune Cell Biol, NIH, Bethesda, MD 20892 USA.
RP Ashwell, JD (reprint author), NCI, Lab Immune Cell Biol, NIH, Bethesda, MD 20892 USA.
EM jda@pop.nci.nih.gov
NR 11
TC 4
Z9 4
U1 0
U2 1
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 18
PY 2011
VL 44
IS 4
BP 511
EP 512
DI 10.1016/j.molcel.2011.11.004
PG 2
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 852WI
UT WOS:000297387800002
PM 22099299
ER
PT J
AU Lee, WS
Kang, C
Drayna, D
Kornfeld, S
AF Lee, Wang-Sik
Kang, Changsoo
Drayna, Dennis
Kornfeld, Stuart
TI Analysis of Mannose 6-Phosphate Uncovering Enzyme Mutations Associated
with Persistent Stuttering
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ALPHA-N-ACETYLGLUCOSAMINIDASE
AB GlcNAc-1-phosphodiester-N-acetylglucosaminidase ("uncovering enzyme" (UCE); EC 3.1.4.45) is a Golgi enzyme that mediates the second step in the synthesis of the mannose 6-phosphate lysosomal targeting signal on acid hydrolases. Recently, three mutations (two missense and one deletion/frameshift) in the NAGPA gene that encodes UCE have been identified in individuals with persistent stuttering. We now demonstrate that each mutation leads to lower cellular UCE activity. The p.R328C mutation impairs folding in the endoplasmic reticulum, resulting in degradation of a significant portion by the proteasomal system. The p.H84Q mutation also impairs folding and, in addition, decreases the specific activity of the enzyme that folds sufficiently to traffic to the Golgi. The p.F513SfsX113 frameshift mutation adds 113 amino acids to the C terminus of the cytoplasmic tail of the protein, including a VWLL sequence that causes rapid degradation via the proteasomal system. These biochemical findings extend the genetic data implicating mutations
C1 [Lee, Wang-Sik; Kornfeld, Stuart] Washington Univ, Sch Med, Dept Internal Med, St Louis, MO 63110 USA.
[Kang, Changsoo; Drayna, Dennis] NIDCD, NIH, Bethesda, MD 20892 USA.
RP Kornfeld, S (reprint author), Washington Univ, Sch Med, Dept Internal Med, St Louis, MO 63110 USA.
EM skornfel@wustl.edu
FU National Institutes of Health (NIH), NIDCD [Grant Z01-00046-11]; NIH
[CA08759]
FX This work was supported, in whole or in part, by National Institutes of
Health (NIH), NIDCD, Grant Z01-00046-11 (to D. D.) and by NIH Grant
CA08759 (to S. K.).
NR 13
TC 11
Z9 12
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
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 18
PY 2011
VL 286
IS 46
BP 39786
EP 39793
DI 10.1074/jbc.M111.295899
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 846TI
UT WOS:000296925700012
PM 21956109
ER
PT J
AU Andrew, AJ
Kao, S
Strebel, K
AF Andrew, Amy J.
Kao, Sandra
Strebel, Klaus
TI C-terminal Hydrophobic Region in Human Bone Marrow Stromal Cell Antigen
2 (BST-2)/Tetherin Protein Functions as Second Transmembrane Motif
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; CLATHRIN-MEDIATED ENDOCYTOSIS; ANCHORED
MEMBRANE-PROTEINS; FORMING TOXIN AEROLYSIN; HIV-1 VPU;
GLYCOSYL-PHOSPHATIDYLINOSITOL; PARTICLE RELEASE; MODIFICATION SITES;
MOLECULAR-CLONING; PRION PROTEIN
AB BST-2/CD317/HM1.24/tetherin is a host factor that inhibits the release of HIV-1 and other enveloped viruses. Structurally, tetherin consists of an N-terminal transmembrane (TM) region, a central coiled coil motif, and a putative C-terminal glycosylphosphatidylinositol (GPI) anchor motif. A current working model proposes that BST-2 inhibits virus release by physically tethering viral particles to the cell surface via its TM motif and GPI anchor. Here we analyzed the functional importance of the C-terminal GPI anchor motif in BST-2. We replaced the GPI anchor motif in BST-2 with the TM regions of several surface markers and found that the TM motifs of CD40 and transferrin receptor, but not that of CD45, could functionally substitute for a GPI anchor in BST-2. Conversely, replacing the TM region of CD4 by the putative GPI anchor signal of human BST-2 resulted in proper membrane targeting and surface expression of the chimeric protein, indicating that the BST-2 GPI anchor signal can function as a bona fide TM region. In fact, attempts to demonstrate GPI anchor modification of human BST-2 by biochemical methods failed. Our results demonstrate that the putative C-terminal GPI anchor motif in human BST-2 fulfills the requirements of a bona fide TM motif, leading us to propose that human BST-2 may in fact contain a second TM segment rather than a GPI anchor.
C1 [Andrew, Amy J.; Kao, Sandra; Strebel, Klaus] NIAID, Viral Biochem Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
RP Strebel, K (reprint author), NIAID, Viral Biochem Sect, Mol Microbiol Lab, NIH, Bldg 4,Rm 310,4 Ctr Dr,MSC 0460, Bethesda, MD 20892 USA.
EM kstrebel@nih.gov
FU National Institutes of Health from NIAID [AI000669]
FX This work was supported, in whole or in part, by National Institutes of
Health Grant AI000669 from the Intramural Research Program of NIAID.
NR 51
TC 29
Z9 29
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
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 18
PY 2011
VL 286
IS 46
BP 39967
EP 39981
DI 10.1074/jbc.M111.287011
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 846TI
UT WOS:000296925700030
PM 21937450
ER
PT J
AU Nguyen, TT
Stevens, MV
Kohr, M
Steenbergen, C
Sack, MN
Murphy, E
AF Nguyen, Tiffany T.
Stevens, Mark V.
Kohr, Mark
Steenbergen, Charles
Sack, Michael N.
Murphy, Elizabeth
TI Cysteine 203 of Cyclophilin D Is Critical for Cyclophilin D Activation
of the Mitochondrial Permeability Transition Pore
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ADENINE-NUCLEOTIDE TRANSLOCASE; CYTOCHROME-C RELEASE; S-NITROSYLATION;
NITRIC-OXIDE; CELL-DEATH; ISCHEMIA-REPERFUSION; OXIDATIVE STRESS;
CARDIOPROTECTION; INJURY; RAT
AB The mitochondrial permeability transition pore (mPTP) opening plays a critical role in mediating cell death during ischemia/reperfusion (I/R) injury. Our previous studies have shown that cysteine 203 of cyclophilin D(CypD), a critical mPTP mediator, undergoes protein S-nitrosylation (SNO). To investigate the role of cysteine 203 in mPTP activation, we mutated cysteine 203 of CypD to a serine residue (C203S) and determined its effect on mPTP opening. Treatment of WT mouse embryonic fibroblasts (MEFs) with H2O2 resulted in an 50% loss of the mitochondrial calcein fluorescence, suggesting substantial activation of the mPTP. Consistent with the reported role of CypD in mPTP activation, CypD null (CypD(-/-)) MEFs exhibited significantly less mPTP opening. Addition of a nitric oxide donor, GSNO, to WT but not CypD(-/-) MEFs prior to H2O2 attenuated mPTP opening. To test whether Cys-203 is required for this protection, we infected CypD(-/-) MEFs with a C203S-CypD vector. Surprisingly, C203S-CypD reconstituted MEFs were resistant to mPTP opening in the presence or absence of GSNO, suggesting a crucial role for Cys-203 in mPTP activation. To determine whether mutation of C203S-CypD would alter mPTP in vivo, we injected a recombinant adenovirus encoding C203S-CypD or WT CypD into CypD(-/-) mice via tail vein. Mitochondria isolated from livers of CypD(-/-) mice or mice expressing C203S-CypD were resistant to Ca2+ -induced swelling as compared with WT CypD-reconstituted mice. Our results indicate that the Cys-203 residue of CypD is necessary for redox stress-induced activation of mPTP.
C1 [Nguyen, Tiffany T.; Kohr, Mark; Murphy, Elizabeth] NHLBI, Syst Biol Ctr, NIH, Bethesda, MD 20892 USA.
[Stevens, Mark V.; Sack, Michael N.] NHLBI, Ctr Mol Med, NIH, Bethesda, MD 20892 USA.
[Kohr, Mark; Steenbergen, Charles] Johns Hopkins Univ, Dept Pathol, Baltimore, MD 21257 USA.
RP Murphy, E (reprint author), NHLBI, Syst Biol Ctr, NIH, Bldg 10-8N202,10 Ctr Dr, Bethesda, MD 20892 USA.
EM murphy1@nhlbi.nih.gov
RI Ji, Haofeng/G-6206-2012;
OI Kohr, Mark/0000-0002-6034-5962
FU National Institutes of Health [Z01HL006059, Z01HL002066, 1F32HL096142,
5R01HL039752]
FX This work was supported, in whole or in part, by National Institutes of
Health Grants Z01HL006059 and Z01HL002066 (to T. T. N. and E. M.),
1F32HL096142 (to M. K.) and 5R01HL039752 (to C. S.).
NR 34
TC 76
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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
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 18
PY 2011
VL 286
IS 46
BP 40184
EP 40192
DI 10.1074/jbc.M111.243469
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 846TI
UT WOS:000296925700051
PM 21930693
ER
PT J
AU Ginther, DK
Schaffer, WT
Haak, LL
Kington, R
AF Ginther, Donna K.
Schaffer, Walter T.
Haak, Laurel L.
Kington, Raynard
TI Race Disparity in Grants - Response
SO SCIENCE
LA English
DT Letter
C1 [Ginther, Donna K.] Univ Kansas, Dept Econ, Lawrence, KS 66045 USA.
[Ginther, Donna K.] Univ Kansas, Ctr Sci Technol & Econ Policy, Inst Policy & Social Res, Lawrence, KS 66045 USA.
[Schaffer, Walter T.] NIH, Bethesda, MD 20892 USA.
[Haak, Laurel L.] Discovery Log Thomson Reuters, Rockville, MD 20850 USA.
[Kington, Raynard] Grinnell Coll, Grinnell, IA 50112 USA.
RP Ginther, DK (reprint author), Univ Kansas, Dept Econ, Lawrence, KS 66045 USA.
EM dginther@ku.edu
RI Schaffer, Walter/E-5982-2010; Ginther, Donna/F-7317-2016
OI Schaffer, Walter/0000-0002-2276-4656; Ginther, Donna/0000-0002-0881-7969
NR 6
TC 0
Z9 0
U1 1
U2 7
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD NOV 18
PY 2011
VL 334
IS 6058
BP 899
EP 901
PG 3
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 849CA
UT WOS:000297101800018
ER
PT J
AU Johnson, WD
Muzzio, M
Detrisac, CJ
Kapetanovic, IM
Kopelovich, L
McCormick, DL
AF Johnson, William D.
Muzzio, Miguel
Detrisac, Carol J.
Kapetanovic, Izet M.
Kopelovich, Levy
McCormick, David L.
TI Subchronic oral toxicity and metabolite profiling of the p53 stabilizing
agent, CP-31398, in rats and dogs
SO TOXICOLOGY
LA English
DT Article
DE CP-31398; N
'-[2-[2-(4-Methoxyphenyl)ethenyl]-4-quinazolinyl]-N,N-dimethyl-1,3-propa
nediamine; dihydrochloride; p53; Chemopreventive agent; Chemotherapeutic
agent
ID MUTANT P53; WILD-TYPE; APOPTOSIS; PROTEIN; PATHWAY; GROWTH; GENE;
SUPPRESSION; MUTATIONS; RESCUE
AB CP-31398 (N'-[2-[2-(4-methoxyphenyl)ethenyl]-4-quinazolinyl]-N,N-dimethyl-1,3-propanediamine dihydrochloride) is a styrylquinazoline that stabilizes the DNA binding conformation of p53, thereby maintaining the activity of p53 as a transcription factor and tumor suppressor. In consideration of the potential use of p53 stabilizers for cancer prevention and therapy, 28-day studies (with recovery) were performed to characterize the toxicity of CP-31398 in rats and dogs. In the rat study, groups of 15 CD rats/sex received daily gavage exposure to CP-31398 at 0, 40, 80, or 160 mg/kg/day (0, 240, 480, or 960 mg/m(2)/day). In the dog study, groups of five beagle dogs received daily gavage exposure to CP-31398 at 0, 10, 20, or 40 mg/kg/day (0, 200, 400, or 800 mg/m(2)/day). The high dose of CP-31398 induced mortality in both species: seven male rats and four female rats died as a result of hepatic infarcts, and two female dogs died as a result of hepatic necrosis without evidence of thrombosis. No deaths were seen in the mid- or low-dose groups in either species. In dogs, sporadic emesis was seen in the high dose and mid dose groups, and reductions in body weight gain were observed in all drug-exposed groups. CP-31398 induced mild anemia in both species; clinical pathology data also demonstrated hepatic toxicity, renal toxicity, inflammatory reactions, and coagulopathies in rats in the high dose and mid dose groups. Treatment-related microscopic changes in high dose and mid dose rats were identified in the liver, kidney, heart, bone marrow, lung, adrenals, spleen, thymus, skeletal muscle, and ovary; microscopic changes in the liver, heart, lung, and adrenals persisted through the recovery period. In dogs, microscopic changes were identified in the central nervous system, lung, and liver; changes in all tissues remained at the end of the recovery period. The liver is the primary site of limiting toxicity for CP-31398 in rats, and is also a key site of toxicity in dogs. The maximum tolerated dose (MTD) for subchronic oral administration of CP-31398 is 80 mg/kg/day (480 mg/m(2)/day) in rats and 20 mg/kg/day (400 mg/m(2)/day) in dogs. Although only modest and apparently reversible toxicities (microscopic changes in rats; reductions in body weight gain and alterations in red cell parameters in dogs) were seen in the low dose groups, no observed adverse effect levels (NOAELs) for CP-31398 could not be established for either species. The toxicity of CP-31398 suggests that this agent may not be suitable for use in cancer prevention. However, should in vivo antitumor efficacy be achievable at doses that do not induce limiting toxicity, CP-31398 may have utility as a cancer therapeutic. Modification of the primary sites of CP-31398 metabolism (N-demethylation of the alkyl side chain; hydroxylation and O-demethylation of the styryl benzene group) may result in the development of CP-31398 analogs with comparable pharmacologic activity and reduced toxicity. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
C1 [Johnson, William D.; Muzzio, Miguel; McCormick, David L.] IIT Res Inst, Life Sci Grp, Chicago, IL 60676 USA.
[Detrisac, Carol J.] Charles River Pathol Associates, Chicago, IL 60616 USA.
[Kapetanovic, Izet M.; Kopelovich, Levy] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
RP McCormick, DL (reprint author), IIT Res Inst, Life Sci Grp, 10 W 35th St, Chicago, IL 60676 USA.
EM wjohnson@iitri.org; mmuzzio@iitri.org; Carol.Detrisac@crl.com;
kapetani@mail.nih.gov; kopelovl@mail.nih.gov; dmccormick@iitri.org
FU National Cancer Institute, Division of Health and Human Services
[N01-CN-43304 (HHSN261200433004C)]
FX This work was supported by contract N01-CN-43304 (HHSN261200433004C)
from the National Cancer Institute, Division of Health and Human
Services.
NR 24
TC 5
Z9 5
U1 0
U2 3
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 18
PY 2011
VL 289
IS 2-3
BP 141
EP 150
DI 10.1016/j.tox.2011.08.009
PG 10
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 833OS
UT WOS:000295895400009
PM 21864638
ER
PT J
AU Kochenderfer, JN
Rosenberg, SA
AF Kochenderfer, James N.
Rosenberg, Steven A.
TI Chimeric Antigen Receptor-Modified T Cells in CLL
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
ID CANCER REGRESSION
C1 NCI, Bethesda, MD 20892 USA.
EM kochendj@mail.nih.gov
NR 4
TC 13
Z9 14
U1 0
U2 7
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 17
PY 2011
VL 365
IS 20
BP 1937
EP 1938
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 848HG
UT WOS:000297041900033
PM 22087695
ER
PT J
AU Buice, MA
Chow, CC
AF Buice, Michael A.
Chow, Carson C.
TI Effective stochastic behavior in dynamical systems with incomplete
information
SO PHYSICAL REVIEW E
LA English
DT Article
ID PATH INTEGRAL APPROACH; STATISTICAL MECHANICS; COUPLED OSCILLATORS;
BROWNIAN-MOTION
AB Complex systems are generally analytically intractable and difficult to simulate. We introduce a method for deriving an effective stochastic equation for a high-dimensional deterministic dynamical system for which some portion of the configuration is not precisely specified. We use a response function path integral to construct an equivalent distribution for the stochastic dynamics from the distribution of the incomplete information. We apply this method to the Kuramoto model of coupled oscillators to derive an effective stochastic equation for a single oscillator interacting with a bath of oscillators and also outline the procedure for other systems.
C1 [Buice, Michael A.; Chow, Carson C.] NIDDK, Lab Biol Modeling, NIH, Bethesda, MD 20892 USA.
[Buice, Michael A.] Univ Texas Austin, Ctr Learning & Memory, Austin, TX 78712 USA.
RP Buice, MA (reprint author), NIDDK, Lab Biol Modeling, NIH, Bethesda, MD 20892 USA.
RI Chow, Carson/A-7970-2009
FU NIH/NIDDK
FX This work was supported by the Intramural Program of the NIH/NIDDK.
NR 19
TC 7
Z9 7
U1 0
U2 1
PU AMER PHYSICAL SOC
PI COLLEGE PK
PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA
SN 1539-3755
J9 PHYS REV E
JI Phys. Rev. E
PD NOV 17
PY 2011
VL 84
IS 5
AR 051120
DI 10.1103/PhysRevE.84.051120
PN 1
PG 12
WC Physics, Fluids & Plasmas; Physics, Mathematical
SC Physics
GA 853KG
UT WOS:000297424200003
PM 22181382
ER
PT J
AU Uluisik, I
Kaya, A
Fomenko, DE
Karakaya, HC
Carlson, BA
Gladyshev, VN
Koc, A
AF Uluisik, Irem
Kaya, Alaattin
Fomenko, Dmitri E.
Karakaya, Huseyin C.
Carlson, Bradley A.
Gladyshev, Vadim N.
Koc, Ahmet
TI Boron Stress Activates the General Amino Acid Control Mechanism and
Inhibits Protein Synthesis
SO PLOS ONE
LA English
DT Article
ID TRANSFER-RNA-BINDING; QUORUM-SENSING SIGNAL; SACCHAROMYCES-CEREVISIAE;
TRANSCRIPTIONAL ACTIVATION; TRANSLATIONAL REGULATION; OXIDATIVE STRESS;
MAMMALIAN-CELLS; DIETARY BORON; YEAST; GCN4
AB Boron is an essential micronutrient for plants, and it is beneficial for animals. However, at high concentrations boron is toxic to cells although the mechanism of this toxicity is not known. Atr1 has recently been identified as a boron efflux pump whose expression is upregulated in response to boron treatment. Here, we found that the expression of ATR1 is associated with expression of genes involved in amino acid biosynthesis. These mechanisms are strictly controlled by the transcription factor Gcn4 in response to boron treatment. Further analyses have shown that boron impaired protein synthesis by promoting phosphorylation of eIF2 alpha in a Gcn2 kinase dependent manner. The uncharged tRNA binding domain (HisRS) of Gcn2 is necessary for the phosphorylation of eIF2 alpha in the presence of boron. We postulate that boron exerts its toxic effect through activation of the general amino acid control system and inhibition of protein synthesis. Since the general amino acid control pathway is conserved among eukaryotes, this mechanism of boron toxicity may be of general importance.
C1 [Uluisik, Irem; Kaya, Alaattin; Karakaya, Huseyin C.; Koc, Ahmet] Izmir Inst Technol, Dept Mol Biol & Genet, Izmir, Turkey.
[Kaya, Alaattin; Gladyshev, Vadim N.] Harvard Univ, Sch Med, Boston, MA USA.
[Kaya, Alaattin; Gladyshev, Vadim N.] Brigham & Womens Hosp, Dept Med, Div Genet, Boston, MA 02115 USA.
[Fomenko, Dmitri E.] Univ Nebraska, Dept Biochem, Lincoln, NE 68583 USA.
[Carlson, Bradley A.] NCI, Mol Biol Selenium Sect, Lab Canc Prevent, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Uluisik, I (reprint author), Izmir Inst Technol, Dept Mol Biol & Genet, Izmir, Turkey.
EM ahmetkoc@iyte.edu.tr
RI Gladyshev, Vadim/A-9894-2013;
OI Kaya, Alaattin/0000-0002-6132-5197
FU TUBITAK [104T213, 110T917]; TUBA-GEBIP
FX This work was supported by TUBITAK Grant No. 104T213, 110T917 and
TUBA-GEBIP grant to (A.Koc). The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
NR 43
TC 10
Z9 10
U1 2
U2 26
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 17
PY 2011
VL 6
IS 11
AR e27772
DI 10.1371/journal.pone.0027772
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 855HZ
UT WOS:000297555800033
PM 22114689
ER
PT J
AU Wuchty, S
AF Wuchty, Stefan
TI Computational Prediction of Host-Parasite Protein Interactions between
P. falciparum and H. sapiens
SO PLOS ONE
LA English
DT Article
ID HEAT-SHOCK PROTEINS; PLASMODIUM-FALCIPARUM; INTERACTION NETWORK; MALARIA
PARASITES; INTERACTION DATABASE; MASS-SPECTROMETRY; INFECTION; RESOURCE;
PATHWAY; VIRUS
AB To obtain candidates of interactions between proteins of the malaria parasite Plasmodium falciparum and the human host, homologous and conserved interactions were inferred from various sources of interaction data. Such candidate interactions were assessed by applying a machine learning approach and further filtered according to expression and molecular characteristics, enabling involved proteins to indeed interact. The analysis of predicted interactions indicated that parasite proteins predominantly target central proteins to take control of a human host cell. Furthermore, parasite proteins utilized their protein repertoire in a combinatorial manner, providing a broad connection to host cellular processes. In particular, several prominent pathways of signaling and regulation proteins were predicted to interact with parasite chaperones. Such a result suggests an important role of remodeling proteins in the interaction interface between the human host and the parasite. Identification of such molecular strategies that allow the parasite to take control of the host has the potential to deepen our understanding of the parasite specific remodeling processes of the host cell and illuminate new avenues of disease intervention.
C1 NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA.
RP Wuchty, S (reprint author), NIH, Natl Ctr Biotechnol Informat, Bldg 10, Bethesda, MD 20892 USA.
EM wuchtys@ncbi.nlm.nih.gov
RI Borrmann, Steffen/G-1838-2013
OI Borrmann, Steffen/0000-0001-9189-4393
FU National Institutes of Health/Department of Health and Human Service
(DHHS), (National Library of Medicine)
FX This work was supported by National Institutes of Health/Department of
Health and Human Service (DHHS) (Intramural Research Program of the
National Library of Medicine). The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
NR 47
TC 24
Z9 24
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 17
PY 2011
VL 6
IS 11
AR e26960
DI 10.1371/journal.pone.0026960
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 855HZ
UT WOS:000297555800012
PM 22114664
ER
PT J
AU Wuchty, S
Uzzi, B
AF Wuchty, Stefan
Uzzi, Brian
TI Human Communication Dynamics in Digital Footsteps: A Study of the
Agreement between Self-Reported Ties and Email Networks
SO PLOS ONE
LA English
DT Article
ID SOCIAL NETWORKS; WEAK TIES
AB Digital communication data has created opportunities to advance the knowledge of human dynamics in many areas, including national security, behavioral health, and consumerism. While digital data uniquely captures the totality of a person's communication, past research consistently shows that a subset of contacts makes up a person's "social network" of unique resource providers. To address this gap, we analyzed the correspondence between self-reported social network data and email communication data with the objective of identifying the dynamics in e-communication that correlate with a person's perception of a significant network tie. First, we examined the predictive utility of three popular methods to derive social network data from email data based on volume and reciprocity of bilateral email exchanges. Second, we observed differences in the response dynamics along self-reported ties, allowing us to introduce and test a new method that incorporates time-resolved exchange data. Using a range of robustness checks for measurement and misreporting errors in self-report and email data, we find that the methods have similar predictive utility. Although e-communication has lowered communication costs with large numbers of persons, and potentially extended our number of, and reach to contacts, our case results suggest that underlying behavioral patterns indicative of friendship or professional contacts continue to operate in a classical fashion in email interactions.
C1 [Wuchty, Stefan; Uzzi, Brian] Northwestern Univ, NW Inst Complex Syst & Network Sci NICO, Evanston, IL USA.
[Uzzi, Brian] Northwestern Univ, Kellogg Sch Management, Evanston, IL USA.
[Uzzi, Brian] Northwestern Univ, McCormick Sch Engn, Evanston, IL USA.
RP Wuchty, S (reprint author), NIH, Natl Ctr Biotechnol Informat, Bldg 10, Bethesda, MD 20892 USA.
EM uzzi@northwestern.edu
FU Army Research Laboratory [W911NF-09-2-0053]
FX Research was sponsored by the Army Research Laboratory and was
accomplished under Cooperative Agreement Number W911NF-09-2-0053. The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript. The views and
conclusions contained in this document are those of the authors and
should not be interpreted as representing the official policies, either
expressed or implied, of the Army Research Laboratory or the U.S.
Government. The U.S. Government is authorized to reproduce and
distribute reprints for Government purposes notwithstanding any
copyright notation here on.
NR 31
TC 15
Z9 16
U1 0
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 17
PY 2011
VL 6
IS 11
AR e26972
DI 10.1371/journal.pone.0026972
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 855HZ
UT WOS:000297555800013
PM 22114665
ER
PT J
AU Shurin, SB
AF Shurin, Susan B.
TI Funding mechanisms and program management at the National Heart, Lung,
and Blood Institute: confronting new challenges and exploring new
opportunities
SO BLOOD
LA English
DT Article
AB Over the past 8 years, the National Institutes of Health (NIH) budget appropriation has lost purchasing power, with erosion of the benefits of the doubling of the budget less than a decade ago. For the first time in 40 years, the NIH appropriation in fiscal year 2011 was 1% less than in the previous year. The National Heart, Lung, and Blood Institute (NHLBI) has been closely managing its funds to protect its core functions: support and conduct of research, and training of biomedical research scientists. Rigorous evaluations of funding mechanisms, management of clinical studies, set-aside programs and funding guidelines are designed to help the Institute, in consultation with its advisory council, to minimize the long-term impact of extreme resource limitations on the advance and conduct of science. This report describes some recent actions taken by the NHLBI to maximize support for investigator-initiated research, maintain a balanced portfolio, and provide as much support as possible for established and early-stage investigators. (Blood. 2011;118(20):5380-5382)
C1 NHLBI, NIH, Bethesda, MD 20892 USA.
RP Shurin, SB (reprint author), NHLBI, NIH, Bldg 31,Rm 5A48,31 Ctr Dr MSC 2486, Bethesda, MD 20892 USA.
EM shurinsb@nhlbi.nih.gov
NR 2
TC 2
Z9 2
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 17
PY 2011
VL 118
IS 20
BP 5380
EP 5382
DI 10.1182/blood-2011-08-372367
PG 3
WC Hematology
SC Hematology
GA 851JT
UT WOS:000297265400006
PM 21868577
ER
PT J
AU Furumoto, Y
Charles, N
Olivera, A
Leung, WH
Dillahunt, S
Sargent, JL
Tinsley, K
Odom, S
Scott, E
Wilson, TM
Ghoreschi, K
Kneilling, M
Chen, M
Lee, DM
Bolland, S
Rivera, J
AF Furumoto, Yasuko
Charles, Nicolas
Olivera, Ana
Leung, Wai Hang
Dillahunt, Sandra
Sargent, Jennifer L.
Tinsley, Kevin
Odom, Sandra
Scott, Eric
Wilson, Todd M.
Ghoreschi, Kamran
Kneilling, Manfred
Chen, Mei
Lee, David M.
Bolland, Silvia
Rivera, Juan
TI PTEN deficiency in mast cells causes a mastocytosis-like proliferative
disease that heightens allergic responses and vascular permeability
SO BLOOD
LA English
DT Article
ID SYSTEMIC MASTOCYTOSIS; SIGNALING PATHWAYS; MYELOPROLIFERATIVE DISEASE;
PHOSPHOINOSITIDE 3-KINASE; STAT5 EXPRESSION; KIT; SURVIVAL; IGE;
ACTIVATION; GROWTH
AB Kit regulation of mast cell proliferation and differentiation has been intimately linked to the activation of phosphatidylinositol 3-OH kinase (PI3K). The activating D816V mutation of Kit, seen in the majority of mastocytosis patients, causes a robust activation of PI3K signals. However, whether increased PI3K signaling in mast cells is a key element for their in vivo hyperplasia remains unknown. Here we report that dysregulation of PI3K signaling in mice by deletion of the phosphatase and tensin homolog (Pten) gene (which regulates the levels of the PI3K product, phosphatidylinositol 3,4,5-trisphosphate) caused mast cell hyperplasia and increased numbers in various organs. Selective deletion of Pten in the mast cell compartment revealed that the hyperplasia was intrinsic to the mast cell. Enhanced STAT5 phosphorylation and increased expression of survival factors, such as Bcl-XL, were observed in PTEN-deficient mast cells, and these were further enhanced by stem cell factor stimulation. Mice carrying PTEN-deficient mast cells also showed increased hypersensitivity as well as increased vascular permeability. Thus, Pten deletion in the mast cell compartment results in a mast cell proliferative phenotype in mice, demonstrating that dysregulation of PI3K signals is vital to the observed mast cell hyperplasia. (Blood. 2011;118(20):5466-5475)
C1 [Rivera, Juan] NIAMSD, Immunogenet Mol Lab, NIH, Bethesda, MD 20892 USA.
[Leung, Wai Hang; Bolland, Silvia] NIAID, Immunogenet Lab, NIH, Bethesda, MD 20892 USA.
[Wilson, Todd M.] NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA.
[Ghoreschi, Kamran] NIAMSD, Mol Immunol & Inflammat Branch, Bethesda, MD 20892 USA.
[Kneilling, Manfred] Univ Tubingen, Dept Dermatol, Tubingen, Germany.
[Chen, Mei; Lee, David M.] Brigham & Womens Hosp, Dept Med, Div Rheumatol, Boston, MA 02115 USA.
[Chen, Mei; Lee, David M.] Harvard Univ, Sch Med, Boston, MA USA.
RP Rivera, J (reprint author), NIAMSD, Immunogenet Mol Lab, NIH, Bldg 10,Rm 9C103, Bethesda, MD 20892 USA.
EM juan_rivera@nih.gov
RI Charles, Nicolas/P-5430-2014
OI Charles, Nicolas/0000-0002-5416-5834
FU Laboratory Animal Care and Use Section; Flow Cytometry Section; Light
Imaging Section of the Office of Science and Technology, National
Institute of Arthritis, Musculoskeletal and Skin Diseases; National
Institute of Arthritis, Musculoskeletal and Skin Diseases, National
Institutes of Health
FX The authors thank the Laboratory Animal Care and Use Section, the Flow
Cytometry Section, and the Light Imaging Section of the Office of
Science and Technology, National Institute of Arthritis, Musculoskeletal
and Skin Diseases for their support.; This work was supported by the
intramural program of National Institute of Arthritis, Musculoskeletal
and Skin Diseases, National Institutes of Health.
NR 49
TC 16
Z9 16
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 17
PY 2011
VL 118
IS 20
BP 5466
EP 5475
DI 10.1182/blood-2010-09-309955
PG 10
WC Hematology
SC Hematology
GA 851JT
UT WOS:000297265400017
PM 21926349
ER
PT J
AU Leich, E
Zamo, A
Horn, H
Haralambieva, E
Puppe, B
Gascoyne, RD
Chan, WC
Braziel, RM
Rimsza, LM
Weisenburger, DD
Delabie, J
Jaffe, ES
Fitzgibbon, J
Staudt, LM
Mueller-Hermelink, HK
Calaminici, M
Campo, E
Ott, G
Hernandez, L
Rosenwald, A
AF Leich, Ellen
Zamo, Alberto
Horn, Heike
Haralambieva, Eugenia
Puppe, Bernhard
Gascoyne, Randy D.
Chan, Wing-Chung
Braziel, Rita M.
Rimsza, Lisa M.
Weisenburger, Dennis D.
Delabie, Jan
Jaffe, Elaine S.
Fitzgibbon, Jude
Staudt, Louis M.
Mueller-Hermelink, Hans-Konrad
Calaminici, Mariarita
Campo, Elias
Ott, German
Hernandez, Luis
Rosenwald, Andreas
TI MicroRNA profiles of t(14;18)-negative follicular lymphoma support a
late germinal center B-cell phenotype
SO BLOOD
LA English
DT Article
ID HEPATOCELLULAR-CARCINOMA; EXPRESSION PROFILES; GENE-EXPRESSION; CANCER;
EZH2; APOPTOSIS; SURVIVAL; TCL1; DIFFERENTIATION; IDENTIFICATION
AB A total of 90% of follicular lymphomas (FLs) harbor the translocation t(14;18) leading to deregulated BCL2 expression. Conversely, 10% of FLs lack the t(14;18), and the majority of these FLs do not express BCL2. The molecular features of t(14;18)-negative FLs remain largely unknown. We performed microRNA expression analysis in 32 FL grades 1 to 3A, including 17 t(14;18)-positive FLs, 9 t(14;18)-negative FLs without BCL2 expression, and 6 t(14;18)-negative FLs with BCL2 expression. MicroRNA profiles were correlated with corresponding mRNA expression patterns, and potential targets were investigated by quantitative PCR and immunohistochemistry in an independent validation series of 83 FLs. Statistical analysis identified 17 microRNAs that were differentially expressed between t(14;18)-positive FLs and t(14;18)-negative FLs. The down-regulation of miR-16, miR-26a, miR-101, miR-29c, and miR138 in the t(14;18)-negative FL subset was associated with profound mRNA expression changes of potential target genes involving cell cycle control, apoptosis, and B-cell differentiation. miR-16 target CHEK1 showed increased expression in t(14;18)-negative FLs, whereas TCL1A expression was reduced, in line with a partial loss of the germinal center B-cell phenotype in this FL subset. In conclusion, t(14;18)-negative FL have distinct microRNA profiles that are associated with an increased proliferative capacity and a "late" germinal center B-cell phenotype. (Blood. 2011;118(20):5550-5558)
C1 [Leich, Ellen; Haralambieva, Eugenia; Puppe, Bernhard; Mueller-Hermelink, Hans-Konrad; Rosenwald, Andreas] Univ Wurzburg, Inst Pathol, D-97080 Wurzburg, Germany.
[Zamo, Alberto] Univ Verona, Dept Pathol, I-37100 Verona, Italy.
[Horn, Heike; Ott, German] Robert Bosch Krankenhaus, Dept Clin Pathol, Stuttgart, Germany.
[Horn, Heike; Ott, German] Dr Margarete Fischer Bosch Inst Clin Pharmacol, D-7000 Stuttgart, Germany.
[Gascoyne, Randy D.] Univ British Columbia, British Columbia Canc Agcy, Vancouver, BC V5Z 1M9, Canada.
[Chan, Wing-Chung; Weisenburger, Dennis D.] Univ Nebraska, Med Ctr, Dept Pathol & Microbiol, Omaha, NE USA.
[Braziel, Rita M.] Oregon Hlth & Sci Univ, SW Oncol Grp, Portland, OR 97201 USA.
[Rimsza, Lisa M.] Univ Arizona, Dept Pathol, Tucson, AZ USA.
[Delabie, Jan] Norwegian Radium Hosp, Div Pathol, Oslo, Norway.
[Jaffe, Elaine S.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Fitzgibbon, Jude; Calaminici, Mariarita] Canc Res United Kingdom, St Bartholomews Hosp, London, England.
[Staudt, Louis M.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
[Campo, Elias; Hernandez, Luis] Hosp Clin Barcelona, Dept Pathol, Barcelona, Spain.
RP Rosenwald, A (reprint author), Univ Wurzburg, Inst Pathol, Josef Schneider Str 2, D-97080 Wurzburg, Germany.
EM rosenwald@mail.uni-wuerzburg.de
OI Campo, elias/0000-0001-9850-9793; Delabie, Jan/0000-0001-5023-0689;
Jaffe, Elaine/0000-0003-4632-0301
FU National Cancer Institute [UO1-CA 114778]; Deutsche
Forschungsgemeinschaft; Associazione Italiana per la Ricerca sul Cancro;
Robert-Bosch-Stiftung; Deutsche Krebshilfe; Spanish Ministry of Health;
Direccio d'Estrategia i Coordinacio del Departament de Salut
(Generalitat de Catalunya)
FX This work was supported by the National Cancer Institute Strategic
Partnering to Evaluate Cancer (Signature grant UO1-CA 114778). E. L. was
supported by the Deutsche Forschungsgemeinschaft. A.Z. was supported by
the Associazione Italiana per la Ricerca sul Cancro. G.O. and H. H. were
supported by Robert-Bosch-Stiftung. G.O. and A. R. were supported by the
network project Molecular Mechanisms in Malignant Lymphomas (project M4)
of the Deutsche Krebshilfe. L. H. is a researcher from Institut
d'Investigacions Biomediques August Pi i Sunyer and was supported by the
Spanish Ministry of Health and "programa d'estabilitzacio
d'investigadors" of Direccio d'Estrategia i Coordinacio del Departament
de Salut (Generalitat de Catalunya).
NR 37
TC 28
Z9 28
U1 2
U2 11
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 17
PY 2011
VL 118
IS 20
BP 5550
EP 5558
DI 10.1182/blood-2011-06-361972
PG 9
WC Hematology
SC Hematology
GA 851JT
UT WOS:000297265400025
PM 21960592
ER
PT J
AU Kang, EC
Burdick, KE
Kim, JY
Duan, X
Guo, JU
Sailor, KA
Jung, DE
Ganesan, S
Choi, S
Pradhan, D
Lu, B
Avramopoulos, D
Christian, K
Malhotra, AK
Song, HJ
Ming, GL
AF Kang, Eunchai
Burdick, Katherine E.
Kim, Ju Young
Duan, Xin
Guo, Junjie U.
Sailor, Kurt A.
Jung, Dhong-Eun
Ganesan, Sundar
Choi, Sungkyung
Pradhan, Dennis
Lu, Bai
Avramopoulos, Dimitrios
Christian, Kimberly
Malhotra, Anil K.
Song, Hongjun
Ming, Guo-li
TI Interaction between FEZ1 and DISC1 in Regulation of Neuronal Development
and Risk for Schizophrenia
SO NEURON
LA English
DT Article
ID ADULT NEUROGENESIS; NEURITE OUTGROWTH; STEM-CELL; BRAIN; GENE; PROTEIN;
DISRUPTED-IN-SCHIZOPHRENIA-1; ASSOCIATION; BINDING; TRANSLOCATION
AB Disrupted-in Schizophrenia 1 (DISCI), a susceptibility gene for major mental disorders, encodes a scaffold protein that has a multifaceted impact on neuronal development. How DISC1 regulates different aspects of neuronal development is not well understood. Here, we show that Fasciculation and Elongation Protein Zeta-1 (FEZ1) interacts with DISC1 to synergistically regulate dendritic growth of newborn neurons in the adult mouse hippocampus, and that this pathway complements a parallel DISC1-NDEL1 interaction that regulates cell positioning and morphogenesis of newborn neurons. Furthermore, genetic association analysis of two independent cohorts of schizophrenia patients and healthy controls reveals an epistatic interaction between FEZ1 and DISCI, but not between FEZ1 and NDEL1, for risk of schizophrenia. Our findings support a model in which DISC1 regulates distinct aspects of neuronal development through its interaction with different intracellular partners and such epistasis may contribute to increased risk for schizophrenia.
C1 [Kang, Eunchai; Kim, Ju Young; Duan, Xin; Guo, Junjie U.; Sailor, Kurt A.; Jung, Dhong-Eun; Choi, Sungkyung; Pradhan, Dennis; Christian, Kimberly; Song, Hongjun; Ming, Guo-li] Johns Hopkins Univ, Sch Med, Inst Cell Engn, Baltimore, MD 21205 USA.
[Kang, Eunchai; Avramopoulos, Dimitrios; Song, Hongjun] Johns Hopkins Univ, Sch Med, Predoctoral Training Program Human Genet, Baltimore, MD 21205 USA.
[Kim, Ju Young; Christian, Kimberly; Song, Hongjun; Ming, Guo-li] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
[Duan, Xin; Guo, Junjie U.; Sailor, Kurt A.; Pradhan, Dennis; Song, Hongjun; Ming, Guo-li] Johns Hopkins Univ, Sch Med, Solomon H Snyder Dept Neurosci, Baltimore, MD 21205 USA.
[Avramopoulos, Dimitrios] Johns Hopkins Univ, Sch Med, Inst Med Genet, Baltimore, MD 21205 USA.
[Burdick, Katherine E.; Malhotra, Anil K.] N Shore Long Isl Jewish Hlth Syst, Zucker Hillside Hosp, Div Psychiat Res, Glen Oaks, NY 11004 USA.
[Burdick, Katherine E.; Malhotra, Anil K.] Albert Einstein Coll Med, Dept Psychiat, New York, NY 10461 USA.
[Burdick, Katherine E.; Malhotra, Anil K.] Feinstein Inst Med Res, Manhasset, NY 11004 USA.
[Ganesan, Sundar; Lu, Bai] NIMH, Genes Cognit & Psychosis Program, NIH, Bethesda, MD 20892 USA.
RP Ming, GL (reprint author), Johns Hopkins Univ, Sch Med, Inst Cell Engn, Baltimore, MD 21205 USA.
EM gming1@jhmi.edu
RI Burdick, Katherine/G-6124-2012; Avramopoulos, Dimitrios/J-4392-2012;
Ming, Guo-li/J-7880-2013;
OI Sailor, Kurt/0000-0002-9574-6838
FU NIH [NS048271, HD069184, NS047344, AG024984, MH084018, MH087874];
NARSAD; MSCRF; IMHRO; Johns Hopkins BSI; Donald and Barbara Zucker
Foundation; [MH79800]; [MH080173]; [MH077807]
FX We thank D. Weinberg, D. Valle, and members of Ming and Song
Laboratories for critical comments, L. Liu, Y. Cai, and H. Qasim for
technical support, and A. Sawa and A. Kamiya for anti-NDEL1 antibodies.
This work was supported by NIH (NS048271, HD069184), NARSAD, and MSCRF
to G.-I.M., by NIH (NS047344, AG024984, MH084018, MH087874), IMHRO and
Johns Hopkins BSI to H.S., by MH79800, MH080173 and the Donald and
Barbara Zucker Foundation to A.K.M., and by MH077807 to K.E.B., J.Y.K.,
and K.C. were partially supported by postdoctoral fellowships from
MSCRF.
NR 49
TC 37
Z9 39
U1 1
U2 10
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
J9 NEURON
JI Neuron
PD NOV 17
PY 2011
VL 72
IS 4
BP 559
EP 571
DI 10.1016/j.neuron.2011.09.032
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA 850FI
UT WOS:000297180100008
PM 22099459
ER
PT J
AU Janocha, AJ
Koch, CD
Tiso, M
Ponchia, A
Doctor, A
Gibbons, L
Gaston, B
Beall, CM
Erzurum, SC
AF Janocha, Allison J.
Koch, Carl D.
Tiso, Mauro
Ponchia, Andrea
Doctor, Allan
Gibbons, Lindsey
Gaston, Benjamin
Beall, Cynthia M.
Erzurum, Serpil C.
TI Nitric Oxide during Altitude Acclimatization
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
ID HEMOGLOBIN
C1 [Janocha, Allison J.; Koch, Carl D.; Erzurum, Serpil C.] Cleveland Clin, Cleveland, OH 44106 USA.
[Tiso, Mauro] NIH, Bethesda, MD 20892 USA.
[Ponchia, Andrea] Univ Padua, Padua, Italy.
[Doctor, Allan; Gibbons, Lindsey] Washington Univ, St Louis, MO USA.
[Gaston, Benjamin] Univ Virginia, Sch Med, Charlottesville, VA 22908 USA.
[Beall, Cynthia M.] Case Western Reserve Univ, Cleveland, OH 44106 USA.
RP Janocha, AJ (reprint author), Cleveland Clin, Cleveland, OH 44106 USA.
EM erzurus@ccf.org
OI Doctor, Allan/0000-0002-6096-6400; Beall, Cynthia/0000-0003-1462-8299
FU NCRR NIH HHS [1UL1RR024989, 1UL1RR024992, UL1 RR024989, UL1 RR024992];
NHLBI NIH HHS [HL59337, HL60917, P01 HL103453, R01 HL059337, R01
HL060917, R37 HL060917, R56 HL059337, T32 HL083823, T32HL083823, P01
HL101871]
NR 4
TC 24
Z9 27
U1 1
U2 6
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 17
PY 2011
VL 365
IS 20
BP 1942
EP 1944
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 848HG
UT WOS:000297041900029
PM 22087700
ER
PT J
AU Lorenzen, ED
Nogues-Bravo, D
Orlando, L
Weinstock, J
Binladen, J
Marske, KA
Ugan, A
Borregaard, MK
Gilbert, MTP
Nielsen, R
Ho, SYW
Goebel, T
Graf, KE
Byers, D
Stenderup, JT
Rasmussen, M
Campos, PF
Leonard, JA
Koepfli, KP
Froese, D
Zazula, G
Stafford, TW
Aaris-Sorensen, K
Batra, P
Haywood, AM
Singarayer, JS
Valdes, PJ
Boeskorov, G
Burns, JA
Davydov, SP
Haile, J
Jenkins, DL
Kosintsev, P
Kuznetsova, T
Lai, XL
Martin, LD
McDonald, HG
Mol, D
Meldgaard, M
Munch, K
Stephan, E
Sablin, M
Sommer, RS
Sipko, T
Scott, E
Suchard, MA
Tikhonov, A
Willerslev, R
Wayne, RK
Cooper, A
Hofreiter, M
Sher, A
Shapiro, B
Rahbek, C
Willerslev, E
AF Lorenzen, Eline D.
Nogues-Bravo, David
Orlando, Ludovic
Weinstock, Jaco
Binladen, Jonas
Marske, Katharine A.
Ugan, Andrew
Borregaard, Michael K.
Gilbert, M. Thomas P.
Nielsen, Rasmus
Ho, Simon Y. W.
Goebel, Ted
Graf, Kelly E.
Byers, David
Stenderup, Jesper T.
Rasmussen, Morten
Campos, Paula F.
Leonard, Jennifer A.
Koepfli, Klaus-Peter
Froese, Duane
Zazula, Grant
Stafford, Thomas W., Jr.
Aaris-Sorensen, Kim
Batra, Persaram
Haywood, Alan M.
Singarayer, Joy S.
Valdes, Paul J.
Boeskorov, Gennady
Burns, James A.
Davydov, Sergey P.
Haile, James
Jenkins, Dennis L.
Kosintsev, Pavel
Kuznetsova, Tatyana
Lai, Xulong
Martin, Larry D.
McDonald, H. Gregory
Mol, Dick
Meldgaard, Morten
Munch, Kasper
Stephan, Elisabeth
Sablin, Mikhail
Sommer, Robert S.
Sipko, Taras
Scott, Eric
Suchard, Marc A.
Tikhonov, Alexei
Willerslev, Rane
Wayne, Robert K.
Cooper, Alan
Hofreiter, Michael
Sher, Andrei
Shapiro, Beth
Rahbek, Carsten
Willerslev, Eske
TI Species-specific responses of Late Quaternary megafauna to climate and
humans
SO NATURE
LA English
DT Article
ID PLEISTOCENE EXTINCTIONS; POPULATION-DYNAMICS; WOOLLY MAMMOTHS; STEPPE;
INFERENCE; PATTERNS; AMERICA; DECLINE; RECORD; CANADA
AB Despite decades of research, the roles of climate and humans in driving the dramatic extinctions of large-bodied mammals during the Late Quaternary period remain contentious. Here we use ancient DNA, species distribution models and the human fossil record to elucidate how climate and humans shaped the demographic history of woolly rhinoceros, woolly mammoth, wild horse, reindeer, bison and musk ox. We show that climate has been a major driver of population change over the past 50,000 years. However, each species responds differently to the effects of climatic shifts, habitat redistribution and human encroachment. Although climate change alone can explain the extinction of some species, such as Eurasian musk ox and woolly rhinoceros, a combination of climatic and anthropogenic effects appears to be responsible for the extinction of others, including Eurasian steppe bison and wild horse. We find no genetic signature or any distinctive range dynamics distinguishing extinct from surviving species, emphasizing the challenges associated with predicting future responses of extant mammals to climate and human-mediated habitat change.
C1 [Lorenzen, Eline D.; Orlando, Ludovic; Weinstock, Jaco; Binladen, Jonas; Gilbert, M. Thomas P.; Stenderup, Jesper T.; Rasmussen, Morten; Campos, Paula F.; Stafford, Thomas W., Jr.; Aaris-Sorensen, Kim; Haile, James; Meldgaard, Morten; Willerslev, Eske] Univ Copenhagen, Ctr GeoGenet, DK-1350 Copenhagen K, Denmark.
[Nogues-Bravo, David; Marske, Katharine A.; Borregaard, Michael K.; Rahbek, Carsten] Univ Copenhagen, Dept Biol, Ctr Macroecol Evolut & Climate, DK-2100 Copenhagen O, Denmark.
[Ugan, Andrew] Smithsonian Trop Res Inst, Ancon, Punama, Panama.
[Nielsen, Rasmus] Univ Calif Berkeley, Dept Integrat Biol, Berkeley, CA 94720 USA.
[Nielsen, Rasmus] Univ Calif Berkeley, Dept Stat, Berkeley, CA 94720 USA.
[Nielsen, Rasmus] Univ Copenhagen, Dept Biol, DK-2200 Copenhagen, Denmark.
[Ho, Simon Y. W.] Univ Sydney, Sch Biol Sci, Sydney, NSW 2006, Australia.
[Goebel, Ted; Graf, Kelly E.] Texas A&M Univ, Dept Anthropol, Ctr Study Amer 1, College Stn, TX 77843 USA.
[Byers, David] Missouri State Univ, Dept Sociol & Anthropol, Springfield, MO 65807 USA.
[Leonard, Jennifer A.] Uppsala Univ, Dept Evolutionary Biol, S-75236 Uppsala, Sweden.
[Leonard, Jennifer A.] EBD CSIC, Conservat & Evolutionary Genet Grp, Seville 41092, Spain.
[Koepfli, Klaus-Peter; Wayne, Robert K.] Univ Calif Los Angeles, Dept Ecol & Evolutionary Biol, Los Angeles, CA 90095 USA.
[Koepfli, Klaus-Peter] NCI, Lab Genom Divers, Frederick, MD 21702 USA.
[Froese, Duane] Univ Alberta, Dept Earth & Atmospher Sci, Edmonton, AB T6G 2E3, Canada.
[Zazula, Grant] Govt Yukon, Dept Tourism & Culture, Yukon Palaeontol Program, Whitehorse, YT Y1A 2C6, Canada.
[Stafford, Thomas W., Jr.] Stafford Res Inc, Lafayette, CO 80026 USA.
[Batra, Persaram] Mt Holyoke Coll, Dept Earth & Environm, S Hadley, MA 01075 USA.
[Haywood, Alan M.] Univ Leeds, Sch Earth & Environm, Leeds LS2 9JT, W Yorkshire, England.
[Singarayer, Joy S.; Valdes, Paul J.] Univ Bristol, Sch Geog Sci, Bristol BS8 1SS, Avon, England.
[Boeskorov, Gennady] Russian Acad Sci, Siberian Branch, Diamond & Precious Met Geol Inst, Yakutsk 677891, Russia.
[Burns, James A.] Royal Alberta Museum, Edmonton, AB T5N 0M6, Canada.
[Burns, James A.] Manitoba Museum, Winnipeg, MB R3B 0N2, Canada.
[Davydov, Sergey P.] Russian Acad Sci, Far E Branch, Pacific Inst Geog, NE Sci Stn, Chersky 678830, Russia.
[Jenkins, Dennis L.] Univ Oregon, Museum Nat & Cultural Hist, Eugene, OR 97403 USA.
[Kosintsev, Pavel] Russian Acad Sci, Ural Branch, Inst Plant & Anim Ecol, Ekaterinburg 620144, Russia.
[Kuznetsova, Tatyana] Moscow MV Lomonosov State Univ, Moscow 119899, Russia.
[Lai, Xulong] China Univ Geosci, State Key Lab Biogeol & Environm Geol, Wuhan 430074, Hubei, Peoples R China.
[Martin, Larry D.] Univ Kansas, Museum Nat Hist, Lawrence, KS 66045 USA.
[McDonald, H. Gregory] Natl Pk Serv, Pk Museum Management Program, Ft Collins, CO 80525 USA.
[Mol, Dick] Nat Hist Museum, Rotterdam, Netherlands.
[Munch, Kasper] Aarhus Univ, BiRC, DK-8000 Aarhus C, Denmark.
[Stephan, Elisabeth] Landesamt Denkmalpflege, Regierungsprasidium Stuttgart, D-78467 Constance, Germany.
[Sablin, Mikhail; Tikhonov, Alexei] Russian Acad Sci, Inst Zool, St Petersburg 199034, Russia.
[Sommer, Robert S.] Univ Kiel, Inst Nat & Resource Conservat, Dept Landscape Ecol, D-24098 Kiel, Germany.
[Sipko, Taras; Sher, Andrei] Russian Acad Sci, Inst Ecol & Evolut, Moscow 119071, Russia.
[Scott, Eric] San Bernardino Cty Museum, Div Geol Sci, Redlands, CA 92374 USA.
[Suchard, Marc A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Biomath Genet, Los Angeles, CA 90095 USA.
[Suchard, Marc A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Human Genet, Los Angeles, CA 90095 USA.
[Suchard, Marc A.] Univ Calif Los Angeles, Sch Publ Hlth, Dept Biostat, Los Angeles, CA 90095 USA.
[Willerslev, Rane] Univ Oslo, Museum Cultural Hist, N-0130 Oslo, Norway.
[Cooper, Alan] Univ Adelaide, Australian Ctr Ancient DNA, Adelaide, SA 5005, Australia.
[Hofreiter, Michael] Univ York, Dept Biol, Area 2, York YO10 5DD, N Yorkshire, England.
[Shapiro, Beth] Penn State Univ, Dept Biol, University Pk, PA 16802 USA.
[Ugan, Andrew] Univ Utah, Dept Anthropol, Salt Lake City, UT 84112 USA.
[Ugan, Andrew] Museo Hist Nat San Rafael, Mendoza, Argentina.
RP Willerslev, E (reprint author), Univ Copenhagen, Ctr GeoGenet, Oster Voldgade 5-7, DK-1350 Copenhagen K, Denmark.
EM ewillerslev@snm.ku.dk
RI CSIC, EBD Donana/C-4157-2011; Borregaard, Michael/B-8442-2008; Leonard,
Jennifer/A-7894-2010; publist, CMEC/C-3010-2012; Hofreiter,
Michael/A-3996-2017; publicationpage, cmec/B-4405-2017; Munch,
Kasper/A-1434-2010; Gilbert, Marcus/A-8936-2013; Ho, Simon/A-8417-2008;
Campos, Paula/B-1634-2010; Koroleva, Olga/C-1306-2012; Cooper,
Alan/E-8171-2012; Lorenzen, Eline/D-1442-2012; Orlando,
Ludovic/A-8932-2013; Nielsen, Rasmus/D-4405-2009; Valdes,
Paul/C-4129-2013; Rahbek, Carsten/D-9372-2013; Rahbek,
Carsten/L-1129-2013; Marske, Katharine/J-5962-2014
OI Shapiro, Beth/0000-0002-2733-7776; CSIC, EBD Donana/0000-0003-4318-6602;
Borregaard, Michael/0000-0002-8146-8435; Leonard,
Jennifer/0000-0003-0291-7819; Hofreiter, Michael/0000-0003-0441-4705;
Sablin, Mikhail/0000-0002-2773-7454; Munch, Kasper/0000-0003-2880-6252;
Gilbert, Marcus/0000-0002-5805-7195; Ho, Simon/0000-0002-0361-2307;
Campos, Paula/0000-0003-1285-4671; Cooper, Alan/0000-0002-7738-7851;
Lorenzen, Eline/0000-0002-6353-2819; Orlando,
Ludovic/0000-0003-3936-1850; Nielsen, Rasmus/0000-0003-0513-6591;
Marske, Katharine/0000-0002-9837-9367
FU Leverhulme Trust [F/757/A]; McDonald Grants and Awards Fund; NSF
[ARC-0909456]; Danish National Research Foundation; Lundbeck Foundation;
Danish Council for Independent Research; US National Science Foundation
FX This paper is in memory of our friend and colleague Andrei Sher, who was
a contributor to this study. Dr Sher died unexpectedly, but his major
contributions to the field of Quaternary science will be remembered and
appreciated for many years. We are grateful to A. Lister and T. Stuart
for guidance and discussions. We thank T. B. Brandt, B. Hockett and A.
Telka for laboratory help and samples, and L. M. R. Thrane for his work
on the megafauna locality database. Data taken from the Stage 3 project
were partly funded by grant F/757/A from the Leverhulme Trust, and a
grant from the McDonald Grants and Awards Fund. B. S. was supported by
NSF ARC-0909456. We acknowledge the Danish National Research Foundation,
the Lundbeck Foundation, the Danish Council for Independent Research and
the US National Science Foundation for financial support.
NR 42
TC 217
Z9 220
U1 51
U2 398
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 17
PY 2011
VL 479
IS 7373
BP 359
EP U195
DI 10.1038/nature10574
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 848OA
UT WOS:000297059700037
PM 22048313
ER
PT J
AU Vivian, JP
Duncan, RC
Berry, R
O'Connor, GM
Reid, HH
Beddoe, T
Gras, S
Saunders, PM
Olshina, MA
Widjaja, JML
Harpur, CM
Lin, J
Maloveste, SM
Price, DA
Lafont, BAP
McVicar, DW
Clements, CS
Brooks, AG
Rossjohn, J
AF Vivian, Julian P.
Duncan, Renee C.
Berry, Richard
O'Connor, Geraldine M.
Reid, Hugh H.
Beddoe, Travis
Gras, Stephanie
Saunders, Philippa M.
Olshina, Maya A.
Widjaja, Jacqueline M. L.
Harpur, Christopher M.
Lin, Jie
Maloveste, Sebastien M.
Price, David A.
Lafont, Bernard A. P.
McVicar, Daniel W.
Clements, Craig S.
Brooks, Andrew G.
Rossjohn, Jamie
TI Killer cell immunoglobulin-like receptor 3DL1-mediated recognition of
human leukocyte antigen B
SO NATURE
LA English
DT Article
ID COMPLEX CLASS-I; HLA-B; CRYSTAL-STRUCTURE; PEPTIDE; ACTIVATION;
MOLECULES; KIR3DL1; POLYMORPHISMS; PROGRESSION; SELECTION
AB Members of the killer cell immunoglobulin-like receptor (KIR) family, a large group of polymorphic receptors expressed on natural killer (NK) cells, recognize particular peptide-laden human leukocyte antigen (pHLA) class I molecules and have a pivotal role in innate immune responses(1). Allelic variation and extensive polymorphism within the three-domain KIR family (KIR3D, domains D0-D1-D2) affects pHLA binding specificity and is linked to the control of viral replication and the treatment outcome of certain haematological malignancies(1-3). Here we describe the structure of a human KIR3DL1 receptor bound to HLA-B*5701 complexed with a self-peptide. KIR3DL1 clamped around the carboxy-terminal end of the HLA-B*5701 antigen-binding cleft, resulting in two discontinuous footprints on the pHLA. First, the D0 domain, a distinguishing feature of the KIR3D family, extended towards beta 2-microglobulin and abutted a region of the HLA molecule with limited polymorphism, thereby acting as an 'innate HLA sensor' domain. Second, whereas the D2-HLAB*5701 interface exhibited a high degree of complementarity, the D1-pHLA-B*5701 contacts were suboptimal and accommodated a degree of sequence variation both within the peptide and the polymorphic region of the HLA molecule. Although the two-domain KIR (KIR2D) and KIR3DL1 docked similarly onto HLA-C(4,5) and HLA-B respectively, the corresponding D1-mediated interactions differed markedly, thereby providing insight into the specificity of KIR3DL1 for discrete HLA-A and HLA-B allotypes. Collectively, in association with extensive mutagenesis studies at the KIR3DL1-pHLA-B*5701 interface, we provide a framework for understanding the intricate interplay between peptide variability, KIR3D and HLA polymorphism in determining the specificity requirements of this essential innate interaction that is conserved across primate species.
C1 [Saunders, Philippa M.; Widjaja, Jacqueline M. L.; Harpur, Christopher M.; Lin, Jie; Brooks, Andrew G.] Univ Melbourne, Dept Microbiol & Immunol, Parkville, Vic 3010, Australia.
[Vivian, Julian P.; Duncan, Renee C.; Berry, Richard; Reid, Hugh H.; Beddoe, Travis; Gras, Stephanie; Olshina, Maya A.; Clements, Craig S.; Rossjohn, Jamie] Monash Univ, Sch Biomed Sci, Dept Biochem & Mol Biol, Clayton, Vic 3800, Australia.
[O'Connor, Geraldine M.; McVicar, Daniel W.] NCI, Canc & Inflammat Program, Frederick, MD 21702 USA.
[Maloveste, Sebastien M.; Lafont, Bernard A. P.] NIAID, Nonhuman Primate Immunogenet & Cellular Immunol U, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Price, David A.; Rossjohn, Jamie] Cardiff Univ, Sch Med, Dept Infect Immun & Biochem, Cardiff CF14 4XN, S Glam, Wales.
[Price, David A.] NIAID, Human Immunol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Brooks, AG (reprint author), Univ Melbourne, Dept Microbiol & Immunol, Parkville, Vic 3010, Australia.
EM agbrooks@unimelb.edu.au; jamie.rossjohn@monash.edu
RI McVicar, Daniel/G-1970-2015; gras, stephanie/C-8307-2013; Rossjohn,
Jamie/F-9032-2013; Lafont, Bernard/B-7236-2014; Beddoe,
Travis/F-3415-2014; Price, David/C-7876-2013
OI Rossjohn, Jamie/0000-0002-2020-7522; Beddoe, Travis/0000-0003-4550-2277;
Brooks, Andrew/0000-0002-4085-9683; Price, David/0000-0001-9416-2737
FU National Health and Medical Research Council of Australia (NHMRC);
Australian Research Council (ARC); National Cancer Institute, National
Institutes of Health; National Institute of Allergy and Infectious
Diseases, National Institutes of Health; National Institutes of Health;
NHMRC; Medical Research Council (UK); ARC QEII
FX We thank the staff at the MX2 beamline of the Australian synchrotron for
assistance with data collection. We thank A. Radu Aricescu for the gift
of the pHLsec vector. This research was supported by the National Health
and Medical Research Council of Australia (NHMRC), the Australian
Research Council (ARC) and the Intramural Research Programs of the
National Cancer Institute and the National Institute of Allergy and
Infectious Diseases, National Institutes of Health. D. W. M. and
G.M.O'C. were supported by the Intramural AIDS Targeted Antiviral
Program of the National Institutes of Health. J.P.V. is supported by an
NHMRC Peter Doherty Research Fellowship; D. A. P. is supported by a
Medical Research Council (UK) Senior Clinical Fellowship; B. A. P. L. is
supported by the Intramural Research Program of the National Institute
of Allergy and Infectious Diseases, National Institutes of Health; C. S.
C. is supported by an ARC QEII Fellowship; J.R. is supported by an ARC
Federation Fellowship.
NR 29
TC 92
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U1 0
U2 15
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 17
PY 2011
VL 479
IS 7373
BP 401
EP U155
DI 10.1038/nature10517
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 848OA
UT WOS:000297059700046
PM 22020283
ER
PT J
AU Ishizuya-Oka, A
Shi, YB
AF Ishizuya-Oka, Atsuko
Shi, Yun-Bo
TI Evolutionary insights into postembryonic development of adult intestinal
stem cells
SO CELL AND BIOSCIENCE
LA English
DT Article
DE adult stem cell; mammalian suckling-to-weaning transition; amphibian
metamorphosis; thyroid hormone
ID XENOPUS-LAEVIS; THYROID-HORMONE; GUT
AB In the adult vertebrate intestine, multi-potent stem cells continuously generate all of the epithelial cells throughout the adulthood. While it has long been known that the frog intestine is formed via the development of adult intestinal stem cells during thyroid hormone (TH)-dependent metamorphosis, the basic structure of the adult intestine is formed by birth in mammals and it is unclear if the subsequent maturation of the intestine involves any changes in the intestinal stem cells. Two recent papers showing that B lymphocyte-induced maturation protein 1 (Blimp1) regulates postnatal epithelial stem cell reprogramming during mouse intestinal maturation support the model that adult intestinal stem cells are developed during postembryonic development in mammals, in a TH-dependent process similar to intestinal remodeling during amphibian metamorphosis. Since the formation of the adult intestine in both mammals and amphibians is closely associated with the adaptation from aquatic to terrestrial life during the peak of endogenous TH levels, the molecular mechanisms by which the adult stem cells are developed are likely evolutionally conserved.
C1 [Ishizuya-Oka, Atsuko] Nippon Med Sch, Dept Biol, Kawasaki, Kanagawa 2110063, Japan.
[Shi, Yun-Bo] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Mol Morphogenesis, Lab Gene Regulat & Dev, Program Cellular Regulat & Metab PCRM,NIH, Bethesda, MD 20892 USA.
RP Ishizuya-Oka, A (reprint author), Nippon Med Sch, Dept Biol, Kawasaki, Kanagawa 2110063, Japan.
EM a-oka@nms.ac.jp; shi@helix.nih.gov
FU NICHD, NIH; JSPS [20570060]
FX This research was supported in part by the Intramural Research Program
of NICHD, NIH and the JSPS Grants-in-Aid for Scientific Research (C)
(Grant number 20570060 to AI-O).
NR 10
TC 26
Z9 26
U1 1
U2 5
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 16
PY 2011
VL 1
AR 37
DI 10.1186/2045-3701-1-37
PG 3
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 982QA
UT WOS:000307059300001
PM 22087560
ER
PT J
AU Fu, JD
Rushing, SN
Lieu, DK
Chan, CW
Kong, CW
Geng, L
Wilson, KD
Chiamvimonvat, N
Boheler, KR
Wu, JC
Keller, G
Hajjar, RJ
Li, RA
AF Fu, Ji-Dong
Rushing, Stephanie N.
Lieu, Deborah K.
Chan, Camie W.
Kong, Chi-Wing
Geng, Lin
Wilson, Kitchener D.
Chiamvimonvat, Nipavan
Boheler, Kenneth R.
Wu, Joseph C.
Keller, Gordon
Hajjar, Roger J.
Li, Ronald A.
TI Distinct Roles of MicroRNA-1 and-499 in Ventricular Specification and
Functional Maturation of Human Embryonic Stem Cell-Derived
Cardiomyocytes
SO PLOS ONE
LA English
DT Article
ID MUSCLE-SPECIFIC MICRORNA; TRANSCRIPTION FACTOR; CARDIAC-HYPERTROPHY;
PROGENITOR CELLS; MICROARRAY DATA; GENE-TRANSFER; HCN CHANNELS;
DIFFERENTIATION; TARGETS; EXPRESSION
AB Background: MicroRNAs (miRs) negatively regulate transcription and are important determinants of normal heart development and heart failure pathogenesis. Despite the significant knowledge gained in mouse studies, their functional roles in human (h) heart remain elusive.
Methods and Results: We hypothesized that miRs that figure prominently in cardiac differentiation are differentially expressed in differentiating, developing, and terminally mature human cardiomyocytes (CMs). As a first step, we mapped the miR profiles of human (h) embryonic stem cells (ESCs), hESC-derived (hE), fetal (hF) and adult (hA) ventricular (V) CMs. 63 miRs were differentially expressed between hESCs and hE-VCMs. Of these, 29, including the miR-302 and -371/372/373 clusters, were associated with pluripotency and uniquely expressed in hESCs. Of the remaining miRs differentially expressed in hE-VCMs, 23 continued to express highly in hF- and hA-VCMs, with miR-1, -133, and -499 displaying the largest fold differences; others such as miR-let-7a, -let-7b, -26b, -125a and -143 were non-cardiac specific. Functionally, LV-miR-499 transduction of hESC-derived cardiovascular progenitors significantly increased the yield of hE-VCMs (to 72% from 48% of control; p < 0.05) and contractile protein expression without affecting their electrophysiological properties (p > 0.05). By contrast, LV-miR-1 transduction did not bias the yield (p > 0.05) but decreased APD and hyperpolarized RMP/MDP in hE-VCMs due to increased I(to), I(Ks) and I(Kr), and decreased If (p < 0.05) as signs of functional maturation. Also, LV-miR-1 but not 499 augmented the immature Ca(2+) transient amplitude and kinetics. Molecular pathway analyses were performed for further insights.
Conclusion: We conclude that miR-1 and -499 play differential roles in cardiac differentiation of hESCs in a context-dependent fashion. While miR-499 promotes ventricular specification of hESCs, miR-1 serves to facilitate electrophysiological maturation.
C1 [Fu, Ji-Dong; Rushing, Stephanie N.; Lieu, Deborah K.; Chan, Camie W.; Chiamvimonvat, Nipavan; Li, Ronald A.] Univ Calif Davis, Sch Med, Davis, CA 95616 USA.
[Rushing, Stephanie N.; Lieu, Deborah K.; Hajjar, Roger J.; Li, Ronald A.] Mt Sinai Sch Med, Ctr Cardiovasc Res, New York, NY USA.
[Chan, Camie W.; Kong, Chi-Wing; Li, Ronald A.] Univ Hong Kong, Dept Med, Hong Kong, Hong Kong, Peoples R China.
[Chan, Camie W.] Univ Hong Kong, Dept Anat, Hong Kong, Hong Kong, Peoples R China.
[Li, Ronald A.] Univ Hong Kong, Dept Physiol, Hong Kong, Hong Kong, Peoples R China.
[Kong, Chi-Wing; Geng, Lin; Boheler, Kenneth R.; Li, Ronald A.] Univ Hong Kong, Stem Cell & Regenerat Med Consortium, Hong Kong, Hong Kong, Peoples R China.
[Kong, Chi-Wing; Li, Ronald A.] Univ Hong Kong, LKS Fac Med, Heart Brain Hormone & Hlth Aging Res Ctr, Hong Kong, Hong Kong, Peoples R China.
[Wilson, Kitchener D.; Wu, Joseph C.] Stanford Univ, Dept Med, Palo Alto, CA 94304 USA.
[Wilson, Kitchener D.; Wu, Joseph C.] Stanford Univ, Dept Radiol, Palo Alto, CA 94304 USA.
[Boheler, Kenneth R.] NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA.
[Keller, Gordon] Univ Hlth Network, McEwen Cent Regenerat Med, Toronto, ON, Canada.
RP Fu, JD (reprint author), Univ Calif Davis, Sch Med, Davis, CA 95616 USA.
EM ronald.li@mssm.edu
RI Fu, Jidong/E-8173-2012; Wilson, Kitchener/A-7146-2016
FU National Institutes of Health [R01 HL72857, 5R33HL089027-05,
1DP2OD004437-01, T32]; California Institute for Regenerative Medicine;
WCC Foundation; Council of HKSAR [T13-706/11]; NIH, National Institute
on Aging; VistaGen Therapeutics, Inc., South San Francisco
FX This work was supported by extramural grants from the National
Institutes of Health (R01 HL72857 to RAL, 5R33HL089027-05 and
1DP2OD004437-01 to JCW, T32 to SR), the California Institute for
Regenerative Medicine (to JDF and RAL), the WCC Foundation Stem Cell
Fund (to RAL), Research Grant Council of HKSAR (T13-706/11) and by the
Intramural Research Program of the NIH, National Institute on Aging
(KRB). This work has received partial support from VistaGen
Therapeutics, Inc., South San Francisco, CA. The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.; This work has received support from
VistaGen Therapeutics, Inc., South San Francisco, CA. There are no
patents, products in development or marketed products to declare. This
does not alter the authors' adherence to all the PLoS ONE policies on
sharing data and materials, as detailed online in the guide for authors.
NR 53
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U2 16
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 16
PY 2011
VL 6
IS 11
AR e27417
DI 10.1371/journal.pone.0027417
PG 15
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 855HV
UT WOS:000297555400043
PM 22110643
ER
PT J
AU Manoukis, NC
Baber, I
Diallo, M
Sogoba, N
Ribeiro, JMC
AF Manoukis, Nicholas C.
Baber, Ibrahima
Diallo, Moussa
Sogoba, Nafomon
Ribeiro, Jose M. C.
TI Seasonal Climate Effects Anemotaxis in Newly Emerged Adult Anopheles
gambiae Giles in Mali, West Africa
SO PLOS ONE
LA English
DT Article
ID MALARIA TRANSMISSION; MOSQUITOS DIPTERA; CARBON-DIOXIDE; FLIGHT; WIND;
ORIENTATION; CULICIDAE; BEHAVIOR; VILLAGE; ABSENCE
AB The direction and magnitude of movement by the malaria vector Anopheles gambiae Giles has been of great interest to medical entomologists for over 70 years. This direction of movement is likely to be affected by many factors, from environmental conditions and stage of life history of the mosquito to the existence of attractants in the vicinity. We report here the direction of movement of newly emerged An. gambiae in nature, around the village of Doneguebougou, Mali. We assessed the direction of movement for individual mosquitoes by placing them in a novel enclosure with exit traps oriented in the direction of the cardinal and intermediate points of the compass. We consistently found predominantly Southward directions of movement during 2009 and 2010, with an additional Eastward component during the dry season and a Westward one during the wet season. Our data indicate that wind has an important effect on the direction of movement, but that this effect varied by season: Average directions of movement were downwind during the dry season and upwind during the wet season. A switch in anemotactic response suggests that the direction of movement of An. gambiae relative to the wind immediately after emergence under varying conditions of humidity should be further investigated under controlled conditions.
C1 [Manoukis, Nicholas C.] ARS, US Pacific Basin Agr Res Ctr, USDA, Hilo, HI 96720 USA.
[Baber, Ibrahima; Diallo, Moussa; Sogoba, Nafomon] Univ Mali, Malaria Res & Training Ctr, Fac Med Pharm & Odontostomatol, Bamako, Mali.
[Ribeiro, Jose M. C.] NIAID, Sect Vector Biol, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
RP Manoukis, NC (reprint author), ARS, US Pacific Basin Agr Res Ctr, USDA, Hilo, HI 96720 USA.
EM nicholas.manoukis@ars.usda.gov
RI Ribeiro, Jose/J-7011-2015;
OI Manoukis, Nicholas/0000-0001-5062-7256; Ribeiro,
Jose/0000-0002-9107-0818
FU NIAID/NIH
FX This work was supported by the intramural program of the NIAID/NIH.
These funds paid for fuel, materials and lodging. The funders had no
role in study design, data collection and analysis, decision to publish,
or preparation of the manuscript.
NR 34
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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 16
PY 2011
VL 6
IS 11
AR e26910
DI 10.1371/journal.pone.0026910
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 855HV
UT WOS:000297555400016
PM 22114663
ER
PT J
AU Zudaire, E
Gambardella, L
Kurcz, C
Vermeren, S
AF Zudaire, Enrique
Gambardella, Laure
Kurcz, Christopher
Vermeren, Sonja
TI A Computational Tool for Quantitative Analysis of Vascular Networks
SO PLOS ONE
LA English
DT Article
ID BLOOD-VESSELS; ANGIOGENESIS; PI3K; P110-ALPHA; INHIBITOR; ALLANTOIS;
KINASES; MICE
AB Angiogenesis is the generation of mature vascular networks from pre-existing vessels. Angiogenesis is crucial during the organism' development, for wound healing and for the female reproductive cycle. Several murine experimental systems are well suited for studying developmental and pathological angiogenesis. They include the embryonic hindbrain, the postnatal retina and allantois explants. In these systems vascular networks are visualised by appropriate staining procedures followed by microscopical analysis. Nevertheless, quantitative assessment of angiogenesis is hampered by the lack of readily available, standardized metrics and software analysis tools. Non-automated protocols are being used widely and they are, in general, time - and labour intensive, prone to human error and do not permit computation of complex spatial metrics. We have developed a light-weight, user friendly software, AngioTool, which allows for quick, hands-off and reproducible quantification of vascular networks in microscopic images. AngioTool computes several morphological and spatial parameters including the area covered by a vascular network, the number of vessels, vessel length, vascular density and lacunarity. In addition, AngioTool calculates the so-called "branching index" ( branch points / unit area), providing a measurement of the sprouting activity of a specimen of interest. We have validated AngioTool using images of embryonic murine hindbrains, post-natal retinas and allantois explants. AngioTool is open source and can be downloaded free of charge.
C1 [Zudaire, Enrique] NCI, Angiogenesis Core Facil, Radiat Oncol Branch, NIH, Gaithersburg, MD USA.
[Gambardella, Laure; Vermeren, Sonja] Babraham Inst, Inositide Lab, Cambridge, England.
[Kurcz, Christopher] Sci Applicat Int Corp Frederick Inc, Adv Biomed Comp Ctr, Informat Syst Program, Frederick, MD USA.
RP Zudaire, E (reprint author), NCI, Angiogenesis Core Facil, Radiat Oncol Branch, NIH, Gaithersburg, MD USA.
EM zudairee@mail.nih.gov; sonja.vermeren@babraham.ac.uk
OI Vermeren, Sonja/0000-0002-8460-0884
FU Medical Research Council [G0700740]; Biotechnology and Biological
Sciences Research Council [BB/C520712]
FX This work was supported by an grant from the Medical Research Council
(G0700740; http://www.mrc.ac.uk). SV holds a Biotechnology and
Biological Sciences Research Council David Phillips Fellowship
(BB/C520712; http://www.bbsrc.ac.uk/). The funders had no role in study
design, data collection and analysis, decision to publish or preparation
of the manuscript.
NR 30
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U1 2
U2 8
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 16
PY 2011
VL 6
IS 11
AR e27385
DI 10.1371/journal.pone.0027385
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 855HV
UT WOS:000297555400041
PM 22110636
ER
PT J
AU Shi, C
Geders, TW
Park, SW
Wilson, DJ
Boshoff, HI
Abayomi, O
Barry, CE
Schnappinger, D
Finzel, BC
Aldrich, CC
AF Shi, Ce
Geders, Todd W.
Park, Sae Woong
Wilson, Daniel J.
Boshoff, Helena I.
Abayomi, Orishadipe
Barry, Clifton E., III
Schnappinger, Dirk
Finzel, Barry C.
Aldrich, Courtney C.
TI Mechanism-based Inactivation by Aromatization of the Transaminase BioA
Involved in Biotin Biosynthesis in Mycobaterium tuberculosis
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID AMINOBUTYRIC-ACID AMINOTRANSFERASE; MYCOBACTERIUM-TUBERCULOSIS;
(S)-4-AMINO-4,5-DIHYDRO-2-THIOPHENECARBOXYLIC ACID;
(S)-4-AMINO-4,5-DIHYDRO-2-FURANCARBOXYLIC ACID;
ASPARTATE-AMINOTRANSFERASE; ENANTIOMERIC PURITY; RING HETEROCYCLES;
AROMATICITY INDEX; AMICLENOMYCIN; INHIBITION
AB BioA catalyzes the second step of biotin biosynthesis, and this enzyme represents a potential target to develop new antitubercular agents. Herein we report the design, synthesis, and biochemical characterization of a mechanism-based inhibitor (1) featuring a 3,6-dihydropyrid-2-one heterocycle that covalently modifies the pyridoxal S'-phosphate (PLP) cofactor of BioA through aromatization. The structure of the PLP adduct was confirmed by MS/MS and X-ray crystallography at 1.94 angstrom resolution. Inactivation of BioA by 1 was time- and concentration-dependent and protected by substrate. We used a conditional knock-down mutant of M. tuberculosis to demonstrate the antitubercular activity of 1 correlated with BioA expression, and these results provide support for the designed mechanism of action.
C1 [Shi, Ce; Wilson, Daniel J.; Aldrich, Courtney C.] Univ Minnesota, Acad Hlth Ctr, Ctr Drug Design, Minneapolis, MN 55455 USA.
[Geders, Todd W.; Finzel, Barry C.] Univ Minnesota, Dept Med Chem, Minneapolis, MN 55455 USA.
[Park, Sae Woong; Schnappinger, Dirk] Weill Cornell Med Coll, Dept Microbiol & Immunol, New York, NY 10065 USA.
[Boshoff, Helena I.; Abayomi, Orishadipe; Barry, Clifton E., III] NIAID, TB Res Sect, Bethesda, MD 20892 USA.
RP Aldrich, CC (reprint author), Univ Minnesota, Acad Hlth Ctr, Ctr Drug Design, Minneapolis, MN 55455 USA.
EM aldri015@umn.edu
RI Barry, III, Clifton/H-3839-2012; Shi, Ce/G-6523-2013;
OI Shi, Ce/0000-0002-5793-6841; Finzel, Barry/0000-0001-8761-3384
FU Bill and Melinda Gates foundation; Wellcome Trust through the Grand
Challenges in Global Health Initiative; National Institutes of Health
[AI091790]; NIAID, NIH
FX This research was supported by a grant from the Bill and Melinda Gates
foundation and the Wellcome Trust through the Grand Challenges in Global
Health Initiative (to Douglas Young, Imperial College), the National
Institutes of Health (AI091790 to D.S. and C.C.A.) and the Intramural
Research Program of the NIAID, NIH (to C.E.B.). We thank Dr. Lorraine
Anderson for assistance in MS/MS experiments, Kathryn Gustafson for
assistance in purification and crystallization experiments, and Dr. Anja
Meissner for performing cytotoxicity assays. We are grateful for
resources from the University of Minnesota Supercomputing Institute.
NR 61
TC 15
Z9 15
U1 4
U2 22
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD NOV 16
PY 2011
VL 133
IS 45
BP 18194
EP 18201
DI 10.1021/ja204036t
PG 8
WC Chemistry, Multidisciplinary
SC Chemistry
GA 852TU
UT WOS:000297381200042
PM 21988601
ER
PT J
AU Bateman, DA
Tycko, R
Wickner, RB
AF Bateman, David A.
Tycko, Robert
Wickner, Reed B.
TI Experimentally Derived Structural Constraints for Amyloid Fibrils of
Wild-Type Transthyretin
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID BETA-SHEET STRUCTURE; RETINOL-BINDING PROTEIN; SENILE SYSTEMIC
AMYLOIDOSIS; PRE-ALBUMIN; IN-VITRO; PREALBUMIN; PRION; POLYNEUROPATHY;
THYROXINE; CORE
AB Transthyretin (TTR) is a largely beta-sheet serum protein responsible for transporting thyroxine and vitamin A. TTR is found in amyloid deposits of patients with senile systemic amyloidosis. TTR mutants lead to familial amyloidotic polyneuropathy and familial amyloid cardiomyopathy, with an earlier age of onset. Studies of amyloid fibrils of familial amyloidotic polyneuropathy mutant TTR suggest a structure similar to the native state with only a simple opening of a beta-strand-loop-strand region exposing the two main beta-sheets of the protein for fibril elongation. However, we find that the wild-type TTR sequence forms amyloid fibrils that are considerably different from the previously suggested amyloid structure. Using protease digestion with mass spectrometry, we observe the amyloid core to be primarily composed of the C-terminal region, starting around residue 50. Solid-state NMR measurements prove that TTR differs from other pathological amyloids in not having an in-register parallel beta-sheet architecture. We also find that the TTR amyloid is incapable of binding thyroxine as monitored by either isothermal calorimetry or 1,8-anilinonaphthalene sulfonate competition. Taken together, our experiments are consistent with a significantly different configuration of the beta-sheets compared to the previously suggested structure.
C1 [Bateman, David A.; Wickner, Reed B.] NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
[Tycko, Robert] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Wickner, RB (reprint author), NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
EM wickner@helix.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases
FX This work was supported by the Intramural Program of the National
Institute of Diabetes and Digestive and Kidney Diseases.
NR 46
TC 14
Z9 14
U1 0
U2 12
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD NOV 16
PY 2011
VL 101
IS 10
BP 2485
EP 2492
DI 10.1016/j.bpj.2011.10.009
PG 8
WC Biophysics
SC Biophysics
GA 849RT
UT WOS:000297143500024
PM 22098747
ER
PT J
AU Graydon, CW
Cho, S
Li, GL
Kachar, B
von Gersdorff, H
AF Graydon, Cole W.
Cho, Soyoun
Li, Geng-Lin
Kachar, Bechara
von Gersdorff, Henrique
TI Sharp Ca2+ Nanodomains beneath the Ribbon Promote Highly Synchronous
Multivesicular Release at Hair Cell Synapses
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID PRESYNAPTIC ACTIVE ZONES; RETINAL BIPOLAR NEURONS; AUDITORY-NERVE
FIBERS; SYNAPTIC VESICLE; CALCIUM-DEPENDENCE; FREQUENCY-SELECTIVITY;
TRANSMITTER RELEASE; AFFERENT SYNAPSE; CAPACITANCE MEASUREMENTS;
ELECTRON TOMOGRAPHY
AB Hair cell ribbon synapses exhibit several distinguishing features. Structurally, a dense body, or ribbon, is anchored to the presynaptic membrane and tethers synaptic vesicles; functionally, neurotransmitter release is dominated by large EPSC events produced by seemingly synchronous multivesicular release. However, the specific role of the synaptic ribbon in promoting this form of release remains elusive. Using complete ultrastructural reconstructions and capacitance measurements of bullfrog amphibian papilla hair cells dialyzed with high concentrations of a slow Ca2+ buffer (10 mM EGTA), we found that the number of synaptic vesicles at the base of the ribbon correlated closely to those vesicles that released most rapidly and efficiently, while the rest of the ribbon-tethered vesicles correlated to a second, slower pool of vesicles. Combined with the persistence of multivesicular release in extreme Ca2+ buffering conditions (10 mM BAPTA), our data argue against the Ca2+-dependentcompoundfusion of ribbon-tethered vesicles at hair cell synapses. Moreover, during hair cell depolarization, our results suggest that elevated Ca2+ levels enhance vesicle pool replenishment rates. Finally, using Ca2+ diffusion simulations, we propose that the ribbon and its vesicles define a small cytoplasmic volume where Ca2+ buffer is saturated, despite 10 mM BAPTA conditions. This local buffer saturation permits fast and large Ca2+ rises near release sites beneath the synaptic ribbon that can trigger multiquantal EPSCs. We conclude that, by restricting the available presynaptic volume, the ribbon may be creating conditions for the synchronous release of a small cohort of docked vesicles.
C1 [Graydon, Cole W.; Kachar, Bechara] Natl Inst Deafness & Other Commun Disorders, NIH, Bethesda, MD 20892 USA.
[Graydon, Cole W.] Brown Univ, Dept Neurosci, Brown NIH Grad Partnerships Program, Providence, RI 02906 USA.
[Cho, Soyoun; Li, Geng-Lin; von Gersdorff, Henrique] Oregon Hlth & Sci Univ, Vollum Inst, Portland, OR 97239 USA.
RP Kachar, B (reprint author), Natl Inst Deafness & Other Commun Disorders, NIH, 50 S Dr,MSC 8027, Bethesda, MD 20892 USA.
EM kacharb@nidcd.nih.gov; vongersd@ohsu.edu
RI Li, Geng-Lin/I-7998-2014
OI Li, Geng-Lin/0000-0001-7053-4284
FU NIDCD [DC04274]; Deafness Research Foundation; Tartar Fellowship; NIDCD
Division of Intramural Research
FX This work was supported by NIDCD Grant DC04274 (H. v. G.), a Deafness
Research Foundation Grant and a Tartar Fellowship (S. C.), a K99
Research Award from NIDCD (G.-L. L.), and the NIDCD Division of
Intramural Research (C. W. G., B. K.). We thank Will Grimes and Gary
Matthews for discussions.
NR 80
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Z9 64
U1 0
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 16
PY 2011
VL 31
IS 46
BP 16637
EP 16650
DI 10.1523/JNEUROSCI.1866-11.2011
PG 14
WC Neurosciences
SC Neurosciences & Neurology
GA 850RK
UT WOS:000297215200017
PM 22090491
ER
PT J
AU Kon, M
Kiffin, R
Koga, H
Chapochnick, J
Macian, F
Varticovski, L
Cuervo, AM
AF Kon, Maria
Kiffin, Roberta
Koga, Hiroshi
Chapochnick, Javier
Macian, Fernando
Varticovski, Lyuba
Cuervo, Ana Maria
TI Chaperone-Mediated Autophagy Is Required for Tumor Growth
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Article
ID RAT-LIVER LYSOSOMES; SELECTIVE PATHWAY; OXIDATIVE STRESS;
ALPHA-SYNUCLEIN; DEGRADATION; PROTEIN; TUMORIGENESIS; PROTEOLYSIS;
METABOLISM; ACTIVATION
AB The cellular process of autophagy (literally "self-eating") is important for maintaining the homeostasis and bioenergetics of mammalian cells. Two of the best-studied mechanisms of autophagy are macroautophagy and chaperone-mediated autophagy (CMA). Changes in macroautophagy activity have been described in cancer cells and in solid tumors, and inhibition of macroautophagy promotes tumorigenesis. Because normal cells respond to inhibition of macroautophagy by up-regulation of the CMA pathway, we aimed to characterize the CMA status in different cancer cells and to determine the contribution of changes in CMA to tumorigenesis. Here, we show consistent up-regulation of CMA in different types of cancer cells regardless of the status of macroautophagy. We also demonstrate an increase in CMA components in human cancers of different types and origins. CMA is required for cancer cell proliferation in vitro because it contributes to the maintenance of the metabolic alterations characteristic of malignant cells. Using human lung cancer xenografts in mice, we confirmed the CMA dependence of cancer cells in vivo. Inhibition of CMA delays xenograft tumor growth, reduces the number of cancer metastases, and induces regression of existing human lung cancer xenografts in mice. The fact that similar manipulations of CMA also reduce tumor growth of two different melanoma cell lines suggests that targeting this autophagic pathway may have broad antitumorigenic potential.
C1 [Kon, Maria; Kiffin, Roberta; Koga, Hiroshi; Cuervo, Ana Maria] Albert Einstein Coll Med, Dept Dev & Mol Biol, Bronx, NY 10461 USA.
[Chapochnick, Javier] Albert Einstein Coll Med, Dept Surg, Bronx, NY 10461 USA.
[Macian, Fernando] Albert Einstein Coll Med, Dept Pathol, Bronx, NY 10461 USA.
[Macian, Fernando; Cuervo, Ana Maria] Albert Einstein Coll Med, Inst Aging Studies, Bronx, NY 10461 USA.
[Varticovski, Lyuba] NCI, Lab Receptor Biol & Gene Express, Ctr Canc Res, Bethesda, MD 20892 USA.
[Cuervo, Ana Maria] Albert Einstein Coll Med, Finstein Canc Ctr, Bronx, NY 10461 USA.
RP Cuervo, AM (reprint author), Albert Einstein Coll Med, Dept Dev & Mol Biol, Bronx, NY 10461 USA.
EM ana-maria.cuervo@einstein.yu.edu
OI Macian, Fernando/0000-0003-2666-035X
FU NIH [AG021904, AG031782]; Hirschl/Weill-Caulier Career Scientist Award;
CTSA [UL1 RR025750]; Albert Einstein Cancer Center [NCI PO1 13330,
TG32GM007288]
FX Supported by NIH grants AG021904 (A.M.C.) and AG031782 (A.M.C. and
F.M.), a Hirschl/Weill-Caulier Career Scientist Award (A.M.C.), a CTSA
(UL1 RR025750), the Albert Einstein Cancer Center grant NCI PO1 13330,
and TG32GM007288 (M.K.).
NR 47
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U1 4
U2 20
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 16
PY 2011
VL 3
IS 109
AR 109ra117
DI 10.1126/scitranslmed.3003182
PG 13
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 850SL
UT WOS:000297218300005
PM 22089453
ER
PT J
AU Traverse, JH
Henry, TD
Ellis, SG
Pepine, CJ
Willerson, JT
Zhao, DXM
Forder, JR
Byrne, BJ
Hatzopoulos, AK
Penn, MS
Perin, EC
Baran, KW
Chambers, J
Lambert, C
Raveendran, G
Simon, DI
Vaughan, DE
Simpson, LM
Gee, AP
Taylor, DA
Cogle, CR
Thomas, JD
Silva, GV
Jorgenson, BC
Olson, RE
Bowman, S
Francescon, J
Geither, C
Handberg, E
Smith, DX
Baraniuk, S
Piller, LB
Loghin, C
Aguilar, D
Richman, S
Zierold, C
Bettencourt, J
Sayre, SL
Vojvodic, RW
Skarlatos, SI
Gordon, DJ
Ebert, RF
Kwak, M
Moye, LA
Simari, RD
AF Traverse, Jay H.
Henry, Timothy D.
Ellis, Stephen G.
Pepine, Carl J.
Willerson, James T.
Zhao, David X. M.
Forder, John R.
Byrne, Barry J.
Hatzopoulos, Antonis K.
Penn, Marc S.
Perin, Emerson C.
Baran, Kenneth W.
Chambers, Jeffrey
Lambert, Charles
Raveendran, Ganesh
Simon, Daniel I.
Vaughan, Douglas E.
Simpson, Lara M.
Gee, Adrian P.
Taylor, Doris A.
Cogle, Christopher R.
Thomas, James D.
Silva, Guilherme V.
Jorgenson, Beth C.
Olson, Rachel E.
Bowman, Sherry
Francescon, Judy
Geither, Carrie
Handberg, Eileen
Smith, Deirdre X.
Baraniuk, Sarah
Piller, Linda B.
Loghin, Catalin
Aguilar, David
Richman, Sara
Zierold, Claudia
Bettencourt, Judy
Sayre, Shelly L.
Vojvodic, Rachel W.
Skarlatos, Sonia I.
Gordon, David J.
Ebert, Ray F.
Kwak, Minjung
Moye, Lemuel A.
Simari, Robert D.
CA Cardiovasc Cell Therapy Res Networ
TI Effect of Intracoronary Delivery of Autologous Bone Marrow Mononuclear
Cells 2 to 3 Weeks Following Acute Myocardial Infarction on Left
Ventricular Function The LateTIME Randomized Trial
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID ENDOTHELIAL PROGENITOR CELLS; MESENCHYMAL STEM-CELLS; RESEARCH NETWORK
CCTRN; CARDIAC REPAIR; DOUBLE-BLIND; EJECTION FRACTION; PILOT TRIAL;
THERAPY; INFUSION; DETERMINANTS
AB Context Clinical trial results suggest that intracoronary delivery of autologous bone marrow mononuclear cells (BMCs) may improve left ventricular (LV) function when administered within the first week following myocardial infarction (MI). However, because a substantial number of patients may not present for early cell delivery, the efficacy of autologous BMC delivery 2 to 3 weeks post-MI warrants investigation.
Objective To determine if intracoronary delivery of autologous BMCs improves global and regional LV function when delivered 2 to 3 weeks following first MI.
Design, Setting, and Patients A randomized, double-blind, placebo-controlled trial (LateTIME) of the National Heart, Lung, and Blood Institute-sponsored Cardiovascular Cell Therapy Research Network of 87 patients with significant LV dysfunction (LV ejection fraction [LVEF] <= 45%) following successful primary percutaneous coronary intervention (PCI) between July 8, 2008, and February 28, 2011.
Interventions Intracoronary infusion of 150 x 10(6) autologous BMCs (total nucleated cells) or placebo (BMC: placebo, 2:1) was performed within 12 hours of bone marrow aspiration after local automated cell processing.
Main Outcome Measures Changes in global (LVEF) and regional (wall motion) LV function in the infarct and border zone between baseline and 6 months, measured by cardiac magnetic resonance imaging. Secondary end points included changes in LV volumes and infarct size.
Results A total of 87 patients were randomized (mean [SD] age, 57 [11] years; 83% men). Harvesting, processing, and intracoronary delivery of BMCs in this setting was feasible. Change between baseline and 6 months in the BMC group vs placebo for mean LVEF (48.7% to 49.2% vs 45.3% to 48.8%; between-group mean difference, -3.00; 95% CI, -7.05 to 0.95), wall motion in the infarct zone (6.2 to 6.5 mm vs 4.9 to 5.9 mm; between-group mean difference, -0.70; 95% CI, -2.78 to 1.34), and wall motion in the border zone (16.0 to 16.6 mm vs 16.1 to 19.3 mm; between-group mean difference, -2.60; 95% CI, -6.03 to 0.77) were not statistically significant. No significant change in LV volumes and infarct volumes was observed; both groups decreased by a similar amount at 6 months vs baseline.
Conclusion Among patients with MI and LV dysfunction following reperfusion with PCI, intracoronary infusion of autologous BMCs vs intracoronary placebo infusion, 2 to 3 weeks after PCI, did not improve global or regional function at 6 months.
C1 [Traverse, Jay H.; Henry, Timothy D.; Jorgenson, Beth C.; Olson, Rachel E.] Abbott NW Hosp, Minneapolis Heart Inst Fdn, Minneapolis, MN 55407 USA.
[Traverse, Jay H.; Henry, Timothy D.; Raveendran, Ganesh; Taylor, Doris A.; Zierold, Claudia] Univ Minnesota, Sch Med, Minneapolis, MN 55455 USA.
[Ellis, Stephen G.; Thomas, James D.; Geither, Carrie] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Forder, John R.] Univ Florida, Coll Med, Dept Radiol, Gainesville, FL 32610 USA.
[Willerson, James T.; Perin, Emerson C.; Silva, Guilherme V.; Smith, Deirdre X.] St Lukes Episcopal Hosp, Texas Heart Inst, Houston, TX USA.
[Zhao, David X. M.; Hatzopoulos, Antonis K.; Bowman, Sherry; Francescon, Judy] Vanderbilt Univ, Sch Med, Nashville, TN 37212 USA.
[Penn, Marc S.] Summa Cardiovasc Inst, Akron, OH USA.
[Baran, Kenneth W.] United Heart & Vasc Clin, St Paul, MN USA.
[Chambers, Jeffrey] Mercy Hosp, Coon Rapids, MN USA.
[Lambert, Charles] Florida Hosp Tampa, Pepin Heart Inst, Tampa, FL USA.
[Simon, Daniel I.] Univ Hosp Case Med Ctr, Cleveland, OH USA.
[Vaughan, Douglas E.] Northwestern Univ, Chicago, IL 60611 USA.
[Loghin, Catalin] Univ Texas Houston, Sch Med, Houston, TX 77030 USA.
[Simpson, Lara M.; Baraniuk, Sarah; Piller, Linda B.; Bettencourt, Judy; Sayre, Shelly L.; Vojvodic, Rachel W.; Moye, Lemuel A.] Univ Texas Houston, Sch Publ Hlth, Houston, TX 77030 USA.
[Gee, Adrian P.; Aguilar, David; Richman, Sara] Baylor Coll Med, Houston, TX 77030 USA.
[Skarlatos, Sonia I.; Gordon, David J.; Ebert, Ray F.; Kwak, Minjung] NHLBI, Bethesda, MD 20892 USA.
[Simari, Robert D.] Mayo Clin, Rochester, MN USA.
RP Moye, LA (reprint author), Univ Texas Houston, Sch Publ Hlth, 1200 Herman Pressler,Ste E815, Houston, TX 77030 USA.
EM lemmoye@msn.com
RI Hatzopoulos, Antonis/D-2049-2010; Cogle, Christopher/H-1746-2016
OI Cogle, Christopher/0000-0001-5422-6863
FU National Heart, Lung, and Blood Institute (NHLBI) [5 U01 HL087318-04,
N01-HB-37164, HHSN268201000008C, N01-HB-37163, HHSN268201000007C];
Athersys
FX All authors have completed and submitted the ICMJE Form for Disclosure
of Potential Conflicts of Interest and none were reported. Dr Penn
reported being a consultant for Juventas Therapeutics and Aastrom
Biosciences and receiving grant funding for his institution from
Athersys. No other authors reported any financial disclosures.; This
study was supported by the National Heart, Lung, and Blood Institute
(NHLBI) under the cooperative agreement 5 U01 HL087318-04 and in part by
the NHLBI contracts N01-HB-37164 and HHSN268201000008C to the Molecular
and Cellular Therapeutics Facility, University of Minnesota, and
N01-HB-37163 and HHSN268201000007C to the Cell Processing Facility,
Baylor College of Medicine.
NR 38
TC 182
Z9 191
U1 2
U2 12
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 16
PY 2011
VL 306
IS 19
BP 2110
EP 2119
DI 10.1001/jama.2011.1670
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 847YU
UT WOS:000297013000017
PM 22084195
ER
PT J
AU Lauer, MS
AF Lauer, Michael S.
TI Cardiovascular Science in the Service of National Strength
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
ID HYPERTENSION
C1 NHLBI, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
RP Lauer, MS (reprint author), NHLBI, Div Cardiovasc Sci, 6701 Rockledge Dr,Room 8128, Bethesda, MD 20892 USA.
EM lauerm@nhlbi.nih.gov
RI Lauer, Michael/L-9656-2013
OI Lauer, Michael/0000-0002-9217-8177
NR 10
TC 9
Z9 9
U1 0
U2 2
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 16
PY 2011
VL 306
IS 19
BP 2145
EP 2146
DI 10.1001/jama.2011.1669
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 847YU
UT WOS:000297013000021
PM 22089722
ER
PT J
AU Shi, GB
Ji, XH
AF Shi, Genbin
Ji, Xinhua
TI New ways to derivatize at position 6 of 7,7-dimethyl-7,8-dihydropterin
SO TETRAHEDRON LETTERS
LA English
DT Article
DE Pterin; Carboxylation; Bromination; Ester; Aldehyde
ID 6-HYDROXYMETHYL-7,8-DIHYDROPTERIN PYROPHOSPHOKINASE; VITAMIN
BIOSYNTHESIS; INHIBITORS; MECHANISM
AB Reported are the synthesis of two intermediates for derivatization at position 6 of 7,7-dimethyl-7,8-dihydropterin: 6-carboxylic acid ethyl ester-7,7-dimethyl-7,8-dihydropterin, which is a novel compound, and 6-aldehyde-7,7-dimethyl-7,8-dihydropterin, which is synthesized by a new method with a yield of 90%. Published by Elsevier Ltd.
C1 [Shi, Genbin; Ji, Xinhua] NCI, Biomol Struct Sect, Macromol Crystallog Lab, Frederick, MD 21702 USA.
RP Ji, XH (reprint author), NCI, Biomol Struct Sect, Macromol Crystallog Lab, 1050 Boyles St, Frederick, MD 21702 USA.
EM jix@mail.nih.gov
RI Ji, Xinhua/C-9664-2012
OI Ji, Xinhua/0000-0001-6942-1514
FU NIH; National Cancer Institute; Center for Cancer Research; NIAID
[Y3-RC-8007-01]
FX We thank Dr. Larry Keefer for critical reading of the manuscript. This
research was supported by the Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research and the Trans
NIH/FDA Intramural Biodenfense Program Y3-RC-8007-01 from the NIAID.
Mass spectrometry experiments were conducted with an Agilent 1100 series
LC/Mass Selective Detector maintained by the Biophysics Resource in the
Structural Biophysics Laboratory, an Agilent 1200 LC/MSD-SL system in
the Chemical Biology Laboratory, and a Thermoquest Surveyor Finnigan LCQ
deca maintained by the Comparative Carcinogenesis Laboratory of National
Cancer Institute at Frederick.
NR 28
TC 2
Z9 2
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 16
PY 2011
VL 52
IS 46
BP 6174
EP 6176
DI 10.1016/j.tetlet.2011.09.047
PG 3
WC Chemistry, Organic
SC Chemistry
GA 847QX
UT WOS:000296988700031
PM 22125346
ER
PT J
AU Lega, BC
Kahana, MJ
Jaggi, J
Baltuch, GH
Zaghloul, K
AF Lega, Bradley C.
Kahana, Michael J.
Jaggi, Jurg
Baltuch, Gordon H.
Zaghloul, Kareem
TI Neuronal and oscillatory activity during reward processing in the human
ventral striatum
SO NEUROREPORT
LA English
DT Article
DE deep brain stimulation; nucleus accumbens; reward; ventral striatum
ID DEEP BRAIN-STIMULATION; DEPRESSION; CIRCUITRY
AB Accumulated evidence from animal studies implicates the ventral striatum in the processing of reward information. Recently, deep brain stimulation (DBS) surgery has enabled researchers to analyze neurophysiological recordings from humans engaged in reward tasks. We present data recorded from the human ventral striatum during deep brain stimulation surgery as a participant played a video game coupled to the receipt of visual reward images. To our knowledge, we identify the first instances of reward-sensitive single unit activity in the human ventral striatum. Local field potential data suggest that alpha oscillations are sensitive to positive feedback, whereas beta oscillations exhibit significantly higher power during unrewarded trials. We report evidence of alpha-gamma cross-frequency coupling that differentiates between positive and negative feedback. NeuroReport 22:795-800 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
C1 [Lega, Bradley C.; Jaggi, Jurg; Baltuch, Gordon H.] Univ Penn, Dept Neurosurg, Philadelphia, PA 19104 USA.
[Kahana, Michael J.] Univ Penn, Dept Psychol, Philadelphia, PA 19104 USA.
[Zaghloul, Kareem] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
RP Lega, BC (reprint author), Univ Penn, Dept Neurosurg, 3401 Walnut St Entrance C,Room 303, Philadelphia, PA 19104 USA.
EM bradlega@gmail.com
FU Dana Foundation
FX This study was supported by a grant from the Dana Foundation. The
authors would also like to acknowledge the contributions of Marie Kerr
for her assistance in maintaining IRB documents.
NR 25
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U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0959-4965
J9 NEUROREPORT
JI Neuroreport
PD NOV 16
PY 2011
VL 22
IS 16
BP 795
EP 800
DI 10.1097/WNR.0b013e32834b2975
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA 832SS
UT WOS:000295828200002
PM 21975313
ER
PT J
AU Pallikkuth, S
Rogers, K
Villinger, F
Dosterll, M
Vaccari, M
Franchini, G
Pahwa, R
Pahwa, S
AF Pallikkuth, Suresh
Rogers, Kenneth
Villinger, Francois
Dosterll, Melvin
Vaccari, Monica
Franchini, Genoveffa
Pahwa, Rajendra
Pahwa, Savita
TI Interleukin-21 administration to rhesus macaques chronically infected
with simian immunodeficiency virus increases cytotoxic effector
molecules in T cells and NK cells and enhances B cell function without
increasing immune activation or viral replication
SO VACCINE
LA English
DT Article
DE Interleukin-21; T cells; B cells; Natural killer cells; Rhesus macaques;
SIV
ID HIV-1 INFECTION; PERFORIN EXPRESSION; FLOW-CYTOMETRY; DNA VACCINE;
METASTATIC MELANOMA; NONHUMAN-PRIMATES; HUMAN NAIVE; IL-21; RESPONSES;
CD4(+)
AB We have previously shown that interleukin-21, a pleiotropic C gamma-chain signaling cytokine, induces the expression of the cytotoxic molecules granzyme B (GrB) and perforin in vitro in CD8 T cells and NK cells of chronically HIV infected individuals. In this pilot study, four chronically SIV infected rhesus macaques (RM) in late-stage disease were given two doses of recombinant MamulL-21, 50 mu g/kg, intravenously 7 days apart, followed by one subcutaneous dose, 100 mu g/kg, 23 days after the second dose. Three animals served as controls. After each dose of IL-21, increases were noted in frequency and mean fluorescence intensity of GrB and perforin expression in memory and effector subsets of CD8 T cells in peripheral blood (PB), in peripheral and mesenteric lymph node (LN) cells, in PB memory and effector CD4 T cells and in NK cells. Frequencies of SIV-gag specific CD107a(+)IFN-gamma(+) CD8 T cells increased 3.8-fold in PB and 1.8-fold in LN. In addition, PB CD27(+) memory B cells were 2-fold higher and serum SIV antibodies increased significantly after IL-21 administration. No changes were observed in markers of T cell activation, T cell proliferation or plasma virus load. Thus, administration of IL-21 to chronically SIV infected viremic animals was safe, well tolerated and could augment the cytotoxic potential of T cells and NK cells, promote B cell differentiation with increases in SIV antibody titers without discernable increase in cellular activation. Further studies are warranted to elucidate the effects and potential benefit of IL-21 administration in the context of SIV/HIV infection and in SIV/HIV vaccine design. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Pallikkuth, Suresh; Pahwa, Savita] Univ Miami, Miller Sch Med, Dept Microbiol & Immunol, Dev Ctr AIDS Res D CFAR, Miami, FL 33136 USA.
[Rogers, Kenneth; Villinger, Francois] Emory Univ, Dept Pathol & Lab Med, Yerkes Natl Primate Res Ctr, Atlanta, GA 30322 USA.
[Dosterll, Melvin; Vaccari, Monica; Franchini, Genoveffa] NCI, Vaccine Branch, Anim Models & Retroviral Vaccine Sect, Bethesda, MD 20892 USA.
[Pahwa, Rajendra] Max Healthcare Super Specialty Hosp, Saket New Delhi 110017, India.
[Pahwa, Rajendra] Max Res Inst, Saket New Delhi 110017, India.
RP Pahwa, S (reprint author), Univ Miami, Miller Sch Med, Dept Microbiol & Immunol, Dev Ctr AIDS Res D CFAR, 1580 NW 10th Ave,BCRI 712, Miami, FL 33136 USA.
EM spahwa@med.miami.edu
FU NIH [A1077501, R24RR016988, RR00165]
FX We thank the Laboratory Sciences Core of the Developmental Center for
AIDS Research and Sylvester Comprehensive Cancer Center, University of
Miami Miller School of Medicine for flow cytometry. We acknowledge the
animal facilities at Advanced BioScience Laboratories, Inc. and Yerkes
National Primate Research Center for the study. This work was supported
by NIH grant A1077501 (SP), R24RR016988 (FV) and RR00165 (Yerkes NPRC).
NR 68
TC 31
Z9 31
U1 0
U2 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
J9 VACCINE
JI Vaccine
PD NOV 15
PY 2011
VL 29
IS 49
BP 9229
EP 9238
DI 10.1016/j.vaccine.2011.09.118
PG 10
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 854WM
UT WOS:000297525500016
PM 21996099
ER
PT J
AU Van Eperen, L
Marincola, FM
AF Van Eperen, Laura
Marincola, Francesco M.
TI How scientists use social media to communicate their research
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Editorial Material
AB Millions of people all over the world are constantly sharing an extremely wide range of fascinating, quirky, funny, irrelevant and important content all at once. Even scientists are no strangers to this trend. Social media has enabled them to communicate their research quickly and efficiently throughout each corner of the world. But which social media platforms are they using to communicate this research and how are they using them? One thing is clear: the range of social media platforms that scientists are using is relatively vast and dependent on discipline and sentiment. While the future of social media is unknown, a combination of educated speculation and persuasive fact points to the industry's continual growth and influence. Thus, is that not only are scientists utilizing social media to communicate their research, they must. The ability to communicate to the masses via social media is critical to the distribution of scientific information amongst professionals in the field and to the general population.
C1 [Van Eperen, Laura] Van Eperen & Co, Strateg Commun Consulting, Bethesda, MD 20817 USA.
[Marincola, Francesco M.] Natl Inst Hlth Bethesda, Infect Dis & Immunogenet Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD USA.
[Marincola, Francesco M.] Natl Inst Hlth Bethesda, Trans NIH Ctr Human Immunol, Bethesda, MD USA.
RP Van Eperen, L (reprint author), Van Eperen & Co, Strateg Commun Consulting, Bethesda, MD 20817 USA.
EM laurav@veandco.com
NR 1
TC 14
Z9 16
U1 4
U2 16
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD NOV 15
PY 2011
VL 9
AR 199
DI 10.1186/1479-5876-9-199
PG 3
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 857NX
UT WOS:000297726400001
PM 22085450
ER
PT J
AU Kilimnik, G
Zhao, B
Jo, JH
Periwal, V
Witkowski, P
Misawa, R
Hara, M
AF Kilimnik, German
Zhao, Billy
Jo, Junghyo
Periwal, Vipul
Witkowski, Piotr
Misawa, Ryosuke
Hara, Manami
TI Altered Islet Composition and Disproportionate Loss of Large Islets in
Patients with Type 2 Diabetes
SO PLOS ONE
LA English
DT Article
ID BETA-CELL MASS; PANCREATIC-ISLETS; ARCHITECTURE; ALPHA; MICE; MELLITUS
AB Human islets exhibit distinct islet architecture with intermingled alpha-and beta-cells particularly in large islets. In this study, we quantitatively examined pathological changes of the pancreas in patients with type 2 diabetes (T2D). Specifically, we tested a hypothesis that changes in endocrine cell mass and composition are islet-size dependent. A large-scale analysis of cadaveric pancreatic sections from T2D patients (n = 12) and non-diabetic subjects (n = 14) was carried out combined with semi-automated analysis to quantify changes in islet architecture. The method provided the representative islet distribution in the whole pancreas section that allowed us to examine details of endocrine cell composition in individual islets. We observed a preferential loss of large islets (>60 mu m in diameter) in T2D patients compared to non-diabetic subjects. Analysis of islet cell composition revealed that the beta-cell fraction in large islets was decreased in T2D patients. This change was accompanied by a reciprocal increase in alpha-cell fraction, however total alpha-cell area was decreased along with beta-cells in T2D. Delta-cell fraction and area remained unchanged. The computer-assisted quantification of morphological changes in islet structure minimizes sampling bias. Significant beta-cell loss was observed in large islets in T2D, in which alpha-cell ratio reciprocally increased. However, there was no alpha-cell expansion and the total alpha-cell area was also decreased. Changes in islet architecture were marked in large islets. Our method is widely applicable to various specimens using standard immunohistochemical analysis that may be particularly useful to study large animals including humans where large organ size precludes manual quantitation of organ morphology.
C1 [Kilimnik, German; Zhao, Billy; Hara, Manami] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
[Jo, Junghyo; Periwal, Vipul] NIDDKD, Lab Biol Modeling, NIH, Bethesda, MD 20892 USA.
[Witkowski, Piotr; Misawa, Ryosuke] Univ Chicago, Dept Surg, Chicago, IL 60637 USA.
RP Kilimnik, G (reprint author), Univ Chicago, Dept Med, 5841 S Maryland Ave, Chicago, IL 60637 USA.
EM mhara@midway.uchicago.edu
RI Periwal, Vipul/I-1728-2012; Jo, Junghyo/D-4889-2011
FU United States of America Public Health Service [DK-081527, DK-072473,
DK-042086, DK-20595]; Kovler Family Foundation; National Institutes of
Health, National Institute of Diabetes and Digestive and Kidney Diseases
FX The study is supported by United States of America Public Health Service
Grant DK-081527, DK-072473, DK-042086 and DK-20595 to the University of
Chicago Diabetes Research and Training Center (Animal Models Core), a
gift from the Kovler Family Foundation (to MH); and the Intramural
Research Program of the National Institutes of Health, National
Institute of Diabetes and Digestive and Kidney Diseases (to JJ and VP).
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 27
TC 34
Z9 36
U1 0
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 15
PY 2011
VL 6
IS 11
AR e27445
DI 10.1371/journal.pone.0027445
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 855HU
UT WOS:000297555300022
PM 22102895
ER
PT J
AU Steidl, S
Miller, AD
Blaha, CD
Yeomans, JS
AF Steidl, Stephan
Miller, Anthony D.
Blaha, Charles D.
Yeomans, John S.
TI M-5 Muscarinic Receptors Mediate Striatal Dopamine Activation by Ventral
Tegmental Morphine and Pedunculopontine Stimulation in Mice
SO PLOS ONE
LA English
DT Article
ID NUCLEUS-LESIONED RATS; SUBSTANTIA-NIGRA; CHOLINERGIC STIMULATION;
GLUTAMATE RECEPTORS; EXCITOTOXIC LESIONS; D-AMPHETAMINE; NEURONS; AREA;
EFFLUX; ACETYLCHOLINE
AB Opiates, like other addictive drugs, elevate forebrain dopamine levels and are thought to do so mainly by inhibiting GABA neurons near the ventral tegmental area (VTA), in turn leading to a disinhibition of dopamine neurons. However, cholinergic inputs from the laterodorsal (LDT) and pedunculopontine (PPT) tegmental nucleus to the VTA and substantia nigra (SN) importantly contribute, as either LDT or PPT lesions strongly attenuate morphine-induced forebrain dopamine elevations. Pharmacological blockade of muscarinic acetylcholine receptors in the VTA or SN has similar effects. M-5 muscarinic receptors are the only muscarinic receptor subtype associated with VTA and SN dopamine neurons. Here we tested the contribution of M-5 muscarinic receptors to morphine-induced dopamine elevations by measuring nucleus accumbens dopamine efflux in response to intra-VTA morphine infusion using in vivo chronoamperometry. Intra-VTA morphine increased nucleus accumbens dopamine efflux in urethane-anesthetized wildtype mice starting at 10 min after infusion. These increases were absent in M-5 knockout mice and were similarly blocked by pre-treatment with VTA scopolamine in wildtype mice. Furthermore, in wildtype mice electrical stimulation of the PPT evoked an initial, short-lasting increase in striatal dopamine efflux, followed 5 min later by a second prolonged increase in dopamine efflux. In M-5 knockout mice, or following systemic pre-treatment with scopolamine in wildtype mice, the prolonged increase in striatal dopamine efflux was absent. The time course of increased accumbal dopamine efflux in wildtype mice following VTA morphine was consistent with both the prolonged M-5-mediated excitation of striatal dopamine efflux following PPT electrical stimulation and accumbal dopamine efflux following LDT electrical stimulation. Therefore, M-5 receptors appear critical for prolonged PPT excitation of dopamine efflux and for dopamine efflux induced by intra-VTA morphine.
C1 [Steidl, Stephan; Yeomans, John S.] Univ Toronto, Dept Psychol, Toronto, ON M5S 1A1, Canada.
[Miller, Anthony D.; Blaha, Charles D.] Univ Memphis, Dept Psychol, Memphis, TN 38152 USA.
[Steidl, Stephan; Yeomans, John S.] Univ Toronto, Ctr Biol Timing & Cognit, Toronto, ON, Canada.
RP Steidl, S (reprint author), Natl Inst Drug Abuse, Behav Neurosci Res Branch, NIH, Baltimore, MD USA.
EM ssteidl@nida.nih.gov
OI Blaha, Charles/0000-0001-5155-1505
FU Canadian Institutes of Health Research (CIHR); Natural Sciences and
Engineering Research Council of Canada (NSERC)
FX This work was supported by a Canadian Institutes of Health Research
(CIHR) grant to JSY and a Natural Sciences and Engineering Research
Council of Canada Graduate Scholar doctoral scholarship (NSERC CGS-D) to
SS. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 38
TC 19
Z9 20
U1 1
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 15
PY 2011
VL 6
IS 11
AR e27538
DI 10.1371/journal.pone.0027538
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 855HU
UT WOS:000297555300027
PM 22102904
ER
PT J
AU Tilahun, ME
Kwan, A
Natarajan, K
Quinn, M
Tilahun, AY
Xie, C
Margulies, DH
Osborne, BA
Goldsby, RA
Rajagopalan, G
AF Tilahun, Mulualem E.
Kwan, Alan
Natarajan, Kannan
Quinn, Megan
Tilahun, Ashenafi Y.
Xie, Chen
Margulies, David H.
Osborne, Barbara A.
Goldsby, Richard A.
Rajagopalan, Govindarajan
TI Chimeric Anti-Staphylococcal Enterotoxin B Antibodies and Lovastatin Act
Synergistically to Provide In Vivo Protection against Lethal Doses of
SEB
SO PLOS ONE
LA English
DT Article
ID TOXIC-SHOCK-SYNDROME; II TRANSGENIC MICE; T-CELL-ACTIVATION; BACTERIAL
SUPERANTIGENS; INTRAVENOUS IMMUNOGLOBULIN; STAPHYLOCOCCAL ENTEROTOXINS;
RECEPTOR MIMICS; TOXOID VACCINES; STATINS; STIMULATION
AB Staphylococcal enterotoxin B (SEB) is one of a family of toxins secreted by Staphylococcus aureus that act as superantigens, activating a large fraction of the T-cell population and inducing production of high levels of inflammatory cytokines that can cause toxic shock syndrome (TSS) and death. Extracellular engagement of the TCR of T-cells and class II MHC of antigen presenting cells by SEB triggers the activation of many intracellular signaling processes. We engineered chimeric antibodies to block the extracellular engagement of cellular receptors by SEB and used a statin to inhibit intracellular signaling. Chimeric human-mouse antibodies directed against different neutralizing epitopes of SEB synergistically inhibited its activation of human T-cells in vitro. In the in vivo model of lethal toxic shock syndrome (TSS) in HLA-DR3 transgenic mice, two of these antibodies conferred significant partial protection when administered individually, but offered complete protection in a synergistic manner when given together. Similarly, in vivo, lovastatin alone conferred only partial protection from TSS similar to single anti-SEB antibodies. However, used in combination with one chimeric neutralizing anti-SEB antibody, lovastatin provided complete protection against lethal TSS in HLA-DR3 transgenic mice. These experiments demonstrate that in vivo protection against lethal doses of SEB can be achieved by a statin of proven clinical safety and chimeric human-mouse antibodies, agents now widely used and known to be of low immunogenicity in human hosts.
C1 [Tilahun, Mulualem E.; Kwan, Alan; Quinn, Megan; Xie, Chen; Goldsby, Richard A.] Amherst Coll, Dept Biol, Amherst, MA 01002 USA.
[Tilahun, Mulualem E.; Osborne, Barbara A.; Goldsby, Richard A.] Univ Massachusetts, Dept Vet & Anim Sci, Amherst, MA 01003 USA.
[Tilahun, Ashenafi Y.; Rajagopalan, Govindarajan] Mayo Clin, Coll Med, Dept Immunol, Rochester, MA USA.
[Natarajan, Kannan; Margulies, David H.] NIAID, Mol Biol Sect, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Tilahun, ME (reprint author), Amherst Coll, Dept Biol, Amherst, MA 01002 USA.
EM ragoldsby@amherst.edu; Rajagopalan.Govindarajan@mayo.edu
RI Margulies, David/H-7089-2013;
OI Margulies, David/0000-0001-8530-7375
FU NIH [AI057652, AI076944, AI068741]
FX This work was supported by NIH grants AI057652, AI076944, and AI068741.
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 57
TC 6
Z9 7
U1 0
U2 8
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 15
PY 2011
VL 6
IS 11
AR e27203
DI 10.1371/journal.pone.0027203
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 855HU
UT WOS:000297555300012
PM 22102880
ER
PT J
AU Kasprzak, KS
Diwan, BA
Kaczmarek, MZ
Logsdon, DL
Fivash, MJ
Salnikow, K
AF Kasprzak, Kazimierz S.
Diwan, Bhalchandra A.
Kaczmarek, Monika Z.
Logsdon, Daniel L.
Fivash, Mathew J.
Salnikow, Konstantin
TI Effects of ascorbic acid on carcinogenicity and acute toxicity of nickel
subsulfide, and on tumor transplants growth in gulonolactone oxidase
knock-out mice and wild-type C57BL mice
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE Ascorbate; Gulonolactone oxidase; Gulo-/- mice; Nickel carcinogenesis
ID DEPLETION; METALS
AB The aim of this study was to test a hypothesis that ascorbate depletion could enhance carcinogenicity and acute toxicity of nickel. Homozygous L-gulono-gamma -lactone oxidase gene knock-out mice (Gulo-/- mice) unable to produce ascorbate and wild-type C57BL mice (WT mice) were injected intramuscularly with carcinogenic nickel subsulfide (Ni3S2), and observed for the development of injection site tumors for 57 weeks. Small pieces of one of the induced tumors were transplanted subcutaneously into separate groups of Gulo-/- and WT mice and the growth of these tumors was measured for up to 3 months. The two strains of mice differed significantly with regard to (1) Ni3S2 carcinogenesis: Gulo-/- mice were 40% more susceptible than WT mice; and (2) transplanted tumors development: Gulo-/- mice were more receptive to tumor growth than WT mice, but only in terms of a much shorter tumor latency; later in the exponential phase of growth, the growth rates were the same. And, with adequate ascorbate supplementation, the two strains were equally susceptible to acute toxicity of Ni3S2. Statistically significant effects of dietary ascorbate dosing levels were the following: (1) reduction in ascorbate supplementation increased acute toxicity of Ni3S2 in Gulo-/- mice; (2) ascorbate supplementation extended the latency of transplanted tumors in WT mice. In conclusion, the lack of endogenous ascorbate synthesis makes Gulo-/- mice more susceptible to Ni3S2 carcinogenesis. Dietary ascorbate tends to attenuate acute toxicity of Ni3S2 and to extend the latency of transplanted tumors. The latter effects may be of practical importance to humans and thus deserve further studies. Published by Elsevier Inc.
C1 [Kasprzak, Kazimierz S.; Kaczmarek, Monika Z.; Salnikow, Konstantin] NCI, Comparat Carcinogenesis Lab, Frederick, MD 21702 USA.
[Diwan, Bhalchandra A.] NCI, Basic Res Program, Sci Applicat Int Corp, Frederick Inc, Frederick, MD 21702 USA.
[Logsdon, Daniel L.] NCI, Lab Anim Sci Program,Sci, Sci Applicat Int Corp, Frederick Inc, Frederick, MD 21702 USA.
[Fivash, Mathew J.] NCI, Data Management Serv, Frederick, MD 21702 USA.
RP Salnikow, K (reprint author), NCI, Div Canc Biol, Bethesda, MD 20892 USA.
EM salnikok@mail.nih.gov
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; NIH, National Cancer Institute, Center for Cancer
Research
FX This publication has been funded in part with Federal funds from the
National Cancer Institute, National Institutes of Health, under contract
HHSN261200800001E. This research was supported in part by the Intramural
Research Program of the NIH, National Cancer Institute, Center for
Cancer Research. The content of this publication does not necessarily
reflect the views or policies of the Department of Health and Human
Services, nor does mention of trade names, commercial products, or
organizations imply endorsement by the U.S. Government. The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 29
TC 4
Z9 5
U1 1
U2 7
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 2011
VL 257
IS 1
BP 32
EP 37
DI 10.1016/j.taap.2011.08.015
PG 6
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 855YV
UT WOS:000297603100004
PM 21878346
ER
PT J
AU Fabre, KM
Saito, K
DeGraff, W
Sowers, AL
Thetford, A
Cook, JA
Krishna, MC
Mitchell, JB
AF Fabre, Kristin M.
Saito, Keita
DeGraff, William
Sowers, Anastasia L.
Thetford, Angela
Cook, John A.
Krishna, Murali C.
Mitchell, James B.
TI The effects of resveratrol and selected metabolites on the radiation and
antioxidant response
SO CANCER BIOLOGY & THERAPY
LA English
DT Article
DE resveratrol; piceatannol; antioxidants; oxidative stress; peroxide;
ionizing radiation; quinones
ID DOUBLE-STRAND BREAKS; IONIZING-RADIATION; INDUCED APOPTOSIS; CELL LINES;
OXIDATIVE STRESS; MAMMALIAN-CELLS; FREE-RADICALS; CANCER; DAMAGE;
MECHANISMS
AB Excess reactive oxygen species (ROS) generated from ionizing radiation (IR) or endogenous sources like cellular respiration and inflammation produce cytotoxic effects that can lead to carcinogenesis. Resveratrol (RSV), a polyphenol with antioxidant and anticarcinogenic capabilities, has shown promise as a potential radiation modifier. The present study focuses on examining the effects of RSV or RSV metabolites as a radiation modifier in normal tissue. RSV or a RSV metabolite, piceatannol (PIC) did not protect human lung fibroblasts (1522) from the radiation-induced cell killing. Likewise, neither RSV nor PIC afforded protection against lethal total body IR in C3H mice. Additional research has shown protection in cells against hydrogen peroxide when treated with RSV. Therefore, clonogenic survival was measured in 1522 cells with RSV and RSV metabolites. Only the RSV derivative, piceatannol (PIC), showed protection against hydrogen peroxide mediated cytotoxicity; whereas, RSV enhanced hydrogen peroxide sensitivity at a 50 mu M concentration; the remaining metabolites evaluated had little to no effect on survival. PIC also showed enhancement to peroxide exposure at a higher concentration (150 mu M). A potential mechanism for RSV-induced sensitivity to peroxides could be its ability to block 1522 cells in the S-phase, which is most sensitive to hydrogen peroxide treatment. In addition, both RSV and PIC can be oxidized to phenoxyl radicals and quinones, which may exert cytotoxic effects. These cytotoxic effects were abolished when HBED, a metal chelator, was added. Taken together RSV and many of its metabolic derivatives are not effective as chemical radioprotectors and should not be considered for clinical use.
C1 [Fabre, Kristin M.; Saito, Keita; DeGraff, William; Sowers, Anastasia L.; Thetford, Angela; Cook, John A.; Krishna, Murali C.; Mitchell, James B.] NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Fabre, KM (reprint author), NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM fabrek@mail.nih.gov
FU Center of Cancer Research, National Cancer Institute, National
Institutes of Health
FX This research was supported by the Intramural Research Program of the
Center of Cancer Research, National Cancer Institute, National
Institutes of Health.
NR 50
TC 11
Z9 11
U1 0
U2 12
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4047
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD NOV 15
PY 2011
VL 12
IS 10
BP 915
EP 923
DI 10.4161/cbt.12.10.17714
PG 9
WC Oncology
SC Oncology
GA 849ZW
UT WOS:000297165200008
PM 22024758
ER
PT J
AU Jeang, KT
AF Jeang, Kuan-Teh
TI Human T cell leukemia virus type 1 (HTLV-1) latency: Death signaling
awakens the sleeping retrovirus
SO CELL CYCLE
LA English
DT News Item
C1 NIAID, NIH, Bethesda, MD 20892 USA.
RP Jeang, KT (reprint author), NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM kjeang@nih.gov
RI Jeang, Kuan-Teh/A-2424-2008
NR 9
TC 1
Z9 1
U1 0
U2 0
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
J9 CELL CYCLE
JI Cell Cycle
PD NOV 15
PY 2011
VL 10
IS 22
BP 3824
EP 3825
DI 10.4161/cc.10.22.18233
PG 2
WC Cell Biology
SC Cell Biology
GA 850BE
UT WOS:000297168600015
PM 22142857
ER
PT J
AU Kim, YJ
Guzman-Hernandez, ML
Balla, T
AF Kim, Yeun Ju
Guzman-Hernandez, Maria Luisa
Balla, Tamas
TI A Highly Dynamic ER-Derived Phosphatidylinositol-Synthesizing Organelle
Supplies Phosphoinositides to Cellular Membranes
SO DEVELOPMENTAL CELL
LA English
DT Article
ID CDP-DIACYLGLYCEROL SYNTHASE; PROTEIN-KINASE-C; PHOSPHOLIPASE-C;
PLASMA-MEMBRANE; SUBCELLULAR-DISTRIBUTION; ENDOPLASMIC-RETICULUM;
CONTACT SITES; CORTEX SLICES; CELLS; YEAST
AB Polyphosphoinositides are lipid signaling molecules generated from phosphatidylinositol (PtdIns) with critical roles in vesicular trafficking and signaling. It is poorly understood where PtdIns is located within cells and how it moves around between membranes. Here we identify a hitherto-unrecognized highly mobile membrane compartment as the site of Ptdlns synthesis and a likely source of PtdIns of all membranes. We show that the PtdIns-synthesizing enzyme PIS associates with a rapidly moving compartment of ER origin that makes ample contacts with other membranes. In contrast, CDP-diacylglycerol synthases that provide PIS with its substrate reside in the tubular ER. Expression of a PtdIns-specific bacterial PLC generates diacylglycerol also in rapidly moving cytoplasmic objects. We propose a model in which PtdIns is synthesized in a highly mobile lipid distribution platform and is delivered to other membranes during multiple contacts by yet-to-be-defined lipid transfer mechanisms.
C1 [Kim, Yeun Ju; Guzman-Hernandez, Maria Luisa; Balla, Tamas] NICHD, Sect Mol Signal Transduct, Program Dev Neurosci, NIH, Bethesda, MD 20892 USA.
RP Balla, T (reprint author), NICHD, Sect Mol Signal Transduct, Program Dev Neurosci, NIH, Bethesda, MD 20892 USA.
EM ballat@mail.nih.gov
OI Balla, Tamas/0000-0002-9077-3335
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development of the National Institutes of Health
FX Confocal imaging was performed at the Microscopy & Imaging Core of the
National Institute of Child Health and Human Development, National
Institutes of Health with the kind assistance of Drs. Vincent Schram and
James T. Russell. The enthusiastic contribution of Miss Anna
Mezey-Brownstein to this project during her Summer Internship is greatly
appreciated. We are also grateful to Dr. Howard Goldfine (University of
Pennsylvania) for Listens strains. This research was supported by the
Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development of the National
Institutes of Health.
NR 48
TC 64
Z9 65
U1 1
U2 6
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1534-5807
J9 DEV CELL
JI Dev. Cell
PD NOV 15
PY 2011
VL 21
IS 5
BP 813
EP 824
DI 10.1016/j.devce1.2011.09.005
PG 12
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA 850XU
UT WOS:000297233700005
PM 22075145
ER
PT J
AU Mohebtash, M
Tsang, KY
Madan, RA
Huen, NY
Poole, DJ
Jochems, C
Jones, J
Ferrara, T
Heery, CR
Arlen, PM
Steinberg, SM
Pazdur, M
Rauckhorst, M
Jones, EC
Dahut, WL
Schlom, J
Gulley, JL
AF Mohebtash, Mahsa
Tsang, Kwong-Yok
Madan, Ravi A.
Huen, Ngar-Yee
Poole, Diane J.
Jochems, Caroline
Jones, Jacquin
Ferrara, Theresa
Heery, Christopher R.
Arlen, Philip M.
Steinberg, Seth M.
Pazdur, Mary
Rauckhorst, Myrna
Jones, Elizabeth C.
Dahut, William L.
Schlom, Jeffrey
Gulley, James L.
TI A Pilot Study of MUC-1/CEA/TRICOM Poxviral-Based Vaccine in Patients
with Metastatic Breast and Ovarian Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID RESISTANT PROSTATE-CANCER; COLONY-STIMULATING FACTOR; REGULATORY
T-CELLS; ANTIGEN-PRESENTING CELLS; RANDOMIZED PHASE-II;
IMMUNE-RESPONSES; SIPULEUCEL-T; CARCINOEMBRYONIC ANTIGEN; DIVERSIFIED
PRIME; TUMOR-ANTIGEN
AB Purpose: PANVAC is a recombinant poxviral vaccine that contains transgenes for MUC-1, CEA, and 3 T-cell costimulatory molecules. This study was conducted to obtain preliminary evidence of clinical response in metastatic breast and ovarian cancer patients.
Experimental design: Twenty-six patients were enrolled and given monthly vaccinations. Clinical and immune outcomes were evaluated.
Results: These patients were heavily pretreated, with 21 of 26 patients having 3 or more prior chemotherapy regimens. Side effects were largely limited to mild injection-site reactions. For the 12 breast cancer patients enrolled, median time to progression was 2.5 months (1-37+) and median overall survival was 13.7 months. Four patients had stable disease. One patient had a complete response by RECIST and remained on study for 37 months or more, with a significant drop in serum interleukin (IL)-6 and IL-8 by day 71. Another patient with metastatic disease confined to the mediastinum had a 17% reduction in mediastinal mass and was on study for 10 months. Patients with stable or responding disease had fewer prior therapies and lower tumor marker levels than patients with no evidence of response. For the ovarian cancer patients (n = 14), the median time to progression was 2 months (1-6) and median overall survival was 15.0 months. Updated data are presented here for one patient treated with this vaccine in a previous trial, with a time to progression of 38 months.
Conclusions: Some patients who had limited tumor burden with minimal prior chemotherapy seemed to benefit from the vaccine. Further studies to confirm these results are warranted. Clin Cancer Res; 17(22); 7164-73. (C) 2011 AACR.
C1 [Gulley, James L.] NCI, Lab Tumor Immunol & Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Mohebtash, Mahsa; Madan, Ravi A.; Jones, Jacquin; Heery, Christopher R.; Arlen, Philip M.; Dahut, William L.; Gulley, James L.] NCI, Med Oncol Branch, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, Bethesda, MD 20892 USA.
[Jones, Elizabeth C.] NIH, Radiol & Imaging Sci Clin Ctr, Bethesda, MD 20892 USA.
RP Gulley, JL (reprint author), NCI, Lab Tumor Immunol & Biol, Ctr Canc Res, NIH, 10 Ctr Dr,Room 8B09, Bethesda, MD 20892 USA.
EM gulleyj@mail.nih.gov
RI Gulley, James/K-4139-2016
OI Gulley, James/0000-0002-6569-2912
FU Intramural NIH HHS [Z01 BC010666-04]
NR 45
TC 58
Z9 61
U1 1
U2 8
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 15
PY 2011
VL 17
IS 22
BP 7164
EP 7173
DI 10.1158/1078-0432.CCR-11-0649
PG 10
WC Oncology
SC Oncology
GA 849XK
UT WOS:000297158500023
PM 22068656
ER
PT J
AU Bayulkem, K
Lopez, G
AF Bayulkem, Kemal
Lopez, Grisel
TI Clinical approach to nonmotor sensory fluctuations in Parkinson's
disease
SO JOURNAL OF THE NEUROLOGICAL SCIENCES
LA English
DT Article; Proceedings Paper
CT 7th International Congress on Mental Dysfunction and other Non-Motor
Features in Parkinsons Disease and Related Disorders
CY DEC 09-12, 2010
CL Barcelona, SPAIN
DE Parkinson's disease; Nonmotor sensory fluctuations; "On" and "off'
periods
ID RESTLESS LEGS SYNDROME; APOMORPHINE; AKATHISIA; PAIN; SYMPTOMS;
DYSTONIA; LEVODOPA; CHOREA; MOTOR
AB Many nonmotor fluctuations (NMFs) may occur in addition to the classic motor fluctuations (MFs) in patients with Parkinson's disease (PD) within several years of initiation of dopaminergic treatment. Patients can experience these NMFs in the "on" and/or "off' periods. NMFs can be divided into three groups: Autonomic, cognitive/psychiatric, and sensory. Nonmotor sensory fluctuations (NMSFs) occurring in association with "on" period are more frequently recognized than those in the "off' state. NMSFs commonly reported include pain, numbness, paresthesia/dysesthesia, akathisia, rest-legs syndrome (RLS), dyspnea, and internal tremor (IT)
Proposed treatments of NMSFs are based on whether they occur during "off' or "on" state. These include reduction of dopaminergic medication, use of long-acting dopamine agonists or controlled released levodopa (LD), surgical intervention, and/or targeted pharmacological intervention to minimize dopaminergic side effects. NMSFs might be related to dopaminergic mechanisms although difficulty in managing these symptoms with dopaminergic therapy suggests a different pathway. Conclusion: Recognition of NMSFs is important in the care of patients with Parkinson disease to prevent unnecessary interventions and for appropriate medication regimen adjustments. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Bayulkem, Kemal] Natl Inst Neurol Disorders & Stroke, NIH, Bethesda, MD 20892 USA.
[Lopez, Grisel] NHGRI, NIH, Bethesda, MD 20892 USA.
RP Bayulkem, K (reprint author), Natl Inst Neurol Disorders & Stroke, NIH, Bethesda, MD 20892 USA.
EM kemal.bayulkem@gmail.com; glopez@mail.nih.gov
NR 40
TC 14
Z9 15
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0022-510X
J9 J NEUROL SCI
JI J. Neurol. Sci.
PD NOV 15
PY 2011
VL 310
IS 1-2
SI SI
BP 82
EP 85
DI 10.1016/j.jns.2011.07.056
PG 4
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 846UA
UT WOS:000296927500021
PM 21872276
ER
PT J
AU Goldstein, DS
Sewell, L
Sharabi, Y
AF Goldstein, David S.
Sewell, LaToya
Sharabi, Yehonatan
TI Autonomic dysfunction in PD: A window to early detection?
SO JOURNAL OF THE NEUROLOGICAL SCIENCES
LA English
DT Article; Proceedings Paper
CT 7th International Congress on Mental Dysfunction and other Non-Motor
Features in Parkinsons Disease and Related Disorders
CY DEC 09-12, 2010
CL Barcelona, SPAIN
DE Parkinson; Syuclein; Orthostatic hypotension; Autonomic; Sympathetic
ID CARDIAC SYMPATHETIC DENERVATION; MULTIPLE SYSTEM ATROPHY; LEWY BODY
DISEASE; PARKINSONS-DISEASE; ORTHOSTATIC HYPOTENSION; ALPHA-SYNUCLEIN;
DOPAMINE; I-123-MIBG; METABOLITE; OXIDATION
AB It has been suggested that autonomic dysfunction constitutes a biomarker for early detection of the disease process in Parkinson disease (PD). Recent findings based on cardiac sympathetic and striatal dopaminergic imaging in the same patients indicate that this view is overly simple. Although evidence of cardiac sympathetic denervation is associated with other non-motor manifestations such as anosmia, REM behavior disorder, dementia, baroreflex failure, and orthostatic hypotension (OH), across individual patients the severities of OH and of the cardiac sympathetic lesion (indicated by thoracic 6-[(18)F]fluorodopamine PET scanning) are unrelated to the severity of the putamen dopaminergic lesion (indicated by brain 6-[(18)F] fluorodopa PET scanning). Moreover, whereas cases have been reported with neuroimaging evidence of cardiac sympathetic denervation several years before motor onset of PD, in other cases loss of cardiac sympathetic innervation progresses approximately concurrently with the movement disorder or can even occur as a late finding. Bases for independent sympathetic noradrenergic and striatal dopaminergic lesions in Lewy body diseases remain poorly understood. In elderly patients with unexplained OH or other evidence of autonomic failure, it is reasonable for clinicians to look for subtle signs of parkinsonism, such as masked facies, cogwheel rigidity, and shuffling gate. Published by Elsevier B.V.
C1 [Goldstein, David S.; Sewell, LaToya] NINDS, Clin Neurocardiol Sect, NIH, Bethesda, MD 20892 USA.
[Sharabi, Yehonatan] Chaim Sheba Med Ctr, Hypertens Unit, IL-52621 Tel Hashomer, Israel.
RP Goldstein, DS (reprint author), NINDS, Clin Neurocardiol Sect, NIH, 10 Ctr Dr,MSC 1620,Bldg 10,Room 5N220, Bethesda, MD 20892 USA.
EM goldsteind@ninds.nih.gov
FU Intramural NIH HHS
NR 29
TC 22
Z9 22
U1 0
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0022-510X
J9 J NEUROL SCI
JI J. Neurol. Sci.
PD NOV 15
PY 2011
VL 310
IS 1-2
SI SI
BP 118
EP 122
DI 10.1016/j.jns.2011.04.011
PG 5
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 846UA
UT WOS:000296927500028
PM 21529844
ER
PT J
AU Sharabi, Y
Goldstein, DS
AF Sharabi, Yehonatan
Goldstein, David S.
TI Mechanisms of orthostatic hypotension and supine hypertension in
Parkinson disease
SO JOURNAL OF THE NEUROLOGICAL SCIENCES
LA English
DT Article; Proceedings Paper
CT 7th International Congress on Mental Dysfunction and other Non-Motor
Features in Parkinsons Disease and Related Disorders
CY DEC 09-12, 2010
CL Barcelona, SPAIN
DE Parkinson; Supine hypertension; Orthostatic hypotension; Baroreflex;
Blood pressure; Autonomic
ID CARDIAC SYMPATHETIC DENERVATION; BLOOD-PRESSURE VARIABILITY; MULTIPLE
SYSTEM ATROPHY; AUTONOMIC FAILURE; NONMOTOR SYMPTOMS; MANAGEMENT;
ATHEROSCLEROSIS; ABNORMALITIES; DYSAUTONOMIA; MORTALITY
AB Non-motor aspects of Parkinson disease (PD) are now recognized to be important both clinically and scientifically. Among these facets are abnormalities in blood pressure regulation. As much as 40% of PD patients have orthostatic hypotension (OH), which is usually associated with supine hypertension (SH). Symptoms of OH range from light-headedness to falls with serious trauma. SH, while typically asymptomatic, poses a significant increased risk for cardiovascular morbidity and mortality. Neuroimaging, neurochemical, and neuropharmacological studies indicate cardiac and extra-cardiac sympathetic noradrenergic denervation and baroreflex failure in virtually all PD patients with OH, and cardiac sympathetic denervation has been confirmed histopathologically. Mechanisms of SH in PD + OH remain poorly understood. The diurnal blood pressure profile shows increased variability that is correlated with decreased baroreflex gain and with increased morbidity and mortality. Treatment should be individually tailored according to the timing of OH or SH, using primarily short-acting sympathomimetic medications in the daytime for OH and short-acting antihypertensive in the nighttime for SH. Future research is needed to understand better and attenuate blood pressure fluctuations through manipulations that improve baroreflex function. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Sharabi, Yehonatan] Tel Aviv Univ, Hypertens Unit, Sackler Fac Med, Chaim Sheba Med Ctr, IL-52621 Tel Hashomer, Israel.
[Sharabi, Yehonatan; Goldstein, David S.] NINDS, Clin Neurocardiol Sect, NIH, Bethesda, MD 20892 USA.
RP Sharabi, Y (reprint author), Tel Aviv Univ, Hypertens Unit, Sackler Fac Med, Chaim Sheba Med Ctr, IL-52621 Tel Hashomer, Israel.
EM sharabiy@sheba.health.gov.il
FU Intramural NIH HHS [Z01 NS003033-01, Z99 NS999999]
NR 43
TC 30
Z9 35
U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0022-510X
J9 J NEUROL SCI
JI J. Neurol. Sci.
PD NOV 15
PY 2011
VL 310
IS 1-2
SI SI
BP 123
EP 128
DI 10.1016/j.jns.2011.06.047
PG 6
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 846UA
UT WOS:000296927500029
PM 21762927
ER
PT J
AU Hallett, M
AF Hallett, Mark
TI Psychogenic parkinsonism
SO JOURNAL OF THE NEUROLOGICAL SCIENCES
LA English
DT Article; Proceedings Paper
CT 7th International Congress on Mental Dysfunction and other Non-Motor
Features in Parkinsons Disease and Related Disorders
CY DEC 09-12, 2010
CL Barcelona, SPAIN
DE Parkinson's disease; Psychogenic movement disorder; Conversion; Tremor;
Bradykinesia; Rigidity; Gait disorder; DAT scan
ID MOVEMENT-DISORDERS; TREMORS; DISEASE; FREQUENCY
AB Parkinsonism can be psychogenic, and psychogenic parkinsonism is about 10% of psychogenic movement disorder patients. Patients can present with any feature or combination of features of organic Parkinson's disease. There are clinical clues that can lead to the correct diagnosis, and laboratory testing with clinical neurophysiology or DAT (dopamine transporter) scanning can be helpful as well. Patients may have both organic Parkinson's disease and psychogenic parkinsonism, and this might be considered a psychologically induced aggravation of the organic disorder. Published by Elsevier B.V.
C1 NINDS, Human Motor Control Sect, NIH, Bethesda, MD 20892 USA.
RP Hallett, M (reprint author), NINDS, Human Motor Control Sect, NIH, Bldg 10,Rm 7D37,10 Ctr Dr MSC 1428, Bethesda, MD 20892 USA.
EM hallettm@ninds.nih.gov
FU Intramural NIH HHS [ZIA NS002667-26]
NR 19
TC 8
Z9 8
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0022-510X
J9 J NEUROL SCI
JI J. Neurol. Sci.
PD NOV 15
PY 2011
VL 310
IS 1-2
SI SI
BP 163
EP 165
DI 10.1016/j.jns.2011.03.019
PG 3
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 846UA
UT WOS:000296927500036
PM 21458829
ER
PT J
AU Djamshidian, A
Averbeck, BB
Lees, AJ
O'Sullivan, SS
AF Djamshidian, Atbin
Averbeck, Bruno B.
Lees, Andrew J.
O'Sullivan, Sean S.
TI Clinical aspects of impulsive compulsive behaviours in Parkinson's
disease
SO JOURNAL OF THE NEUROLOGICAL SCIENCES
LA English
DT Article; Proceedings Paper
CT 7th International Congress on Mental Dysfunction and Other Non-Motor
Features in Parkinson's Disease and Related Disorders
CY DEC 09-12, 2010
CL Barcelona, SPAIN
DE Parkinson's disease; Impulse control disorders; Impulsive-compulsive
behaviours; Addiction
ID DOPAMINE DYSREGULATION SYNDROME; HEDONISTIC HOMEOSTATIC DYSREGULATION;
SUBTHALAMIC NUCLEUS STIMULATION; IMPAIRED DECISION-MAKING; CONTROL
DISORDERS; SENSATION SEEKING; BASAL GANGLIA; RISK-FACTORS; DRUG-USE;
PREVALENCE
AB Impulsive-compulsive behaviours (ICBs) are an increasingly well-recognised adverse-effect of dopaminergic medications used to treat Parkinson's disease. ICBs include pathological gambling, compulsive sexual behaviour, compulsive buying, and binge eating, together with punding and the addiction-like compulsive use of dopamine replacement therapy, or dopamine dysregulation syndrome. The prevalence of ICBs was approximately 14% in a large study undertaken in specialist movement disorder clinics.
Dopamine dysregulation syndrome is more associated with compulsive L-dopa use, whereas other ICBs are more linked with oral dopamine agonist use. Other mechanisms implicated in the development and perpetuation of ICBs in PD include aberrant learning from reward-related situations, including decreased learning from negative feedback, increased measures of impulsivity or sensation seeking, and strong preference for immediate over future rewards.
Treatment options for impulsive-compulsive behaviours include pharmacological, surgical and psychological interventions. The early recognition and prevention of ICBs, coupled with awareness of clinical risk factors for the development of these behaviours is of paramount importance, given the lack of specific treatments for these sometimes debilitating behaviours. (C) 2011 Elsevier B.V. All rights reserved.
C1 [O'Sullivan, Sean S.] St George Hosp, Movement Disorders Unit, Dept Neurol, London, England.
[Djamshidian, Atbin; Lees, Andrew J.; O'Sullivan, Sean S.] Univ London, Dept Mol Neurosci, London, England.
[Djamshidian, Atbin; Lees, Andrew J.; O'Sullivan, Sean S.] Univ London, Reta Lila Weston Inst Neurol Studies, London, England.
[Averbeck, Bruno B.] UCL, Inst Neurol, Sobell Dept Motor Neurosci & Movement Disorders, London WC1N 3BG, England.
[Averbeck, Bruno B.] NIMH, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA.
RP O'Sullivan, SS (reprint author), St George Hosp, Movement Disorders Unit, Dept Neurol, London, England.
EM seano'sullivan@nhs.net
RI O'Sullivan, Sean/C-9333-2012; Lees, Andrew/A-6605-2009;
OI O'Sullivan, Sean/0000-0002-0583-7956; Djamshidian,
Atbin/0000-0001-7174-6000
FU Intramural NIH HHS
NR 98
TC 22
Z9 23
U1 1
U2 10
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0022-510X
J9 J NEUROL SCI
JI J. Neurol. Sci.
PD NOV 15
PY 2011
VL 310
IS 1-2
SI SI
BP 183
EP 188
DI 10.1016/j.jns.2011.07.031
PG 6
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 846UA
UT WOS:000296927500040
PM 21839478
ER
PT J
AU Gillet, JP
Calcagno, AM
Varma, S
Marino, M
Green, LJ
Vora, MI
Patel, C
Orina, JN
Eliseeva, TA
Singal, V
Padmanabhan, R
Davidson, B
Ganapathi, R
Sood, AK
Rueda, BR
Ambudkar, SV
Gottesman, MM
AF Gillet, Jean-Pierre
Calcagno, Anna Maria
Varma, Sudhir
Marino, Miguel
Green, Lisa J.
Vora, Meena I.
Patel, Chirayu
Orina, Josiah N.
Eliseeva, Tatiana A.
Singal, Vineet
Padmanabhan, Raji
Davidson, Ben
Ganapathi, Ram
Sood, Anil K.
Rueda, Bo R.
Ambudkar, Suresh V.
Gottesman, Michael M.
TI Redefining the relevance of established cancer cell lines to the study
of mechanisms of clinical anti-cancer drug resistance
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE gene signature; NCI-60 panel; translational medicine; gene expression
profiling assay; cell culture model
ID BINDING CASSETTE TRANSPORTERS; OVARIAN-CANCER; MULTIDRUG-RESISTANCE;
GENE-EXPRESSION; CROSS-RESISTANCE; MYELOID-LEUKEMIA; CHEMOTHERAPY;
MICROARRAY; AGENTS; P53
AB Although in vitro models have been a cornerstone of anti-cancer drug development, their direct applicability to clinical cancer research has been uncertain. Using a state-of-the-art Taqman-based quantitative RT-PCR assay, we investigated the multidrug resistance (MDR) transcriptome of six cancer types, in established cancer cell lines (grown in monolayer, 3D scaffold, or in xenograft) and clinical samples, either containing >75% tumor cells or micro-dissected. The MDR transcriptome was determined a priori based on an extensive curation of the literature published during the last three decades, which led to the enumeration of 380 genes. No correlation was found between clinical samples and established cancer cell lines. As expected, we found up-regulation of genes that would facilitate survival across all cultured cancer cell lines evaluated. More troubling, however, were data showing that all of the cell lines, grown either in vitro or in vivo, bear more resemblance to each other, regardless of the tissue of origin, than to the clinical samples they are supposed to model. Although cultured cells can be used to study many aspects of cancer biology and response of cells to drugs, this study emphasizes the necessity for new in vitro cancer models and the use of primary tumor models in which gene expression can be manipulated and small molecules tested in a setting that more closely mimics the in vivo cancer microenvironment so as to avoid radical changes in gene expression profiles brought on by extended periods of cell culture.
C1 [Gillet, Jean-Pierre; Calcagno, Anna Maria; Marino, Miguel; Green, Lisa J.; Patel, Chirayu; Orina, Josiah N.; Eliseeva, Tatiana A.; Singal, Vineet; Padmanabhan, Raji; Ambudkar, Suresh V.; Gottesman, Michael M.] NCI, Cell Biol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Varma, Sudhir] NIAID, Bioinformat & Computat Biosci Branch, Off Cyber Infrastruct & Computat Biol, Off Sci Management & Operat,NIH, Bethesda, MD 20892 USA.
[Vora, Meena I.] Biophase Syst, Fremont, CA 94539 USA.
[Davidson, Ben] Oslo Univ Hosp, Div Pathol, Norwegian Radium Hosp, N-0310 Oslo, Norway.
[Davidson, Ben] Univ Oslo, Fac Med, N-0310 Oslo, Norway.
[Ganapathi, Ram] Cleveland Clin, Taussig Canc Inst, Cleveland, OH 44195 USA.
[Sood, Anil K.] Univ Texas MD Anderson Canc Ctr, Dept Gynecol Oncol, Houston, TX 77030 USA.
[Sood, Anil K.] Univ Texas MD Anderson Canc Ctr, Dept Canc Biol, Houston, TX 77030 USA.
[Sood, Anil K.] Univ Texas MD Anderson Canc Ctr, Ctr RNA Interference & Noncoding RNA, Houston, TX 77030 USA.
[Rueda, Bo R.] Massachusetts Gen Hosp, Vincent Ctr Reprod Biol, Vincent Dept Obstet & Gynecol, Boston, MA 02114 USA.
RP Gottesman, MM (reprint author), NCI, Cell Biol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
EM mgottesman@nih.gov
RI gillet, jean-pierre/A-3714-2012; Calcagno, Anna Maria/A-5617-2012;
Varma, Sudhir/N-8763-2014; 木子, 瑞/N-8882-2015;
OI Varma, Sudhir/0000-0002-4096-4782; Calcagno, Anna
Maria/0000-0002-0804-2753
FU NIH, Center for Cancer Research, NCI
FX We thank the Developmental Therapeutics Program for the total RNA from
the NCI-60 cell panel; George Leiman for editorial assistance; and L.
Stenke, M. Lindberg, M. Bjorkholm, J. Sjoberg, K. Viktorsson, R.
Lewensohn (Karolinska Institutet), S. A. Rosenberg [Tumor Immunology
Section Branch, National Cancer Institute (NCI), National Institutes of
Health (NIH)], T. Waldman (Lombardi Comprehensive Cancer Center,
Georgetown University), C. Harris, A. Schetter (Laboratory of Human
Carcinogenesis, NCI, NIH), J. Keller (Laboratory of Cancer Prevention,
NCI, NIH), P. Liu (Genetics and Molecular Biology Branch, National Human
Genome Research Institute, NIH), L. Wolff (Laboratory of Cellular
Oncology, NCI, NIH), T. Fojo, and L. Mickley Huff (Medical Oncology
Branch, NCI, NIH) for generously providing clinical cancer samples. The
BRB-ArrayTools were developed by Richard Simon and colleagues (Biometric
Research Branch, National Cancer Institute). This research was supported
by the Intramural Research Program of the NIH, Center for Cancer
Research, NCI.
NR 45
TC 112
Z9 115
U1 3
U2 24
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 15
PY 2011
VL 108
IS 46
BP 18708
EP 18713
DI 10.1073/pnas.1111840108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 847XQ
UT WOS:000297008900037
PM 22068913
ER
PT J
AU Matsuda, E
Sugioka-Sugiyama, R
Mizuguchi, T
Mehta, S
Cui, BC
Grewal, SIS
AF Matsuda, Emiko
Sugioka-Sugiyama, Rie
Mizuguchi, Takeshi
Mehta, Sameet
Cui, Bowen
Grewal, Shiv I. S.
TI A homolog of male sex-determining factor SRY cooperates with a
transposon-derived CENP-B protein to control sex-specific directed
recombination
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE development; transposition; directionality; yeast
ID MATING-TYPE INTERCONVERSION; YEAST SCHIZOSACCHAROMYCES-POMBE;
MOBILITY-GROUP BOX; FISSION YEAST; REGULATES DIRECTIONALITY;
HETEROCHROMATIN DOMAIN; TRANSCRIPTION FACTOR; DETERMINING REGION;
GENE-EXPRESSION; CHROMOSOME-III
AB Schizosaccharomyces pombe cells switch mating type by replacing genetic information at the expressed mat1 locus with sequences copied from mat2-P or mat3-M silent donor loci. The choice of donor locus is dictated by cell type, such that mat2 is the preferred donor in M cells and mat3 is the preferred donor in P cells. Donor choice involves a recombination-promoting complex (RPC) containing Swi2 and Swi5. In P cells, the RPC localizes to a specific DNA element located adjacent to mat3, but in M cells it spreads across the silent mating-type region, including mat2-P. This differential distribution of the RPC regulates nonrandom choice of donors. However, cell-type-specific differences in RPC localization are not understood. Here we show that the mat1-M-encoded factor Mc, which shares structural and functional similarities with the male sex-determining factor SRY, is highly enriched at the swi2 and swi5 loci and promotes elevated levels of RPC components. Loss of Mc reduces Swi2 and Swi5 to levels comparable to those in P cells and disrupts RPC spreading across the mat2/3 region. Mc also localizes to loci expressed preferentially in M cells and to retrotransposon LTRs. We demonstrate that Mc localization at LTRs and at swi2 requires Abp1, a homolog of transposon-derived CENP-B protein and that loss of Abp1 impairs Swi2 protein expression and the donor choice mechanism. These results suggest that Mc modulates levels of recombination factors, which is important for mating-type donor selection and for the biased gene conversion observed during meiosis, where M cells serve as preferential donors of genetic information.
C1 [Matsuda, Emiko; Sugioka-Sugiyama, Rie; Mizuguchi, Takeshi; Mehta, Sameet; Cui, Bowen; Grewal, Shiv I. S.] NCI, Lab Biochem & Mol Biol, NIH, Bethesda, MD 20892 USA.
RP Grewal, SIS (reprint author), NCI, Lab Biochem & Mol Biol, NIH, Bethesda, MD 20892 USA.
EM grewals@mail.nih.gov
OI Mehta, Sameet/0000-0002-3029-3217
FU National Institutes of Health, National Cancer Institute, Center for
Cancer Research
FX We thank H. Cam and S. Jia for their helpful contributions. We also
thank M. Lichten, F. Reyes-Turcu, N. Grewal, and K. Zhang for comments
on the manuscript. This research was supported by the Intramural
Research Program of the National Institutes of Health, National Cancer
Institute, Center for Cancer Research.
NR 50
TC 5
Z9 5
U1 0
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 15
PY 2011
VL 108
IS 46
BP 18754
EP 18759
DI 10.1073/pnas.1109988108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 847XQ
UT WOS:000297008900045
PM 22042869
ER
PT J
AU Fernandez-Lima, FA
Post, J
DeBord, JD
Eller, MJ
Verkhoturov, SV
Dela-Negra, S
Woods, AS
Schweikert, EA
AF Fernandez-Lima, Francisco A.
Post, Jeremy
DeBord, John D.
Eller, Michael J.
Verkhoturov, Stanislav V.
Dela-Negra, Serge
Woods, Amina S.
Schweikert, Emile A.
TI Analysis of Native Biological Surfaces Using a 100 kV Massive Gold
Cluster Source
SO ANALYTICAL CHEMISTRY
LA English
DT Article
ID SITU STRUCTURAL-CHARACTERIZATION; SECONDARY-ION EMISSION; BRAIN-TISSUE;
PROJECTILE SIZE; MALDI-MS/MS; SPECTROMETRY; MATRIX; ENERGY; LIPIDS;
NANOPARTICLES
AB In the present work, the advantages of a new, 100 kV platform equipped with a massive gold cluster source for the analysis of native biological surfaces are shown. Inspection of the molecular ion emission as a function of projectile size demonstrates a secondary ion yield increase of similar to 100x for 520 keV Au-400(4+) as compared to 130 keV Au-3(1+) and 43 keV C-60. In particular, yields of tens of percent of molecular ions per projectile impact for the most abundant components can be observed with the 520 keV Au-400(4+) probe. A comparison between 520 keV Au-400(4+) time-of-flight-secondary ion mass spectrometry (TOF-SIMS) and matrix assisted laser desorption ionization-mass spectrometry (MALDI-MS) data showed a similar pattern and similar relative intensities of lipid components across a rat brain sagittal section. The abundant secondary ion yield of analyte-specific ions makes 520 keV Au-400(4+) projectiles an attractive probe for submicrometer molecular mapping of native surfaces.
C1 [Fernandez-Lima, Francisco A.; DeBord, John D.; Eller, Michael J.; Verkhoturov, Stanislav V.; Schweikert, Emile A.] Texas A&M Univ, Dept Chem, College Stn, TX 77843 USA.
[Post, Jeremy; Woods, Amina S.] NIDA IRP, Struct Biol Unit, NIH, Baltimore, MD 21224 USA.
[Dela-Negra, Serge] Inst Phys Nucl Orsay, F-91406 Orsay, France.
RP Schweikert, EA (reprint author), Texas A&M Univ, Dept Chem, 3255 TAMU, College Stn, TX 77842 USA.
EM schweikert@chem.tamu.edu
RI Eller, Michael/M-2223-2014;
OI Eller, Michael/0000-0002-9069-2180; Schweikert,
Emile/0000-0003-3964-7998
FU National Science Foundation [CHE-0750377]; National Institute of Health
[1K99RR030188-01]
FX This work was supported by the National Science Foundation (Grant
CHE-0750377). F.A.F.-L. acknowledges the National Institute of Health
support (Grant No. 1K99RR030188-01)
NR 39
TC 16
Z9 16
U1 0
U2 18
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0003-2700
J9 ANAL CHEM
JI Anal. Chem.
PD NOV 15
PY 2011
VL 83
IS 22
BP 8448
EP 8453
DI 10.1021/ac201481r
PG 6
WC Chemistry, Analytical
SC Chemistry
GA 845NQ
UT WOS:000296830200014
PM 21967684
ER
PT J
AU Taylor, JG
AF Taylor, James G.
TI Therapy-Related Acute Myelogenous Leukemia in a Hydroxyurea-Treated
Patient With Sickle Cell Anemia
SO ANNALS OF INTERNAL MEDICINE
LA English
DT Letter
ID DISEASE
C1 NIH, Bldg 10, Bethesda, MD 20892 USA.
RP Taylor, JG (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
OI Taylor, James/0000-0002-4421-1809
FU Intramural NIH HHS [ZIA HL006012-04]
NR 5
TC 4
Z9 4
U1 0
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 15
PY 2011
VL 155
IS 10
BP 722
EP 724
DI 10.7326/0003-4819-155-10-201111150-00024
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 849EI
UT WOS:000297108000017
PM 22084346
ER
PT J
AU van Eggermond, MCJA
Boom, DR
Klous, P
Schooten, E
Marquez, VE
Wierda, RJ
Holling, TM
van den Eisen, PJ
AF van Eggermond, Marja C. J. A.
Boom, Daniel R.
Klous, Petra
Schooten, Erik
Marquez, Victor E.
Wierda, Rutger J.
Holling, Tjadine M.
van den Eisen, Peter J.
TI Epigenetic regulation of CIITA expression in human T-cells
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Article
DE Class II TransActivator (CIITA); MHC class II (MHC-II); Epigenetic
regulation; T-cells; T-leukemia; T-lymphoma
ID CLASS-II TRANSACTIVATOR; HISTONE LYSINE METHYLATION; BREAST-CANCER
CELLS; GROUP PROTEIN EZH2; IFN-GAMMA; DNA METHYLATION; TRANSCRIPTIONAL
REGULATION; ANTIGEN PRESENTATION; B-LYMPHOCYTES; PROMOTER-III
AB In humans, T-cells accomplish expression of MHC-II molecules through induction of CIITA upon activation. Here we show that CIITA promoter accessibility in T-cells is epigenetically regulated. In unstimulated T-cells, CIITA-PIII chromatin displays relative high levels of repressive histone methylation marks (3Me-K27-H3 and 3Me-K20-H4) and low levels of acetylated histones H3 (Ac-H3) and H4 (Ac-H4). These repressive histone marks are replaced by histone methylation marks associated with transcriptional active genes (3Me-K4-H3) and high levels of Ac-H3 and Ac-H4 in activated T-cells. This is associated with concomitant recruitment of RNA polymerase II. In T-leukemia cells, devoid of CIITA expression, similar repressive histone methylation marks and low levels of acetylated histone H3 correlated with lack of CIITA expression. This in contrast to CIITA expressing T-lymphoma cells, which display high levels of Ac-H3 and 3Me-K4-H3, and relative low levels of the 3Me-K27-H3 and 3Me-K20-H4 marks. Of interest was the observation that the levels of histone acetylation and methylation modifications in histones H3 and H4 were also noted in chromatin of the downstream CIITA-PIV promoter as well as the upstream CIITA-PI and CIITA-PII promoters both in normal T-cells and in malignant T-cells. Together our data show that CIITA chromatin in T-cells expressing CIITA display similar histone acetylation and methylation characteristics associated with an open chromatin structure. The opposite is true for T-cells lacking CIITA expression, which display histone modifications characteristic of condensed chromatin. (C) 2011 Elsevier Inc. All rights reserved.
C1 [van den Eisen, Peter J.] Leiden Univ, Med Ctr, Div Mol Biol, Dept Immunohematol & Blood Transfus, NL-2333 ZA Leiden, Netherlands.
[Marquez, Victor E.] NCI, Med Chem Lab, Ctr Canc Res, Frederick, MD 21701 USA.
[van den Eisen, Peter J.] Vrije Univ Amsterdam, Med Ctr, Dept Pathol, Amsterdam, Netherlands.
RP van den Eisen, PJ (reprint author), Leiden Univ, Med Ctr, Div Mol Biol, Dept Immunohematol & Blood Transfus, Albinusdreef 2, NL-2333 ZA Leiden, Netherlands.
EM pjvdelsen@lumc.nl
RI Wierda, Rutger/C-1031-2009;
OI Van den Elsen, Peter/0000-0002-5196-0082
FU Leiden University Medical Center; Dutch Cancer Society
FX We thank Yi Zhang and Vittorio Sartorelli for advice, Thomas Jenuwein
for the generous gift of the 3Me-K27-H3 antibody and Victor E. Marquez
for the generous gift of zebularine and DZNep. We also thank Sacha B.
Geutskens for critically reading of the manuscript. This research is
supported by grants from the Leiden University Medical Center and the
Dutch Cancer Society.
NR 43
TC 4
Z9 4
U1 0
U2 5
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD NOV 15
PY 2011
VL 82
IS 10
SI SI
BP 1430
EP 1437
DI 10.1016/j.bcp.2011.05.026
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 840BX
UT WOS:000296414400018
PM 21664896
ER
PT J
AU Barbieri, F
Wurth, R
Favoni, RE
Pattarozzi, A
Gatti, M
Ratto, A
Ferrari, A
Bajetto, A
Florio, T
AF Barbieri, Federica
Wuerth, Roberto
Favoni, Roberto E.
Pattarozzi, Alessandra
Gatti, Monica
Ratto, Alessandra
Ferrari, Angelo
Bajetto, Adriana
Florio, Tullio
TI Receptor tyrosine kinase inhibitors and cytotoxic drugs affect pleural
mesothelioma cell proliferation: insight into EGFR and ERK1/2 as
antitumor targets
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Article
DE EGFR; Mesothelioma; Proliferation; Tyrosine-kinase inhibitors
ID GROWTH-FACTOR-RECEPTOR; HUMAN-MALIGNANT MESOTHELIOMA;
SOUTHWEST-ONCOLOGY-GROUP; LUNG-CANCER; PHASE-II; IMATINIB MESYLATE;
EXPRESSION; GEFITINIB; GEMCITABINE; CISPLATIN
AB Malignant pleural mesothelioma (MPM) is an aggressive chemotherapy-resistant cancer. Up-regulation of epidermal growth factor receptor (EGFR) plays an important role in MPM development and EGFR-tyrosine kinase inhibitors (TKIs) may represent novel therapeutic options. We tested the effects of the EGFR TKIs gefitinib and erlotinib and TKIs targeted to other growth factors (VEGFR and PDGFR), in comparison to standard antineoplastic agents, in two human MPM cell lines, IST-Mes2 and ZL55. All drugs showed IC50 values in the micromolar range: TKIs induced cytostatic effects at concentrations up to the IC50, while conventional drug growth-inhibitory activity was mainly cytotoxic. Moreover, the treatment of IST-Mes2 with TKIs (gefitinib and imatinib mesylate) in combination with cisplatin and gemcitabine did not show additivity. Focusing on the molecular mechanisms underlying the antiproliferative and pro-apoptotic effects of EGFR-TKIs, we observed that gefitinib induced the formation and stabilization of inactive EGFR homodimers, even in absence of EGF, as demonstrated by EGFR B-max and number of sites/cell. The analysis of downstream effectors of EGFR signaling demonstrated that EGF-induced proliferation, reverted by gefitinib, involved ERK1/2 activation, independently from Akt pathway. Gefitinib inhibits MPM cell growth and survival, preventing EGF-dependent activation of ERK1/2 pathway by blocking EGFR-TK phosphorylation and stabilizing inactive EGFR dimers. Along with the molecular definition of TKIs pharmacological efficacy in vitro, these results may contribute to delve deep into the promising but still controversial role for targeted and conventional drugs in the therapy of MPM. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Barbieri, Federica; Wuerth, Roberto; Pattarozzi, Alessandra; Gatti, Monica; Bajetto, Adriana; Florio, Tullio] Univ Genoa, Pharmacol Lab, Dept Oncol Biol & Genet, I-16132 Genoa, Italy.
[Favoni, Roberto E.] Natl Canc Inst, Dept Translat Oncol, I-16132 Genoa, Italy.
[Ratto, Alessandra; Ferrari, Angelo] Ist Zooprofilatt Sperimentale Piemonte, I-16129 Genoa, Italy.
RP Florio, T (reprint author), Univ Genoa, Pharmacol Lab, Dept Oncol Biol & Genet, Viale Benedetto XV 2, I-16132 Genoa, Italy.
EM federica.barbieri@unige.it; roberto.wurth@uni-ge.it;
roberto.favoni@istge.it; alpat25@hotmail.com; monica.gatti@unige.it;
cerovec@izsto.it; Angelo.Ferrari@izsto.it; adriana.bajetto@unige.it;
tullio.florio@unige.it
RI Florio, Tullio/A-2211-2012; Barbieri, Federica/L-8753-2015;
OI Florio, Tullio/0000-0002-2394-996X; Barbieri,
Federica/0000-0001-8988-6896; Monica, Gatti/0000-0002-2016-0285; Ratto,
Alessandra/0000-0003-0445-2306
FU Italian Association for Cancer Research [IG9089]
FX This work was supported by grant from the Italian Association for Cancer
Research (2009 AIRC Program no. IG9089) to TF.
NR 44
TC 10
Z9 10
U1 0
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD NOV 15
PY 2011
VL 82
IS 10
SI SI
BP 1467
EP 1477
DI 10.1016/j.bcp.2011.07.073
PG 11
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 840BX
UT WOS:000296414400021
PM 21787763
ER
PT J
AU Shay, JW
Cucinotta, FA
Sulzman, FM
Coleman, CN
Minna, JD
AF Shay, Jerry W.
Cucinotta, Francis A.
Sulzman, Frank M.
Coleman, C. Norman
Minna, John D.
TI From Mice and Men to Earth and Space: Joint NASA-NCI Workshop on Lung
Cancer Risk Resulting from Space and Terrestrial Radiation
SO CANCER RESEARCH
LA English
DT Editorial Material
AB On June 27-28, 2011, scientists from the National Cancer Institute (NCI), NASA, and academia met in Bethesda to discuss major lung cancer issues confronting each organization. For NASA, available data suggest that lung cancer is the largest potential cancer risk from space travel for both men and women and quantitative risk assessment information for mission planning is needed. In space, the radiation risk is from high energy and charge (HZE) nuclei (such as Fe) and high-energy protons from solar flares and not from gamma radiation. In contrast, the NCI is endeavoring to estimate the increased lung cancer risk from the potential widespread implementation of computed tomographic (CT) screening in individuals at high risk for developing lung cancer based on the National Lung Cancer Screening Trial (NLST). For the latter, exposure will be X-rays from CT scans from the screening (which uses "low-dose" CT scans) and also from follow-up scans used to evaluate abnormalities found during initial screening. Topics discussed included the risk of lung cancer arising after HZE particle, proton, and low-dose exposure to Earth's radiation. The workshop examined preclinical models, epidemiology, molecular markers, "omics" technology, radiobiology issues, and lung stem cells that relate to the development of lung cancer. Cancer Res; 71(22); 6926-9. (C)2011 AACR.
C1 [Shay, Jerry W.; Minna, John D.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Cucinotta, Francis A.; Sulzman, Frank M.] NASA, Lyndon B Johnson Space Ctr, Houston, TX 77058 USA.
[Coleman, C. Norman] NCI, Radiat Res Program, Bethesda, MD 20892 USA.
RP Shay, JW (reprint author), Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
EM Jerry.Shay@utsouthwestern.edu
FU NCI NIH HHS [P50 CA070907, T32 CA124334, P50 CA070907-10, T32
CA124334-05]
NR 0
TC 9
Z9 9
U1 0
U2 6
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD NOV 15
PY 2011
VL 71
IS 22
BP 6926
EP 6929
DI 10.1158/0008-5472.CAN-11-2546
PG 4
WC Oncology
SC Oncology
GA 847NS
UT WOS:000296980200003
PM 21900398
ER
PT J
AU Patel, V
Marsh, CA
Dorsam, RT
Mikelis, CM
Masedunskas, A
Amornphimoltham, P
Nathan, CA
Singh, B
Weigert, R
Molinolo, AA
Gutkind, JS
AF Patel, Vyomesh
Marsh, Christina A.
Dorsam, Robert T.
Mikelis, Constantinos M.
Masedunskas, Andrius
Amornphimoltham, Panomwat
Nathan, Cherie Ann
Singh, Bhuvanesh
Weigert, Roberto
Molinolo, Alfredo A.
Gutkind, J. Silvio
TI Decreased Lymphangiogenesis and Lymph Node Metastasis by mTOR Inhibition
in Head and Neck Cancer
SO CANCER RESEARCH
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMA; MAMMALIAN TARGET; GROWTH-FACTOR; TUMOR
LYMPHANGIOGENESIS; MEDICAL PROGRESS; TONGUE CANCER; RAPAMYCIN;
ACTIVATION; CARCINOGENESIS; STATISTICS
AB Despite our improved understanding of cancer, the 5-year survival rate for head and neck squamous cell carcinomas (HNSCC) patients remains relatively unchanged at 50% for the past three decades. HNSCCs often metastasize to locoregional lymph nodes, and lymph node involvement represents one of the most important prognostic factors of poor clinical outcome. Among the multiple dysregulated molecular mechanism in HNSCCs, emerging basic, preclinical, and clinical findings support the importance of the mTOR signaling route in HNSCC progression. Indeed, we observed here that the activation of mTOR is a widespread event in clinical specimens of HNSCCs invading locoregional lymph nodes. We developed an orthotopic model of HNSCC consisting of the implantation of HNSCC cells into the tongues of immunocompromised mice. These orthotopic tumors spontaneously metastasize to the cervical lymph nodes, where the presence of HNSCC cells can be revealed by histologic and immunohistochemical evaluation. Both primary and metastatic experimental HNSCC lesions exhibited elevated mTOR activity. The ability to monitor and quantitate lymph node invasion in this model system enabled us to explore whether the blockade of mTOR could impact HNSCC metastasis. We found that inhibition of mTOR with rapamycin and the rapalog RAD001 diminished lymphangiogenesis in the primary tumors and prevented the dissemination of HNSCC cancer cells to the cervical lymph nodes, thereby prolonging animal survival. These findings may provide a rationale for the future clinical evaluation of mTOR inhibitors, including rapamycin and its analogues, as part of a molecular-targeted metastasis preventive strategy for the treatment of patients with HNSCC. Cancer Res; 71(22); 7103-12. (C)2011 AACR.
C1 [Patel, Vyomesh; Marsh, Christina A.; Dorsam, Robert T.; Mikelis, Constantinos M.; Masedunskas, Andrius; Amornphimoltham, Panomwat; Weigert, Roberto; Molinolo, Alfredo A.; Gutkind, J. Silvio] NIDR, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA.
[Nathan, Cherie Ann] Louisiana State Univ, Hlth Sci Ctr, Dept Otolaryngol Head & Neck Surg, Shreveport, LA 71105 USA.
[Singh, Bhuvanesh] Mem Sloan Kettering Canc Ctr, Lab Epithelial Canc Biol, Head & Neck Serv, New York, NY 10021 USA.
RP Gutkind, JS (reprint author), Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, 30 Convent Dr,Bldg 30,Room 211, Bethesda, MD 20892 USA.
EM sg39v@nih.gov
RI Gutkind, J. Silvio/A-1053-2009;
OI Masedunskas, Andrius/0000-0002-4533-5467
FU National Institute of Dental and Craniofacial Research, NIH
FX This work was supported by the Intramural Program of the National
Institute of Dental and Craniofacial Research, NIH.
NR 42
TC 74
Z9 75
U1 0
U2 11
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD NOV 15
PY 2011
VL 71
IS 22
BP 7103
EP 7112
DI 10.1158/0008-5472.CAN-10-3192
PG 10
WC Oncology
SC Oncology
GA 847NS
UT WOS:000296980200021
PM 21975930
ER
PT J
AU Nakashima, H
Terabe, M
Berzofsky, JA
Husain, SR
Puri, RK
AF Nakashima, Hideyuki
Terabe, Masaki
Berzofsky, Jay A.
Husain, Syed R.
Puri, Raj K.
TI A Novel Combination Immunotherapy for Cancer by IL-13R alpha 2-Targeted
DNA Vaccine and Immunotoxin in Murine Tumor Models
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID MYELOID SUPPRESSOR-CELLS; RECEPTOR-ALPHA CHAIN; INTERLEUKIN-13 RECEPTOR;
PSEUDOMONAS EXOTOXIN; T-CELLS; CHEMOKINE; IMMUNITY; PROTEIN; EXPRESSION;
CARCINOMA
AB Optimum efficacy of therapeutic cancer vaccines may require combinations that generate effective antitumor immune responses, as well as overcome immune evasion and tolerance mechanisms mediated by progressing tumor. Previous studies showed that IL-13R alpha 2, a unique tumor-associated Ag, is a promising target for cancer immunotherapy. A targeted cytotoxin composed of IL-13 and mutated Pseudomonas exotoxin induced specific killing of IL-13Ra2(+) tumor cells. When combined with IL-13R alpha 2 DNA cancer vaccine, surprisingly, it mediated synergistic antitumor effects on tumor growth and metastasis in established murine breast carcinoma and sarcoma tumor models. The mechanism of synergistic activity involved direct killing of tumor cells and cell-mediated immune responses, as well as elimination of myeloid-derived suppressor cells and, consequently, regulatory T cells. These novel results provide a strong rationale for combining immunotoxins with cancer vaccines for the treatment of patients with advanced cancer. The Journal of Immunology, 2011, 187: 4935-4946.
C1 [Nakashima, Hideyuki; Husain, Syed R.; Puri, Raj K.] NIH, Tumor Vaccines & Biotechnol Branch, Div Cellular & Gene Therapies, Ctr Biol Evaluat & Res,US Food & Drug Adm, Bethesda, MD 20892 USA.
[Terabe, Masaki; Berzofsky, Jay A.] NCI, Vaccine Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Puri, RK (reprint author), NIH, Tumor Vaccines & Biotechnol Branch, Div Cellular & Gene Therapies, Ctr Biol Evaluat & Res,US Food & Drug Adm, Bldg 29B,Room 2NN20,29 Lincoln Dr, Bethesda, MD 20892 USA.
EM raj.puri@fda.hhs.gov
FU Intramural NIH HHS [Z99 OD999999]
NR 46
TC 12
Z9 13
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD NOV 15
PY 2011
VL 187
IS 10
BP 4935
EP 4946
DI 10.4049/jimmunol.1102095
PG 12
WC Immunology
SC Immunology
GA 844SJ
UT WOS:000296767300002
PM 22013118
ER
PT J
AU Qi, HY
Daniels, MP
Liu, YQ
Chen, LY
Alsaaty, S
Levine, SJ
Shelhamer, JH
AF Qi, Hai-Yan
Daniels, Mathew P.
Liu, Yueqin
Chen, Li-Yuan
Alsaaty, Sara
Levine, Stewart J.
Shelhamer, James H.
TI A Cytosolic Phospholipase A(2)-Initiated Lipid Mediator Pathway Induces
Autophagy in Macrophages
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID ADAPTIVE IMMUNITY; LEUKOTRIENES; ACTIVATION; A(2); INFLAMMATION;
RECEPTOR; INNATE; ROLES; ATG5; PROSTAGLANDINS
AB Autophagy delivers cytoplasmic constituents to autophagosomes and is involved in innate and adaptive immunity. Cytosolic phospholipase (cPLA(2))-initiated proinflammatory lipid mediator pathways play a critical role in host defense and inflammation. The crosstalk between the two pathways remains unclear. In this study, we report that cPLA(2) and its metabolite lipid mediators induced autophagy in the RAW246.7 macrophage cell line and in primary monocytes. IFN-gamma-triggered autophagy involves activation of cPLA(2). Cysteinyl leukotrienes D-4 and E-4 and PGD(2) also induced these effects. The autophagy is independent of changes in mTOR or autophagic flux. cPLA(2) and lipid mediator-induced autophagy is ATG5 dependent. These data suggest that lipid mediators play a role in the regulation of autophagy, demonstrating a connection between the two seemingly separate innate immune responses, induction of autophagy and lipid mediator generation. The Journal of Immunology, 2011, 187: 5286-5292.
C1 [Qi, Hai-Yan; Liu, Yueqin; Chen, Li-Yuan; Alsaaty, Sara; Shelhamer, James H.] NHLBI, Dept Crit Care Med, Ctr Clin, NIH, Bethesda, MD 20892 USA.
[Daniels, Mathew P.] NHLBI, Electron Microscopy Core Facil, NIH, Bethesda, MD 20892 USA.
[Levine, Stewart J.] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
RP Shelhamer, JH (reprint author), NHLBI, Dept Crit Care Med, Ctr Clin, NIH, Bldg 10,Room 2C145, Bethesda, MD 20892 USA.
EM jshelhamer@nih.gov
FU Clinical Center, National Institutes of Health
FX This work was supported by the intramural research program of the
Clinical Center, National Institutes of Health.
NR 34
TC 7
Z9 9
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD NOV 15
PY 2011
VL 187
IS 10
BP 5286
EP 5292
DI 10.4049/jimmunol.1004004
PG 7
WC Immunology
SC Immunology
GA 844SJ
UT WOS:000296767300037
PM 22003202
ER
PT J
AU Weinberg, CR
Shi, M
Umbach, DM
AF Weinberg, Clarice R.
Shi, Min
Umbach, David M.
TI A Sibling-augmented Case-only Approach for Assessing Multiplicative
Gene-Environment Interactions
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE environment; epidemiologic methods; family; genes; logistic models;
population
ID CASE-PARENT TRIADS; ASSOCIATION; JOINT; POWER
AB Family-based designs protect analyses of genetic effects from bias that is due to population stratification. Investigators have assumed that this robustness extends to assessments of gene-environment interaction. Unfortunately, this assumption fails for the common scenario in which the genotyped variant is related to risk through linkage with a causative allele. Bias also plagues other methods of assessment of gene-environment interaction. When testing against multiplicative joint effects, the case-only design offers excellent power, but it is invalid if genotype and exposure are correlated in the population. The authors describe 4 mechanisms that produce genotype-exposure dependence: exposure-related genetic population stratification, effects of family history on behavior, genotype effects on exposure, and selective attrition. They propose a sibling-augmented case-only (SACO) design that protects against the former 2 mechanisms and is therefore valid for studying young-onset disease in which genotype does not influence exposure. A SACO design allows the ascertainment of genotype and exposure for cases and exposure for 1 or more unaffected siblings selected randomly. Conditional logistic regression permits assessment of exposure effects and gene-environment interactions. Via simulations, the authors compare the likelihood-based inference on interactions using the SACO design with that based on other designs. They also show that robust analyses of interactions using tetrads or disease-discordant sibling pairs are equivalent to analyses using the SACO design.
C1 [Weinberg, Clarice R.; Shi, Min; Umbach, David M.] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
RP Weinberg, CR (reprint author), NIEHS, Biostat Branch, MD A3-03,POB 12233, Res Triangle Pk, NC 27709 USA.
EM weinber2@niehs.nih.gov
FU National Institutes of Health, National Institute of Environmental
Health Sciences [Z01 ES040007, Z01 ES045002]
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Environmental
Health Sciences, under project numbers Z01 ES040007 and Z01 ES045002.
NR 11
TC 3
Z9 3
U1 0
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD NOV 15
PY 2011
VL 174
IS 10
BP 1183
EP 1189
DI 10.1093/aje/kwr231
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 842WK
UT WOS:000296632300010
PM 22021562
ER
PT J
AU Abraham, B
Hicks, W
Jia, YP
Baek, JH
Miller, JL
Alayash, AI
AF Abraham, Bindu
Hicks, Wayne
Jia, Yiping
Baek, Jin Hyen
Miller, Jeffery L.
Alayash, Abdu I.
TI Isolated Hb Providence beta 82Asn and beta 82Asp Fractions Are More
Stable than Native HbA(0) under Oxidative Stress Conditions
SO BIOCHEMISTRY
LA English
DT Article
ID HUMAN HEMOGLOBIN; HYDROGEN-PEROXIDE; BLOOD SUBSTITUTES;
ESCHERICHIA-COLI; OXYGEN-TRANSPORT; NITRIC-OXIDE; MYOGLOBIN; HEME;
BINDING; STABILITY
AB We have previously shown that hydrogen peroxide (H2O2) triggers irreversible oxidation of amino acids exclusive to the beta-chains of purified human hemoglobin (HbAo). However, it is not clear, whether alpha- or beta-subunit Hb variants exhibit different oxidative resistance to H2O2 when compared to their native HbAo. Hb Providence contains two beta-subunit variants with single amino acid mutations at beta Lys82 -> Asp (beta K82D) and at beta Lys82 -> Asn (beta K82N) positions and binds oxygen at lower affinity than wild type HbA. We have separated Hb Providence into its 3 component fractions, and contrasted oxidative reactions of its beta-mutant fractions with HbAo. Relative to HbAo, both beta K82N and beta K82D fractions showed similar autoxidation kinetics and similar initial oxidation reaction rates with H2O2. However, a more profound pattern of changes was seen in HbAo than in the two Providence fractions. The structural changes in HbAo include a collapse of beta-subunits, and alpha-alpha dimer formation in the presence of excess H2O2. Mass spectrometric and amino acid analysis revealed that beta Cys93 and beta Cys112 were oxidized in the HbAo fraction, consistent with oxidative pathways driven by a ferrylHb and its protein radical. These amino acids were oxidized at a lesser extent in beta K82D fraction. While the 3 isolated components of Hb Providence exhibited similar ligand binding and oxidation reaction kinetics, the variant fractions were more effective in consuming H2O2 and safely internalizing radicals through the ferric/ferryl pseudoperoxidase cycle.
C1 [Abraham, Bindu; Hicks, Wayne; Jia, Yiping; Baek, Jin Hyen; Alayash, Abdu I.] US FDA, Lab Biochem & Vasc Biol, Div Hematol, CBER, Bethesda, MD 20892 USA.
[Miller, Jeffery L.] NIDDK, NIH, Bethesda, MD 20892 USA.
RP Alayash, AI (reprint author), US FDA, Lab Biochem & Vasc Biol, Div Hematol, CBER, Bethesda, MD 20892 USA.
EM abdu.alayash@fda.hhs.gov
FU CBER
FX This work was supported in part by CBER Critical Path Research Program.
NR 43
TC 7
Z9 7
U1 0
U2 10
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD NOV 15
PY 2011
VL 50
IS 45
BP 9752
EP 9766
DI 10.1021/bi200876e
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 842KK
UT WOS:000296598100007
PM 21977904
ER
PT J
AU Parvin, MN
Turner, RJ
AF Parvin, Most Nahid
Turner, R. James
TI Identification of Key Residues Involved in the Dimerization of the
Secretory Na+-K+-2Cl(-) Cotransporter NKCC1
SO BIOCHEMISTRY
LA English
DT Article
ID K-CL COTRANSPORTER; CATION-CHLORIDE COTRANSPORTERS; FUNCTIONAL
EXPRESSION; MOLECULAR-CLONING; STRUCTURAL UNIT; ACCUMULATION; HOMODIMER;
DOMAIN
AB The "secretory" Na+-K+-2Cl(-) cotransporter, NKCC1, belongs to the SLC12 gene family of electroneutral cation-chloride cotransporters. A number of these proteins, including NKCC1 itself, exist as homodimers in the membrane, suggesting that this may be a common feature of the SLC12 family. We have previously demonstrated that replacing the C-terminus of NKCC1 with that of its close homologue NKCC2 produced a fully functional chimeric protein that formed homodimers but did not dimerize with NKCC1. Here we employ a novel co-immunoprecipitation assay to study the dimerization interaction of NKCC1 using additional NKCC1/NKCC2 C-terminal chimeras and point mutants. Our results indicate that the substitution of a number of regions of the C-terminus of NKCC1 with the corresponding sequence from NKCC2 results in weakened dimerization with wild-type NKCC1, demonstrating that various residues play a role in this interaction. Most interestingly, however, we find that the replacement of a single NKCC1 residue, G812, with cysteine, the corresponding amino acid in NKCC2, results in a point mutant that displays no significant dimerization with the wild-type protein. In addition to this effect on heterodimer formation, we also find that G812 mutants can nevertheless form homodimers but that this interaction can be weaker than that observed for wild-type NKCC1. We demonstrate that our results are consistent with at least one established mechanism of protein dimer formation, that of "domain swapping", as well as with a recently reported crystal structure of the C-terminus of a bacterial SLC12 homologue.
C1 [Parvin, Most Nahid; Turner, R. James] Natl Inst Dent & Craniofacial Res, Membrane Biol Sect, Mol Physiol & Therapeut Branch, NIH,DHHS, Bethesda, MD 20892 USA.
RP Turner, RJ (reprint author), Natl Inst Dent & Craniofacial Res, Membrane Biol Sect, Mol Physiol & Therapeut Branch, NIH,DHHS, Bethesda, MD 20892 USA.
EM rjturner@nih.gov
FU National Institute of Dental and Craniofacial Research, National
Institutes of Health, Bethesda, MD
FX This research was supported by the Intramural Research Program of the
National Institute of Dental and Craniofacial Research, National
Institutes of Health, Bethesda, MD.
NR 27
TC 4
Z9 4
U1 0
U2 10
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD NOV 15
PY 2011
VL 50
IS 45
BP 9857
EP 9864
DI 10.1021/bi201498y
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 842KK
UT WOS:000296598100017
PM 21970294
ER
PT J
AU Kostova, MB
Myers, CJ
Beck, TN
Plotkin, BJ
Green, JM
Boshoff, HIM
Barry, CE
Deschamps, JR
Konaklieva, MI
AF Kostova, Maya B.
Myers, Carey J.
Beck, Tim N.
Plotkin, Balbina J.
Green, Jacalyn M.
Boshoff, Helena I. M.
Barry, Clifton E., III
Deschamps, Jeffrey R.
Konaklieva, Monika I.
TI C4-Alkylthiols with activity against Moraxella catarrhalis and
Mycobacterium tuberculosis
SO BIOORGANIC & MEDICINAL CHEMISTRY
LA English
DT Article
DE Mycobacterium tuberculosis; Moraxella catarrhalis; beta-Lactams;
Antimicrobial resistance
ID POLYMER-BOUND TRIPHENYLPHOSPHINE; BETA-LACTAM INHIBITORS;
ESCHERICHIA-COLI; HETEROCYCLES; DISULFIDES; GENERATION; PROTEASES;
ALCOHOLS; WATER
AB Antimicrobial resistance represents a global threat to healthcare. The ability to adequately treat infectious diseases is increasingly under siege due to the emergence of drug-resistant microorganisms. New approaches to drug development are especially needed to target organisms that exhibit broad antibiotic resistance due to expression of beta-lactamases which is the most common mechanism by which bacteria become resistant to beta-lactam antibiotics. We designed and synthesized 20 novel monocyclic beta-lactams with alkyl-and aryl-thio moieties at C4, and subsequently tested these for antibacterial activity. These compounds demonstrated intrinsic activity against serine beta-lactamase producing Mycobacterium tuberculosis wild type strain (Mtb) and multiple (n = 6) beta-lactamase producing Moraxella catarrhalis clinical isolates. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Kostova, Maya B.; Myers, Carey J.; Beck, Tim N.; Konaklieva, Monika I.] American Univ, Dept Chem, Washington, DC 20016 USA.
[Plotkin, Balbina J.] Midwestern Univ, Dept Microbiol & Immunol, Downers Grove, IL 60515 USA.
[Green, Jacalyn M.] Midwestern Univ, Dept Biochem, Downers Grove, IL 60515 USA.
[Boshoff, Helena I. M.; Barry, Clifton E., III] NIAID, TB Res Sect, LCID, NIH, Bethesda, MD 20892 USA.
[Deschamps, Jeffrey R.] USN, Res Lab, Washington, DC 20375 USA.
RP Konaklieva, MI (reprint author), American Univ, Dept Chem, Washington, DC 20016 USA.
EM mkonak@american.edu
RI Barry, III, Clifton/H-3839-2012;
OI Deschamps, Jeffrey/0000-0001-5845-0010
FU Research Corporation Cottrell; American University; Department of
Chemistry at American University, Washington, DC; Midwestern University;
NIH, NIAID
FX We express our sincere thanks and appreciation to the donors of The
Research Corporation Cottrell, for the financial support of this
research project. This work was funded in part, by the American
University Research Grant and the Department of Chemistry at American
University, Washington, DC and by Midwestern University. We are grateful
to Joyce Tjhio of Loyola University Stritch School of Medicine for
generously providing us with the Moraxella catarrhalis clinical
isolates. This research was supported in part by the Intramural Research
Program of the NIH, NIAID.
NR 33
TC 7
Z9 7
U1 0
U2 8
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0968-0896
J9 BIOORGAN MED CHEM
JI Bioorg. Med. Chem.
PD NOV 15
PY 2011
VL 19
IS 22
BP 6842
EP 6852
DI 10.1016/j.bmc.2011.09.030
PG 11
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry,
Organic
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 841TI
UT WOS:000296535900034
PM 22014754
ER
PT J
AU Gore, AV
Swift, MR
Cha, YR
Lo, B
McKinney, MC
Li, WL
Castranova, D
Davis, A
Mukouyama, YS
Weinstein, BM
AF Gore, Aniket V.
Swift, Matthew R.
Cha, Young R.
Lo, Brigid
McKinney, Mary C.
Li, Wenling
Castranova, Daniel
Davis, Andrew
Mukouyama, Yoh-suke
Weinstein, Brant M.
TI Rspo1/Wnt signaling promotes angiogenesis via Vegfc/Vegfr3
SO DEVELOPMENT
LA English
DT Article
DE Angiogenesis; Vegfc; Zebrafish
ID ENDOTHELIAL-GROWTH-FACTOR; VASCULAR DEVELOPMENT; DEVELOPING ZEBRAFISH;
MOUSE EMBRYOS; VEGF-C; NEGATIVE REGULATOR; WNT; PATHWAY; CELLS;
MORPHOGENESIS
AB Here, we show that a novel Rspo1-Wnt-Vegfc-Vegfr3 signaling pathway plays an essential role in developmental angiogenesis. A mutation in R-spondin1 (rspo1), a Wnt signaling regulator, was uncovered during a forward-genetic screen for angiogenesis-deficient mutants in the zebrafish. Embryos lacking rspo1 or the proposed rspo1 receptor kremen form primary vessels by vasculogenesis, but are defective in subsequent angiogenesis. Endothelial cell-autonomous inhibition of canonical Wnt signaling also blocks angiogenesis in vivo. The pro-angiogenic effects of Rspo1/Wnt signaling are mediated by Vegfc/Vegfr3(Flt4) signaling. Vegfc expression is dependent on Rspo1 and Wnt, and Vegfc and Vegfr3 are necessary to promote angiogenesis downstream from Rspo1-Wnt. As all of these molecules are expressed by the endothelium during sprouting stages, these results suggest that Rspo1-Wnt-VegfC-Vegfr3 signaling plays a crucial role as an endothelial-autonomous permissive cue for developmental angiogenesis.
C1 [Gore, Aniket V.; Swift, Matthew R.; Cha, Young R.; Lo, Brigid; McKinney, Mary C.; Castranova, Daniel; Davis, Andrew; Weinstein, Brant M.] NICHHD, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
[Li, Wenling; Mukouyama, Yoh-suke] NHLBI, Lab Stem Cell & Neuro Vasc Biol, Genet & Dev Biol Ctr, NIH, Bethesda, MD 20892 USA.
RP Weinstein, BM (reprint author), NICHHD, Program Genom Differentiat, NIH, 6B 3B309, Bethesda, MD 20892 USA.
EM flyingfish2@nih.gov
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [HD001011]; Leducq Foundation
FX This research was supported by the intramural program of the Eunice
Kennedy Shriver National Institute of Child Health and Human Development
[HD001011 to B. W.] and by the Leducq Foundation [to B. W.]. Deposited
in PMC for release after 12 months.
NR 77
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U1 2
U2 10
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0950-1991
J9 DEVELOPMENT
JI Development
PD NOV 15
PY 2011
VL 138
IS 22
BP 4875
EP 4886
DI 10.1242/dev.068460
PG 12
WC Developmental Biology
SC Developmental Biology
GA 842EZ
UT WOS:000296576700007
PM 22007135
ER
PT J
AU Charu, V
Chowell, G
Mejia, LSP
Echevarria-Zuno, S
Borja-Aburto, VH
Simonsen, L
Miller, MA
Viboud, C
AF Charu, Vivek
Chowell, Gerardo
Palacio Mejia, Lina Sofia
Echevarria-Zuno, Santiago
Borja-Aburto, Victor H.
Simonsen, Lone
Miller, Mark A.
Viboud, Cecile
TI Mortality Burden of the A/H1N1 Pandemic in Mexico: A Comparison of
Deaths and Years of Life Lost to Seasonal Influenza
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID RESPIRATORY SYNCYTIAL VIRUS; A H1N1 VIRUS; UNITED-STATES; EXCESS
MORTALITY; AGE DISTRIBUTION; A(H1N1) 2009; IMPACT; HOSPITALIZATIONS;
VACCINATION; INFECTION
AB Background. The mortality burden of the 2009 A/H1N1 influenza pandemic remains controversial, in part because of delays in reporting of vital statistics that are traditionally used to measure influenza-related excess mortality. Here, we compare excess mortality rates and years of life lost (YLL) for pandemic and seasonal influenza in Mexico and evaluate laboratory-confirmed death reports.
Methods. Monthly age-and cause-specific death rates from January 2000 through April 2010 and population-based surveillance of influenza virus activity were used to estimate excess mortality and YLL in Mexico. Age-stratified laboratory-confirmed A/H1N1 death reports were obtained from an active surveillance system covering 40% of the population.
Results. The A/H1N1 pandemic was associated with 11.1 excess all-cause deaths per 100 000 population and 445 000 YLL during the 3 waves of virus activity in Mexico, April-December 2009. The pandemic mortality burden was 0.6-2.6 times that of a typical influenza season and lower than that of the severe 2003-2004 influenza epidemic. Individuals aged 5-19 and 20-59 years were disproportionately affected relative to their experience with seasonal influenza. Laboratory-confirmed deaths captured 1 of 7 pandemic excess deaths overall but only 1 of 41 deaths in persons >60 years of age in 2009. A recrudescence of excess mortality was observed in older persons during winter 2010, in a period when influenza and respiratory syncytial virus cocirculated.
Conclusions. Mexico experienced higher 2009 A/H1N1 pandemic mortality burden than other countries for which estimates are available. Further analyses of detailed vital statistics are required to assess geographical variation in the mortality patterns of this pandemic.
C1 [Charu, Vivek; Chowell, Gerardo; Simonsen, Lone; Miller, Mark A.; Viboud, Cecile] NIH, Div Int Epidemiol & Populat Studies, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Chowell, Gerardo] Arizona State Univ, Sch Human Evolut & Social Change, Tempe, AZ USA.
[Palacio Mejia, Lina Sofia] Ctr Informac Decisiones Salud Publ, Inst Nacl Salud Publ, Cuernavaca, Morelos, Mexico.
[Echevarria-Zuno, Santiago; Borja-Aburto, Victor H.] Inst Mexicano Seguro Social, Mexico City, DF, Mexico.
[Simonsen, Lone] George Washington Univ, Sch Publ Hlth & Hlth Serv, Dept Global Hlth, Washington, DC USA.
RP Viboud, C (reprint author), NIH, Div Int Epidemiol & Populat Studies, Fogarty Int Ctr, 16 Ctr Dr, Bethesda, MD 20892 USA.
EM viboudc@mail.nih.gov
RI Chowell, Gerardo/F-5038-2012; Palacio Mejia, Lina Sofia/C-8725-2014;
OI Chowell, Gerardo/0000-0003-2194-2251; Palacio Mejia, Lina
Sofia/0000-0003-3203-9420; Simonsen, Lone/0000-0003-1535-8526
FU Division of International Epidemiology and Population Studies;
International Influenza Unit; Office of Global Affairs; Department of
Health and Human Services; Department of Homeland Security; Fogarty
International Center; National Institutes of Health
FX This work was supported by 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 International Influenza Unit, Office of Global Affairs,
Department of Health and Human Services, and by the RAPIDD program of
the Science and Technology Directorate, Department of Homeland Security
(to L.S.).
NR 39
TC 47
Z9 47
U1 0
U2 12
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD NOV 15
PY 2011
VL 53
IS 10
BP 985
EP 993
DI 10.1093/cid/cir644
PG 9
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 834CV
UT WOS:000295937100005
PM 21976464
ER
PT J
AU Kapogiannis, BG
Soe, MM
Nesheim, SR
Abrams, EJ
Carter, RJ
Farley, J
Palumbo, P
Koenig, LJ
Bulterys, M
AF Kapogiannis, Bill G.
Soe, Minn M.
Nesheim, Steven R.
Abrams, Elaine J.
Carter, Rosalind J.
Farley, John
Palumbo, Paul
Koenig, Linda J.
Bulterys, Marc
TI Mortality Trends in the US Perinatal AIDS Collaborative Transmission
Study (1986-2004)
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID ACTIVE ANTIRETROVIRAL THERAPY; HIV-INFECTED CHILDREN;
IMMUNODEFICIENCY-VIRUS-INFECTION; DISEASE PROGRESSION; OPPORTUNISTIC
INFECTIONS; HIV-1-INFECTED CHILDREN; PREDICT MORTALITY; VIRAL LOAD;
UNINFECTED CHILDREN; CHANGING PATTERNS
AB Background. Highly active antiretroviral therapy (HAART) has improved human immunodeficiency virus (HIV)-associated morbidity and mortality. The bimodal mortality distribution in HIV-infected children makes it important to evaluate temporal effects of HAART among a birth cohort with long-term, prospective follow-up.
Methods. Perinatal AIDS Collaborative Transmission Study (PACTS)/PACTS-HIV Follow-up of Perinatally Exposed Children (HOPE) study was a Centers for Disease Control and Prevention-sponsored multicenter, prospective birth cohort study of HIV-exposed uninfected and infected infants from 1985 until 2004. Mortality was evaluated for the no/monotherapy, mono-/dual-therapy, and HAART eras, that is, 1 January 1986 through 31 December 1990, from 1 January 1991 through 31 December 1996, and 1 January 1997 through 31 December 2004.
Results. Among 364 HIV-infected children, 56% were female and 69% black non-Hispanic. Of 98 deaths, 79 (81%) and 61 (62%) occurred in children < 3 and < 2 years old, respectively. The median age at death increased significantly across the eras (P < .0001). The average annual mortality rates were 18 (95% confidence interval [CI], 11.6-26.8), 6.9 (95% CI, 5.4-8.8), and 0.8 (95% CI, 0.4-1.5) events per 100 person-years for the no/monotherapy, mono-/dual-therapy and HAART eras, respectively. The corresponding 6-year survival rates for children born in these eras were 57%, 76%, and 91%, respectively (P < .0001). Among children who received HAART in the first 6 months of age, the probability of 6-year survival was 94%. Ten-year survival rates for HAART and non-HAART recipients were 94% and 45% (P < .05). HAART-associated reductions in mortality remained significant after adjustment for confounders (hazard ratio, 0.3; 95% CI, .08-.76). Opportunistic infections (OIs) caused 31.8%, 16.9%, and 9.1% of deaths across the respective eras (P = .051).
Conclusions. A significant decrease in annual mortality and a prolongation in survival were seen in this US perinatal cohort of HIV-infected children. Temporal decreases in OI-associated mortality resulted in relative proportional increases of non-OI-associated deaths.
C1 [Kapogiannis, Bill G.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Ctr Res Mothers & Children, Pediat Adolescent & Maternal AIDS Branch, NIH, Bethesda, MD 20892 USA.
[Kapogiannis, Bill G.; Nesheim, Steven R.] Emory Univ, Sch Med, Dept Pediat, Div Infect Dis, Atlanta, GA USA.
[Kapogiannis, Bill G.] Emory Univ, Sch Med, Dept Med, Atlanta, GA USA.
[Soe, Minn M.; Nesheim, Steven R.; Koenig, Linda J.; Bulterys, Marc] Ctr Dis Control & Prevent, Div HIV AIDS Prevent, Natl Ctr HIV AIDS Viral Hepatitis STD & TB Preven, Atlanta, GA USA.
[Abrams, Elaine J.] Columbia Univ, Dept Pediat, Harlem Hosp Ctr, New York, NY 10027 USA.
[Abrams, Elaine J.; Carter, Rosalind J.] Columbia Univ, Mailman Sch Publ Hlth, ICAP, New York, NY USA.
[Carter, Rosalind J.] Med & Hlth Res Assoc, New York, NY USA.
[Farley, John] Univ Maryland, Dept Pediat, Baltimore, MD 21201 USA.
[Farley, John] US FDA, Ctr Drug Evaluat & Res, Silver Spring, MD USA.
[Palumbo, Paul] Dartmouth Coll, Dept Pediat, Hanover, NH 03755 USA.
[Palumbo, Paul] Univ Med & Dent New Jersey, Dept Pediat, Newark, NJ 07103 USA.
RP Kapogiannis, BG (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Ctr Res Mothers & Children, Pediat Adolescent & Maternal AIDS Branch, NIH, 6100 Execut Blvd,Room 4B11J, Bethesda, MD 20892 USA.
EM kapogiannisb@mail.nih.gov
FU CDC (Medical and Health Research Association of New York City)
[U64/CCU207228]; University of Medicine and Dentistry of New Jersey-New
Jersey Medical School [U64/CCU202219]; University of Maryland School of
Medicine [U64/CCU306825]; Emory University School of Medicine
[U64/CCU404456]
FX PACTS and PACTS-HOPE were funded between 1985 and 2004 by the CDC
through cooperative agreements U64/CCU207228 (Medical and Health
Research Association of New York City), U64/CCU202219 (University of
Medicine and Dentistry of New Jersey-New Jersey Medical School),
U64/CCU306825 (University of Maryland School of Medicine), and
U64/CCU404456 (Emory University School of Medicine).; B. G. K. and S. R.
N. were funded by a grant to Emory University School of Medicine, J. F.
by a grant to the University of Maryland School of Medicine, and P. P.
by a grant to the University of Medicine and Dentistry of New Jersey.
All other authors report no potential conflicts.
NR 66
TC 29
Z9 29
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD NOV 15
PY 2011
VL 53
IS 10
BP 1024
EP 1034
DI 10.1093/cid/cir641
PG 11
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 834CV
UT WOS:000295937100012
PM 22002982
ER
PT J
AU Baysal, BE
McKay, SE
Kim, YJ
Zhang, ZM
Alila, L
Willett-Brozick, JE
Pacak, K
Kim, TH
Shadel, GS
AF Baysal, Bora E.
McKay, Sharen E.
Kim, Yoon Jung
Zhang, Zimei
Alila, Linda
Willett-Brozick, Joan E.
Pacak, Karel
Kim, Tae Hoon
Shadel, Gerald S.
TI Genomic imprinting at a boundary element flanking the SDHD locus
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID MITOCHONDRIAL BIOGENESIS; HEREDITARY PARAGANGLIOMA; NONCODING RNAS;
BINDING SITES; WIDE ANALYSIS; GENE; PHEOCHROMOCYTOMA; METHYLATION;
EXPRESSION; HYPOXIA
AB Germline mutations in SDHD, a mitochondrial complex II (succinate dehydrogenase) subunit gene at chromosome band 11q23, cause highly penetrant paraganglioma (PGL) tumors when transmitted through fathers. In contrast, maternal transmission rarely, if ever, leads to tumor development. The mechanism underlying this unusual monogenic tumor predisposition pattern is poorly understood. Here, we describe identification of imprinted methylation within an alternative promoter for a large intergenic non-coding RNA located at a distant gene desert boundary flanking SDHD. Methylation at this site primarily occurs within two consecutive HpaII restriction enzyme sites in a tissue-specific manner, most commonly in the adrenal gland. Informative fetal tissues and PGL tumors demonstrate maternal allelic hypermethylation. While a strong binding site for the enhancer-blocking protein CTCF within the alternative promoter shows no evidence of methylation, hyper-methylated adrenal tissues show increased binding of the chromatin-looping factor cohesin relative to the hypo-methylated tissues. These results suggest that the differential allelic methylation we observe at this locus is associated with altered chromatin architectures. These results provide molecular evidence for imprinting at a boundary element flanking the SDHD locus and suggest that epigenetic suppression of the maternal allele is the underlying mechanism of the imprinted penetrance of SDHD mutations.
C1 [Baysal, Bora E.; McKay, Sharen E.; Zhang, Zimei; Alila, Linda; Shadel, Gerald S.] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06510 USA.
[Kim, Yoon Jung; Kim, Tae Hoon; Shadel, Gerald S.] Yale Univ, Sch Med, Dept Genet, New Haven, CT 06510 USA.
[Kim, Tae Hoon; Shadel, Gerald S.] Yale Comprehens Canc Ctr, New Haven, CT 06510 USA.
[Willett-Brozick, Joan E.] Univ Pittsburgh, Sch Med, Dept Obstet Gynecol & Reprod Sci, Pittsburgh, PA 15213 USA.
[Pacak, Karel] Eunice Shriver Kennedy Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
RP Baysal, BE (reprint author), Yale Univ, Sch Med, Dept Pathol, 333 Cedar St, New Haven, CT 06510 USA.
EM bora.baysal@roswellpark.org; gerald.shadel@yale.edu
OI Kim, Tae Hoon/0000-0003-3950-7557
FU National Institutes of Health [R01CA11236, R01CA140485]; Chairman's
Challenge Award; Rita Allen Foundation; Sidney Kimmel Foundation; NIH
[R01HL059655]
FX This work is supported by National Institutes of Health (R01CA11236 and
R01CA140485); Chairman's Challenge Award; Rita Allen Foundation; and
Sidney Kimmel Foundation. Portions of this study were also supported by
NIH grant R01HL059655 to G.S.S.
NR 33
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U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD NOV 15
PY 2011
VL 20
IS 22
BP 4452
EP 4461
DI 10.1093/hmg/ddr376
PG 10
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 836IB
UT WOS:000296103800014
PM 21862453
ER
PT J
AU Chen, F
Chen, GK
Millikan, RC
John, EM
Ambrosone, CB
Bernstein, L
Zheng, W
Hu, JJ
Ziegler, RG
Deming, SL
Bandera, EV
Nyante, S
Palmer, JR
Rebbeck, TR
Ingles, SA
Press, MF
Rodriguez-Gil, JL
Chanock, SJ
Le Marchand, L
Kolonel, LN
Henderson, BE
Stram, DO
Haiman, CA
AF Chen, Fang
Chen, Gary K.
Millikan, Robert C.
John, Esther M.
Ambrosone, Christine B.
Bernstein, Leslie
Zheng, Wei
Hu, Jennifer J.
Ziegler, Regina G.
Deming, Sandra L.
Bandera, Elisa V.
Nyante, Sarah
Palmer, Julie R.
Rebbeck, Timothy R.
Ingles, Sue A.
Press, Michael F.
Rodriguez-Gil, Jorge L.
Chanock, Stephen J.
Le Marchand, Loic
Kolonel, Laurence N.
Henderson, Brian E.
Stram, Daniel O.
Haiman, Christopher A.
TI Fine-mapping of breast cancer susceptibility loci characterizes genetic
risk in African Americans
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; COMMON VARIANTS; CONFER SUSCEPTIBILITY; PROTEIN
HZIMP10; MULTIPLE LOCI; 8Q24; POLYMORPHISMS; POPULATION; WOMEN;
EPIDEMIOLOGY
AB Genome-wide association studies (GWAS) have revealed 19 common genetic variants that are associated with breast cancer risk. Testing of the index signals found through GWAS and fine-mapping of each locus in diverse populations will be necessary for characterizing the role of these risk regions in contributing to inherited susceptibility. In this large study of breast cancer in African-American women (3016 cases and 2745 controls), we tested the 19 known risk variants identified by GWAS and replicated associations (P < 0.05) with only 4 variants. Through fine-mapping, we identified markers in four regions that better capture the association with breast cancer risk in African Americans as defined by the index signal (2q35, 5q11, 10q26 and 19p13). We also identified statistically significant associations with markers in four separate regions (8q24, 10q22, 11q13 and 16q12) that are independent of the index signals and may represent putative novel risk variants. In aggregate, the more informative markers found in the study enhance the association of these risk regions with breast cancer in African Americans [per allele odds ratio (OR) 5 1.18, P = 2.8 3 10(-24) versus OR =1.04, P = 6.1 x 10(-5)]. In this detailed analysis of the known breast cancer risk loci, we have validated and improved upon markers of risk that better characterize their association with breast cancer in women of African ancestry.
C1 [Press, Michael F.] Univ So Calif, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
[Press, Michael F.] Univ So Calif, Keck Sch Med, Dept Pathol, Los Angeles, CA 90033 USA.
[Chen, Fang; Chen, Gary K.; Ingles, Sue A.; Henderson, Brian E.; Stram, Daniel O.; Haiman, Christopher A.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Millikan, Robert C.; Nyante, Sarah] Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Epidemiol, Chapel Hill, NC USA.
[Millikan, Robert C.; Nyante, Sarah] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[John, Esther M.] No Calif Canc Ctr, Fremont, CA USA.
[John, Esther M.] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
[John, Esther M.] Stanford Univ, Stanford Canc Ctr, Stanford, CA 94305 USA.
[Ambrosone, Christine B.] Roswell Pk Canc Inst, Dept Canc Prevent & Control, Buffalo, NY 14263 USA.
[Bernstein, Leslie] Beckman Res Inst, Dept Populat Sci, Div Canc Etiol, City Of Hope, CA USA.
[Zheng, Wei; Deming, Sandra L.] Vanderbilt Univ, Sch Med, Vanderbilt Epidemiol Ctr, Div Epidemiol,Dept Med, Nashville, TN 37212 USA.
[Zheng, Wei; Deming, Sandra L.] Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr, Nashville, TN 37212 USA.
[Hu, Jennifer J.; Rodriguez-Gil, Jorge L.] Univ Miami, Miller Sch Med, Sylvester Comprehens Canc Ctr, Miami, FL 33136 USA.
[Hu, Jennifer J.; Rodriguez-Gil, Jorge L.] Univ Miami, Miller Sch Med, Dept Epidemiol & Publ Hlth, Miami, FL 33136 USA.
[Ziegler, Regina G.; Chanock, Stephen J.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Bandera, Elisa V.] Canc Inst New Jersey, New Brunswick, NJ USA.
[Palmer, Julie R.] Boston Univ, Slone Epidemiol Ctr, Boston, MA 02215 USA.
[Rebbeck, Timothy R.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Le Marchand, Loic; Kolonel, Laurence N.] Univ Hawaii, Canc Res Ctr, Program Epidemiol, Honolulu, HI 96813 USA.
RP Haiman, CA (reprint author), Harlyne Norris Res Tower,1450 Biggy St,Room 1504, Los Angeles, CA 90033 USA.
EM haiman@usc.edu
RI Bandera, Elisa/M-4169-2014;
OI Bandera, Elisa/0000-0002-8789-2755; Palmer, Julie/0000-0002-6534-335X
FU Department of Defense Breast Cancer [W81XWH-08-1-0383]; National
Institute of Health [R01-CA132839, R01-CA63464, R37-CA54281]; Norris
Foundation; California Breast Cancer Research Program [15UB-8402];
National Institute for Child Health and Development [NO1-HD-3-3175]; US
Army Medical Research and Material Command (USAMRMC)
[DAMD-17-01-0-0334]; National Institutes of Health [R01-CA100598,
R01-CA77305, U01-CA69417, P50-CA58223, R01-CA100374, R01-CA73629, RFA
CA-95-011]; Breast Cancer Research Foundation; United States Army
Medical Research [DAMD17-96-6071]; Center for Environmental Health and
Susceptibility, National Institute of Environmental Health Sciences,
National Institutes of Health [P30-ES10126]; National Cancer Institute,
National Institutes of Health
FX This work was supported by a Department of Defense Breast Cancer
Research Program Era of Hope Scholar Award to C.A.H. (W81XWH-08-1-0383),
a National Institute of Health grant to C.A.H. (R01-CA132839), the
Norris Foundation, and a grant from the California Breast Cancer
Research Program to D.O.S. (15UB-8402). Each of the participating
studies was supported by the following grants: MEC: by National
Institutes of Health (R01-CA63464 and R37-CA54281); CARE: by National
Institute for Child Health and Development (NO1-HD-3-3175), WCHS: by US
Army Medical Research and Material Command (USAMRMC)
(DAMD-17-01-0-0334); the National Institutes of Health (R01-CA100598);
and the Breast Cancer Research Foundation; SFBCS: by National Institutes
of Health R01-CA77305) and United States Army Medical Research Program
(DAMD17-96-6071); NC-BCFR: by National Institutes of Health
(U01-CA69417); CBCS: by National Institutes of Health Specialized
Program of Research Excellence in Breast Cancer (P50-CA58223) and Center
for Environmental Health and Susceptibility, National Institute of
Environmental Health Sciences, National Institutes of Health
(P30-ES10126); PLCO: by Intramural Research Program, National Cancer
Institute, National Institutes of Health; NBHS: by National Institutes
of Health (R01-CA100374); WFBC: by National Institutes of Health
(R01-CA73629). The Breast Cancer Family Registry (BCFR) was supported by
the National Cancer Institute, National Institutes of Health under (RFA
CA-95-011) and through cooperative agreements with members of the Breast
Cancer Family Registry and Principal Investigators.
NR 55
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PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD NOV 15
PY 2011
VL 20
IS 22
BP 4491
EP 4503
DI 10.1093/hmg/ddr367
PG 13
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 836IB
UT WOS:000296103800017
PM 21852243
ER
PT J
AU Beigi, R
Noguchi, L
Parsons, T
Macio, I
Ayudhya, RPKN
Chen, JM
Hendrix, CW
Masse, B
Valentine, M
Piper, J
Watts, DH
AF Beigi, Richard
Noguchi, Lisa
Parsons, Teresa
Macio, Ingrid
Ayudhya, Ratiya P. Kunjara Na
Chen, Jianmeng
Hendrix, Craig W.
Masse, Benoit
Valentine, Megan
Piper, Jeanna
Watts, D. Heather
TI Pharmacokinetics and Placental Transfer of Single-Dose Tenofovir 1%
Vaginal Gel in Term Pregnancy
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; SAFETY; HIV
AB Tenofovir (TFV) 1% vaginal gel has been found to decrease sexual transmission of human immunodeficiency virus. To initiate investigations during pregnancy, 16 healthy pregnant women scheduled for cesarean delivery received a single application of TFV gel preoperatively. Maternal serum drug concentrations were determined and fetal cord blood, amniotic fluid, placental tissue, and endometrial tissue specimens were collected. The median maternal peak concentration and cord blood TFV concentrations were 4.3 and 1.9 ng/mL, respectively (similar to 100- and 40-fold lower than after TFV oral dosing, respectively). No adverse events were related to the use of TFV gel. These findings support ongoing and future investigations of TFV gel in pregnancy.
C1 [Beigi, Richard; Macio, Ingrid] UPMC, Magee Womens Hosp, Dept OB GYN RS, Div Reprod Infect Dis, Pittsburgh, PA 15213 USA.
[Beigi, Richard; Noguchi, Lisa; Ayudhya, Ratiya P. Kunjara Na] Magee Womens Res Inst, Microbicide Trials Network, Pittsburgh, PA USA.
[Parsons, Teresa; Chen, Jianmeng; Hendrix, Craig W.] Johns Hopkins Univ, Sch Med, Dept Med Clin Pharmacol, Baltimore, MD USA.
[Noguchi, Lisa] Johns Hopkins Univ, Sch Publ Hlth, Baltimore, MD USA.
[Piper, Jeanna] NIAID, Div AIDS, NIH, Bethesda, MD 20892 USA.
[Watts, D. Heather] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Masse, Benoit] Fred Hutchinson Canc Res Ctr, Stat Ctr HIV Res & Prevent SCHARP AIDS15, Seattle, WA 98104 USA.
[Valentine, Megan] FHI, Res Triangle Pk, NC USA.
[Masse, Benoit] Univ Montreal, CHU St Justine Res Ctr, Quebec City, PQ, Canada.
RP Beigi, R (reprint author), UPMC, Magee Womens Hosp, Dept OB GYN RS, Div Reprod Infect Dis, 300 Halket St, Pittsburgh, PA 15213 USA.
EM rbeigi@mail.magee.edu
RI Hendrix, Craig/G-4182-2014;
OI Hendrix, Craig/0000-0002-5696-8665; Masse, Benoit/0000-0002-4944-8098
FU Division of AIDS; US National Institute of Allergy and Infectious
Diseases; US Eunice Kennedy Shriver National Institute of Child Health
and Human Development; National Institute of Mental Health; US National
Institutes of Health [1-U01-AI068633-0]; CONRAD (Arlington, Virginia)
FX This work was supported by the Division of AIDS, US National Institute
of Allergy and Infectious Diseases, the US Eunice Kennedy Shriver
National Institute of Child Health and Human Development, the National
Institute of Mental Health, US National Institutes of Health (grant
1-U01-AI068633-0); and CONRAD (Arlington, Virginia).
NR 15
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U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD NOV 15
PY 2011
VL 204
IS 10
BP 1527
EP 1531
DI 10.1093/infdis/jir562
PG 5
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 834UU
UT WOS:000295990400009
PM 21930612
ER
PT J
AU Baden, LR
Blattner, WA
Morgan, C
Huang, YD
Defawe, OD
Sobieszczyk, ME
Kochar, N
Tomaras, GD
McElrath, MJ
Russell, N
Brandariz, K
Cardinali, M
Graham, BS
Barouch, DH
Dolin, R
AF Baden, Lindsey R.
Blattner, William A.
Morgan, Cecilia
Huang, Yunda
Defawe, Olivier D.
Sobieszczyk, Magdalena E.
Kochar, Nidhi
Tomaras, Georgia D.
McElrath, M. Juliana
Russell, Nina
Brandariz, Kara
Cardinali, Massimo
Graham, Barney S.
Barouch, Dan H.
Dolin, Raphael
CA NIAID HIV Vaccine Trials Network
TI Timing of Plasmid Cytokine (IL-2/Ig) Administration Affects HIV-1
Vaccine Immunogenicity in HIV-Seronegative Subjects
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; T-CELL RESPONSES; DNA CANDIDATE VACCINE;
IMMUNE-RESPONSES; RHESUS-MONKEYS; MEDIATED-IMMUNITY; PHASE-1 SAFETY;
INFECTION; VIREMIA; INTERLEUKIN-2
AB Background. To investigate the potential immunostimulatory effect of interleukin (IL) 2 as a human immunodeficiency virus type 1 (HIV-1) vaccine adjuvant, we conducted a study of a plasmid coding for a fusion protein of IL-2 and immunoglobulin (IL-2/Ig).
Methods. This phase I trial evaluated an HIV-1 DNA vaccine with the plasmid cytokine adjuvant (IL-2/Ig) in 70 HIV-negative adults. Subjects received placebo (group C), adjuvant alone (group A), vaccine alone (group D), increasing doses of adjuvant concurrent with vaccine (groups T1-T4), or adjuvant given 2 days after vaccine (group T5).
Results. No significant differences in adverse events were observed between treatment groups. Cellular immune responses to envelope protein EnvA peptides were detected by interferon (IFN) gamma and IL-2 enzyme-linked immunospot (ELISPOT) assays in 50% and 40% of subjects, respectively, in T4, and in 100% and 80% in T5. The median responses for groups T4 and T5, respectively, were 90 and 193 spot-forming cells (SFCs)/10(6) peripheral blood mononuclear cells (P = .004; T4 vs T5) for the IL-2 ELISPOT assay and 103 and 380 SFCs/10(6) PBMCs (P = .003; T4 vs T5) for the IFN-gamma ELISPOT assay. A trend to more durable cellular immune responses in T5 was observed at 1 year (T5 vs T4/D; P = .07). Higher anti-Env antibody responses were detected with T5 than with T4.
Conclusions. Plasmid IL-2/Ig significantly increased immune responses when administered 2 days after the DNA vaccine, compared with simultaneous administration. These observations have important implications for the development of cytokine augmentation strategies.
C1 [Baden, Lindsey R.] Brigham & Womens Hosp, Div Infect Dis, Dept Med, Boston, MA 02115 USA.
[Brandariz, Kara; Barouch, Dan H.; Dolin, Raphael] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Med, Boston, MA 02215 USA.
[Blattner, William A.] Univ Maryland, Dept Med, Inst Human Virol, Div Epidemiol, Baltimore, MD 21201 USA.
[Cardinali, Massimo] NIAID, Div AIDS, NIH, Bethesda, MD 20892 USA.
[Graham, Barney S.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Morgan, Cecilia; Defawe, Olivier D.; McElrath, M. Juliana] Fred Hutchinson Canc Res Ctr, Vaccine & Infect Dis Div, Seattle, WA 98104 USA.
[Huang, Yunda; Kochar, Nidhi] Fred Hutchinson Canc Res Ctr, Stat Ctr HIV AIDS Res & Prevent SCHARP, Seattle, WA 98104 USA.
[Russell, Nina] Bill & Melinda Gates Fdn, Global Hlth Program, Seattle, WA USA.
[Sobieszczyk, Magdalena E.] Columbia Univ, Med Ctr, New York, NY USA.
[Sobieszczyk, Magdalena E.] Coll Phys & Surg, Div Infect Dis, New York, NY USA.
[Tomaras, Georgia D.] Duke Univ, Sch Med, Human Vaccine Inst, Durham, NC USA.
RP Baden, LR (reprint author), Brigham & Womens Hosp, Div Infect Dis, Dept Med, 15 Francis S,P-BBA4, Boston, MA 02115 USA.
EM lbaden@partners.org
RI Tomaras, Georgia/J-5041-2016
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health
FX This work was funded by the National Institute of Allergy and Infectious
Diseases, National Institutes of Health.
NR 42
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U1 0
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD NOV 15
PY 2011
VL 204
IS 10
BP 1541
EP 1549
DI 10.1093/infdis/jir615
PG 9
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 834UU
UT WOS:000295990400011
PM 21940420
ER
PT J
AU Memoli, MJ
Davis, AS
Proudfoot, K
Chertow, DS
Hrabal, RJ
Bristol, T
Taubenberger, JK
AF Memoli, Matthew J.
Davis, A. Sally
Proudfoot, Kathleen
Chertow, Daniel S.
Hrabal, Rachel J.
Bristol, Tyler
Taubenberger, Jeffery K.
TI Parenteral Peramivir Treatment for Oseltamivir-Resistant 2009 Pandemic
Influenza A H1N1 Viruses Reply
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Letter
ID RAPID SELECTION
C1 [Memoli, Matthew J.; Davis, A. Sally; Proudfoot, Kathleen; Chertow, Daniel S.; Hrabal, Rachel J.; Bristol, Tyler; Taubenberger, Jeffery K.] NIAID, Viral Pathogenesis & Evolut Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Memoli, MJ (reprint author), NIAID, Viral Pathogenesis & Evolut Sect, Infect Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM memolim@niaid.nih.gov
NR 10
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U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD NOV 15
PY 2011
VL 204
IS 10
BP 1642
EP 1643
DI 10.1093/infdis/jir617
PG 2
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 834UU
UT WOS:000295990400023
ER
PT J
AU Cabarcas, SM
Mathews, LA
Farrar, WL
AF Cabarcas, Stephanie M.
Mathews, Lesley A.
Farrar, William L.
TI The cancer stem cell niche-there goes the neighborhood?
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE cancer stem cell; niche; microenvironment; inflammation; hypoxia;
angiogenesis; vascular niche; EMT; tumor dormancy
ID HUMAN EMBRYONIC STEM; EPITHELIAL-MESENCHYMAL TRANSITION;
TUMOR-INITIATING CELLS; SINGLE-MOUSE BLASTOMERES; PATHWAY INHIBITOR
TFPI; TISSUE FACTOR PATHWAY; PROSTATE-CANCER; SELF-RENEWAL; HUMAN
BREAST; ANTICANCER THERAPY
AB The niche is the environment in which stem cells reside and is responsible for the maintenance of unique stem cell properties such as self-renewal and an undifferentiated state. The heterogeneous populations which constitute a niche include both stem cells and surrounding differentiated cells. This network of heterogeneity is responsible for the control of the necessary pathways that function in determining stem cell fate. The concept that cancer stem cells, a subpopulation of cells responsible for tumor initiation and formation, reside in their own unique niche is quickly evolving and it is of importance to understand and identify the processes occurring within this environment. The necessary intrinsic pathways that are utilized by this cancer stem cell population to maintain both self-renewal and the ability to differentiate are believed to be a result of the environment where cancer stem cells reside. The ability of a specific cancer stem cell niche to provide the environment in which this population can flourish is a critical aspect of cancer biology that mandates intense investigation. This review focuses on current evidence demonstrating that homeostatic processes such as inflammation, epithelial to mesenchymal transition, hypoxia and angiogenesis contribute to the maintenance and control of cancer stem cell fate by providing the appropriate signals within the microenvironment. It is necessary to understand the key processes occurring within this highly specialized cancer stem cell niche to identify potential therapeutic targets that can serve as the basis for development of more effective anticancer treatments.
C1 [Cabarcas, Stephanie M.; Mathews, Lesley A.; Farrar, William L.] NIH, Canc Stem Cell Sect, Lab Canc Prevent, Ctr Canc Res, Frederick, MD USA.
RP Farrar, WL (reprint author), NIH, Canc Stem Cell Sect, Lab Canc Prevent, Ctr Canc Res, Frederick, MD USA.
EM wf31i@nih.gov
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; NIH
FX Grant sponsor: National Cancer Institute, National Institutes of Health
(federal funds); Grant number: HHSN261200800001E; Grant sponsor:
Intramural Research Program (NIH)
NR 136
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U1 1
U2 31
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD NOV 15
PY 2011
VL 129
IS 10
BP 2315
EP 2327
DI 10.1002/ijc.26312
PG 13
WC Oncology
SC Oncology
GA 824VT
UT WOS:000295231000003
PM 21792897
ER
PT J
AU Cropp, CD
Simpson, CL
Wahlfors, T
Ha, N
George, A
Jones, MS
Harper, U
Ponciano-Jackson, D
Green, TA
Tammela, TLJ
Bailey-Wilson, J
Schleutker, J
AF Cropp, Cheryl D.
Simpson, Claire L.
Wahlfors, Tiina
Ha, Nati
George, Asha
Jones, MaryPat S.
Harper, Ursula
Ponciano-Jackson, Damaris
Green, Tiffany A.
Tammela, Teuvo L. J.
Bailey-Wilson, Joan
Schleutker, Johanna
TI Genome-wide linkage scan for prostate cancer susceptibility in Finland:
evidence for a novel locus on 2q37.3 and confirmation of signal on
17q21-q22
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE prostate cancer; genome-wide linkage; Finland; 17q; 2q
ID INTERNATIONAL CONSORTIUM; ERROR PROBABILITIES; SUGGESTIVE EVIDENCE;
SEQUENCE VARIANTS; I ERROR; ASSOCIATION; GENE; FAMILIES; DISEQUILIBRIUM;
RISK
AB Genome-wide linkage studies have been used to localize rare and highly penetrant prostate cancer (PRCA) susceptibility genes. Linkage studies performed in different ethnic backgrounds and populations have been somewhat disparate, resulting in multiple, often irreproducible signals because of genetic heterogeneity and high sporadic background of the disease. Our first genome-wide linkage study and subsequent fine-mapping study of Finnish hereditary prostate cancer (HPC) families gave evidence of linkage to one region. Here, we conducted subsequent scans with microsatellites and SNPs in a total of 69 Finnish HPC families. GENEHUNTER-PLUS was used for parametric and nonparametric analyses. Our microsatellite genome-wide linkage study provided evidence of linkage to 17q12-q23, with a heterogeneity LOD (HLOD) score of 3.14 in a total of 54 of the 69 families. Genome-wide SNP analysis of 59 of the 69 families gave a highest HLOD score of 3.40 at 2q37.3 under a dominant high penetrance model. Analyzing all 69 families by combining microsatellite and SNP maps also yielded HLOD scores of > 3.3 in two regions (2q37.3 and 17q12-q21.3). These significant linkage peaks on chromosome 2 and 17 confirm previous linkage evidence of a locus on 17q from other populations and provide a basis for continued research into genetic factors involved in PRCA. Fine-mapping analysis of these regions is ongoing and candidate genes at linked loci are currently under analysis.
C1 [Wahlfors, Tiina; Ha, Nati; Schleutker, Johanna] Univ Tampere, Inst Biomed Technol, Tampere 33014, Finland.
[Cropp, Cheryl D.; Simpson, Claire L.; George, Asha; Green, Tiffany A.; Bailey-Wilson, Joan] NHGRI, Inherited Dis Res Branch, NIH, Baltimore, MD USA.
[Wahlfors, Tiina; Ha, Nati; Schleutker, Johanna] Tampere Univ Hosp, Ctr Lab Med, Tampere, Finland.
[George, Asha] Fox Chase Canc Ctr, Div Populat Sci, Philadelphia, PA 19111 USA.
[Jones, MaryPat S.; Harper, Ursula; Ponciano-Jackson, Damaris] NHGRI, Genom Core Genome Technol Branch, NIH, Rockville, MD USA.
[Green, Tiffany A.] Johns Hopkins Bloomberg Sch Publ, Dept Epidemiol, Baltimore, MD USA.
[Tammela, Teuvo L. J.] Univ Tampere, Tampere Univ Hosp, Dept Urol, Tampere 33014, Finland.
RP Schleutker, J (reprint author), Univ Tampere, Inst Biomed Technol, Biokatu 8, Tampere 33014, Finland.
EM Johanna.Schleutker@uta.fi
OI Simpson, Claire/0000-0003-2244-7690; Bailey-Wilson,
Joan/0000-0002-9153-2920
FU National Human Genome Research Institute, National Institutes of Health,
Academy of Finland [118413, 126714]; Sigrid Juselius Foundation; Finnish
Cancer Organizations, Competitive Research Funding of the Tampere
University Hospital [9K119]; International Consortium for Prostate
Cancer Genetics (ICPCG), Consortium's Data Coordinating Center (DCC),
National Institutes of Health [U01 CA89600]; Center for Inherited
Disease Research (NIH) [N01-HG-65403]
FX Grant sponsor: Intramural Program of the National Human Genome Research
Institute, National Institutes of Health, Academy of Finland; Grant
numbers: 118413, 126714; Grant sponsors: Sigrid Juselius Foundation,
Finnish Cancer Organizations, Competitive Research Funding of the
Tampere University Hospital; Grant number: 9K119; Grant sponsor: The
International Consortium for Prostate Cancer Genetics (ICPCG),
Consortium's Data Coordinating Center (DCC), National Institutes of
Health; Grant number: U01 CA89600; Grant sponsor: Center for Inherited
Disease Research (NIH); Grant number: N01-HG-65403
NR 48
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U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD NOV 15
PY 2011
VL 129
IS 10
BP 2400
EP 2407
DI 10.1002/ijc.25906
PG 8
WC Oncology
SC Oncology
GA 824VT
UT WOS:000295231000011
PM 21207418
ER
PT J
AU Borstnik, U
Miller, BT
Brooks, BR
Janezic, D
AF Borstnik, Urban
Miller, Benjamin T.
Brooks, Bernard R.
Janezic, Dusanka
TI The Distributed Diagonal Force Decomposition Method for Parallelizing
Molecular Dynamics Simulations
SO JOURNAL OF COMPUTATIONAL CHEMISTRY
LA English
DT Article
DE parallelization; parallel methods; force decomposition; parallel
molecular dynamics simulations; dynamic load balancing
ID PAIRWISE PARTICLE INTERACTIONS; ALGORITHM; POTENTIALS; PROTEINS;
PROGRAM; NETWORK
AB Parallelization is an effective way to reduce the computational time needed for molecular dynamics simulations. We describe a new parallelization method, the distributed-diagonal force decomposition method, with which we extend and improve the existing force decomposition methods. Our new method requires less data communication during molecular dynamics simulations than replicated data and current force decomposition methods, increasing the parallel efficiency. It also dynamically load-balances the processors' computational load throughout the simulation. The method is readily implemented in existing molecular dynamics codes and it has been incorporated into the CHARMM program, allowing its immediate use in conjunction with the many molecular dynamics simulation techniques that are already present in the program. We also present the design of the Force Decomposition Machine, a cluster of personal computers and networks that is tailored to running molecular dynamics simulations using the distributed diagonal force decomposition method. The design is expandable and provides various degrees of fault resilience. This approach is easily adaptable to computers with Graphics Processing Units because it is independent of the processor type being used. (C) 2011 Wiley Periodicals, Inc. J Comput Chem 32: 3005-3013, 2011
C1 [Borstnik, Urban; Janezic, Dusanka] Natl Inst Chem, SI-1000 Ljubljana, Slovenia.
[Miller, Benjamin T.; Brooks, Bernard R.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Janezic, Dusanka] Univ Primorska, Fac Math Nat Sci & Informat Technol, SI-6000 Koper, Slovenia.
RP Borstnik, U (reprint author), Natl Inst Chem, Hajdrihova 19, SI-1000 Ljubljana, Slovenia.
EM dusa@cmm.ki.si
OI Miller, Benjamin/0000-0003-1647-0122
FU Slovenian Research Agency [P1-0002]; NIH, NHLBI
FX Contract/grant sponsor: Slovenian Research Agency; Contract/grant
number: P1-0002; Contract/grant sponsor: Intramural Research Program
(NIH, NHLBI)
NR 43
TC 4
Z9 4
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0192-8651
J9 J COMPUT CHEM
JI J. Comput. Chem.
PD NOV 15
PY 2011
VL 32
IS 14
BP 3005
EP 3013
DI 10.1002/jcc.21882
PG 9
WC Chemistry, Multidisciplinary
SC Chemistry
GA 823LE
UT WOS:000295123000007
PM 21793007
ER
PT J
AU Mashalidis, EH
Mukherjee, T
Sledz, P
Matak-Vinkovic, D
Boshoff, H
Abell, C
Barry, CE
AF Mashalidis, Ellene H.
Mukherjee, Tathagata
Sledz, Pawel
Matak-Vinkovic, Dijana
Boshoff, Helena
Abell, Chris
Barry, Clifton E., III
TI Rv2607 from Mycobacterium tuberculosis Is a Pyridoxine 5 '-Phosphate
Oxidase with Unusual Substrate Specificity
SO PLOS ONE
LA English
DT Article
ID BRAIN PYRIDOXINE-5-PHOSPHATE OXIDASE; VITAMIN-B6 BIOSYNTHESIS; GENOME
SEQUENCE; RABBIT LIVER; PURIFICATION; 5-PHOSPHATE; METABOLISM; INSIGHTS;
FMN
AB Despite intensive effort, the majority of the annotated Mycobacterium tuberculosis genome consists of genes encoding proteins of unknown or poorly understood function. For example, there are seven conserved hypothetical proteins annotated as homologs of pyridoxine 5'-phosphate oxidase (PNPOx), an enzyme that oxidizes pyridoxine 59-phosphate (PNP) or pyridoxamine 5'-phosphate (PMP) to form pyridoxal 5'-phosphate (PLP). We have characterized the function of Rv2607 from Mycobacterium tuberculosis H37Rv and shown that it encodes a PNPOx that oxidizes PNP to PLP. The k(cat) and K(M) for this reaction were 0.01 s(-1) and 360 mu M, respectively. Unlike many PNPOx enzymes, Rv2607 does not recognize PMP as a substrate.
C1 [Mashalidis, Ellene H.; Mukherjee, Tathagata; Boshoff, Helena; Barry, Clifton E., III] NIAID, NIH, Bethesda, MD 20892 USA.
[Mashalidis, Ellene H.; Sledz, Pawel; Matak-Vinkovic, Dijana; Abell, Chris] Univ Cambridge, Dept Chem, Cambridge CB2 1EW, England.
RP Mashalidis, EH (reprint author), NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM ca26@cam.ac.uk; clifton_barry@nih.gov
RI Barry, III, Clifton/H-3839-2012
FU National Institute of Allergy and Infectious Disease, National
Institutes of Health
FX This work was funded by the Intramural Research Program of the National
Institute of Allergy and Infectious Disease, National Institutes of
Health. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 26
TC 5
Z9 5
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 14
PY 2011
VL 6
IS 11
AR e27643
DI 10.1371/journal.pone.0027643
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 855HK
UT WOS:000297554300043
PM 22110704
ER
PT J
AU Lin, FR
Niparko, JK
Ferrucci, L
AF Lin, Frank R.
Niparko, John K.
Ferrucci, Luigi
TI Hearing Loss Prevalence in the United States
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Letter
ID IMPAIRMENT; ADULTS
C1 [Lin, Frank R.; Niparko, John K.] Johns Hopkins Sch Med, Dept Otolaryngol & Neck Surg, Baltimore, MD USA.
[Lin, Frank R.] Johns Hopkins Med Inst, Ctr Aging & Hlth, Baltimore, MD 21205 USA.
[Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD 21224 USA.
RP Lin, FR (reprint author), Johns Hopkins Ctr Aging & Hlth, Dept Otolaryngol Head& Neck Surg, 2024 E Monument St,Ste 2-700, Baltimore, MD 21205 USA.
EM flin1@jhmi.edu
FU NIDCD NIH HHS [K23 DC011279, K23DC011279]
NR 8
TC 115
Z9 119
U1 1
U2 16
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9926
J9 ARCH INTERN MED
JI Arch. Intern. Med.
PD NOV 14
PY 2011
VL 171
IS 20
BP 1851
EP 1852
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 848MS
UT WOS:000297056300014
PM 22083573
ER
PT J
AU Ascierto, PA
Marincola, FM
Ribas, A
AF Ascierto, Paolo A.
Marincola, Francesco M.
Ribas, Antoni
TI Anti-CTLA4 monoclonal antibodies: the past and the future in clinical
application
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Editorial Material
ID METASTATIC MELANOMA; PHASE-II; T-CELLS; IPILIMUMAB; TREMELIMUMAB; TRIAL;
COMBINATION; THERAPY; CANCER
AB Recently, two studies using ipilimumab, an anti-CTLA-4 monoclonal antibody (mab) demonstrated improvements in overall survival in the treatment of advanced melanoma. These studies utilized two different schedules of treatment in different patient categories (first and second line of treatment). However, the results were quite similar despite of different dosage used and the combination with dacarbazine in the first line treatment. We reviewed the result of randomized phase II-III clinical studies testing anti-CTLA-4 antibodies (ipilimumab and tremelimumab) for the treatment of melanoma to focus on practical or scientific questions related to the broad utilization of these products in the clinics. These analyses raised some considerations about the future of these compounds, their potential application, dosage, the importance of the schedule (induction/manteinance compared to induction alone) and their role as adjuvants. Anti-CTLA-4 antibody therapy represents the start of a new era in the treatment of advanced melanoma but we are on the steep slope of the learning curve toward the optimization of their utilization either a single agents or in combination.
C1 [Ascierto, Paolo A.] Ist Nazl Tumori Fdn Pascale, Unit Med Oncol & Innovat Therapies, Naples, Italy.
[Marincola, Francesco M.] NIH, IDIS, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Marincola, Francesco M.] NIH, CHI, Bethesda, MD 20892 USA.
[Ribas, Antoni] Univ Calif Los Angeles, Dept Med, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90024 USA.
RP Ascierto, PA (reprint author), Ist Nazl Tumori Fdn Pascale, Unit Med Oncol & Innovat Therapies, Naples, Italy.
EM paolo.ascierto@gmail.com
NR 22
TC 33
Z9 35
U1 5
U2 9
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD NOV 13
PY 2011
VL 9
AR 196
DI 10.1186/1479-5876-9-196
PG 5
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 893GW
UT WOS:000300345300001
PM 22077981
ER
PT J
AU Taiwo, B
Zheng, L
Gallien, S
Matining, RM
Kuritzkes, DR
Wilson, CC
Berzins, BI
Acosta, EP
Bastow, B
Kim, PS
Eron, JJ
AF Taiwo, Babafemi
Zheng, Lu
Gallien, Sebastien
Matining, Roy M.
Kuritzkes, Daniel R.
Wilson, Cara C.
Berzins, Baiba I.
Acosta, Edward P.
Bastow, Barbara
Kim, Peter S.
Eron, Joseph J., Jr.
CA ACTG A5262 Team
TI Efficacy of a nucleoside-sparing regimen of darunavir/ritonavir plus
raltegravir in treatment-naive HIV-1-infected patients (ACTG A5262)
SO AIDS
LA English
DT Article
DE antiretroviral therapy; darunavir; nucleoside sparing; raltegravir
ID ANTIRETROVIRAL DRUG-RESISTANCE; ONCE-DAILY DARUNAVIR/RITONAVIR; HIV-1
VIRAL LOAD; INITIAL TREATMENT; LOPINAVIR/RITONAVIR; INFECTION; SAFETY;
THERAPY; COMBINATION; TENOFOVIR
AB Objective: To explore darunavir/ritonavir (DRV/r) plus raltegravir (RAL) combination therapy in antiretroviral-naive patients.
Design: Phase IIb, single-arm, open-label, multicenter study.
Methods: One hundred and twelve antiretroviral-naive, HIV-1-infected patients received DRV/r 800/100 mg once daily and RAL 400 mg twice daily. Primary endpoint was virologic failure by week 24. Virologic failure was defined as confirmed viral load of 1000 copies/ml or more at week 12, or an increase of more than 0.5 log(10) copies/ml in viral load from week 4 to 12, or a confirmed viral load of more than 50 copies/ml at or after week 24. Protease and integrase genes were sequenced in patients experiencing virologic failure.
Results: Virologic failure rate was 16% [95% confidence interval (CI) 10-24] by week 24 and 26% (95% CI 19-36) by week 48 in an intent-to-treat analysis. Viral load at virologic failure was 51-200 copies/ml in 17/28 failures. Adjusting for age and sex, virologic failure was associated with baseline viral load of more than 100 000 copies/ml [hazard ratio 3.76, 95% CI (1.52-9.31), P = 0.004] and lower CD4 cell count [0.77 per 100 cells/mu l increase (95% CI 0.61-0.98), P - 0.037]. When trough RAL concentrations were included as a time-varying covariate in the analysis, virologic failure remained associated with baseline viral load more than 100 000 copies/ml [hazard ratio = 4.67 (95% CI 1.93-11.25), P < 0.001], whereas RAL level below detection limit in plasma at one or more previous visits was associated with increased hazard [hazard ratio = 3.42 (95% CI 1.41-8.26), P = 0.006]. All five participants with integrase mutations during virologic failure had baseline viral load more than 100 000 copies/ml.
Conclusion: DRV/r plus RAL was effective and well tolerated in most patients, but virologic failure and integrase resistance were common, particularly in patients with baseline viral load more than 100 000 copies/ml. (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins
C1 [Taiwo, Babafemi; Berzins, Baiba I.] Northwestern Univ, Div Infect Dis, Chicago, IL 60611 USA.
[Zheng, Lu; Matining, Roy M.] Harvard Univ, Sch Publ Hlth, Stat Data Anal Ctr, Boston, MA 02115 USA.
[Gallien, Sebastien; Kuritzkes, Daniel R.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Sect Retroviral Therapeut, Boston, MA 02115 USA.
[Wilson, Cara C.] Univ Colorado, Hlth Sci Ctr, Div Infect Dis, Denver, CO USA.
[Acosta, Edward P.] Univ Alabama, Div Clin Pharmacol, Dept Pharmacol & Toxicol, Birmingham, AL 35294 USA.
[Kim, Peter S.] NIAID, Div Aids, NIH, Bethesda, MD 20892 USA.
[Bastow, Barbara] Social & Sci Syst Inc, ACTG Operat Ctr, Silver Spring, MD USA.
[Eron, Joseph J., Jr.] Univ N Carolina, Div Infect Dis, Chapel Hill, NC USA.
RP Taiwo, B (reprint author), Northwestern Univ, Div Infect Dis, Chicago, IL 60611 USA.
EM b-taiwo@northwestern.edu
RI Gallien, Sebastien/F-9930-2015
OI Gallien, Sebastien/0000-0002-8033-0936
FU National Institute of Allergy and Infectious Diseases [U01AI068636,
U01AI68634]; National Institute of Mental Health (NIMH); National
Institute of Dental and Craniofacial Research (NIDCR); National Center
for Research Resources; Tibotec; GlaxoSmithKline; Merck; Northwestern
University [AI069471]; University of California San Diego [AI 69432];
Ohio State University [AI069474]; MetroHealth Medical Center
[AI-069501]; Alabama Therapeutics CRS [U01 AI069452]; University of
Pennsylvania [U01-AI-69467-05, P30-AI-045008-12]; UCSF AIDS CRS [5UO1
AI069502]; Washington University in St. Louis [AI 069495]; Duke
University Medical Center CRS [5U01 AI069484]; University of Cincinnati
[1U01AI069513]; UNC AIDS Clinical Trials Unit UNC AIDS CRS [5-U01
AI069423, UL 1RR 025747, AI50410]; Houston AIDS Research (HART)
[1U01AI069503]; Beth Israel Deaconess (Partners/Harvard) CRS [U01
AI069472-05]; Stanford University AIDS CTU [AI069556]; Georgetown
University [5U01AI069494]; AIDS Care [U01AI069511-02, UL1 RR 024160];
Vanderbilt Therapeutics CRS [AI-069439, RR-024975]; Pittsburgh CRS [1
UO1 AI 069494-01]; Case CRS [AI69501]
FX The project described was supported by Award Number U01AI068636 and
U01AI68634 from the National Institute of Allergy and Infectious
Diseases and supported by the National Institute of Mental Health (NIMH)
and National Institute of Dental and Craniofacial Research (NIDCR). The
content is solely the responsibility of the authors and does not
necessarily represent the official views of the National Institute of
Allergy and Infectious Diseases or the National Institutes of Health.
The project is supported in part by grants funded by the National Center
for Research Resources. The authors would like to thank the study
volunteers. We also thank Merck for providing raltegravir and Tibotec
Therapeutics for providing darunavir.; B.T. has served as an advisor and
received research support and honoraria from Tibotec. E. P. A. has
served as a consultant to Tibotec and Merck. D. R. K. is a consultant to
Merck and has received honoraria and research support from the company.
J.J.E is a consultant to Abbott, GlaxoSmithKline, Merck, ViiV and
Tibotec, and has received research support (to UNC) from GlaxoSmithKline
and Merck.; ACTG site investigators: Karen Coleman and Meredith Rathert
[Northwestern University (Site 2701) CTU Grant AI069471]; Edward
Seefried and Leticia Muttera [University of California San Diego (Site
701) CTU Grant number AI 69432]; Michael F. Para and Heather Harber [The
Ohio State University (Site 2301) CTU Grant AI069474]; Robert Kalayjian
and Ann Marie Anderson [MetroHealth Medical Center (Site 2503) CTU Grant
AI-069501]; Kerry Upton and Jenna White [Alabama Therapeutics CRS (Site
5801) CTU Grant U01 AI069452]; Pablo Tebas and Aleshia Thomas
[University of Pennsylvania (Site 6201) CTU Grant U01-AI-69467-05, CFAR
Grant P30-AI-045008-12]; Annie Luetkemeyer and Jay Dwyer [UCSF AIDS CRS
(Site 801) CTU Grant 5UO1 AI069502]; Mariea Snell and James Conner
[Washington University in St. Louis (Site 2101) CTU Grant AI 069495];
Nathan M. Thielman and Jacquelin Granholm [Duke University Medical
Center CRS (Site 1601) CTU Grant 5U01 AI069484]; Carl J Fichtenbaum and
Eva Moore [University of Cincinnati (Site 2401) CTU Grant 1U01AI069513];
David Currin and Megan Avots [UNC AIDS Clinical Trials Unit UNC AIDS CRS
(Site 3201) CTU Grant 5-U01 AI069423, CTSA Grant UL 1RR 025747, CFAR
Grant AI50410]; Roberto C. Arduino and Maria Laura Martinez [Houston
AIDS Research (HART) (Site 31473) CTU Grant 1U01AI069503]; Mary Albrecht
and Amanda Youmans [Beth Israel Deaconess (Partners/Harvard) CRS (Site
103) CTU Grant U01 AI069472-05]; Debbie Slamowitz and Sandra Valle
[Stanford University AIDS CTU (Site 501) CTU Grant AI069556]; Princy N.
Kumar and Joseph Timpone [Georgetown University (Site 1008) Grant
5U01AI069494]; Christine Hurley and Roberto Corales [AIDS Care (Site
1108) CTU Grant U01AI069511-02 (as of 2/12/08), CTSI Grant UL1 RR
024160]; Vicki Bailey and Husamettin Erdem [Vanderbilt Therapeutics CRS
(Site 3652) CTU Grant AI-069439, Grant RR-024975]; Sharon Riddler and
Sally McNulty [Pittsburgh CRS (Site 1001) CTU Grant 1 UO1 AI 069494-01];
Barbara Philpotts and Dawn Antosh [Case CRS (Site 2501) CTU Grant
AI69501].
NR 30
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U1 0
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0269-9370
J9 AIDS
JI Aids
PD NOV 13
PY 2011
VL 25
IS 17
BP 2113
EP 2122
DI 10.1097/QAD.0b013e32834bbaa9
PG 10
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 841QG
UT WOS:000296526900008
PM 21857490
ER
PT J
AU Jain, M
Zhang, LS
Patterson, EE
Kebebew, E
AF Jain, Meenu
Zhang, Lisa
Patterson, Erin E.
Kebebew, Electron
TI KIAA0101 Is Overexpressed, and Promotes Growth and Invasion in Adrenal
Cancer
SO PLOS ONE
LA English
DT Article
ID PCNA-ASSOCIATED FACTOR; ADRENOCORTICAL TUMORS; HEPATOCELLULAR-CARCINOMA;
EXPRESSION; GENE; MALIGNANCY; P15(PAF); PREDICTS; CELLS
AB Background: KIAA0101 is a proliferating cell nuclear antigen-associated factor that is overexpressed in some human malignancies. Adrenocortical neoplasm is one of the most common human neoplasms for which the molecular causes are poorly understood. Moreover, it is difficult to distinguish between localized benign and malignant adrenocortical tumors. For these reasons, we studied the expression, function and possible mechanism of dysregulation of KIAA0101 in human adrenocortical neoplasm.
Methodology/Principal Findings: KIAA0101 mRNA and protein expression levels were determined in 112 adrenocortical tissue samples (21 normal adrenal cortex, 80 benign adrenocortical tumors, and 11 adrenocortical carcinoma (ACC). SiRNA knockdown was used to determine the functional role of KIAA0101 on cell proliferation, cell cycle, apoptosis, soft agar anchorage independent growth and invasion in the ACC cell line, NCI-H295R. In addition, we explored the mechanism of KIAA0101 dysregulation by examining the mutational status. KIAA0101 mRNA (9.7 fold) and protein expression were significantly higher in ACC (p<0.0001). KIAA0101 had sparse protein expression in only a few normal adrenal cortex samples, which was confined to adrenocortical progenitor cells. KIAA0101 expression levels were 84% accurate for distinguishing between ACC and normal and benign adrenocortical tumor samples. Knockdown of KIAA0101 gene expression significantly decreased anchorage independent growth by 80% and invasion by 60% (p = 0.001; p = 0.006). We found no mutations in KIAA0101 in ACC.
Conclusions/Significance: KIAA0101 is overexpressed in ACC. Our data supports that KIAA0101 is a marker of cellular proliferation, promotes growth and invasion, and is a good diagnostic marker for distinguishing benign from malignant adrenocortical neoplasm.
C1 [Jain, Meenu; Zhang, Lisa; Patterson, Erin E.; Kebebew, Electron] NCI, Endocrine Oncol Sect, Surg Branch, Bethesda, MD 20892 USA.
RP Jain, M (reprint author), NCI, Endocrine Oncol Sect, Surg Branch, Bethesda, MD 20892 USA.
EM kebebewe@mail.nih.gov
FU Center for Cancer Research, National Cancer Institute, National
Institutes of Health
FX This research was supported by the Intramural Research Program, Center
for Cancer Research, National Cancer Institute, National Institutes of
Health. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 30
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Z9 23
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 11
PY 2011
VL 6
IS 11
AR e26866
DI 10.1371/journal.pone.0026866
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 855HG
UT WOS:000297553900012
PM 22096502
ER
PT J
AU Shin, DM
Lee, CH
Morse, HC
AF Shin, Dong-Mi
Lee, Chang-Hoon
Morse, Herbert C., III
TI IRF8 Governs Expression of Genes Involved in Innate and Adaptive
Immunity in Human and Mouse Germinal Center B Cells
SO PLOS ONE
LA English
DT Article
ID SEQUENCE-BINDING-PROTEIN; INTERFERON REGULATORY FACTOR-8; LEUKEMIA-LIKE
SYNDROME; TRANSCRIPTION FACTORS; DENDRITIC CELLS; IN-VIVO; TARGET GENES;
FACTOR PU.1; ACTIVATION; FAMILY
AB IRF8 (Interferon Regulatory Factor 8) is a transcription factor expressed throughout B cell differentiation except for mature plasma cells. Previous studies showed it is part of the transcriptional network governing B cell specification and commitment in the bone marrow, regulates the distribution of mature B cells into the splenic follicular and marginal zone compartments, and is expressed at highest levels in germinal center (GC) B cells. Here, we investigated the transcriptional programs and signaling pathways affected by IRF8 in human and mouse GC B cells as defined by ChIP-chip analyses and transcriptional profiling. We show that IRF8 binds a large number of genes by targeting two distinct motifs, half of which are also targeted by PU.1. Over 70% of the binding sites localized to proximal and distal promoter regions with similar to 25% being intragenic. There was significant enrichment among targeted genes for those involved in innate and adaptive immunity with over 30% previously defined as interferon stimulated genes. We also showed that IRF8 target genes contributes to multiple aspects of the biology of mature B cells including critical components of the molecular crosstalk among GC B cells, T follicular helper cells, and follicular dendritic cells.
C1 [Shin, Dong-Mi; Lee, Chang-Hoon; Morse, Herbert C., III] NIAID, Immunopathol Lab, NIH, Rockville, MD USA.
RP Shin, DM (reprint author), NIAID, Immunopathol Lab, NIH, Rockville, MD USA.
EM hmorse@niaid.nih.gov
OI Morse, Herbert/0000-0002-9331-3705
FU National Institutes of Health (NIH), National Institute of Allergy and
Infectious Diseases
FX This work was supported by the Intramural Research Program of the
National Institutes of Health (NIH), National Institute of Allergy and
Infectious Diseases. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 51
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U1 0
U2 0
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 11
PY 2011
VL 6
IS 11
AR e27384
DI 10.1371/journal.pone.0027384
PG 13
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 855HG
UT WOS:000297553900039
PM 22096565
ER
PT J
AU Sivakumaran, S
Agakov, F
Theodoratou, E
Prendergast, JG
Zgaga, L
Manolio, T
Rudan, I
McKeigue, P
Wilson, JF
Campbell, H
AF Sivakumaran, Shanya
Agakov, Felix
Theodoratou, Evropi
Prendergast, James G.
Zgaga, Lina
Manolio, Teri
Rudan, Igor
McKeigue, Paul
Wilson, James F.
Campbell, Harry
TI Abundant Pleiotropy in Human Complex Diseases and Traits
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; JUVENILE IDIOPATHIC ARTHRITIS;
GENETIC-ANALYSIS; ANGIOTENSIN-II; SCHIZOPHRENIA; CHOLESTEROL; LOCUS;
SCAN; ALLOPURINOL; DEFICIENCY
AB We present a systematic review of pleiotropy among SNPs and genes reported to show genome-wide association with common complex diseases and traits. We find abundant evidence of pleiotropy; 233 (16.9%) genes and 77 (4.6%) SNPs show pleiotropic effects. SNP pleiotropic status was associated with gene location (p = 0.024; pleiotropic SNPs more often exonic 114.5% versus 4.9% for nonpleiotropic, trait-associated SNPs] and less often intergenic [15.8% versus 23.6%]), "predicted transcript consequence" (p = 0.001; pleiotropic SNPs more often predicted to be structurally deleterious [5% versus 0.4%] but not more often in regulatory sequences), and certain disease classes. We develop a method to calculate the likelihood that pleiotropic links between traits occurred more often than expected and demonstrate that this approach can identify etiological links that are already known (such as between fetal hemoglobin and malaria risk) and those that are not yet established (e.g., between plasma campesterol levels and gallstones risk; and between immunoglobulin A and juvenile idiopathic arthritis). Examples of pleiotropy will accumulate over time, but it is already clear that pleiotropy is a common property of genes and SNPs associated with disease traits, and this will have implications for identification of molecular targets for drug development, future genetic risk-profiling, and classification of diseases.
C1 [Sivakumaran, Shanya; Agakov, Felix; Theodoratou, Evropi; Zgaga, Lina; Rudan, Igor; McKeigue, Paul; Wilson, James F.; Campbell, Harry] Univ Edinburgh, Ctr Populat Hlth Sci, Edinburgh EH8 9AG, Midlothian, Scotland.
[Agakov, Felix] Pharmatics Ltd, Edinburgh EH15 3LZ, Midlothian, Scotland.
[Prendergast, James G.] Inst Genet & Mol Med, MRC Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland.
[Zgaga, Lina] Univ Zagreb, Sch Med, Andrija Stampar Sch Publ Hlth, Zagreb 10000, Croatia.
[Manolio, Teri] NHGRI, Off Populat Genom, Bethesda, MD 20892 USA.
RP Campbell, H (reprint author), Univ Edinburgh, Ctr Populat Hlth Sci, Edinburgh EH8 9AG, Midlothian, Scotland.
EM harry.campbell@ed.ac.uk
RI Rudan, Igor/I-1467-2012; Theodoratou, Evropi/C-3430-2014; Wilson, James
F/A-5704-2009;
OI Rudan, Igor/0000-0001-6993-6884; Theodoratou,
Evropi/0000-0001-5887-9132; Wilson, James F/0000-0001-5751-9178; Zgaga,
Lina/0000-0003-4089-9703; Prendergast, James/0000-0001-8916-018X
FU Cancer Research UK [C31250/A10107]
FX E.T. is funded by Cancer Research UK Fellowship C31250/A10107.
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U1 4
U2 33
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD NOV 11
PY 2011
VL 89
IS 5
BP 607
EP 618
DI 10.1016/j.ajhg.2011.10.004
PG 12
WC Genetics & Heredity
SC Genetics & Heredity
GA 848YD
UT WOS:000297090100002
PM 22077970
ER
PT J
AU Ohtani, K
Vlachojannis, GJ
Koyanagi, M
Boeckel, JN
Urbich, C
Farcas, R
Bonig, H
Marquez, VE
Zeiher, AM
Dimmeler, S
AF Ohtani, Kisho
Vlachojannis, Georgios J.
Koyanagi, Masamichi
Boeckel, Jes-Niels
Urbich, Carmen
Farcas, Ruxandra
Bonig, Halvard
Marquez, Victor E.
Zeiher, Andreas M.
Dimmeler, Stefanie
TI Epigenetic Regulation of Endothelial Lineage Committed Genes in
Pro-Angiogenic Hematopoietic and Endothelial Progenitor Cells
SO CIRCULATION RESEARCH
LA English
DT Article
DE Jmjd3; eNOS; hypoxia; proangiogenic cells
ID NITRIC-OXIDE SYNTHASE; DNA METHYLATION; GROWTH-FACTOR; EXPRESSION;
PROMOTER; HYPOXIA; JMJD3; STEM; TRANSCRIPTION; MOBILIZATION
AB Rationale: Proangiogenic hematopoietic and endothelial progenitor cells (EPCs) contribute to postnatal neovascularization, but the mechanisms regulating differentiation to the endothelial lineage are unclear.
Objective: To elucidate the epigenetic control of endothelial gene expression in proangiogenic cells and EPCs.
Methods and Results: Here we demonstrate that the endothelial nitric oxide synthase (eNOS) promoter is epigenetically silenced in proangiogenic cells (early EPCs), CD34(+) cells, and mesoangioblasts by DNA methylation and prominent repressive histone H3K27me3 marks. In order to reverse epigenetic silencing to facilitate endothelial commitment, we used 3-deazaneplanocin A, which inhibits the histone methyltransferase enhancer of zest homolog 2 and, thereby, reduces H3K27me3. 3-Deazaneplanocin A was not sufficient to increase eNOS expression, but the combination of 3-deazaneplanocin A and the histone deacetylase inhibitor Trichostatin A augmented eNOS expression, indicating that the concomitant inhibition of silencing histone modification and enhancement of activating histone modification facilitates eNOS expression. In ischemic tissue, hypoxia plays a role in recruiting progenitor cells. Therefore, we examined the effect of hypoxia on epigenetic modifications. Hypoxia modulated the balance of repressive to active histone marks and increased eNOS mRNA expression. The reduction of repressive H3K27me3 was associated with an increase of the histone demethylase Jmjd3. Silencing of Jmjd3 induced apoptosis and senescence in proangiogenic cells and inhibited hypoxia-mediated up-regulation of eNOS expression in mesoangioblasts.
Conclusions: These findings provide evidence that histone modifications epigenetically control the eNOS promoter in proangiogenic cells. (Circ Res. 2011; 109: 1219-1229.)
C1 [Dimmeler, Stefanie] Goethe Univ Frankfurt, Ctr Mol Med, Inst Cardiovasc Regenerat, D-60590 Frankfurt, Germany.
[Vlachojannis, Georgios J.; Zeiher, Andreas M.] Goethe Univ Frankfurt, Ctr Mol Med, Dept Cardiol, D-60590 Frankfurt, Germany.
[Bonig, Halvard] German Red Cross Blood Serv, Dept Cellular Therapeut Cell Proc, Frankfurt, Germany.
[Marquez, Victor E.] NCI, Biol Chem Lab, Ctr Canc Res, Frederick, MD 21701 USA.
RP Dimmeler, S (reprint author), Goethe Univ Frankfurt, Ctr Mol Med, Inst Cardiovasc Regenerat, Theodor Stern Kai 7, D-60590 Frankfurt, Germany.
EM dimmeler@em.uni-frankfurt.de
OI Bonig, Halvard/0000-0003-0088-2675
FU NIH, National Cancer Institute, Center for Cancer Research; Sankyo
Foundation of Life Science; European Community [LSHM-CT-2005-018630,
8260020]; Excellence Cluster Cardio-Pulmonary System; [SFB834]; [B4]
FX We thank Britta Kluge, Ariane Fischer, and Marion Muhly-Reinholz
(Institute of Cardiovascular Regeneration, Centre for Molecular
Medicine, University of Frankfurt, Germany) for their excellent
technical assistance and Dr Ulrike Koehl (Pediatric Hematology and
Oncology, University Hospital Frankfurt, Frankfurt, Germany) who
generously provided immunomagnetically selected CD34+ cells.
This research was supported in part by the Intramural Research Program
of the NIH, National Cancer Institute, Center for Cancer Research.; This
work is supported by the Sankyo Foundation of Life Science (to K.O.) and
the European Community's Sixth Framework Programme contract
("HeartRepair") LSHM-CT-2005-018630, and Angioscaff (8260020). Stefanie
Dimmeler is supported by the Excellence Cluster Cardio-Pulmonary System
and the SFB834 (project B4). This research was supported in part by the
Intramural Research Program of the National Institutes of Health, Center
for Cancer Research, National Cancer Institute.
NR 35
TC 47
Z9 51
U1 0
U2 13
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7330
J9 CIRC RES
JI Circ.Res.
PD NOV 11
PY 2011
VL 109
IS 11
BP 1219
EP U71
DI 10.1161/CIRCRESAHA.111.247304
PG 20
WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Hematology
GA 846BM
UT WOS:000296872200009
PM 21980126
ER
PT J
AU Kane, LA
Youle, RJ
AF Kane, Lesley A.
Youle, Richard J.
TI PINK1 and Parkin Flag Miro to Direct Mitochondrial Traffic
SO CELL
LA English
DT Editorial Material
ID GTPASE
AB The Parkinson's disease proteins PINK1 and Parkin are proposed guardians of mitochondrial fidelity, targeting damaged mitochondria for degradation by mitophagy. In this issue of Cell, Wang et al. (2011) now show that PINK1 and Parkin also regulate mitochondrial trafficking and quarantine damaged mitochondria by severing their connection to the microtubule network.
C1 [Kane, Lesley A.; Youle, Richard J.] NINDS, NIH, Bethesda, MD 20892 USA.
RP Youle, RJ (reprint author), NINDS, NIH, Bethesda, MD 20892 USA.
EM youle@helix.nih.gov
NR 9
TC 11
Z9 11
U1 1
U2 14
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD NOV 11
PY 2011
VL 147
IS 4
BP 721
EP 723
DI 10.1016/j.cell.2011.10.028
PG 4
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 846LM
UT WOS:000296902300007
PM 22078873
ER
PT J
AU Yen, JH
Kocieda, VP
Jing, HE
Ganea, D
AF Yen, Jui-Hung
Kocieda, Virginia P.
Jing, Huie
Ganea, Doina
TI Prostaglandin E2 Induces Matrix Metalloproteinase 9 Expression in
Dendritic Cells through Two Independent Signaling Pathways Leading to
Activator Protein 1 (AP-1) Activation
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID NECROSIS-FACTOR-ALPHA; IV COLLAGENASE GENE; FACTOR-KAPPA-B; MATRIX
METALLOPROTEINASES; MMP-9 EXPRESSION; UP-REGULATION; TRANSCRIPTIONAL
ACTIVITY; PROSTANOID RECEPTORS; REGULATED KINASES; LANGERHANS CELLS
AB Dendritic Cells (DCs) play an important role in the initiation of the immune response by migrating to regional lymph nodes and presenting antigen processed at the inflammatory site to antigen-specific naive T cells. Prostaglandin E2 (PGE2) has been reported to play an essential role in DC migration. We reported previously that PGE2 induces matrix metalloproteinase 9 (MMP-9) expression in DCs and that PGE2-induced MMP-9 is required for DC migration in vivo and in vitro. In this study, we investigated the signaling mechanisms involved in PGE2-induced MMP-9 expression in DCs. We show that PGE2-induced MMP-9 expression is mediated primarily through the EP2/EP4 -> cAMP -> protein kinase A (PKA)/PI3K -> ERK signaling pathway, leading to c-Fos expression, and through JNK-mediated activation of c-Jun in a PKA/PI3K/ERK-independent manner. EP2 and EP4 receptor agonists, as well as cAMP analogs, mimic the up-regulation of MMP-9 by PGE2. PKA, PI3K, and ERK inhibitors abolished PGE2- and cAMP-induced c-Fos and MMP-9 up-regulation, and ERK activation was required for the binding of activator protein 1 (AP-1) transcription factor to the MMP-9 promoter. Our results describe a new molecular mechanism for the effect of PGE2 on MMP-9 production in DCs that could lead to future therapeutic approaches using ERK inhibitors to regulate DC migration.
C1 [Yen, Jui-Hung; Kocieda, Virginia P.; Ganea, Doina] Temple Univ, Sch Med, Dept Microbiol & Immunol, Philadelphia, PA 19140 USA.
[Jing, Huie] NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA.
RP Yen, JH (reprint author), Temple Univ, Sch Med, Dept Microbiol & Immunol, Philadelphia, PA 19140 USA.
EM doina.ganea@temple.edu
NR 49
TC 39
Z9 40
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
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 11
PY 2011
VL 286
IS 45
BP 38913
EP 38923
DI 10.1074/jbc.M111.252932
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 844PO
UT WOS:000296759800010
PM 21940623
ER
PT J
AU Logue, JS
Whiting, JL
Tunquist, B
Sacks, DB
Langeberg, LK
Wordeman, L
Scott, JD
AF Logue, Jeremy S.
Whiting, Jennifer L.
Tunquist, Brian
Sacks, David B.
Langeberg, Lorene K.
Wordeman, Linda
Scott, John D.
TI AKAP220 Protein Organizes Signaling Elements That Impact Cell Migration
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID KINASE ANCHORING PROTEIN; DYNAMIC INSTABILITY; EPITHELIAL-CELLS;
IN-VIVO; MICROTUBULE; IQGAP1; ASSOCIATION; ADHESION; GROWTH;
PHOSPHORYLATION
AB Cell movement requires the coordinated reception, integration, and processing of intracellular signals. We have discovered that the protein kinase A anchoring protein AKAP220 interacts with the cytoskeletal scaffolding protein IQGAP1 to influence cell motility. AKAP220/IQGAP1 networks receive and integrate calcium and cAMP second messenger signals and position signaling enzymes near their intended substrates at leading edges of migrating cells. IQGAP1 supports calcium/calmodulin-dependent association of factors that modulate microtubule dynamics. AKAP220 suppresses GSK-3 beta and positions this kinase to allow recruitment of the plus-end microtubule tracking protein CLASP2. Gene silencing of AKAP220 alters the rate of microtubule polymerization and the lateral tracking of growing microtubules and retards cell migration in metastatic human cancer cells. This reveals an unappreciated role for this anchored kinase/microtubule effector protein network in the propagation of cell motility.
C1 [Logue, Jeremy S.; Whiting, Jennifer L.; Tunquist, Brian; Langeberg, Lorene K.; Scott, John D.] Univ Washington, Sch Med, Howard Hughes Med Inst, Seattle, WA 98195 USA.
[Whiting, Jennifer L.; Langeberg, Lorene K.; Scott, John D.] Univ Washington, Sch Med, Dept Pharmacol, Seattle, WA 98195 USA.
[Logue, Jeremy S.] Univ Washington, Sch Med, Mol & Cellular Biol Program, Seattle, WA 98195 USA.
[Wordeman, Linda] Univ Washington, Sch Med, Dept Physiol & Biophys, Seattle, WA 98195 USA.
[Sacks, David B.] NIH, Dept Lab Med, Bethesda, MD 20892 USA.
RP Scott, JD (reprint author), Univ Washington, Sch Med, Howard Hughes Med Inst, 1959 Pacific Ave NE,Box 357750, Seattle, WA 98195 USA.
EM scottjdw@u.washington.edu
OI Sacks, David/0000-0003-3100-0735
FU National Institutes of Health [DK54441, GM69429, CA93645]
FX This work was supported, in whole or in part, by National Institutes of
Health Grants DK54441 (to J. D. S.), GM69429 (to L. W.), and CA93645 (to
D. B. S.).
NR 42
TC 17
Z9 17
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 11
PY 2011
VL 286
IS 45
BP 39269
EP 39281
DI 10.1074/jbc.M111.277756
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 844PO
UT WOS:000296759800045
PM 21890631
ER
PT J
AU Bonocora, RP
Decker, PK
Glass, S
Knipling, L
Hinton, DM
AF Bonocora, Richard P.
Decker, Phillip K.
Glass, Stephanie
Knipling, Leslie
Hinton, Deborah M.
TI Bacteriophage T4 MotA Activator and the beta-Flap Tip of RNA Polymerase
Target the Same Set of sigma(70) Carboxyl-terminal Residues
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID TRANSCRIPTIONAL ACTIVATOR; PROTEIN-PROTEIN; PROMOTER RECOGNITION;
ABORTIVE INITIATION; ANGSTROM RESOLUTION; MUTATIONAL ANALYSIS;
CRYSTAL-STRUCTURE; STRUCTURAL BASIS; OPEN-COMPLEX; REGION 4
AB Sigma factors, the specificity subunits of RNA polymerase, are involved in interactions with promoter DNA, the core subunits of RNA polymerase, and transcription factors. The bacteriophage T4-encoded activator, MotA, is one such factor, which engages the C terminus of the Escherichia coli housekeeping sigma factor, sigma(70). MotA functions in concert with a phage-encoded co-activator, AsiA, as a molecular switch. This process, termed sigma appropriation, inhibits host transcription while activating transcription from a class of phage promoters. Previous work has demonstrated that MotA contacts the C terminus of sigma(70), H5, a region that is normally bound within RNA polymerase by its interaction with the beta-flap tip. To identify the specific sigma(70) residues responsible for interacting with MotA and the beta-flap tip, we generated single substitutions throughout the C terminus of sigma(70). We find that MotA targets H5 residues that are normally engaged by the beta-flap. In two-hybrid assays, the interaction of sigma(70) with either the beta-flap tip or MotA is impaired by alanine substitutions at residues Leu-607, Arg-608, Phe-610, Leu-611, and Asp-613. Transcription assays identify Phe-610 and Leu-611 as the key residues for MotA/AsiA-dependent transcription. Phe-610 is a crucial residue in the H5/beta-flap tip interaction using promoter clearance assays with RNA polymerase alone. Our results show how the actions of small transcriptional factors on a defined local region of RNA polymerase can fundamentally change the specificity of polymerase.
C1 [Bonocora, Richard P.; Decker, Phillip K.; Glass, Stephanie; Knipling, Leslie; Hinton, Deborah M.] NIDDK, Gene Express & Regulat Sect, Lab Cell & Mol Biol, NIH, Bethesda, MD 20892 USA.
RP Hinton, DM (reprint author), NIDDK, Gene Express & Regulat Sect, Lab Cell & Mol Biol, NIH, Bldg 8,Rm 2A-13, Bethesda, MD 20892 USA.
EM dhinton@helix.nih.gov
FU NIDDK, National Institutes of Health
FX This work was supported, in whole or in part, by the Intramural Research
Program of the NIDDK, National Institutes of Health.
NR 47
TC 4
Z9 4
U1 1
U2 4
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 11
PY 2011
VL 286
IS 45
BP 39290
EP 39296
DI 10.1074/jbc.M111.278762
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 844PO
UT WOS:000296759800047
PM 21911499
ER
PT J
AU Valdes, JL
Tang, JR
McDermott, MI
Kuo, JC
Zimmerman, SP
Wincovitch, SM
Waterman, CM
Milgram, SL
Playford, MP
AF Valdes, Julie L.
Tang, Jingrong
McDermott, Mark I.
Kuo, Jean-Cheng
Zimmerman, Seth P.
Wincovitch, Stephen M.
Waterman, Clare M.
Milgram, Sharon L.
Playford, Martin P.
TI Sorting Nexin 27 Protein Regulates Trafficking of a p21-activated Kinase
(PAK) Interacting Exchange Factor (beta-Pix)-G Protein-coupled Receptor
Kinase Interacting Protein (GIT) Complex via a PDZ Domain Interaction
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID FOCAL ADHESION KINASE; BETA-PIX; CELL-MIGRATION; MEMBRANE; FAMILY;
IDENTIFICATION; ACTIVATION; BINDING; ROLES; ACTIN
AB Sorting nexin 27 (SNX27) is a 62-kDa protein localized to early endosomes and known to regulate the intracellular trafficking of ion channels and receptors. In addition to a PX domain, SNX27 is the only sorting family member that contains a PDZ domain. To identify novel SNX27-PDZ binding partners, we performed a proteomic screen in mouse principal kidney cortical collecting duct cells using a GST-SNX27 fusion construct as bait. We found that beta-Pix (p21-activated kinase-interactive exchange factor), a guanine nucleotide exchange factor for the Rho family of small GTPases known to regulate cell motility directly interacted with SNX27. The association of beta-Pix and SNX27 is specific for beta-Pix isoforms terminating in the type-1 PDZ binding motif (ETNL). In the same screen we also identified Git1/2 as a potential SNX27 interacting protein. The interaction between SNX27 and Git1/2 is indirect and mediated by beta-Pix. Furthermore, we show recruitment of the beta-Pix.Git complex to endosomal sites in a SNX27-dependent manner. Finally, migration assays revealed that depletion of SNX27 from HeLa and mouse principal kidney cortical collecting duct cells significantly decreases cell motility. We propose a model by which SNX27 regulates trafficking of beta-Pix to focal adhesions and thereby influences cell motility.
C1 [Valdes, Julie L.; Tang, Jingrong; McDermott, Mark I.; Kuo, Jean-Cheng; Zimmerman, Seth P.; Wincovitch, Stephen M.; Waterman, Clare M.; Milgram, Sharon L.; Playford, Martin P.] NHLBI, Cell Biol & Physiol Ctr, NIH, Bethesda, MD 20982 USA.
[Kuo, Jean-Cheng] Natl Yang Ming Univ, Inst Biochem & Mol Biol, Taipei 112, Taiwan.
RP Playford, MP (reprint author), NIH, Bldg 10,Rm 6N256,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM playfordmp@nhlbi.nih.gov
OI Waterman, Clare/0000-0001-6142-6775
FU National Institutes of Health; NHLBI
FX This work was supported, in whole or in part, by a National Institutes
of Health grant from the NHLBI.
NR 44
TC 17
Z9 19
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
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 11
PY 2011
VL 286
IS 45
BP 39403
EP 39416
DI 10.1074/jbc.M111.260802
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 844PO
UT WOS:000296759800058
PM 21926430
ER
PT J
AU Weisz, A
Mazzola, EP
Ito, Y
AF Weisz, Adrian
Mazzola, Eugene P.
Ito, Yoichiro
TI Preparative separation of 1,3,6-pyrenetrisulfonic acid trisodium salt
from the color additive D&C Green No. 8 (pyranine) by pH-zone-refining
counter-current chromatography
SO JOURNAL OF CHROMATOGRAPHY A
LA English
DT Article; Proceedings Paper
CT 242nd ACS National Meeting
CY AUG 28-SEP 01, 2011
CL Denver, CO
SP ACS
DE Counter-current chromatography; pH-zone-refining CCC; Pyranine; D&C
Green No. 8; Dyes; 8-Hydroxy-1,3,6-pyrenetrisulfonic acid;
1,3,6-Pyrenetrisulfonic acid
ID QUINOLINE YELLOW; PURIFICATION
AB In developing analytical methods for batch certification of the color additive D&C Green No.8 (G8), the U.S. Food and Drug Administration needed the trisodium salt of 1,3.6-pyrenetrisulfonic acid (P3S) for use as a reference material. Since P3S was not commercially available, preparative quantities of it were separated from portions of a sample of G8 that contained similar to 3.5% P3S. The separations were performed by pH-zone-refining counter-current chromatography using dodecylamine (DA) as the hydrophobic counterion. The added DA enabled partitioning of the polysulfonated components into the organic stationary phase of the two-phase solvent system used, 1-butanol-water (1:1). Thus, a typical separation that involved 20.3 g of G8, using sulfuric acid as the retainer acid and 20% DA in the stationary phase and 0.1 M sodium hydroxide as the mobile phase, resulted in similar to 0.58 g of P3S of greater than 99% purity. The identification and characterization of the separated P3S were performed by elemental analyses, proton nuclear magnetic resonance, high-resolution mass spectrometry, ultra-violet spectra, and high-performance liquid chromatography. Published by Elsevier B.V.
C1 [Weisz, Adrian] US FDA, Off Cosmet & Colors, Ctr Food Safety & Appl Nutr, College Pk, MD 20740 USA.
[Mazzola, Eugene P.] US FDA, Off Regulatory Sci, Ctr Food Safety & Appl Nutr, College Pk, MD 20740 USA.
[Ito, Yoichiro] NHLBI, Biochem & Biophys Ctr, NIH, Bethesda, MD 20892 USA.
RP Weisz, A (reprint author), US FDA, Off Cosmet & Colors, Ctr Food Safety & Appl Nutr, HFS 106,5100 Paint Branch Pkwy, College Pk, MD 20740 USA.
EM adrian.weisz@fda.hhs.gov
FU Intramural NIH HHS [ZIA HL005107-04]
NR 23
TC 13
Z9 14
U1 1
U2 17
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0021-9673
J9 J CHROMATOGR A
JI J. Chromatogr. A
PD NOV 11
PY 2011
VL 1218
IS 45
BP 8249
EP 8254
DI 10.1016/j.chroma.2011.09.049
PG 6
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 846XV
UT WOS:000296937400013
PM 21982993
ER
PT J
AU James, S
Simmons, CP
James, AA
AF James, Stephanie
Simmons, Cameron P.
James, Anthony A.
TI Mosquito Trials
SO SCIENCE
LA English
DT Editorial Material
ID TRANSMISSION
C1 [James, Stephanie] Fdn NIH, Bethesda, MD 20814 USA.
[Simmons, Cameron P.] Univ Oxford, Clin Res Unit, Hosp Trop Dis, Wellcome Trust Major Overseas Program, Ho Chi Minh City, Vietnam.
[James, Anthony A.] Univ Calif Irvine, Dept Microbiol & Mol Genet, Irvine, CA 92697 USA.
[James, Anthony A.] Univ Calif Irvine, Dept Mol Biol & Biochem, Irvine, CA 92697 USA.
RP James, S (reprint author), Fdn NIH, Bethesda, MD 20814 USA.
EM sjames@fnih.org; csimmons@oucru.org; aajames@uci.edu
OI Simmons, Cameron P./0000-0002-9039-7392
NR 6
TC 19
Z9 19
U1 2
U2 24
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 11
PY 2011
VL 334
IS 6057
BP 771
EP 772
DI 10.1126/science.1213798
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 845US
UT WOS:000296849600036
PM 22076370
ER
PT J
AU Simmons, G
Glynn, SA
Komaroff, AL
Mikovits, JA
Tobler, LH
Hackett, J
Tang, N
Switzer, WM
Heneine, W
Hewlett, IK
Zhao, JQ
Lo, SC
Alter, HJ
Linnen, JM
Gao, K
Coffin, JM
Kearney, MF
Ruscetti, FW
Pfost, MA
Bethel, J
Kleinman, S
Holmberg, JA
Busch, MP
AF Simmons, Graham
Glynn, Simone A.
Komaroff, Anthony L.
Mikovits, Judy A.
Tobler, Leslie H.
Hackett, John, Jr.
Tang, Ning
Switzer, William M.
Heneine, Walid
Hewlett, Indira K.
Zhao, Jiangqin
Lo, Shyh-Ching
Alter, Harvey J.
Linnen, Jeffrey M.
Gao, Kui
Coffin, John M.
Kearney, Mary F.
Ruscetti, Francis W.
Pfost, Max A.
Bethel, James
Kleinman, Steven
Holmberg, Jerry A.
Busch, Michael P.
CA Blood XMRV Sci Res Working Grp
TI Failure to Confirm XMRV/MLVs in the Blood of Patients with Chronic
Fatigue Syndrome: A Multi-Laboratory Study
SO SCIENCE
LA English
DT Article
ID VIRUS-RELATED VIRUS; RETROVIRUS XMRV; CELLS; CONTAMINATION; SEQUENCES;
ABSENCE; DONORS; DETECT
AB Murine leukemia viruses (MLVs), including xenotropic-MLV-related virus (XMRV), have been controversially linked to chronic fatigue syndrome (CFS). To explore this issue in greater depth, we compiled coded replicate samples of blood from 15 subjects previously reported to be XMRV/MLV-positive (14 with CFS) and from 15 healthy donors previously determined to be negative for the viruses. These samples were distributed in a blinded fashion to nine laboratories, which performed assays designed to detect XMRV/MLV nucleic acid, virus replication, and antibody. Only two laboratories reported evidence of XMRV/MLVs; however, replicate sample results showed disagreement, and reactivity was similar among CFS subjects and negative controls. These results indicate that current assays do not reproducibly detect XMRV/MLV in blood samples and that blood donor screening is not warranted.
C1 [Simmons, Graham; Tobler, Leslie H.; Busch, Michael P.] Blood Syst Res Inst, San Francisco, CA 94118 USA.
[Simmons, Graham; Tobler, Leslie H.; Busch, Michael P.] Univ Calif San Francisco, San Francisco, CA 94118 USA.
[Glynn, Simone A.] NHLBI, Transfus Med & Cellular Therapeut Branch, NIH, Bethesda, MD 20892 USA.
[Komaroff, Anthony L.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Komaroff, Anthony L.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Mikovits, Judy A.; Pfost, Max A.] Univ Nevada, Whittemore Peterson Inst, Reno, NV 89557 USA.
[Hackett, John, Jr.; Tang, Ning] Abbott Labs, Abbott Pk, IL 60064 USA.
[Switzer, William M.; Heneine, Walid] Ctr Dis Control & Prevent, Div HIV AIDS Prevent, Atlanta, GA 30333 USA.
[Hewlett, Indira K.; Zhao, Jiangqin] US FDA, Off Blood Res, Rockville, MD 20852 USA.
[Lo, Shyh-Ching] US FDA, Off Cellular Tissue & Gene Therapies Review, Bethesda, MD 20892 USA.
[Alter, Harvey J.] NIH, Dept Transfus Med, Bethesda, MD 20892 USA.
[Linnen, Jeffrey M.; Gao, Kui] Gen Probe, San Diego, CA 92121 USA.
[Coffin, John M.] Tufts Univ, Dept Mol Biol & Microbiol, Boston, MA 02111 USA.
[Kearney, Mary F.; Ruscetti, Francis W.] NCI, Frederick, MD 21702 USA.
[Bethel, James] WESTAT Corp, Rockville, MD 20850 USA.
[Kleinman, Steven] Univ British Columbia, Dept Pathol, Victoria, BC V9A4W4, Canada.
[Holmberg, Jerry A.] US Dept HHS, Rockville, MD 20852 USA.
RP Busch, MP (reprint author), Blood Syst Res Inst, San Francisco, CA 94118 USA.
EM mbusch@bloodsystems.org
RI Simmons, Graham/G-3523-2012; Haleyur Giri Setty, Mohan Kumar/F-5841-2014
OI Simmons, Graham/0000-0002-9615-7023; Haleyur Giri Setty, Mohan
Kumar/0000-0001-6423-1420
FU National Heart, Lung, and Blood Institute REDS-II Central Laboratory
[N01 HB-57181]; F. M. Kirby Foundation
FX The authors acknowledge the tremendous effort contributed by all Blood
XMRV Scientific Research Working Group (SRWG) members; the roster of the
SRWG is listed as supporting material on Science Online. The authors
acknowledge the many laboratory members from all of the contributing
laboratories, including I. Steffen, I. Wilson, L. Pitina, K. Murcia, P.
Loanzon, S. Ng, and N. Gefter at the Blood Systems Research Institute;
H. Zheng, H. Jia, S. Tang, and A. Shankar at CDC; C. Puccinelli, S.
Rawat, A. McKenzie, K. Hagen, and D. T. Cramer at WPI; J. Carrick at
Gen-Probe; D. Bertolette, Y. Huang, and C. Sadowski at NCI/Ruscetti; E.
Anderson, J. Spindler, and A. Wiegand at DRP; K. Devadas, M. K. H. G.
Setty, S. Tang, P. H. Zhang, and D. S. Gaddam in the Office of Blood
Research and Review, FDA; B. Li, N. Pripuzova, and G.-C. Hung in the
Office of Cellular, Tissue and Gene Therapies, FDA; R. Wang from the
clinical center NIH; G. Leckie at Abbott Molecular; and X. Qiu at Abbott
Diagnostics. The laboratory work was funded by the National Heart, Lung,
and Blood Institute REDS-II Central Laboratory Contract to Blood Systems
Research Institute (N01 HB-57181). J.M.C. was a research professor of
the American Cancer Society with support from the F. M. Kirby
Foundation. The findings and conclusions in this report are those of the
authors and do not necessarily represent the views of the NIH, CDC, FDA,
or the Department of Health and Human Services. M. P. B. is a member of
the Scientific Advisory Board of Gen-Probe, which provides blood
screening assays for pathogen nucleic acids. S. K. is a paid consultant
to Novartis Diagnostics, a distributor of blood donor screening assays,
and to Cerus Corporation, a manufacturer of pathogen inactivation
systems for blood components. WPI has filed patent applications related
to methods of testing XMRVs and variants in blood. Abbott Laboratories
has filed patent applications relating to detection of XMRV by use of
immunoassays and molecular-based assays. Gen-Probe has filed patent
applications relating to the assays they performed in this paper.
NR 21
TC 53
Z9 55
U1 1
U2 13
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD NOV 11
PY 2011
VL 334
IS 6057
BP 814
EP 817
DI 10.1126/science.1213841
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 845US
UT WOS:000296849600049
PM 21940862
ER
PT J
AU Clayton-Smith, J
O'Sullivan, J
Daly, S
Bhaskar, S
Day, R
Anderson, B
Voss, AK
Thomas, T
Biesecker, LG
Smith, P
Fryer, A
Chandler, KE
Kerr, B
Tassabehji, M
Lynch, SA
Krajewska-Walasek, M
McKee, S
Smith, J
Sweeney, E
Mansour, S
Mohammed, S
Donnai, D
Black, G
AF Clayton-Smith, Jill
O'Sullivan, James
Daly, Sarah
Bhaskar, Sanjeev
Day, Ruth
Anderson, Beverley
Voss, Anne K.
Thomas, Tim
Biesecker, Leslie G.
Smith, Philip
Fryer, Alan
Chandler, Kate E.
Kerr, Bronwyn
Tassabehji, May
Lynch, Sally-Ann
Krajewska-Walasek, Malgorzata
McKee, Shane
Smith, Janine
Sweeney, Elizabeth
Mansour, Sahar
Mohammed, Shehla
Donnai, Dian
Black, Graeme
TI Whole-Exome-Sequencing Identifies Mutations in Histone Acetyltransferase
Gene KAT6B in Individuals with the Say-Barber-Biesecker Variant of Ohdo
Syndrome
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID MENTAL-RETARDATION; BLEPHAROPHIMOSIS SYNDROME; HYPOPLASTIC TEETH;
SIMPSON TYPE; MORF; QUERKOPF; FACIES; MICE
AB Say-Barber-Biesecker-Young-Simpson syndrome (SBBYSS or Ohdo syndrome) is a multiple anomaly syndrome characterized by severe intellectual disability, blepharophimosis, and a mask-like facial appearance. A number of individuals with SBBYSS also have thyroid abnormalities and cleft palate. The condition usually occurs sporadically and is therefore presumed to be due in most cases to new dominant mutations. In individuals with SBBYSS, a whole-exome sequencing approach was used to demonstrate de novo protein-truncating mutations in the highly conserved histone acetyltransferase gene KAT6B (MYST4/MORF)) in three out of four individuals sequenced. Sanger sequencing was used to confirm truncating mutations of KAT6B, clustering in the final exon of the gene in all four individuals and in a further nine persons with typical SBBYSS. Where parental samples were available, the mutations were shown to have occurred de novo. During mammalian development KAT6B is upregulated specifically in the developing central nervous system, facial structures, and limb buds. The phenotypic features seen in the Qkf mouse, a hypomorphic Kat6b mutant, include small eyes, ventrally placed ears and long first digits that mirror the human phenotype. This is a further example of how perturbation of a protein involved in chromatin modification might give rise to a multisystem developmental disorder.
C1 [Clayton-Smith, Jill; O'Sullivan, James; Daly, Sarah; Bhaskar, Sanjeev; Day, Ruth; Anderson, Beverley; Smith, Philip; Chandler, Kate E.; Kerr, Bronwyn; Tassabehji, May; Donnai, Dian; Black, Graeme] Univ Manchester, St Marys Hosp, Manchester Acad Hlth Sci Ctr, Sch Biomed, Manchester M13 9WL, Lancs, England.
[Voss, Anne K.; Thomas, Tim] Walter & Eliza Hall Inst Med Res, Div Mol Med, Parkville, Vic 3052, Australia.
[Voss, Anne K.] Univ Melbourne, Dept Med Biol, Parkville, Vic 3052, Australia.
[Biesecker, Leslie G.] NHGRI, Genet Dis Res Branch, Bethesda, MD 20892 USA.
[Fryer, Alan; Sweeney, Elizabeth] Alder Hey Hosp, Cheshire & Merseyside Genet Serv, Liverpool L12 2AP, Merseyside, England.
[Lynch, Sally-Ann] Our Ladys Hosp Sick Children, Natl Ctr Med Genet, Dublin 12, Ireland.
[Krajewska-Walasek, Malgorzata] Childrens Mem Hlth Inst, Dept Med Genet, PL-04730 Warsaw, Poland.
[McKee, Shane] Belfast City Hosp, Dept Med Genet, No Ireland Reg Genet Serv, Belfast BT9 7AB, Antrim, North Ireland.
[Smith, Janine] Childrens Hosp Westmead, Dept Clin Genet, Westmead, NSW 2145, Australia.
[Mansour, Sahar] St Georges Med Sch, Dept Med Genet, London SW17 0RE, England.
[Mohammed, Shehla] Guys Hosp, Dept Clin Genet, London SE1 9RT, England.
RP Clayton-Smith, J (reprint author), Univ Manchester, St Marys Hosp, Manchester Acad Hlth Sci Ctr, Sch Biomed, Manchester M13 9WL, Lancs, England.
EM jill.clayton-smith@cmft.nhs.uk
RI Voss, Anne/F-5110-2013;
OI Voss, Anne/0000-0002-3853-9381; Black, Graeme/0000-0001-8727-6592
FU Manchester Biomedical Research Centre; National Institute for Health
Research; Healing Foundation; National Institute of Health; Australian
NHMRC; Victorian government
FX Clinical and Laboratory work carried out within the Genetic Medicine
Department at St Mary's Hospital was supported by the Manchester
Biomedical Research Centre funded by the National Institute for Health
Research. Research into clefting syndromes in Manchester is supported by
the Healing Foundation. The Clinseq project was funded by the National
Institute of Health. A.K.V. and T.T. were supported by project grants
and research fellowships from the Australian NHMRC as well as through
infrastructure funding from the Victorian government.
NR 25
TC 70
Z9 75
U1 3
U2 15
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD NOV 11
PY 2011
VL 89
IS 5
BP 675
EP 681
DI 10.1016/j.ajhg.2011.10.008
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA 848YD
UT WOS:000297090100010
PM 22077973
ER
PT J
AU Chen, SP
Chahar, HS
Abraham, S
Wu, HQ
Pierson, TC
Wang, XZA
Manjunath, N
AF Chen, Shuiping
Chahar, Harendra S.
Abraham, Sojan
Wu, Haoquan
Pierson, Theodore C.
Wang, Xiaozhong A.
Manjunath, N.
TI Ago-2-Mediated Slicer Activity Is Essential for Anti-Flaviviral Efficacy
of RNAi
SO PLOS ONE
LA English
DT Article
ID CELLULAR MICRORNAS; HIV-1 REPLICATION; VIRUS-INFECTION; CODING REGIONS;
WEST-NILE; P-BODIES; EXPRESSION; CELLS; INTERFERES; SUPPRESSION
AB RNA interference can be mediated by fully complementary siRNA or partially complementary miRNA. siRNAs are widely used to suppress viral replication and the fully complementary siRNA bound Ago-2 in the RISC is known to degrade the target RNA. Although other argonaute proteins lacking slicer activity can also bind oligonucleotides with both si and miRNA structures, whether they can also contribute to antiviral effects is not entirely clear. We tested si and miRNA structured oligos for target repression in dual luciferase assays as well as for inhibition of Dengue and West Nile virus replication in ES cells expressing individual Ago proteins. In luciferase assays, both fully complementary and partially complementary oligos effectively repressed their targets in all individual Ago expressing cell lines, although the efficacy with fully complementary oligos was higher in Ago-2+ cells. However, partially complementary oligos had no effect on virus replication in any cell line, while fully complementary siRNAs were highly effective in Ago-2 expressing, but not in cells expressing other Ago proteins. This occurred irrespective of whether the target sequences were located in the coding region or 39UTR of the virus. We conclude that Ago-2 slicer activity is essential for anti-viral efficacy of siRNAs and miRNA-mediated translational repression/transcript destabilization is too weak to suppress the abundantly expressed flaviviral proteins.
C1 [Chen, Shuiping; Chahar, Harendra S.; Abraham, Sojan; Wu, Haoquan; Manjunath, N.] Texas Tech Univ Hlth Sci Ctr, Dept Biomed Sci, Ctr Excellence Infect Dis Res, Paul L Foster Sch Med, El Paso, TX 79905 USA.
[Pierson, Theodore C.] NIAID, Viral Pathogenesis Sect, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
[Wang, Xiaozhong A.] Northwestern Univ, Dept Biochem Mol Biol & Cell Biol, Evanston, IL USA.
RP Chen, SP (reprint author), Texas Tech Univ Hlth Sci Ctr, Dept Biomed Sci, Ctr Excellence Infect Dis Res, Paul L Foster Sch Med, El Paso, TX 79905 USA.
EM manjunath.swamy@ttuhsc.edu
FU National Institutes of Health/National Institute of Allergy and
Infectious Diseases [U01AI075419]
FX National Institutes of Health/National Institute of Allergy and
Infectious Diseases grant U01AI075419. The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 38
TC 6
Z9 6
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 10
PY 2011
VL 6
IS 11
AR e27551
DI 10.1371/journal.pone.0027551
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 852HQ
UT WOS:000297348800033
PM 22102908
ER
PT J
AU Koga, F
Yoshida, S
Tatokoro, M
Kawakami, S
Fujii, Y
Kumagai, J
Neckers, L
Kihara, K
AF Koga, Fumitaka
Yoshida, Soichiro
Tatokoro, Manabu
Kawakami, Satoru
Fujii, Yasuhisa
Kumagai, Jiro
Neckers, Len
Kihara, Kazunori
TI ErbB2 and NF kappa B Overexpression as Predictors of Chemoradiation
Resistance and Putative Targets to Overcome Resistance in
Muscle-Invasive Bladder Cancer
SO PLOS ONE
LA English
DT Article
ID SELECTIVE ORGAN PRESERVATION; THERAPY-ONCOLOGY-GROUP; SHOCK-PROTEIN 90;
RADIATION-THERAPY; UROTHELIAL CARCINOMA; TRANSURETHRAL RESECTION;
ESOPHAGEAL-CARCINOMA; RADICAL CYSTECTOMY; LOCAL-CONTROL; EXPRESSION
AB Radical cystectomy for muscle-invasive bladder cancer (MIBC) patients frequently impairs their quality of life (QOL) due to urinary diversion. To improve their QOL, a bladder-sparing alternative strategy using chemoradiation has been developed. In bladder-sparing protocols, complete response (CR) to induction chemoradiation is a prerequisite for bladder preservation and favorable survival. Thus predicting chemoradiation resistance and overcoming it would increase individual MIBC patients' chances of bladder preservation. The aim of this study is to investigate putative molecular targets for treatment aimed at improving chemoradiation response. Expression levels of erbB2, NF kappa B, p53, and survivin were evaluated immunohistochemically in pretreatment biopsy samples from 35 MIBC patients in whom chemoradiation sensitivity had been pathologically evaluated in cystectomy specimens, and associations of these expression levels with chemoradiation sensitivity and cancer-specific survival (CSS) were investigated. Of the 35 patients, 11 (31%) achieved pathological CR, while tumors in the remaining 24 patients (69%) were chemoradiation-resistant. Multivariate analysis identified erbB2 and NF kappa B overexpression and hydronephrosis as significant and independent risk factors for chemoradiation resistance with respective relative risks of 11.8 (P = 0.014), 15.4 (P = 0.024) and 14.3 (P = 0.038). The chemoradiation resistance rate was 88.5% for tumors overexpressing erbB2 and/or NF kappa B, but only 11.1% for those negative for both (P <0.0001). The 5-year CSS rate was 74% overall. Through multivariate analysis, overexpression of erbB2 and/or NFkB was identified as an independent risk factor for bladder cancer death with marginal significance (hazard ratio 21.5, P = 0.056) along with chemoradiation resistance (P = 0.003) and hydronephrosis (P = 0.018). The 5-year CSS rate for the 11 patients achieving pathological CR was 100%, while that for the 24 with chemoradiation-resistant disease was 61% (P = 0.018). Thus, erbB2 and NFkB overexpression are relevant to chemoradiation resistance and are putative targets aimed at overcoming chemoradiation resistance in MIBC.
C1 [Koga, Fumitaka; Yoshida, Soichiro; Tatokoro, Manabu; Kawakami, Satoru; Fujii, Yasuhisa; Kihara, Kazunori] Tokyo Med & Dent Univ, Dept Urol, Grad Sch, Tokyo, Japan.
[Kumagai, Jiro] Tokyo Med & Dent Univ, Dept Surg Pathol, Grad Sch, Tokyo, Japan.
[Neckers, Len] NCI, Urol Oncol Branch, Bethesda, MD 20892 USA.
RP Koga, F (reprint author), Tokyo Med & Dent Univ, Dept Urol, Grad Sch, Tokyo, Japan.
EM f-koga.uro@tmd.ac.jp
FU Ministry of Education, Culture, Sports, Science and Technology of Japan
[19791102, 19791103]
FX This work was supported, in part, by grants-in-aids for scientific
research (19791102, 19791103), from the Ministry of Education, Culture,
Sports, Science and Technology of Japan. 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 36
TC 17
Z9 17
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 10
PY 2011
VL 6
IS 11
AR e27616
DI 10.1371/journal.pone.0027616
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 852HQ
UT WOS:000297348800037
PM 22102915
ER
PT J
AU Plechanovova, A
Byun, Y
Alquicer, G
Skultetyova, L
Mlcochova, P
Nemcova, A
Kim, HJ
Navratil, M
Mease, R
Lubkowski, J
Pomper, M
Konvalinka, J
Rulisek, L
Barinka, C
AF Plechanovova, Anna
Byun, Youngjoo
Alquicer, Glenda
Skultetyova, L'ubica
Mlcochova, Petra
Nemcova, Adriana
Kim, Hyung-Joon
Navratil, Michal
Mease, Ronnie
Lubkowski, Jacek
Pomper, Martin
Konvalinka, Jan
Rulisek, Lubomir
Barinka, Cyril
TI Novel Substrate-Based Inhibitors of Human Glutamate Carboxypeptidase II
with Enhanced Lipophilicity
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID UREA-BASED INHIBITORS; MEMBRANE ANTIGEN; PROSTATE-CANCER;
DIABETIC-NEUROPATHY; MORPHINE-TOLERANCE; NUCLEIC-ACIDS; ACTIVE-SITE;
BASIS-SETS; GCP-II; NAALADASE
AB Virtually all low molecular weight inhibitors of human glutamate carboxypeptidase II (GCPII) are highly polar compounds that have limited use in settings where more lipophilic molecules are desired. Here we report the identification and characterization of GCPII inhibitors with enhanced liphophilicity that are derived from a series of newly identified dipeptidic GCPII substrates featuring nonpolar aliphatic side chains at the C-terminus. To analyze the interactions governing the substrate recognition by GCPII, we determined crystal structures of the inactive GCPII(E424A) mutant in complex with selected dipeptides and complemented the structural data with quantum mechanics/molecular mechanics calculations. Results reveal the importance of nonpolar interactions governing GCPII affinity toward novel substrates as well as formerly unnoticed plasticity of the S1' specificity pocket. On the basis of those data, we designed, synthesized, and evaluated a series of novel GCPII inhibitors with enhanced lipophilicity, with the best candidates having low nanomolar inhibition constants and clogD > -0.3. Our findings offer new insights into the design of more lipophilic inhibitors targeting GCPII.
C1 [Alquicer, Glenda; Skultetyova, L'ubica; Barinka, Cyril] Acad Sci Czech Republic, Inst Biotechnol, Prague 14200 4, Czech Republic.
[Plechanovova, Anna; Mlcochova, Petra; Nemcova, Adriana; Navratil, Michal; Konvalinka, Jan; Rulisek, Lubomir] Acad Sci Czech Republic, Inst Organ Chem & Biochem, Gilead Sci Res Ctr, IOCB, CR-16610 Prague 6, Czech Republic.
[Plechanovova, Anna; Mlcochova, Petra; Navratil, Michal; Konvalinka, Jan] Charles Univ Prague, Dept Biochem, Fac Nat Sci, Prague 2030, Czech Republic.
[Byun, Youngjoo; Kim, Hyung-Joon; Mease, Ronnie; Pomper, Martin] Johns Hopkins Med Inst, Russell H Morgan Dept Radiol & Radiol Sci, Baltimore, MD 21231 USA.
[Byun, Youngjoo] Korea Univ, Coll Pharm, Yeongi Gun 339700, Chungnam, South Korea.
[Lubkowski, Jacek] NCI, Ctr Canc Res, Frederick, MD 21702 USA.
RP Barinka, C (reprint author), Acad Sci Czech Republic, Inst Biotechnol, Videnska 1083, Prague 14200 4, Czech Republic.
EM cyril.barinka@img.cas.cz
RI Alquicer Barrera, Glenda /F-6834-2014; Rulisek, Lubomir/G-5277-2014;
Konvalinka, Jan/G-7518-2014; Barinka, Cyril/G-9803-2014; Skultetyova,
Lubica/H-3053-2014;
OI Konvalinka, Jan/0000-0003-0695-9266
FU EMBO [1978]; Ministry of Education, Youth and Sports of the Czech
Republic [ME10031, LC 512]; IBT [AV0Z-50520701]; IOCB [AV0Z40550506];
NIH, National Cancer Institute, Center for Cancer Research; U.S.
Department of Energy, Office of Science, Office of Basic Energy Sciences
[W-31-109-Eng38]; [R21/R33 MH080580]
FX The authors thank Jana Starkova for excellent technical assistance.
Financial support from EMBO (Installation Grant No. 1978), Ministry of
Education, Youth and Sports of the Czech Republic (Projects ME10031, LC
512), IBT (Grant AV0Z-50520701), and IOCB (Grant AV0Z40550506) is
gratefully acknowledged. This work was also supported in part by the
Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research (J.L. and C.B.) and by Grant R21/R33 MH080580
(M.P.). Use of the Advanced Photon Source was supported by the U.S.
Department of Energy, Office of Science, Office of Basic Energy
Sciences, under Contract No. W-31-109-Eng38.
NR 53
TC 9
Z9 9
U1 1
U2 16
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 10
PY 2011
VL 54
IS 21
BP 7535
EP 7546
DI 10.1021/jm200807m
PG 12
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 839ZN
UT WOS:000296408100010
PM 21923190
ER
PT J
AU Sisirak, V
Vey, N
Vanbervliet, B
Duhen, T
Puisieux, I
Homey, B
Bowman, EP
Trinchieri, G
Dubois, B
Kaiserlian, D
Lira, SA
Puisieux, A
Blay, JY
Caux, C
Bendriss-Vermare, N
AF Sisirak, Vanja
Vey, Nelly
Vanbervliet, Beatrice
Duhen, Thomas
Puisieux, Isabelle
Homey, Bernhard
Bowman, Edward P.
Trinchieri, Giorgio
Dubois, Bertrand
Kaiserlian, Dominique
Lira, Sergio A.
Puisieux, Alain
Blay, Jean-Yves
Caux, Christophe
Bendriss-Vermare, Nathalie
TI CCR6/CCR10-mediated plasmacytoid dendritic cell recruitment to inflamed
epithelia after instruction in lymphoid tissues
SO BLOOD
LA English
DT Article
ID CUTANEOUS LUPUS-ERYTHEMATOSUS; INTERFERON-PRODUCING CELLS; CHEMOKINE
RECEPTOR 6; T-CELLS; CXCR3 LIGANDS; CUTTING EDGE; SKIN INFLAMMATION;
IMMUNE-RESPONSES; IN-VIVO; EXPRESSION
AB Absent in peripheral tissues during homeostasis, human plasmacytoid dendritic cells (pDCs) are described in inflamed skin or mucosa. Here, we report that, unlike blood pDCs, a subset of tonsil pDCs express functional CCR6 and CCR10, and their respective ligands CCL20 and CCL27 are detected in inflamed epithelia contacting blood dendritic cell antigen 2(+) pDCs. Moreover, pDCs are recruited to imiquimod-treated skin tumors in WT but not CCR6-deficient mice, and competitive adoptive transfers reveal that CCR6-deficient pDCs are impaired in homing to inflamed skin tumors after intravenous transfer. On IL-3 culture, CCR6 and CCR10 expression is induced on human blood pDCs that become responsive to CCL20 and CCL27/CCL28, respectively. Interestingly, unlike myeloid DC, blood pDCs initially upregulate CCR7 expression and CCL19 responsiveness on IL-3 +/- CpG-B and then acquire functional CCR6 and CCR10. Finally, IL-3-differentiated CCR6(+) CCR10(+) pDCs secrete high levels of IFN-alpha in response to virus. Overall, we propose an unexpected pDCs migratory model that may best apply for mucosal-associated lymphoid tissues. After CCR7-mediated extravasation into lymphoid tissues draining inflamed epithelia, blood pDCs may be instructed to up-regulate CCR6 and/or CCR10 allowing their homing into inflamed epithelia (in mucosae or skin). At this site, pDCs can then produce IFN-alpha contributing to pathogen clearance and/ or local inflammation. (Blood. 2011;118(19):5130-5140)
C1 [Sisirak, Vanja; Vey, Nelly; Vanbervliet, Beatrice; Puisieux, Isabelle; Puisieux, Alain; Blay, Jean-Yves; Caux, Christophe; Bendriss-Vermare, Nathalie] Univ Lyon 1, Inst Sci Pharmaceut & Biol, F-69365 Lyon, France.
[Sisirak, Vanja; Vey, Nelly; Vanbervliet, Beatrice; Puisieux, Isabelle; Puisieux, Alain; Blay, Jean-Yves; Caux, Christophe; Bendriss-Vermare, Nathalie] Ctr Rech Cancerol Lyon, INSERM, U1052, Lyon, France.
[Sisirak, Vanja; Vey, Nelly; Vanbervliet, Beatrice; Puisieux, Isabelle; Puisieux, Alain; Blay, Jean-Yves; Caux, Christophe; Bendriss-Vermare, Nathalie] Ctr Rech Cancerol Lyon, Ctr Natl Rech Sci, UMR 5286, Lyon, France.
[Sisirak, Vanja; Vey, Nelly; Puisieux, Isabelle; Puisieux, Alain; Blay, Jean-Yves; Caux, Christophe; Bendriss-Vermare, Nathalie] LabEx DEVweCAN, Lyon, France.
[Duhen, Thomas] Benaroya Res Inst, Program Immunol, Seattle, WA USA.
[Homey, Bernhard] Univ Dusseldorf, Dept Dermatol, D-4000 Dusseldorf, Germany.
[Bowman, Edward P.] Schering Plough Biopharma, Dept Immunol, Palo Alto, CA USA.
[Trinchieri, Giorgio] NCI, Canc & Inflammat Program, Ctr Canc Res, NIH, Frederick, MD 21701 USA.
[Dubois, Bertrand; Kaiserlian, Dominique] Inst Federatif Rech, INSERM, Equipe Immunite Infect & Vaccinat, U851, Lyon, France.
[Lira, Sergio A.] Mt Sinai Sch Med, Inst Immunol, New York, NY USA.
[Puisieux, Alain] Inst Univ France, Paris, France.
RP Bendriss-Vermare, N (reprint author), Ctr Leon Berard, Ctr Rech Cancerol Lyon, INSERM, Ctr Natl Rech Sci 5286,UMR 1052, 28 Rue Laennec, F-69373 Lyon 08, France.
EM nathalie.bendriss-vermare@lyon.unicancer.fr
RI Dubois, Bertrand/D-4446-2013; Caux, Christophe/G-2851-2013; KAISERLIAN,
Dominique/G-3325-2013; Blay, Jean-Yves/N-3966-2016; Sisirak,
Vanja/O-9393-2016
OI Blay, Jean-Yves/0000-0001-7190-120X; Sisirak, Vanja/0000-0003-3070-6533
FU Association pour la Recherche contre le Cancer; Comites departementaux
de Saone-et-Loire et du Rhone de la Ligue nationale contre le cancer;
Institut National du Cancer [INCA ACI-63-04, ACI 2007-2009, PL116,
PL-969-017]; Breast Cancer Research Foundation; BioPole program DEMINAP;
Region Rhone-Alpes and Association pour la Recherche sur le Cancer
FX This work was supported by Association pour la Recherche contre le
Cancer, Comites departementaux de Saone-et-Loire et du Rhone de la Ligue
nationale contre le cancer, Institut National du Cancer (grants INCA
ACI-63-04, ACI 2007-2009, PL116, and PL-969-017), Breast Cancer Research
Foundation, and BioPole program DEMINAP. V.S. was supported by the
Region Rhone-Alpes and Association pour la Recherche sur le Cancer.
NR 56
TC 23
Z9 27
U1 0
U2 6
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 10
PY 2011
VL 118
IS 19
BP 5130
EP 5140
DI 10.1182/blood-2010-07-295626
PG 11
WC Hematology
SC Hematology
GA 845ZN
UT WOS:000296867100014
PM 21937703
ER
PT J
AU Boasso, A
Royle, CM
Doumazos, S
Aquino, VN
Biasin, M
Piacentini, L
Tavano, B
Fuchs, D
Mazzotta, F
Lo Caputo, S
Shearer, GM
Clerici, M
Graham, DR
AF Boasso, Adriano
Royle, Caroline M.
Doumazos, Spyridon
Aquino, Veronica N.
Biasin, Mara
Piacentini, Luca
Tavano, Barbara
Fuchs, Dietmar
Mazzotta, Francesco
Lo Caputo, Sergio
Shearer, Gene M.
Clerici, Mario
Graham, David R.
TI Overactivation of plasmacytoid dendritic cells inhibits antiviral T-cell
responses: a model for HIV immunopathogenesis
SO BLOOD
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; APOPTOSIS-INDUCING LIGAND; IMMUNE
ACTIVATION; INDOLEAMINE 2,3-DIOXYGENASE; TRYPTOPHAN CATABOLISM; I
INTERFERON; LIPID RAFTS; INFECTION; RECEPTOR; INNATE
AB Adelicate balance between immunostimulatory and immunosuppressive signals mediated by dendritic cells (DCs) and other antigen-presenting cells (APCs) regulates the strength and efficacy of antiviral T-cell responses. HIV is a potent activator of plasmacytoid DCs (pDCs), and chronic pDC activation by HIV promotes the pathogenesis of AIDS. Cholesterol is pivotal in maintaining HIV envelope integrity and allowing HIV-cell interaction. By depleting envelope-associated cholesterol to different degrees, we generated virions with reduced ability to activate pDCs. We found that APC activation was dissociated from the induction of type I IFN-alpha/beta and indoleamine-2,3-dioxygenase (IDO)-mediated immunosuppression in vitro. Extensive cholesterol withdrawal, resulting in partial protein and RNA loss from the virions, rendered HIV a more powerful recall immunogen for stimulating memory CD8 T-cell responses in HIV-exposed, uninfected individuals. These enhanced responses were dependent on the inability of cholesterol-depleted HIV to induce IFN alpha/beta. (Blood. 2011;118(19):5152-5162)
C1 [Boasso, Adriano; Royle, Caroline M.; Doumazos, Spyridon] Univ London Imperial Coll Sci Technol & Med, Immunol Sect, Chelsea & Westminster Hosp, Div Infect Dis,Dept Med,Fac Med, London SW10 9NH, England.
[Aquino, Veronica N.; Graham, David R.] Johns Hopkins Univ, Retrovirus Lab, Dept Mol & Comparat Pathobiol, Sch Med, Baltimore, MD USA.
[Biasin, Mara; Piacentini, Luca; Tavano, Barbara; Clerici, Mario] Univ Milan, Cattedra Immunol, Milan, Italy.
[Fuchs, Dietmar] Innsbruck Med Univ, Div Biol Chem Bioctr, Innsbruck, Austria.
[Mazzotta, Francesco; Lo Caputo, Sergio] Osped SM Annunziata, Div Malattie Infett, Florence, Italy.
[Shearer, Gene M.] NCI, Expt Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Clerici, Mario] Fdn Don C Gnocchi, Ist Ricovero & Cura Carattere Sci, Milan, Italy.
RP Boasso, A (reprint author), Univ London Imperial Coll Sci Technol & Med, Immunol Sect, Chelsea & Westminster Hosp, Div Infect Dis,Dept Med,Fac Med, 369 Fulham Rd, London SW10 9NH, England.
EM a.boasso@imperial.ac.uk; dgraham@jhmi.edu
RI biasin, mara/G-7426-2012; Piacentini, Luca/K-8908-2016;
OI Piacentini, Luca/0000-0003-1022-4481; Boasso,
Adriano/0000-0001-9673-6319; Clerici, Mario/0000-0001-5920-6191
FU Wellcome Trust [085164/Z/08/Z]; National Institutes of Health
[1R01MH087233-01A1, 2P01MH070306-06]
FX This work was supported by a Wellcome Trust award (085164/Z/08/Z to A.B.
and C.M.R.) and by National Institutes of Health grants
(1R01MH087233-01A1 and 2P01MH070306-06 to D.R.G. and V.N.A.).
NR 45
TC 29
Z9 30
U1 0
U2 9
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 10
PY 2011
VL 118
IS 19
BP 5152
EP 5162
DI 10.1182/blood-2011-03-344218
PG 11
WC Hematology
SC Hematology
GA 845ZN
UT WOS:000296867100016
PM 21931112
ER
PT J
AU Yang, D
Tao, J
Li, L
Kedei, N
Toth, ZE
Czap, A
Velasquez, JF
Mihova, D
Michalowski, AM
Yuspa, SH
Blumberg, PM
AF Yang, D.
Tao, J.
Li, L.
Kedei, N.
Toth, Z. E.
Czap, A.
Velasquez, J. F.
Mihova, D.
Michalowski, A. M.
Yuspa, S. H.
Blumberg, P. M.
TI RasGRP3, a Ras activator, contributes to signaling and the tumorigenic
phenotype in human melanoma
SO ONCOGENE
LA English
DT Article
DE Ras activator; Akt; HGF; melanoma; cell transformation; guanine
nucleotide exchange factor
ID POLYMERASE-CHAIN-REACTION; PHORBOL ESTERS; KINASE ACTIVATION; B-RAF;
FUNCTIONAL-ANALYSIS; CELL PROLIFERATION; COLORECTAL TUMORS; REGULATED
KINASE; BRAF MUTATIONS; PHOSPHORYLATION
AB RasGRP3, an activator for H-Ras, R-Ras and Ras-associated protein-1/2, has emerged as an important mediator of signaling downstream from receptor coupled phosphoinositide turnover in B and T cells. Here, we report that RasGRP3 showed a high level of expression in multiple human melanoma cell lines as well as in a subset of human melanoma tissue samples. Suppression of endogenous RasGRP3 expression in these melanoma cell lines reduced Ras-GTP formation as well as c-Met expression and Akt phosphorylation downstream from hepatocyte growth factor (HGF) or epidermal growth factor (EGF) stimulation. RasGRP3 suppression also inhibited cell proliferation and reduced both colony formation in soft agar and xenograft tumor growth in immunodeficient mice, demonstrating the importance of RasGRP3 for the transformed phenotype of the melanoma cells. Reciprocally, overexpression of RasGRP3 in human primary melanocytes altered cellular morphology, markedly enhanced cell proliferation and rendered the cells tumorigenic in a mouse xenograft model. Suppression of RasGRP3 expression in these cells inhibited downstream RasGRP3 responses and suppressed cell growth, confirming the functional role of RasGRP3 in the altered behavior of these cells. The identification of the role of RasGRP3 in melanoma highlights its importance, as a Ras activator, in the phosphoinositide signaling pathway in human melanoma and provides a new potential therapeutic target. Oncogene (2011) 30, 4590-4600; doi: 10.1038/onc.2011.166; published online 23 May 2011
C1 [Yang, D.; Tao, J.; Li, L.; Kedei, N.; Czap, A.; Velasquez, J. F.; Mihova, D.; Michalowski, A. M.; Yuspa, S. H.; Blumberg, P. M.] NCI, Lab Canc Biol & Genet, Ctr Canc Res, Bethesda, MD 20892 USA.
[Toth, Z. E.] Semmelweis Univ, Dept Anat Histol & Embryol, Neuromorphol & Neuroendocrine Res Lab, Budapest, Hungary.
[Toth, Z. E.] Hungarian Acad Sci, Budapest, Hungary.
RP Blumberg, PM (reprint author), NCI, Lab Canc Biol & Genet, Ctr Canc Res, Room 4048,Bldg 37,37 Convent Dr MSC 4255, Bethesda, MD 20892 USA.
EM blumberp@dc37a.nci.nih.gov
FU NIH, Center for Cancer Research, National Cancer Institute [Z1A BC
005270]; ETT [495/09]; Bolyai fellowship
FX This research was supported in part by the intramural program of the
NIH, Center for Cancer Research, National Cancer Institute (project
number Z1A BC 005270) and in part by grant ETT 495/09. ZE Toth is
supported by the Bolyai fellowship. We thank Glenn Merlino for helpful
comments.
NR 54
TC 16
Z9 17
U1 1
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD NOV 10
PY 2011
VL 30
IS 45
BP 4590
EP 4600
DI 10.1038/onc.2011.166
PG 11
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA 846IO
UT WOS:000296890700006
PM 21602881
ER
PT J
AU Chaturvedi, AK
Engels, EA
Pfeiffer, RM
Hernandez, BY
Xiao, WH
Kim, E
Jiang, B
Goodman, MT
Sibug-Saber, M
Cozen, W
Liu, LH
Lynch, CF
Wentzensen, N
Jordan, RC
Altekruse, S
Anderson, WF
Rosenberg, PS
Gillison, ML
AF Chaturvedi, Anil K.
Engels, Eric A.
Pfeiffer, Ruth M.
Hernandez, Brenda Y.
Xiao, Weihong
Kim, Esther
Jiang, Bo
Goodman, Marc T.
Sibug-Saber, Maria
Cozen, Wendy
Liu, Lihua
Lynch, Charles F.
Wentzensen, Nicolas
Jordan, Richard C.
Altekruse, Sean
Anderson, William F.
Rosenberg, Philip S.
Gillison, Maura L.
TI Human Papillomavirus and Rising Oropharyngeal Cancer Incidence in the
United States
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMA; HPV VACCINATION; ORAL-CANCER; NECK-CANCER;
RISK-FACTOR; HEAD; SURVIVAL; INFECTION; THERAPY; SMOKING
AB Purpose
Recent increases in incidence and survival of oropharyngeal cancers in the United States have been attributed to human papillomavirus (HPV) infection, but empirical evidence is lacking.
Patients and Methods
HPV status was determined for all 271 oropharyngeal cancers (1984-2004) collected by the three population-based cancer registries in the Surveillance, Epidemiology, and End Results (SEER) Residual Tissue Repositories Program by using polymerase chain reaction and genotyping (Inno-LiPA), HPV16 viral load, and HPV16 mRNA expression. Trends in HPV prevalence across four calendar periods were estimated by using logistic regression. Observed HPV prevalence was reweighted to all oropharyngeal cancers within the cancer registries to account for nonrandom selection and to calculate incidence trends. Survival of HPV-positive and HPV-negative patients was compared by using Kaplan-Meier and multivariable Cox regression analyses.
Results
HPV prevalence in oropharyngeal cancers significantly increased over calendar time regardless of HPV detection assay (P trend < .05). For example, HPV prevalence by Inno-LiPA increased from 16.3% during 1984 to 1989 to 71.7% during 2000 to 2004. Median survival was significantly longer for HPV-positive than for HPV-negative patients (131 v 20 months; log-rank P < .001; adjusted hazard ratio, 0.31; 95% CI, 0.21 to 0.46). Survival significantly increased across calendar periods for HPV-positive (P = .003) but not for HPV-negative patients (P = .18). Population-level incidence of HPV-positive oropharyngeal cancers increased by 225% (95% CI, 208% to 242%) from 1988 to 2004 (from 0.8 per 100,000 to 2.6 per 100,000), and incidence for HPV-negative cancers declined by 50% (95% CI, 47% to 53%; from 2.0 per 100,000 to 1.0 per 100,000). If recent incidence trends continue, the annual number of HPV-positive oropharyngeal cancers is expected to surpass the annual number of cervical cancers by the year 2020.
Conclusion
Increases in the population-level incidence and survival of oropharyngeal cancers in the United States since 1984 are caused by HPV infection. J Clin Oncol 29: 4294-4301. (C) 2011 by American Society of Clinical Oncology
C1 [Chaturvedi, Anil K.] NCI, NIH, Rockville, MD 20852 USA.
[Altekruse, Sean] NCI, Surveillance Epidemiol & End Results Program, Rockville, MD 20852 USA.
[Hernandez, Brenda Y.; Goodman, Marc T.] Canc Res Ctr Hawaii, Honolulu, HI 96813 USA.
[Xiao, Weihong; Kim, Esther; Jiang, Bo; Gillison, Maura L.] Ohio State Univ, Columbus, OH 43210 USA.
[Sibug-Saber, Maria; Cozen, Wendy; Liu, Lihua] Univ So Calif, Los Angeles, CA USA.
[Jordan, Richard C.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Jordan, Richard C.] Radiat Therapy Oncol Grp Biospecimen Resource, San Francisco, CA USA.
[Lynch, Charles F.] Univ Iowa, Iowa City, IA USA.
RP Chaturvedi, AK (reprint author), NCI, NIH, 6120 Execut Blvd,EPS 7072, Rockville, MD 20852 USA.
EM chaturva@mail.nih.gov
RI Chaturvedi, Anil/J-2024-2015
OI Chaturvedi, Anil/0000-0003-2696-8899
FU National Cancer Institute, National Institutes of Health; The James
Comprehensive Cancer Center; The Ohio State University; Oral Cancer
Foundation; Merck
FX Supported by the Intramural Research Program of the National Cancer
Institute, National Institutes of Health; The James Comprehensive Cancer
Center; The Ohio State University; and the Oral Cancer Foundation.;
Brenda Y. Hernandez, Merck; Maura L. Gillison, Merck
NR 36
TC 882
Z9 890
U1 12
U2 71
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2011
VL 29
IS 32
BP 4294
EP 4301
DI 10.1200/JCO.2011.36.4596
PG 8
WC Oncology
SC Oncology
GA 845BJ
UT WOS:000296797500020
PM 21969503
ER
PT J
AU Rusch, VW
Hawes, D
Decker, PA
Martin, SE
Abati, A
Landreneau, RJ
Patterson, GA
Inculet, RI
Jones, DR
Malthaner, RA
Cohen, RG
Ballman, K
Putnam, JB
Cote, RJ
AF Rusch, Valerie W.
Hawes, Debra
Decker, Paul A.
Martin, Sue Ellen
Abati, Andrea
Landreneau, Rodney J.
Patterson, G. Alexander
Inculet, Richard I.
Jones, David R.
Malthaner, Richard A.
Cohen, Robbin G.
Ballman, Karla
Putnam, Joe B., Jr.
Cote, Richard J.
TI Occult Metastases in Lymph Nodes Predict Survival in Resectable
Non-Small-Cell Lung Cancer: Report of the ACOSOG Z0040 Trial
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID BONE-MARROW MICROMETASTASIS; POLYMERASE-CHAIN-REACTION; CIRCULATING
TUMOR-CELLS; BREAST-CANCER; IMMUNOHISTOCHEMICAL DETECTION;
MESSENGER-RNA; CARCINOMA; MARKERS; CLASSIFICATION; FREQUENCY
AB Purpose
The survival of patients with non-small-cell lung cancer (NSCLC), even when resectable, remains poor. Several small studies suggest that occult metastases (OMs) in pleura, bone marrow (BM), or lymph nodes (LNs) are present in early-stage NSCLC and are associated with a poor outcome. We investigated the prevalence of OMs in resectable NSCLC and their relationship with survival.
Patients and Methods
Eligible patients had previously untreated, potentially resectable NSCLC. Saline lavage of the pleural space, performed before and after pulmonary resection, was examined cytologically. Rib BM and all histologically negative LNs (N0) were examined for OM, diagnosed by cytokeratin immunohistochemistry (IHC). Survival probabilities were estimated using the Kaplan-Meier method. The log-rank test and Cox proportional hazards regression model were used to compare survival of groups of patients. P < .05 was considered significant.
Results
From July 1999 to March 2004, 1,047 eligible patients (538 men and 509 women; median age, 67.2 years) were entered onto the study, of whom 50% had adenocarcinoma and 66% had stage I NSCLC. Pleural lavage was cytologically positive in only 29 patients. OMs were identified in 66 (8.0%) of 821 BM specimens and 130 (22.4%) of 580 LN specimens. In univariate and multivariable analyses OMs in LN but not BM were associated with significantly worse disease-free survival (hazard ratio [HR], 1.50; P = .031) and overall survival (HR, 1.58; P = .009).
Conclusion
In early-stage NSCLC, LN OMs detected by IHC identify patients with a worse prognosis. Future clinical trials should test the role of IHC in identifying patients for adjuvant therapy. J Clin Oncol 29: 4313-4319. (C) 2011 by American Society of Clinical Oncology
C1 [Rusch, Valerie W.] Mem Sloan Kettering Canc Ctr, Thorac Surg Serv, New York, NY 10065 USA.
[Hawes, Debra; Martin, Sue Ellen; Cohen, Robbin G.; Ballman, Karla] Univ So Calif, Los Angeles, CA USA.
[Decker, Paul A.] Mayo Clin, Rochester, MN USA.
[Abati, Andrea] NCI, NIH, Bethesda, MD 20892 USA.
[Landreneau, Rodney J.] Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA.
[Patterson, G. Alexander] Washington Univ, Sch Med, St Louis, MO USA.
[Jones, David R.] Univ Virginia Hlth Syst, Charlottesville, VA USA.
[Putnam, Joe B., Jr.] Vanderbilt Univ, Nashville, TN USA.
[Cote, Richard J.] Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
[Inculet, Richard I.; Malthaner, Richard A.] London Hlth Sci Ctr, London, ON, Canada.
RP Rusch, VW (reprint author), Mem Sloan Kettering Canc Ctr, Thorac Surg Serv, 1275 York Ave, New York, NY 10065 USA.
EM ruschv@mskcc.org
FU National Cancer Institute [U10 CA076001, R01 CA84339]; University of
California [8RT-0061]
FX Supported in part by National Cancer Institute Grants No. U10 CA076001
and R01 CA84339 (R.J.C.) and University of California Tobacco-Related
Disease Research Program Grant No. 8RT-0061 (R.J.C.).
NR 39
TC 33
Z9 35
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2011
VL 29
IS 32
BP 4313
EP 4319
DI 10.1200/JCO.2011.35.2500
PG 7
WC Oncology
SC Oncology
GA 845BJ
UT WOS:000296797500023
PM 21990404
ER
PT J
AU Song, JY
Strom, T
Raffeld, M
Pittaluga, S
Jaffe, ES
AF Song, Joo Y.
Strom, Ted
Raffeld, Mark
Pittaluga, Stefania
Jaffe, Elaine S.
TI Peripheral T-Cell Lymphoma With Aberrant Expression of CD30, CD15, and
CD20
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID MARKERS; CD79A
C1 [Song, Joo Y.; Raffeld, Mark; Pittaluga, Stefania; Jaffe, Elaine S.] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Strom, Ted] Memphis VA Med Ctr, Memphis, TN USA.
[Strom, Ted] Univ Tennessee, Hlth Sci Ctr, Memphis, TN USA.
RP Song, JY (reprint author), NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RI Song, Joo/E-5356-2016;
OI Song, Joo/0000-0003-3497-2513; Jaffe, Elaine/0000-0003-4632-0301
NR 8
TC 4
Z9 4
U1 0
U2 3
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2011
VL 29
IS 32
BP E789
EP E791
DI 10.1200/JCO.2011.36.9280
PG 3
WC Oncology
SC Oncology
GA 845BJ
UT WOS:000296797500003
PM 21990402
ER
PT J
AU Scheinberg, P
Young, NS
AF Scheinberg, Philip
Young, Neal S.
TI Horse versus Rabbit Antithymocyte Globulin in Aplastic Anemia REPLY
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
ID TRIAL; THYMOGLOBULIN; MULTICENTER; THERAPY; ATGAM
C1 [Scheinberg, Philip; Young, Neal S.] NHLBI, Bethesda, MD 20892 USA.
RP Scheinberg, P (reprint author), NHLBI, Bldg 10, Bethesda, MD 20892 USA.
EM scheinbp@mail.nih.gov
RI Scheinberg, Phillip/H-5251-2012
NR 5
TC 0
Z9 0
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
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 10
PY 2011
VL 365
IS 19
BP 1843
EP 1844
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 844QQ
UT WOS:000296762800023
ER
PT J
AU Wang, SS
Lu, YN
Rothman, N
Abdou, AM
Cerhan, JR
De Roos, A
Davis, S
Severson, RK
Cozen, W
Chanock, SJ
Bernstein, L
Morton, LM
Hartge, P
AF Wang, Sophia S.
Lu, Yani
Rothman, Nathaniel
Abdou, Amr M.
Cerhan, James R.
De Roos, Anneclaire
Davis, Scott
Severson, Richard K.
Cozen, Wendy
Chanock, Stephen J.
Bernstein, Leslie
Morton, Lindsay M.
Hartge, Patricia
TI Variation in Effects of Non-Hodgkin Lymphoma Risk Factors According to
the Human Leukocyte Antigen (HLA)-DRB1*01:01 Allele and Ancestral
Haplotype 8.1
SO PLOS ONE
LA English
DT Article
ID EPIDEMIOLOGY CONSORTIUM INTERLYMPH; NECROSIS-FACTOR TNF; POOLED
ANALYSIS; SUN EXPOSURE; POLYMORPHISMS; MALIGNANCIES; IL10
AB Genetic variations in human leukocyte antigens (HLA) are critical in host responses to infections, transplantation, and immunological diseases. We previously identified associations with non-Hodgkin lymphoma (NHL) and the HLA-DRB1*01:01 allele and extended ancestral haplotype (AH) 8.1 (HLA-A*01-B*08-DR*03-TNF-308A). To illuminate how HLA alleles and haplotypes may influence NHL etiology, we examined potential interactions between HLA-DRB1*01:01 and AH 8.1, and a wide range of NHL risk factors among 685 NHL cases and 646 controls from a United States population-based case-control study. We calculated odds ratios and 95% confidence intervals by HLA allele or haplotype status, adjusted for sex, age, race and study center for NHL and two major subtypes using polychotomous unconditional logistic regression models. The previously reported elevation in NHL risk associated with exposures to termite treatment and polychlorinated biphenyls were restricted to individuals who did not possess HLA-DRB1*01:01. Previous associations for NHL and DLBCL with decreased sun exposure, higher BMI, and autoimmune conditions were statistically significant only among those with AH 8.1, and null among those without AH 8.1. Our results suggest that NHL risk factors vary in their association based on HLA-DRB1*01:01 and AH 8.1 status. Our results further suggest that certain NHL risk factors may act through a common mechanism to alter NHL risk. Finally, control participants with either HLA-DRB1*01:01 or AH 8.1 reported having a family history of NHL twice as likely as those who did not have either allele or haplotype, providing the first empirical evidence that HLA associations may explain some of the well-established relationship between family history and NHL risk.
C1 [Wang, Sophia S.; Lu, Yani; Bernstein, Leslie] Beckman Res Inst & City Hope, Div Canc Etiol, Dept Populat Sci, Duarte, CA USA.
[Rothman, Nathaniel; Chanock, Stephen J.; Morton, Lindsay M.; Hartge, Patricia] NCI, Div Canc Epidemiol & Genet, NIH, US Dept HHS, Rockville, MD USA.
[Abdou, Amr M.] Natl Res Ctr, Dept Microbiol & Immunol, Cairo, Egypt.
[Cerhan, James R.] Mayo Clin, Div Epidemiol, Coll Med, Rochester, MN USA.
[De Roos, Anneclaire; Davis, Scott] Univ Washington, Fred Hutchinson Canc Res Ctr, Seattle, WA 98195 USA.
[Severson, Richard K.] Wayne State Univ, Dept Family Med & Publ Hlth Sci, Karmanos Canc Inst, Detroit, MI USA.
[Cozen, Wendy] Univ So Calif, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
RP Wang, SS (reprint author), Beckman Res Inst & City Hope, Div Canc Etiol, Dept Populat Sci, Duarte, CA USA.
EM sowang@coh.org
RI Morton, Lindsay/B-5234-2015;
OI Morton, Lindsay/0000-0001-9767-2310; Abdou, Amr/0000-0002-3373-2406;
Cerhan, James/0000-0002-7482-178X
FU National Institutes of Health (NHI) National Cancer Institute (NCI)
[HHSN261200800001E]; Public Health Service (PHS) [N01-PC-65064,
N01-PC-67008, N01-PC-67009, N01-PC-67010, N02-PC-71105]; NIH, National
Cancer Institute, Center for Cancer Research
FX The NCI-SEER study was supported by the Intramural Research Program of
the National Institutes of Health (NHI) National Cancer Institute (NCI),
and by Public Health Service (PHS) contracts N01-PC-65064, N01-PC-67008,
N01-PC-67009, N01-PC-67010, and N02-PC-71105. HLA typing for the study
was funded in part with federal funds from the National Cancer
Institute, National Institutes of Health, under Contract No.
HHSN261200800001E and in part by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research. 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 United States Government. The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
NR 26
TC 2
Z9 2
U1 0
U2 0
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 9
PY 2011
VL 6
IS 11
AR e26949
DI 10.1371/journal.pone.0026949
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 852II
UT WOS:000297350800017
PM 22096508
ER
PT J
AU Tremblay, ME
Stevens, B
Sierra, A
Wake, H
Bessis, A
Nimmerjahn, A
AF Tremblay, Marie-Eve
Stevens, Beth
Sierra, Amanda
Wake, Hiroaki
Bessis, Alain
Nimmerjahn, Axel
TI The Role of Microglia in the Healthy Brain
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID ADULT HIPPOCAMPAL NEUROGENESIS; CENTRAL-NERVOUS-SYSTEM; IN-VIVO;
VISUAL-CORTEX; SYNAPSE ELIMINATION; PYRAMIDAL NEURONS; DENDRITIC SPINES;
MAMMALIAN BRAIN; MOUSE-BRAIN; D-SERINE
AB Microglia were recently shown to play unexpected roles in normal brain development and adult physiology. This has begun to dramatically change our view of these resident "immune" cells. Here, we briefly review topics covered in our 2011 Society for Neuroscience minisymposium "The Role of Microglia in the Healthy Brain." This summary is not meant to be a comprehensive review of microglia physiology, but rather to share new results and stimulate further research into the cellular and molecular mechanisms by which microglia influence postnatal development, adult neuronal plasticity, and circuit function.
C1 [Tremblay, Marie-Eve] Univ Wisconsin, Dept Psychiat, Madison, WI 53719 USA.
[Stevens, Beth] Childrens Hosp, Dept Neurol, FM Kirby Neurobiol Ctr, Boston, MA 02115 USA.
[Stevens, Beth] Harvard Univ, Sch Med, Program Neurosci, Boston, MA 02115 USA.
[Sierra, Amanda] Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA.
[Wake, Hiroaki] NICHHD, Nervous Syst Dev & Plast Sect, NIH, Bethesda, MD 20892 USA.
[Bessis, Alain] Ecole Normale Super, Inst Biol, Inst Natl Sante & Rech Med 1024, CNRS 8197, F-75005 Paris, France.
[Nimmerjahn, Axel] Salk Inst Biol Studies, Waitt Adv Biophoton Ctr, La Jolla, CA 92037 USA.
RP Tremblay, ME (reprint author), Univ Wisconsin, Dept Psychiat, 6001 Res Pk Blvd, Madison, WI 53719 USA.
EM tremblay2@wisc.edu
RI Sierra, Amanda/E-3305-2010;
OI Sierra, Amanda/0000-0001-8415-096X; Tremblay,
Marie-Eve/0000-0003-2863-9626
FU Fonds de la Recherche en Sante du Quebec; Canadian Institutes of Health
Research; Smith Family Foundation; Dana Foundation; seventh European
Framework Program Moodinflame; Rita Allen Foundation; Whitehall
Foundation; Mirjana Maletic-Savatic; Farish Foundation
FX This work was supported by Fonds de la Recherche en Sante du Quebec and
Canadian Institutes of Health Research postdoctoral fellowships (M.-E.
T.), the Smith Family Foundation and the Dana Foundation (B. S.), the
seventh European Framework Program Moodinflame (A. B.), and the Rita
Allen Foundation Scholars Program and the Whitehall Foundation (A.N.).
We apologize to all colleagues whose important work was not directly
cited due to space limitations. A.S. is grateful to Juan M. Encinas for
critical reading and Mirjana Maletic-Savatic and the Farish Foundation
for funding support. H. W. is grateful to R. Douglas Fields and Philip
R. Lee for critical reading.
NR 77
TC 289
Z9 299
U1 8
U2 56
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 9
PY 2011
VL 31
IS 45
BP 16064
EP 16069
DI 10.1523/JNEUROSCI.4158-11.2011
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA 845CE
UT WOS:000296799700004
PM 22072657
ER
PT J
AU Meissner, K
Bingel, U
Colloca, L
Wager, TD
Watson, A
Flaten, MA
AF Meissner, Karin
Bingel, Ulrike
Colloca, Luana
Wager, Tor D.
Watson, Alison
Flaten, Magne Arve
TI The Placebo Effect: Advances from Different Methodological Approaches
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID CAFFEINE-ASSOCIATED STIMULI; BOWEL-SYNDROME PATIENTS; NOCEBO RESPONSES;
BRAIN ACTIVITY; FUNCTIONAL-SIGNIFICANCE; DISPOSITIONAL OPTIMISM;
CINGULATE CORTEX; OPIOID ACTIVITY; PAIN; ANALGESIA
AB There is accumulating evidence from different methodological approaches that the placebo effect is a neurobiological phenomenon. Behavioral, psychophysiological, and neuroimaging results have largely contributed to accepting the placebo response as real. A major aspect of recent and future advances in placebo research is to demonstrate linkages between behavior, brain, and bodily responses. This article provides an overview of the processes involved in the formation of placebo responses by combining research findings from behavioral, psychophysiological, and neuroimaging methods. The integration of these different methodological approaches is a key objective, motivating our scientific pursuits toward a placebo research that can inform and guide important future scientific knowledge.
C1 [Flaten, Magne Arve] Univ Tromso, Fac Hlth Sci, Dept Psychol, N-9037 Tromso, Norway.
[Meissner, Karin] Univ Munich, Inst Med Psychol, D-80336 Munich, Germany.
[Meissner, Karin] Tech Univ Munich, Inst Gen Practice, D-81776 Munich, Germany.
[Bingel, Ulrike] Univ Med Ctr Hamburg Eppendorf, Dept Neurol, D-20246 Hamburg, Germany.
[Colloca, Luana] NIH, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
[Colloca, Luana] NIH, Dept Bioeth, Bethesda, MD 20892 USA.
[Wager, Tor D.] Univ Colorado, Dept Psychol, Boulder, CO 80309 USA.
[Watson, Alison] Univ Manchester, Human Pain Res Grp, Manchester M13 9PT, Lancs, England.
RP Flaten, MA (reprint author), Univ Tromso, Fac Hlth Sci, Dept Psychol, N-9037 Tromso, Norway.
EM luana.colloca@nih.gov; magne.flaten@uit.no
RI Flaten, Magne Arve/A-2029-2014;
OI Colloca, Luana/0000-0002-6503-4709
FU intramural NCCAM; International Association for the Study of Pain
(IASP); European Federation of IASP; Bial Foundation [186/10]; NIMH
[R01MH076136]; NIDA [1RC1DA028608]; German Federal Ministry of Education
and Research [01GQ0808]; German Research Foundation [FO-1328]
FX This work has been funded in part by generous support from intramural
NCCAM (L. C.), International Association for the Study of Pain (IASP)
and European Federation of IASP Chapters research grants (L. C.), The
Bial Foundation Grant 186/10 (M. A. F.), NIMH Grant R01MH076136 (T. D.
W.), NIDA Grant 1RC1DA028608 (T. D. W.), the German Federal Ministry of
Education and Research (01GQ0808) (U. B.), and the German Research
Foundation (FO-1328) (U.B.).
NR 94
TC 62
Z9 65
U1 3
U2 32
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 9
PY 2011
VL 31
IS 45
BP 16117
EP 16124
DI 10.1523/JNEUROSCI.4099-11.2011
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 845CE
UT WOS:000296799700011
PM 22072664
ER
PT J
AU Tu, HW
Hampton, RR
Murray, EA
AF Tu, Hsiao-Wei
Hampton, Robert R.
Murray, Elisabeth A.
TI Perirhinal Cortex Removal Dissociates Two Memory Systems in
Matching-to-Sample Performance in Rhesus Monkeys
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID OBJECT-DISCRIMINATION; RHINAL CORTEX; UNCONSCIOUS INFLUENCES; INTERTRIAL
INTERVALS; VISUAL RECOGNITION; NEUROTOXIC LESIONS; MACACA-MULATTA; HUMAN
AMNESIA; AREA TE; INDEPENDENCE
AB Dissociations of memory systems are typically made using independent cognitive tests. For example, in monkeys habits have been inferred from performance in object discrimination tests, while non-matching-to-sample tests are thought to measure familiarity resulting from single exposures. Such tests cannot measure individual memory processes accurately when more than one memory process contributes to performance. In process dissociation procedures (PDPs), two memory processes cooperate and compete in the performance of a single cognitive task, allowing quantitative estimates of the contributions of each process. We used PDP to measure the contributions of habits and one-trial memory to visual matching-to-sample performance. Sets of test images were shown only once in each daily testing session but were repeated day after day. To produce habits, high-frequency images were correct more frequently than other images across days. Habits were manifest in the extent to which choices in the test phase of matching-to-sample trials were made to the high-frequency images, regardless of which image had been presented as the sample. One-trial memory was measured by the extent to which choices at test were made to the image that had appeared as the sample on that trial, regardless of habit. Perirhinal cortex removal reduced the contribution of one-trial memory to matching performance, but left both habits and the ability to discriminate images intact. PDP can be applied in monkeys in a way that parallels its use in humans, providing a new tool for investigating the neurobiology of memory in nonhuman animals and for comparing memory across species.
C1 [Tu, Hsiao-Wei; Hampton, Robert R.] Emory Univ, Dept Psychol, Atlanta, GA 30322 USA.
[Tu, Hsiao-Wei; Hampton, Robert R.] Emory Univ, Yerkes Natl Primate Res Ctr, Atlanta, GA 30322 USA.
[Murray, Elisabeth A.] NIMH, Sect Neurobiol Learning & Memory, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA.
RP Tu, HW (reprint author), Emory Univ, Yerkes Natl Primate Res Ctr, 954 Gatewood Rd, Atlanta, GA 30329 USA.
EM hsiaowei.tu@emory.edu
OI Murray, Elisabeth/0000-0003-1450-1642
FU National Institute of Mental Health (NIMH) [R01MH082819]; National
Science Foundation [0745573]; Yerkes Center [RR-00165]
FX This work was supported by the Intramural Research Program of the
National Institute of Mental Health (NIMH). Additional support was
provided by NIMH Grant R01MH082819, National Science Foundation Grant
0745573, and Yerkes Center Base Grant RR-00165, which was awarded by the
Animal Resources Program of the National Institutes of Health. We thank
Sparky Zivin for assistance with testing animals and animal care; Rick
Duntz for assistance in surgery; and Jeanette Black and Renee Hill of
the NIH In Vivo Nuclear Magnetic Resonance Research Center for technical
assistance.
NR 47
TC 9
Z9 9
U1 2
U2 11
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 9
PY 2011
VL 31
IS 45
BP 16336
EP 16343
DI 10.1523/JNEUROSCI.2338-11.2011
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 845CE
UT WOS:000296799700032
PM 22072685
ER
PT J
AU Giri, J
Li, WJ
Tuan, RS
Cicerone, MT
AF Giri, Jyotsnendu
Li, Wan-Ju
Tuan, Rocky S.
Cicerone, Marcus T.
TI Stabilization of Proteins by Nanoencapsulation in Sugar-Glass for Tissue
Engineering and Drug Delivery Applications
SO ADVANCED MATERIALS
LA English
DT Article
ID GROWTH-FACTOR DELIVERY; AOT REVERSE MICELLES; BIODEGRADABLE
MICROSPHERES; POLY(ETHYLENE GLYCOL); CONTROLLED-RELEASE; PLGA
MICROSPHERES; ENCAPSULATION; STABILITY; SYSTEMS; ASSAY
AB A novel sugar-glass-nanoparticle (SGnP) system is developed to stabilize biomolecules for incorporation and delivery from a drug delivery system. It yields excellent protection from process-related stresses with little or no degradation, very good encapsulation efficiency, and storage stability, as well as giving burst-free sustained release for essentially any protein and polymer system of interest.
C1 [Giri, Jyotsnendu; Cicerone, Marcus T.] NIST, Div Polymers, Gaithersburg, MD 20899 USA.
[Giri, Jyotsnendu; Tuan, Rocky S.] Natl Inst Arthrit & Musculoskeletal & Skin Dis, NIH, Bethesda, MD 20892 USA.
[Li, Wan-Ju] Univ Wisconsin Madison, Dept Orthopaed & Rehabil, Madison, WI 53705 USA.
[Li, Wan-Ju] Univ Wisconsin Madison, Dept Biomed Engn, Madison, WI 53705 USA.
[Tuan, Rocky S.] Univ Pittsburgh, Sch Med, Ctr Cellular & Mol Engn, Dept Orthoped Surg, Pittsburgh, PA 15219 USA.
RP Cicerone, MT (reprint author), NIST, Div Polymers, Gaithersburg, MD 20899 USA.
EM cicerone@nist.gov
FU NIH/NIBIB [R01 EB006398-01A1]; National Research Council of the National
Academy of Sciences in the Joint NIH/NIST
FX The authors acknowledge funding from NIH/NIBIB under grant R01
EB006398-01A1. J.G. acknowledges postdoctoral fellowship support from
the National Research Council of the National Academy of Sciences in the
Joint NIH/NIST Postdoctoral Programs. The authors gratefully acknowledge
assistance from Steve Hudson (NIST) for TEM imaging. This article, a
contribution of NIST, is not subject to US copyright.
NR 37
TC 11
Z9 11
U1 1
U2 33
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA BOSCHSTRASSE 12, D-69469 WEINHEIM, GERMANY
SN 0935-9648
J9 ADV MATER
JI Adv. Mater.
PD NOV 9
PY 2011
VL 23
IS 42
BP 4861
EP 4867
DI 10.1002/adma.201102267
PG 7
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
Nanotechnology; Materials Science, Multidisciplinary; Physics, Applied;
Physics, Condensed Matter
SC Chemistry; Science & Technology - Other Topics; Materials Science;
Physics
GA 848HH
UT WOS:000297042000004
PM 21953536
ER
PT J
AU Yamashita, S
Lukacik, P
Barnard, TJ
Noinaj, N
Felek, S
Tsang, TM
Krukonis, ES
Hinnebusch, BJ
Buchanan, SK
AF Yamashita, Satoshi
Lukacik, Petra
Barnard, Travis J.
Noinaj, Nicholas
Felek, Suleyman
Tsang, Tiffany M.
Krukonis, Eric S.
Hinnebusch, B. Joseph
Buchanan, Susan K.
TI Structural Insights into Ail-Mediated Adhesion in Yersinia pestis
SO STRUCTURE
LA English
DT Article
ID OUTER-MEMBRANE PROTEIN; ESCHERICHIA-COLI; YOP DELIVERY;
EXTRACELLULAR-MATRIX; PLAGUE VIRULENCE; HOST-CELLS; RESISTANCE;
INVASION; ENTEROCOLITICA; EXPRESSION
AB Ail is an outer membrane protein from Yersinia pestis that is highly expressed in a rodent model of bubonic plague, making it a good candidate for vaccine development. Ail is important for attaching to host cells and evading host immune responses, facilitating rapid progression of a plague infection. Binding to host cells is important for injection of cytotoxic Yersinia outer proteins. To learn more about how Ail mediates adhesion, we solved two high-resolution crystal structures of Ail, with no ligand bound and in complex with a heparin analog called sucrose octasulfate. We identified multiple adhesion targets, including laminin and heparin, and showed that a 40 kDa domain of laminin called LG4-5 specifically binds to Ail. We also evaluated the contribution of laminin to delivery of Yops to HEp-2 cells. This work constitutes a structural description of how a bacterial outer membrane protein uses a multivalent approach to bind host cells.
C1 [Yamashita, Satoshi; Lukacik, Petra; Barnard, Travis J.; Noinaj, Nicholas; Buchanan, Susan K.] NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Felek, Suleyman; Krukonis, Eric S.] Univ Michigan, Sch Dent, Dept Biol & Mat Sci, Ann Arbor, MI 48109 USA.
[Tsang, Tiffany M.; Krukonis, Eric S.] Univ Michigan, Sch Med, Dept Microbiol & Immunol, Ann Arbor, MI 48109 USA.
[Hinnebusch, B. Joseph] NIAID, Lab Zoonot Pathogens, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
RP Buchanan, SK (reprint author), NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM skbuchan@helix.nih.gov
FU NIH, National Institute of Diabetes and Digestive and Kidney Diseases;
NIH, National Institute of Allergy and Infectious Diseases; NIH
[R21AI090194]; U. S. Department of Energy, Office of Science, Office of
Basic Energy Sciences [W-31-109-Eng-38]
FX The authors thank N. Suzuki for providing samples, technical support,
and discussions, and H. Bernstein and J. Fairman for reading the
manuscript. S.Y., P.L., T.J.B., N.N., and S.K.B. are supported by the
Intramural Research Program of the NIH, National Institute of Diabetes
and Digestive and Kidney Diseases. B.J.H. is supported by the Intramural
Research Program of the NIH, National Institute of Allergy and
Infectious Diseases. S.F., T.M.T., and E.S.K. are supported by NIH Grant
R21AI090194 to E.S.K. Data were collected at Southeast Regional
Collaborative Access Team (SER-CAT) beamline 22-ID at the Advanced
Photon Source, Argonne National Laboratory. Supporting institutions may
be found at http://www.ser-cat.org/members.html. Use of the Advanced
Photon Source 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.
NR 31
TC 27
Z9 29
U1 0
U2 7
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0969-2126
J9 STRUCTURE
JI Structure
PD NOV 9
PY 2011
VL 19
IS 11
BP 1672
EP 1682
DI 10.1016/j.str.2011.08.010
PG 11
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 847VD
UT WOS:000296999700018
PM 22078566
ER
PT J
AU Miller, FG
Pearson, SD
AF Miller, Franklin G.
Pearson, Steven D.
TI Linking Insurance Coverage for Innovative Invasive Procedures With
Participation in Clinical Research
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
ID STENOSIS; STROKE
C1 [Miller, Franklin G.; Pearson, Steven D.] NIH, Dept Bioeth, Ctr Clin, Bethesda, MD 20892 USA.
RP Miller, FG (reprint author), NIH, Dept Bioeth, Ctr Clin, Bldg 10,Room 1C118, Bethesda, MD 20892 USA.
EM fmiller@nih.gov
FU Intramural NIH HHS
NR 9
TC 3
Z9 3
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 9
PY 2011
VL 306
IS 18
BP 2024
EP 2025
DI 10.1001/jama.2011.1631
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 843VT
UT WOS:000296704300027
PM 22068996
ER
PT J
AU Ma, HY
Sullivan-Halley, J
Smith, AW
Neuhouser, ML
Alfano, CM
Meeske, K
George, SM
McTiernan, A
McKean-Cowdin, R
Baumgartner, KB
Ballard-Barbash, R
Bernstein, L
AF Ma, Huiyan
Sullivan-Halley, Jane
Smith, Ashley W.
Neuhouser, Marian L.
Alfano, Catherine M.
Meeske, Kathleen
George, Stephanie M.
McTiernan, Anne
McKean-Cowdin, Roberta
Baumgartner, Kathy B.
Ballard-Barbash, Rachel
Bernstein, Leslie
TI Estrogenic botanical supplements, health-related quality of life,
fatigue, and hormone-related symptoms in breast cancer survivors: a HEAL
study report
SO BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE
LA English
DT Article
ID ALPHA-LINOLENIC ACID; POSTMENOPAUSAL WOMEN; LONG-TERM; CONTROLLED-TRIAL;
DOUBLE-BLIND; HOT FLASHES; ALTERNATIVE MEDICINE; ENDOGENOUS HORMONES;
SOY PHYTOESTROGENS; PHYSICAL-ACTIVITY
AB Background: It remains unclear whether estrogenic botanical supplement (EBS) use influences breast cancer survivors' health-related outcomes.
Methods: We examined the associations of EBS use with health-related quality of life (HRQOL), with fatigue, and with 15 hormone-related symptoms such as hot flashes and night sweats among 767 breast cancer survivors participating in the Health, Eating, Activity, and Lifestyle (HEAL) Study. HRQOL was measured by the Medical Outcomes Study short form-36 physical and mental component scale summary score. Fatigue was measured by the Revised-Piper Fatigue Scale score.
Results: Neither overall EBS use nor the number of EBS types used was associated with HRQOL, fatigue, or hormone-related symptoms. However, comparisons of those using each specific type of EBS with non-EBS users revealed the following associations. Soy supplements users were more likely to have a better physical health summary score (odds ratio [OR] = 1.66, 95% confidence interval [CI] = 1.02-2.70). Flaxseed oil users were more likely to have a better mental health summary score (OR = 1.76, 95% CI = 1.05-2.94). Ginseng users were more likely to report severe fatigue and several hormone-related symptoms (all ORs >= 1.7 and all 95% CIs exclude 1). Red clover users were less likely to report weight gain, night sweats, and difficulty concentrating (all OR approximately 0.4 and all 95% CIs exclude 1). Alfalfa users were less likely to experience sleep interruption (OR = 0.28, 95% CI = 0.12-0.68). Dehydroepiandrosterone users were less likely to have hot flashes (OR = 0.33, 95% CI = 0.14-0.82).
Conclusions: Our findings indicate that several specific types of EBS might have important influences on a woman's various aspects of quality of life, but further verification is necessary.
C1 [Ma, Huiyan; Sullivan-Halley, Jane; Bernstein, Leslie] City Hope Natl Med Ctr, Beckman Res Inst, Dept Populat Sci, Div Canc Etiol, Duarte, CA 91010 USA.
[Smith, Ashley W.; Alfano, Catherine M.; Ballard-Barbash, Rachel] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Neuhouser, Marian L.; McTiernan, Anne] Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA.
[Meeske, Kathleen] Childrens Hosp Los Angeles, Childrens Ctr Canc & Blood Dis, Los Angeles, CA 90027 USA.
[George, Stephanie M.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[McKean-Cowdin, Roberta] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90089 USA.
[Baumgartner, Kathy B.] Univ Louisville, Sch Publ Hlth & Informat Sci, Louisville, KY 40202 USA.
RP Ma, HY (reprint author), City Hope Natl Med Ctr, Beckman Res Inst, Dept Populat Sci, Div Canc Etiol, Duarte, CA 91010 USA.
EM hma@coh.org
FU National Cancer Institute [N01-CN-5036-20, N01-CN-05228,
N01-PC-67010/N01-PC-35139, N01-PC-67007/N01-PC-35138,
N01-PC-67009/N01-PC-35142, T32 CA09661]; NIH [M01-RR-00037]; National
Institute of Child Health and Human Development [N01-HD-3-3175];
California Department of Health Services [050Q-8709-S1528]
FX National Cancer Institute contracts N01-CN-5036-20, N01-CN-05228,
N01-PC-67010/N01-PC-35139, N01-PC-67007/N01-PC-35138 and
N01-PC-67009/N01-PC-35142, and training grant T32 CA09661. A portion of
this work was conducted through the Clinical Research Center at the
University of Washington and supported by the NIH grant M01-RR-00037.
Data collection for the Women's Contraceptive and Reproductive
Experiences Study at the University of Southern California was supported
by the National Institute of Child Health and Human Development contract
N01-HD-3-3175. Patient identification was supported in part by the
California Department of Health Services grant 050Q-8709-S1528.
NR 71
TC 11
Z9 11
U1 2
U2 7
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 8
PY 2011
VL 11
AR 109
DI 10.1186/1472-6882-11-109
PG 11
WC Integrative & Complementary Medicine
SC Integrative & Complementary Medicine
GA 858HU
UT WOS:000297787500001
PM 22067368
ER
PT J
AU Neddens, J
Buonanno, A
AF Neddens, Joerg
Buonanno, Andres
TI Expression of the Neuregulin Receptor ErbB4 in the Brain of the Rhesus
Monkey (Macaca mulatta)
SO PLOS ONE
LA English
DT Article
ID LONG-TERM POTENTIATION; PARVALBUMIN-POSITIVE INTERNEURONS;
CENTRAL-NERVOUS-SYSTEM; TYROSINE KINASE; DIFFERENTIAL EXPRESSION;
GABAERGIC INTERNEURONS; SEXUAL DEVELOPMENT; RETICULAR NUCLEUS;
PREFRONTAL CORTEX; RAT HIPPOCAMPUS
AB We demonstrated recently that frontal cortical expression of the Neuregulin (NRG) receptor ErbB4 is restricted to interneurons in rodents, macaques, and humans. However, little is known about protein expression patterns in other areas of the brain. In situ hybridization studies have shown high ErbB4 mRNA levels in various subcortical areas, suggesting that ErbB4 is also expressed in cell types other than cortical interneurons. Here, using highly-specific monoclonal antibodies, we provide the first extensive report of ErbB4 protein expression throughout the cerebrum of primates. We show that ErbB4 immunoreactivity is high in association cortices, intermediate in sensory cortices, and relatively low in motor cortices. The overall immunoreactivity in the hippocampal formation is intermediate, but is high in a subset of interneurons. We detected the highest overall immunoreactivity in distinct locations of the ventral hypothalamus, medial habenula, intercalated nuclei of the amygdala and structures of the ventral forebrain, such as the islands of Calleja, olfactory tubercle and ventral pallidum, and medium expression in the reticular thalamic nucleus. While this pattern is generally consistent with ErbB4 mRNA expression data, further investigations are needed to identify the exact cellular and subcellular sources of mRNA and protein expression in these areas. In contrast to in situ hybridization in rodents, we detected only low levels of ErbB4-immunoreactivity in mesencephalic dopaminergic nuclei but a diffuse pattern of immunofluorescence that was medium in the dorsal striatum and high in the ventral forebrain, suggesting that most ErbB4 protein in dopaminergic neurons could be transported to axons. We conclude that the NRG-ErbB4 signaling pathway can potentially influence many functional systems throughout the brain of primates, and suggest that major sites of action are areas of the "corticolimbic" network. This interpretation is functionally consistent with the genetic association of NRG1 and ERBB4 with schizophrenia.
C1 [Neddens, Joerg; Buonanno, Andres] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Mol Neurobiol Sect, NIH, Bethesda, MD USA.
RP Neddens, J (reprint author), JSW Life Sci GmbH, Dept Histol, Grambach, Austria.
EM jneddens@jsw-lifesciences.com
FU Eunice Kennedy Shriver National Institutes of Child Health and Human
Development (NICHD), National Institutes of Health
FX The research was supported by the Intramural Research Program of the
Eunice Kennedy Shriver National Institutes of Child Health and Human
Development (NICHD), National Institutes of Health. Neither institution
had a role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 69
TC 8
Z9 8
U1 2
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 8
PY 2011
VL 6
IS 11
AR e27337
DI 10.1371/journal.pone.0027337
PG 20
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 852HZ
UT WOS:000297349700033
PM 22087295
ER
PT J
AU Rostami, E
Krueger, F
Zoubak, S
Dal Monte, O
Raymont, V
Pardini, M
Hodgkinson, CA
Goldman, D
Risling, M
Grafman, J
AF Rostami, Elham
Krueger, Frank
Zoubak, Serguei
Dal Monte, Olga
Raymont, Vanessa
Pardini, Matteo
Hodgkinson, Colin A.
Goldman, David
Risling, Marten
Grafman, Jordan
TI BDNF Polymorphism Predicts General Intelligence after Penetrating
Traumatic Brain Injury
SO PLOS ONE
LA English
DT Article
ID NEUROTROPHIC FACTOR GENE; FACTOR VAL66MET POLYMORPHISM; FAMILY-BASED
ASSOCIATION; TRKB MESSENGER-RNA; BIPOLAR DISORDER; HEAD-INJURY;
APOLIPOPROTEIN-E; CONFERS SUSCEPTIBILITY; HIPPOCAMPAL-FORMATION;
ALZHEIMERS-DISEASE
AB Neuronal plasticity is a fundamental factor in cognitive outcome following traumatic brain injury. Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, plays an important role in this process. While there are many ways to measure cognitive outcome, general cognitive intelligence is a strong predictor of everyday decision-making, occupational attainment, social mobility and job performance. Thus it is an excellent measure of cognitive outcome following traumatic brain injury (TBI). Although the importance of the single-nucleotide polymorphisms polymorphism on cognitive function has been previously addressed, its role in recovery of general intelligence following TBI is unknown. We genotyped male Caucasian Vietnam combat veterans with focal penetrating TBI (pTBI) (n = 109) and non-head injured controls (n = 38) for 7 BDNF single-nucleotide polymorphisms. Subjects were administrated the Armed Forces Qualification Test (AFQT) at three different time periods: pre-injury on induction into the military, Phase II (10-15 years post-injury, and Phase III (30-35 years post-injury). Two single-nucleotide polymorphisms, rs7124442 and rs1519480, were significantly associated with post-injury recovery of general cognitive intelligence with the most pronounced effect at the Phase II time point, indicating lesion-induced plasticity. The genotypes accounted for 5% of the variance of the AFQT scores, independently of other significant predictors such as pre-injury intelligence and percentage of brain volume loss. These data indicate that genetic variations in BDNF play a significant role in lesion-induced recovery following pTBI. Identifying the underlying mechanism of this brain-derived neurotrophic factor effect could provide insight into an important aspect of post-traumatic cognitive recovery.
C1 [Rostami, Elham; Risling, Marten] Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
[Krueger, Frank] George Mason Univ, Dept Mol Neurosci, Fairfax, VA 22030 USA.
[Krueger, Frank] George Mason Univ, Dept Psychol, Fairfax, VA 22030 USA.
[Dal Monte, Olga] Natl Inst Neurol Disorders & Stroke, Cognit Neurosci Sect, NIH, Bethesda, MD USA.
[Zoubak, Serguei; Hodgkinson, Colin A.; Goldman, David] NIAAA, Neurogenet Lab, NIH, Bethesda, MD USA.
[Zoubak, Serguei] Uniformed Serv Univ Hlth Sci, Ctr Neurosci & Regenerat Med, Bethesda, MD 20814 USA.
[Pardini, Matteo] Univ Genoa, Dept Neurosci Ophtalmol & Genet, Genoa, Italy.
[Pardini, Matteo] Univ Genoa, Magnet Resonance Res Ctr Nervous Syst Dis, Genoa, Italy.
[Zoubak, Serguei] Henry Jackson Fdn Adv Mil Med, Rockville, MD USA.
[Grafman, Jordan] Kessler Fdn Res Ctr, Traumat Brain Injury Res Lab, W Orange, NJ USA.
[Raymont, Vanessa] Johns Hopkins Univ, Dept Radiol, Baltimore, MD USA.
[Raymont, Vanessa] Univ London Imperial Coll Sci Technol & Med, Dept Med, London, England.
RP Rostami, E (reprint author), Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
EM jgrafman@kesslerfoundation.org
RI Pardini, Matteo/F-8414-2010; Goldman, David/F-9772-2010;
OI Pardini, Matteo/0000-0002-4740-1982; Goldman, David/0000-0002-1724-5405;
Grafman, Jordan H./0000-0001-8645-4457
FU U.S. National Institute of Neurological Disorders and Stroke; U.S. Army
Medical Research and Material Command
FX This work was supported by the U.S. National Institute of Neurological
Disorders and Stroke intramural research program and a project grant
from the U.S. Army Medical Research and Material Command administrated
by the Henry M. Jackson Foundation (Vietnam Head Injury Study Phase III:
a 30-year post-injury follow-up study). No external funding was received
for this study. The funders had no role in study design, data collection
and analysis, decision to publish, or preparation of the manuscript.
NR 97
TC 19
Z9 21
U1 1
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 8
PY 2011
VL 6
IS 11
AR e27389
DI 10.1371/journal.pone.0027389
PG 13
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 852HZ
UT WOS:000297349700038
PM 22087305
ER
PT J
AU Talisman, IJ
Kumar, V
Deschamps, JR
Frisch, M
Malhotra, SV
AF Talisman, Ian J.
Kumar, Vineet
Deschamps, Jeffrey R.
Frisch, Mark
Malhotra, Sanjay V.
TI Application of silver N-heterocyclic carbene complexes in
O-glycosidation reactions
SO CARBOHYDRATE RESEARCH
LA English
DT Article
DE O-Glycosidation; Silver N-heterocyclic carbene complex; Carbohydrates
ID FACILE SYNTHESIS; LIQUIDS; CANCER; AGENTS; DRUGS; BOND
AB We report the efficient O-glycosidation of glycosyl bromides with therapeutically relevant acceptors facilitated by silver N-heterocyclic carbene (Ag-NHC) complexes. A set of four Ag-NHC complexes was synthesized and evaluated as promoters for glycosidation reactions. Two new bis-Ag-NHC complexes derived from ionic liquids 1-benzyl-3-methyl-1H-imidazolium chloride and 1-(2-methoxyethyl)-3-methylimidazolium chloride were found to efficiently promote glycosidation, whereas known mono-Ag complexes of 1,3-bis(2,4,6-trimethylphenyl)imidazolium chloride and 1,3-bis(2,6-di-isopropylphenyl)imidazolium chloride failed to facilitate the reaction. The structures of the promoters were established by X-ray crystallography and these complexes were employed in the glycosidation of different glycosyl bromide donors with biologically valuable acceptors, such as estrone, estradiol, and various flavones. The products were obtained in yields considered good to excellent, and all reactions were highly selective for the 13 isomer regardless of neighboring group effects. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Talisman, Ian J.; Kumar, Vineet; Malhotra, Sanjay V.] NCI, Lab Synthet Chem, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Deschamps, Jeffrey R.; Frisch, Mark] USN, Res Lab, Washington, DC 20375 USA.
RP Malhotra, SV (reprint author), NCI, Lab Synthet Chem, SAIC Frederick Inc, 1050 Boyles St, Frederick, MD 21702 USA.
EM malhotrasa@mail.nih.gov
RI yan, peifang/G-2730-2011;
OI Deschamps, Jeffrey/0000-0001-5845-0010
FU NCI, National Institutes of Health [HSN261200800001E]; NIDA [Y1-DA1101]
FX This project has been funded in whole or in part with federal funds from
the NCI, National Institutes of Health, under Contract No.
HSN261200800001E. X-ray studies were supported by NIDA under interagency
agreement Y1-DA1101. The authors would like to thank Dr. Que N. Van for
the HBMC of compound 31.
NR 34
TC 6
Z9 6
U1 1
U2 11
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0008-6215
J9 CARBOHYD RES
JI Carbohydr. Res.
PD NOV 8
PY 2011
VL 346
IS 15
BP 2337
EP 2341
DI 10.1016/j.carres.2011.07.025
PG 5
WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA 847CV
UT WOS:000296950400003
PM 21911215
ER
PT J
AU Brodie, BR
Pokharel, Y
Hansen, C
Kissling, G
Milks, S
Cooper, M
McAlhany, C
Stuckey, T
AF Brodie, Bruce R.
Pokharel, Yashashwi
Hansen, Charles
Kissling, Grace
Milks, Sally
Cooper, Michael
McAlhany, Chris
Stuckey, Thomas
TI Incidence and Predictors of Early or Late and Very Late Stent Thrombosis
following Primary PCI with BMS and DES for STEMI: A 16 year Single
Center Experience
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 23rd Annual Transcatheter Cardiovascular Therapeutics (TCT) Symposium
CY NOV 07-11, 2011
CL San Francisco, CA
C1 [Brodie, Bruce R.; Milks, Sally; Cooper, Michael; McAlhany, Chris; Stuckey, Thomas] Cone Heart & Vasc Ctr, Greensboro, NC USA.
[Pokharel, Yashashwi; Hansen, Charles] Univ N Carolina, Internal Med Residency Program, Greensboro, NC 27412 USA.
[Kissling, Grace] NIEHS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 8
PY 2011
VL 58
IS 20
SU B
BP B21
EP B22
PG 2
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 846IZ
UT WOS:000296891900094
ER
PT J
AU Wang, W
Yang, J
Liu, H
Lu, D
Chen, XF
Zenonos, Z
Campos, LS
Rad, R
Guo, G
Zhang, SJ
Bradley, A
Liu, PT
AF Wang, Wei
Yang, Jian
Liu, Hui
Lu, Dong
Chen, Xiongfeng
Zenonos, Zenon
Campos, Lia S.
Rad, Roland
Guo, Ge
Zhang, Shujun
Bradley, Allan
Liu, Pentao
TI Rapid and efficient reprogramming of somatic cells to induced
pluripotent stem cells by retinoic acid receptor gamma and liver
receptor homolog 1
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE embryonic stem cell; RAREoct; piggyBac transposition; SH-iPSC
ID GROUND-STATE PLURIPOTENCY; NUCLEAR RECEPTORS; HUMAN FIBROBLASTS;
GENE-EXPRESSION; DEFINED FACTORS; BREAST-CANCER; SELF-RENEWAL; MOUSE
CLONES; GENERATION; PIGGYBAC
AB Somatic cells can be reprogrammed to induced pluripotent stem cells (iPSCs) by expressing four transcription factors: Oct4, Sox2, Klf4, and c-Myc. Here we report that enhancing RA signaling by expressing RA receptors (RARs) or by RA agonists profoundly promoted reprogramming, but inhibiting it using a RAR-alpha dominant-negative form completely blocked it. Coexpressing Rarg (RAR-gamma) and Lrh-1 (liver receptor homologue 1; Nr5a2) with the four factors greatly accelerated reprogramming so that reprogramming of mouse embryonic fibroblast cells to ground-state iPSCs requires only 4 d induction of these six factors. The six-factor combination readily reprogrammed primary human neonatal and adult fibroblast cells to exogenous factor-independent iPSCs, which resembled ground-state mouse ES cells in growth properties, gene expression, and signaling dependency. Our findings demonstrate that signaling through RARs has critical roles in molecular reprogramming and that the synergistic interaction between Rarg and Lrh1 directs reprogramming toward ground-state pluripotency. The human iPSCs described here should facilitate functional analysis of the human genome.
C1 [Wang, Wei; Yang, Jian; Liu, Hui; Lu, Dong; Zenonos, Zenon; Campos, Lia S.; Rad, Roland; Bradley, Allan; Liu, Pentao] Wellcome Trust Sanger Inst, Hinxton CB10 1HH, S Cambs, England.
[Liu, Hui; Zhang, Shujun] Huazhong Agr Univ, Coll Anim Sci & Technol, Wuhan 430070, Peoples R China.
[Chen, Xiongfeng] Sci Applicat Int Corporat Frederick, Frederick, MD 21701 USA.
[Chen, Xiongfeng] NCI, Frederick, MD 21701 USA.
[Guo, Ge] Univ Cambridge, Wellcome Trust Ctr Stem Cell Res, Cambridge CB2 1QR, England.
RP Liu, PT (reprint author), Wellcome Trust Sanger Inst, Hinxton CB10 1HH, S Cambs, England.
EM pl2@sanger.ac.uk
FU Wellcome Trust [077186/Z/05/Z]; China Scholarship Council
FX We thank Prof. Austin Smith for the Oct4-Puro-IRES-EGFP cassette and for
the Oct4-GFP MEFs, Dr. Fangtang Yang and Beiyun Fu for spectral
karyotyping human iPSCs, Dr. Yali Xue for helping genotype human Y
chromosome polymorphisms, and the RSF staff of the Sanger Institute for
their assistance on the mouse work. We thank Dr. Peter W. Andrews for
the human ES cell antibodies. P.L. thanks Prof. Mike Stratton, Prof.
Janet Rossant, and Drs. Bill Skarnes, Derek Stemple, Andy Futreal, and
Carol Smee for comments and suggestions on this manuscript. This work
was supported by the Wellcome Trust (077186/Z/05/Z) (to P.L.) and by the
China Scholarship Council (H.L.).
NR 49
TC 97
Z9 106
U1 4
U2 24
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 8
PY 2011
VL 108
IS 45
BP 18283
EP 18288
DI 10.1073/pnas.1100893108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 843UT
UT WOS:000296700000031
PM 21990348
ER
PT J
AU Hassan, H
Sakaguchi, S
Tenno, M
Kopf, A
Boucheron, N
Carpenter, AC
Egawa, T
Taniuchi, I
Ellmeier, W
AF Hassan, Hammad
Sakaguchi, Shinya
Tenno, Mari
Kopf, Aglaja
Boucheron, Nicole
Carpenter, Andrea C.
Egawa, Takeshi
Taniuchi, Ichiro
Ellmeier, Wilfried
TI Cd8 enhancer E8(I) and Runx factors regulate CD8 alpha expression in
activated CD8(+) T cells
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE epigenetic marks; transcriptional control; cytotoxic T lymphocytes
ID GENE-EXPRESSION; DIFFERENTIATION; THYMOCYTES; CHROMATIN; COMMITMENT;
LINEAGE; BINDING; REPRESSION; PROTEINS; DELETION
AB Cd8a and Cd8b1 coreceptor gene (Cd8) expression is tightly controlled during T-cell development by the activity of five Cd8 enhancers (E8(I)-E8(V)). Here we demonstrate a unique transcriptional program regulating CD8 expression during CD8(+) effector T-cell differentiation. The Cd8 enhancer E8(I) and Runx/core-binding factor-beta (CBF beta) complexes were required for the establishment of this regulatory circuit, because E8(I)-, Runx3-, or CBF beta-deficient CD8(+) T cells down-regulated CD8 alpha expression during activation. This finding correlated with enhanced repressive histone marks at the Cd8a promoter in the absence of E8(I), and the down-regulation of CD8 alpha expression could be blocked by treating E8I-, Runx3-, or CBF beta-deficient CD8(+) T cells with the histone deacetylase inhibitor trichostatin A. Moreover, Runx/CBF beta complexes bound the Cd8ab gene cluster in activated CD8(+) T cells, suggesting direct control of the Cd8a locus. However, CD8(+) effector T cells maintained high levels of CD8 alpha when CBF beta was conditionally deleted after activation. Thus, our data suggest an E8(I)- and Runx3/CBF beta-dependent epigenetic programming of the Cd8a locus during T-cell activation, leading to Runx/CBF beta complex-independent maintenance of CD8 alpha expression in effector T cells.
C1 [Hassan, Hammad; Sakaguchi, Shinya; Kopf, Aglaja; Boucheron, Nicole; Ellmeier, Wilfried] Med Univ Vienna, Inst Immunol, Ctr Pathophysiol Infectiol & Immunol, Div Immunobiol, A-1090 Vienna, Austria.
[Tenno, Mari; Taniuchi, Ichiro] RIKEN Res Ctr Allergy & Immunol, Lab Transcript Regulat, Kanagawa 2300045, Japan.
[Carpenter, Andrea C.] NCI, Lab Immune Cell Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Egawa, Takeshi] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA.
RP Ellmeier, W (reprint author), Med Univ Vienna, Inst Immunol, Ctr Pathophysiol Infectiol & Immunol, Div Immunobiol, A-1090 Vienna, Austria.
EM wilfried.ellmeier@meduniwien.ac.at
RI Taniuchi, Ichiro/N-6399-2015;
OI Taniuchi, Ichiro/0000-0002-9853-9068; Ellmeier,
Wilfried/0000-0001-8192-8481; Boucheron, Nicole/0000-0002-4979-8311
FU Austrian Science Fund [P16708, P19930, I698]; Austrian Ministry of
Science and Research (BM:WF) [Y-163]; High Education Commission of
Pakistan; Leukemia and Lymphoma Society; RIKEN Research Center for
Allergy and Immunology
FX We thank Dagmar Stoiber-Sakaguchi, Olivia Simma, and Winfried Pickl
(Medical University of Vienna) for technical help. This study was
supported by the Austrian Science Fund (research Grants P16708, P19930,
and I698), and by the START Program (Project Y-163) of the Austrian
Ministry of Science and Research (BM:WF) (to W.E.); a PhD fellowship of
the High Education Commission of Pakistan (to H.H.); a Leukemia and
Lymphoma Society Special Fellowship (to T.E.); and a RIKEN Research
Center for Allergy and Immunology International collaboration award (to
I.T. and W.E.).
NR 30
TC 20
Z9 20
U1 0
U2 1
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 8
PY 2011
VL 108
IS 45
BP 18330
EP 18335
DI 10.1073/pnas.1105835108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 843UT
UT WOS:000296700000039
PM 22025728
ER
PT J
AU Allen, JA
Yost, JM
Setola, V
Chen, X
Sassano, MF
Chen, M
Peterson, S
Yadav, PN
Huang, XP
Feng, B
Jensen, NH
Che, X
Bai, X
Frye, SV
Wetsel, WC
Caron, MG
Javitch, JA
Roth, BL
Jin, J
AF Allen, John A.
Yost, Julianne M.
Setola, Vincent
Chen, Xin
Sassano, Maria F.
Chen, Meng
Peterson, Sean
Yadav, Prem N.
Huang, Xi-ping
Feng, Bo
Jensen, Niels H.
Che, Xin
Bai, Xu
Frye, Stephen V.
Wetsel, William C.
Caron, Marc G.
Javitch, Jonathan A.
Roth, Bryan L.
Jin, Jian
TI Discovery of beta-Arrestin-Biased Dopamine D-2 Ligands for Probing
Signal Transduction Pathways Essential for Antipsychotic Efficacy
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE functional selectivity; ligand bias
ID RECEPTOR FUNCTIONAL SELECTIVITY; DRUG; SEROTONIN; ARIPIPRAZOLE;
PHARMACOLOGY; OPC-14597; SCHIZOPHRENIA; BEHAVIOR
AB Elucidating the key signal transduction pathways essential for both antipsychotic efficacy and side-effect profiles is essential for developing safer and more effective therapies. Recent work has highlighted noncanonical modes of dopamine D-2 receptor (D2R) signaling via beta-arrestins as being important for the therapeutic actions of both antipsychotic and antimanic agents. We thus sought to create unique D2R agonists that display signaling bias via beta-arrestinergic signaling. Through a robust diversity-oriented modification of the scaffold represented by aripiprazole (1), we discovered UNC9975 (2), UNC0006 (3), and UNC9994 (4) as unprecedented beta-arrestin-biased D2R ligands. These compounds also represent unprecedented beta-arrestin-biased ligands for a Gi-coupled G protein-coupled receptor (GPCR). Significantly, UNC9975, UNC0006, and UNC9994 are simultaneously antagonists of Gi-regulated cAMP production and partial agonists for D2R/beta-arrestin-2 interactions. Importantly, UNC9975 displayed potent antipsychotic-like activity without inducing motoric side effects in inbred C57BL/6 mice in vivo. Genetic deletion of beta-arrestin-2 simultaneously attenuated the antipsychotic actions of UNC9975 and transformed it into a typical antipsychotic drug with a high propensity to induce catalepsy. Similarly, the antipsychotic-like activity displayed by UNC9994, an extremely beta-arrestin-biased D2R agonist, in wild-type mice was completely abolished in beta-arrestin-2 knockout mice. Taken together, our results suggest that beta-arrestin signaling and recruitment can be simultaneously a significant contributor to antipsychotic efficacy and protective against motoric side effects. These functionally selective, beta-arrestin-biased D2R ligands represent valuable chemical probes for further investigations of D2R signaling in health and disease.
C1 [Allen, John A.; Setola, Vincent; Sassano, Maria F.; Yadav, Prem N.; Huang, Xi-ping; Jensen, Niels H.; Roth, Bryan L.] Univ N Carolina, Dept Pharmacol, Chapel Hill, NC 27599 USA.
[Allen, John A.; Setola, Vincent; Sassano, Maria F.; Yadav, Prem N.; Huang, Xi-ping; Jensen, Niels H.; Roth, Bryan L.] Univ N Carolina, Natl Inst Mental Hlth Psychoact Drug, Screening Program, Sch Med, Chapel Hill, NC 27599 USA.
[Yost, Julianne M.; Chen, Xin; Frye, Stephen V.; Jin, Jian] Univ N Carolina, Ctr Integrat Chem Biol & Drug Discovery, Div Chem Biol & Med Chem, Eshelman Sch Pharm, Chapel Hill, NC 27599 USA.
[Chen, Meng; Wetsel, William C.] Duke Univ, Med Ctr, Dept Psychiat & Behav Sci, Dept Cell Biol, Durham, NC 27710 USA.
[Chen, Meng; Peterson, Sean; Wetsel, William C.; Caron, Marc G.] Duke Univ, Med Ctr, Dept Neurobiol, Durham, NC 27710 USA.
[Peterson, Sean; Caron, Marc G.] Duke Univ, Med Ctr, Dept Cell Biol, Dept Med, Durham, NC 27710 USA.
[Feng, Bo; Javitch, Jonathan A.] Columbia Univ, Coll Phys & Surg, Ctr Mol Recognit, New York, NY 10032 USA.
[Feng, Bo; Javitch, Jonathan A.] Columbia Univ, Coll Phys & Surg, Dept Psychiat, New York, NY 10032 USA.
[Feng, Bo; Javitch, Jonathan A.] Columbia Univ, Coll Phys & Surg, Dept Pharmacol, New York, NY 10032 USA.
[Che, Xin; Bai, Xu] Jilin Univ, Ctr Combinatorial Chem & Drug Discovery, Changchun 130012, Jilin, Peoples R China.
RP Roth, BL (reprint author), Univ N Carolina, Dept Pharmacol, Chapel Hill, NC 27599 USA.
EM bryan_roth@med.unc.edu; jianjin@email.unc.edu
RI Peterson, Sean/J-9498-2012; sassano, maria/G-4941-2013; Roth,
Bryan/F-3928-2010; Allen, John/D-6141-2011
FU National Institutes of Health [U19MH082441S1, U19MH082441, R01MH61887,
R01MH73853, R01DA022413, R01MH054137]; Lieber Center for Schizophrenia
Research and Treatment; National Institute of Mental Health
FX We thank Dr. J. Martin Herold for critical reading of synthetic
procedures and characterization data and Dr. Gilad Barnea (Brown
University) for supplying cells and cDNA for the Tango assay. We thank
the National Institutes of Health (Grants U19MH082441S1, U19MH082441,
R01MH61887, R01MH73853, R01DA022413, and R01MH054137) and the Lieber
Center for Schizophrenia Research and Treatment for financial support
and the National Institute of Mental Health Psychoactive Drug Screen
Program for selectivity assay support.
NR 42
TC 121
Z9 123
U1 4
U2 26
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 8
PY 2011
VL 108
IS 45
BP 18488
EP 18493
DI 10.1073/pnas.1104807108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 843UT
UT WOS:000296700000066
PM 22025698
ER
PT J
AU Klaiber, M
Dankworth, B
Kruse, M
Hartmann, M
Nikolaev, VO
Yang, RB
Volker, K
Gassner, B
Oberwinkler, H
Feil, R
Freichel, M
Groschner, K
Skryabin, BV
Frantz, S
Birnbaumer, L
Pongs, O
Kuhn, M
AF Klaiber, Michael
Dankworth, Beatrice
Kruse, Martin
Hartmann, Michael
Nikolaev, Viacheslav O.
Yang, Ruey-Bing
Voelker, Katharina
Gassner, Birgit
Oberwinkler, Heike
Feil, Robert
Freichel, Marc
Groschner, Klaus
Skryabin, Boris V.
Frantz, Stefan
Birnbaumer, Lutz
Pongs, Olaf
Kuhn, Michaela
TI A cardiac pathway of cyclic GMP-independent signaling of guanylyl
cyclase A, the receptor for atrial natriuretic peptide
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID PROTEIN-KINASE-G; EXTRACELLULAR DOMAIN; TRPC CHANNELS; EXPRESSION;
HYPERTROPHY; CELLS; PHOSPHORYLATION; INHIBITION; HEART; MICE
AB Cardiac atrial natriuretic peptide (ANP) regulates arterial blood pressure, moderates cardiomyocyte growth, and stimulates angiogenesis and metabolism. ANP binds to the transmembrane guanylyl cyclase (GC) receptor, GC-A, to exert its diverse functions. This process involves a cGMP-dependent signaling pathway preventing pathological [Ca(2+)](i) increases in myocytes. In chronic cardiac hypertrophy, however, ANP levels are markedly increased and GC-A/cGMP responses to ANP are blunted due to receptor desensitization. Here we show that, in this situation, ANP binding to GC-A stimulates a unique cGMP-independent signaling pathway in cardiac myocytes, resulting in pathologically elevated intracellular Ca(2+) levels. This pathway involves the activation of Ca(2+)-permeable transient receptor potential canonical 3/6 (TRPC3/C6) cation channels by GC-A, which forms a stable complex with TRPC3/C6 channels. Our results indicate that the resulting cation influx activates voltage-dependent L-type Ca(2+) channels and ultimately increases myocyte Ca(i)(2+) levels. These observations reveal a dual role of the ANP/GCA- signaling pathway in the regulation of cardiac myocyte Ca(i)(2+) homeostasis. Under physiological conditions, activation of a cGMP-dependent pathway moderates the Ca(i)(2+)-enhancing action of hypertrophic factors such as angiotensin II. By contrast, a cGMP-independent pathway predominates under pathophysiological conditions when GC-A is desensitized by high ANP levels. The concomitant rise in [Ca(2+)](i) might increase the propensity to cardiac hypertrophy and arrhythmias.
C1 [Klaiber, Michael; Dankworth, Beatrice; Hartmann, Michael; Voelker, Katharina; Gassner, Birgit; Oberwinkler, Heike; Kuhn, Michaela] Univ Wurzburg, Inst Physiol, D-97070 Wurzburg, Germany.
[Nikolaev, Viacheslav O.] Univ Wurzburg, Inst Pharmacol, D-97070 Wurzburg, Germany.
[Kruse, Martin; Pongs, Olaf] Univ Hamburg, Inst Neurale Signalverarbeitung, Zentrum Mol Neurobiol, D-20251 Hamburg, Germany.
[Nikolaev, Viacheslav O.] Univ Gottingen, Emmy Noether Grp, Deutsch Forschungsgemeinschaft, Dept Cardiol & Pneumol, D-37075 Gottingen, Germany.
[Yang, Ruey-Bing] Acad Sinica, Inst Biomed Sci, Taipei 114, Taiwan.
[Feil, Robert] Univ Tubingen, Interfak Inst Biochem, D-72076 Tubingen, Germany.
[Freichel, Marc] Univ Saarland, D-66421 Homburg, Germany.
[Groschner, Klaus] Graz Univ, Inst Pharmaceut Sci, A-8010 Graz, Austria.
[Skryabin, Boris V.] Univ Munster, Inst Expt Pathol, D-48149 Munster, Germany.
[Frantz, Stefan] Univ Hosp Wurzburg, Dept Internal Med 1, D-97080 Wurzburg, Germany.
[Birnbaumer, Lutz] NIEHS, NIH, Dept Human & Hlth Serv, Res Triangle Pk, NC 27709 USA.
RP Kuhn, M (reprint author), Univ Wurzburg, Inst Physiol, D-97070 Wurzburg, Germany.
EM michaela.kuhn@mail.uni-wuerzburg.de
RI Frantz, Stefan/G-1723-2012; Feil, Robert/B-8918-2014
OI Feil, Robert/0000-0002-7335-4841
FU Deutsche Forschungsgemeinschaft [SFB 487, SFB 688]; Interdisziplin res
Zentrum fur Klinische Forschung-Wurzburg; National Institutes of Health
[NS08174]
FX We thank Karina Zimmermann for neonatal rat cardiomyocyte isolation and
Prof. Veit Flockerzi (Experimentelle und Klinische Pharmakologie und
Toxikologie, Universitat des Saarlandes, Homburg, Germany) for the
plasmids for expression of TRPC3/C4/C5/C6 channels in HEK293 cells and
for specific antibodies for detection of TRPC4 and TRPC5. This work was
funded by Deutsche Forschungsgemeinschaft (SFB 487 and 688) and
Interdisziplin res Zentrum fur Klinische Forschung-Wurzburg (to M.
Kuhn). M. Kruse was partly supported by National Institutes of Health
Grant NS08174.
NR 25
TC 21
Z9 23
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 8
PY 2011
VL 108
IS 45
BP 18500
EP 18505
DI 10.1073/pnas.1103300108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 843UT
UT WOS:000296700000068
PM 22027011
ER
PT J
AU Ryan, TM
Griffin, MDW
Bailey, MF
Schuck, P
Howlett, GJ
AF Ryan, Timothy M.
Griffin, Michael D. W.
Bailey, Michael F.
Schuck, Peter
Howlett, Geoffrey J.
TI NBD-Labeled Phospholipid Accelerates Apolipoprotein C-II Amyloid Fibril
Formation but Is Not Incorporated into Mature Fibrils
SO BIOCHEMISTRY
LA English
DT Article
ID SODIUM DODECYL-SULFATE; FIBRILLIZATION IN-VITRO; A-I; ATHEROSCLEROTIC
PLAQUES; SYSTEMIC AMYLOIDOSIS; PROTEIN INTERACTIONS; NEUTRAL PH; INDUCE;
ASSOCIATION; BETA
AB Human apolipoprotein (apo) C-II is one of several lipid-binding proteins that self-assemble into fibrils and accumulate in disease-related amyloid deposits. A general characteristic of these amyloid deposits is the presence of lipids, known to modulate individual steps in amyloid fibril formation. ApoC-II fibril formation is activated by submicellar phospholipids but inhibited by micellar lipids. We examined the mechanism for the activation by submicellar lipids using the fluorescently labeled, short-chain phospholipid 1-dodecyl-[(7-nitro-2-1,3-benzoxadiazol-4-yl)amino]-2-hydroxyglycero-3-phosphocholine (NBD-lyso-12-PC). Addition of submicellar NBD-lyso-12-PC increased the rate of fibril formation by apoC-II approximately 2-fold. Stopped flow kinetic analysis using fluorescence detection and low, non-fibril-forming concentrations of apoC-II indicated NBD-lyso-12-PC binds rapidly, on the millisecond time scale, followed by the slower formation of discrete apoC-II tetramers. Sedimentation velocity analysis showed NBD-lyso-12-PC binds to both apoC-II monomers and tetramers at approximately five sites per monomer with an average dissociation constant of approximately 10 mu M. Mature apoC-II fibrils formed in the presence of NBD-lyso-12-PC were devoid of lipid, indicating a purely catalytic role for submicellar lipids in the activation of apoC-II fibril formation. These studies demonstrate the catalytic potential of small amphiphilic molecules in controlling protein folding and fibril assembly pathways.
C1 [Ryan, Timothy M.; Griffin, Michael D. W.; Bailey, Michael F.; Howlett, Geoffrey J.] Univ Melbourne, Dept Biochem & Mol Biol, Mol Sci & Biotechnol Inst Bio21, Melbourne, Vic 3010, Australia.
[Schuck, Peter] Natl Inst Biomed Imaging & Bioengn, Dynam Macromol Assembly Sect, Lab Cellular Imaging & Macromol Biophys, NIH, Bethesda, MD 20892 USA.
RP Howlett, GJ (reprint author), Univ Melbourne, Dept Biochem & Mol Biol, Mol Sci & Biotechnol Inst Bio21, Melbourne, Vic 3010, Australia.
EM ghowlett@unimelb.edu.au
OI Schuck, Peter/0000-0002-8859-6966; /0000-0001-9845-7735
FU Australian Research Council [DP0984565, DP110103528]; National Institute
of Biomedical Imaging and Bioengineering, National Institutes of Health
FX This research was supported under the Australian Research Council's
Discovery Projects funding scheme (Project DP0984565). M.D.W.G. is the
recipient of an Australian Research Council Post Doctoral Fellowship
(Project DP110103528). This work was supported in part by the Intramural
Research Program of the National Institute of Biomedical Imaging and
Bioengineering, National Institutes of Health.
NR 46
TC 7
Z9 7
U1 1
U2 13
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD NOV 8
PY 2011
VL 50
IS 44
BP 9579
EP 9586
DI 10.1021/bi201192r
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 838PH
UT WOS:000296304200016
PM 21985034
ER
PT J
AU Bulut, G
Fallen, S
Beauchamp, EM
Drebing, LE
Sun, JF
Berry, DL
Kallakury, B
Crum, CP
Toretsky, JA
Schlegel, R
Uren, A
AF Bulut, Guelay
Fallen, Shannon
Beauchamp, Elspeth M.
Drebing, Lauren E.
Sun, Junfeng
Berry, Deborah L.
Kallakury, Bhaskar
Crum, Christopher P.
Toretsky, Jeffrey A.
Schlegel, Richard
Ueren, Aykut
TI Beta-Catenin Accelerates Human Papilloma Virus Type-16 Mediated Cervical
Carcinogenesis in Transgenic Mice
SO PLOS ONE
LA English
DT Article
ID EPIGENETIC INACTIVATION; SQUAMOUS CARCINOGENESIS; UTERINE CERVIX; RODENT
DIETS; WNT PATHWAY; SFRP GENES; CANCER; CARCINOMA; TRANSFORMATION; E6
AB Human papilloma virus (HPV) is the principal etiological agent of cervical cancer in women, and its DNA is present in virtually all of these tumors. However, exposure to the high-risk HPV types alone is insufficient for tumor development. Identifying specific collaborating factors that will lead to cervical cancer remains an unanswered question, especially because millions of women are exposed to HPV. Our earlier work using an in vitro model indicated that activation of the canonical Wnt pathway in HPV-positive epithelial cells was sufficient to induce anchorage independent growth. We therefore hypothesized that constitutive activation of this pathway might function as the "second hit." To address this possibility, we developed two double-transgenic (DT) mouse models, K14-E7/Delta N87 beta cat and K14-HPV16/Delta N87 beta cat that express either the proteins encoded by the E7 oncogene or the HPV16 early region along with constitutively active beta-catenin, which was expressed by linking it to the keratin-14 (K14) promoter. We initiated tumor formation by treating all groups with estrogen for six months. Invasive cervical cancer was observed in 11% of the K14-Delta N87 beta cat mice, expressing activated beta-catenin and in 50% of the animals expressing the HPV16 E7 oncogene. In double-transgenic mice, coexpression of beta-catenin and HPV16 E7 induced invasive cervical cancer at about 7 months in 94% of the cases. We did not observe cervical cancer in any group unless the mice were treated with estrogen. In the second model, K14-HPV16 mice suffered cervical dysplasias, but this phenotype was not augmented in HPV16/Delta N87 beta cat mice. In summary, the phenotypes of the K14-E7/Delta N87 beta cat mice support the hypothesis that activation of the Wnt/beta-catenin pathway in HPV-associated premalignant lesions plays a functional role in accelerating cervical carcinogenesis.
C1 [Bulut, Guelay; Fallen, Shannon; Beauchamp, Elspeth M.; Drebing, Lauren E.; Toretsky, Jeffrey A.; Ueren, Aykut] Georgetown Univ, Med Ctr, Lombardi Comprehens Canc Ctr, Washington, DC 20007 USA.
[Sun, Junfeng] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
[Kallakury, Bhaskar; Schlegel, Richard] Georgetown Univ, Med Ctr, Dept Pathol, Washington, DC 20007 USA.
[Crum, Christopher P.] Harvard Univ, Dept Pathol, Boston, MA 02115 USA.
RP Fallen, S (reprint author), Georgetown Univ, Med Ctr, Lombardi Comprehens Canc Ctr, Washington, DC 20007 USA.
EM au26@georgetown.edu
RI BULUT, GULAY/J-3180-2012
FU National Institutes of Health (NIH) [CA108641]; Cancer Center [P30
CA051008]; NIH ARRA [1G20 RR025828-01]
FX This study was supported by grants from the National Institutes of
Health (NIH) CA108641 (to AU), Cancer Center Support Grant P30 CA051008
for use of Shared Resources (H&E and IHC stainings) and NIH ARRA Grant
1G20 RR025828-01 for use of Rodent Barrier Facility Equipment (between
7/20/2009 to 7/19/2011). The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 31
TC 28
Z9 28
U1 0
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 7
PY 2011
VL 6
IS 11
AR e27243
DI 10.1371/journal.pone.0027243
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 852HH
UT WOS:000297347700030
PM 22087269
ER
PT J
AU Charu, V
Viboud, C
Simonsen, L
Sturm-Ramirez, K
Shinjoh, M
Chowell, G
Miller, M
Sugaya, N
AF Charu, Vivek
Viboud, Cecile
Simonsen, Lone
Sturm-Ramirez, Katharine
Shinjoh, Masayoshi
Chowell, Gerardo
Miller, Mark
Sugaya, Norio
TI Influenza-Related Mortality Trends in Japanese and American Seniors:
Evidence for the Indirect Mortality Benefits of Vaccinating
Schoolchildren
SO PLOS ONE
LA English
DT Article
ID UNITED-STATES; SEASONAL INFLUENZA; CHILDREN; IMPACT; IMMUNIZATION; LIVE;
POPULATION; PREVENTION; MORBIDITY; INFECTION
AB Background: The historical Japanese influenza vaccination program targeted at schoolchildren provides a unique opportunity to evaluate the indirect benefits of vaccinating high-transmitter groups to mitigate disease burden among seniors. Here we characterize the indirect mortality benefits of vaccinating schoolchildren based on data from Japan and the US.
Methods: We compared age-specific influenza-related excess mortality rates in Japanese seniors aged >= 65 years during the schoolchildren vaccination program (1978-1994) and after the program was discontinued (1995-2006). Indirect vaccine benefits were adjusted for demographic changes, socioeconomics and dominant influenza subtype; US mortality data were used as a control.
Results: We estimate that the schoolchildren vaccination program conferred a 36% adjusted mortality reduction among Japanese seniors (95% CI: 17-51%), corresponding to similar to 1,000 senior deaths averted by vaccination annually (95% CI: 400-1,800). In contrast, influenza-related mortality did not change among US seniors, despite increasing vaccine coverage in this population.
Conclusions: The Japanese schoolchildren vaccination program was associated with substantial indirect mortality benefits in seniors.
C1 [Charu, Vivek; Viboud, Cecile; Simonsen, Lone; Sturm-Ramirez, Katharine; Chowell, Gerardo; Miller, Mark] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Simonsen, Lone] George Washington Univ, Sch Publ Hlth & Hlth Serv, Dept Global Hlth, Washington, DC USA.
[Shinjoh, Masayoshi] Keio Univ, Sch Med, Dept Pediat, Tokyo, Japan.
[Chowell, Gerardo] Arizona State Univ, Sch Human Evolut & Social Change, Tempe, AZ 85287 USA.
[Sugaya, Norio] Keiyu Hosp, Dept Pediat, Yokohama, Kanagawa, Japan.
RP Charu, V (reprint author), NIH, Fogarty Int Ctr, Bldg 10, Bethesda, MD 20892 USA.
EM vcharu@gmail.com
RI Chowell, Gerardo/F-5038-2012;
OI Chowell, Gerardo/0000-0003-2194-2251; Simonsen, Lone/0000-0003-1535-8526
FU Division of International Epidemiology and Population Studies; Fogarty
International Center; National Institutes of Health; International
Influenza Unit; Office of Global Affairs; Office of the Secretary of the
Department of Health and Human Services; Department of Homeland Security
FX Financial support provided by the Division of International Epidemiology
and Population Studies, Fogarty International Center, National
Institutes of Health and International Influenza Unit, Office of Global
Affairs, Office of the Secretary of the Department of Health and Human
Services. LS acknowledges support by the RAPIDD program of the Science &
Technology Directorate, Department of Homeland Security, and Fogarty
International Center, National Institutes of Health. The funders had no
role in study design, data collection and analysis, decision to publish,
or preparation of the manuscript.
NR 45
TC 9
Z9 9
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 7
PY 2011
VL 6
IS 11
AR e26282
DI 10.1371/journal.pone.0026282
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 852HH
UT WOS:000297347700005
PM 22087226
ER
PT J
AU Huda, A
Tyagi, E
Marino-Ramirez, L
Bowen, NJ
Jjingo, D
Jordan, IK
AF Huda, Ahsan
Tyagi, Eishita
Marino-Ramirez, Leonardo
Bowen, Nathan J.
Jjingo, Daudi
Jordan, I. King
TI Prediction of Transposable Element Derived Enhancers Using Chromatin
Modification Profiles
SO PLOS ONE
LA English
DT Article
ID UCSC GENOME BROWSER; GENE-EXPRESSION; HISTONE MODIFICATIONS;
HYPERSENSITIVE SITES; CAP ANALYSIS; SELFISH DNA; STEM-CELLS; EVOLUTION;
IDENTIFICATION; MOUSE
AB Experimentally characterized enhancer regions have previously been shown to display specific patterns of enrichment for several different histone modifications. We modelled these enhancer chromatin profiles in the human genome and used them to guide the search for novel enhancers derived from transposable element (TE) sequences. To do this, a computational approach was taken to analyze the genome-wide histone modification landscape characterized by the ENCODE project in two human hematopoietic cell types, GM12878 and K562. We predicted the locations of 2,107 and 1,448 TE-derived enhancers in the GM12878 and K562 cell lines respectively. A vast majority of these putative enhancers are unique to each cell line; only 3.5% of the TE-derived enhancers are shared between the two. We evaluated the functional effect of TE-derived enhancers by associating them with the cell-type specific expression of nearby genes, and found that the number of TE-derived enhancers is strongly positively correlated with the expression of nearby genes in each cell line. Furthermore, genes that are differentially expressed between the two cell lines also possess a divergent number of TE-derived enhancers in their vicinity. As such, genes that are up-regulated in the GM12878 cell line and down-regulated in K562 have significantly more TE-derived enhancers in their vicinity in the GM12878 cell line and vice versa. These data indicate that human TE-derived sequences are likely to be involved in regulating cell-type specific gene expression on a broad scale and suggest that the enhancer activity of TE-derived sequences is mediated by epigenetic regulatory mechanisms.
C1 [Huda, Ahsan; Tyagi, Eishita; Bowen, Nathan J.; Jjingo, Daudi; Jordan, I. King] Georgia Inst Technol, Sch Biol, Atlanta, GA 30332 USA.
[Marino-Ramirez, Leonardo] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
[Marino-Ramirez, Leonardo; Jordan, I. King] PanAmer Bioinformat Inst, Santa Marta, Magdalena, Colombia.
[Bowen, Nathan J.] Georgia Inst Technol, Ovarian Canc Inst, Atlanta, GA 30332 USA.
RP Huda, A (reprint author), Georgia Inst Technol, Sch Biol, Atlanta, GA 30332 USA.
EM king.jordan@biology.gatech.edu
RI Marino-Ramirez, Leonardo/I-5759-2013
OI Marino-Ramirez, Leonardo/0000-0002-5716-8512
FU Alfred P. Sloan Research Fellowship in Computational and Evolutionary
Molecular Biology [BR-4839]; Georgia Institute of Technology; Integrated
Cancer Research Center at the Georgia Institute of Technology; NIH, NLM,
NCBI; Corporacion Colombiana de Investigacion Agropucuaria CORPOICA
FX IKJ and AH were supported by an Alfred P. Sloan Research Fellowship in
Computational and Evolutionary Molecular Biology (BR-4839)
(http://www.sloan.org/). Eishita Tyagi was supported by the
Bioinformatics program at the Georgia Institute of Technology
(http://www.bioinformatics.biology.gatech.edu/). NJB was supported by
the Integrated Cancer Research Center at the Georgia Institute of
Technology (http://ovariancancerinstitute.org/). This research was
supported in part by the Intramural Research Program of the NIH, NLM,
NCBI (http://www.ncbi.nlm.nih.gov/). LMR is supported by Corporacion
Colombiana de Investigacion Agropucuaria CORPOICA
(http://www.corpoica.org.co/SitioWeb/). The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 41
TC 9
Z9 10
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 7
PY 2011
VL 6
IS 11
AR e27513
DI 10.1371/journal.pone.0027513
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 852HH
UT WOS:000297347700061
PM 22087331
ER
PT J
AU Schuetz, A
Haule, A
Reither, K
Ngwenyama, N
Rachow, A
Meyerhans, A
Maboko, L
Koup, RA
Hoelscher, M
Geldmacher, C
AF Schuetz, Alexandra
Haule, Antelmo
Reither, Klaus
Ngwenyama, Njabulo
Rachow, Andrea
Meyerhans, Andreas
Maboko, Leonard
Koup, Richard A.
Hoelscher, Michael
Geldmacher, Christof
TI Monitoring CD27 Expression to Evaluate Mycobacterium Tuberculosis
Activity in HIV-1 Infected Individuals In Vivo
SO PLOS ONE
LA English
DT Article
ID T-CELLS; PULMONARY TUBERCULOSIS; INFECTION; HIV; PREVALENCE; RESPONSES;
GAMMA; CD4
AB The level of bacterial activity is only poorly defined during asymptomatic Mycobacterium tuberculosis (MTB) infection. The objective was to study the capacity of a new biomarker, the expression of the T cell maturation marker CD27 on MTB-specific CD4 T cells, to identify active tuberculosis (TB) disease in subjects from a MTB and HIV endemic region. The frequency and CD27 expression of circulating MTB-specific CD4 T cells was determined in 96 study participants after stimulation with purified protein derivative (PPD) using intracellular cytokine staining for IFNgamma (IFN gamma). Subjects were then stratified by their TB and HIV status. Within PPD responders, a CD27(-) phenotype was associated with active TB in HIV- (p = 0.0003) and HIV+ (p = 0.057) subjects, respectively. In addition, loss of CD27 expression preceded development of active TB in one HIV seroconverter. Interestingly, in contrast to HIV- subjects, MTB-specific CD4 T cell populations from HIV+ TB-asymptomatic subjects were often dominated by CD27(-) cells. These data indicate that down-regulation of CD27 on MTB-specific CD4 T cell could be used as a biomarker of active TB, potentially preceding clinical TB disease. Furthermore, these data are consistent with the hypothesis that late, chronic HIV infection is frequently associated with increased mycobacterial activity in vivo. The analysis of T cell maturation and activation markers might thus be a useful tool to monitor TB disease progression.
C1 [Schuetz, Alexandra; Haule, Antelmo; Reither, Klaus; Rachow, Andrea; Maboko, Leonard] Referral Hosp, NIMR Mbeya Med Res Programme, Mbeya, Tanzania.
[Reither, Klaus; Rachow, Andrea; Hoelscher, Michael; Geldmacher, Christof] Klinikum Univ Munich, Dept Infect Dis & Trop Med, Munich, Germany.
[Ngwenyama, Njabulo; Koup, Richard A.; Geldmacher, Christof] NIAID, Immunol Lab, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Meyerhans, Andreas] Univ Saarland, Inst Infect Med, Inst Virol, D-6650 Homburg, Germany.
RP Schuetz, A (reprint author), USAMC AFRIMS, Henry M Jackson Fdn Adv Mil Med, Walter Reed Program, Dept Retrovirol, Bangkok, Thailand.
EM alexandra.schuetz@afrims.org
RI Hoelscher, Michael/D-3436-2012; Meyerhans, Andreas/D-3382-2014
OI Meyerhans, Andreas/0000-0003-0620-5317
FU European Commission [ERBICA4-CT-2002-10035, SANTE/2004/078-545/130]
FX The work was supported by grants from the European Commission (DG XII,
INCO-DC, ERBICA4-CT-2002-10035 and DG X, EuropeAID
SANTE/2004/078-545/130). The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 16
TC 20
Z9 20
U1 0
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 7
PY 2011
VL 6
IS 11
AR e27284
DI 10.1371/journal.pone.0027284
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 852HH
UT WOS:000297347700034
PM 22087280
ER
PT J
AU Zuo, LJ
Zhang, CK
Wang, F
Li, CSR
Zhao, HY
Lu, LG
Zhang, XY
Lu, L
Zhang, HP
Zhang, FY
Krystal, JH
Luo, XG
AF Zuo, Lingjun
Zhang, Clarence K.
Wang, Fei
Li, Chiang-Shan R.
Zhao, Hongyu
Lu, Lingeng
Zhang, Xiang-Yang
Lu, Lin
Zhang, Heping
Zhang, Fengyu
Krystal, John H.
Luo, Xingguang
TI A Novel, Functional and Replicable Risk Gene Region for Alcohol
Dependence Identified by Genome-Wide Association Study
SO PLOS ONE
LA English
DT Article
ID POLYMORPHISMS; POPULATION; EXPRESSION; FINGER
AB Several genome-wide association studies (GWASs) reported tens of risk genes for alcohol dependence, but most of them have not been replicated or confirmed by functional studies. The present study used a GWAS to search for novel, functional and replicable risk gene regions for alcohol dependence. Associations of all top-ranked SNPs identified in a discovery sample of 681 African-American (AA) cases with alcohol dependence and 508 AA controls were retested in a primary replication sample of 1,409 European-American (EA) cases and 1,518 EA controls. The replicable associations were then subjected to secondary replication in a sample of 6,438 Australian family subjects. A functional expression quantitative trait locus (eQTL) analysis of these replicable risk SNPs was followed-up in order to explore their cis-acting regulatory effects on gene expression. We found that within a 90 Mb region around PHF3-PTP4A1 locus in AAs, a linkage disequilibrium (LD) block in PHF3-PTP4A1 formed the only peak associated with alcohol dependence at p<10(-4). Within this block, 30 SNPs associated with alcohol dependence in AAs (1.6x10(-5) <= p <= 0.050) were replicated in EAs (1.3x10(-3)<= p <= 0.038), and 18 of them were also replicated in Australians (1.8x10(-3)<= p <= 0.048). Most of these risk SNPs had strong cis-acting regulatory effects on PHF3-PTP4A1 mRNA expression across three HapMap samples. The distributions of -log(p) values for association and functional signals throughout this LD block were highly consistent across AAs, EAs, Australians and three HapMap samples. We conclude that the PHF3-PTP4A1 region appears to harbor a causal locus for alcohol dependence, and proteins encoded by PHF3 and/or PTP4A1 might play a functional role in the disorder.
C1 [Zuo, Lingjun; Wang, Fei; Li, Chiang-Shan R.; Krystal, John H.; Luo, Xingguang] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT 06520 USA.
[Zuo, Lingjun; Krystal, John H.; Luo, Xingguang] Vet Affairs Connecticut Healthcare Syst, West Haven, CT USA.
[Zhang, Clarence K.; Zhao, Hongyu; Lu, Lingeng; Zhang, Heping] Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA.
[Wang, Fei] China Med Univ, Affiliated Hosp 1, Dept Psychiat, Shenyang, Peoples R China.
[Zhang, Xiang-Yang] Baylor Coll Med, Menninger Dept Psychiat & Behav Sci, Houston, TX 77030 USA.
[Lu, Lin] Peking Univ, Natl Inst Drug Dependence, Beijing 100871, Peoples R China.
[Zhang, Fengyu] NIMH, Gene Cognit & Psychosis Program, NIH, Bethesda, MD 20892 USA.
RP Zuo, LJ (reprint author), Yale Univ, Sch Med, Dept Psychiat, New Haven, CT 06520 USA.
EM Lingjun.Zuo@yale.edu; Xingguang.Luo@yale.edu
RI Li, Chiang-Shan/J-2813-2016
OI Li, Chiang-Shan/0000-0002-9393-1212
FU National Institute on Drug Abuse (NIDA) [K01 DA029643, K24 DA017899, R01
DA016750, K02 DA026990, R01 DA013423]; National Institute on Alcohol
Abuse and Alcoholism (NIAAA) [R01 AA016015, R21 AA020319, R21 AA018004,
K24 AA013736, R01 AA11330, R01 AA017535, P50 AA012870, U10 AA008401];
National Alliance for Research on Schizophrenia and Depression (NARSAD)
Award [17616]; Department of Veterans Affairs through VA Alcohol
Research Center; VA National Center for PTSD; Depression REAP; National
Institutes of Health (NIH) Genes, Environment and Health Initiative
(GEI) [U01 HG004422, U01HG004438]; GENEVA Coordinating Center [U01
HG004446]; National Cancer Institute [P01 CA089392]; NIH
[HHSN268200782096C]
FX This work was supported in part by National Institute on Drug Abuse
(NIDA) grants K01 DA029643, K24 DA017899, R01 DA016750 and K02 DA026990,
National Institute on Alcohol Abuse and Alcoholism (NIAAA) grants R01
AA016015, R21 AA020319, R21 AA018004, K24 AA013736, R01 AA11330, R01
AA017535, and P50 AA012870 and the National Alliance for Research on
Schizophrenia and Depression (NARSAD) Award 17616 (L.Z.). This work also
received support from the Department of Veterans Affairs through its
support of the VA Alcohol Research Center, the VA National Center for
PTSD, and the Depression REAP. The authors thank National Institutes of
Health GWAS Data Repository, the Contributing Investigator(s) (Drs.
Bierut and Edenberg) who contributed the phenotype and genotype data
(SAGE and COGA) from his/her original study, and the primary funding
organization that supported the contributing study. Funding support for
SAGE and COGA was provided through the National Institutes of Health
(NIH) Genes, Environment and Health Initiative (GEI) Grant U01 HG004422
and U01HG004438; the GENEVA Coordinating Center (U01 HG004446); the
National Institute on Alcohol Abuse and Alcoholism (U10 AA008401); the
National Institute on Drug Abuse (R01 DA013423); the National Cancer
Institute (P01 CA089392); and the NIH contract "High throughput
genotyping for studying the genetic contributions to human disease"
(HHSN268200782096C). Assistance with data cleaning was provided by the
National Center for Biotechnology Information. Genotyping was performed
at the Johns Hopkins University Center for Inherited Disease Research or
at deCODE. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 28
TC 29
Z9 30
U1 0
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 7
PY 2011
VL 6
IS 11
AR e26726
DI 10.1371/journal.pone.0026726
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 852HH
UT WOS:000297347700009
PM 22096494
ER
PT J
AU Pitzer, VE
Viboud, C
Lopman, BA
Patel, MM
Parashar, UD
Grenfell, BT
AF Pitzer, Virginia E.
Viboud, Cecile
Lopman, Ben A.
Patel, Manish M.
Parashar, Umesh D.
Grenfell, Bryan T.
TI Influence of birth rates and transmission rates on the global
seasonality of rotavirus incidence
SO JOURNAL OF THE ROYAL SOCIETY INTERFACE
LA English
DT Article
DE rotavirus; seasonality; vaccination; infectious disease modelling
ID HOSPITAL-BASED SURVEILLANCE; AGED LESS-THAN-5 YEARS; TIME-SERIES
ANALYSIS; 1ST 2 YEARS; MOLECULAR EPIDEMIOLOGY; DEVELOPING-COUNTRIES;
UNITED-STATES; DOUBLE-BLIND; CHILDREN; DIARRHEA
AB Rotavirus is a major cause of mortality in developing countries, and yet the dynamics of rotavirus in such settings are poorly understood. Rotavirus is typically less seasonal in the tropics, although recent observational studies have challenged the universality of this pattern. While numerous studies have examined the association between environmental factors and rotavirus incidence, here we explore the role of intrinsic factors. By fitting a mathematical model of rotavirus transmission dynamics to published age distributions of cases from 15 countries, we obtain estimates of local transmission rates. Model-predicted patterns of seasonal incidence based solely on differences in birth rates and transmission rates are significantly correlated with those observed (Spearman's rho = 0.65, p < 0.05). We then examine seasonal patterns of rotavirus predicted across a range of different birth rates and transmission rates and explore how vaccination may impact these patterns. Our results suggest that the relative lack of rotavirus seasonality observed in many tropical countries may be due to the high birth rates and transmission rates typical of developing countries rather than being driven primarily by environmental conditions. While vaccination is expected to decrease the overall burden of disease, it may increase the degree of seasonal variation in the incidence of rotavirus in some settings.
C1 [Pitzer, Virginia E.; Grenfell, Bryan T.] Princeton Univ, Dept Ecol & Evolutionary Biol, Princeton, NJ 08544 USA.
[Grenfell, Bryan T.] Princeton Univ, Woodrow Wilson Sch Publ & Int Affairs, Princeton, NJ 08544 USA.
[Pitzer, Virginia E.; Viboud, Cecile; Grenfell, Bryan T.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Lopman, Ben A.; Patel, Manish M.; Parashar, Umesh D.] Ctr Dis Control & Prevent, Epidemiol Branch, Div Viral Dis, Natl Ctr Immunizat & Resp Dis, Atlanta, GA 30033 USA.
RP Pitzer, VE (reprint author), Princeton Univ, Dept Ecol & Evolutionary Biol, Princeton, NJ 08544 USA.
EM vepitzer@princeton.edu
OI Pitzer, Virginia/0000-0003-1015-2289
FU National Institutes of Health [R01 GM083983-01]; Bill and Melinda Gates
Foundation; RAPIDD programme of the Science and Technology Directorate;
Department of Homeland Security; Fogarty International Center, National
Institutes of Health
FX This work was supported by the National Institutes of Health (R01
GM083983-01), the Bill and Melinda Gates Foundation, and the RAPIDD
programme of the Science and Technology Directorate, Department of
Homeland Security, and the Fogarty International Center, National
Institutes of Health (V. E. P and B. G.). The findings and conclusions
in this report are those of the authors and do not necessarily represent
the views of the Centers for Disease Control and Prevention (CDC).
NR 59
TC 33
Z9 33
U1 1
U2 11
PU ROYAL SOC
PI LONDON
PA 6-9 CARLTON HOUSE TERRACE, LONDON SW1Y 5AG, ENGLAND
SN 1742-5689
J9 J R SOC INTERFACE
JI J. R. Soc. Interface
PD NOV 7
PY 2011
VL 8
IS 64
BP 1584
EP 1593
DI 10.1098/rsif.2011.0062
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 824OJ
UT WOS:000295211200005
PM 21508015
ER
PT J
AU Sando, L
Henriques, ST
Foley, F
Simonsen, SM
Daly, NL
Hall, KN
Gustafson, KR
Aguilar, MI
Craik, DJ
AF Sando, Lillian
Henriques, Sonia Troeira
Foley, Fiona
Simonsen, Shane M.
Daly, Norelle L.
Hall, Kristopher N.
Gustafson, Kirk R.
Aguilar, Marie-Isabel
Craik, David J.
TI A Synthetic Mirror Image of Kalata B1 Reveals that Cyclotide Activity Is
Independent of a Protein Receptor
SO CHEMBIOCHEM
LA English
DT Article
DE anti-HIV; chirality; cyclic peptides; membranes; proteins
ID CYCLIC-CYSTINE-KNOT; HELICAL ANTIMICROBIAL PEPTIDES; ANTI-HIV
CYCLOTIDES; PLANT CYCLOTIDES; MACROCYCLIC PEPTIDES; OLDENLANDIA-AFFINIS;
MOLECULAR-INTERACTIONS; MEMBRANE INTERACTIONS; BIOLOGICAL-ACTIVITY; DRUG
DESIGN
AB Featuring a circular, knotted structure and diverse bioactivities, cyclotides are a fascinating family of peptides that have inspired applications in drug design. Most likely evolved to protect plants against pests and herbivores, cyclotides also exhibit anti-cancer, anti-HIV, and hemolytic activities. In all of these activities, cell membranes appear to play an important role. However, the question of whether the activity of cyclotides depends on the recognition of chiral receptors or is primarily modulated by the lipid-bilayer environment has remained unknown. To determine the importance of lipid membranes on the activity of the prototypic cyclotide, kalata B1, we synthesized its all-D enantiomer and assessed its bioactivities. After the all-D enantiomer had been confirmed by (1)H NMR to be the structural mirror image of the native kalata B1, it was tested for anti-HIV activity, cytotoxicity, and hemolytic properties. The all-D peptide is active in these assays, albeit with less efficiency; this reveals that kalata B1 does not require chiral recognition to be active. The lower activity than the native peptide correlates with a lower affinity for phospholipid bilayers in model membranes. These results exclude a chiral receptor mechanism and support the idea that interaction with phospholipid membranes plays a role in the activity of kalata B1. In addition, studies with mixtures of L and D enantiomers of kalata B1 suggested that biological activity depends on peptide oligomerization at the membrane surface, which determines affinity for membranes by modulating the association-dissociation equilibrium.
C1 [Sando, Lillian; Henriques, Sonia Troeira; Foley, Fiona; Simonsen, Shane M.; Daly, Norelle L.; Craik, David J.] Univ Queensland, Inst Mol Biosci, Brisbane, Qld 4072, Australia.
[Henriques, Sonia Troeira] Univ Lisbon, Fac Med, Inst Mol Med, P-1649028 Lisbon, Portugal.
[Hall, Kristopher N.; Aguilar, Marie-Isabel] Monash Univ, Dept Biochem & Mol Biol, Clayton, Vic 3800, Australia.
[Gustafson, Kirk R.] NCI, Mol Targets Lab, Ctr Canc Res, Frederick, MD 21702 USA.
RP Craik, DJ (reprint author), Univ Queensland, Inst Mol Biosci, Brisbane, Qld 4072, Australia.
EM d.craik@imb.uq.edu.au
RI Daly, Norelle/D-4302-2013; Craik, David/B-1695-2010; Troeira Henriques,
Sonia/J-3500-2016
OI Craik, David/0000-0003-0007-6796; Troeira Henriques,
Sonia/0000-0001-9564-9651
FU Australian Research Council [ARC-DP0880105]; National Health and Medical
Research Council (NHMRC); European Commission (EU) [PIOF-GA-2008-220318]
FX Studies in our laboratory on cyclotides are supported by grants from the
Australian Research Council (ARC-DP0880105) and the National Health and
Medical Research Council (NHMRC). D.J.C. is an NHMRC Professorial
Fellow. S.T.H. is a Marie Curie Postdoctoral Fellow awarded by European
Commission (EU) (PIOF-GA-2008-220318). N.L.D. is a Queensland Smart
State Fellow.
NR 51
TC 24
Z9 24
U1 2
U2 12
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1439-4227
J9 CHEMBIOCHEM
JI ChemBioChem
PD NOV 4
PY 2011
VL 12
IS 16
BP 2456
EP 2462
DI 10.1002/cbic.201100450
PG 7
WC Biochemistry & Molecular Biology; Chemistry, Medicinal
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 849YB
UT WOS:000297160300012
PM 21928440
ER
PT J
AU Fowler, T
Sen, R
Roy, AL
AF Fowler, Trent
Sen, Ranjan
Roy, Ananda L.
TI Regulation of Primary Response Genes
SO MOLECULAR CELL
LA English
DT Review
ID RNA-POLYMERASE-II; CHROMATIN-REMODELING COMPLEX; TRANSCRIPTION FACTORS;
C-FOS; MESSENGER-RNA; GROWTH-FACTOR; DEPENDENT TRANSCRIPTION; HISTONE
ACETYLATION; SIGNAL-TRANSDUCTION; NEURONAL-ACTIVITY
AB Primary response genes (PRGs) are a set of genes that are induced in response to both cell-extrinsic and cell-intrinsic signals and do not require de novo protein synthesis for their expression. These "first responders" in the waves of transcription of signal-responsive genes play pivotal roles in a wide range of biological responses, including neuronal survival and plasticity, cardiac stress response, innate and adaptive immune responses, glucose metabolism, and oncogeneic transformation. Here we bring together recent advances and our current understanding of the signal-induced transcriptional and epigenetic regulation of PRGs.
C1 [Fowler, Trent; Roy, Ananda L.] Tufts Univ, Sch Med, Sackler Sch Biomed Sci, Dept Pathol, Boston, MA 02111 USA.
[Roy, Ananda L.] Tufts Univ, Sch Med, Sackler Sch Biomed Sci, Genet Program, Boston, MA 02111 USA.
[Roy, Ananda L.] Tufts Univ, Sch Med, Sackler Sch Biomed Sci, Program Immunol, Boston, MA 02111 USA.
[Sen, Ranjan] NIA, Lab Mol Biol & Immunol, Biomed Res Ctr, Baltimore, MD 21224 USA.
RP Roy, AL (reprint author), Tufts Univ, Sch Med, Sackler Sch Biomed Sci, Dept Pathol, 150 Harrison Ave, Boston, MA 02111 USA.
EM ananda.roy@tufts.edu
FU National Institute on Aging (Baltimore); National Institutes of Health
[AI079206]
FX We apologize to colleagues whose work could not be cited here due to
space constraints. R.S is supported by the Intramural Research Program
of the National Institute on Aging (Baltimore). A.L.R. is supported in
part by a grant from the National Institutes of Health (AI079206).
NR 100
TC 62
Z9 63
U1 1
U2 16
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 4
PY 2011
VL 44
IS 3
BP 348
EP 360
DI 10.1016/j.molce1.2011.09.014
PG 13
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 844OE
UT WOS:000296756100004
PM 22055182
ER
PT J
AU Li, ZW
Potts-Kant, EN
Garantziotis, S
Foster, WM
Hollingsworth, JW
AF Li, Zhuowei
Potts-Kant, Erin N.
Garantziotis, Stavros
Foster, W. Michael
Hollingsworth, John W.
TI Hyaluronan Signaling during Ozone-Induced Lung Injury Requires TLR4,
MyD88, and TIRAP
SO PLOS ONE
LA English
DT Article
ID TOLL-LIKE RECEPTOR-4; AIRWAY HYPERRESPONSIVENESS; CUTTING EDGE; MOUSE
LUNG; MICE; INFLAMMATION; MORTALITY; SUSCEPTIBILITY; EXPOSURE; ASTHMA
AB Ozone exposure is associated with exacerbation of reactive airways disease. We have previously reported that the damage-associated molecular pattern, hyaluronan, is required for the complete biological response to ambient ozone and that hyaluronan fragments signal through toll-like receptor 4 (TLR4). In this study, we further investigated the role of TLR4 adaptors in ozone-induced airway hyperresponsiveness (AHR) and the direct response to hyaluronan fragments (HA). Using a murine model of AHR, C57BL/6J, TLR4(-/-), MyD88(-/-), and TIRAP(-/-) mice were characterized for AHR after exposure to either ozone (1 ppmx3 h) or HA fragments. Animals were characterized for AHR with methacholine challenge, cellular inflammation, lung injury, and production of pro-inflammatory cytokines. Ozone-exposed C57BL/6J mice developed cellular inflammation, lung injury, pro-inflammatory cytokines, and AHR, while mice deficient in TLR4, MyD88 or TIRAP demonstrated both reduced AHR and reduced levels of pro-inflammatory cytokines including TNF alpha, IL-1 beta, MCP-1, IL-6 and KC. The level of hyaluronan was increased after inhalation of ozone in each strain of mice. Direct challenge of mice to hyaluronan resulted in AHR in C57BL/6J mice, but not in TLR4(-/-), MyD88(-/-), or TIRAP(-/-) mice. HA-induced cytokine production in wild-type mice was significantly reduced in TLR4(-/-), MyD88(-/-), or TIRAP(-/-) mice. In conclusion, our findings support that ozone-induced airway hyperresponsiveness is dependent on the HA-TLR4-MyD88-TIRAP signaling pathway.
C1 [Li, Zhuowei; Potts-Kant, Erin N.; Foster, W. Michael; Hollingsworth, John W.] Duke Univ, Dept Med, Durham, NC 27710 USA.
[Hollingsworth, John W.] Duke Univ, Dept Immunol, Durham, NC USA.
[Garantziotis, Stavros] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
RP Li, ZW (reprint author), Duke Univ, Dept Med, Durham, NC 27710 USA.
EM john.hollingsworth@duke.edu
RI Dennis, Allison/A-7654-2014; Garantziotis, Stavros/A-6903-2009
OI Garantziotis, Stavros/0000-0003-4007-375X
FU National Institute of Environmental Health Sciences [ES016126, ES020426]
FX This work was supported by the National Institute of Environmental
Health Sciences (ES016126, ES020426). The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 50
TC 29
Z9 30
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 4
PY 2011
VL 6
IS 11
AR e27137
DI 10.1371/journal.pone.0027137
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 850MH
UT WOS:000297198200038
PM 22073274
ER
PT J
AU Liao, LM
Brennan, P
van Bemmel, DM
Zaridze, D
Matveev, V
Janout, V
Kollarova, H
Bencko, V
Navratilova, M
Szeszenia-Dabrowska, N
Mates, D
Rothman, N
Boffetta, P
Chow, WH
Moore, LE
AF Liao, Linda M.
Brennan, Paul
van Bemmel, Dana M.
Zaridze, David
Matveev, Vsevolod
Janout, Vladimir
Kollarova, Hellena
Bencko, Vladimir
Navratilova, Marie
Szeszenia-Dabrowska, Neonila
Mates, Dana
Rothman, Nathaniel
Boffetta, Paolo
Chow, Wong-Ho
Moore, Lee E.
TI LINE-1 Methylation Levels in Leukocyte DNA and Risk of Renal Cell Cancer
SO PLOS ONE
LA English
DT Article
ID KIDNEY CANCER; COLORECTAL ADENOMA; VEGETABLE INTAKE; BLADDER-CANCER;
CENTRAL-EUROPE; LIFE-STYLE; SERUM DNA; HYPOMETHYLATION; GENES;
HYPERMETHYLATION
AB Purpose: Leukocyte global DNA methylation levels are currently being considered as biomarkers of cancer susceptibility and have been associated with risk of several cancers. In this study, we aimed to examine the association between long interspersed nuclear elements (LINE-1) methylation levels, as a biomarker of global DNA methylation in blood cell DNA, and renal cell cancer risk.
Experimental Design: LINE-1 methylation of bisulfite-converted genomic DNA isolated from leukocytes was quantified by pyrosequencing measured in triplicate, and averaged across 4 CpG sites. A total of 328 RCC cases and 654 controls frequency-matched(2:1) on age(+/- 5years), sex and study center, from a large case-control study conducted in Central and Eastern Europe were evaluated.
Results: LINE-1 methylation levels were significantly higher in RCC cases with a median of 81.97% (interquartile range[IQR]: 80.84-83.47) compared to 81.67% (IQR: 80.35-83.03) among controls (p = 0.003, Wilcoxon). Compared to the lowest LINE-1 methylation quartile(Q1), the adjusted ORs for increasing methylation quartiles were as follows: OR(Q2) = 1.84(1.20-2.81), OR(Q3) = 1.72(1.11-2.65) and OR(Q4) = 2.06(1.34-3.17), with a p-trend = 0.004. The association was stronger among current smokers (p-trend<0.001) than former or never smokers (p-interaction = 0.03). To eliminate the possibility of selection bias among controls, the relationship between LINE-1 methylation and smoking was evaluated and confirmed in a case-only analysis, as well.
Conclusions: Higher levels of LINE-1 methylation appear to be positively associated with RCC risk, particularly among current smokers. Further investigations using both post-and pre-diagnostic genomic DNA is warranted to confirm findings and will be necessary to determine whether the observed differences occur prior to, or as a result of carcinogenesis.
C1 [Liao, Linda M.; van Bemmel, Dana M.; Rothman, Nathaniel; Chow, Wong-Ho; Moore, Lee E.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Zaridze, David; Matveev, Vsevolod] Inst Carcinogenesis, Moscow, Russia.
[Brennan, Paul] Int Agcy Res Canc, F-69372 Lyon, France.
[Janout, Vladimir; Kollarova, Hellena] Palacky Univ, CR-77147 Olomouc, Czech Republic.
[Bencko, Vladimir] Charles Univ Prague, Prague, Czech Republic.
[Navratilova, Marie] Masaryk Mem Canc Inst, Brno, Czech Republic.
[Szeszenia-Dabrowska, Neonila] Inst Occupat Med, Lodz, Poland.
[Mates, Dana] Inst Publ Hlth, Bucharest, Romania.
[Boffetta, Paolo] Mt Sinai Sch Med, Tisch Canc Inst, New York, NY USA.
[Boffetta, Paolo] Int Prevent Res Inst, Lyon, France.
RP Liao, LM (reprint author), NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
EM liaolm@mail.nih.gov
RI Liao, Linda/B-3960-2011; Zaridze, David/K-5605-2013; Janout,
Vladimir/M-5133-2014; Szeszenia-Dabrowska, Neonila/F-7190-2010;
OI Liao, Linda/0000-0002-1923-5294; mates, dana/0000-0002-6219-9807
FU National Institutes of Health, National Cancer Institute, Division of
Cancer Epidemiology and Genetics (Bethesda, MD, USA)
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 (Bethesda, MD, USA). The funders had no
role in study design, data collection and analysis, decision to publish,
or preparation of the manuscript.
NR 47
TC 33
Z9 33
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 4
PY 2011
VL 6
IS 11
AR e27361
DI 10.1371/journal.pone.0027361
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 850MH
UT WOS:000297198200069
PM 22076155
ER
PT J
AU Teng, CT
Li, Y
Stockton, P
Foley, J
AF Teng, Christina T.
Li, Yin
Stockton, Pat
Foley, Julie
TI Fasting Induces the Expression of PGC-1 alpha and ERR Isoforms in the
Outer Stripe of the Outer Medulla (OSOM) of the Mouse Kidney
SO PLOS ONE
LA English
DT Article
ID ERYTHROPOIETIN-PRODUCING CELLS; HORMONE RESPONSE ELEMENT; ALPHA
GENE-EXPRESSION; RECEPTOR-GAMMA; COACTIVATOR-1-ALPHA PGC-1-ALPHA;
TRANSCRIPTIONAL COACTIVATOR; HEPATIC GLUCONEOGENESIS; JUXTAMEDULLARY
CORTEX; ESTROGEN-RECEPTOR; METABOLIC-CONTROL
AB Background: Peroxisome proliferator-activated receptor-gamma co-activator-1 alpha (PGC-1 alpha) is a member of the transcriptional coactivator family that plays a central role in the regulation of cellular energy metabolism under various physiological stimuli. During fasting, PGC-1 alpha is induced in the liver and together with estrogen-related receptor a and gamma (ERR alpha and ERR gamma, orphan nuclear receptors with no known endogenous ligand, regulate sets of genes that participate in the energy balance program. We found that PGC-1 alpha, ERR alpha and ERR gamma was highly expressed in human kidney HK2 cells and that PGC-1 alpha induced dynamic protein interactions on the ERR alpha chromatin. However, the effect of fasting on the expression of endogenous PG-C1 alpha, ERR alpha and ERR gamma in the kidney is not known.
Methodology/Principal Findings: In this study, we demonstrated by qPCR that the expression of PGC-1 alpha, ERR alpha and ERR gamma was increased in the mouse kidney after fasting. By using immunohistochemistry (IHC), we showed these three proteins are co-localized in the outer stripe of the outer medulla (OSOM) of the mouse kidney. We were able to collect this region from the kidney using the Laser Capture Microdissection (LCM) technique. The qPCR data showed significant increase of PGC-1 alpha, ERR alpha and ERR gamma mRNA in the LCM samples after fasting for 24 hours. Furthermore, the known ERR alpha target genes, mitochondrial oxidative phosphorylation gene COX8H and the tricarboxylic acid (TCA) cycle gene IDH3A also showed an increase. Taken together, our data suggest that fasting activates the energy balance program in the OSOM of the kidney.
C1 [Teng, Christina T.] NIEHS, Biomol Screening Branch, NIH, Res Triangle Pk, NC 27709 USA.
[Li, Yin] NIEHS, Natl Toxicol Program, NIH, Res Triangle Pk, NC 27709 USA.
[Li, Yin] NIEHS, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Stockton, Pat; Foley, Julie] NIEHS, Cellular & Mol Pathol Branch, NIH, Res Triangle Pk, NC 27709 USA.
RP Teng, CT (reprint author), NIEHS, Biomol Screening Branch, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM teng1@niehs.nih.gov
FU National Institutes of Health; National Institute of Environmental
Health Sciences [Z01-ES 070067]
FX The work was supported by the Intramural Research Program of the
National Institutes of Health and by the National Institute of
Environmental Health Sciences Project Z01-ES 070067 to C.T.T. No current
external funding sources for this study. The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 50
TC 4
Z9 5
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 4
PY 2011
VL 6
IS 11
AR e26961
DI 10.1371/journal.pone.0026961
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 850MH
UT WOS:000297198200026
PM 22073226
ER
PT J
AU Sandtner, W
Egwolf, B
Khalili-Araghi, F
Sanchez-Rodriguez, JE
Roux, B
Bezanilla, F
Holmgren, M
AF Sandtner, Walter
Egwolf, Bernhard
Khalili-Araghi, Fatemeh
Sanchez-Rodriguez, Jorge E.
Roux, Benoit
Bezanilla, Francisco
Holmgren, Miguel
TI Ouabain Binding Site in a Functioning Na+/K+ ATPase
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID FAMILIAL HEMIPLEGIC MIGRAINE; NA,K-ATPASE ALPHA-SUBUNIT;
SODIUM-POTASSIUM PUMP; CARDIAC GLYCOSIDE BINDING; BETA-SUBUNIT; DIRECTED
MUTAGENESIS; CRYSTAL-STRUCTURE; EXTRACELLULAR DOMAIN; STRUCTURAL
INSIGHTS; NA+,K+-ATPASE PUMP
AB The Na+/K+ ATPase is an almost ubiquitous integral membrane protein within the animal kingdom. It is also the selective target for cardiotonic derivatives, widely prescribed inhibitors for patients with heart failure. Functional studies revealed that ouabain-sensitive residues distributed widely throughout the primary sequence of the protein. Recently, structural work has brought some consensus to the functional observations. Here, we use a spectroscopic approach to estimate distances between a fluorescent ouabain and a lanthanide binding tag (LBT), which was introduced at five different positions in the Na+/K+ ATPase sequence. These five normally functional LBT-Na+/K+ ATPase constructs were expressed in the cell membrane of Xenopus laevis oocytes, operating under physiological internal and external ion conditions. The spectroscopic data suggest two mutually exclusive distances between the LBT and the fluorescent ouabain. From the estimated distances and using homology models of the LBT-Na+/K+ ATPase constructs, approximate ouabain positions could be determined. Our results suggest that ouabain binds at two sites along the ion permeation pathway of the Na+/K+ ATPase. The external site (low apparent affinity) occupies the same region as previous structural findings. The high apparent affinity site is, however, slightly deeper toward the intracellular end of the protein. Interestingly, in both cases the lactone ring faces outward. We propose a sequential ouabain binding mechanism that is consistent with all functional and structural studies.
C1 Med Univ Vienna, Dept Pharmacol, A-1090 Vienna, Austria.
[Egwolf, Bernhard] Max Planck Inst Biophys Chem, Dept Theoret & Computat Biophys, D-37077 Gottingen, Germany.
[Khalili-Araghi, Fatemeh; Sanchez-Rodriguez, Jorge E.; Roux, Benoit; Bezanilla, Francisco] Univ Chicago, Gordon Ctr Integrat Sci, Dept Biochem & Mol Biol, Chicago, IL 60637 USA.
[Holmgren, Miguel] NINDS, Mol Neurophysiol Sect, Porter Neurosci Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Roux, B (reprint author), 929 E 57 St, Chicago, IL 60637 USA.
EM roux@uchicago.edu; fbezanilla@uchicago.edu; holmgren@ninds.nih.gov
FU National Institutes of Health [R01-GM062342, R01-GM030376,
U54-GM087519]; NINDS, National Institutes of Health; Consejo Nacional de
Ciencia y TecnologIa (Mexico)
FX This work was supported, in whole or in part, by National Institutes of
Health Grants R01-GM062342, R01-GM030376, and U54-GM087519. This work
was also supported by the Intramural Research Program NINDS, National
Institutes of Health.; Recipient of a postdoctoral fellowship from
Consejo Nacional de Ciencia y TecnologIa (Mexico).
NR 46
TC 25
Z9 28
U1 0
U2 12
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 4
PY 2011
VL 286
IS 44
BP 38177
EP 38183
DI 10.1074/jbc.M111.267682
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 842JD
UT WOS:000296594200031
PM 21911500
ER
PT J
AU Das, S
Rericha, EC
Bagorda, A
Parent, CA
AF Das, Satarupa
Rericha, Erin C.
Bagorda, Anna
Parent, Carole A.
TI Direct Biochemical Measurements of Signal Relay during Dictyostelium
Development
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID PROTEIN-COUPLED RECEPTORS; COLLECTIVE CELL-MIGRATION; CYCLIC 3',5'-AMP
RELAY; CHEMOATTRACTANT RECEPTOR; MEDIATED ACTIVATION; ADENYLYL-CYCLASE;
DOWN-REGULATION; CAMP RECEPTOR; INDUCED PHOSPHORYLATION; DISCOIDEUM
AB Upon starvation, individual Dictyostelium discoideum cells enter a developmental program that leads to collective migration and the formation of a multicellular organism. The process is mediated by extracellular cAMP binding to the G protein-coupled cAMP receptor 1, which initiates a signaling cascade leading to the activation of adenylyl cyclase A (ACA), the synthesis and secretion of additional cAMP, and an autocrine and paracrine activation loop. The release of cAMP allows neighboring cells to polarize and migrate directionally and form characteristic chains of cells called streams. We now report that cAMP relay can be measured biochemically by assessing ACA, ERK2, and TORC2 activities at successive time points in development after stimulating cells with subsaturating concentrations of cAMP. We also find that the activation profiles of ACA, ERK2, and TORC2 change in the course of development, with later developed cells showing a loss of sensitivity to the relayed signal. We examined mutants in PKA activity that have been associated with precocious development and find that this loss in responsiveness occurs earlier in these mutants. Remarkably, we show that this loss in sensitivity correlates with a switch in migration patterns as cells transition from streams to aggregates. We propose that as cells proceed through development, the cAMP-induced desensitization and down-regulation of cAMP receptor 1 impacts the sensitivities of chemotactic signaling cascades leading to changes in migration patterns.
C1 [Das, Satarupa; Bagorda, Anna; Parent, Carole A.] NCI, Cellular & Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Rericha, Erin C.] Univ Maryland, Inst Res Elect & Appl Phys, College Pk, MD 20742 USA.
RP Parent, CA (reprint author), NCI, Cellular & Mol Biol Lab, Ctr Canc Res, NIH, 37 Convent Dr,Bldg 37,Rm 2066, Bethesda, MD 20892 USA.
EM parentc@mail.nih.gov
OI Das, Satarupa/0000-0002-4217-9972
FU National Institutes of Health NCI of the Center for Cancer Research;
Burroughs Wellcome fund
FX This work was supported, in whole or in part, by the National Institutes
of Health NCI Intramural Research Program of the Center for Cancer
Research.; Recipient of a Career Award at the Scientific Interface from
the Burroughs Wellcome fund.
NR 50
TC 7
Z9 7
U1 0
U2 9
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 4
PY 2011
VL 286
IS 44
BP 38649
EP 38658
DI 10.1074/jbc.M111.284182
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 842JD
UT WOS:000296594200077
PM 21911494
ER
PT J
AU Busillo, JM
Azzam, KM
Cidlowski, JA
AF Busillo, John M.
Azzam, Kathleen M.
Cidlowski, John A.
TI Glucocorticoids Sensitize the Innate Immune System through Regulation of
the NLRP3 Inflammasome
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID NALP3 INFLAMMASOME; ENDOTHELIAL-CELLS; INDUCED APOPTOSIS; OXIDATIVE
STRESS; CUTTING EDGE; RECEPTOR; ACTIVATION; ATP; RELEASE; GENE
AB Glucocorticoids have long been recognized as powerful anti-inflammatory compounds that are one of the most widely prescribed classes of drugs in the world. However, their role in the regulation of innate immunity is not well understood. We sought to examine the effects of glucocorticoids on the NOD-like receptors (NLRs), a central component of the inflammasome and innate immunity. Surprisingly, we show that glucocorticoids induce both NLRP3 messenger RNA and protein, which is a critical component of the inflammasome. The glucocorticoid-dependent induction of NLRP3 sensitizes the cells to extracellular ATP and significantly enhances the ATP-mediated release of proinflammatory molecules, including mature IL-1 beta, TNF-alpha, and IL-6. This effect was specific for glucocorticoids and dependent on the glucocorticoid receptor. These studies demonstrate a novel role for glucocorticoids in sensitizing the initial inflammatory response by the innate immune system.
C1 [Busillo, John M.; Cidlowski, John A.] NIEHS, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA.
[Azzam, Kathleen M.] NIEHS, Lab Resp Biol, Dept Hlth & Human Serv, NIH, Res Triangle Pk, NC 27709 USA.
RP Cidlowski, JA (reprint author), 111 TW Alexander Dr,Rm F349, Res Triangle Pk, NC 27709 USA.
EM cidlows1@niehs.nih.gov
FU National Institutes of Health of the NIEHS [1ZIAES090057-15]
FX This work was supported, in whole or in part, by a National Institutes
of Health grant 1ZIAES090057-15 (intramural research program of the
NIEHS).
NR 61
TC 60
Z9 62
U1 3
U2 12
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 4
PY 2011
VL 286
IS 44
BP 38703
EP 38713
DI 10.1074/jbc.M111.275370
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 842JD
UT WOS:000296594200082
PM 21940629
ER
PT J
AU Qian, WJ
Liu, F
Burke, TR
AF Qian, Wenjian
Liu, Fa
Burke, Terrence R., Jr.
TI Investigation of Unanticipated Alkylation at the N(pi) Position of a
Histidyl Residue Under Mitsunobu Conditions and Synthesis of
Orthogonally Protected Histidine Analogues
SO JOURNAL OF ORGANIC CHEMISTRY
LA English
DT Article
ID POLO-LIKE KINASES; SMALL-MOLECULE INHIBITOR; CANCER-THERAPY; IONIC
LIQUIDS; BOX DOMAIN; PLK1; POLO-LIKE-KINASE-1; IMIDAZOLE
AB We had previously reported that Mitsunobu-based introduction of alkyl substituents onto the imidazole N(pi)-position of a key histidine residue in phosphothreonine-containing peptides can impart high binding affinity against the polo-box domain of polo-like kinase 1. Our current paper investigates the mechanism leading to this N(pi)-alkylation and provides synthetic methodologies that permit the facile synthesis of histidine N(pi)-modified peptides. These agents represent new and potentially important tools for biological studies.
C1 [Qian, Wenjian; Liu, Fa; Burke, Terrence R., Jr.] NCI, Biol Chem Lab, Mol Discovery Program, Ctr Canc Res,NIH, Frederick, MD 21702 USA.
RP Burke, TR (reprint author), NCI, Biol Chem Lab, Mol Discovery Program, Ctr Canc Res,NIH, Frederick, MD 21702 USA.
EM tburke@helix.nih.gov
RI Burke, Terrence/N-2601-2014
FU NIH, Center for Cancer Research; NCI-Frederick; National Cancer
Institute, National Institutes of Health
FX This work was supported in part by the Intramural Research Program of
the NIH, Center for Cancer Research, NCI-Frederick, and the National
Cancer Institute, National Institutes of Health.
NR 31
TC 13
Z9 13
U1 0
U2 15
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-3263
J9 J ORG CHEM
JI J. Org. Chem.
PD NOV 4
PY 2011
VL 76
IS 21
BP 8885
EP 8890
DI 10.1021/jo201599c
PG 6
WC Chemistry, Organic
SC Chemistry
GA 837LY
UT WOS:000296206400030
PM 21950469
ER
PT J
AU Dong, SW
Cahill, KJ
Kang, MI
Colburn, NH
Henrich, CJ
Wilson, JA
Beutler, JA
Johnson, RP
Porco, JA
AF Dong, Suwei
Cahill, Katharine J.
Kang, Moon-Il
Colburn, Nancy H.
Henrich, Curtis J.
Wilson, Jennifer A.
Beutler, John A.
Johnson, Richard P.
Porco, John A., Jr.
TI Microwave-Based Reaction Screening: Tandem Retro-Diels Alder/Diels-Alder
Cycloadditions of o-Quinol Dimers
SO JOURNAL OF ORGANIC CHEMISTRY
LA English
DT Article
ID ASSISTED ORGANIC-SYNTHESIS; ENANTIOSELECTIVE SYNTHESIS; DIMERIZATION
CASCADE; COPE REARRANGEMENT; HEATING ELEMENTS; DENSITY;
CYCLOHEXA-2,4-DIENONES; CYCLOHEXADIENONES; DEAROMATIZATION;
PHOTOREACTION
AB We have accomplished a parallel screen of cycloaddition partners for o-quinols utilizing a plate-based microwave system. Microwave irradiation improves the efficiency of retro-Diels-Alder/Diels-Alder cascades of o-quinol dimers which generally proceed in a diastereoselective fashion. Computational studies indicate that asynchronous transition states are favored in Diels-Alder cycloadditions of o-quinols. Subsequent biological evaluation of a collection of cycloadducts has identified an inhibitor of activator protein-1 (AP-1), an oncogenic transcription factor.
C1 [Cahill, Katharine J.; Johnson, Richard P.] Univ New Hampshire, Dept Chem, Durham, NH 03824 USA.
[Dong, Suwei; Porco, John A., Jr.] Boston Univ, Dept Chem, Boston, MA 02215 USA.
[Dong, Suwei; Porco, John A., Jr.] Boston Univ, Ctr Chem Methodol & Lib Dev CMLD BU, Boston, MA 02215 USA.
[Kang, Moon-Il; Colburn, Nancy H.; Henrich, Curtis J.; Wilson, Jennifer A.; Beutler, John A.] NCI, Ctr Canc Res, Lab Canc Prevent, Frederick, MD 21702 USA.
[Kang, Moon-Il; Colburn, Nancy H.; Henrich, Curtis J.; Wilson, Jennifer A.; Beutler, John A.] NCI, Ctr Canc Res, Mol Targets Lab, Frederick, MD 21702 USA.
RP Johnson, RP (reprint author), Univ New Hampshire, Dept Chem, Durham, NH 03824 USA.
EM richard.johnson@unh.edu; porco@bu.edu
RI Beutler, John/B-1141-2009;
OI Beutler, John/0000-0002-4646-1924; Johnson, Richard/0000-0002-1100-6235
FU NIGMS CMLD Initiative [P50 GM067041]; National Science Foundation
[CHE-0910826]; NIH, National Cancer Institute, Center for Cancer
Research; National Cancer Institute, National Institutes of Health
[HHSN261200800001E]
FX This work was generously supported by the NIGMS CMLD Initiative (P50
GM067041, J.A.P.), the National Science Foundation (CHE-0910826,
R.P.J.), and the Intramural Research Program of the NIH, National Cancer
Institute, Center for Cancer Research. This project has been funded in
part with federal funds from the National Cancer Institute, National
Institutes of Health, under contract HHSN261200800001E. The content of
this publication does not necessarily reflect the views or policies of
the Department of Health and Human Services, nor does mention of trade
names, commercial products or organizations imply endorsement by the
U.S. Government. We thank Dr. Emil Lobkovsky (Cornell University) for
X-ray crystal structure analysis and Anton Paar Corp., CEM Corp., and
Waters Corp. for assistance with instrumentation.
NR 56
TC 17
Z9 17
U1 3
U2 15
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-3263
J9 J ORG CHEM
JI J. Org. Chem.
PD NOV 4
PY 2011
VL 76
IS 21
BP 8944
EP 8954
DI 10.1021/jo201658y
PG 11
WC Chemistry, Organic
SC Chemistry
GA 837LY
UT WOS:000296206400036
PM 21942286
ER
PT J
AU Mahnke, YD
Saqr, A
Hazenfeld, S
Brady, RC
Roederer, M
Subbramanian, RA
AF Mahnke, Yolanda D.
Saqr, Areej
Hazenfeld, Staci
Brady, Rebecca C.
Roederer, Mario
Subbramanian, Ramu A.
TI Age-related changes in durability and function of vaccine-elicited
influenza-specific CD4(+) T-cell responses
SO VACCINE
LA English
DT Article
DE Hemagglutinin; Durability; T-cell quality; Proliferation
ID VIRUS-INFECTION; A VIRUS; AVIAN INFLUENZA; REPLICATIVE SENESCENCE;
ANTIBODY-RESPONSE; CROSS-PROTECTION; IMMUNITY; MEMORY; HEMAGGLUTININ;
EXPRESSION
AB The major antigenic component of licensed influenza vaccines, hemagglutinin (HA), elicits predominantly type-specific antibody responses, thus necessitating frequent antigenic updates to the annual vaccine. However, accumulating evidence suggests that influenza vaccines can also induce significant cross-reactive T-cell responses to highly divergent, heterosubtypic HA antigens not included in the vaccine. Influenza vaccines are less effective among the elderly and studies that characterize cross-reactive T-cell immunity in this vulnerable population are much needed. Here, we systematically compare the ex vivo frequency, cytokine profile and phenotype of vaccine-elicited HA-specific T-cell responses among a cohort of young (18-49 years old) and elderly (>= 70 years old) vaccinees, as well as the maturation and activation phenotype of total CD4(+) and CD8(+) T-cells. IFN-gamma production after in vitro expansion and HA-specific Ab titers were also determined. We find that vaccine-elicited ex vivo frequencies of CD4+ T-cells elicited by vaccination reactive to any given homo- or heterosubtypic Ag were comparable across the two age groups. While, no differences were observed between age groups in the phenotype of Ag-specific or total CD4(+) T-cells, PBMC from young adults were superior at producing IFN-gamma after short-term Ag-specific culture. Significantly, while vaccine-elicited T-cell responses were durable among the younger vaccinees, they were short-lived among the elderly. These results have important ramifications for our understanding of vaccine-induced changes in the magnitude and functionality of HA-specific CD4(+) T-cells, as well as age-related alterations in response kinetics. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Saqr, Areej; Hazenfeld, Staci; Brady, Rebecca C.; Subbramanian, Ramu A.] Cincinnati Childrens Hosp Med Ctr, Div Infect Dis, Dept Pediat, Cincinnati, OH 45229 USA.
[Mahnke, Yolanda D.; Roederer, Mario] NIAID, ImmunoTechnol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Subbramanian, RA (reprint author), Cincinnati Childrens Hosp Med Ctr, Div Infect Dis, Dept Pediat, MLC 7017,3333 Burnet Ave, Cincinnati, OH 45229 USA.
EM ramu.subbramanian@gmail.com
FU National Institute for Allergy and Infectious Diseases, NIH
FX The authors would like to thank Dr. Alex Klimov and Dr. Xiyan Xu at the
Center for Disease Control and Prevention (CDC), as well as BEI
Resources for the influenza reagents. We thank Dr. David Bernstein,
Tarek Shata and Saleem Basha for discussions; Tara Foltz for clinical
study coordination; and Joanne Yu for preparation of Ab-conjugates. We
also thank Dr. Martha Nason for help with statistical analysis and power
calculations. This work was supported by the Intramural Research Program
of the National Institute for Allergy and Infectious Diseases, NIH. The
funding bodies did not have any involvement in the actual research.
NR 62
TC 12
Z9 12
U1 0
U2 13
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
J9 VACCINE
JI Vaccine
PD NOV 3
PY 2011
VL 29
IS 47
BP 8606
EP 8614
DI 10.1016/j.vaccine.2011.09.019
PG 9
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 848GA
UT WOS:000297037400019
PM 21939709
ER
PT J
AU Nikolic, DS
Lehmann, M
Felts, R
Garcia, E
Blanchet, FP
Subramaniam, S
Piguet, V
AF Nikolic, Damjan S.
Lehmann, Martin
Felts, Richard
Garcia, Eduardo
Blanchet, Fabien P.
Subramaniam, Sriram
Piguet, Vincent
TI HIV-1 activates Cdc42 and induces membrane extensions in immature
dendritic cells to facilitate cell-to-cell virus propagation
SO BLOOD
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; DC-SIGN; VIROLOGICAL SYNAPSE; TARGET-CELL;
TRANSMISSION; FILOPODIA; PROTEIN; IDENTIFICATION; VISUALIZATION;
REPLICATION
AB HIV-1 cell-to-cell transmission confers a strong advantage as it increases efficiency of transfer up to 100-fold compared with a cell-free route. Mechanisms of HIV-1 cell-to-cell transmission are still unclear and can in part be explained by the presence of actin-containing cellular protrusions. Such protrusions have been shown to facilitate cell-to-cell viral dissemination. Using fluorescence microscopy, electron tomography, and ion abrasion scanning electron microscopy we show that HIV-1 induces membrane extensions in immature dendritic cells through activation of Cdc42. We demonstrate that these extensions are induced after engagement of DC-SIGN by HIV-1(env) via a cascade that involves Src kinases, Cdc42, Pak1, and Wasp. Silencing of Cdc42 or treatment with a specific Cdc42 inhibitor, Secramine A, dramatically reduced the number of membrane protrusions visualized on the cell surface and decreased HIV-1 transfer via infectious synapses. Ion abrasion scanning electron microscopy of cell-cell contact regions showed that cellular extensions from immature dendritic cells that have the appearance of thin filopodia in thin section images are indeed extended membranous sheets with a narrow cross section. Our results demonstrate that HIV-1 binding on immature dendritic cells enhances the formation of membrane extensions that facilitate HIV-1 transfer to CD4(+) T lymphocytes. (Blood. 2011;118(18):4841-4852)
C1 [Piguet, Vincent] Cardiff Univ, Dept Dermatol & Wound Healing, Welsh Inst Dermatol, Sch Med, Cardiff CF14 4XN, S Glam, Wales.
[Blanchet, Fabien P.; Piguet, Vincent] Univ Wales Hosp, Cardiff CF14 4XN, S Glam, Wales.
[Nikolic, Damjan S.; Lehmann, Martin; Garcia, Eduardo; Blanchet, Fabien P.; Piguet, Vincent] Univ Hosp & Med Sch Geneva, Dept Dermatol & Venerol, Geneva, Switzerland.
[Nikolic, Damjan S.; Lehmann, Martin; Garcia, Eduardo; Blanchet, Fabien P.; Piguet, Vincent] Univ Hosp & Med Sch Geneva, Dept Microbiol, Geneva, Switzerland.
[Nikolic, Damjan S.; Lehmann, Martin; Garcia, Eduardo; Blanchet, Fabien P.; Piguet, Vincent] Univ Hosp & Med Sch Geneva, Dept Mol Med, Geneva, Switzerland.
[Felts, Richard; Subramaniam, Sriram] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Piguet, V (reprint author), Cardiff Univ, Dept Dermatol & Wound Healing, Welsh Inst Dermatol, Sch Med, 3rd Floor,Glamorgan House,Heath Pk, Cardiff CF14 4XN, S Glam, Wales.
EM piguetv@cardiff.ac.uk
FU Swiss National Science Foundation; Human Science Frontier Program;
Cardiff University; National Cancer Institute; National Institute of
General Medical Sciences; MD-PhD scholarship
FX This work was supported by the Swiss National Science Foundation, the
Human Science Frontier Program, and Cardiff University (V.P.), the
National Cancer Institute (S.S.), an MD-PhD scholarship (D.S.N.), and
the National Institute of General Medical Sciences (Pharmacology
Research Associate Fellowship; R.F.).
NR 38
TC 31
Z9 31
U1 0
U2 7
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 3
PY 2011
VL 118
IS 18
BP 4841
EP 4852
DI 10.1182/blood-2010-09-305417
PG 12
WC Hematology
SC Hematology
GA 843YS
UT WOS:000296714500014
PM 21562048
ER
PT J
AU McDermott, DH
Liu, Q
Ulrick, J
Kwatemaa, N
Anaya-O'Brien, S
Penzak, SR
Oliveira, J
Priel, DAL
Kelly, C
Garofalo, M
Littel, P
Marquesen, MM
Hilligoss, D
DeCastro, R
Fleisher, TA
Kuhns, DB
Malech, HL
Murphy, PM
AF McDermott, David H.
Liu, Qian
Ulrick, Jean
Kwatemaa, Nana
Anaya-O'Brien, Sandra
Penzak, Scott R.
Oliveira Filho, Joao
Priel, Debra A. Long
Kelly, Corin
Garofalo, Mary
Littel, Patricia
Marquesen, Martha M.
Hilligoss, Diane
DeCastro, Rosamma
Fleisher, Thomas A.
Kuhns, Douglas B.
Malech, Harry L.
Murphy, Philip M.
TI The CXCR4 antagonist plerixafor corrects panleukopenia in patients with
WHIM syndrome
SO BLOOD
LA English
DT Article
ID CHEMOKINE RECEPTOR CXCR4; BONE-MARROW; MEMORY CD4(+); T-CELLS;
MYELOKATHEXIS; DISEASE; HYPOGAMMAGLOBULINEMIA; GRANULOCYTOPENIA;
PHARMACOKINETICS; DESENSITIZATION
AB WHIM syndrome is a rare congenital immunodeficiency disorder characterized by warts, hypogammaglobulinemia, infections, and myelokathexis (neutropenia because of impaired egress from the BM); most patients also have severe panleukopenia. Because WHIM syndrome is caused by mutations in the chemokine receptor CXCR4 that result in increased agonist-dependent signaling, we hypothesized that the CXCR4 antagonist plerixafor (Mozobil [Genyzme Corporation], AMD3100), might be an effective treatment. To test this, we enrolled 3 unrelated adult patients with the most common WHIM mutation, CXCR4(R334X), in a phase 1 dose-escalation study. Plerixafor increased absolute lymphocyte, monocyte, and neutrophil counts in blood to normal without significant side effects in all 3 patients. Peak responses occurred at 3-12 hours after injection and waned by 24 hours after injection which tracked the drug's pharmacokinetics. All 3 cell types increased in a dose-dependent manner with the rank order of responsiveness absolute lymphocyte > monocyte > neutrophil. These data provide the first pharmacologic evidence that panleukopenia in WHIM syndrome is caused by CXCL12-CXCR4 signaling-dependent leukocyte sequestration, and support continued study of plerixafor as mechanism-based therapy in this disease. This study is registered at http://www.clinicaltrials.gov as NCT00967785. (Blood. 2011;118(18):4957-4962)
C1 [McDermott, David H.; Liu, Qian; Murphy, Philip M.] NIAID, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Ulrick, Jean; Kwatemaa, Nana; Anaya-O'Brien, Sandra; Kelly, Corin; Garofalo, Mary; Littel, Patricia; Marquesen, Martha M.; Hilligoss, Diane; DeCastro, Rosamma; Malech, Harry L.] NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA.
[Penzak, Scott R.] NIH, Ctr Clin, Dept Pharm, Bethesda, MD 20892 USA.
[Oliveira Filho, Joao; Fleisher, Thomas A.] NIH, Ctr Clin, Div Lab Med, Bethesda, MD 20892 USA.
[Priel, Debra A. Long; Kuhns, Douglas B.] NCI, Clin Serv Program, SAIC Frederick Inc, Frederick, MD 21701 USA.
RP McDermott, DH (reprint author), 9000 Rockville Pike,Bldg 10,Rm 11N107, Bethesda, MD 20892 USA.
EM dmcdermott@nih.gov
OI Malech, Harry/0000-0001-5874-5775; McDermott, David/0000-0001-6978-0867
FU Division of Intramural Research of the National Institute of Allergy and
Infectious Diseases; Office of Rare Diseases Research, National
Institutes of Health; National Cancer Institute, National Institutes of
Health [HHSN261200800001E]
FX This work was supported by the Division of Intramural Research of the
National Institute of Allergy and Infectious Diseases and the Office of
Rare Diseases Research, National Institutes of Health, and was funded in
part with federal funds from the National Cancer Institute, National
Institutes of Health under Contract number HHSN261200800001E. Plerixafor
was provided at no cost for the study by Genzyme Corporation.
NR 29
TC 53
Z9 53
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 3
PY 2011
VL 118
IS 18
BP 4957
EP 4962
DI 10.1182/blood-2011-07-368084
PG 6
WC Hematology
SC Hematology
GA 843YS
UT WOS:000296714500025
PM 21890643
ER
PT J
AU Dayan, E
Cohen, LG
AF Dayan, Eran
Cohen, Leonardo G.
TI Neuroplasticity Subserving Motor Skill Learning
SO NEURON
LA English
DT Review
ID TRANSCRANIAL MAGNETIC STIMULATION; EXPERIENCE-DEPENDENT PLASTICITY;
WHITE-MATTER ARCHITECTURE; IMAGING BRAIN PLASTICITY; VOXEL-BASED
MORPHOMETRY; LONG-TERM POTENTIATION; CORTICAL PLASTICITY;
PROTEIN-SYNTHESIS; CONTEXTUAL INTERFERENCE; MEMORY CONSOLIDATION
AB Recent years have seen significant progress in our understanding of the neural substrates of motor skill learning. Advances in neuroimaging provide new insight into functional reorganization associated with the acquisition, consolidation, and retention of motor skills. Plastic changes involving structural reorganization in gray and white matter architecture that occur over shorter time periods than previously thought have been documented as well. Data from experimental animals provided crucial information on plausible cellular and molecular substrates contributing to brain reorganization underlying skill acquisition in humans. Here, we review findings demonstrating functional and structural plasticity across different spatial and temporal scales that mediate motor skill learning while identifying converging areas of interest and possible avenues for future research.
C1 [Dayan, Eran; Cohen, Leonardo G.] Natl Inst Neurol Disorders & Stroke, Human Cort Physiol & Stroke Neurorehabil Sect, NIH, Bethesda, MD 20892 USA.
RP Cohen, LG (reprint author), Natl Inst Neurol Disorders & Stroke, Human Cort Physiol & Stroke Neurorehabil Sect, NIH, Bethesda, MD 20892 USA.
EM cohenl@ninds.nih.gov
RI Dayan, Eran/C-3449-2009;
OI Dayan, Eran/0000-0001-9710-9210
FU National Institute of Neurological Disorders and Stroke, National
Institutes of Health
FX We would like to thank Barry Richmond, Sunbin Song, and Nitzan Censor
for providing useful suggestions. This work was supported by the
Intramural Research Program of the National Institute of Neurological
Disorders and Stroke, National Institutes of Health.
NR 137
TC 246
Z9 249
U1 11
U2 121
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
J9 NEURON
JI Neuron
PD NOV 3
PY 2011
VL 72
IS 3
BP 443
EP 454
DI 10.1016/j.neuron.2011.10.008
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 845ME
UT WOS:000296826000003
PM 22078504
ER
PT J
AU Shukla, S
Kavak, E
Gregory, M
Imashimizu, M
Shutinoski, B
Kashlev, M
Oberdoerffer, P
Sandberg, R
Oberdoerffer, S
AF Shukla, Sanjeev
Kavak, Ersen
Gregory, Melissa
Imashimizu, Masahiko
Shutinoski, Bojan
Kashlev, Mikhail
Oberdoerffer, Philipp
Sandberg, Rickard
Oberdoerffer, Shalini
TI CTCF-promoted RNA polymerase II pausing links DNA methylation to
splicing
SO NATURE
LA English
DT Article
ID INSULATOR PROTEIN CTCF; HUMAN GENOME; TRANSCRIPTION ELONGATION;
BINDING-SITES; ZINC FINGERS; IN-VIVO; CD45; CANCER; EXONS; SEQ
AB Alternative splicing of pre-messenger RNA is a key feature of transcriptome expansion in eukaryotic cells, yet its regulation is poorly understood. Spliceosome assembly occurs co-transcriptionally, raising the possibility that DNA structure may directly influence alternative splicing. Supporting such an association, recent reports have identified distinct histone methylation patterns, elevated nucleosome occupancy and enriched DNA methylation at exons relative to introns. Moreover, the rate of transcription elongation has been linked to alternative splicing. Here we provide the first evidence that a DNA-binding protein, CCCTC-binding factor (CTCF), can promote inclusion of weak upstream exons by mediating local RNA polymerase II pausing both in a mammalian model system for alternative splicing, CD45, and genome-wide. We further show that CTCF binding to CD45 exon 5 is inhibited by DNA methylation, leading to reciprocal effects on exon 5 inclusion. These findings provide a mechanistic basis for developmental regulation of splicing outcome through heritable epigenetic marks.
C1 [Shukla, Sanjeev; Gregory, Melissa; Shutinoski, Bojan; Oberdoerffer, Philipp; Oberdoerffer, Shalini] Natl Canc Inst Frederick, Ctr Canc Res, Mouse Canc Genet Program, Frederick, MD 21702 USA.
[Kavak, Ersen; Sandberg, Rickard] Karolinska Inst, Dept Cell & Mol Biol, SE-17177 Stockholm, Sweden.
[Kavak, Ersen; Sandberg, Rickard] Ludwig Inst Canc Res, SE-17177 Stockholm, Sweden.
[Imashimizu, Masahiko; Kashlev, Mikhail] Natl Canc Inst Frederick, Ctr Canc Res, Gene Regulat & Chromosome Biol Lab, Frederick, MD 21702 USA.
RP Oberdoerffer, S (reprint author), Natl Canc Inst Frederick, Ctr Canc Res, Mouse Canc Genet Program, Frederick, MD 21702 USA.
EM shalini.oberdoerffer@nih.gov
RI Shutinoski, Bojan/M-5260-2016;
OI Shutinoski, Bojan/0000-0003-4669-5656; Sandberg,
Rickard/0000-0001-6473-1740
FU NIH, the National Cancer Institute, The Center for Cancer Research;
Swedish Research Council Foundation; Foundation for Strategic Research
FX We thank A. Rao, C. Burge and K. Lynch for critical reading of this
manuscript. We also thank A. Rao for reagents and K. Nyswaner and M.
Prigge for technical assistance. This work is supported by the
Intramural Research Program of NIH, the National Cancer Institute, The
Center for Cancer Research (S.O., P.O., M. K.), and the Swedish Research
Council Foundation and the Foundation for Strategic Research (R.S.).
NR 54
TC 373
Z9 388
U1 2
U2 60
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 3
PY 2011
VL 479
IS 7371
BP 74
EP U99
DI 10.1038/nature10442
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 840FA
UT WOS:000296422600034
PM 21964334
ER
PT J
AU Zhu, L
Ghosh, K
King, M
Cellmer, T
Bakajin, O
Lapidus, LJ
AF Zhu, Li
Ghosh, Kingshuk
King, Michael
Cellmer, Troy
Bakajin, Olgica
Lapidus, Lisa J.
TI Evidence of Multiple Folding Pathways for the Villin Headpiece Subdomain
SO JOURNAL OF PHYSICAL CHEMISTRY B
LA English
DT Article
ID MICROFLUIDIC MIXER; MOLECULAR-DYNAMICS; HELICAL SUBDOMAIN; SPEED LIMIT;
PROTEIN; KINETICS; SIMULATIONS; SPECTROSCOPY; FUNNELS; STATES
AB The defining property of two-state models of protein folding is that the measured relaxation rates are independent of the starting conditions and only depend on the final conditions. In this work we compare the kinetics of the very fast folding villin subdomain measured after a large change in denaturant concentration using an ultrarapid microfluidic mixer with the kinetics measured after a small temperature change in a laser T-jump experiment and find a significant difference in the observed folding kinetics. The final conditions of temperature and denaturant concentration and the use of tryptophan fluorescence as a probe are the same in both experiments, while the initial conditions are very different. The slower mixing kinetics show no evidence of the faster phase in T-jump experiments, which would support models of on- or off-pathway intermediates. Rather we interpret the combined mixer and T-jump experiments as evidence of an ensemble of unfolded states, some of which are traps. The ensemble after dilution from high denaturant is more expanded than the ensemble after an increase in temperature and, on average, takes longer to reach the native state.
C1 [Zhu, Li; King, Michael; Lapidus, Lisa J.] Michigan State Univ, Dept Phys & Astron, E Lansing, MI 48824 USA.
[Zhu, Li] Southeast Univ, Adv Photon Ctr, Nanjing 210096, Peoples R China.
[Ghosh, Kingshuk] Univ Denver, Dept Phys & Astron, Denver, CO 80208 USA.
[Cellmer, Troy] NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
[Bakajin, Olgica] Univ Calif Davis, Ctr Biophoton Sci & Technol, Sacramento, CA 95817 USA.
RP Lapidus, LJ (reprint author), Michigan State Univ, Dept Phys & Astron, E Lansing, MI 48824 USA.
RI Zhu, Li/H-4746-2011
FU National Science Foundation FIBR [NSF EF-0623664, 0623664]; Burroughs
Welcome Fund
FX We thank William Eaton, Ken Dill, and Vijay Pande for many helpful
discussions. This work is supported by National Science Foundation FIBR
(NSF EF-0623664). This work was partially supported by funding from
National Science Foundation FIBR Grant 0623664 administered by the
Center for Biophotonics, an NSF Science and Technology Center, managed
by the University of California, Davis, under Cooperative Agreement PHY
0120999. The research of L.L., Ph.D. is supported in part by a Career
Award at the Scientific Interface from the Burroughs Welcome Fund.
NR 37
TC 16
Z9 16
U1 2
U2 13
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 3
PY 2011
VL 115
IS 43
BP 12632
EP 12637
DI 10.1021/jp206238y
PG 6
WC Chemistry, Physical
SC Chemistry
GA 837CY
UT WOS:000296169900036
PM 21923150
ER
PT J
AU Francis, DM
Rozycki, B
Tortajada, A
Hummer, G
Peti, W
Page, R
AF Francis, Dana M.
Rozycki, Bartosz
Tortajada, Antoni
Hummer, Gerhard
Peti, Wolfgang
Page, Rebecca
TI Resting and Active States of the ERK2:HePTP Complex
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID PROTEIN-TYROSINE-PHOSPHATASE; MAP KINASE ERK2; PTP-SL; DOCKING
INTERACTIONS; SIGNALING PATHWAYS; STRUCTURAL BASIS; IN-VITRO;
ACTIVATION; SPECIFICITY; MECHANISMS
AB The MAP kinase ERK2 (ERK2, extracellular signal-regulated kinase 2) is regulated by numerous phosphatases that tightly control its activity. For example, the hematopoietic tyrosine phosphatase (HePTP) negatively regulates T cell activation in lymphocytes via ERK2 dephosphorylation. However, only very limited structural information is available for these biologically important complexes. Here, we use small-angle X-ray scattering combined with EROS ensemble refinement to characterize the structures of the resting and active states of ERK2:HePTP complexes. Our data show that the resting state ERIC2:HePTP complex adopts a highly extended, dynamic conformation that becomes compact and ordered in the active state complex. This work experimentally demonstrates that these complexes undergo significant dynamic structural changes in solution and provides the first structural insight into an active state MAPK complex.
C1 [Tortajada, Antoni; Page, Rebecca] Brown Univ, Dept Mol Biol Cell Biol & Biochem, Providence, RI 02912 USA.
[Francis, Dana M.; Peti, Wolfgang] Brown Univ, Dept Mol Pharmacol Physiol & Biotechnol, Providence, RI 02912 USA.
[Rozycki, Bartosz; Hummer, Gerhard] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Page, R (reprint author), Brown Univ, Dept Mol Biol Cell Biol & Biochem, Providence, RI 02912 USA.
EM Rebecca_Page@brown.edu
RI Rozycki, Bartosz/B-7005-2009; Hummer, Gerhard/A-2546-2013; Peti,
Wolfgang/L-3492-2014
OI Rozycki, Bartosz/0000-0001-5938-7308; Hummer,
Gerhard/0000-0001-7768-746X;
FU American Cancer Society [RSG-08-067-01-LIB]; European Community;
National Institute of Diabetes and Digestive and Kidney Diseases, NIH;
U.S. DOE, Office of Science [DE-AC02-98CH10886]
FX The authors thank Drs. Lin Yang and Marc Allaire (NSLS, X9) for their
support. The project was supported by Grant RSG-08-067-01-LIB from the
American Cancer Society to R.P. B.R. was supported by a Marie Curie
International Outgoing Fellowship within the 7th European Community
Framework Program. B.R. and G.H. were supported by the Intramural
Research Program of the National Institute of Diabetes and Digestive and
Kidney Diseases, NIH. Use of the NSLS was supported by the U.S. DOE,
Office of Science under Contract No. DE-AC02-98CH10886. Simulations were
performed on the Biowulf computing cluster at NIH.
NR 33
TC 17
Z9 17
U1 0
U2 9
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD NOV 2
PY 2011
VL 133
IS 43
BP 17138
EP 17141
DI 10.1021/ja2075136
PG 4
WC Chemistry, Multidisciplinary
SC Chemistry
GA 852TR
UT WOS:000297380900010
PM 21985012
ER
PT J
AU Cousins, MM
Laeyendecker, O
Beauchamp, G
Brookmeyer, R
Towler, WI
Hudelson, SE
Khaki, L
Koblin, B
Chesney, M
Moore, RD
Kelen, GD
Coates, T
Celum, C
Buchbinder, SP
Seage, GR
Quinn, TC
Donnell, D
Eshleman, SH
AF Cousins, Matthew M.
Laeyendecker, Oliver
Beauchamp, Geetha
Brookmeyer, Ronald
Towler, William I.
Hudelson, Sarah E.
Khaki, Leila
Koblin, Beryl
Chesney, Margaret
Moore, Richard D.
Kelen, Gabor D.
Coates, Thomas
Celum, Connie
Buchbinder, Susan P.
Seage, George R., III
Quinn, Thomas C.
Donnell, Deborah
Eshleman, Susan H.
TI Use of a High Resolution Melting (HRM) Assay to Compare Gag, Pol, and
Env Diversity in Adults with Different Stages of HIV Infection
SO PLOS ONE
LA English
DT Article
ID VIRUS TYPE-1 INFECTION; GENETIC DIVERSITY; PROGRESSION; EVOLUTION;
IDENTIFICATION; SEROCONVERSION; POLYMORPHISM; CHALLENGES; PLASMA; DONORS
AB Background: Cross-sectional assessment of HIV incidence relies on laboratory methods to discriminate between recent and non-recent HIV infection. Because HIV diversifies over time in infected individuals, HIV diversity may serve as a biomarker for assessing HIV incidence. We used a high resolution melting (HRM) diversity assay to compare HIV diversity in adults with different stages of HIV infection. This assay provides a single numeric HRM score that reflects the level of genetic diversity of HIV in a sample from an infected individual.
Methods: HIV diversity was measured in 203 adults: 20 with acute HIV infection (RNA positive, antibody negative), 116 with recent HIV infection (tested a median of 189 days after a previous negative HIV test, range 14-540 days), and 67 with non-recent HIV infection (HIV infected >2 years). HRM scores were generated for two regions in gag, one region in pol, and three regions in env.
Results: Median HRM scores were higher in non-recent infection than in recent infection for all six regions tested. In multivariate models, higher HRM scores in three of the six regions were independently associated with non-recent HIV infection.
Conclusions: The HRM diversity assay provides a simple, scalable method for measuring HIV diversity. HRM scores, which reflect the genetic diversity in a viral population, may be useful biomarkers for evaluation of HIV incidence, particularly if multiple regions of the HIV genome are examined.
C1 [Cousins, Matthew M.; Towler, William I.; Hudelson, Sarah E.; Khaki, Leila; Eshleman, Susan H.] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
[Laeyendecker, Oliver; Moore, Richard D.; Quinn, Thomas C.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Laeyendecker, Oliver; Quinn, Thomas C.] NIAID, Immunoregulat Lab, NIH, Baltimore, MD USA.
[Beauchamp, Geetha; Donnell, Deborah] Fred Hutchinson Canc Res Ctr, Stat Ctr HIV AIDS Res & Prevent, Seattle, WA 98104 USA.
[Brookmeyer, Ronald] Univ Calif Los Angeles, Dept Biostat, Los Angeles, CA USA.
[Koblin, Beryl] New York Blood Ctr, Lab Infect Dis Prevent, New York, NY 10021 USA.
[Chesney, Margaret; Buchbinder, Susan P.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Kelen, Gabor D.] Johns Hopkins Univ, Sch Med, Dept Emergency Med, Baltimore, MD 21205 USA.
[Coates, Thomas] Univ Calif Los Angeles, Program Global Hlth, Los Angeles, CA USA.
[Celum, Connie] Univ Washington, Dept Med, Seattle, WA USA.
[Buchbinder, Susan P.] San Francisco Dept Publ Hlth, San Francisco, CA USA.
[Seage, George R., III] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
RP Cousins, MM (reprint author), Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
EM seshlem@jhmi.edu
RI Laeyendecker, Oliver/B-9331-2009;
OI Kelen, Gabor/0000-0002-3236-8286; Laeyendecker,
Oliver/0000-0002-6429-4760; Donnell, Deborah/0000-0002-0587-7480
FU HIV Network for Prevention Trials (HIVNET); U.S. National Institute of
Allergy and Infectious Diseases (NIAID); National Institutes of Health
(NIH); Dept. of Health and Human Services (DHHS) [NO1-AI35176,
N01-AI35173, N01-AI45200, U01-AI046745, U01-AI068613, UM1-AI068613];
National Institute on Drug Abuse (NIDA) [R01-DA011602]; National
Institute of Mental Health; Office of AIDS Research of the NIH; National
Institute of Alcohol Abuse and Alcoholism [R01-AA016893]; Emergency
Medicine Foundation (Center of Excellence); NIAID [R01-AI095068];
Division of Intramural Research, NIAID, NIH
FX This work was supported by: (1) the HIV Network for Prevention Trials
(HIVNET) and sponsored by the U.S. National Institute of Allergy and
Infectious Diseases (NIAID), the National Institutes of Health (NIH),
and Dept. of Health and Human Services (DHHS) (NO1-AI35176; N01-AI35173;
N01-AI45200; U01-AI046745), (2) the HIV Prevention Trials Network (HPTN)
sponsored by the NIAID, the National Institute on Drug Abuse (NIDA), the
National Institute of Mental Health, and the Office of AIDS Research of
the NIH and DHHS (U01-AI068613 and UM1-AI068613) (3) NIDA
(R01-DA011602), (4) the National Institute of Alcohol Abuse and
Alcoholism (R01-AA016893), (5) the Emergency Medicine Foundation (Center
of Excellence grant), (6) NIAID (R01-AI095068), and (7) the Division of
Intramural Research, NIAID, NIH. The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 39
TC 24
Z9 24
U1 1
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 2
PY 2011
VL 6
IS 11
AR e27211
DI 10.1371/journal.pone.0027211
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 849WB
UT WOS:000297154900090
PM 22073290
ER
PT J
AU Gonzalez, JM
Dong, Z
Romero, R
Girardi, G
AF Gonzalez, Juan M.
Dong, Zhong
Romero, Roberto
Girardi, Guillermina
TI Cervical Remodeling/Ripening at Term and Preterm Delivery: The Same
Mechanism Initiated by Different Mediators and Different Effector Cells
SO PLOS ONE
LA English
DT Article
ID UTERINE CERVIX; PARTURITION; EXPRESSION; PREGNANCY; BIRTH; FIBROBLASTS;
MATRIX-METALLOPROTEINASE-9; ACTIVATION; LEUKOCYTES; WOMEN
AB Background: Premature cervical remodeling/ripening is believed to contribute to preterm delivery (PTD), the leading cause of perinatal morbidity and mortality. Despite considerable research, the causes of term and PTD remain unclear, and there is no effective treatment for PTD. We previously demonstrated that complement activation plays a causative role in cervical remodeling that leads to PTD in mice.
Methodology/Principal Findings: Here we found that complement activation is not required for the physiological process that leads to term delivery in mice. Neither increased C3 cervical deposition nor increased C3a and C5a serum levels were observed at term. In addition, macrophages infiltration was found in PTD in contrast to term delivery were no leukocytes were found. Despite the different role of complement and different cellular effector cells, PTD and term delivery share a common dowsntream pathway characterized by increased metalloproteinases (MMPs) release and increased collagen degradation. However, different sources of MMPs were identified. Macrophages are the source of MMPs in PTD while cervical fibroblasts and columnar epithelial cells synthesize MMPs at term delivery. A dramatic diminution in serum progesterone levels precedes parturition at term but not in PTD, suggesting that progesterone withdrawal initiates cervical remodeling at term. On the other hand, MMPs release in PTD is triggered by C5a.
Conclusion and Significance: In conclusion, preterm and term cervical remodeling occur through the same mechanism but they are initiated by different mediators and effector cells. That complement activation is required for PTD but not for the physiological process that leads to term delivery, suggests that complement is a potential specific biomarker and selective target to prevent PTD and thus avert neonatal mortality and morbidity.
C1 [Gonzalez, Juan M.; Dong, Zhong; Romero, Roberto] NICHHD, Perinatol Res Branch, NIH, Bethesda, MD 20892 USA.
[Girardi, Guillermina] CUNY, York Coll, New York, NY 10021 USA.
RP Gonzalez, JM (reprint author), NICHHD, Perinatol Res Branch, NIH, Bethesda, MD 20892 USA.
EM Guillermina.Girardi@ed.ac.uk
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development, NIH, DHHS
FX These studies were supported by the Intramural Research Program of the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development, NIH, DHHS. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 29
TC 27
Z9 29
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 2
PY 2011
VL 6
IS 11
AR e26877
DI 10.1371/journal.pone.0026877
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 849WB
UT WOS:000297154900050
PM 22073213
ER
PT J
AU Hornstra, HM
Priestley, RA
Georgia, SM
Kachur, S
Birdsell, DN
Hilsabeck, R
Gates, LT
Samuel, JE
Heinzen, RA
Kersh, GJ
Keim, P
Massung, RF
Pearson, T
AF Hornstra, Heidie M.
Priestley, Rachael A.
Georgia, Shalamar M.
Kachur, Sergey
Birdsell, Dawn N.
Hilsabeck, Remy
Gates, Lauren T.
Samuel, James E.
Heinzen, Robert A.
Kersh, Gilbert J.
Keim, Paul
Massung, Robert F.
Pearson, Talima
TI Rapid Typing of Coxiella burnetii
SO PLOS ONE
LA English
DT Article
ID AMPLIFICATION MUTATION ASSAY; PCR; GENE
AB Coxiella burnetii has the potential to cause serious disease and is highly prevalent in the environment. Despite this, epidemiological data are sparse and isolate collections are typically small, rare, and difficult to share among laboratories as this pathogen is governed by select agent rules and fastidious to culture. With the advent of whole genome sequencing, some of this knowledge gap has been overcome by the development of genotyping schemes, however many of these methods are cumbersome and not readily transferable between institutions. As comparisons of the few existing collections can dramatically increase our knowledge of the evolution and phylogeography of the species, we aimed to facilitate such comparisons by extracting SNP signatures from past genotyping efforts and then incorporated these signatures into assays that quickly and easily define genotypes and phylogenetic groups. We found 91 polymorphisms (SNPs and indels) among multispacer sequence typing (MST) loci and designed 14 SNP-based assays that could be used to type samples based on previously established phylogenetic groups. These assays are rapid, inexpensive, real-time PCR assays whose results are unambiguous. Data from these assays allowed us to assign 43 previously untyped isolates to established genotypes and genomic groups. Furthermore, genotyping results based on assays from the signatures provided here are easily transferred between institutions, readily interpreted phylogenetically and simple to adapt to new genotyping technologies.
C1 [Hornstra, Heidie M.; Georgia, Shalamar M.; Kachur, Sergey; Birdsell, Dawn N.; Hilsabeck, Remy; Gates, Lauren T.; Keim, Paul; Pearson, Talima] No Arizona Univ, Ctr Microbial Genet & Genom, Flagstaff, AZ 86011 USA.
[Priestley, Rachael A.; Kersh, Gilbert J.; Massung, Robert F.] Ctr Dis Control & Prevent, Rickettsial Zoonoses Branch, Atlanta, GA USA.
[Samuel, James E.] Texas A&M Hlth Sci Ctr, Dept Microbial & Mol Pathogenesis, College Stn, TX USA.
[Heinzen, Robert A.] NIAID, Intracellular Parasites Lab, Rocky Mt Labs, NIH, Hamilton, MT USA.
[Keim, Paul] Translat Genom Res Inst, Pathogen Genom Div, Phoenix, AZ USA.
RP Hornstra, HM (reprint author), No Arizona Univ, Ctr Microbial Genet & Genom, Flagstaff, AZ 86011 USA.
EM rfm2@cdc.gov; talima.pearson@nau.edu
FU U.S. Department of Homeland Security ST CB Division
FX This work was supported by the U.S. Department of Homeland Security S&T
CB Division Bioforensics R&D Program. The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 21
TC 28
Z9 28
U1 1
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 2
PY 2011
VL 6
IS 11
AR e26201
DI 10.1371/journal.pone.0026201
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 849WB
UT WOS:000297154900015
PM 22073151
ER
PT J
AU Utani, K
Okamoto, A
Shimizu, N
AF Utani, Koh-ichi
Okamoto, Atsushi
Shimizu, Noriaki
TI Generation of Micronuclei during Interphase by Coupling between
Cytoplasmic Membrane Blebbing and Nuclear Budding
SO PLOS ONE
LA English
DT Article
ID EXTRACHROMOSOMALLY AMPLIFIED DNA; GENE AMPLIFICATION; DOUBLE MINUTES;
CANCER-CELLS; HL-60 CELLS; MOLECULAR-MECHANISMS; MYC GENES; S PHASE;
C-MYC; CHROMATIN
AB Micronucleation, mediated by interphase nuclear budding, has been repeatedly suggested, but the process is still enigmatic. In the present study, we confirmed the previous observation that there are lamin B1-negative micronuclei in addition to the positive ones. A large cytoplasmic bleb was found to frequently entrap lamin B1-negative micronuclei, which were connected to the nucleus by a thin chromatin stalk. At the bottom of the stalk, the nuclear lamin B1 structure appeared broken. Chromatin extrusion through lamina breaks has been referred to as herniation or a blister of the nucleus, and has been observed after the expression of viral proteins. A cell line in which extrachromosomal double minutes and lamin B1 protein were simultaneously visualized in different colors in live cells was established. By using these cells, time-lapse microscopy revealed that cytoplasmic membrane blebbing occurred simultaneously with the extrusion of nuclear content, which generated lamin B1-negative micronuclei during interphase. Furthermore, activation of cytoplasmic membrane blebbing by the addition of fresh serum or camptothecin induced nuclear budding within 1 to 10 minutes, which suggested that blebbing might be the cause of the budding. After the induction of blebbing, the frequency of lamin-negative micronuclei increased. The budding was most frequent during S phase and more efficiently entrapped small extrachromosomal chromatin than the large chromosome arm. Based on these results, we suggest a novel mechanism in which cytoplasmic membrane dynamics pulls the chromatin out of the nucleus through the lamina break. Evidence for such a mechanism was obtained in certain cancer cell lines including human COLO 320 and HeLa. The mechanism could significantly perturb the genome and influence cancer cell phenotypes.
C1 [Utani, Koh-ichi; Okamoto, Atsushi; Shimizu, Noriaki] Hiroshima Univ, Grad Sch Biosphere Sci, Higashihiroshima, Hiroshima 724, Japan.
RP Utani, K (reprint author), NCI, Mol Pharmacol Lab, NIH, Bethesda, MD 20892 USA.
EM shimizu@hiroshima-u.ac.jp
FU Japan Society for the Promotion of Science [17370002, 21657051];
Ministry of Education, Science, Sports and Culture of Japan [19038016]
FX This work was supported in part by a Grant-in-Aid for Scientific
Research (B) [grant number 17370002] and a Grant-in-Aid for Challenging
Exploratory Research [grant number 21657051] both from the Japan Society
for the Promotion of Science to NS and a Grant-in-Aid for Scientific
Research on Priority Areas - Nuclear dynamics [grant number 19038016]
from the Ministry of Education, Science, Sports and Culture of Japan to
NS. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 47
TC 10
Z9 10
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 2
PY 2011
VL 6
IS 11
AR e27233
DI 10.1371/journal.pone.0027233
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 849WB
UT WOS:000297154900093
PM 22073297
ER
PT J
AU Va, P
Yang, WS
Nechuta, S
Chow, WH
Cai, H
Yang, G
Gao, S
Gao, YT
Zheng, W
Shu, XO
Xiang, YB
AF Va, Puthiery
Yang, Wan-Shui
Nechuta, Sarah
Chow, Wong-Ho
Cai, Hui
Yang, Gong
Gao, Shan
Gao, Yu-Tang
Zheng, Wei
Shu, Xiao-Ou
Xiang, Yong-Bing
TI Marital Status and Mortality among Middle Age and Elderly Men and Women
in Urban Shanghai
SO PLOS ONE
LA English
DT Article
ID BREAST-CANCER; GENDER-DIFFERENCES; PHYSICAL-ACTIVITY; SOCIAL-CONTROL;
HEART-DISEASE; HEALTH; COHORT; MARRIAGE; PATTERNS; ASSOCIATION
AB Background: Previous studies have suggested that marital status is associated with mortality, but few studies have been conducted in China where increasing aging population and divorce rates may have major impact on health and total mortality.
Methods: We examined the association of marital status with mortality using data from the Shanghai Women's Health Study (1996-2009) and Shanghai Men's Health Study (2002-2009), two population-based cohort studies of 74,942 women aged 40-70 years and 61,500 men aged 40-74 years at the study enrollment. Deaths were identified by biennial home visits and record linkage with the vital statistics registry. Marital status was categorized as married, never married, divorced, widowed, and all unmarried categories combined. Cox regression models were used to derive hazard ratios (HR) and 95% confidence interval (CI).
Results: Unmarried and widowed women had an increased all-cause HR = 1.11, 95% CI: 1.03, 1.21 and HR = 1.10, 95% CI: 1.02, 1.20 respectively) and cancer (HR = 1.17, 95% CI: 1.04, 1.32 and HR = 1.18, 95% CI: 1.04, 1.34 respectively) mortality. Never married women had excess all-cause mortality (HR = 1.46, 95% CI: 1.03, 2.09). Divorce was associated with elevated cardiovascular disease (CVD) mortality in women (HR = 1.47, 95% CI: 1.01, 2.13) and elevated all-cause mortality (HR = 2.45, 95% CI: 1.55, 3.86) in men. Amongst men, not being married was associated with excess all-cause (HR = 1.45, 95% CI: 1.12, 1.88) and CVD (HR = 1.65, 95% CI: 1.07, 2.54) mortality.
Conclusions: Marriage is associated with decreased all cause mortality and CVD mortality, in particular, among both Chinese men and women.
C1 [Va, Puthiery] Univ New England, Coll Osteopath Med, Biddeford, ME USA.
[Yang, Wan-Shui; Gao, Shan; Xiang, Yong-Bing] Shanghai Jiao Tong Univ, Renji Hosp, Shanghai Canc Inst, State Key Lab Oncogene & Related Genes,Sch Med, Shanghai 200030, Peoples R China.
[Yang, Wan-Shui; Gao, Shan; Gao, Yu-Tang; Xiang, Yong-Bing] Shanghai Jiao Tong Univ, Renji Hosp, Dept Epidemiol, Shanghai Canc Inst,Sch Med, Shanghai 200030, Peoples R China.
[Nechuta, Sarah; Cai, Hui; Yang, Gong; Zheng, Wei; Shu, Xiao-Ou] Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr, Div Epidemiol,Dept Med,Vanderbilt Epidemiol Ctr, Nashville, TN 37212 USA.
[Chow, Wong-Ho] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
RP Va, P (reprint author), Univ New England, Coll Osteopath Med, Biddeford, ME USA.
EM ybxiang@shsci.org
FU US National Institutes of Health [R37 CA070867, R01 CA82729, R01
HL095931]; funds of state key project specialized for infectious
diseases of China [2008ZX10002-015]; Fogarty International Clinical
Research Scholars; Vanderbilt Institute for Global Health; Fogarty
International Center, NIH [R24TW007988]
FX This study was supported by grants from the US National Institutes of
Health (R37 CA070867, R01 CA82729, and R01 HL095931) and the funds of
state key project specialized for infectious diseases of China (No.
2008ZX10002-015). Puthiery Va is supported by the Fogarty International
Clinical Research Scholars and Fellows Support Center at the Vanderbilt
Institute for Global Health, funded by the Fogarty International Center,
NIH, through an R24 Training Grant (Grant number: R24TW007988). The
funders had no role study design, data collection and analysis, decision
to publish, or preparation of the manuscript.
NR 64
TC 6
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U1 1
U2 15
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 2
PY 2011
VL 6
IS 11
AR e26600
DI 10.1371/journal.pone.0026600
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 849WB
UT WOS:000297154900026
PM 22073174
ER
PT J
AU Nandal, A
Ruiz, JC
Subramanian, P
Ghimire-Rijal, S
Sinnamon, RA
Stemmler, TL
Bruick, RK
Philpott, CC
AF Nandal, Anjali
Ruiz, Julio C.
Subramanian, Poorna
Ghimire-Rijal, Sudipa
Sinnamon, Ruth Ann
Stemmler, Timothy L.
Bruick, Richard K.
Philpott, Caroline C.
TI Activation of the HIF Prolyl Hydroxylase by the Iron Chaperones PCBP1
and PCBP2
SO CELL METABOLISM
LA English
DT Article
ID HYPOXIA-INDUCIBLE FACTOR; FAMILY; DIOXYGENASES; PROTEINS; CLUSTER;
DOMAIN; ALPHA
AB Mammalian cells express dozens of iron-containing proteins, yet little is known about the mechanism of metal ligand incorporation. Human poly (rC) binding protein 1 (PCBP1) is an iron chaperone that binds iron and delivers it to ferritin, a cytosolic iron storage protein. We have identified the iron-dependent prolyl hydroxylases (PHDs) and asparaginyl hydroxylase (FIH1) that modify hypoxia-inducible factor alpha (HIF alpha) as targets of PCBP1. Depletion of PCBP1 or PCBP2 in cells led to loss of PHD activity, manifested by reduced prolyl hydroxylation of HIF1 alpha, impaired degradation of HIF1 alpha through the VHL/proteasome pathway, and accumulation of active HIFI transcription factor. PHD activity was restored in vitro by addition of excess Fe(II), or purified Fe-PCBP1, and PCBP1 bound to PHD2 and FIH1 in vivo. These data indicated that PCBP1 was required for iron incorporation into PHD and suggest a broad role for PCBP1 and 2 in delivering iron to cytosolic nonheme iron enzymes.
C1 [Nandal, Anjali; Philpott, Caroline C.] NIDDKD, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
[Ruiz, Julio C.; Bruick, Richard K.] Univ Texas SW Med Ctr Dallas, Dept Biochem, Dallas, TX 75390 USA.
[Subramanian, Poorna; Ghimire-Rijal, Sudipa; Sinnamon, Ruth Ann; Stemmler, Timothy L.] Wayne State Univ, Sch Med, Dept Biochem & Mol Biol, Detroit, MI 48201 USA.
RP Philpott, CC (reprint author), NIDDKD, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
EM carolinep@intra.niddk.nih.gov
RI Nandal, Anjali/A-5376-2013
FU NIDDK, NIH; NIH [DK068139, CA115962]; Burroughs Wellcome Fund; National
Center for Research Resources [C06-RR15437-01]; Sara and Frank McKnight
Fund for Biomedical Research
FX We thank Olga Aprelikova, Hye-sik Kong, and Len Neckers for generously
providing technical suggestions, cell lines, plasmids, and antibodies.
These studies were supported by the Intramural Research Program of
NIDDK, NIH (A.N. and C.C.P), and NIH DK068139 (P.S., S.G.-R., and
T.L.S.). R.K.B. is the Michael L. Rosenberg Scholar in Medical Research
and was supported by the Burroughs Wellcome Fund, NIH grant CA115962,
and a National Center for Research Resources Grant (C06-RR15437-01).
J.C.R. was supported by the Sara and Frank McKnight Fund for Biomedical
Research.
NR 30
TC 60
Z9 62
U1 0
U2 12
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1550-4131
J9 CELL METAB
JI Cell Metab.
PD NOV 2
PY 2011
VL 14
IS 5
BP 647
EP 657
DI 10.1016/j.cmet.2011.08.015
PG 11
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 849RG
UT WOS:000297142200010
PM 22055506
ER
PT J
AU Sedlacek, M
Tipton, PW
Brenowitz, SD
AF Sedlacek, Miloslav
Tipton, Philip W.
Brenowitz, Stephan D.
TI Sustained Firing of Cartwheel Cells in the Dorsal Cochlear Nucleus
Evokes Endocannabinoid Release and Retrograde Suppression of Parallel
Fiber Synapses
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID METABOTROPIC GLUTAMATE RECEPTORS; TERM SYNAPTIC PLASTICITY;
COMPLEX-SPIKING NEURONS; AUDITORY BRAIN-STEM; ENDOGENOUS CANNABINOIDS;
POSTTETANIC POTENTIATION; PURKINJE-CELLS; INHIBITORY INTERNEURONS;
CALCIUM INFLUX; HELD SYNAPSE
AB Neurons in many brain regions release endocannabinoids from their dendrites that act as retrograde signals to transiently suppress neurotransmitter release from presynaptic terminals. Little is known, however, about the physiological mechanisms of short-term endocannabinoid-mediated plasticity under physiological conditions. Here we investigate calcium-dependent endocannabinoid release from cartwheel cells (CWCs) of the mouse dorsal cochlear nucleus (DCN) in the auditory brainstem that provide feedforward inhibition onto DCN principal neurons. We report that sustained action potential firing by CWCs evokes endocannabinoid release in response to submicromolar elevation of dendritic calcium that transiently suppresses their parallel fiber (PF) inputs by >70%. Basal spontaneous CWC firing rates are insufficient to evoke tonic suppression of PF synapses. However, elevating CWC firing rates by stimulating PFs triggers the release of endocannabinoids and heterosynaptic suppression of PF inputs. Spike-evoked suppression by endocannabinoids selectively suppresses excitatory synapses, but glycinergic/GABAergic inputs onto CWCs are not affected. Our findings demonstrate a mechanism of transient plasticity mediated by endocannabinoids that heterosynaptically suppresses subsets of excitatory presynaptic inputs to CWCs that regulates feedforward inhibition of DCN principal neurons and may influence the output of the DCN.
C1 [Sedlacek, Miloslav; Tipton, Philip W.; Brenowitz, Stephan D.] Natl Inst Deafness & Other Commun Disorders, Sect Synapt Transmiss, NIH, Bethesda, MD 20892 USA.
RP Brenowitz, SD (reprint author), Natl Inst Deafness & Other Commun Disorders, Sect Synapt Transmiss, NIH, Bldg 50,Room 4152,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM brenowitzs@nidcd.nih.gov
OI Tipton, Philip/0000-0003-4084-2248
FU National Institute on Deafness and Other Communication Disorders
FX This work was supported by the National Institute on Deafness and Other
Communication Disorders Intramural Research Program. We thank Drs. Jeff
Diamond, David Lovinger, Ron Petralia, and Shan He for comments on the
manuscript.
NR 60
TC 13
Z9 13
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 2
PY 2011
VL 31
IS 44
BP 15807
EP 15817
DI 10.1523/JNEUROSCI.4088-11.2011
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 844ES
UT WOS:000296731100019
PM 22049424
ER
PT J
AU Monosov, IE
Sheinberg, DL
Thompson, KG
AF Monosov, Ilya E.
Sheinberg, David L.
Thompson, Kirk G.
TI The Effects of Prefrontal Cortex Inactivation on Object Responses of
Single Neurons in the Inferotemporal Cortex during Visual Search
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID FRONTAL EYE FIELD; INFERIOR TEMPORAL CORTEX; SPATIAL SELECTION; SUPERIOR
COLLICULUS; TOP-DOWN; AREAS V4; ATTENTION; SIGNALS; MICROSTIMULATION;
RECOGNITION
AB Inferotemporal cortex (IT) is believed to be directly involved in object processing and necessary for accurate and efficient object recognition. The frontal eye field (FEF) is an area in the primate prefrontal cortex that is involved in visual spatial selection and is thought to guide spatial attention and eye movements. We show that object-selective responses of IT neurons and behavioral performance are affected by changes in frontal eye field activity. This was found in monkeys performing a search classification task by temporarily inactivating subregions of FEF while simultaneously recording the activity from single neurons in IT. The effect on object selectivity and performance was specific, occurring in a predictable spatially dependent manner and was strongest when the IT neuron's preferred target was presented in the presence of distractors. FEF inactivation did not affect IT responses on trials in which the nonpreferred target was presented in the search array.
C1 [Monosov, Ilya E.; Thompson, Kirk G.] NEI, Sensorimotor Res Lab, NIH, Bethesda, MD 20892 USA.
[Sheinberg, David L.] Brown Univ, Dept Neurosci, Providence, RI 02906 USA.
RP Monosov, IE (reprint author), NEI, Sensorimotor Res Lab, NIH, Bldg 49,Room 2A50, Bethesda, MD 20892 USA.
EM ilya.monosov@gmail.com
FU National Eye Institute-National Institutes of Health; NEI [R01-EY14681]
FX This work was supported by the Intramural Research Program of the
National Eye Institute-National Institutes of Health as well as NEI
Grant R01-EY14681 (D. L. S.). We thank Drs. Jeffrey Schall, David
Leopold, Okihide Hikosaka, Bruce Cumming, Michael Schmid, Ethan
Bromberg-Martin, Christian Quaia, Robert Wurtz, Susheel Vijayraghavan,
Shinya Yamamoto, and Masaharu Yasuda for valuable comments; and Charles
Zhu and Neal Phipps for excellent MRI services.
NR 41
TC 8
Z9 8
U1 1
U2 5
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 2
PY 2011
VL 31
IS 44
BP 15956
EP 15961
DI 10.1523/JNEUROSCI.2995-11.2011
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA 844ES
UT WOS:000296731100033
PM 22049438
ER
PT J
AU Cohen, JI
Fauci, AS
Varmus, H
Nabel, GJ
AF Cohen, Jeffrey I.
Fauci, Anthony S.
Varmus, Harold
Nabel, Gary J.
TI Epstein-Barr Virus: An Important Vaccine Target for Cancer Prevention
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Editorial Material
ID PHASE-I TRIAL; INFECTIOUS-MONONUCLEOSIS; GP350 VACCINE; LYMPHOMA
AB Participants at the February 2011 meeting at the U.S. National Institutes of Health on Epstein-Barr virus (EBV) vaccine research recommend that future clinical trials have two goals: prevention of infectious mononucleosis and EBV-associated cancers, facilitated by identification of disease-predictive surrogate markers.
C1 [Cohen, Jeffrey I.; Fauci, Anthony S.; Nabel, Gary J.] NIAID, US Natl Inst Hlth NIH, Bethesda, MD 20892 USA.
[Varmus, Harold] NCI, NIH, Bethesda, MD 20892 USA.
[Nabel, Gary J.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Cohen, JI (reprint author), NIAID, US Natl Inst Hlth NIH, Bethesda, MD 20892 USA.
EM jcohen@niaid.nih.gov
FU Vaccine Research Center; NIAID; National Cancer Institute at NIH
FX The views expressed herein represent those of the authors and not
necessarily those of their institutions or of other meeting participants
and do not constitute an endorsement of a specific commercial product.
This meeting was sponsored by the Vaccine Research Center, an intramural
research program of NIAID, and by the National Cancer Institute at NIH.
NR 9
TC 49
Z9 51
U1 0
U2 8
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1946-6234
J9 SCI TRANSL MED
JI Sci. Transl. Med.
PD NOV 2
PY 2011
VL 3
IS 107
AR 107fs7
DI 10.1126/scitranslmed.3002878
PG 3
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 844MD
UT WOS:000296750400001
PM 22049067
ER
PT J
AU Volkow, ND
AF Volkow, Nora D.
TI Epigenetics of Nicotine: Another Nail in the Coughing
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Article
ID ADDICTION; MARIJUANA; FOSB; INHIBITION; SMOKING; GATEWAY; TOBACCO;
BRAIN; DRUGS; YOUTH
AB In a mouse model, chronic nicotine exposure before cocaine use exacerbated the epigenetic, gene-expression, electrophysiological, and behavioral effects that occur during the transition from acute to chronic responses to cocaine that have been linked with the addictive process. Nicotine enhancement of the effects can be mimicked with an inhibitor of chromatin-modifying enzymes (class I and II histone deacetylases). These findings may spur the discovery of therapeutics for the treatment of addiction.
C1 Natl Inst Drug Abuse, NIH, Bethesda, MD 20892 USA.
RP Volkow, ND (reprint author), Natl Inst Drug Abuse, NIH, Bethesda, MD 20892 USA.
EM nvolkow@nida.nih.gov
FU U.S. National Institute on Drug Abuse
FX The author is the director of the U.S. National Institute on Drug Abuse,
which administered a grant awarded to carry out some of the work
discussed herein.
NR 23
TC 0
Z9 0
U1 1
U2 19
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1946-6234
J9 SCI TRANSL MED
JI Sci. Transl. Med.
PD NOV 2
PY 2011
VL 3
IS 107
AR 107ps43
DI 10.1126/scitranslmed.3003278
PG 4
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 844MD
UT WOS:000296750400002
PM 22049068
ER
PT J
AU Aguda, BD
Kim, YJ
Kim, HS
Friedman, A
Fine, HA
AF Aguda, Baltazar D.
Kim, Yangjin
Kim, Hong Sug
Friedman, Avner
Fine, Howard A.
TI Qualitative Network Modeling of the Myc-p53 Control System of Cell
Proliferation and Differentiation
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID EMBRYONIC STEM-CELLS; PTEN TUMOR-SUPPRESSOR; HUMAN CANCER GENES; P53
TARGET GENES; C-MYC; SELF-RENEWAL; IN-VIVO; PATHWAYS; GLIOBLASTOMA;
PROTEIN
AB A kinetic model of a molecular control system for the cellular decision to proliferate or differentiate is formulated and analyzed for the purpose of understanding how the system can break down in cancer cells. The proposed core of this control system is composed of the transcription factors Myc and p53. The network of interactions between these factors involves negative and positive feedback loops that are linked to pathways involved in differentiation, cell cycle, and apoptosis. Understanding the dynamics of the Myc-p53 control system is aided by the postulate that there exists a cancer zone defined as a range of oncogenic Myc activities where the probability of initiating cancer is high. We propose that an essential role of p53 is to prevent the system from entering or staying too long in the cancer zone by downregulating Myc or, when Myc activity somehow becomes too high, by inducing apoptosis, cell cycle arrest, or differentiation. Kinetic modeling illustrates how deletions or aberrations in PTEN, MDM2, and ARF (genes implicated in various cancers, including glioma) affect the Myc-p53 control system. In addition, computer simulations demonstrate how this control system generates different cellular phenotypes characterized by rates of cellular differentiation and proliferation.
C1 [Aguda, Baltazar D.; Kim, Hong Sug; Fine, Howard A.] NCI, Neurooncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Fine, Howard A.] Natl Inst Neurol Disorder & Stroke, NIH, Bethesda, MD USA.
[Kim, Yangjin] Univ Michigan, Dept Math & Stat, Dearborn, MI 48128 USA.
[Friedman, Avner] Ohio State Univ, Math Biosci Inst, Columbus, OH 43210 USA.
RP Aguda, BD (reprint author), NCI, Neurooncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM agudabd@mail.nih.gov
RI Kim, Yangjin/C-9681-2014
FU National Institutes of Health, National Cancer Institute; University of
Michigan-Dearborn
FX Funding was provided by the Intramural Research Program of the National
Institutes of Health, National Cancer Institute. Y.K. was supported by a
Faculty Research Grant from the University of Michigan-Dearborn.
NR 57
TC 11
Z9 12
U1 0
U2 11
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD NOV 2
PY 2011
VL 101
IS 9
BP 2082
EP 2091
DI 10.1016/j.bpj.2011.09.052
PG 10
WC Biophysics
SC Biophysics
GA 843KD
UT WOS:000296669800002
PM 22067145
ER
PT J
AU Hu, KN
McGlinchey, RP
Wickner, RB
Tycko, R
AF Hu, Kan-Nian
McGlinchey, Ryan P.
Wickner, Reed B.
Tycko, Robert
TI Segmental Polymorphism in a Functional Amyloid
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID SOLID-STATE NMR; NUCLEAR-MAGNETIC-RESONANCE; PARALLEL BETA-SHEET; HUMAN
PRION PROTEIN; ALPHA-SYNUCLEIN; REPEAT DOMAIN; LIMITED PROTEOLYSIS;
SECONDARY-STRUCTURE; STRUCTURAL BASIS; ROTATING SOLIDS
AB Although amyloid fibrils are generally considered to be causative or contributing agents in amyloid diseases, several amyloid fibrils are also believed to have biological functions. Among these are fibrils formed by Pmel17 within melanosomes, which act as a template for melanin deposition. We use solid-state NMR to show that the molecular structures of fibrils formed by the 130-residue pseudo-repeat domain Pmel17:RPT are polymorphic even within the biologically relevant pH range. Thus, biological function in amyloid fibrils does not necessarily imply a unique molecular structure. Solid-state NMR spectra of three Pmel17:RPT polymorphs show that in all cases, only a subset (similar to 30%) of the full amino acid sequence contributes to the immobilized fibril core. Although the repetitive nature of the sequence and incomplete spectral resolution prevent the determination of unique chemical shift assignments from two- and three-dimensional solid-state NMR spectra, we use a Monte Carlo assignment algorithm to identify protein segments that are present in or absent from the fibril core. The results show that the identity of the core-forming segments varies from one polymorph to another, a phenomenon known as segmental polymorphism.
C1 [Hu, Kan-Nian; Tycko, Robert] Natl Inst Diabet Digest & Kidney Dis, Chem Phys Lab, NIH, Bethesda, MD USA.
[McGlinchey, Ryan P.; Wickner, Reed B.; Tycko, Robert] Natl Inst Diabet Digest & Kidney Dis, Lab Biochem & Genet, NIH, Bethesda, MD USA.
RP Tycko, R (reprint author), Natl Inst Diabet Digest & Kidney Dis, Chem Phys Lab, NIH, Bethesda, MD USA.
EM robertty@mail.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health.
NR 61
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Z9 28
U1 0
U2 25
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD NOV 2
PY 2011
VL 101
IS 9
BP 2242
EP 2250
DI 10.1016/j.bpj.2011.09.051
PG 9
WC Biophysics
SC Biophysics
GA 843KD
UT WOS:000296669800021
PM 22067164
ER
PT J
AU Oken, MM
Hocking, WG
Kvale, PA
Andriole, GL
Buys, SS
Church, TR
Crawford, ED
Fouad, MN
Isaacs, C
Reding, DJ
Weissfeld, JL
Yokochi, LA
O'Brien, B
Ragard, LR
Rathmell, JM
Riley, TL
Wright, P
Caparaso, N
Hu, P
Izmirlian, G
Pinsky, PF
Prorok, PC
Kramer, BS
Miller, AB
Gohagan, JK
Berg, CD
AF Oken, Martin M.
Hocking, Willam G.
Kvale, Paul A.
Andriole, Gerald L.
Buys, Saundra S.
Church, Timothy R.
Crawford, E. David
Fouad, Mona N.
Isaacs, Claudine
Reding, Douglas J.
Weissfeld, Joel L.
Yokochi, Lance A.
O'Brien, Barbara
Ragard, Lawrence R.
Rathmell, Joshua M.
Riley, Thomas L.
Wright, Patrick
Caparaso, Neil
Hu, Ping
Izmirlian, Grant
Pinsky, Paul F.
Prorok, Philip C.
Kramer, Barnett S.
Miller, Anthony B.
Gohagan, John K.
Berg, Christine D.
CA PLCO Project Team
TI Screening by Chest Radiograph and Lung Cancer Mortality The Prostate,
Lung, Colorectal, and Ovarian (PLCO) Randomized Trial
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
AB Context The effect on mortality of screening for lung cancer with modern chest radiographs is unknown.
Objective To evaluate the effect on mortality of screening for lung cancer using radiographs in the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial.
Design, Setting, and Participants Randomized controlled trial that involved 154 901 participants aged 55 through 74 years, 77 445 of whom were assigned to annual screenings and 77 456 to usual care at 1 of 10 screening centers across the United States between November 1993 and July 2001. The data from a subset of eligible participants for the National Lung Screening Trial (NLST), which compared chest radiograph with spiral computed tomographic (CT) screening, were analyzed.
Intervention Participants in the intervention group were offered annual postero-anterior view chest radiograph for 4 years. Diagnostic follow-up of positive screening results was determined by participants and their health care practitioners. Participants in the usual care group were offered no interventions and received their usual medical care. All diagnosed cancers, deaths, and causes of death were ascertained through the earlier of 13 years of follow-up or until December 31, 2009.
Main Outcome Measures Mortality from lung cancer. Secondary outcomes included lung cancer incidence, complications associated with diagnostic procedures, and all-cause mortality.
Results Screening adherence was 86.6% at baseline and 79% to 84% at years 1 through 3; the rate of screening use in the usual care group was 11%. Cumulative lung cancer incidence rates through 13 years of follow-up were 20.1 per 10 000 person-years in the intervention group and 19.2 per 10 000 person-years in the usual care group (rate ratio [RR]; 1.05, 95% CI, 0.98-1.12). A total of 1213 lung cancer deaths were observed in the intervention group compared with 1230 in usual care group through 13 years (mortality RR, 0.99; 95% CI, 0.87-1.22). Stage and histology were similar between the 2 groups. The RR of mortality for the subset of participants eligible for the NLST, over the same 6-year follow-up period, was 0.94 (95% CI, 0.81-1.10).
Conclusion Annual screening with chest radiograph did not reduce lung cancer mortality compared with usual care.
C1 [Hu, Ping; Izmirlian, Grant; Pinsky, Paul F.; Prorok, Philip C.; Berg, Christine D.] NCI, Biometry Res Grp, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
[Hu, Ping; Izmirlian, Grant; Pinsky, Paul F.; Prorok, Philip C.; Berg, Christine D.] NCI, Early Detect Res Grp, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
[Kramer, Barnett S.] NCI, Phys Data Query Screening & Prevent Editorial Boa, NIH, Bethesda, MD 20892 USA.
[Oken, Martin M.; Church, Timothy R.] Univ Minnesota, Sch Publ Hlth, Minneapolis, MN USA.
[Hocking, Willam G.; Reding, Douglas J.] Marshfield Clin Fdn Med Res & Educ, Marshfield, WI 54449 USA.
[Kvale, Paul A.] Henry Ford Hlth Syst, Detroit, MI USA.
[Andriole, Gerald L.] Washington Univ, St Louis, MO USA.
[Buys, Saundra S.] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT USA.
[Crawford, E. David] Univ Colorado, Denver, CO 80202 USA.
[Fouad, Mona N.] Univ Alabama, Sch Med, Birmingham, AL USA.
[Isaacs, Claudine] Georgetown Univ, Lombardi Canc Ctr, Washington, DC USA.
[Weissfeld, Joel L.] Univ Pittsburgh, Med Ctr Canc Pavil, Pittsburgh, PA USA.
[Yokochi, Lance A.] Pacific Hlth Res & Educ Inst, Honolulu, HI USA.
[O'Brien, Barbara; Ragard, Lawrence R.] Westat Corp, Rockville, MD USA.
[Rathmell, Joshua M.; Riley, Thomas L.; Wright, Patrick] Informat Management Serv Inc, Rockville, MD USA.
[Caparaso, Neil] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Miller, Anthony B.] Univ Toronto, Dalla Lana Sch Publ Hlth, Toronto, ON, Canada.
[Gohagan, John K.] NIH, Off Dis Prevent, Bethesda, MD 20892 USA.
RP Prorok, PC (reprint author), NCI, Biometry Res Grp, Canc Prevent Div, NIH, 6130 Execut Blvd, Bethesda, MD 20892 USA.
EM prorokp@mail.nih.gov
RI Berg , Christine/K-1047-2014;
OI Church, Timothy R./0000-0003-3292-5035; Hocking,
William/0000-0002-0690-3759
FU National Cancer Institute (NCI); National Institute of Diabetes and
Digestive and Kidney Diseases; Division of Cancer Prevention of the NCI;
Division of Cancer Epidemiology and Genetics NCI, National Institutes of
Health, Department of Health and Human Services
FX All authors have completed and submitted the ICMJE Form for Disclosure
of Potential Conflicts of Interest. Mr Hocking reported receiving grant
support and travel support for himself and his institution from the
National Cancer Institute (NCI). Dr Kvale reported receiving
institutional support and travel expenses from the NCI. Dr Andriole
reported receiving institutional grant support from the NCI; serving as
a consultant for Amarex, Amgen, Augmenix, Bayer, Bristol-Myers Squib,
Cambridge Endo, Caris, GlaxoSmithKline, Janssen Biotech Inc, Myriad
Genetics Steba Biotech, Ortho-Clinical Diagnostics, and Viking Medical;
having pending institutional grants from the NCI and National Institute
of Diabetes and Digestive and Kidney Diseases; receiving royalties;
receiving payment for developing educational presentations for Amgen;
owning stocks or stock options from Augmenix, Cambridge Endo,
Envisioning Medical, and Viking Medical; and receiving travel expenses
from Amarex, Amgen, Augmenix, Bayer, Bristol-Myers Squibb, Cambridge
Endo, Caris, Myriad Genetics, Ortho-Clinical Diagnostics, and Steba
Biotech. Dr Buys reported receiving institutional support from the NCI.
Dr Crawford reported receiving institutional grant and travel support
and pending grants from the NCI. Dr Fouad reported receiving
institutional grant support and travel support from the NCI. Dr Isaacs
reported receiving institutional grant and travel support from the NCI.
Dr Redding reported receiving institutional grant support from the NCI.
Dr Weissfeld reported receiving institutional grant and travel support
and compensation for participation for in review activites for the NCI.
Dr Miller reported receiving travel support and compensation for
participation in review activities for the NCI. No other disclosures
were reported.; The NCI funded the Prostate, Lung, Colorectal and
Ovarian (PLCO) Cancer Screening Trial. This research also was supported
by contracts from the Division of Cancer Prevention of the NCI and by
the Intramural Research Program of the Division of Cancer Epidemiology
and Genetics NCI, National Institutes of Health, Department of Health
and Human Services. Role of the Sponsor: The NCI was responsible for the
design and conduct of the study; collection, management, analysis, and
interpretation of the data; and in the preparation, review, or approval
of the manuscript.
NR 19
TC 187
Z9 197
U1 2
U2 17
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 2
PY 2011
VL 306
IS 17
BP 1865
EP 1873
DI 10.1001/jama.2011.1591
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 839OD
UT WOS:000296376200020
PM 22031728
ER
PT J
AU Engels, EA
Pfeiffer, RM
Fraumeni, JF
Kasiske, BL
Israni, AK
Snyder, JJ
Wolfe, RA
Goodrich, NP
Bayakly, AR
Clarke, CA
Copeland, G
Finch, JL
Fleissner, ML
Goodman, MT
Kahn, A
Koch, L
Lynch, CF
Madeleine, MM
Pawlish, K
Rao, C
Williams, MA
Castenson, D
Curry, M
Parsons, R
Fant, G
Lin, M
AF Engels, Eric A.
Pfeiffer, Ruth M.
Fraumeni, Joseph F., Jr.
Kasiske, Bertram L.
Israni, Ajay K.
Snyder, Jon J.
Wolfe, Robert A.
Goodrich, Nathan P.
Bayakly, A. Rana
Clarke, Christina A.
Copeland, Glenn
Finch, Jack L.
Fleissner, Mary Lou
Goodman, Marc T.
Kahn, Amy
Koch, Lori
Lynch, Charles F.
Madeleine, Margaret M.
Pawlish, Karen
Rao, Chandrika
Williams, Melanie A.
Castenson, David
Curry, Michael
Parsons, Ruth
Fant, Gregory
Lin, Monica
TI Spectrum of Cancer Risk Among US Solid Organ Transplant Recipients
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID UNITED-STATES; KIDNEY-TRANSPLANTATION; BRONCHOGENIC-CARCINOMA;
LIVER-TRANSPLANTATION; RENAL-TRANSPLANTATION; LUNG TRANSPLANTATION; CELL
CARCINOMA; DISEASE; PEOPLE; AGENTS
AB Context Solid organ transplant recipients have elevated cancer risk due to immunosuppression and oncogenic viral infections. Because most prior research has concerned kidney recipients, large studies that include recipients of differing organs can inform cancer etiology.
Objective To describe the overall pattern of cancer following solid organ transplantion.
Design, Setting, and Participants Cohort study using linked data on solid organ transplant recipients from the US Scientific Registry of Transplant Recipients (1987-2008) and 13 state and regional cancer registries.
Main Outcome Measures Standardized incidence ratios (SIRs) and excess absolute risks (EARs) assessing relative and absolute cancer risk in transplant recipients compared with the general population.
Results The registry linkages yielded data on 175 732 solid organ transplants (58.4% for kidney, 21.6% for liver, 10.0% for heart, and 4.0% for lung). The overall cancer risk was elevated with 10 656 cases and an incidence of 1375 per 100 000 person-years (SIR, 2.10 [95% CI, 2.06-2.14]; EAR, 719.3 [95% CI, 693.3-745.6] per 100 000 person-years). Risk was increased for 32 different malignancies, some related to known infections (eg, anal cancer, Kaposi sarcoma) and others unrelated (eg, melanoma, thyroid and lip cancers). The most common malignancies with elevated risk were non-Hodgkin lymphoma (n=1504; incidence: 194.0 per 100 000 person-years; SIR, 7.54 [95% CI, 7.17-7.93]; EAR, 168.3 [95% CI, 158.6-178.4] per 100 000 person-years) and cancers of the lung (n=1344; incidence: 173.4 per 100 000 person-years; SIR, 1.97 [95% CI, 1.86-2.08]; EAR, 85.3 [95% CI, 76.2-94.8] per 100 000 person-years), liver (n= 930; incidence: 120.0 per 100 000 person-years; SIR, 11.56 [95% CI, 10.83-12.33]; EAR, 109.6 [95% CI, 102.0-117.6] per 100 000 person-years), and kidney (n= 752; incidence: 97.0 per 100 000 person-years; SIR, 4.65 [95% CI, 4.32-4.99]; EAR, 76.1 [95% CI, 69.3-83.3] per 100 000 person-years). Lung cancer risk was most elevated in lung recipients (SIR, 6.13 [95% CI, 5.18-7.21]) but also increased among other recipients (kidney: SIR, 1.46 [95% CI, 1.34-1.59]; liver: SIR, 1.95 [95% CI, 1.74-2.19]; and heart: SIR, 2.67 [95% CI, 2.40-2.95]). Liver cancer risk was elevated only among liver recipients (SIR, 43.83 [95% CI, 40.90-46.91]), who manifested exceptional risk in the first 6 months (SIR, 508.97 [95% CI, 474.16-545.66]) and a 2-fold excess risk for 10 to 15 years thereafter (SIR, 2.22 [95% CI, 1.57-3.04]). Among kidney recipients, kidney cancer risk was elevated (SIR, 6.66 [95% CI, 6.12-7.23]) and bimodal in onset time. Kidney cancer risk also was increased in liver recipients (SIR, 1.80 [95% CI, 1.40-2.29]) and heart recipients (SIR, 2.90 [95% CI, 2.32-3.59]).
Conclusion Compared with the general population, recipients of a kidney, liver, heart, or lung transplant have an increased risk for diverse infection-related and unrelated cancers. JAMA. 2011; 306(17): 1891-1901
C1 [Engels, Eric A.; Pfeiffer, Ruth M.; Fraumeni, Joseph F., Jr.] NCI, Rockville, MD 20892 USA.
[Kasiske, Bertram L.; Israni, Ajay K.; Snyder, Jon J.] Sci Registry Transplant Recipients, Minneapolis, MN USA.
[Kasiske, Bertram L.; Israni, Ajay K.; Snyder, Jon J.] Minneapolis Med Res Fdn Inc, Minneapolis, MN USA.
[Wolfe, Robert A.; Goodrich, Nathan P.] Sci Registry Transplant Recipients, Ann Arbor, MI USA.
[Wolfe, Robert A.; Goodrich, Nathan P.] Arbor Res Collaborat Hlth, Ann Arbor, MI USA.
[Bayakly, A. Rana] Georgia Comprehens Canc Registry, Atlanta, GA USA.
[Clarke, Christina A.] Canc Prevent Inst Calif, Fremont, CA USA.
[Copeland, Glenn] Michigan Dept Community Hlth, Lansing, MI USA.
[Finch, Jack L.] Colorado Cent Canc Registry, Denver, CO USA.
[Fleissner, Mary Lou] Connecticut Tumor Registry, Hartford, CT USA.
[Goodman, Marc T.] Univ Hawaii, Program Epidemiol, Honolulu, HI 96822 USA.
[Kahn, Amy] New York State Canc Registry, Albany, NY USA.
[Koch, Lori] Illinois State Canc Registry, Springfield, IL USA.
[Lynch, Charles F.] Univ Iowa, Dept Epidemiol, Iowa City, IA USA.
[Madeleine, Margaret M.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Pawlish, Karen] New Jersey Dept Hlth & Senior Serv, Trenton, NJ USA.
[Rao, Chandrika] N Carolina Cent Canc Registry, Raleigh, NC USA.
[Williams, Melanie A.] Texas Dept State Hlth Serv, Austin, TX USA.
[Castenson, David; Curry, Michael; Parsons, Ruth] Informat Management Serv Inc, Rockville, MD USA.
[Fant, Gregory; Lin, Monica] US Hlth Resources & Serv Adm, Rockville, MD 20857 USA.
RP Engels, EA (reprint author), NCI, 6120 Execut Blvd,EPS 7076, Rockville, MD 20892 USA.
EM engelse@exchange.nih.gov
FU Bristol-Myers Squibb; Roche; Genzyme; American Society of Nephrology;
RTI International; Arbor Research Collaborative for Health
[HHSH234200537009C]; Minneapolis Medical Research Foundation
[HHSH250201000018C]; Centers for Disease Control and Prevention:
California [1U58 DP000807-01]; Centers for Disease Control and
Prevention: Colorado [U58 DP000848-04]; Centers for Disease Control and
Prevention: Georgia [5U58DP000817-05]; Centers for Disease Control and
Prevention: Illinois [5658DP000805-04]; Centers for Disease Control and
Prevention: Michigan [5U58DP000812-03]; Centers for Disease Control and
Prevention: New Jersey [5U58/DP000808-03]; Centers for Disease Control
and Prevention: NewYork [15-0351]; Centers for Disease Control and
Prevention: North Carolina [U58DP000832]; Centers for Disease Control
and Prevention: Texas [5U58DP000824-04]; National Cancer Institute:
California [HHSN261201000036C, HHSN261201000035C, HHSN261201000034C];
National Cancer Institute: Connecticut [HHSN261201000024C]; National
Cancer Institute: Hawaii [HHSN261201000037C, N01-PC35137, N01-PC-35139];
National Cancer Institute: Iowa [N01-PC35143]; National Cancer
Institute: New Jersey [HHSN261200544005C ADB, N01-PC-54405]; National
Cancer Institute: Seattle-Puget Sound [N01-PC-35142]; National Cancer
Institute
FX All authors have completed and submitted the ICMJE Form for Disclosure
of Potential Conflicts of Interest. Dr Kasiske reported that he receives
grant funding from Bristol-Myers Squibb. Dr Israni reported that he
receives grant funding from Bristol-Myers Squibb, Roche, and Genzyme. Dr
Snyder reported that he receives consultancy fees from Genzyme for his
participation on a scientific review board; research support is paid to
his institution by Bristol-Myers Squibb and Genzyme; and he has received
payment from the American Society of Nephrology for his work as an
invited educational speaker. Mr Finch reported that consulting fees were
paid to his institution by RTI International; he received travel
expenses from RTI International for his work in Michigan to assist with
electronic data match. No other disclosures were reported.; During most
of the period in which the study was conducted, the Scientific Registry
of Transplant Recipients was managed by Arbor Research Collaborative for
Health (contract HHSH234200537009C). Beginning in September 2010, the
Scientific Registry of Transplant Recipients was managed by Minneapolis
Medical Research Foundation (contract HHSH250201000018C). The following
cancer registries were supported by the National Program of Cancer
Registries of the Centers for Disease Control and Prevention: California
(agreement 1U58 DP000807-01), Colorado (agreement U58 DP000848-04),
Georgia (agreement 5U58DP000817-05), Illinois (agreement
5658DP000805-04), Michigan (agreement 5U58DP000812-03), New Jersey
(agreement 5U58/DP000808-03), NewYork (agreement 15-0351), North
Carolina (agreement U58DP000832), and Texas (agreement 5U58DP000824-04).
The following cancer registries were supported by the Surveillance,
Epidemiology and End Results Program of the National Cancer Institute:
California (contracts HHSN261201000036C, HHSN261201000035C, and
HHSN261201000034C), Connecticut (contract HHSN261201000024C), Hawaii
(contracts HHSN261201000037C, N01-PC35137, and N01-PC-35139), Iowa
(contract N01-PC35143), New Jersey (contract HHSN261200544005C ADB No.
N01-PC-54405), and Seattle-Puget Sound (contract N01-PC-35142).
Additional support was provided by California, Colorado, Connecticut,
Illinois, Iowa, New Jersey, and New York (Cancer Surveillance
Improvement Initiative No. 14-2491), Texas, and Washington, as well as
the Fred Hutchinson Cancer Research Center. This research was supported
in part by the Intramural Research Program of the National Cancer
Institute.
NR 39
TC 352
Z9 358
U1 3
U2 28
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 2
PY 2011
VL 306
IS 17
BP 1891
EP 1901
DI 10.1001/jama.2011.1592
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 839OD
UT WOS:000296376200023
PM 22045767
ER
PT J
AU Soler Artigas, M
Loth, DW
Wain, LV
Gharib, SA
Obeidat, M
Tang, WB
Zhai, GJ
Zhao, JH
Smith, AV
Huffman, JE
Albrecht, E
Jackson, CM
Evans, DM
Cadby, G
Fornage, M
Manichaikul, A
Lopez, LM
Johnson, T
Aldrich, MC
Aspelund, T
Barroso, I
Campbell, H
Cassano, PA
Couper, DJ
Eiriksdottir, G
Franceschini, N
Garcia, M
Gieger, C
Gislason, GK
Grkovic, I
Hammond, CJ
Hancock, DB
Harris, TB
Ramasamy, A
Heckbert, SR
Heliovaara, M
Homuth, G
Hysi, PG
Alan, L
Jankovic, S
Joubert, BR
Karrasch, S
Klopp, N
Koch, B
Kritchevsky, SB
Launer, LJ
Liu, YM
Loehr, LR
Lohman, K
Loos, RJF
Lumley, T
Al Balushi, KA
Ang, WQ
Barr, RG
Beilby, J
Blakey, JD
Boban, M
Boraska, V
Brisman, J
Britton, JR
Brusselle, GG
Cooper, C
Curjuric, I
Dahgam, S
Deary, IJ
Ebrahim, S
Eijgelsheim, M
Francks, C
Gaysina, D
Granell, R
Gu, XJ
Hankinson, JL
Hardy, R
Harris, SE
Henderson, J
Henry, A
Hingorani, AD
Hofman, A
Holt, PG
Hui, JN
Hunter, ML
Imboden, M
Jameson, KA
Kerr, SM
Kolcic, I
Kronenberg, F
Liu, JZ
Marchini, J
McKeever, T
Morris, AD
Olin, AC
Porteous, DJ
Postma, DS
Rich, SS
Ring, SM
Rivadeneira, F
Rochat, T
Sayer, AA
Sayers, I
Sly, PD
Smith, GD
Sood, A
Starr, JM
Uitterlinden, AG
Vonk, JM
Wannamethee, SG
Whincup, PH
Wijmenga, C
Williams, OD
Wong, A
Mangino, M
Marciante, KD
McArdle, WL
Meibohm, B
Morrison, AC
North, KE
Omenaas, E
Palmer, LJ
Pietilainen, KH
Pin, I
Polasek, O
Pouta, A
Psaty, BM
Hartikainen, AL
Rantanen, T
Ripatti, S
Rotter, JI
Rudan, I
Rudnicka, AR
Schulz, H
Shin, SY
Spector, TD
Surakka, I
Vitart, V
Volzke, H
Wareham, NJ
Warrington, NM
Wichmann, HE
Wild, SH
Wilk, JB
Wjst, M
Wright, AF
Zgaga, L
Zemunik, T
Pennell, CE
Nyberg, F
Kuh, D
Holloway, JW
Boezen, HM
Lawlor, DA
Morris, RW
Probst-Hensch, N
Kaprio, J
Wilson, JF
Hayward, C
Kahonen, M
Heinrich, J
Musk, AW
Jarvis, DL
Glaser, S
Jarvelin, MR
Stricker, BHC
Elliott, P
O'Connor, GT
Strachan, DP
London, SJ
Hall, IP
Gudnason, V
Tobin, MD
AF Soler Artigas, Maria
Loth, Daan W.
Wain, Louise V.
Gharib, Sina A.
Obeidat, Ma'en
Tang, Wenbo
Zhai, Guangju
Zhao, Jing Hua
Smith, Albert Vernon
Huffman, Jennifer E.
Albrecht, Eva
Jackson, Catherine M.
Evans, David M.
Cadby, Gemma
Fornage, Myriam
Manichaikul, Ani
Lopez, Lorna M.
Johnson, Toby
Aldrich, Melinda C.
Aspelund, Thor
Barroso, Ines
Campbell, Harry
Cassano, Patricia A.
Couper, David J.
Eiriksdottir, Gudny
Franceschini, Nora
Garcia, Melissa
Gieger, Christian
Gislason, Gauti Kjartan
Grkovic, Ivica
Hammond, Christopher J.
Hancock, Dana B.
Harris, Tamara B.
Ramasamy, Adaikalavan
Heckbert, Susan R.
Heliovaara, Markku
Homuth, Georg
Hysi, Pirro G.
James, Alan L.
Jankovic, Stipan
Joubert, Bonnie R.
Karrasch, Stefan
Klopp, Norman
Koch, Beate
Kritchevsky, Stephen B.
Launer, Lenore J.
Liu, Yongmei
Loehr, Laura R.
Lohman, Kurt
Loos, Ruth J. F.
Lumley, Thomas
Al Balushi, Khalid A.
Ang, Wei Q.
Barr, R. Graham
Beilby, John
Blakey, John D.
Boban, Mladen
Boraska, Vesna
Brisman, Jonas
Britton, John R.
Brusselle, Guy G.
Cooper, Cyrus
Curjuric, Ivan
Dahgam, Santosh
Deary, Ian J.
Ebrahim, Shah
Eijgelsheim, Mark
Francks, Clyde
Gaysina, Darya
Granell, Raquel
Gu, Xiangjun
Hankinson, John L.
Hardy, Rebecca
Harris, Sarah E.
Henderson, John
Henry, Amanda
Hingorani, Aroon D.
Hofman, Albert
Holt, Patrick G.
Hui, Jennie
Hunter, Michael L.
Imboden, Medea
Jameson, Karen A.
Kerr, Shona M.
Kolcic, Ivana
Kronenberg, Florian
Liu, Jason Z.
Marchini, Jonathan
McKeever, Tricia
Morris, Andrew D.
Olin, Anna-Carin
Porteous, David J.
Postma, Dirkje S.
Rich, Stephen S.
Ring, Susan M.
Rivadeneira, Fernando
Rochat, Thierry
Sayer, Avan Aihie
Sayers, Ian
Sly, Peter D.
Smith, George Davey
Sood, Akshay
Starr, John M.
Uitterlinden, Andre G.
Vonk, Judith M.
Wannamethee, S. Goya
Whincup, Peter H.
Wijmenga, Cisca
Williams, O. Dale
Wong, Andrew
Mangino, Massimo
Marciante, Kristin D.
McArdle, Wendy L.
Meibohm, Bernd
Morrison, Alanna C.
North, Kari E.
Omenaas, Ernst
Palmer, Lyle J.
Pietilainen, Kirsi H.
Pin, Isabelle
Polasek, Ozren
Pouta, Anneli
Psaty, Bruce M.
Hartikainen, Anna-Liisa
Rantanen, Taina
Ripatti, Samuli
Rotter, Jerome I.
Rudan, Igor
Rudnicka, Alicja R.
Schulz, Holger
Shin, So-Youn
Spector, Tim D.
Surakka, Ida
Vitart, Veronique
Voelzke, Henry
Wareham, Nicholas J.
Warrington, Nicole M.
Wichmann, H-Erich
Wild, Sarah H.
Wilk, Jemma B.
Wjst, Matthias
Wright, Alan F.
Zgaga, Lina
Zemunik, Tatijana
Pennell, Craig E.
Nyberg, Fredrik
Kuh, Diana
Holloway, John W.
Boezen, H. Marike
Lawlor, Debbie A.
Morris, Richard W.
Probst-Hensch, Nicole
Kaprio, Jaakko
Wilson, James F.
Hayward, Caroline
Kahonen, Mika
Heinrich, Joachim
Musk, Arthur W.
Jarvis, Deborah L.
Glaeser, Sven
Jarvelin, Marjo-Riitta
Stricker, Bruno H. Ch
Elliott, Paul
O'Connor, George T.
Strachan, David P.
London, Stephanie J.
Hall, Ian P.
Gudnason, Vilmundur
Tobin, Martin D.
CA Int Lung Canc Consortium
GIANT Consortium
TI Genome-wide association and large-scale follow up identifies 16 new loci
influencing lung function
SO NATURE GENETICS
LA English
DT Article
ID OBSTRUCTIVE PULMONARY-DISEASE; GENETIC-VARIATION; BLOOD-PRESSURE;
VARIANTS; METAANALYSIS; RISK; PROTEIN; POLYMORPHISMS; POPULATION;
EXPRESSION
AB Pulmonary function measures reflect respiratory health and are used in the diagnosis of chronic obstructive pulmonary disease. We tested genome-wide association with forced expiratory volume in 1 second and the ratio of forced expiratory volume in 1 second to forced vital capacity in 48,201 individuals of European ancestry with follow up of the top associations in up to an additional 46,411 individuals. We identified new regions showing association (combined P < 5 x 10(-8)) with pulmonary function in or near MFAP2, TGFB2, HDAC4, RARB, MECOM (also known as EVI1), SPATA9, ARMC2, NCR3, ZKSCAN3, CDC123, C10orf11, LRP1, CCDC38, MMP15, CFDP1 and KCNE2. Identification of these 16 new loci may provide insight into the molecular mechanisms regulating pulmonary function and into molecular targets for future therapy to alleviate reduced lung function.
C1 [Soler Artigas, Maria; Wain, Louise V.; Tobin, Martin D.] Univ Leicester, Dept Hlth Sci, Leicester, Leics, England.
[Soler Artigas, Maria; Wain, Louise V.; Tobin, Martin D.] Univ Leicester, Dept Genet, Leicester LE1 7RH, Leics, England.
[Loth, Daan W.; Eijgelsheim, Mark; Hofman, Albert; Rivadeneira, Fernando; Uitterlinden, Andre G.; Stricker, Bruno H. Ch] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
[Loth, Daan W.; Stricker, Bruno H. Ch] Inspectorate Healthcare, The Hague, Netherlands.
[Gharib, Sina A.] Univ Washington, Ctr Lung Biol, Seattle, WA 98195 USA.
[Gharib, Sina A.; Marciante, Kristin D.; Psaty, Bruce M.] Univ Washington, Dept Med, Seattle, WA USA.
[Obeidat, Ma'en; Launer, Lenore J.; Al Balushi, Khalid A.; Blakey, John D.; Henry, Amanda; Sayers, Ian; Hall, Ian P.] Univ Nottingham Hosp, Nottingham Resp Biomed Res Unit, Div Therapeut & Mol Med, London, England.
[Tang, Wenbo; Cassano, Patricia A.] Cornell Univ, Div Nutr Sci, Ithaca, NY 14853 USA.
[Zhai, Guangju; Hammond, Christopher J.; Hysi, Pirro G.; Mangino, Massimo; Spector, Tim D.] Kings Coll London, Dept Twin Res & Genet Epidemiol, London WC2R 2LS, England.
[Zhai, Guangju] Mem Univ Newfoundland, Fac Med, Discipline Genet, St John, NF, Canada.
[Zhao, Jing Hua; Loos, Ruth J. F.; Wareham, Nicholas J.] Addenbrookes Hosp, Inst Metab Sci, Epidemiol Unit, MRC, Cambridge, England.
[Smith, Albert Vernon; Aspelund, Thor; Eiriksdottir, Gudny; Gislason, Gauti Kjartan; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
[Smith, Albert Vernon; Aspelund, Thor; Gudnason, Vilmundur] Univ Iceland, Reykjavik, Iceland.
[Huffman, Jennifer E.; Vitart, Veronique; Wright, Alan F.; Hayward, Caroline] Western Gen Hosp, Inst Genet & Mol Med, MRC, Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland.
[Albrecht, Eva; Gieger, Christian] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Genet Epidemiol, Neuherberg, Germany.
[Jackson, Catherine M.] Univ St Andrews, Sch Med, St Andrews, Fife, Scotland.
[Evans, David M.; Smith, George Davey; Lawlor, Debbie A.] Univ Bristol, Sch Social & Community Med, MRC, Ctr Causal Anal Translat Epidemiol, Bristol, Avon, England.
[Cadby, Gemma; Palmer, Lyle J.] Ontario Inst Canc Res, Toronto, ON, Canada.
[Cadby, Gemma; Palmer, Lyle J.; Warrington, Nicole M.] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Prosserman Ctr Hlth Res, Toronto, ON M5G 1X5, Canada.
[Fornage, Myriam; Gu, Xiangjun] Univ Texas Houston, Brown Fdn Inst Mol Med, Houston, TX USA.
[Fornage, Myriam; Morrison, Alanna C.] Univ Texas Houston, Sch Publ Hlth, Ctr Human Genet, Houston, TX USA.
[Manichaikul, Ani; Rich, Stephen S.] Univ Virginia, Ctr Publ Hlth Genom, Charlottesville, VA USA.
[Manichaikul, Ani] Univ Virginia, Div Biostat & Epidemiol, Dept Publ Hlth Sci, Charlottesville, VA USA.
[Lopez, Lorna M.; Deary, Ian J.; Harris, Sarah E.; Starr, John M.] Univ Edinburgh, Ctr Cognit Ageing & Cognit Epidemiol, Edinburgh, Midlothian, Scotland.
[Lopez, Lorna M.; Deary, Ian J.] Univ Edinburgh, Dept Psychol, Edinburgh, Midlothian, Scotland.
[Johnson, Toby] Queen Mary Univ London, Barts & London Sch Med & Dent, William Harvey Res Inst, Clin Pharmacol & Genome Ctr, London, England.
[Aldrich, Melinda C.] Vanderbilt Univ, Dept Thorac Surg, Nashville, TN USA.
[Aldrich, Melinda C.] Vanderbilt Univ, Div Epidemiol, Nashville, TN USA.
[Barroso, Ines; Shin, So-Youn] Wellcome Trust Sanger Inst, Cambridge, England.
[Barroso, Ines] Univ Cambridge, Addenbrookes Hosp, Inst Metab Sci, Metab Res Labs, Cambridge CB2 2QQ, England.
[Campbell, Harry; Rudan, Igor; Wild, Sarah H.; Zgaga, Lina; Wilson, James F.] Univ Edinburgh, Ctr Populat Hlth Sci, Edinburgh, Midlothian, Scotland.
[Couper, David J.] Univ N Carolina, Dept Biostat, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
[Franceschini, Nora; Loehr, Laura R.; North, Kari E.] Univ N Carolina, Dept Epidemiol, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
[Garcia, Melissa; Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
[Grkovic, Ivica; Jankovic, Stipan; Rudan, Igor] Univ Split, Sch Med, Croatian Ctr Global Hlth, Split, Croatia.
[Hancock, Dana B.; Joubert, Bonnie R.; London, Stephanie J.] NIEHS, Epidemiol Branch, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA.
[Hancock, Dana B.] Res Triangle Inst Int, Behav Hlth Epidemiol Program, Res Triangle Pk, NC USA.
[Ramasamy, Adaikalavan; Jarvelin, Marjo-Riitta; Elliott, Paul] Univ London Imperial Coll Sci Technol & Med, Dept Epidemiol & Biostat, London, England.
[Ramasamy, Adaikalavan] Kings Coll London, Guys Hosp, Dept Med & Mol Genet, London WC2R 2LS, England.
[Heckbert, Susan R.; Marciante, Kristin D.; Psaty, Bruce M.] Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Heckbert, Susan R.; Psaty, Bruce M.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Heckbert, Susan R.; Psaty, Bruce M.] Grp Hlth Cooperat Puget Sound, Grp Hlth Res Inst, Seattle, WA USA.
[Heliovaara, Markku; Kaprio, Jaakko] Natl Inst Hlth & Welf, Helsinki, Finland.
[Homuth, Georg] Ernst Moritz Arndt Univ Greifswald, Interfac Inst Genet & Funct Genom, Greifswald, Germany.
[James, Alan L.] Sir Charles Gairdner Hosp, Dept Pulm Physiol & Sleep Med, W Australian Sleep Disorders Res Inst, Nedlands, WA 6009, Australia.
[James, Alan L.; Musk, Arthur W.] Univ Western Australia, Sch Med & Pharmacol, Perth, WA 6009, Australia.
[James, Alan L.; Hui, Jennie; Hunter, Michael L.; Musk, Arthur W.] Sir Charles Gairdner Hosp, Dept Resp Med, Busselton Populat Med Res Fdn, Nedlands, WA 6009, Australia.
[Karrasch, Stefan] Univ Munich, Inst & Outpatient Clin Occupat Social & Environm, Munich, Germany.
[Klopp, Norman] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Unit Mol Epidemiol, Neuherberg, Germany.
[Koch, Beate] Univ Hosp Greifswald, Dept Internal Med B, Greifswald, Germany.
[Kritchevsky, Stephen B.] Wake Forest Sch Med, Sticht Ctr Aging, Winston Salem, NC USA.
[Lohman, Kurt] Wake Forest Univ, Bowman Gray Sch Med, Div Publ Hlth Sci, Dept Biostat Sci, Winston Salem, NC USA.
[Liu, Yongmei; Ang, Wei Q.; Warrington, Nicole M.; Pennell, Craig E.] Univ Western Australia, Sch Womens & Infants Hlth, Perth, WA 6009, Australia.
[Lumley, Thomas] Univ Auckland, Dept Stat, Auckland 1, New Zealand.
[Barr, R. Graham] Columbia Univ, Med Ctr, Dept Med, New York, NY USA.
[Beilby, John] Univ Western Australia, Dept Surg & Pathol, Nedlands, WA 6009, Australia.
[Beilby, John; Hui, Jennie] Queen Elizabeth II Med Ctr, PathW Lab Med Western Australia, Nedlands, WA, Australia.
[Boban, Mladen; Boraska, Vesna; Kolcic, Ivana; Polasek, Ozren; Zemunik, Tatijana] Univ Split, Fac Med, Split, Croatia.
[Brisman, Jonas; Dahgam, Santosh; Olin, Anna-Carin; Nyberg, Fredrik] Univ Gothenburg, Sahlgrenska Acad, Inst Med, Dept Publ Hlth & Community Med, Gothenburg, Sweden.
[Britton, John R.; McKeever, Tricia] Univ Nottingham, Sch Community Hlth Sci, Div Epidemiol & Publ Hlth, Nottingham NG7 2RD, England.
[Britton, John R.; McKeever, Tricia] Univ Nottingham, Nottingham Resp Biomed Res Unit, Nottingham NG7 2RD, England.
[Cooper, Cyrus; Jameson, Karen A.; Sayer, Avan Aihie] Univ Southampton, MRC Lifecourse Epidemiol Unit, Southampton, Hants, England.
[Curjuric, Ivan; Imboden, Medea; Probst-Hensch, Nicole] Swiss Trop & Publ Hlth TPH Inst, Basel, Switzerland.
[Brusselle, Guy G.] Ghent Univ Hosp, Dept Resp Med, B-9000 Ghent, Belgium.
[Curjuric, Ivan; Imboden, Medea; Probst-Hensch, Nicole] Univ Basel, CH-4003 Basel, Switzerland.
[Ebrahim, Shah] London Sch Hyg & Trop Med, Dept Epidemiol & Populat Hlth, Noncommun Dis Epidemiol Unit, London WC1, England.
[Ebrahim, Shah] S Asia Ctr Chron Dis, New Delhi, India.
[Francks, Clyde] Max Planck Inst Psycholinguist, Nijmegen, Netherlands.
[Gaysina, Darya; Hardy, Rebecca; Wong, Andrew; Kuh, Diana] MRC Unit Lifelong Hlth & Ageing, London, England.
[Granell, Raquel; Henderson, John; Ring, Susan M.; McArdle, Wendy L.] Univ Bristol, Sch Social & Community Med, Bristol, Avon, England.
[Hankinson, John L.] Hankinson Consulting Inc, Athens, GA USA.
[Harris, Sarah E.] Univ Edinburgh, Med Genet Sect, Edinburgh, Midlothian, Scotland.
[Hingorani, Aroon D.] UCL, Dept Epidemiol & Publ Hlth, London, England.
[Holt, Patrick G.; Sly, Peter D.] Univ Western Australia, Telethon Inst Child Hlth Res, Perth, WA 6009, Australia.
[Holt, Patrick G.; Sly, Peter D.] Univ Western Australia, Ctr Child Hlth Res, Perth, WA 6009, Australia.
[Hui, Jennie] Univ Western Australia, Sch Pathol & Lab Med, Nedlands, WA 6009, Australia.
[Hui, Jennie; Hunter, Michael L.; Musk, Arthur W.] Univ Western Australia, Sch Populat Hlth, Nedlands, WA 6009, Australia.
[Kerr, Shona M.; Porteous, David J.] Univ Edinburgh, Inst Genet & Mol Med, Mol Med Ctr, Edinburgh, Midlothian, Scotland.
[Kronenberg, Florian] Innsbruck Med Univ, Dept Med Genet Mol & Clin Pharmacol, Div Genet Epidemiol, Innsbruck, Austria.
[Liu, Jason Z.; Marchini, Jonathan] Univ Oxford, Dept Stat, Oxford OX1 3TG, England.
[Morris, Andrew D.] Univ Dundee, Inst Med Res, Dundee, Scotland.
[Postma, Dirkje S.] Univ Groningen, Univ Med Ctr Groningen, Dept Pulmonol, Groningen, Netherlands.
[Rivadeneira, Fernando; Uitterlinden, Andre G.; Stricker, Bruno H. Ch] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
[Rochat, Thierry] Univ Hosp Geneva, Div Pulm Med, Geneva, Switzerland.
[Sood, Akshay] Univ New Mexico, Dept Med, Albuquerque, NM 87131 USA.
[Starr, John M.] Univ Edinburgh, Geriatr Med Unit, Edinburgh, Midlothian, Scotland.
[Vonk, Judith M.; Boezen, H. Marike] Univ Groningen, Univ Med Ctr Groningen, Dept Epidemiol, Groningen, Netherlands.
[Wannamethee, S. Goya; Morris, Richard W.] UCL, Dept Primary Care & Populat Hlth, London, England.
[Whincup, Peter H.; Rudnicka, Alicja R.; Strachan, David P.] St Georges Univ London, Div Populat Hlth Sci & Educ, London, England.
[Wijmenga, Cisca] Univ Groningen, Univ Med Ctr Groningen, Dept Genet, Groningen, Netherlands.
[Williams, O. Dale] Univ Alabama Birmingham, Div Prevent Med, Birmingham, AL USA.
[Meibohm, Bernd] Univ Tennessee, Ctr Hlth Sci, Coll Pharm, Memphis, TN 38163 USA.
[Omenaas, Ernst] Haukeland Hosp, Clin Res Ctr, N-5021 Bergen, Norway.
[Pietilainen, Kirsi H.] Univ Helsinki, Cent Hosp, Obes Res Unit, Dept Med,Div Internal Med, Helsinki, Finland.
[Pietilainen, Kirsi H.; Kaprio, Jaakko] Univ Helsinki, Dept Publ Hlth, Hjelt Inst, Helsinki, Finland.
[Pietilainen, Kirsi H.; Ripatti, Samuli; Surakka, Ida; Kaprio, Jaakko] Univ Helsinki, Inst Mol Med, Helsinki, Finland.
[Pin, Isabelle] CHU Grenoble, F-38043 Grenoble, France.
[Pin, Isabelle] Ctr Rech Albert Bonniot, INSERM, U823, Grenoble, France.
[Pin, Isabelle] Univ Grenoble 1, Grenoble, France.
[Polasek, Ozren; Rudan, Igor] Gen Info Ltd, Zagreb, Croatia.
[Pouta, Anneli; Jarvelin, Marjo-Riitta] Natl Inst Hlth & Welf, Dept Children Young People & Families, Oulu, Finland.
[Hartikainen, Anna-Liisa] Univ Oulu, Inst Clin Med, Oulu, Finland.
[Rantanen, Taina] Univ Jyvaskyla, Dept Hlth Sci, Ctr Gerontol Res, Jyvaskyla, Finland.
[Ripatti, Samuli; Surakka, Ida] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Publ Hlth Genom Unit, Helsinki, Finland.
[Rotter, Jerome I.] Cedars Sinai Med Ctr, Inst Med Genet, Los Angeles, CA 90048 USA.
[Schulz, Holger; Wichmann, H-Erich; Heinrich, Joachim] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 1, Neuherberg, Germany.
[Voelzke, Henry] Ernst Moritz Arndt Univ Greifswald, Inst Community Med, Study Hlth Pomerania SHIP Clin Epidemiol Res, Greifswald, Germany.
[Wichmann, H-Erich] Univ Munich, Chair Epidemiol, Inst Med Informat Biometry & Epidemiol, Munich, Germany.
[Wichmann, H-Erich] Univ Munich, Klinikum Grosshadern, D-8000 Munich, Germany.
[Wilk, Jemma B.] Brigham & Womens Hosp, Dept Med, Div Aging, Boston, MA 02115 USA.
[Wilk, Jemma B.] Harvard Univ, Sch Med, Boston, MA USA.
[Wjst, Matthias] Helmholtz Zentrum Munchen, Comprehens Pneumol Ctr, Inst Lung Biol & Dis, Neuherberg, Germany.
[Wjst, Matthias] Tech Univ Munich, IMSE, Munich, Germany.
[Zgaga, Lina] Univ Zagreb, Fac Med, Andrija Stampar Sch Publ Hlth, Zagreb 41000, Croatia.
[Nyberg, Fredrik] AstraZeneca Res & Dev, Molndal, Sweden.
[Holloway, John W.] Univ Southampton, Fac Med, Southampton SO9 5NH, Hants, England.
[Kahonen, Mika] Univ Tampere, Dept Clin Physiol, FIN-33101 Tampere, Finland.
[Kahonen, Mika] Tampere Univ Hosp, Tampere, Finland.
[Musk, Arthur W.] Sir Charles Gairdner Hosp, Dept Resp Med, Nedlands, WA 6009, Australia.
[Jarvis, Deborah L.; Jarvelin, Marjo-Riitta; Elliott, Paul] Univ London Imperial Coll Sci Technol & Med, MRC Hlth Protect Agcy HPA Ctr Environm & Hlth, London, England.
[Glaeser, Sven] Univ Hosp Greifswald, Dept Internal Med B, Greifswald, Germany.
[Jarvelin, Marjo-Riitta] Univ Oulu, Inst Hlth Sci, Oulu, Finland.
[Jarvelin, Marjo-Riitta] Univ Oulu, Bioctr Oulu, Oulu, Finland.
[Stricker, Bruno H. Ch] Erasmus MC, Dept Med Informat, Rotterdam, Netherlands.
[O'Connor, George T.] Boston Univ, Sch Med, Ctr Pulm, Boston, MA 02118 USA.
[O'Connor, George T.] NHLBI, Framingham Heart Study, Framingham, MA USA.
RP Tobin, MD (reprint author), Univ Leicester, Dept Hlth Sci, Leicester, Leics, England.
EM london2@niehs.nih.gov; mt47@leicester.ac.uk
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Taina/O-6579-2016; Wong, Andrew/M-8899-2016; Davey Smith,
George/A-7407-2013; Boraska Perica, Vesna/D-8230-2017; Grkovic,
Ivica/D-8728-2017; Boban, Mladen/E-2777-2017; Kolcic, Ivana/E-2713-2017;
Aihie Sayer, Avan/A-4359-2012; Gaysina, Darya/J-5720-2013; Soler
Artigas, Maria/L-6529-2013; PIN, Isabelle/N-3020-2013; Kronenberg,
Florian/B-1736-2008; Wijmenga, Cisca/D-2173-2009; Palmer,
Lyle/K-3196-2014; Warrington, Nicole/P-4868-2014; Schulz,
Holger/J-5643-2015; Gudnason, Vilmundur/K-6885-2015; Ripatti,
Samuli/H-9446-2014; Wilson, James F/A-5704-2009; Sly, Peter/F-1486-2010;
jackson, cathy/H-4869-2013; Holloway, John/B-5424-2009; Evans,
David/H-6325-2013; Hancock, Dana/D-8577-2012; Rudan, Igor/I-1467-2012;
Lopez, Lorna/F-7265-2010; Aspelund, Thor/C-5983-2008; Francks,
Clyde/E-1384-2012; Hunter, Michael/B-3213-2013; Porteous,
David/C-7289-2013; Aldrich, Melinda/C-7783-2013; Deary, Ian/C-6297-2009;
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Gieger, Christian/0000-0001-6986-9554
FU Academy of Finland [104781, 120315, 129269, 1114194]; Center of
Excellence in Complex Disease Genetics [213506, 129680]; SALVE; Althingi
(Icelandic Parliament); Arthritis Research Campaign; Asthma UK;
AstraZeneca; AXA; Biotechnology and Biological Sciences Research Council
(BBSRC) [BB/F019394/1, G20234]; British Heart Foundation [PG/97012,
PG/06/154/22043, FS05/125]; British Lung Foundation; Research United
Kingdom; Chief Scientist Office, Scottish Government Health Directorate
[CZD/16/6]; Croatian Institute for Public Health; UK Department of
Health; Dutch Kidney Foundation; Erasmus Medical Center and Erasmus
University, Rotterdam; Estonian Genome Center, University of Tartu,
Estonia [SF0180142s08]; EU [018996, QLK4-CT-1999-01237]; European
Commission [QLG1-CT-2000-01643, LSHB-CT-2006-018996, LSHG-CT2006- 01894,
QLG2-CT-2002-01254, HEALTH-F2-2008-201865, HEALTH-F2-2008-35627,
HEALTH-F4-2007-201413]; Finnish Foundation for Cardiovascular Research;
Flight Attendant Medical Research Institute (FAMRI); German Asthma and
COPD Network (COSYCONET: BMBF) [01GI0883]; German Bundesministerium fuer
Forschung und Technology [01 AK 803 A-H, 01 IG 07015 G]; German Federal
Ministry of Education and Research (BMBF); German National Genome
Research Network; German Ministry of Cultural Affairs; GlaxoSmithKline;
Gyllenberg Foundations; Healthway, Western Australia; Helmholtz Zentrum
Munchen, German Research Center for Environmental Health, Neuherberg,
Germany; East Midlands Development Agency; European Regional Development
Fund; Higher Education Funding Council for England (HEFCE); Hjartavernd
(Icelandic Heart Association); Innsbruck Medical University; Institute
for Anthropological Research in Zagreb; International Osteoporosis
Foundation; NIH, National Institute on Aging and National Institute of
Environmental Health Sciences; Jalmari and Rauha Ahokas Foundation;
Juvenile Diabetes Research Foundation International (JDRF); Lifelong
Health and Wellbeing Initiative [G0700704/84698]; Medical Research
Council UK [G1000861, G0501942, G0902313, G0000934, G0800582, G0500539,
G0600705, G9901462]; Tampere University Hospital; Ministry of Science,
Education and Sport of the Republic of Croatia [108-1080315-0302];
Medical Research Council Human Genetics Unit; Medisearch-The Leicester
Medical Research Foundation; Munich Center of Health Sciences (MC
Health) as part of LMUinnovativ; National Health and Medical Research
Council of Australia [ID 403981, ID 003209]; National Human Genome
Research Institute (NHGRI) [U01-HG-004729, U01-HG-004402]; National
Institute for Health Research (NIHR) Comprehensive Biomedical Research
Centres (Guy's & St. Thomas' NHS Foundation Trust; King's College London
and Cambridge University Hospitals NHS Foundation Trust; University of
Cambridge; Netherlands Genomics Initiative (NGI)/Netherlands
Organisation for Scientific Research (NWO) [050-060-810]; Netherlands
Organization for the Health Research and Development (ZonMw);
Netherlands Organization of Scientific Research NOW [1750102007006,
175.010.2005.011, 911-03-012]; Northern Netherlands Collaboration of
Provinces (SNN); Norwegian University of Science and Technology; Novo
Nordisk; Ontario Institute of Cancer Research and Canadian Cancer
Society Research Institute [CCSRI 020214]; Republic of Croatia Ministry
of Science, Education and Sports [108-1080315-0302]; Research Institute
for Diseases in the Elderly (RIDE) [014-93-015]; Research Into Ageing
[251]; Siemens Healthcare, Erlangen, Germany; Federal State of
Mecklenburg-West Pomerania; Social Ministry of the Federal State of
Mecklenburg-West Pomerania; Structure Enhancing Fund (FES) of the Dutch
government; Swedish Heart and Lung Foundation [20050561]; Swedish
Research Council for Worklife and Social research (FAS) [2001-0263,
2003-0139]; Swiss National Science Foundation [4026-28099,
3347CO-108796, 3247BO-104283, 3247BO-104288, 3247BO-104284, 32-65896.01,
32-59302.99, 32-52720.97, 32-4253.94]; Asthma, Allergy and Inflammation
Research Trust; Great Wine Estates of the Margaret River region of
Western Australia; Netherlands' Ministry of Economic Affairs, Ministry
of Education, Culture and Science and Ministry for Health, Welfare and
Sports; Royal Society; University of Split and Zagreb Medical Schools;
Tromso University [U01 DK062418]; UBS Wealth Foundation [BA29s8Q7-DZZ];
University Hospital Oulu, Biocenter, University of Oulu, Finland
[75617]; University Medical Center Groningen; University of Bristol;
University of Leicester; University of Nottingham; US National
Institutes of Health (NIH) [1P50 CA70907, RO1 CA121197, U19 CA148127,
CA55769, CA127219, R01HL071051, R01HL071205, R01HL071250, R01HL071251,
R01HL071252, R01HL071258, R01HL071259, UL1RR025005, HHSN268200625226C,
HHSN268200782096C, R01-HL084099]; US NIH National Cancer Institute
[RO1CA111703]; US NIH National Center for Research Resources
[M01-RR00425, 5M01 RR00997]; US NIH National Eye Institute (NEI); US NIH
National Heart, Lung and Blood Institute [N01-HC-85079, N01-HC-85086,
N01-HC-35129, N01 HC-15103, N01 HC-55222]; US NIH National Institute of
Allergy and Infectious Diseases (NIAID); US NIH National Institute of
Child Health and Human Development (NICHD); US NIH National Institute of
Diabetes and Digestive and Kidney Diseases (NIDDK) [DK063491]; US NIH
National Institute of Environmental Health Sciences (NIEHS) [ZO1
ES49019, ES015794]; US NIH National Institute of Mental Health (NIMH)
[5R01MH63706: 02]; US NIH National Institute of Neurological Disorders
and Stroke (NINDD); US NIH National Institute on Aging (NIA) [R01
AG032098, RC1 AG035835, N01AG12100, N01AG62101, N01AG62103, N01AG62106,
1R01AG032098-01A1, AG-023269, AG-15928, AG-20098, AG-027058]; Wellcome
Trust [077016/Z/05/Z, GR069224, 068545/Z/02, 076113/B/04/Z, 079895]
FX We thank the many colleagues who contributed to collection and
phenotypic characterization of the clinical sampling, genotyping and
analysis of the data. We especially thank those who kindly agreed to
participate in the studies. Major funding for this work is from the
following sources (alphabetical): Academy of Finland (project grants
104781, 120315, 129269, 1114194, Center of Excellence in Complex Disease
Genetics (213506 and 129680) and SALVE); Althingi (Icelandic
Parliament); Arthritis Research Campaign; Asthma UK; AstraZeneca; AXA
Research Fund; Biotechnology and Biological Sciences Research Council
(BBSRC) (BB/F019394/1, G20234); British Heart Foundation (PG/97012,
PG/06/154/22043, FS05/125); British Lung Foundation; Canadian Institutes
of Health Research (Grant ID MOP-82893); Cancer Research United Kingdom;
Chief Scientist Office, Scottish Government Health Directorate
(CZD/16/6); Croatian Institute for Public Health; UK Department of
Health; Dutch Kidney Foundation; Erasmus Medical Center and Erasmus
University, Rotterdam; Estonian Genome Center, University of Tartu,
Estonia (SF0180142s08); EU funding (GABRIEL GRANT Number: 018996, ECRHS
II Coordination Number: QLK4-CT-1999-01237); European Commission (DG
XII, EURO-BLCS, FP-5 QLG1-CT-2000-01643, FP-6 LSHB-CT-2006-018996
(GABRIEL), FP-6 LSHG-CT2006- 018947 (EUROSPAN), FP-6 GenomEUtwin project
QLG2-CT-2002-01254, FP7/2007-2013: HEALTH-F2-2008-201865, GEFOS,
HEALTH-F2-2008-35627, TREAT-OA, HEALTH-F4-2007-201413 (ENGAGE)); Finnish
Foundation for Cardiovascular Research; Flight Attendant Medical
Research Institute (FAMRI); German Asthma and COPD Network (COSYCONET:
BMBF grant 01GI0883); German Bundesministerium fuer Forschung und
Technology (01 AK 803 A-H, 01 IG 07015 G); German Federal Ministry of
Education and Research (BMBF) (03ZIK012, 01ZZ9603, 01ZZ0103 and
01ZZ0403): German National Genome Research Network (NGFN-2 and
NGFN-plus); German Ministry of Cultural Affairs; GlaxoSmithKline;
Gyllenberg Foundations; Healthway, Western Australia; Helmholtz Zentrum
Munchen, German Research Center for Environmental Health, Neuherberg,
Germany; Healthcare and Bioscience iNet (funded by the East Midlands
Development Agency, partially financed by the European Regional
Development Fund, delivered by Medilink East Midlands); Higher Education
Funding Council for England (HEFCE); Hjartavernd (Icelandic Heart
Association); Innsbruck Medical University; Institute for
Anthropological Research in Zagreb; International Osteoporosis
Foundation; Intramural Research Program of the NIH, National Institute
on Aging and National Institute of Environmental Health Sciences;
Jalmari and Rauha Ahokas Foundation; Juvenile Diabetes Research
Foundation International (JDRF); Lifelong Health and Wellbeing
Initiative (G0700704/84698); Medical Research Council UK (G1000861,
G0501942, G0902313, G0000934, G0800582, G0500539, G0600705,
PrevMetSyn/SALVE, G9901462); Medical Research Fund of the Tampere
University Hospital; Ministry of Science, Education and Sport of the
Republic of Croatia (108-1080315-0302); Medical Research Council Human
Genetics Unit; Medisearch-The Leicester Medical Research Foundation;
Munich Center of Health Sciences (MC Health) as part of LMUinnovativ;
National Health and Medical Research Council of Australia (Grant ID
403981 and ID 003209); National Human Genome Research Institute (NHGRI)
(U01-HG-004729, U01-HG-004402); National Institute for Health Research
(NIHR) Comprehensive Biomedical Research Centres (Guy's & St.; Thomas'
NHS Foundation Trust in partnership with King's College London and
Cambrdge University Hospitals NHS Foundation Trust in partnership with
the University of Cambridge); Netherlands Genomics Initiative
(NGI)/Netherlands Organisation for Scientific Research (NWO)
(050-060-810); Netherlands Organization for the Health Research and
Development (ZonMw); Netherlands Organization of Scientific Research NOW
(1750102007006, 175.010.2005.011, 911-03-012); Northern Netherlands
Collaboration of Provinces (SNN); Norwegian University of Science and
Technology; Novo Nordisk; Ontario Institute of Cancer Research and
Canadian Cancer Society Research Institute (CCSRI 020214); Republic of
Croatia Ministry of Science, Education and Sports research grants
(108-1080315-0302); Research Institute for Diseases in the Elderly
(RIDE) (014-93-015: RIDE2); Research Into Ageing (251); Siemens
Healthcare, Erlangen, Germany and the Federal State of Mecklenburg-West
Pomerania; Social Ministry of the Federal State of Mecklenburg-West
Pomerania; Structure Enhancing Fund (FES) of the Dutch government;
Swedish Heart and Lung Foundation grant 20050561; Swedish Research
Council for Worklife and Social research (FAS), grants 2001-0263,
2003-0139; Swiss National Science Foundation (grants no.
4026-28099,3347CO-108796, 3247BO-104283, 3247BO-104288, 3247BO-104284,
32-65896.01,32-59302.99, 32-52720.97, 32-4253.; 94); The Asthma, Allergy
and Inflammation Research Trust; The Great Wine Estates of the Margaret
River region of Western Australia; The Netherlands' Ministry of Economic
Affairs, Ministry of Education, Culture and Science and Ministry for
Health, Welfare and Sports; The Royal Society; The University of Split
and Zagreb Medical Schools; Tromso University; U01 DK062418; UBS Wealth
Foundation Grant BA29s8Q7-DZZ; UK Department of Health Policy Research
Programme; University Hospital Oulu, Biocenter, University of Oulu,
Finland (75617); University Medical Center Groningen; University of
Bristol; University of Leicester HEFCE CIF award; University of
Nottingham; US National Institutes of Health (NIH) (1P50 CA70907, RO1
CA121197, U19 CA148127, CA55769, CA127219, R01HL071051, R01HL071205,
R01HL071250, R01HL071251, R01HL071252, R01HL071258, R01HL071259,
UL1RR025005, contracts HHSN268200625226C, HHSN268200782096C,
R01-HL084099); US NIH National Cancer Institute (RO1CA111703); US NIH
National Center for Research Resources (grants M01-RR00425 and 5M01
RR00997); US NIH National Eye Institute (NEI); US NIH National Heart,
Lung and Blood Institute (contracts N01-HC-85079 through N01-HC-85086,
N01-HC-35129, N01 HC-15103, N01 HC-55222, N01-HC-75150, N01-HC-45133,
N01-HC-95095, N01-HC-48047, N01-HC-48048, N01-HC-48049, N01-HC-48050,
N01-HC-45134, N01-HC-05187, N01-HC-45205, N01-HC-45204, N01 HC-25195,
N01-HC-95159 through N01-HC-95169, RR-024156, N02-HL-6-4278, R01
HL-071022, R01 HL-077612, R01 HL-074104, RC1 HL100543,
HHSN268201100005C, HHSN268201100006C, HHSN268201100007C,
HHSN268201100008C, HHSN268201100009C, HHSN268201100010C,
HHSN268201100011C and HHSN268201100012C, grants HL080295, HL087652,
HL105756, R01-HL-084099, R01HL087641, R01HL59367, R01HL086694, HL088133,
HL075336 5R01HL087679-02 through the STAMPEED program (1RL1MH083268-01),
1K23HL094531-01); US NIH National Institute of Allergy and Infectious
Diseases (NIAID); US NIH National Institute of Child Health and Human
Development (NICHD); US NIH National Institute of Diabetes and Digestive
and Kidney Diseases (NIDDK) (DK063491); US NIH National Institute of
Environmental Health Sciences (NIEHS) (ZO1 ES49019, ES015794); US IH
National Institute of Mental Health (NIMH) (5R01MH63706: 02); US NIH
National Institute of Neurological Disorders and Stroke (NINDD); US NIH
National Institute on Aging (NIA) (R01 AG032098, RC1 AG035835,
N01AG12100, N01AG62101, N01AG62103, N01AG62106, 1R01AG032098-01A1,
AG-023269, AG-15928, AG-20098, AG-027058); Wellcome Trust
(077016/Z/05/Z, GR069224, 068545/Z/02, 076113/B/04/Z, 079895).
NR 55
TC 35
Z9 35
U1 3
U2 47
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD NOV
PY 2011
VL 43
IS 11
BP 1082
EP 1090
DI 10.1038/ng.941
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 842GS
UT WOS:000296584000011
PM 21946350
ER
PT J
AU Tarabeux, J
Kebir, O
Gauthier, J
Hamdan, FF
Xiong, L
Piton, A
Spiegelman, D
Henrion, E
Millet, B
Fathalli, F
Joober, R
Rapoport, JL
DeLisi, LE
Fombonne, E
Mottron, L
Forget-Dubois, N
Boivin, M
Michaud, JL
Drapeau, P
Lafreniere, RG
Rouleau, GA
Krebs, MO
AF Tarabeux, J.
Kebir, O.
Gauthier, J.
Hamdan, F. F.
Xiong, L.
Piton, A.
Spiegelman, D.
Henrion, E.
Millet, B.
Fathalli, F.
Joober, R.
Rapoport, J. L.
DeLisi, L. E.
Fombonne, E.
Mottron, L.
Forget-Dubois, N.
Boivin, M.
Michaud, J. L.
Drapeau, P.
Lafreniere, R. G.
Rouleau, G. A.
Krebs, M-O
CA S2D Team
TI Rare mutations in N-methyl-D-aspartate glutamate receptors in autism
spectrum disorders and schizophrenia
SO TRANSLATIONAL PSYCHIATRY
LA English
DT Article
DE autism; mutation; NMDA; schizophrenia
ID MHC CLASS-I; NMDA-RECEPTOR; MENTAL-RETARDATION; NOVO MUTATIONS; COMMON
VARIANTS; GENE; ASSOCIATION; EXPRESSION; SUBUNITS; ENCEPHALITIS
AB Pharmacological, genetic and expression studies implicate N-methyl-D-aspartate (NMDA) receptor hypofunction in schizophrenia (SCZ). Similarly, several lines of evidence suggest that autism spectrum disorders (ASD) could be due to an imbalance between excitatory and inhibitory neurotransmission. As part of a project aimed at exploring rare and/or de novo mutations in neurodevelopmental disorders, we have sequenced the seven genes encoding for NMDA receptor subunits (NMDARs) in a large cohort of individuals affected with SCZ or ASD (n = 429 and 428, respectively), parents of these subjects and controls (n 568). Here, we identified two de novo mutations in patients with sporadic SCZ in GRIN2A and one de novo mutation in GRIN2B in a patient with ASD. Truncating mutations in GRIN2C, GRIN3A and GRIN3B were identified in both subjects and controls, but no truncating mutations were found in the GRIN1, GRIN2A, GRIN2B and GRIN2D genes, both in patients and controls, suggesting that these subunits are critical for neurodevelopment. The present results support the hypothesis that rare de novo mutations in GRIN2A or GRIN2B can be associated with cases of sporadic SCZ or ASD, just as it has recently been described for the related neurodevelopmental disease intellectual disability. The influence of genetic variants appears different, depending on NMDAR subunits. Functional compensation could occur to counteract the loss of one allele in GRIN2C and GRIN3 family genes, whereas GRIN1, GRIN2A, GRIN2B and GRIN2D appear instrumental to normal brain development and function. Translational Psychiatry (2011) 1, e55; doi: 10.1038/tp.2011.52; published online 15 November 2011
C1 [Tarabeux, J.; Gauthier, J.; Xiong, L.; Piton, A.; Spiegelman, D.; Henrion, E.; Lafreniere, R. G.; Rouleau, G. A.] Univ Montreal, Dept Med, Montreal, PQ H3C 3J7, Canada.
[Tarabeux, J.; Gauthier, J.; Xiong, L.; Piton, A.; Spiegelman, D.; Henrion, E.; Lafreniere, R. G.; Rouleau, G. A.] Univ Montreal, CRCHUM, CENUM, Montreal, PQ, Canada.
[Tarabeux, J.; Kebir, O.; Millet, B.; Krebs, M-O] Sainte Anne Hosp, INSERM, Lab Pathophysiol Psychiat Dis, Ctr Psychiat & Neurosci,U894, Paris, France.
[Tarabeux, J.; Kebir, O.; Krebs, M-O] Univ Paris 05, Fac Med Paris Descartes, Ctr Evaluat & Rech Clin, Sainte Anne Hosp, Paris, France.
[Hamdan, F. F.; Michaud, J. L.] CHU Sainte Justine, Ctr Rech, CENUM, Montreal, PQ, Canada.
[Drapeau, P.] Univ Montreal, Grp Rech Syst Nerveux Cent, Montreal, PQ, Canada.
[Drapeau, P.; S2D Team] Univ Montreal, Dept Pathol & Cell Biol, Montreal, PQ, Canada.
[Fathalli, F.; Joober, R.] McGill Univ, Dept Psychiat, Douglas Mental Hlth Univ Inst, Montreal, PQ, Canada.
[Rapoport, J. L.] NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA.
[DeLisi, L. E.] Harvard Univ, Sch Med, Boston VA Healthcare Syst, Brockton, MA USA.
[Fombonne, E.] McGill Univ, Montreal Childrens Hosp, Dept Psychiat, Montreal, PQ H3H 1P3, Canada.
[Mottron, L.] Hop Riviere des Prairies, CETEDUM, Montreal, PQ, Canada.
[Forget-Dubois, N.; Boivin, M.] Univ Laval, Res Unit Childrens Psychosocial Maladjustment, Quebec City, PQ, Canada.
[Boivin, M.] Canada Res Chair Child Social Dev, Quebec City, PQ, Canada.
RP Rouleau, GA (reprint author), CHUM Res Ctr, 2099 Alexandre De Seve St,Rm Y-3633, Montreal, PQ H2L 2W5, Canada.
EM guy.rouleau@umontreal.ca; marie-odile.krebs@inserm.fr
RI Boivin, Michel/J-3652-2013; Forget-Dubois, Nadine/A-4811-2013; piton,
amelie/F-1201-2013;
OI Forget-Dubois, Nadine/0000-0002-4285-3293; piton,
amelie/0000-0003-0408-7468; Fombonne, Eric/0000-0002-8605-3538
FU Genome Canada and Genome Quebec; Universitede Montreal for the 'Synapse
to Disease' (S2D) project; Canadian Foundation for Innovation;
UniversiteParis Descartes; Fondation Pierre Deniker
FX We would like to thank all the families involved in this study. This
work was supported by Genome Canada and Genome Quebec, and received
co-funding from Universitede Montreal for the 'Synapse to Disease' (S2D)
project, as well as funding from the Canadian Foundation for Innovation.
JT receives a scholarship from the UniversiteParis Descartes (joint
program UniversiteParis Descartes - Universitede Montreal). GAR holds
the Canada Research Chair in Genetics of the Nervous System and a
Jeanne-et-J.-Louis-Levesque Chair for the Genetics of Brain Diseases. PD
holds the Canada Research Chair in Neuroscience. JLM is a recipient of
the Clinical Investigator Award of CIHR (Canadian Institutes of Health
Research). The S2D team is composed of the following additional members:
Isabelle Bachand, Marjolaine Chicoine, Melanie Cote, Kathleen Daignault,
Anne Desjarlais, Ousmane Diallo, Sylvia Dobrzeniecka, Joannie Duguay,
Marina Drits, Philippe Jolivet, Liliane Karamera, Frederic Kuku, Karine
Lachapelle, Guy Laliberte, Sandra Laurent, Annie Levert, Meijiang Liao,
Claude Marineau, Carlos Marino, Anne Noreau, Huashan Peng, Annie
Raymond, Annie Reynolds, Daniel Rochefort, Judith St-Onge, Pascale
Thibodeau, Kazuya Tsurudome, Yan Yang, Sophie Leroy, Narjes Bendjemaa,
Katia Ossian, Melanie Chayet and Fayc, al Mouaffak. We would also like
to thank Dr Chawki Benkelfat for several helpful discussions. A portion
of the schizophrenia cohort was collected through the Collaborative
Network for Family Study in Psychiatry ('Reseau d'etude familiale en
Psychiatry', REFAPSY), supported by the Fondation Pierre Deniker. We
also acknowledge the efforts of the members of the Genome Quebec
Innovation Centre Sequencing (Pierre Lepage, Sebastien Brunet and Hao
Fan Yam) and Bioinformatic (Louis Letourneau and Louis Dumond Joseph)
groups.
NR 61
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U1 4
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PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 2158-3188
J9 TRANSL PSYCHIAT
JI Transl. Psychiatr.
PD NOV
PY 2011
VL 1
AR e55
DI 10.1038/tp.2011.52
PG 7
WC Psychiatry
SC Psychiatry
GA 971PR
UT WOS:000306216800004
PM 22833210
ER
PT J
AU Ferrucci, L
AF Ferrucci, L.
TI SECULAR TRENDS IN BODY WEIGHT AND COMPOSITION: RESULTS FROM THE
BALTIMORE LONGITUDINAL STUDY OF AGING
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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 15
EP 15
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000068
ER
PT J
AU Sanders, J
Fitzpatrick, A
Boudreau, R
Arnold, A
Aviv, A
Fried, LF
Harris, TB
Newman, AB
AF Sanders, J.
Fitzpatrick, A.
Boudreau, R.
Arnold, A.
Aviv, A.
Fried, L. F.
Harris, T. B.
Newman, A. B.
TI LEUKOCYTE TELOMERE LENGTH IS ASSOCIATED WITH AGE-RELATED CHRONIC DISEASE
BURDEN IN OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Sanders, J.; Boudreau, R.; Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Fitzpatrick, A.; Arnold, A.] Univ Washington, Seattle, WA 98195 USA.
[Aviv, A.] Univ Med & Dent New Jersey, Newark, NJ 07103 USA.
[Fried, L. F.] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Harris, 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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 22
EP 23
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000105
ER
PT J
AU Patel, K
Koster, A
Caserotti, P
Van Domelen, DR
Harris, TB
AF Patel, K.
Koster, A.
Caserotti, P.
Van Domelen, D. R.
Harris, T. B.
TI ASSOCIATION OF FREE-LIVING PHYSICAL ACTIVITY AND SEDENTARY BEHAVIOR WITH
THE RED CELL DISTRIBUTION WIDTH
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Patel, K.; Koster, A.; Caserotti, P.; Van Domelen, D. R.; Harris, T. B.] 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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 23
EP 24
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000109
ER
PT J
AU Glynn, NW
Santanasto, AJ
Goodpaster, B
Mackey, DC
Newman, AB
Simonsick, EM
AF Glynn, N. W.
Santanasto, A. J.
Goodpaster, B.
Mackey, D. C.
Newman, A. B.
Simonsick, E. M.
TI ASSESSMENT AND ASSOCIATION OF FATIGUE AND FATIGABILITY WITH FUNCTION,
FITNESS AND ENERGY EXPENDITURE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Glynn, N. W.; Santanasto, A. J.; Goodpaster, B.; Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Mackey, D. C.] Calif Pacific Med Ctr, San Francisco, CA USA.
[Simonsick, E. M.] 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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 72
EP 73
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000325
ER
PT J
AU Schrack, JA
Simonsick, EM
Ferrucci, L
AF Schrack, J. A.
Simonsick, E. M.
Ferrucci, L.
TI WALKING EFFICIENCY AS AN INDICATOR OF FATIGABILITY AND RISK FACTOR FOR
MOBILITY LIMITATION
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, NIH, 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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 72
EP 72
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000324
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 ASSESSING FATIGABILITY: CONSTRUCT AND PREDICTIVE VALIDITY OF TWO
PERFORMANCE-BASED METHODS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Simonsick, E. M.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
[Simonsick, E. M.; Schrack, J. A.] Johns Hopkins Univ Med Inst, Baltimore, MD USA.
[Glynn, N. W.] Univ Pittsburgh, Pittsburgh, PA 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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 72
EP 72
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000323
ER
PT J
AU Santanasto, AJ
Coen, PM
Simonsick, EM
Conley, KE
Newman, AB
Goodpaster, B
Glynn, W
AF Santanasto, A. J.
Coen, P. M.
Simonsick, E. M.
Conley, K. E.
Newman, A. B.
Goodpaster, B.
Glynn, W.
TI RELATIONSHIP BETWEEN FATIGABILITY AND MITOCHONDRIAL FUNCTION IN OLDER
ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Santanasto, A. J.; Coen, P. M.; Newman, A. B.; Goodpaster, B.; Glynn, W.] Univ Pittsburgh, Pittsburgh, PA 21224 USA.
[Simonsick, E. M.] NIA, Baltimore, MD USA.
[Conley, K. E.] Univ Washington, Seattle, WA 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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 73
EP 73
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000326
ER
PT J
AU Siggeirsdottir, K
Aspelund, T
Mogensen, B
Jonsson, B
Harris, TB
Launer, LJ
Sigurdsson, G
Gudnason, V
AF Siggeirsdottir, K.
Aspelund, T.
Mogensen, B.
Jonsson, B.
Harris, T. B.
Launer, L. J.
Sigurdsson, G.
Gudnason, V.
TI EFFECT OF OSTEOPOROTIC FRACTURES ON FUNCTION, QUALITY OF LIFE AND
HOSPITALIZATION. THE AGES-REYKJAVIK STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Siggeirsdottir, K.; Aspelund, T.; Gudnason, V.] Iceland Heart Assoc, Kopavogur, Iceland.
[Jonsson, B.] Malmo Univ Hosp, Malmo, Sweden.
[Mogensen, B.; Sigurdsson, G.] Natl Univ Hosp Reykjavik, Reykjavik, Iceland.
[Harris, T. B.; Launer, L. J.] NIA, Bethesda, MD 20892 USA.
[Aspelund, T.; Mogensen, B.; Sigurdsson, G.; 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
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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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 109
EP 109
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000492
ER
PT J
AU Bean, JF
Kiely, DK
Leveille, SG
Phillips, CL
Ferrucci, L
Guralnik, JM
Bandinelli, S
AF Bean, J. F.
Kiely, D. K.
Leveille, S. G.
Phillips, C. L.
Ferrucci, L.
Guralnik, J. M.
Bandinelli, S.
TI THE RELEVANCE OF LEG SPEED, LEG STRENGTH AND OTHER PHYSICAL ATTRIBUTES
TO SUCCESSFUL WALKING SKILLS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Bean, J. F.] Spaulding Rehabil Hosp, Cambridge, MA USA.
[Bean, J. F.] Harvard Univ, Sch Med, Boston, MA USA.
[Kiely, D. K.] Hebrew SeniorLife, Boston, MA USA.
[Leveille, S. G.] UMASS Boston, Boston, MA USA.
[Phillips, C. L.; Ferrucci, L.] NIA, Bethesda, MD 20892 USA.
[Guralnik, J. M.] Univ Maryland, Baltimore, MD 21201 USA.
[Bandinelli, S.] Univ Florence, Florence, Italy.
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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 112
EP 112
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000507
ER
PT J
AU Ward, RE
Caserotti, P
Faulkner, K
Boudreau, R
Cawthon, PM
Newman, AB
Cauley, JA
Strotmeyer, ES
AF Ward, R. E.
Caserotti, P.
Faulkner, K.
Boudreau, R.
Cawthon, P. M.
Newman, A. B.
Cauley, J. A.
Strotmeyer, E. S.
TI PERIPHERAL NERVE FUNCTION AND LOWER EXTREMITY MUSCLE POWER IN OLDER MEN
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ward, R. E.; Boudreau, R.; Newman, A. B.; Cauley, J. A.; Strotmeyer, E. S.] Univ Pittsburgh, Pittsburgh, PA USA.
[Caserotti, P.] NIA, Lab Epidemiol Biometry & Demog, NIH, Bethesda, MD 20892 USA.
[Faulkner, K.] NIOSH, Natl Personal Protect Technol Lab, Ctr Dis Control, Pittsburgh, PA USA.
[Cawthon, P. M.] Calif Pacific Med Ctr, San Francisco, CA USA.
RI Strotmeyer, Elsa/F-3015-2014
NR 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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 112
EP 112
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000506
ER
PT J
AU Cappola, A
Sun, K
Fried, LP
Dalal, MS
Ferrucci, L
Semba, R
AF Cappola, A.
Sun, K.
Fried, L. P.
Dalal, M. S.
Ferrucci, L.
Semba, R.
TI KLOTHO AND HORMONES INVOLVED IN MINERAL METABOLISM
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Cappola, A.] Univ Penn, Philadelphia, PA 19104 USA.
[Sun, K.; Dalal, M. S.; Semba, R.] Johns Hopkins Univ, Baltimore, MD USA.
[Fried, L. P.] Columbia Univ, New York, NY USA.
[Ferrucci, L.] NIA, NIH, Baltimore, MD 21224 USA.
NR 0
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U1 0
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PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 113
EP 113
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000512
ER
PT J
AU Crasto, C
Cappola, A
Sun, K
Bandinelli, S
Ferrucci, L
Semba, R
AF Crasto, C.
Cappola, A.
Sun, K.
Bandinelli, S.
Ferrucci, L.
Semba, R.
TI KLOTHO AND SKELETAL MUSCLE STRENGTH
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Crasto, C.; Sun, K.; Semba, R.] Johns Hopkins, Baltimore, MD USA.
[Cappola, A.] Univ Penn, Philadelphia, PA 19104 USA.
[Bandinelli, S.] Azienda Sanit Firenze, Florence, Italy.
[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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 113
EP 113
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000513
ER
PT J
AU Ferrucci, L
AF Ferrucci, L.
TI KLOTHO AND AGING: PERSPECTIVES FROM MICE TO HUMANS
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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 113
EP 113
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000510
ER
PT J
AU Semba, R
Cappola, A
Sun, K
Bandinelli, S
Guralnik, J
Ferrucci, L
AF Semba, R.
Cappola, A.
Sun, K.
Bandinelli, S.
Guralnik, J.
Ferrucci, L.
TI PLASMA KLOTHO, CARDIOVASCULAR DISEASE, AND MORTALITY IN OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Semba, R.; Sun, K.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Cappola, A.] Univ Penn, Philadelphia, PA 19104 USA.
[Bandinelli, S.] Azienda Sanit Firenze, Florence, Italy.
[Guralnik, J.; 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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 113
EP 113
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000511
ER
PT J
AU Barr, RA
AF Barr, R. A.
TI A RUN THROUGH THE NIA MECHANISM MAZE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Barr, R. A.] NIA, Div Extramural Act, 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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 120
EP 120
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000553
ER
PT J
AU Harden, J
AF Harden, J.
TI NIA SYMPOSIUM: INTERACTIVE ROUNDTABLE DISCUSSIONS ON LIFESTYLE,
LIFESPAN, AND ADVANCES AND OPPORTUNITIES IN AGING RESEARCH
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Harden, J.] 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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 120
EP 121
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000554
ER
PT J
AU Ungvari, Z
Bailey-Downs, L
Sosnowska, D
Gautam, T
Ballabh, P
De Cabo, R
Sonntag, W
Csiszar, A
AF Ungvari, Z.
Bailey-Downs, L.
Sosnowska, D.
Gautam, T.
Ballabh, P.
De Cabo, R.
Sonntag, W.
Csiszar, A.
TI VASCULAR OXIDATIVE STRESS IN AGING: HOMEOSTATIC FAILURE VIA
DYSREGULATION OF NRF2-MEDIATED ANTIOXIDANT RESPONSE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ungvari, Z.; Bailey-Downs, L.; Sosnowska, D.; Gautam, T.; Sonntag, W.; Csiszar, A.] Univ Oklahoma, Hlth Sci Ctr, Dept Geriatr Med, Reynolds Oklahoma Ctr Aging, Oklahoma City, OK USA.
[Ballabh, P.] New York Med Coll, Westchester Med Ctr, Dept Pediat, Valhalla, NY 10595 USA.
[Ballabh, P.] New York Med Coll, Westchester Med Ctr, Dept Anat & Cell Biol, Valhalla, NY 10595 USA.
[De Cabo, R.] NIA, Lab Expt Gerontol, 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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 121
EP 121
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000558
ER
PT J
AU Barry, LC
Thorpe, R
Yaffe, K
Penninx, B
Womack, CR
Newman, AB
Simonsick, EM
AF Barry, L. C.
Thorpe, R.
Yaffe, K.
Penninx, B.
Womack, C. R.
Newman, A. B.
Simonsick, E. M.
TI RACE, DEPRESSION, AND PERFORMANCE-BASED MOBILITY OVER TIME: THE HEALTH,
AGING, AND BODY COMPOSITION STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Barry, L. C.] Yale Univ, Sch Med, New Haven, CT USA.
[Thorpe, R.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Yaffe, K.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Penninx, B.] Vrije Univ Amsterdam, Med Ctr, Amsterdam, Netherlands.
[Womack, C. R.] Univ Tennessee, Memphis, TN USA.
[Newman, A. B.] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA USA.
[Newman, A. B.] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
[Simonsick, E. M.] 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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 147
EP 147
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000668
ER
PT J
AU Metti, AL
Cauley, JA
Ayonayon, HN
Rosano, C
Williamson, J
Harris, TB
Yaffe, K
AF Metti, A. L.
Cauley, J. A.
Ayonayon, H. N.
Rosano, C.
Williamson, J.
Harris, T. B.
Yaffe, K.
TI THE DEMOGRAPHIC AND MEDICAL CORRELATES OF PLASMA A beta 42 AND A beta
42/A beta 40
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Metti, A. L.; Cauley, J. A.; Rosano, C.] Univ Pittsburgh, Pittsburgh, PA USA.
[Ayonayon, H. N.; Yaffe, K.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Harris, T. B.] NIA, Bethesda, MD 20892 USA.
[Williamson, J.] Wake Forest Univ, Baptist Med Ctr, Winston Salem, NC 27109 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
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 163
EP 163
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602001057
ER
EF