FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Choisy, M
Rohani, P
AF Choisy, Marc
Rohani, Pejman
TI Changing spatial epidemiology of pertussis in continental USA
SO PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES
LA English
DT Article
DE pertussis; spatial dynamics; infectious disease re-emergence
ID UNITED-STATES; WAVELET ANALYSIS; TRAVELING-WAVES; INFLUENZA; DYNAMICS;
SYNCHRONY; PATTERNS; TRANSMISSION; VACCINATION; HIERARCHIES
AB Prediction and control of the geographical spread of emerging pathogens has become a central public health issue. Because these infectious diseases are by definition novel, there are few data to characterize their dynamics. One possible solution to this problem is to apply lessons learnt from analyses of historical data on familiar and epidemiologically similar pathogens. However, the portability of the spatial ecology of an infectious disease in a different epoch to other infections remains unexamined. Here, we study this issue by taking advantage of the recent re-emergence of pertussis in the United States to compare its spatial transmission dynamics throughout the 1950s with the past decade. We report 4-year waves, sweeping across the continent in the 1950s. These waves are shown to emanate from highly synchronous foci in the northwest and northeast coasts. In contrast, the recent resurgence of the disease is characterized by 5.5-year epidemics with no particular spatial structure. We interpret this to be the result of dramatic changes in patterns of human movement over the second half of the last century, together with changing age distribution of pertussis. We conclude that extrapolation regarding the spatial spread of contemporaneous pathogens based on analyses of historical incidence may be potentially very misleading.
C1 [Choisy, Marc] Ctr IRD, MIVEGEC UM1 UM2 CNRS 5290 IRD 224, F-34394 Montpellier 5, France.
[Rohani, Pejman] Univ Michigan, Dept Ecol & Evolutionary Biol, Ctr Study Complex Syst, Ann Arbor, MI 48109 USA.
[Rohani, Pejman] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Choisy, M (reprint author), Ctr IRD, MIVEGEC UM1 UM2 CNRS 5290 IRD 224, 911 Ave Agropolis,BP 64501, F-34394 Montpellier 5, France.
EM marc.choisy@ird.fr
RI Choisy, Marc/J-7131-2016
OI Choisy, Marc/0000-0002-5187-6390
FU IRD; CNRS; Vaccine Modeling Initiative of the Bill and Melinda Gates
Foundation; Research and Policy in Infectious Disease Dynamics program
of the Science and Technology Directorate, Department of Homeland
Security; Fogarty International Center, National Institutes of Health;
National Institutes of Health [1R01AI101155]
FX We thank Aaron King and two anonymous reviewers for comments on this
paper. M.C. was funded by IRD and CNRS. M.C. and P.R. were supported by
the Vaccine Modeling Initiative of the Bill and Melinda Gates Foundation
and the Research and Policy in Infectious Disease Dynamics program of
the Science and Technology Directorate, Department of Homeland Security,
and the Fogarty International Center, National Institutes of Health, and
by a grant from the National Institutes of Health 1R01AI101155.
NR 42
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U1 0
U2 12
PU ROYAL SOC
PI LONDON
PA 6-9 CARLTON HOUSE TERRACE, LONDON SW1Y 5AG, ENGLAND
SN 0962-8452
EI 1471-2954
J9 P ROY SOC B-BIOL SCI
JI Proc. R. Soc. B-Biol. Sci.
PD NOV 22
PY 2012
VL 279
IS 1747
BP 4574
EP 4581
DI 10.1098/rspb.2012.1761
PG 8
WC Biology; Ecology; Evolutionary Biology
SC Life Sciences & Biomedicine - Other Topics; Environmental Sciences &
Ecology; Evolutionary Biology
GA 025TU
UT WOS:000310218400008
PM 23015623
ER
PT J
AU Schneider, P
Bell, AS
Sim, DG
O'Donnell, AJ
Blanford, S
Paaijmans, KP
Read, AF
Reece, SE
AF Schneider, Petra
Bell, Andrew S.
Sim, Derek G.
O'Donnell, Aidan J.
Blanford, Simon
Paaijmans, Krijn P.
Read, Andrew F.
Reece, Sarah E.
TI Virulence, drug sensitivity and transmission success in the rodent
malaria, Plasmodium chabaudi
SO PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES
LA English
DT Article
DE competition; drug resistance; fitness; genetically diverse infection;
transmission; virulence evolution
ID REVERSE-TRANSCRIPTION PCR; PUBLIC-HEALTH IMPACT; PARASITIC NEMATODES;
RESISTANCE; FALCIPARUM; ARTEMISININ; EVOLUTION; INFECTIONS; TOLERANCE;
RECRUDESCENCE
AB Here, we test the hypothesis that virulent malaria parasites are less susceptible to drug treatment than less virulent parasites. If true, drug treatment might promote the evolution of more virulent parasites (defined here as those doing more harm to hosts). Drug-resistance mechanisms that protect parasites through interactions with drug molecules at the sub-cellular level are well known. However, parasite phenotypes associated with virulence might also help parasites survive in the presence of drugs. For example, rapidly replicating parasites might be better able to recover in the host if drug treatment fails to eliminate parasites. We quantified the effects of drug treatment on the in-host survival and between-host transmission of rodent malaria (Plasmodium chabaudi) parasites which differed in virulence and had never been previously exposed to drugs. In all our treatment regimens and in single- and mixed-genotype infections, virulent parasites were less sensitive to pyrimethamine and artemisinin, the two antimalarial drugs we tested. Virulent parasites also achieved disproportionately greater transmission when exposed to pyrimethamine. Overall, our data suggest that drug treatment can select for more virulent parasites. Drugs targeting transmission stages (such as artemisinin) may minimize the evolutionary advantage of virulence in drug-treated infections.
C1 [Schneider, Petra; Reece, Sarah E.] Univ Edinburgh, Sch Biol Sci, Ctr Immun Infect & Evolut, Edinburgh EH9 3JT, Midlothian, Scotland.
[Schneider, Petra; O'Donnell, Aidan J.; Reece, Sarah E.] Univ Edinburgh, Sch Biol Sci, Inst Evolut, Edinburgh EH9 3JT, Midlothian, Scotland.
[Schneider, Petra; O'Donnell, Aidan J.; Reece, Sarah E.] Univ Edinburgh, Sch Biol Sci, Inst Immunol & Infect Res, Edinburgh EH9 3JT, Midlothian, Scotland.
[Bell, Andrew S.; Sim, Derek G.; Blanford, Simon; Paaijmans, Krijn P.; Read, Andrew F.] Penn State Univ, Dept Biol, Ctr Infect Dis Dynam, University Pk, PA 16802 USA.
[Bell, Andrew S.; Sim, Derek G.; Blanford, Simon; Paaijmans, Krijn P.; Read, Andrew F.] Penn State Univ, Dept Entomol, Ctr Infect Dis Dynam, University Pk, PA 16802 USA.
[Read, Andrew F.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Schneider, P (reprint author), Univ Edinburgh, Sch Biol Sci, Ctr Immun Infect & Evolut, Edinburgh EH9 3JT, Midlothian, Scotland.
EM petra.schneider@ed.ac.uk
RI Reece, Sarah/C-9447-2009;
OI Schneider, Petra/0000-0002-2616-237X
FU Wellcome Trust [WT082234MA]; Wissenschaftskolleg zu Berlin; Centre for
Immunity, Infection and Evolution, Edinburgh; National Institute of
General Medical Sciences [R01GM089932]; Pennsylvania Department of
Health using Tobacco Settlement Funds
FX We thank R. Mooney, B. Chan and D. Kroczynski for assistance during the
experiments; L. Ross and J. Hadfield for statistical advice on MCMCglmm;
P. Hunt for providing primers and protocols for classical resistance
genotyping; and N. Mideo, L. Pollitt, A. Rowe and laboratory members,
the co-evolution discussion group at Ashworth Laboratories, and members
of the RAPIDD program of the Science and Technology Directorate,
Department of Homeland Security, and the Fogarty International Center,
National Institutes of Health, for discussion. For funding, we thank the
Wellcome Trust (WT082234MA) and Wissenschaftskolleg zu Berlin (S.E.R.),
the Centre for Immunity, Infection and Evolution, Edinburgh (P.S.), the
National Institute of General Medical Sciences (R01GM089932) and a grant
from the Pennsylvania Department of Health using Tobacco Settlement
Funds (A.F.R.). The funders had no role in study design, data collection
and analysis, decision to publish or preparation of the manuscript.
NR 51
TC 14
Z9 14
U1 1
U2 22
PU ROYAL SOC
PI LONDON
PA 6-9 CARLTON HOUSE TERRACE, LONDON SW1Y 5AG, ENGLAND
SN 0962-8452
J9 P ROY SOC B-BIOL SCI
JI Proc. R. Soc. B-Biol. Sci.
PD NOV 22
PY 2012
VL 279
IS 1747
BP 4677
EP 4685
DI 10.1098/rspb.2012.1792
PG 9
WC Biology; Ecology; Evolutionary Biology
SC Life Sciences & Biomedicine - Other Topics; Environmental Sciences &
Ecology; Evolutionary Biology
GA 025TU
UT WOS:000310218400021
PM 23015626
ER
PT J
AU Kolb, P
Phan, K
Gao, ZG
Marko, AC
Sali, A
Jacobson, KA
AF Kolb, Peter
Phan, Khai
Gao, Zhan-Guo
Marko, Adam C.
Sali, Andrej
Jacobson, Kenneth A.
TI Limits of Ligand Selectivity from Docking to Models: In Silico Screening
for A(1) Adenosine Receptor Antagonists
SO PLOS ONE
LA English
DT Article
ID PROTEIN-COUPLED RECEPTORS; DRUG DESIGN; MOLECULAR DOCKING;
CRYSTAL-STRUCTURE; DISCOVERY; PREDICTION; IDENTIFICATION; PHARMACOLOGY;
RADIOLIGAND; DERIVATIVES
AB G protein-coupled receptors (GPCRs) are attractive targets for pharmaceutical research. With the recent determination of several GPCR X-ray structures, the applicability of structure-based computational methods for ligand identification, such as docking, has increased. Yet, as only about 1% of GPCRs have a known structure, receptor homology modeling remains necessary. In order to investigate the usability of homology models and the inherent selectivity of a particular model in relation to close homologs, we constructed multiple homology models for the A(1) adenosine receptor (A(1)AR) and docked similar to 2.2 M lead-like compounds. High-ranking molecules were tested on the A(1)AR as well as the close homologs A(2A)AR and A(3)AR. While the screen yielded numerous potent and novel ligands (hit rate 21% and highest affinity of 400 nM), it delivered few selective compounds. Moreover, most compounds appeared in the top ranks of only one model. These findings have implications for future screens.
C1 [Kolb, Peter; Marko, Adam C.; Sali, Andrej] Univ Calif San Francisco, Dept Pharmaceut Chem, San Francisco, CA USA.
[Phan, Khai; Gao, Zhan-Guo; Jacobson, Kenneth A.] NIDDKD, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Marko, Adam C.; Sali, Andrej] Univ Calif San Francisco, Dept Bioengn & Therapeut Sci, San Francisco, CA 94143 USA.
RP Kolb, P (reprint author), Univ Marburg, Dept Pharmaceut Chem, Marburg, Germany.
EM peter.kolb@uni-marburg.de; kajacobs@helix.nih.gov
RI Jacobson, Kenneth/A-1530-2009; Kolb, Peter/A-3782-2008
OI Jacobson, Kenneth/0000-0001-8104-1493; Kolb, Peter/0000-0003-4089-614X
FU DFG Emmy-Noether Fellowship [KO 4095/1-1]; National Institutes of
Health/National Institute of General Medical Sciences [R01 GM083960];
National Institute of Diabetes and Digestive and Kidney Diseases
Intramural Research Program [1ZIADK031117-24]
FX Funding came from a DFG Emmy-Noether Fellowship KO 4095/1-1 to PK
(www.dfg.de), a National Institutes of Health/National Institute of
General Medical Sciences R01 GM083960 grant to AS (www.nigms.nih.gov),
and a National Institute of Diabetes and Digestive and Kidney Diseases
Intramural Research Program (1ZIADK031117-24) to KAJ
(http://www2.niddk.nih.gov/NIDDKLabs/NIDDKLabsAbout.htm). The funders
had no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 50
TC 22
Z9 22
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 21
PY 2012
VL 7
IS 11
AR e49910
DI 10.1371/journal.pone.0049910
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 047ER
UT WOS:000311821000141
PM 23185482
ER
PT J
AU Nissim, O
Melis, M
Diaz, G
Kleiner, DE
Tice, A
Fantola, G
Zamboni, F
Mishra, L
Farci, P
AF Nissim, Oriel
Melis, Marta
Diaz, Giacomo
Kleiner, David E.
Tice, Ashley
Fantola, Giovanni
Zamboni, Fausto
Mishra, Lopa
Farci, Patrizia
TI Liver Regeneration Signature in Hepatitis B Virus (HBV)-Associated Acute
Liver Failure Identified by Gene Expression Profiling
SO PLOS ONE
LA English
DT Article
ID HEPATOCELLULAR-CARCINOMA; PROGENITOR CELLS; STEM-CELLS; STELLATE CELLS;
GROWTH-FACTOR; ACTIVATION; FIBROSIS; SIMILARITIES; DISEASES; CANCERS
AB Introduction: The liver has inherent regenerative capacity via mitotic division of mature hepatocytes or, when the hepatic loss is massive or hepatocyte proliferation is impaired, through activation of hepatic stem/progenitor cells (HSPC). The dramatic clinical course of acute liver failure (ALF) has posed major limitations to investigating the molecular mechanisms of liver regeneration and the role of HSPC in this setting. We investigated the molecular mechanisms of liver regeneration in 4 patients who underwent liver transplantation for hepatitis B virus (HBV)-associated ALF.
Methods and Findings: Gene expression profiling of 17 liver specimens from the 4 ALF cases and individual specimens from 10 liver donors documented a distinct gene signature for ALF. However, unsupervised multidimensional scaling and hierarchical clustering identified two clusters of ALF that segregated according to histopathological severity massive hepatic necrosis (MHN; 2 patients) and submassive hepatic necrosis (SHN; 2 patients). We found that ALF is characterized by a strong HSPC gene signature, along with ductular reaction, both of which are more prominent in MHN. Interestingly, no evidence of further lineage differentiation was seen in MHN, whereas in SHN we detected cells with hepatocyte-like morphology. Strikingly, ALF was associated with a strong tumorigenesis gene signature. MHN had the greatest upregulation of stem cell genes (EpCAM, CK19, CK7), whereas the most up-regulated genes in SHN were related to cellular growth and proliferation. The extent of liver necrosis correlated with an overriding fibrogenesis gene signature, reflecting the wound-healing process.
Conclusion: Our data provide evidence for a distinct gene signature in HBV-associated ALF whose intensity is directly correlated with the histopathological severity. HSPC activation and fibrogenesis positively correlated with the extent of liver necrosis. Moreover, we detected a tumorigenesis gene signature in ALF, emphasizing the close relationship between liver regeneration and liver cancer.
C1 [Nissim, Oriel; Melis, Marta; Tice, Ashley; Farci, Patrizia] NIAID, Hepat Pathogenesis Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Diaz, Giacomo] Univ Cagliari, Dept Biomed Sci, Cagliari, Italy.
[Kleiner, David E.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Fantola, Giovanni; Zamboni, Fausto] Brotzu Hosp, Liver Transplantat Ctr, Cagliari, Italy.
[Mishra, Lopa] Univ Texas MD Anderson Canc Ctr, Dept Gastroenterol Hepatol & Nutr, Houston, TX 77030 USA.
RP Farci, P (reprint author), NIAID, Hepat Pathogenesis Sect, Infect Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM pfarci@niaid.nih.gov
OI Kleiner, David/0000-0003-3442-4453
FU NIH, National Institute of Allergy and Infectious Diseases and National
Cancer Institute
FX This research was supported by the Intramural Research Program of the
NIH, National Institute of Allergy and Infectious Diseases and National
Cancer Institute. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 44
TC 14
Z9 14
U1 1
U2 11
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 21
PY 2012
VL 7
IS 11
AR e49611
DI 10.1371/journal.pone.0049611
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 047ER
UT WOS:000311821000068
PM 23185381
ER
PT J
AU Britt, JP
Benaliouad, F
McDevitt, RA
Stuber, GD
Wise, RA
Bonci, A
AF Britt, Jonathan P.
Benaliouad, Faiza
McDevitt, Ross A.
Stuber, Garret D.
Wise, Roy A.
Bonci, Antonello
TI Synaptic and Behavioral Profile of Multiple Glutamatergic Inputs to the
Nucleus Accumbens
SO NEURON
LA English
DT Article
ID PREFRONTAL CORTICAL INPUTS; MIDBRAIN DOPAMINE NEURONS; AMPA RECEPTOR
TRAFFICKING; EXCITATORY TRANSMISSION; MOLECULAR-MECHANISMS; PROLONGED
WITHDRAWAL; PROJECTION NEURONS; DIRECTED BEHAVIOR; STRIATAL NEURONS;
COCAINE
AB Excitatory afferents to the nucleus accumbens (NAc) are thought to facilitate reward seeking by encoding reward-associated cues. Selective activation of different glutamatergic inputs to the NAc can produce divergent physiological and behavioral responses, but mechanistic explanations for these pathway-specific effects are lacking. Here, we compared the innervation patterns and synaptic properties of ventral hippocampus, basolateral amygdala, and prefrontal cortex input to the NAc. Ventral hippocampal input was found to be uniquely localized to the medial NAc shell, where it was predominant and selectively potentiated after cocaine exposure. In vivo, bidirectional optogenetic manipulations of this pathway attenuated and enhanced cocaine-induced locomotion. Challenging the idea that any of these inputs encode motivationally neutral information, activation of each discrete pathway reinforced instrumental behaviors. Finally, direct optical activation of medium spiny neurons proved to be capable of supporting self-stimulation, demonstrating that behavioral reinforcement is an explicit consequence of strong excitatory drive to the NAc.
C1 [Bonci, Antonello] Johns Hopkins Univ, Solomon H Snyder Neurosci Inst, Sch Med, Baltimore, MD 21205 USA.
[Britt, Jonathan P.; Benaliouad, Faiza; McDevitt, Ross A.; Wise, Roy A.; Bonci, Antonello] NIDA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Britt, Jonathan P.; Bonci, Antonello] Univ Calif San Francisco, Ernest Gallo Clin & Res Ctr, Emeryville, CA 94608 USA.
[Bonci, Antonello] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA.
[Stuber, Garret D.] Univ N Carolina, Dept Psychiat, UNC Neurosci Ctr, Chapel Hill, NC 27599 USA.
[Stuber, Garret D.] Univ N Carolina, Dept Cell Biol, UNC Neurosci Ctr, Chapel Hill, NC 27599 USA.
[Stuber, Garret D.] Univ N Carolina, Dept Physiol, UNC Neurosci Ctr, Chapel Hill, NC 27599 USA.
RP Bonci, A (reprint author), Johns Hopkins Univ, Solomon H Snyder Neurosci Inst, Sch Med, Baltimore, MD 21205 USA.
EM antonello.bonci@nih.gov
RI Britt, Jonathan/D-8877-2011; Stuber, Garret/E-1160-2011
OI Britt, Jonathan/0000-0003-3044-9565;
FU National Institute on Drug Abuse [DA029325, DA032750]; National
Institutes of Health, National Institute on Drug Abuse
FX We thank Janice Joo, Dhara Patel, Stephanie Chung, Saemi Cho, and
Michael Chiang for technical help. This work was supported by the
National Institute on Drug Abuse (DA029325 and DA032750; G.D.S.) and the
Intramural Research Program of the National Institutes of Health,
National Institute on Drug Abuse.
NR 66
TC 155
Z9 158
U1 2
U2 49
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
J9 NEURON
JI Neuron
PD NOV 21
PY 2012
VL 76
IS 4
BP 790
EP 803
DI 10.1016/j.neuron.2012.09.040
PG 14
WC Neurosciences
SC Neurosciences & Neurology
GA 049JD
UT WOS:000311977900012
PM 23177963
ER
PT J
AU Tachibana, Y
Hikosaka, O
AF Tachibana, Yoshihisa
Hikosaka, Okihide
TI The Primate Ventral Pallidum Encodes Expected Reward Value and Regulates
Motor Action
SO NEURON
LA English
DT Article
ID NIGRA PARS RETICULATA; SACCADIC EYE-MOVEMENTS; BASAL GANGLIA; DOPAMINE
NEURONS; GLOBUS-PALLIDUS; DECISION-MAKING; LATERAL HABENULA; MODULATION;
MOTIVATION; SIGNALS
AB Motor actions are facilitated when expected reward value is high. It is hypothesized that there are neurons that encode expected reward values to modulate impending actions and potentially represent motivation signals. Here, we present evidence suggesting that the ventral pallidum (VP) may participate in this process. We recorded single neuronal activity in the monkey VP using a saccade task with a direction-dependent reward bias. Depending on the amount of the expected reward, VP neurons increased or decreased their activity tonically until the reward was delivered, for both ipsiversive and contraversive saccades. Changes in expected reward values were also associated with changes in saccade performance (latency and velocity). Furthermore, bilateral muscimol-induced inactivation of the VP abolished the reward-dependent changes in saccade latencies. These data suggest that the VP provides expected reward value signals that are used to facilitate or inhibit motor actions.
C1 [Tachibana, Yoshihisa; Hikosaka, Okihide] NEI, Sensorimotor Res Lab, NIH, Bethesda, MD 20892 USA.
[Tachibana, Yoshihisa] Grad Univ Adv Studies, Natl Inst Physiol Sci, Div Syst Neurophysiol, Okazaki, Aichi 4448585, Japan.
[Tachibana, Yoshihisa] Grad Univ Adv Studies, Dept Physiol Sci, Okazaki, Aichi 4448585, Japan.
RP Tachibana, Y (reprint author), NEI, Sensorimotor Res Lab, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM banao@nips.ac.jp; oh@lsr.nei.nih.gov
FU Intramural NIH HHS [ZIA EY000415-09]
NR 50
TC 33
Z9 34
U1 2
U2 11
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
J9 NEURON
JI Neuron
PD NOV 21
PY 2012
VL 76
IS 4
BP 826
EP 837
DI 10.1016/j.neuron.2012.09.030
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 049JD
UT WOS:000311977900015
PM 23177966
ER
PT J
AU Li, G
Cohen, P
Xie, HC
Low, D
Li, DB
Rimner, A
AF Li, Guang
Cohen, Patrice
Xie, Huchen
Low, Daniel
Li, Diana
Rimner, Andreas
TI A novel four-dimensional radiotherapy planning strategy from a
tumor-tracking beam's eye view
SO PHYSICS IN MEDICINE AND BIOLOGY
LA English
DT Article
ID DEFORMABLE IMAGE REGISTRATION; TORSO VOLUME CHANGE; CELL LUNG-CANCER;
RESPIRATORY MOTION; MOVING TARGETS; MONTE-CARLO; REAL-TIME; CT SCANS;
SEGMENTATION; FEASIBILITY
AB To investigate the feasibility of four-dimensional radiotherapy (4DRT) planning from a tumor-tracking beam's eye view (ttBEV) with reliable gross tumor volume (GTV) delineation, realistic normal tissue representation, high planning accuracy and low clinical workload, we propose and validate a novel 4D conformal planning strategy based on a synthesized 3.5D computed tomographic (3.5DCT) image with a motion-compensated tumor. To recreate patient anatomy from a ttBEV in the moving tumor coordinate system for 4DRT planning (or 4D planning), the centers of delineated GTVs in all phase CT images of 4DCT were aligned, and then the aligned CTs were averaged to produce a new 3.5DCT image. This GTV-motion-compensated CT contains a motionless target (with motion artifacts minimized) and motion-blurred normal tissues (with a realistic temporal density average). Semi-automatic threshold-based segmentation of the tumor, lung and body was applied, while manual delineation was used for other organs at risk (OARs). To validate this 3.5DCT-based 4D planning strategy, five patients with peripheral lung lesions of small size (<5 cm(3)) and large motion range (1.2-3.5 cm) were retrospectively studied for stereotactic body radiotherapy (SBRT) using 3D conformal radiotherapy planning tools. The 3.5DCT-based 4D plan (3.5DCT plan) with 9-10 conformal beams was compared with the 4DCT-based 4D plan (4DCT plan). The 4DCT plan was derived from multiple 3D plans based on all phase CT images, each of which used the same conformal beam configuration but with an isocenter shift to aim at the moving tumor and a minor beam aperture and weighting adjustment to maintain plan conformality. The dose-volume histogram (DVH) of the 4DCT plan was created with two methods: one is an integrated DVH (iDVH(4D)), which is defined as the temporal average of all 3D-phase-plan DVHs, and the other (DVH4D) is based on the dose distribution in a reference phase CT image by dose warping from all phase plans using the displacement vector field (DVF) from a free-form deformable image registration (DIR). The DVH3.5D (for the 3.5DCT plan) was compared with both iDVH(4D) and DVH4D. To quantify the DVH difference between the 3.5DCT plan and the 4DCT plan, two methods were used: relative difference (%) of the areas underneath the DVH curves and the volumes receiving more than 20% (V20) and 50% (V50) of prescribed dose of these 4D plans. The volume of the delineated GTV from different phase CTs varied dramatically from 24% to 112% among the five patients, whereas the GTV from 3.5DCT deviated from the averaged GTV in 4DCT by only -6% +/- 6%. For planning tumor volume (PTV) coverage, the difference between the DVH3.5D and iDVH(4D) was negligible (<1% area), whereas the DVH3.5D and DVH4D were quite different, due to DIR uncertainty (similar to 2 mm), which propagates to PTV dose coverage with a pronounced uncertainty for small tumors (0.3-4.0 cm(3)) in stereotactic plans with sharp dose falloff around PTV. For OARs, such as the lung, heart, cord and esophagus, the three DVH curves (DVH3.5D, DVH4D and iDVH(4D)) were found to be almost identical for the same patients, especially in high-dose regions. For the tumor-containing lung, the relative difference of the areas underneath the DVH curves was found to be small (5.3% area on average), of which 65% resulted from the low-dose region (D < 20%). The averaged V20 difference between the two 4D plans was 1.
2% +/- 0.8%. For the mean lung dose (MLD), the 3.5DCT plan differed from the 4DCT plan by -1.1% +/- 1.3%. GTV-motion-compensated CT (3.5DCT) produces an accurate and reliable GTV delineation, which is close to the mean GTV from 4DCT. The 3.5DCT plan is equivalent to the 4DCT plan with <1% dose difference to the PTV and negligible dose difference in OARs. The 3.5DCT approach simplifies 4D planning and provides accurate dose calculation without a substantial increase of clinical workload for motion-tracking delivery to treat small peripheral lung tumors with large motion.
C1 [Li, Guang; Cohen, Patrice; Li, Diana] Mem Sloan Kettering Canc Ctr, Dept Med Phys, New York, NY 10021 USA.
[Xie, Huchen] NCI, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Low, Daniel] Univ Calif Los Angeles, Dept Radiat Oncol, Los Angeles, CA 90024 USA.
[Rimner, Andreas] Mem Sloan Kettering Canc Ctr, Dept Radiat Oncol, New York, NY 10021 USA.
RP Li, G (reprint author), Mem Sloan Kettering Canc Ctr, Dept Med Phys, New York, NY 10021 USA.
EM lig2@mskcc.org
OI Li, Guang/0000-0002-9022-2883
NR 37
TC 4
Z9 4
U1 1
U2 5
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 2012
VL 57
IS 22
BP 7579
EP 7598
DI 10.1088/0031-9155/57/22/75794
PG 20
WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging
SC Engineering; Radiology, Nuclear Medicine & Medical Imaging
GA 033ZA
UT WOS:000310838700025
PM 23103415
ER
PT J
AU Stern, MD
AF Stern, Michael D.
TI Coagulation Makes Waves
SO BIOPHYSICAL JOURNAL
LA English
DT News Item
C1 NIA, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA.
RP Stern, MD (reprint author), NIA, Gerontol Res Ctr, NIH, 4940 Eastern Ave, Baltimore, MD 21224 USA.
EM sternm@grc.nia.nih.gov
NR 3
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U1 0
U2 1
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 21
PY 2012
VL 103
IS 10
BP 2049
EP 2049
DI 10.1016/j.bpj.2012.09.042
PG 1
WC Biophysics
SC Biophysics
GA 041RN
UT WOS:000311419000003
PM 23200038
ER
PT J
AU Vahedi, G
Takahashi, H
Nakayamada, S
Sun, HW
Sartorelli, V
Kanno, Y
O'Shea, JJ
AF Vahedi, Golnaz
Takahashi, Hayato
Nakayamada, Shingo
Sun, Hong-wei
Sartorelli, Vittorio
Kanno, Yuka
O'Shea, John J.
TI STATs Shape the Active Enhancer Landscape of T Cell Populations
SO CELL
LA English
DT Article
ID CHIP-SEQ DATA; TRANSCRIPTION FACTOR; GENE-EXPRESSION; REGULATORY
ELEMENTS; LINEAGE COMMITMENT; RNA-SEQ; BET; DIFFERENTIATION;
IDENTIFICATION; ACCESSIBILITY
AB Signaling pathways are intimately involved in cellular differentiation, allowing cells to respond to their environment by regulating gene expression. Although enhancers are recognized as key elements that regulate selective gene expression, the interplay between signaling pathways and actively used enhancer elements is not clear. Here, we use CD4(+) T cells as a model of differentiation, mapping the activity of cell-type-specific enhancer elements in T helper 1 (Th1) and Th2 cells. Our data establish that STAT proteins have a major impact on the activation of lineage-specific enhancers and the suppression of enhancers associated with alternative cell fates. Transcriptome analysis further supports a functional role for enhancers regulated by STATs. Importantly, expression of lineage-defining master regulators in STAT-deficient cells fails to fully recover the chromatin signature of STAT-dependent enhancers. Thus, these findings point to a critical role of STATs as environmental sensors in dynamically molding the specialized enhancer architecture of differentiating cells.
C1 [Vahedi, Golnaz; Takahashi, Hayato; Nakayamada, Shingo; Kanno, Yuka; O'Shea, John J.] NIAMSD, Lymphocyte Cell Biol Sect, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA.
[Sun, Hong-wei] NIAMSD, Biodata Min & Discovery Sect, NIH, Bethesda, MD 20892 USA.
[Sartorelli, Vittorio] NIAMSD, Lab Muscle Stem Cells & Gene Regulat, NIH, Bethesda, MD 20892 USA.
RP Kanno, Y (reprint author), NIAMSD, Lymphocyte Cell Biol Sect, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA.
EM kannoy@mail.nih.gov
RI Kanno, Yuka/B-5802-2013;
OI Kanno, Yuka/0000-0001-5668-9319
FU Intramural Research Programs of NIAMS
FX The authors thank Drs. K. Zhao, A. Poholek, and K. Ghoreschi for
critically reading this manuscript. We also thank G. Gutierrez-Cruz
(Biodata Mining Core Facility, NIAMS), J. Simone, and J. Lay (Flow
Cytometry Section, NIAMS) for their excellent technical support. This
study utilized the high-performance computational capabilities of the
Biowulf Linux cluster at the NIH. This work was supported by the
Intramural Research Programs of NIAMS.
NR 41
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U1 0
U2 37
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD NOV 21
PY 2012
VL 151
IS 5
BP 981
EP 993
DI 10.1016/j.cell.2012.09.044
PG 13
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 041TG
UT WOS:000311423500012
PM 23178119
ER
PT J
AU Gilliam, JC
Chang, JT
Sandoval, IM
Zhang, YW
Li, TS
Pittler, SJ
Chiu, W
Wensel, TG
AF Gilliam, Jared C.
Chang, Juan T.
Sandoval, Ivette M.
Zhang, Youwen
Li, Tiansen
Pittler, Steven J.
Chiu, Wah
Wensel, Theodore G.
TI Three-Dimensional Architecture of the Rod Sensory Cilium and Its
Disruption in Retinal Neurodegeneration
SO CELL
LA English
DT Article
ID INTRAFLAGELLAR TRANSPORT PROTEIN; BARDET-BIEDL-SYNDROME; CGMP-GATED
CHANNEL; ACID-RICH PROTEINS; CRYOELECTRON TOMOGRAPHY; CILIARY ROOTLET;
BETA-SUBUNIT; BASAL BODY; DISK MORPHOGENESIS; OUTER SEGMENTS
AB Defects in primary cilia lead to devastating disease because of their roles in sensation and developmental signaling but much is unknown about ciliary structure and mechanisms of their formation and maintenance. We used cryo-electron tomography to obtain 3D maps of the connecting cilium and adjacent cellular structures of a modified primary cilium, the rod outer segment, from wild-type and genetically defective mice. The results reveal the molecular architecture of the cilium and provide insights into protein functions. They suggest that the ciliary rootlet is involved in cellular transport and stabilizes the axoneme. A defect in the BBSome membrane coat caused defects in vesicle targeting near the base of the cilium. Loss of the proteins encoded by the Cngb1 gene disrupted links between the disk and plasma membranes. The structures of the outer segment membranes support a model for disk morphogenesis in which basal disks are enveloped by the plasma membrane.
C1 [Gilliam, Jared C.; Chang, Juan T.; Sandoval, Ivette M.; Chiu, Wah; Wensel, Theodore G.] Baylor Coll Med, Verna & Marrs McLean Dept Biochem & Mol Biol, Houston, TX 77030 USA.
[Chang, Juan T.; Chiu, Wah] Baylor Coll Med, Natl Ctr Macromol Imaging, Houston, TX 77030 USA.
[Zhang, Youwen; Pittler, Steven J.] Univ Alabama Birmingham, Dept Vis Sci, Birmingham, AL 35924 USA.
[Li, Tiansen] NEI, Neurobiol Neurodegenerat & Repair Lab, Bethesda, MD 20892 USA.
RP Wensel, TG (reprint author), Baylor Coll Med, Verna & Marrs McLean Dept Biochem & Mol Biol, Houston, TX 77030 USA.
EM twensel@bcm.edu
RI Pittler, Steven/J-7091-2013;
OI Pittler, Steven/0000-0002-8464-9303; Wensel,
Theodore/0000-0003-3518-9352
FU NIH [EY011900, EY07981, P41RR002250, EY018143, EY10309, EY10581,
EY011731, T32EY007001, EY002520]; Robert Welch Foundation [Q-0035,
Q1242]
FX This work was supported in part by grants from the NIH (EY011900 and
EY07981 to T.G.W., P41RR002250 to W. C., EY018143 to S.J.P., EY10309 and
EY10581 to T.L., support for I.M.S. by EY011731, an NIH NRSA trainee
appointment on grant T32EY007001 to J.C.G., and Vision Research Core
Grant EY002520) and by the Robert Welch Foundation (Q-0035 to T.G.W. and
Q1242 to W.C.). We thank Mr. Ralph Nichols for help with electron
microscopy of fixed samples, Dr. Vera Moiseenkova-Bell for help in the
early stages of the project, and Dr. Alecia Gross for helpful
suggestions and pilot experiments.
NR 53
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U1 1
U2 26
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD NOV 21
PY 2012
VL 151
IS 5
BP 1029
EP 1041
DI 10.1016/j.cell.2012.10.038
PG 13
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 041TG
UT WOS:000311423500016
PM 23178122
ER
PT J
AU Yasuda, M
Yamamoto, S
Hikosaka, O
AF Yasuda, Masaharu
Yamamoto, Shinya
Hikosaka, Okihide
TI Robust Representation of Stable Object Values in the Oculomotor Basal
Ganglia
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID NIGRA-PARS-RETICULATA; LONG-TERM-MEMORY; SUBSTANTIA-NIGRA; NEURAL
MECHANISMS; CAUDATE-NUCLEUS; HABIT FORMATION; VISUAL-STIMULI;
EYE-MOVEMENTS; REWARD; STRIATUM
AB Our gaze tends to be directed to objects previously associated with rewards. Such object values change flexibly or remain stable. Here we present evidence that the monkey substantia nigra pars reticulata (SNr) in the basal ganglia represents stable, rather than flexible, object values. After across-day learning of object-reward association, SNr neurons gradually showed a response bias to surprisingly many visual objects: inhibition to high-valued objects and excitation to low-valued objects. Many of these neurons were shown to project to the ipsilateral superior colliculus. This neuronal bias remained intact even after >100 d without further learning. In parallel with the neuronal bias, the monkeys tended to look at high-valued objects. The neuronal and behavioral biases were present even if no value was associated during testing. These results suggest that SNr neurons bias the gaze toward objects that were consistently associated with high values in one's history.
C1 [Yasuda, Masaharu; Yamamoto, Shinya; Hikosaka, Okihide] NEI, Sensorimotor Res Lab, NIH, Bethesda, MD 20892 USA.
[Yamamoto, Shinya] Natl Inst Adv Ind Sci & Technol, Syst Neurosci Grp, Human Technol Res Inst, Tsukuba, Ibaraki 3058568, Japan.
RP Yasuda, M (reprint author), NEI, Sensorimotor Res Lab, NIH, 49 Convent Dr,Bldg 49,Rm 2C28, Bethesda, MD 20892 USA.
EM yasudama@mail.nih.gov
RI Yamamoto, Shinya/S-3134-2016
OI Yamamoto, Shinya/0000-0002-0505-8848
FU Intramural Research Program at the National Institutes of Health,
National Eye Institute
FX This work was supported by the Intramural Research Program at the
National Institutes of Health, National Eye Institute. We thank E.
Bromberg-Martin, H. F. Kim, I. Monosov, S. Hong, and Y. Tachibana for
discussions; and A. M. Nichols, A. V. Hays, B. Nagy, D. Parker, G.
Tansey, J.W. McClurkin, L. P. Jensen, M. K. Smith, and T. W. Ruffner for
technical assistance.
NR 54
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U1 4
U2 17
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 21
PY 2012
VL 32
IS 47
BP 16917
EP 16932
DI 10.1523/JNEUROSCI.3438-12.2012
PG 16
WC Neurosciences
SC Neurosciences & Neurology
GA 041SF
UT WOS:000311420800035
PM 23175843
ER
PT J
AU Parkash, J
Cimino, I
Ferraris, N
Casoni, F
Wray, S
Cappy, H
Prevot, V
Giacobini, P
AF Parkash, Jyoti
Cimino, Irene
Ferraris, Nicoletta
Casoni, Filippo
Wray, Susan
Cappy, Helene
Prevot, Vincent
Giacobini, Paolo
TI Suppression of beta 1-Integrin in Gonadotropin-Releasing Hormone Cells
Disrupts Migration and Axonal Extension Resulting in Severe Reproductive
Alterations
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID HEPATOCYTE GROWTH-FACTOR; NEURONAL MIGRATION; NEURITE OUTGROWTH;
MEDIAN-EMINENCE; GENE-EXPRESSION; GNRH NEURONS; RAT UTERUS; BETA-1-CLASS
INTEGRINS; SENSORY NEURONS; SEMAPHORIN 3F
AB Reproduction in mammals is dependent on the function of hypothalamic neurons whose axons project to the hypothalamic median eminence (ME) where they release gonadotropin-releasing hormone (GnRH) into a specialized capillary network for delivery to the anterior pituitary. These neurons originate prenatally in the nasal placode and migrate into the forebrain along the olfactory-vomeronasal nerves. The complex developmental events leading to the correct establishment of the GnRH system are tightly regulated by the specific spatiotemporal expression patterns of guidance cues and extracellular matrix molecules, the functions of which, in part, are mediated by their binding to beta 1-subunit-containing integrins. To determine the biological role of these cell-surface proteins in reproduction, Cre/LoxP technology was used to generate GnRH neuron-specific beta 1-integrin conditional KO (GnRH-Itgb1(-/-)) mice. Loss of beta 1-integrin signaling impaired migration of GnRH neurons, their axonal extension to the ME, timing of pubertal onset, and fertility in these mice. These results identify beta 1-integrin as a gene involved in normal development of the GnRH system and demonstrate a fundamental role for this protein in acquisition of normal reproductive competence in female mice.
C1 [Giacobini, Paolo] INSERM, U837, Jean Pierre Aubert Res Ctr, Unit 837, F-59045 Lille, France.
[Parkash, Jyoti; Cimino, Irene; Casoni, Filippo; Cappy, Helene; Prevot, Vincent; Giacobini, Paolo] Sch Med, UDSL, F-59045 Lille, France.
[Ferraris, Nicoletta; Giacobini, Paolo] Univ Turin, Dept Human & Anim Biol, I-10123 Turin, Italy.
[Wray, Susan] NINDS, Cellular & Dev Neurobiol Sect, NIH, Bethesda, MD 20892 USA.
RP Giacobini, P (reprint author), INSERM, U837, Jean Pierre Aubert Res Ctr, Unit 837, Pl Verdun, F-59045 Lille, France.
EM paolo.giacobini@inserm.fr
RI Prevot, Vincent/E-5720-2016; Giacobini, Paolo/P-5451-2015
OI Giacobini, Paolo/0000-0002-3075-1441
FU Compagnia di San Paolo, Turin, Italy [2008.1224]; Institut National de
la Sante et de la Recherche Medicale, Inserm, France [U837]; Agence
Nationale de la Recherche, ANR, France [ANR-2010-JCJC-1404-01,
ANR-09-BLAN-0267]; University of Lille 2, Lille, France (Appel a Projets
du Conseil Scientifique de l'Universite Lille 2); Intramural Research
Program of the National Institute of Neurological Disorders and
Stroke-National Institutes of Health
FX This work was supported by Compagnia di San Paolo, Turin, Italy (grant
number 2008.1224 to P. G.); the Institut National de la Sante et de la
Recherche Medicale, Inserm, France (grant number U837); Agence Nationale
de la Recherche, ANR, France (grant numbers ANR-2010-JCJC-1404-01 to P.
G. and ANR-09-BLAN-0267 to V. P.); the University of Lille 2, Lille,
France (Appel a Projets du Conseil Scientifique de l'Universite Lille 2
to P. G.); and the Intramural Research Program of the National Institute
of Neurological Disorders and Stroke-National Institutes of Health. We
thank Meryem Tardivel of the Imaging Core Facility of IFR114 of the
University of Lille 2 for technical assistance, Julien Devassine and
Delphine Cappe (Animal facility-IFR114) for the maintenance of
transgenic mouse lines, the histology facility at University of Lille 2,
Andre Defossez and Claude-Alain Maurage for the histological analyses of
specimens, and Nathalie Jouy from the cytometry core facilities
(BioImaging Center Lille Nord de France-IFR114).
NR 65
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U1 0
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 21
PY 2012
VL 32
IS 47
BP 16992
EP 17002
DI 10.1523/JNEUROSCI.3057-12.2012
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 041SF
UT WOS:000311420800042
PM 23175850
ER
PT J
AU Zafonte, RD
Bagiella, E
Ansel, BM
Novack, TA
Friedewald, WT
Hesdorffer, DC
Timmons, SD
Jallo, J
Eisenberg, H
Hart, T
Ricker, JH
Diaz-Arrastia, R
Merchant, RE
Temkin, NR
Melton, S
Dikmen, SS
AF Zafonte, Ross D.
Bagiella, Emilia
Ansel, Beth M.
Novack, Thomas A.
Friedewald, William T.
Hesdorffer, Dale C.
Timmons, Shelly D.
Jallo, Jack
Eisenberg, Howard
Hart, Tessa
Ricker, Joseph H.
Diaz-Arrastia, Ramon
Merchant, Randall E.
Temkin, Nancy R.
Melton, Sherry
Dikmen, Sureyya S.
TI Effect of Citicoline on Functional and Cognitive Status Among Patients
With Traumatic Brain Injury Citicoline Brain Injury Treatment Trial
(COBRIT)
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID POSTTRAUMATIC-STRESS-DISORDER; MILD HEAD-INJURY; CDP-CHOLINE; MULTIPLE
OUTCOMES; CLINICAL-TRIALS; FOLLOW-UP; HIPPOCAMPAL; SYMPTOMS; RECOVERY;
TBI
AB Context Traumatic brain injury (TBI) is a serious public health problem in the United States, yet no treatment is currently available to improve outcome after TBI. Approved for use in TBI in 59 countries, citicoline is an endogenous substance offering potential neuroprotective properties as well as facilitated neurorepair post injury.
Objective To determine the ability of citicoline to positively affect functional and cognitive status in persons with complicated mild, moderate, and severe TBI.
Design, Setting, and Patients The Citicoline Brain Injury Treatment Trial (COBRIT), a phase 3, double-blind randomized clinical trial conducted between July 20, 2007, and February 4, 2011, among 1213 patients at 8 US level 1 trauma centers to investigate effects of citicoline vs placebo in patients with TBI classified as complicated mild, moderate, or severe.
Intervention Ninety-day regimen of daily enteral or oral citicoline (2000 mg) or placebo.
Main Outcome Measures Functional and cognitive status, assessed at 90 days using the TBI-Clinical Trials Network Core Battery. A global statistical test was used to analyze the 9 scales of the core battery. Secondary outcomes were functional and cognitive improvement, assessed at 30, 90, and 180 days, and examination of the long-term maintenance of treatment effects.
Results Rates of favorable improvement for the Glasgow Outcome Scale-Extended were 35.4% in the citicoline group and 35.6% in the placebo group. For all other scales the rate of improvement ranged from 37.3% to 86.5% in the citicoline group and from 42.7% to 84.0% in the placebo group. The citicoline and placebo groups did not differ significantly at the 90-day evaluation (global odds ratio [OR], 0.98 [95% CI, 0.83-1.15]); in addition, there was no significant treatment effect in the 2 severity subgroups (global OR, 1.14 [95% CI, 0.88-1.49] and 0.89 [95% CI, 0.72-1.49] for moderate/severe and complicated mild TBI, respectively). At the 180-day evaluation, the citicoline and placebo groups did not differ significantly with respect to the primary outcome (global OR, 0.87 [95% CI, 0.72-1.04]).
Conclusion Among patients with traumatic brain injury, the use of citicoline compared with placebo for 90 days did not result in improvement in functional and cognitive status.
C1 [Zafonte, Ross D.] Harvard Univ, Spaulding Rehabil Hosp Network, Sch Med, Dept Phys Med & Rehabil, Boston, MA 02114 USA.
[Zafonte, Ross D.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Bagiella, Emilia] Mt Sinai Sch Med, Dept Hlth Evidence & Policy, New York, NY USA.
[Ansel, Beth M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Novack, Thomas A.; Melton, Sherry] Univ Alabama Birmingham, Dept Phys Med & Rehabil, Birmingham, AL USA.
[Friedewald, William T.] Columbia Univ, Dept Biostat, New York, NY USA.
[Hesdorffer, Dale C.] Columbia Univ, Dept Epidemiol, New York, NY USA.
[Timmons, Shelly D.] Geisinger Med Ctr, Dept Neurosurg, Danville, PA 17822 USA.
[Jallo, Jack] Thomas Jefferson Univ, Div Neurotrauma & Crit Care, Philadelphia, PA 19107 USA.
[Eisenberg, Howard] Univ Maryland, Sch Med, Dept Neurosurg, Baltimore, MD 21201 USA.
[Hart, Tessa] Moss Rehabil Res Inst, Philadelphia, PA USA.
[Ricker, Joseph H.] Univ Pittsburgh, Dept Phys Med & Rehabil, Pittsburgh, PA USA.
[Diaz-Arrastia, Ramon] Uniformed Serv Univ Hlth Sci, Ctr Neurosci & Regenerat Med, Rockville, MD USA.
[Merchant, Randall E.] Virginia Commonwealth Univ, Dept Neurosurg, Richmond, VA 23284 USA.
[Temkin, Nancy R.] Univ Washington, Dept Neurol Surg, Seattle, WA 98195 USA.
[Dikmen, Sureyya S.] Univ Washington, Dept Rehabil Med, Seattle, WA 98195 USA.
RP Zafonte, RD (reprint author), Harvard Univ, Spaulding Rehabil Hosp Network, Sch Med, Dept Phys Med & Rehabil, 125 Nashua St, Boston, MA 02114 USA.
EM rzafonte@partners.org
FU National Institute of Child Health and Human Development at Temple
University [U01HD042738]; National Institute of Child Health and Human
Development at University of Alabama at Birmingham [U01HD042687];
National Institute of Child Health and Human Development at University
of Maryland [U01HD042736]; National Institute of Child Health and Human
Development at University of Pittsburgh [U01HD042678]; National
Institute of Child Health and Human Development at University of
Tennessee Health Sciences Center [U01HD042686]; National Institute of
Child Health and Human Development at University of Texas Southwestern
[U01HD042652]; National Institute of Child Health and Human Development
grants at University of Washington [U01HD042653]; National Institute of
Child Health and Human Development grants at Virginia Commonwealth
University [U01HD042689]; National Institute of Child Health and Human
Development grants at Columbia University [Columbia University
(U01HD042823]
FX This study was supported by National Institute of Child Health and Human
Development grants at the following institutions: Temple University
(U01HD042738); University of Alabama at Birmingham (U01HD042687);
University of Maryland (U01HD042736); University of Pittsburgh
(U01HD042678); University of Tennessee Health Sciences Center
(U01HD042686); University of Texas Southwestern (U01HD042652);
University of Washington (U01HD042653); Virginia Commonwealth University
(U01HD042689); and Columbia University (U01HD042823). Ferrer Grupo
provided the citicoline and identical placebo used in the study.
NR 40
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U1 4
U2 13
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 21
PY 2012
VL 308
IS 19
BP 1993
EP 2000
DI 10.1001/jama.2012.13256
PG 8
WC Medicine, General & Internal
SC General & Internal Medicine
GA 040AQ
UT WOS:000311291400023
PM 23168823
ER
PT J
AU Franco, EL
de Sanjose, S
Broker, TR
Stanley, MA
Chevarie-Davis, M
Isidean, SD
Schiffman, M
AF Franco, Eduardo L.
de Sanjose, Silvia
Broker, Thomas R.
Stanley, Margaret A.
Chevarie-Davis, Myriam
Isidean, Sandra D.
Schiffman, Mark
TI Human Papillomavirus and Cancer Prevention: Gaps in Knowledge and
Prospects for Research, Policy, and Advocacy
SO VACCINE
LA English
DT Review
DE HPV; cancer prevention; policy; advocacy
ID CERVICAL-CANCER; METHYLATION
AB The recognition that human papillomavirus (HPV) infection is the central, necessary cause of cervical cancer paved the way to new fronts of prevention via improved screening methods and HPV vaccination. Much has been learned in all fronts, from the molecular basis of our understanding of how HPV causes disease to the health economics of preventive strategies at the individual and population levels. Progress in other areas of cancer control has yet to show the same multi- and trans-disciplinary gains seen in research on HPV-associated malignancies, which is one of the unequivocal success stories in disease prevention. Yet, as an embarrassment of riches, much more research is needed to fill the gaps in knowledge that remain before we are able to reap the benefits from the knowledge translation from all fronts. Public health research on setting-specific implementation of HPV-based preventive strategies and more concerted advocacy to counter barriers facing the adoption of these strategies are likely to yield major dividends in reducing the burden of HPV-associated diseases. This article forms part of a special supplement entitled "Comprehensive Control of HPV Infections and Related Diseases" Vaccine Volume 30, Supplement 5, 2012. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Franco, Eduardo L.; Chevarie-Davis, Myriam; Isidean, Sandra D.] McGill Univ, Div Canc Epidemiol, Montreal, PQ, Canada.
[de Sanjose, Silvia] Inst Catala Oncol, CERP, Unit Infect & Canc UNIC, Lhospitalet De Llobregat, Barcelona, Spain.
[Broker, Thomas R.] Univ Alabama Birmingham, Dept Biochem & Mol Genet, Birmingham, AL USA.
[Stanley, Margaret A.] Univ Cambridge, Dept Pathol, Cambridge CB2 1QP, England.
[Schiffman, Mark] Natl Canc Inst, Div Canc Epidemiol & Genet, Bethesda, MD USA.
RP Franco, EL (reprint author), McGill Univ, Div Canc Epidemiol, Montreal, PQ, Canada.
EM eduardo.franco@mcgill.ca
RI de Sanjose Llongueras, Silvia/H-6339-2014;
OI Franco, Eduardo/0000-0002-4409-8084
FU European Commission [HEALTH-F3-2010-242061, HEALTH-F2-2011-282562];
Instituto de Salud Carlos III (Spanish Government) [FIS PI10/02995,
RCESP C03/09, RTICESP C03/10, RTIC RD06/0020/0095, CIBERESP]; Agencia de
Gestio d'Ajuts Universitaris i de Recerca - Generalitat de Catalunya
(Catalonian Government) [AGAUR 2005SGR00695, AGAUR 2009SGR126]; Merck;
GlaxoSmithKline; Sanofi Pasteur MSD; Qiagen; GSK
FX The work was partially supported by public grants from the European
Commission (7th Framework Programme grants HEALTH-F3-2010-242061,
PREHDICT and HEALTH-F2-2011-282562, HPV AHEAD), from the Instituto de
Salud Carlos III (Spanish Government) (grants FIS PI10/02995, RCESP
C03/09, RTICESP C03/10, RTIC RD06/0020/0095 and CIBERESP) and from the
Agencia de Gestio d'Ajuts Universitaris i de Recerca - Generalitat de
Catalunya (Catalonian Government) (grants AGAUR 2005SGR00695 and AGAUR
2009SGR126), who had no role in data collection, analysis or
interpretation of results.; EF: Has served as occasional consultant to
companies involved with HPV vaccines (Merck and GSK) and with HPV
diagnostics (Roche, Gen-Probe, BD). He has received an unrestricted
grant from Merck.; SdS: Institutional support: HPV vaccine trials and
epidemiological studies sponsored by GlaxoSmithKline, Merck and Sanofi
Pasteur MSD. Screening and HPV testing trials partially supported by
Qiagen. Personal support: Travel grants to conferences/symposia/meetings
are occasionally granted by either GlaxoSmithKline, Sanofi Pasteur MSD
or Qiagen.; MS: Has received free CareHPV equipment and reagents for an
independent analysis of low-cost HPV testing in Africa. He has also
received free specimen testing from Roche for epidemiologic projects. He
was the NCI co-Project Officer and co-Medical Monitor of an independent
evaluation of GSK HPV vaccine, for which GSK donated vaccine and
financed the regulatory components.
NR 10
TC 20
Z9 20
U1 0
U2 7
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 20
PY 2012
VL 30
SU 5
BP F175
EP F182
DI 10.1016/j.vaccine.2012.06.092
PG 8
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 063CX
UT WOS:000312974900019
PM 23199961
ER
PT J
AU Gillison, ML
Alemany, L
Snijders, PJF
Chaturvedi, A
Steinberg, BM
Schwartz, S
Castellsague, X
AF Gillison, Maura L.
Alemany, Laia
Snijders, Peter J. F.
Chaturvedi, Anil
Steinberg, Bettie M.
Schwartz, Steve
Castellsague, Xavier
TI Human Papillomavirus and Diseases of the Upper Airway: Head and Neck
Cancer and Respiratory Papillomatosis
SO VACCINE
LA English
DT Review
DE Oropharynx; Papillomatosis; Head and neck cancer; HPV; Epidemiology;
Causality
ID SQUAMOUS-CELL-CARCINOMA; ACTIVE HUMAN-PAPILLOMAVIRUS; ORAL HPV
INFECTION; P53 CODON-72 POLYMORPHISM; GENE-EXPRESSION PROFILES;
PHASE-III TRIAL; OROPHARYNGEAL CANCER; RISK-FACTORS; JUVENILE-ONSET;
TONSILLAR CARCINOMA
AB Human papillomavirus (HPV) infection is causally associated with benign and malignant diseases of the upper airway, including respiratory papillomatosis and oropharyngeal cancer. Low-risk HPV types 6 and 11 are the predominant cause of papillomatosis, whereas only HPV16 definitively satisfies both molecular and epidemiological causal criteria as a carcinogenic or high-risk type in the upper airway. HPV16 E6/E7 mRNA expression and integration are observed predominantly among oropharyngeal cancers, and experimental models have shown E6/E7 expression to be necessary for the initiation and maintenance of the malignant phenotype of these cancers. From an epidemiological perspective, a strong and consistent association between markers of HPV16 exposure and oropharyngeal cancer has been demonstrated in numerous case-control studies. HPV-positive oropharyngeal cancers have also been shown to be distinct from HPV-negative head and neck squamous cell cancers with regard to risk-factor profiles, molecular genetic alterations, population-level incidence trends over time, and prognosis. Tumor HPV status (as determined by certain HPV16 in situ hybridization assays or certain p16 immunohistochemistry assays) is the strongest determinant of survival for patients with local-regionally advanced oropharyngeal cancer: patients with HPV-positive cancer have at least a 50% improvement in overall survival at 5 years, which is equivalent to an approximate 30% difference in absolute survival. Thus, HPV status determination is now part of the routine diagnostic evaluation for prognostication. Preliminary evidence indicates that a small proportion of head and neck cancers may be caused by additional HPV types (e.g., 18, 31, 33, 35) and that HPV-caused cancers may rarely arise from non-oropharyngeal sites (e.g., the oral cavity, nasopharynx, and larynx). Whether or not HPV vaccination has the potential to prevent oral HPV infections that lead to cancer or papillomatosis in the upper airway is currently unknown, as is the potential for secondary prevention with HPV detection. This article forms part of a special supplement entitled "Comprehensive Control of HPV Infections and Related Diseases" Vaccine Volume 30, Supplement 5, 2012. (C) 2012 Published by Elsevier Ltd.
C1 [Gillison, Maura L.] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
[Alemany, Laia; Castellsague, Xavier] Catalan Inst Oncol ICO, CERP, Unit Infect & Canc UNIC, Lhospitalet De Llobregat, Barcelona, Spain.
[Snijders, Peter J. F.] Vrije Univ Amsterdam, Med Ctr, Dept Pathol, Amsterdam, Netherlands.
[Chaturvedi, Anil] Natl Canc Inst, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Steinberg, Bettie M.] Feinstein Inst Med Res, Manhasset, NY USA.
[Schwartz, Steve] Fred Hutchinson Canc Res Ctr, Program Epidemiol, Seattle, WA 98104 USA.
RP Gillison, ML (reprint author), Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
EM Maura.gillison@osumc.edu
RI Castellsague Pique, Xavier/N-5795-2014; Chaturvedi, Anil/J-2024-2015;
Steinberg, Bettie/K-3414-2012
OI Castellsague Pique, Xavier/0000-0002-0802-3595; Chaturvedi,
Anil/0000-0003-2696-8899; Steinberg, Bettie/0000-0003-2372-8099
FU European Commission [HEALTH-F3-2010-242061, HEALTH-F2-2011-282562];
Instituto de Salud Carlos III (Spanish Government) [FIS FIS PI10/02995,
FIS PI08/1535, FIS PI11/02096, FIS PI11/02104, RCESP C03/09, RTICESP
C03/10, RTIC RD06/0020/0095, CIBERESP]; Agencia de Gestio d'Ajuts
Universitaris i de Recerca - Generalitat de Catalunya (Catalonian
Government) [AGAUR 2005SGR00695, AGAUR 2009SGR126]; Merck;
GlaxoSmithKline; Sanofi Pasteur MSD; Qiagen
FX The work was partially supported by public grants from the European
Commission (7th Framework Programme grants HEALTH-F3-2010-242061,
PREHDICT and HEALTH-F2-2011-282562, HPV AHEAD), from the Instituto de
Salud Carlos III (Spanish Government) (grants FIS FIS PI10/02995, FIS
PI08/1535, FIS PI11/02096, FIS PI11/02104, RCESP C03/09, RTICESP C03/10,
RTIC RD06/0020/0095 and CIBERESP) and from the Agencia de Gestio d'Ajuts
Universitaris i de Recerca - Generalitat de Catalunya (Catalonian
Government) (grants AGAUR 2005SGR00695 and AGAUR 2009SGR126), who had no
role in data collection, analysis or interpretation of results.; MLG:
Has had scientific collaborations and has received research funding from
Merck. She has acted as a consultant for Merck.; XC: Institutional
support: HPV vaccine trials and epidemiological studies sponsored by
GlaxoSmithKline, Merck and Sanofi Pasteur MSD. Screening and HPV testing
trials partially supported by Qiagen. Personal support: Travel grants to
scientific meetings and honorarium for consultancy are occasionally
granted by either GlaxoSmithKline, Merck, Sanofi Pasteur MSD.; LA:
Institutional support: HPV vaccine trials and epidemiological studies
sponsored by GlaxoSmithKline, Merck and Sanofi Pasteur MSD. Screening
and HPV testing trials partially supported by Qiagen. Personal support:
Travel grants to conferences occasionally granted by Merck and Sanofi
Pasteur MSD.
NR 161
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U1 1
U2 30
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 20
PY 2012
VL 30
SU 5
BP F34
EP F54
DI 10.1016/j.vaccine.2012.05.070
PG 21
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 063CX
UT WOS:000312974900006
PM 23199965
ER
PT J
AU Moscicki, AB
Schiffman, M
Burchell, A
Albero, G
Giuliano, AR
Goodman, MT
Kjaer, SK
Palefsky, J
AF Moscicki, Anna-Barbara
Schiffman, Mark
Burchell, Ann
Albero, Ginesa
Giuliano, Anna R.
Goodman, Marc T.
Kjaer, Susanne K.
Palefsky, Joel
TI Updating the Natural History of Human Papillomavirus and Anogenital
Cancers
SO VACCINE
LA English
DT Review
DE HPV; Natural history; Transmission; Male infections; Anal disease
ID CERVICAL INTRAEPITHELIAL NEOPLASIA; RISK HUMAN-PAPILLOMAVIRUS; HAWAII
HPV COHORT; POPULATION-BASED COHORT; YOUNG-WOMEN; PERSISTENT INFECTIONS;
HETEROSEXUAL COUPLES; UNIVERSITY-STUDENTS; SEXUAL-BEHAVIORS; GRADE 2/3
AB This chapter addresses the natural history of anogenital human papillomavirus (HPV) infection. Cervical infections are the best understood HPV infection. Cervical HPV persistence is the known necessary event for the development of cervical cancer. New infections appearing at any age are benign unless they persist. Several long-term natural history studies have now shed light on the very low risk of cervical intraepithelial neoplasia (CIN) 3+ in women past the peak of HPV acquisition (e.g., 30 or older) who are HPV-negative or clear their HPV. Although data on transmission of HPV are finally emerging, rates of transmission between heterosexual couples vary widely among studies. Factors that affect the calculations of these rates include a) intervals between testing points, b) rates of concordance or discordance at baseline, and c) difficulty in defining established infections versus contamination. Both cervix to anus and anus to cervix autoinoculation in the same woman appears to be quite common. Whether either site serves as a long-term reservoir is unknown. Studies show that anal infections in women and in men who have sex with men are quite common with cumulative rates up to 70-90%. Similarly, clearance of anal HPV is also common, with few individuals showing persistence unless they are human immunodeficiency virus (HIV)-infected. HIV strongly influences the development of anal intraepithelial neoplasia (AIN). The few studies on the natural history of AIN in HIV-infected men suggest that high-grade AIN is a precursor to invasive anal cancer. Although no natural history studies of AIN are available in women, women with other HPV-associated lesions, including CIN3+ and vulvar cancer, have higher rates of anal cancer. Data on the natural history of HPV of the male genitalia are also emerging, although penile intraepithelial neoplasia is poorly understood. Cumulative rates of HPV are extremely high in men and risks are associated with sexual behavior. Unlike women, prevalence rates are steady across all ages, suggesting that men do not develop protection against reinfection. This article forms part of a special supplement entitled "Comprehensive Control of HPV Infections and Related Diseases" Vaccine Volume 30, Supplement 5, 2012. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Moscicki, Anna-Barbara] Univ Calif San Francisco, Dept Pediat, Div Adolescent Med, San Francisco, CA 94143 USA.
[Schiffman, Mark] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Burchell, Ann] Ontario HIV Treatment Network, Toronto, ON, Canada.
[Burchell, Ann] Univ Toronto, Dalla Lana Sch Publ Hlth, Toronto, ON M5S 1A1, Canada.
[Burchell, Ann] McGill Univ, Dept Oncol, Div Canc Epidemiol, Montreal, PQ, Canada.
[Albero, Ginesa] Catalan Inst Oncol ICO, CERP, Unit Infect & Canc UNIC, Barcelona, Spain.
[Albero, Ginesa] CIBER Epidemiol & Salud Publ CIBERESP, Madrid, Spain.
[Giuliano, Anna R.] H Lee Moffitt Canc Ctr & Res Inst, Div Populat Sci, Tampa, FL USA.
[Goodman, Marc T.] Univ Hawaii, Canc Res Ctr, Honolulu, HI 96813 USA.
[Kjaer, Susanne K.] Danish Canc Soc, Res Ctr, Copenhagen, Denmark.
[Kjaer, Susanne K.] Univ Copenhagen, Rigshosp, Juliane Marie Ctr, Dept Gynecol & Obstet, DK-1168 Copenhagen, Denmark.
[Palefsky, Joel] Univ Calif San Francisco, Div Infect Dis, San Francisco, CA USA.
RP Moscicki, AB (reprint author), Univ Calif San Francisco, Dept Pediat, Div Adolescent Med, San Francisco, CA 94143 USA.
EM moscickia@peds.ucsf.edu
RI Albero, Ginesa/G-7248-2015;
OI Albero, Ginesa/0000-0002-9400-1914; Kjaer, Susanne/0000-0002-8347-1398
FU US Public Health Service (National Cancer Institute, National Institutes
of Health, Department of Health and Human Services) [R37 CA51323, NIH
R01 CA098803, R01 CA077318, R01 CA 88739, R01 CA54053]; Canadian
Institutes of Health Research; European Commission
[HEALTH-F3-2010-242061]; Instituto de Salud Carlos III [FIS PI08/1535,
RCESP C03/09, RTICESP C03/10, RTIC RD06/0020/0095, CIBERESP]; Agencia de
Gestio, d'Ajuts Universitaris i de Recerca [AGAUR 2005SGR00695, AGAUR
2009SGR126]; GenProbe; Bectin Dickinson; Merck Canada Ltd.; Qiagen;
GlaxoSmithKline; Merck; Sanofi Pasteur MSD; Roche; GSK; Merck Co., Inc.
FX Dr. Anna-Barbara Moscicki's work is supported by US Public Health
Service grant R37 CA51323 (National Cancer Institute, National
Institutes of Health, Department of Health and Human Services). Dr. Ann
Burchell's work is funded by a Canadian Institutes of Health Research
New Investigator award. Ginesa Albero's work is partially supported by
public grants from the European Commission (7th Framework Programme
grant HEALTH-F3-2010-242061, PREHDICT), from the Instituto de Salud
Carlos III (grants FIS PI08/1535, RCESP C03/09, RTICESP C03/10, RTIC
RD06/0020/0095 and CIBERESP), and from the Agencia de Gestio, d'Ajuts
Universitaris i de Recerca (grants AGAUR 2005SGR00695 and AGAUR
2009SGR126). Dr. Anna Giuliano's work is supported by US Public Health
Service grant NIH R01 CA098803 (National Cancer Institute, National
Institutes of Health, Department of Health and Human Services). Dr. Marc
Goodman's work is supported by US Public Health Service grant R01
CA077318 (National Cancer Institute, National Institutes of Health,
Department of Health and Human Services). Dr. Joel Palefsky's work is
supported by US Public Health Service grants R01 CA 88739 and R01
CA54053 (National Cancer Institute, National Institutes of Health,
Department of Health and Human Services). The authors would like to
thank Anthony Kung for manuscript preparation.; ABM serves as an
advisory board member for Merck and receives support for sexually
transmitted disease testing from GenProbe. She has also received travel
funds and an honorarium for speaking at a symposium supported by Bectin
Dickinson.; In the past, AB received an unrestricted research grant,
speaker fees, and media consultant fees from Merck Canada Ltd., but not
since 2010.; GA: Institutional support: Vaccine trials organized by
GlaxoSmithKline, Merck and Sanofi Pasteur MSD. Screening and HPV testing
trials partially supported by Qiagen. Personal support: Travel grants to
conferences/meetings are occasionally granted by either GlaxoSmithKline,
Merck, Sanofi Pasteur MSD, Roche or Qiagen.; ARG is on the Speakers
Bureau of Merck & Co., Inc., an advisor to Merck & Co., Inc., and has
received research grant support from both GSK and Merck & Co., Inc.; SKK
received lecture fees, advisory board fees, and research grants through
her institution from Merck and Sanofi Pasteur MSD.
NR 86
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U1 3
U2 37
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 20
PY 2012
VL 30
SU 5
BP F24
EP F33
DI 10.1016/j.vaccine.2012.05.089
PG 10
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 063CX
UT WOS:000312974900005
PM 23199964
ER
PT J
AU Schiller, JT
Castellsague, X
Garland, SM
AF Schiller, John T.
Castellsague, Xavier
Garland, Suzanne M.
TI A Review of Clinical Trials of Human Papillomavirus Prophylactic
Vaccines
SO VACCINE
LA English
DT Review
DE HPV; Prophylactic vaccine; Virus-like particle; Gardasil (R); Cervarix
(R); Clinical trials; Cervical cancer; Genital warts; CIN; VIN; VaIN
ID (HPV)-16/18 AS04-ADJUVANTED VACCINE; QUADRIVALENT HPV VACCINE;
CERVICAL-CANCER VACCINE; BLIND PATRICIA TRIAL; VIRUS-LIKE PARTICLES;
OF-STUDY ANALYSIS; AGED 18-45 YEARS; YOUNG-WOMEN; INTRAEPITHELIAL
NEOPLASIA; POOLED ANALYSIS
AB End of study analyses of the phase Ill trials of prophylactic human papillomavirus (HPV) virus-like particle (VLP) vaccines in young women are now largely completed. Two distinct vaccines were evaluated, Gardasil (R) (Merck & Co., Whitehouse Station, NJ USA) a quadrivalent vaccine containing VLPs of types 6, 11, 16 and 18 and Cervarix (R) (GlaxoSmithKline Biologicals, Rixensart, Belgium), a bivalent vaccine containing VLPs of types 16 and 18. Both vaccines exhibited excellent safety and immunogenicity profiles. The vaccines also demonstrated remarkably high and similar efficacy against the vaccine-targeted types for a range of cervical endpoints from persistent infection to cervical intraepithelial neoplasia grade 3 (CIN3) in women naive to the corresponding type at the time of vaccination. However, protection from incident infection or disease from non-vaccine types was restricted, and the vaccines had no effect on prevalent infection or disease. Gardasil (R) also demonstrated strong protection against genital warts and vulvar/vaginal neoplasia associated with the vaccine types. In other trials, Gardasil (R) protected mid-adult women from incident infection and CIN caused by the vaccine types and protected men for incident infection, genital warts and anal intraepithelial neoplasia by the vaccine types. Cervarix (R) protected against vaccine-targeted anal infections in women in an end of study evaluation. For practical reasons, efficacy studies have not been conducted in the primary target populations of current vaccination programs, adolescent girls and boys. However, immunogenicity bridging studies demonstrating excellent safety and strong immune responses in adolescence, coupled with the documentation of durable antibody responses and protection in young adults, leads to an optimistic projection of the effectiveness of the vaccines in adolescent vaccination programs. Taken together, the excellent clinical trial results strongly support the potential of the vaccines as high value public health interventions and justify their widespread implementation to prevent anogenital HPV infections and their associated neoplasia. This article forms part of a special supplement entitled "Comprehensive Control of HPV Infections and Related Diseases" Vaccine Volume 30, Supplement 5, 2012. Published by Elsevier Ltd.
C1 [Schiller, John T.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Castellsague, Xavier] Inst Catala Oncol, Unit Infect & Canc UNIC, CERP, Lhospitalet De Llobregat, Barcelona, Spain.
[Garland, Suzanne M.] Royal Womens Hosp, Reg World Hlth Org Human Papillomavirus Lab, Dept Microbiol & Infect Dis, Melbourne, Vic, Australia.
[Garland, Suzanne M.] Univ Melbourne, Dept Obstet & Gynaecol, Melbourne, Vic 3010, Australia.
[Garland, Suzanne M.] Royal Childrens Hosp, Dept Microbiol, Parkville, Vic, Australia.
[Garland, Suzanne M.] Murdoch Childrens Res Inst, Murdoch, WA, Australia.
RP Schiller, JT (reprint author), NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
EM schillej@mail.nih.gov
RI Castellsague Pique, Xavier/N-5795-2014
OI Castellsague Pique, Xavier/0000-0002-0802-3595
FU European Commission [HEALTH-F3-2010-242061]; Instituto de Salud Carlos
III (Spanish Government) [FIS PI10/02995, RCESP C03/09, RTICESP C03/10,
RTIC RD06/0020/0095, CIBERESP]; Agencia de Gestio d'Ajuts Universitaris
i de Recerca - Generalitat de Catalunya (Catalonian Government) [AGAUR
2005SGR00695, AGAUR 2009SGR126]; GlaxoSmithKline; Merck; Sanofi Pasteur
MSD; Qiagen; Commonwealth Serum Laboratories; Merck Co.
FX The work was partially supported by public grants from the European
Commission (7th Framework Programme grant HEALTH-F3-2010-242061,
PREHDICT), from the Instituto de Salud Carlos III (Spanish Government)
(grants FIS PI10/02995, RCESP C03/09, RTICESP C03/10, RTIC
RD06/0020/0095 and CIBERESP) and from the Agencia de Gestio d'Ajuts
Universitaris i de Recerca - Generalitat de Catalunya (Catalonian
Government) (grants AGAUR 2005SGR00695 and AGAUR 2009SGR126), who had no
role in data collection, analysis or interpretation of results.; XC:
Institutional support: HPV vaccine trials and epidemiological studies
sponsored by GlaxoSmithKline, Merck and Sanofi Pasteur MSD. Screening
and HPV testing trials partially supported by Qiagen. Personal support:
Travel grants to scientific meetings and honorarium for consultancy are
occasionally granted by either GlaxoSmithKline, Merck, Sanofi Pasteur
MSD.; SMG: Has received advisory board fees and grant support from
Commonwealth Serum Laboratories and GlaxoSmithKline, and lecture and
consultancy fees from Merck & Co. She has received grant support through
her institution from Merck & Co. and GlaxoSmithKline to do clinical
trials for HPV/cervical cancer vaccines.
NR 88
TC 227
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U1 20
U2 115
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 20
PY 2012
VL 30
SU 5
BP F123
EP F138
DI 10.1016/j.vaccine.2012.04.108
PG 16
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 063CX
UT WOS:000312974900014
PM 23199956
ER
PT J
AU Stanley, M
Pinto, LA
Trimble, C
AF Stanley, Margaret
Pinto, Ligia A.
Trimble, Connie
TI Human Papillomavirus Vaccines - Immune Responses
SO VACCINE
LA English
DT Review
DE HPV; virus like particle; VLP; antibody; B cells; L1 protein; L2
protein; cell mediated immunity
ID VIRUS-LIKE PARTICLES; HPV VACCINATION PROGRAM; INTRAEPITHELIAL
NEOPLASIA; ANTIBODY-RESPONSES; NATURAL-HISTORY; YOUNG-WOMEN; T-CELLS;
INFECTION; L1; TYPE-16
AB Prophylactic human papillomavirus (HPV) virus-like particle (VLP) vaccines are highly effective. The available evidence suggests that neutralising antibody is the mechanism of protection. However, despite the robust humoral response elicited by VLP vaccines, there is no immune correlate, no minimum level of antibody, or any other immune parameter, that predicts protection against infection or disease. The durability of the antibody response and the importance of antibody isotype, affinity and avidity for vaccine effectiveness are discussed. Once infection and disease are established, then cellular immune responses are essential to kill infected cells. These are complex processes and understanding the local mucosal immune response is a prerequisite for the rational design of therapeutic HPV vaccines. This article forms part of a special supplement entitled "Comprehensive Control of HPV Infections and Related Diseases" Vaccine Volume 30, Supplement 5, 2012. (C) 2012 Published by Elsevier Ltd.
C1 [Stanley, Margaret] Univ Cambridge, Dept Pathol, Cambridge CB2 1QP, England.
[Pinto, Ligia A.] NCI Frederick, HPV Immunol Lab, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Trimble, Connie] Johns Hopkins Univ Hosp, Dept Obstet Gynecol, Baltimore, MD 21287 USA.
[Trimble, Connie] Johns Hopkins Univ Hosp, Dept Oncol, Baltimore, MD 21287 USA.
[Trimble, Connie] Johns Hopkins Univ Hosp, Dept Pathol, Baltimore, MD 21287 USA.
RP Stanley, M (reprint author), Univ Cambridge, Dept Pathol, Tennis Court Rd, Cambridge CB2 1QP, England.
EM mas1001@cam.ac.uk
NR 53
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U1 3
U2 28
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 20
PY 2012
VL 30
SU 5
BP F83
EP F87
DI 10.1016/j.vaccine.2012.04.106
PG 5
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 063CX
UT WOS:000312974900009
PM 23199968
ER
PT J
AU Schotte, F
Cho, HS
Kaila, VRI
Kamikubo, H
Dashdorj, N
Henry, ER
Graber, TJ
Henning, R
Wulff, M
Hummer, G
Kataoka, M
Anfinrud, PA
AF Schotte, Friedrich
Cho, Hyun Sun
Kaila, Ville R. I.
Kamikubo, Hironari
Dashdorj, Naranbaatar
Henry, Eric R.
Graber, Timothy J.
Henning, Robert
Wulff, Michael
Hummer, Gerhard
Kataoka, Mikio
Anfinrud, Philip A.
TI Watching a signaling protein function in real time via 100-ps
time-resolved Laue crystallography
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE time-resolved X-ray diffraction; photoreceptor; light sensor
ID PHOTOACTIVE YELLOW PROTEIN; HALOPHILIC PHOTOTROPHIC BACTERIUM;
ECTOTHIORHODOSPIRA-HALOPHILA; PHOTOCYCLE INTERMEDIATE; PHOTORECEPTOR
PROTEIN; PH-DEPENDENCE; QUANTUM YIELD; E46Q MUTANT; SPECTROSCOPY;
KINETICS
AB To understand how signaling proteins function, it is crucial to know the time-ordered sequence of events that lead to the signaling state. We recently developed on the BioCARS 14-IDB beamline at the Advanced Photon Source the infrastructure required to characterize structural changes in protein crystals with near-atomic spatial resolution and 150-ps time resolution, and have used this capability to track the reversible photocycle of photoactive yellow protein (PYP) following trans-to-cis photoisomerization of its p-coumaric acid (pCA) chromophore over 10 decades of time. The first of four major intermediates characterized in this study is highly contorted, with the pCA carbonyl rotated nearly 90 out of the plane of the phenolate. A hydrogen bond between the pCA carbonyl and the Cys69 backbone constrains the chromophore in this unusual twisted conformation. Density functional theory calculations confirm that this structure is chemically plausible and corresponds to a strained cis intermediate. This unique structure is short-lived (similar to 600 ps), has not been observed in prior cryocrystallography experiments, and is the progenitor of intermediates characterized in previous nanosecond time-resolved Laue crystallography studies. The structural transitions unveiled during the PYP photocycle include trans/cis isomerization, the breaking and making of hydrogen bonds, formation/relaxation of strain, and gated water penetration into the interior of the protein. This mechanistically detailed, near-atomic resolution description of the complete PYP photocycle provides a framework for understanding signal transduction in proteins, and for assessing and validating theoretical/computational approaches in protein biophysics.
C1 [Schotte, Friedrich; Cho, Hyun Sun; Kaila, Ville R. I.; Dashdorj, Naranbaatar; Henry, Eric R.; Hummer, Gerhard; Anfinrud, Philip A.] NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
[Kamikubo, Hironari; Kataoka, Mikio] Nara Inst Sci & Technol, Grad Sch Mat Sci, Nara 6300192, Japan.
[Graber, Timothy J.; Henning, Robert] Univ Chicago, Ctr Adv Radiat Sources, Chicago, IL 60637 USA.
[Wulff, Michael] European Synchrotron Radiat Facil, Expt Div, F-38043 Grenoble, France.
RP Anfinrud, PA (reprint author), NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
EM anfinrud@nih.gov
RI Hummer, Gerhard/A-2546-2013; Henry, Eric/J-3414-2013; Kataoka,
Mikio/H-4402-2011
OI Hummer, Gerhard/0000-0001-7768-746X; Henry, Eric/0000-0002-5648-8696;
FU National Center for Research Resources [5P41RR007707]; National
Institute of General Medical Sciences from NIH [8P41GM103543]; US DOE
[DE-AC02-06CH11357]; Intramural Research Program of the National
Institute of Diabetes and Digestive and Kidney Diseases, NIH; European
Molecular Biology Organization
FX We thank Drs. Keith Moffat, Vukica Srajer, Hyocherl Ihee, and Yang Ouk
Jung for their contributions to earlier, collaborative time-resolved
Laue studies of PYP; Bernard Howder, Jr., for machining many of the
components required for this study; the Biowulf cluster at the National
Institutes of Health (NIH) for computer time; and the Advanced Photon
Source undulator group for reconfiguring and installing two short-period
undulators on the 14-IDB BioCARS beamline. Use of the BioCARS Sector 14
was supported by National Center for Research Resources Grant
5P41RR007707 and National Institute of General Medical Sciences Grant
8P41GM103543 from NIH. Use of the Advanced Photon Source, an Office of
Science User Facility operated for the US Department of Energy (DOE)
Office of Science by Argonne National Laboratory, was supported by US
DOE Contract DE-AC02-06CH11357. The time-resolved setup at Sector 14 was
funded in part through collaboration with P.A.A. This research was
supported by the Intramural Research Program of the National Institute
of Diabetes and Digestive and Kidney Diseases, NIH. V.R.I.K. is the
recipient of a European Molecular Biology Organization Long-Term
Fellowship. VMD was developed by the Theoretical and Computational
Biophysics Group in the Beckman Institute for Advanced Science and
Technology at the University of Illinois at Urbana-Champaign.
NR 36
TC 63
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U1 2
U2 75
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 20
PY 2012
VL 109
IS 47
BP 19256
EP 19261
DI 10.1073/pnas.1210938109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 049PZ
UT WOS:000311997200052
PM 23132943
ER
PT J
AU Furuta, K
Ishido, S
Roche, PA
AF Furuta, Kazuyuki
Ishido, Satoshi
Roche, Paul A.
TI Encounter with antigen-specific primed CD4 T cells promotes MHC class II
degradation in dendritic cells
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE T-cell activation; protein aggregation
ID PEPTIDE COMPLEXES; IN-VIVO; SURFACE; MOLECULES; RAFTS; INTERNALIZATION;
UBIQUITINATION; GLYCOPROTEINS; COMPARTMENTS; CHOLESTEROL
AB Major histocompatibility complex class II molecules (MHC-II) on antigen presenting cells (APCs) engage the TCR on antigen-specific CD4 T cells, thereby providing the specificity required for T cell priming and the induction of an effective immune response. In this study, we have asked whether antigen-loaded dendritic cells (DCs) that have been in contactwith antigen-specific CD4 T cells retain the ability to stimulate additional naive T cells. We show that encounter with antigen-specific primed CD4 T cells induces the degradation of surface MHC-II in antigen-loaded DCs and inhibits the ability of these DCs to stimulate additional naive CD4 T cells. Cross-linking with MHC-II mAb as a surrogate for T-cell engagement also inhibits APC function and induces MHC-II degradation by promoting the clustering of MHC-II present in lipid raft membrane microdomains, a process that leads to MHC-II endocytosis and degradation in lysosomes. Encounter of DCs with antigen-specific primed T cells or engagement of MHC-II with antibodies promotes the degradation of both immunologically relevant and irrelevant MHC-II molecules. These data demonstrate that engagement of MHC-II on DCs after encounter with antigen-specific primed CD4 T cells promotes the down-regulation of cell surface MHC-II in DCs, thereby attenuating additional activation of naive CD4 T cells by these APCs.
C1 [Furuta, Kazuyuki; Roche, Paul A.] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Ishido, Satoshi] RIKEN Res Ctr Allergy & Immunol, Lab Infect Immun, Yokohama, Kanagawa 2300045, Japan.
RP Roche, PA (reprint author), NCI, Expt Immunol Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM rochepa@mail.nih.gov
FU Ministry of Education, Culture, Sports, Science and Technology of Japan;
Japan Society for the Promotion of Science; National Institutes of
Health
FX We thank our many colleagues for the gifts of antibodies used in this
study. This work was supported by the Ministry of Education, Culture,
Sports, Science and Technology of Japan (S. I.), the Japan Society for
the Promotion of Science (S. I.), and the Intramural Research Program of
the National Institutes of Health (P.A.R.).
NR 33
TC 8
Z9 8
U1 1
U2 3
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 20
PY 2012
VL 109
IS 47
BP 19380
EP 19385
DI 10.1073/pnas.1213868109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 049PZ
UT WOS:000311997200073
PM 23129633
ER
PT J
AU Baum, BJ
Alevizos, I
Zheng, CY
Cotrim, AP
Liu, SY
McCullagh, L
Goldsmith, CM
Burbelo, PD
Citrin, DE
Mitchell, JB
Nottingham, LK
Rudy, SF
Van Waes, C
Whatley, MA
Brahim, JS
Chiorini, JA
Danielides, S
Turner, RJ
Patronas, NJ
Chen, CC
Nikolov, NP
Illei, GG
AF Baum, Bruce J.
Alevizos, Ilias
Zheng, Changyu
Cotrim, Ana P.
Liu, Shuying
McCullagh, Linda
Goldsmith, Corinne M.
Burbelo, Peter D.
Citrin, Deborah E.
Mitchell, James B.
Nottingham, Liesl K.
Rudy, Susan F.
Van Waes, Carter
Whatley, Millie A.
Brahim, Jaime S.
Chiorini, John A.
Danielides, Stamatina
Turner, R. James
Patronas, Nicholas J.
Chen, Clara C.
Nikolov, Nikolay P.
Illei, Gabor G.
TI Early responses to adenoviral-mediated transfer of the aquaporin-1 cDNA
for radiation-induced salivary hypofunction
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE gene therapy; radiation damage; salivary glands; dry mouth; water
channel
ID GENE-TRANSFER VECTORS; INCREASED FLUID SECRETION; CYSTIC-FIBROSIS
PATIENTS; PIG PAROTID-GLANDS; PHASE-I; RECOMBINANT ADENOVIRUS;
LOCAL-DELIVERY; INDIVIDUALS; XEROSTOMIA; MANAGEMENT
AB No conventional therapy exists for salivary hypofunction in surviving head and neck cancer patients with Radiation Therapy Oncology Group late grade 2-3 toxicity. We conducted a phase I clinical trial to test the safety and biologic efficacy of serotype 5, adenoviral-mediated aquaporin-1 cDNA transfer to a single previously irradiated parotid gland in 11 subjects using an open label, single-dose, dose-escalation design (AdhAQP1 vector; four dose tiers from 4.8 x 10(7) to 5.8 x 10(9) vector particles per gland). Treated subjects were followed at scheduled intervals. Multiple safety parameters were measured and biologic efficacy was evaluated with measurements of parotid salivary flow rate. Symptoms were assessed with a visual analog scale. All subjects tolerated vector delivery and study procedures well over the 42-d study period reported. No deaths, serious adverse events, or dose-limiting toxicities occurred. Generally, few adverse events occurred, and all were considered mild or moderate. No consistent changes were found in any clinical chemistry and hematology parameters measured. Objective responses were seen in six subjects, all at doses <5.8 x 10(9) vector particles per gland. Five of these six subjects also experienced subjective improvement in xerostomia. AdhAQP1 vector delivery to a single parotid gland was safe and transfer of the hAQP1 cDNA increased parotid flow and relieved symptoms in a subset of subjects.
C1 [Baum, Bruce J.; Alevizos, Ilias; Zheng, Changyu; Cotrim, Ana P.; Liu, Shuying; McCullagh, Linda; Goldsmith, Corinne M.; Chiorini, John A.; Danielides, Stamatina; Turner, R. James; Nikolov, Nikolay P.; Illei, Gabor G.] Natl Inst Dent & Craniofacial Res, Mol Physiol & Therapeut Branch, NIH, Bethesda, MD 20892 USA.
[Burbelo, Peter D.] Natl Inst Dent & Craniofacial Res, Neurobiol & Pain Therapeut Sect, NIH, Bethesda, MD 20892 USA.
[Citrin, Deborah E.] NCI, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Mitchell, James B.] NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Nottingham, Liesl K.; Rudy, Susan F.; Van Waes, Carter] Natl Inst Deafness & Other Commun Disorders, Head & Neck Surg Branch, NIH, Bethesda, MD 20892 USA.
[Whatley, Millie A.; Chen, Clara C.] NIH, Nucl Med Sect, Bethesda, MD 20892 USA.
[Patronas, Nicholas J.] NIH, Sect Neuroradiol Radiol & Imaging Sci, Ctr Clin, Bethesda, MD 20892 USA.
[Brahim, Jaime S.] Univ Maryland, Dept Oral Maxillofacial Surg, Baltimore, MD 21201 USA.
RP Baum, BJ (reprint author), Natl Inst Dent & Craniofacial Res, Mol Physiol & Therapeut Branch, NIH, Bethesda, MD 20892 USA.
EM bbaum@mail.nih.gov
FU The Intramural Research Program of the National Institute of Dental and
Craniofacial Research
FX We thank Dr. Jane Atkinson for many helpful suggestions during this
study. We thank Dr. Sarfaraz Hasni for help in the medical evaluation of
several subjects; Janet Rowan, RN for assistance with many subjects;
multiple physicians, for referring their patients to us; and the 11
study subjects, who gave so generously of their time and themselves,
enabling this trial to be conducted. The Intramural Research Program of
the National Institute of Dental and Craniofacial Research supported
this study.
NR 27
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Z9 54
U1 1
U2 11
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 20
PY 2012
VL 109
IS 47
BP 19403
EP 19407
DI 10.1073/pnas.1210662109
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 049PZ
UT WOS:000311997200077
PM 23129637
ER
PT J
AU Lockwood, WW
Zejnullahu, K
Bradner, JE
Varmus, H
AF Lockwood, William W.
Zejnullahu, Kreshnik
Bradner, James E.
Varmus, Harold
TI Sensitivity of human lung adenocarcinoma cell lines to targeted
inhibition of BET epigenetic signaling proteins
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE drug development; chromatin
ID BROMODOMAIN INHIBITION; C-MYC; TRANSCRIPTION; TUMORIGENESIS; CHROMATIN;
LEUKEMIA; BRD4; EXPRESSION; FAMILY; AP-1
AB Bromodomain and extra terminal domain (BET) proteins function as epigenetic signaling factors that associate with acetylated histones and facilitate transcription of target genes. Inhibitors targeting the activity of BET proteins have shown potent antiproliferative effects in hematological cancers through the suppression of c-MYC and downstream target genes. However, as the epigenetic landscape of a cell varies drastically depending on lineage, transcriptional coactivators such as BETs would be expected to have different targets in cancers derived from different cells of origin, and this may influence the activity and mechanism of action of BET inhibitors. To test this hypothesis, we treated a panel of lung adenocarcinoma (LAC) cell lines with the BET inhibitor JQ1 and found that a subset is acutely susceptible to BET inhibition. In contrast to blood tumors, we showthat LAC cells are inhibited by JQ1 through a mechanism independent of cMYC down-regulation. Through gene expression profiling, we discovered that the oncogenic transcription factor FOSL1 and its targets are suppressed by JQ1 in a dose-dependant manner. Knockdown of BRD4 also decreased FOSL1 levels, and inhibition of FOSL1 phenocopied the effects of JQ1 treatment, suggesting that loss of this transcription factor may be partly responsible for the cytotoxic effects of BET inhibition in LAC cells, although ectopic expression of FOSL1 alone did not rescue the phenotype. Together, these findings suggest that BET inhibitors may be useful in solid tumors and that cell-lineage-specific differences in transcriptional targets of BETs may influence the activity of inhibitors of these proteins in different cancer types.
C1 [Lockwood, William W.; Zejnullahu, Kreshnik; Varmus, Harold] NHGRI, Canc Biol & Genet Sect, Canc Genet Branch, NIH, Bethesda, MD 20892 USA.
[Zejnullahu, Kreshnik] Howard Hughes Med Inst, Chevy Chase, MD 20815 USA.
[Bradner, James E.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[Bradner, James E.] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
RP Lockwood, WW (reprint author), NHGRI, Canc Biol & Genet Sect, Canc Genet Branch, NIH, Bethesda, MD 20892 USA.
EM william.lockwood@nih.gov; harold.varmus@nih.gov
FU National Institutes of Health Intramural Research Program; Canadian
Institutes of Health Research Jean-Francois Saint Denis Fellowship in
Cancer Research
FX We thank Nancy Colburn and Matthew Young for providing the pFB-FRA1
construct. This work was funded by the National Institutes of Health
Intramural Research Program. W. W. L. is supported by the Canadian
Institutes of Health Research Jean-Francois Saint Denis Fellowship in
Cancer Research.
NR 24
TC 120
Z9 120
U1 4
U2 16
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 20
PY 2012
VL 109
IS 47
BP 19408
EP 19413
DI 10.1073/pnas.1216363109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 049PZ
UT WOS:000311997200078
PM 23129625
ER
PT J
AU Lussier, MP
Herring, BE
Nasu-Nishimura, Y
Neutzner, A
Karbowski, M
Youle, RJ
Nicoll, RA
Roche, KW
AF Lussier, Marc P.
Herring, Bruce E.
Nasu-Nishimura, Yukiko
Neutzner, Albert
Karbowski, Mariusz
Youle, Richard J.
Nicoll, Roger A.
Roche, Katherine W.
TI Ubiquitin ligase RNF167 regulates AMPA receptor-mediated synaptic
transmission
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE hippocampus; glutamate receptor; GluA2
ID ACTIVITY-DEPENDENT UBIQUITINATION; VENTRAL NERVE CORD; GLUTAMATE
RECEPTORS; PROTEASOME SYSTEM; C-ELEGANS; DEGRADATION; PROTEINS;
ABUNDANCE; NEURONS
AB AMPA receptors (AMPARs) mediate the majority of fast excitatory neurotransmission, and their density at postsynaptic sites determines synaptic strength. Ubiquitination is a posttranslational modification that dynamically regulates the synaptic expression of many proteins. However, very few of the ubiquitinating enzymes implicated in the process have been identified. In a screen to identify transmembrane RING domain-containing E3 ubiquitin ligases that regulate surface expression of AMPARs, we identified RNF167. Predominantly lysosomal, a subpopulation of RNF167 is located on the surface of cultured neurons. Using a RINGmutant RNF167 or a specific shRNA to eliminate endogenous RNF167, we demonstrate that AMPAR surface expression increases in hippocampal neurons with disrupted RNF167 activity and that RNF167 is involved in activity-dependent ubiquitination of AMPARs. In addition, RNF167 regulates synaptic AMPAR currents, whereas synaptic NMDAR currents are unaffected. Therefore, our study identifies RNF167 as a selective regulator of AMPAR-mediated neurotransmission and expands our understanding of how ubiquitination dynamically regulates excitatory synapses.
C1 [Herring, Bruce E.; Nicoll, Roger A.] Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA.
[Herring, Bruce E.; Nicoll, Roger A.] Univ Calif San Francisco, Dept Physiol, San Francisco, CA 94143 USA.
[Lussier, Marc P.; Nasu-Nishimura, Yukiko; Roche, Katherine W.] NINDS, Receptor Biol Sect, NIH, Bethesda, MD 20892 USA.
[Neutzner, Albert; Karbowski, Mariusz; Youle, Richard J.] NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
RP Nicoll, RA (reprint author), Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA.
EM nicoll@cmp.ucsf.edu; rochek@ninds.nih.gov
OI Neutzner, Albert/0000-0001-9254-5558; Roche,
Katherine/0000-0001-7282-6539
FU The NINDS Intramural Research Program; National Institute of Mental
Health; Le Fond de la Recherche en Sante du Quebec; Brain and Behavior
Research Foundation
FX We thank John D. Badger II for technical assistance, Dr. Dragan Maric
for advice and expertise with the FACS analysis, and the National
Institute of Neurological Disorders and Stroke (NINDS) DNA sequencing
facility. The NINDS Intramural Research Program (K. W. R. and R.J.Y.)
and the National Institute of Mental Health (R.A.N.) supported this
research. M. P. L. is the recipient of a postdoctoral fellowship from Le
Fond de la Recherche en Sante du Quebec, and B. E. H. receives support
from the Brain and Behavior Research Foundation.
NR 33
TC 23
Z9 24
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 20
PY 2012
VL 109
IS 47
BP 19426
EP 19431
DI 10.1073/pnas.1217477109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 049PZ
UT WOS:000311997200081
PM 23129617
ER
PT J
AU Robertson, CE
Martin, A
Baker, CI
Baron-Cohen, S
AF Robertson, Caroline E.
Martin, Alex
Baker, Chris I.
Baron-Cohen, Simon
TI Atypical Integration of Motion Signals in Autism Spectrum Conditions
SO PLOS ONE
LA English
DT Article
ID DORSAL VISUAL PATHWAY; BIOLOGICAL MOTION; PARIETAL CORTEX; PERCEPTUAL
DECISION; DOUBLE DISSOCIATION; TRANSPARENT MOTION; ASPERGER SYNDROME;
JOINT ATTENTION; REACTION-TIME; NEURAL BASIS
AB Vision in Autism Spectrum Conditions (ASC) is characterized by enhanced perception of local elements, but impaired perception of global percepts. Deficits in coherent motion perception seem to support this characterization, but the roots and robustness of such deficits remain unclear. We aimed to investigate the dynamics of the perceptual decision-making network known to support coherent motion perception. In a series of forced-choice coherent motion perception tests, we parametrically varied a single stimulus dimension, viewing duration, to test whether the rate at which evidence is accumulated towards a global decision is atypical in ASC. 40 adult participants (20 ASC) performed a classic motion discrimination task, manually indicating the global direction of motion in a random-dot kinematogram across a range of coherence levels (2-75%) and stimulus-viewing durations (200-1500 ms). We report a deficit in global motion perception at short viewing durations in ASC. Critically, however, we found that increasing the amount of time over which motion signals could be integrated reduced the magnitude of the deficit, such that at the longest duration there was no difference between the ASC and control groups. Further, the deficit in motion integration at the shortest duration was significantly associated with the severity of autistic symptoms in our clinical population, and was independent from measures of intelligence. These results point to atypical integration of motion signals during the construction of a global percept in ASC. Based on the neural correlates of decision-making in global motion perception our findings suggest the global motion deficit observed in ASC could reflect a slower or more variable response from the primary motion area of the brain or longer accumulation of evidence towards a decision-bound in parietal areas.
C1 [Robertson, Caroline E.; Baron-Cohen, Simon] Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge, England.
[Robertson, Caroline E.; Martin, Alex; Baker, Chris I.] NIMH, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
RP Robertson, CE (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge, England.
EM cr419@cam.ac.uk
OI , Caroline/0000-0002-1858-6594; Baker, Chris/0000-0001-6861-8964
FU Intramural Research Program of the National Institute of Mental Health;
Medical Research Council (UK); Gates-Cambridge Trust; NIH-Cambridge
Fellowship
FX This work was supported by the Intramural Research Program of the
National Institute of Mental Health and the Medical Research Council
(UK) (http://www.mrc.ac.uk). CER was supported by the Gates-Cambridge
Trust and the NIH-Cambridge Fellowship. The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 64
TC 16
Z9 16
U1 2
U2 22
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 20
PY 2012
VL 7
IS 11
AR e48173
DI 10.1371/journal.pone.0048173
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 043II
UT WOS:000311535700008
PM 23185249
ER
PT J
AU Saito, K
Matsumoto, S
Yasui, H
Devasahayam, N
Subramanian, S
Munasinghe, JP
Patel, V
Gutkind, JS
Mitchell, JB
Krishna, MC
AF Saito, Keita
Matsumoto, Shingo
Yasui, Hironobu
Devasahayam, Nallathamby
Subramanian, Sankaran
Munasinghe, Jeeva P.
Patel, Vyomesh
Gutkind, J. Silvio
Mitchell, James B.
Krishna, Murali C.
TI Longitudinal Imaging Studies of Tumor Microenvironment in Mice Treated
with the mTOR Inhibitor Rapamycin
SO PLOS ONE
LA English
DT Article
ID ELECTRON-PARAMAGNETIC-RESONANCE; ENDOTHELIAL GROWTH-FACTOR; NECK-CANCER;
MAMMALIAN TARGET; HYPERBARIC-OXYGEN; CYCLING HYPOXIA; VASCULATURE;
PATHWAY; HEAD; ANGIOGENESIS
AB Rapamycin is an allosteric inhibitor of mammalian target of rapamycin, and inhibits tumor growth and angiogenesis. Recent studies suggested a possibility that rapamycin renormalizes aberrant tumor vasculature and improves tumor oxygenation. The longitudinal effects of rapamycin on angiogenesis and tumor oxygenation were evaluated in murine squamous cell carcinoma (SCCVII) by electron paramagnetic resonance imaging (EPRI) and magnetic resonance imaging (MRI) to identify an optimal time after rapamycin treatment for enhanced tumor radioresponse. Rapamycin treatment was initiated on SCCVII solid tumors 8 days after implantation (500-750 mm(3)) and measurements of tumor pO(2) and blood volume were conducted from day 8 to 14 by EPRI/MRI. Microvessel density was evaluated over the same time period by immunohistochemical analysis. Tumor blood volume as measured by MRI significantly decreased 2 days after rapamycin treatment. Tumor pO(2) levels modestly but significantly increased 2 days after rapamycin treatment; whereas, it decreased in non-treated control tumors. Furthermore, the fraction of hypoxic area (pixels with pO(2)<10 mm Hg) in the tumor region decreased 2 days after rapamycin treatments. Immunohistochemical analysis of tumor microvessel density and pericyte coverage revealed that microvessel density decreased 2 days after rapamycin treatment, but pericyte coverage did not change, similar to what was seen with anti-angiogenic agents such as sunitinib which cause vascular renormalization. Collectively, EPRI/MRI co-imaging can provide non-invasive evidence of rapamycin-induced vascular renormalization and resultant transient increase in tumor oxygenation. Improved oxygenation by rapamycin treatment provides a temporal window for anti-cancer therapies to realize enhanced response to radiotherapy.
C1 [Saito, Keita; Matsumoto, Shingo; Yasui, Hironobu; Devasahayam, Nallathamby; Subramanian, Sankaran; Mitchell, James B.; Krishna, Murali C.] NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Yasui, Hironobu] Hokkaido Univ, Grad Sch Vet Med, Dept Environm Vet Sci, Radiat Biol Lab, Sapporo, Hokkaido, Japan.
[Munasinghe, Jeeva P.] Natl Inst Neurol Disorder & Stroke, NIH, Bethesda, MD USA.
[Patel, Vyomesh; Gutkind, J. Silvio] Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD USA.
RP Krishna, MC (reprint author), NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM murali@helix.nih.gov
FU Intramural Research Program, Center for Cancer Research, National Cancer
Institute, National Institutes of Health
FX This work 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 42
TC 14
Z9 14
U1 2
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 20
PY 2012
VL 7
IS 11
AR e49456
DI 10.1371/journal.pone.0049456
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 043II
UT WOS:000311535700034
PM 23185335
ER
PT J
AU Yoneyama, K
Gjesdal, O
Choi, EY
Wu, CO
Hundley, WG
Gomes, AS
Liu, CY
McClelland, RL
Bluemke, DA
Lima, JAC
AF Yoneyama, Kihei
Gjesdal, Ola
Choi, Eui-Young
Wu, Colin O.
Hundley, W. Gregory
Gomes, Antoinette S.
Liu, Chia-Ying
McClelland, Robyn L.
Bluemke, David A.
Lima, Joao A. C.
TI Age, Sex, and Hypertension-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 Article
DE aging; blood pressure; cardiac function; cardiac output; hypertrophy;
magnetic resonance imaging; ventricular remodeling
ID SPECKLE-TRACKING ECHOCARDIOGRAPHY; CANINE LEFT-VENTRICLE; ROTATIONAL
DEFORMATION; MYOCARDIAL-INFARCTION; SYSTOLIC FUNCTION; HEART-FAILURE;
APEX ROTATION; NORMAL VALUES; DOPPLER; RELAXATION
AB Background-The aim of the present study was to evaluate how torsion is influenced by left ventricular (LV) remodeling associated with age, sex, and hypertension in a large community-based population.
Methods and Results-Myocardial shortening and torsion were assessed by tagged cardiac magnetic resonance in 1478 participants without clinically apparent cardiovascular disease in the Multi-Ethnic Study of Atherosclerosis (MESA). Torsion was defined as the difference between apical and basal rotation divided by slice distance. In multivariable linear regression models, older age was associated with lower stroke volume (-3.6 mL per decade; P<0.001) and higher LV mass-to-volume ratio (0.03 g/mL per decade; P<0.001), along with lower circumferential shortening (-0.17% per decade; P<0.05). Torsion, however, was greater at older ages (0.14 degrees per decade; P<0.001) and in women (0.37 degrees/cm versus men; P<0.001). Hypertensive participants had higher LV mass and LV mass-to-volume ratio (15.5 g and 0.07 g/mL, respectively; P<0.001 for both). Circumferential shortening was lower in hypertensive (-0.42%; P<0.01), whereas torsion was higher after adjustment for age and sex (0.17 degrees/cm; P<0.05).
Conclusions-Older age is associated with lower LV volumes and greater relative wall thickness and is accompanied by lower circumferential myocardial shortening, whereas torsion is greater with older age. Hypertensive individuals have greater LV volumes and relative wall thickness and lower circumferential shortening. Torsion, however, is greater in hypertension independently of age and sex. Torsion may therefore represent a compensatory mechanism to maintain an adequate stroke volume and cardiac output in the face of the progressively reduced LV volumes and myocardial shortening associated with hypertension and aging. (Circulation. 2012; 126: 2481-2490.)
C1 [Yoneyama, Kihei; Gjesdal, Ola; Choi, Eui-Young; Liu, Chia-Ying; Lima, Joao A. C.] Johns Hopkins Univ, Dept Cardiol, Baltimore, MD 21287 USA.
[Wu, Colin O.] NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
[Hundley, W. Gregory] Wake Forest Univ Hlth Sci, Dept Internal Med Cardiol, Winston Salem, NC USA.
[Gomes, Antoinette S.] Univ Calif Los Angeles, Sch Med, Dept Radiol, Los Angeles, CA 90024 USA.
[McClelland, Robyn L.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Bluemke, David A.] Natl Inst Biomed Imaging & Bioengn, NIH, Ctr Clin, Bethesda, MD USA.
RP Lima, JAC (reprint author), Johns Hopkins Univ, Johns Hopkins Hosp, Blalock 524D1,600 N Wolfe St, Baltimore, MD 21287 USA.
EM jlima@jhmi.edu
OI Gjesdal, Ola/0000-0003-1913-6445; Bluemke, David/0000-0002-8323-8086
FU National Heart, Lung and Blood Institute [N01-HC-95159, N01-HC-95169];
Fulbright Foundation; Norwegian Medical Association; Norwegian Research
Council
FX This research was supported by contracts N01-HC-95159 through
N01-HC-95169 from the National Heart, Lung and Blood Institute.; Dr
Gjesdal received support from the Fulbright Foundation, the Norwegian
Medical Association, and the Norwegian Research Council.
NR 46
TC 36
Z9 39
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 20
PY 2012
VL 126
IS 21
BP 2481
EP 2490
DI 10.1161/CIRCULATIONAHA.112.093146
PG 10
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 040SF
UT WOS:000311342600013
PM 23147172
ER
PT J
AU Thomas, CG
Li, RH
Smith, HE
Woodruff, GC
Oliver, B
Haag, ES
AF Thomas, Cristel G.
Li, Renhua
Smith, Harold E.
Woodruff, Gavin C.
Oliver, Brian
Haag, Eric S.
TI Simplification and Desexualization of Gene Expression in Self-Fertile
Nematodes
SO CURRENT BIOLOGY
LA English
DT Article
ID CAENORHABDITIS-ELEGANS; LINKED SITES; GENOME SIZE; RNA-SEQ; EVOLUTION;
SELECTION; HERMAPHRODITISM; TRANSCRIPTOME; PHYLOGENY; SEQUENCES
AB Evolutionary transitions between sexual modes could be potent forces in genome evolution [1, 2]. Several Caenorhabditis nematode species have evolved self-fertile hermaphrodites from the obligately outcrossing females of their ancestors [3]. We explored the relationship between sexual mode and global gene expression by comparing two selfing species, C. elegans and C. briggsae, with three phylogenetically informative outcrossing relatives, C. remanei, C. brenneri, and C. japonica. Adult transcriptome assemblies from the selfing species are consistently and strikingly smaller than those of the outcrossing species. Against this background of overall simplification, genes conserved in multiple outcrossing species with strong sex-biased expression are even more likely to be missing from the genomes of the selfing species. In addition, the sexual regulation of remaining transcripts has diverged markedly from the ancestral pattern in both selfing lineages, though in distinct ways. Thus, both the complexity and the sexual specialization of transciptomes are rapidly altered in response to the evolution of self-fertility. These changes may result from the combination of relaxed sexual selection and a recently reported genetic mechanism favoring genome shrinkage [4] in partial selfers.
C1 [Thomas, Cristel G.; Woodruff, Gavin C.; Haag, Eric S.] Univ Maryland, Dept Biol, College Pk, MD 20742 USA.
[Thomas, Cristel G.; Haag, Eric S.] Univ Maryland, Program Mol & Cell Biol, College Pk, MD 20742 USA.
[Li, Renhua; Smith, Harold E.; Oliver, Brian] NIDDKD, NIH, Bethesda, MD 20892 USA.
RP Haag, ES (reprint author), Univ Maryland, Dept Biol, College Pk, MD 20742 USA.
EM ehaag@umd.edu
FU National Institutes of Health (NIH); Ron Ellis for strains; Intramural
Research Program of the NIH; National Institute of Diabetes and
Digestive and Kidney Diseases; NIH [5R01GM079414]
FX The authors wish to thank Ian Korf and WormBase staff for bioinformatics
assistance and the Institute for Bioscience and Biotechnology Research
(IBBR) sequencing core for generating C. briggsae sequencing data. We
thank the Caenorhabditis Genetics Center, which is supported by awards
from the National Institutes of Health (NIH), and Ron Ellis for strains.
This work was supported by the Intramural Research Program of the NIH,
The National Institute of Diabetes and Digestive and Kidney Diseases (to
B.O. and H.E.S.), and NIH grant 5R01GM079414 (to E.S.H.).
NR 32
TC 25
Z9 25
U1 3
U2 21
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0960-9822
EI 1879-0445
J9 CURR BIOL
JI Curr. Biol.
PD NOV 20
PY 2012
VL 22
IS 22
BP 2167
EP 2172
DI 10.1016/j.cub.2012.09.038
PG 6
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 043DT
UT WOS:000311523800027
PM 23103191
ER
PT J
AU Klein, HG
Natanson, C
AF Klein, Harvey G.
Natanson, Charles
TI Red Blood Cell Transfusion
SO ANNALS OF INTERNAL MEDICINE
LA English
DT Letter
C1 [Klein, Harvey G.; Natanson, Charles] NIH, Bethesda, MD 20892 USA.
RP Klein, HG (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
NR 5
TC 2
Z9 2
U1 0
U2 0
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 20
PY 2012
VL 157
IS 10
BP 753
EP 754
DI 10.7326/0003-4819-157-10-201211200-00019
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 043VZ
UT WOS:000311580000026
PM 23165669
ER
PT J
AU Polis, MA
AF Polis, Michael A.
TI Preexposure prophylaxis reduced HIV-1 spread in serodiscordant
heterosexual couples
SO ANNALS OF INTERNAL MEDICINE
LA English
DT Editorial Material
C1 NIAID, Bethesda, MD 20892 USA.
RP Polis, MA (reprint author), NIAID, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 2
TC 1
Z9 1
U1 0
U2 1
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 20
PY 2012
VL 157
IS 10
AR JC5-3
DI 10.7326/0003-4819-157-10-201211200-02003
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 043VZ
UT WOS:000311580000002
PM 23165679
ER
PT J
AU Merchant, MS
Geller, JI
Baird, K
Chou, AJ
Galli, S
Charles, A
Amaoko, M
Rhee, EH
Price, A
Wexler, LH
Meyers, PA
Widemann, BC
Tsokos, M
Mackall, CL
AF Merchant, Melinda S.
Geller, James I.
Baird, Kristin
Chou, Alexander J.
Galli, Susana
Charles, Ava
Amaoko, Martha
Rhee, Eunice H.
Price, Anita
Wexler, Leonard H.
Meyers, Paul A.
Widemann, Brigitte C.
Tsokos, Maria
Mackall, Crystal L.
TI Phase I Trial and Pharmacokinetic Study of Lexatumumab in Pediatric
Patients With Solid Tumors
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID APOPTOSIS-INDUCING LIGAND; TRAIL-INDUCED APOPTOSIS; EWINGS-SARCOMA
FAMILY; CELLS; SENSITIVITY; RESISTANT; TOXICITY; CANCERS
AB Purpose
Lexatumumab is an agonistic, fully human monoclonal antibody against tumor necrosis factor-related apoptosis-inducing ligand receptor 2 with preclinical evidence of activity in pediatric solid tumors.
Patients and Methods
This phase I dose-escalation study examined the safety, tolerability, pharmacokinetics, and immunogenicity of lexatumumab at doses up to, but not exceeding, the adult maximum-tolerated dose (3, 5, 8, and 10 mg/kg), administered once every 2 weeks to patients age <= 21 years with recurrent or progressive solid tumors.
Results
Twenty-four patients received a total of 56 cycles of lexatumumab over all four planned dose levels. One patient had grade 2 pericarditis consistent with radiation recall, and one patient developed grade 3 pneumonia with hypoxia during the second cycle. Five patients experienced stable disease for three to 24 cycles. No patients experienced complete or partial response, but several showed evidence of antitumor activity, including one patient with recurrent progressive osteosarcoma who experienced resolution of clinical symptoms and positron emission tomography activity, ongoing more than 1 year off therapy. One patient with hepatoblastoma showed a dramatic biomarker response.
Conclusion
Pediatric patients tolerate 10 mg/kg of lexatumumab administered once every 14 days, the maximum-tolerated dose identified in adults. The drug seems to mediate some clinical activity in pediatric solid tumors and may work with radiation to enhance antitumor effects.
C1 [Merchant, Melinda S.; Baird, Kristin; Galli, Susana; Widemann, Brigitte C.; Tsokos, Maria; Mackall, Crystal L.] NCI, Bethesda, MD 20892 USA.
[Amaoko, Martha; Rhee, Eunice H.] NIH, Bethesda, MD 20892 USA.
[Chou, Alexander J.; Charles, Ava; Price, Anita; Wexler, Leonard H.; Meyers, Paul A.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Geller, James I.] Cincinnati Childrens Hosp, Cincinnati, OH USA.
RP Merchant, MS (reprint author), 10 Ctr Dr,Bldg 10 CRC,Room 1W-3750, Bethesda, MD 20892 USA.
EM merchanm@mail.nih.gov
OI Price, Anita/0000-0002-3917-6666; Meyers, Paul/0000-0001-6146-6101;
Chou, Alexander/0000-0002-7926-3326
FU Intramural Research Program of the National Cancer Institute, National
Institutes of Health; Clinical Research Training Program, National
Institutes of Health
FX Supported in part by the Intramural Research Program of the National
Cancer Institute, National Institutes of Health, and by the Clinical
Research Training Program, National Institutes of Health (M. A.,
E.H.R.).
NR 24
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U1 0
U2 4
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 2012
VL 30
IS 33
BP 4141
EP 4147
DI 10.1200/JCO.2012.44.1055
PG 7
WC Oncology
SC Oncology
GA 040DF
UT WOS:000311300000024
PM 23071222
ER
PT J
AU Chirinos, JA
Kips, JG
Jacobs, DR
Brumback, L
Duprez, DA
Kronmal, R
Bluemke, DA
Townsend, RR
Vermeersch, S
Segers, P
AF Chirinos, Julio A.
Kips, Jan G.
Jacobs, David R., Jr.
Brumback, Lyndia
Duprez, Daniel A.
Kronmal, Richard
Bluemke, David A.
Townsend, Raymond R.
Vermeersch, Sebastian
Segers, Patrick
TI Arterial Wave Reflections and Incident Cardiovascular Events and Heart
Failure: MESA (Multiethnic Study of Atherosclerosis)
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Article
DE arterial hemodynamics; cardiovascular risk; heart failure; left
ventricular afterload; wave reflections
ID LEFT-VENTRICULAR MASS; INPUT IMPEDANCE; ALL-CAUSE; PRESSURE;
RECLASSIFICATION; PREDICTION; STIFFNESS; VELOCITY; DISEASE; FORMS
AB Objectives This study sought to assess the relationship between central pressure profiles and cardiovascular events (CVEs) in a large community-based sample.
Background Experimental and physiologic data mechanistically implicate wave reflections in the pathogenesis of left ventricular failure and cardiovascular disease, but their association with these outcomes in the general population is unclear.
Methods Aortic pressure waveforms were derived from a generalized transfer function applied to the radial pressure waveform recorded noninvasively from 5,960 participants in the Multiethnic Study of Atherosclerosis. The central pressure waveform was separated into forward and reflected waves using a physiologic flow waveform. Reflection magnitude (RM = [Reflected/Forward wave amplitude] x 100), augmentation index ([Second/First systolic peak] x 100) and pulse pressure amplification ([Radial/aortic pulse pressure] x 100) were assessed as predictors of CVEs and congestive heart failure (CHF) during a median follow-up of 7.61 years.
Results After adjustment for established risk factors, aortic AIx independently predicted hard CVEs (hazard ratio [HR] per 10% increase: 1.08; 95% confidence interval [CI]: 1.01 to 1.14; p = 0.016), whereas PPA independently predicted all CVEs (HR per 10% increase: 0.82; 95% CI: 0.70 to 0.96; p = 0.012). RM was independently predictive of all CVEs (HR per 10% increase: 1.34; 95% CI: 1.08 to 1.67; p = 0.009) and hard CVEs (HR per 10% increase: 1.46; 95% CI: 1.12 to 1.90; p = 0.006) and was strongly predictive of new-onset CHF (HR per 10% increase: 2.69; 95% CI: 1.79 to 4.04; p < 0.0001), comparing favorably to other risk factors for CHF as per various measures of model performance, reclassification, and discrimination. In a fully adjusted model, compared to nonhypertensive subjects with low RM, the HRs (95% CI) for hypertensive subjects with low RM, nonhypertensive subjects with high RM, and hypertensive subjects with high RM were 1.81 (0.85 to 3.86), 2.16 (1.07 to 5.01), and 3.98 (1.96 to 8.05), respectively.
Conclusions Arterial wave reflections represent a novel strong risk factor for CHF in the general population. (J Am Coll Cardiol 2012;60:2170-7) (C) 2012 by the American College of Cardiology Foundation
C1 [Chirinos, Julio A.] Univ Penn, Sch Med, Dept Cardiol, Philadelphia, PA 19104 USA.
[Chirinos, Julio A.; Townsend, Raymond R.] Philadelphia VA Med Ctr, Philadelphia, PA USA.
[Kips, Jan G.; Vermeersch, Sebastian; Segers, Patrick] Univ Ghent, IBiTech, B-9000 Ghent, Belgium.
[Jacobs, David R., Jr.] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Jacobs, David R., Jr.] Univ Oslo, Dept Nutr, Oslo, Norway.
[Brumback, Lyndia; Kronmal, Richard] Univ Washington, Sch Publ Hlth, Dept Biostat, Seattle, WA 98195 USA.
[Duprez, Daniel A.] Univ Minnesota, Sch Med, Div Cardiol, Minneapolis, MN 55455 USA.
[Bluemke, David A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
RP Chirinos, JA (reprint author), Univ Penn, Sch Med, Dept Cardiol, Rm 8B111,Univ & Woodland Ave, Philadelphia, PA 19104 USA.
EM julio.chirinos@uphs.upenn.edu
OI Bluemke, David/0000-0002-8323-8086
FU National Heart, Lung, and Blood Institute [N01-HC-95159, N01-HC-95169];
American Heart Association grants [0885031N, R01-HL-098382]; Atcor
Medical; Cardiodynamics; APC cardiovascular; Novartis; Genentech;
Amarin; Merck; Pfizer; Boehringer Ingelheim; [RR-024156]
FX This research was supported by contracts N01-HC-95159 through
N01-HC-95169 from the National Heart, Lung, and Blood Institute and
RR-024156 as well as American Heart Association grants 0885031N and
R01-HL-098382. Dr. Chirinos has received minor support (equipment loans)
from Atcor Medical, Cardiodynamics, and APC cardiovascular. Dr. Duprez
has received research grants from Novartis, Genentech, and Amarin; and
speakers' fees from Merck, Pfizer, Novartis, and Boehringer Ingelheim.
All other authors have reported that they have no relationships relevant
to the contents of this paper to disclose.
NR 34
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U1 4
U2 13
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
EI 1558-3597
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 20
PY 2012
VL 60
IS 21
BP 2170
EP 2177
DI 10.1016/j.jacc.2012.07.054
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 037CC
UT WOS:000311077600007
PM 23103044
ER
PT J
AU Danaher, MR
Schisterman, EF
Roy, A
Albert, PS
AF Danaher, M. R.
Schisterman, E. F.
Roy, A.
Albert, P. S.
TI Estimation of gene-environment interaction by pooling biospecimens
SO STATISTICS IN MEDICINE
LA English
DT Article
DE allele frequency measurements; case-control study; cost efficiency;
logistic regression; power
ID SNP ALLELE FREQUENCIES; POOLED DNA SAMPLES; SINGLE-NUCLEOTIDE
POLYMORPHISMS; TOF MASS-SPECTROMETRY; PRIMER EXTENSION; DISEASE; DESIGN;
ASSOCIATION; BIOMARKERS; DHPLC
AB Case-control studies are prone to low power for testing geneenvironment interactions (GXE) given the need for a sufficient number of individuals on each strata of disease, gene, and environment. We propose a new study design to increase power by strategically pooling biospecimens. Pooling biospecimens allows us to increase the number of subjects significantly, thereby providing substantial increase in power. We focus on a special, although realistic case, where disease and environmental statuses are binary, and gene status is ordinal with each individual having 0, 1, or 2 minor alleles. Through pooling, we obtain an allele frequency for each level of disease and environmental status. Using the allele frequencies, we develop a new methodology for estimating and testing GXE that is comparable to the situation when we have complete data on gene status for each individual. We also explore the measurement process and its effect on the GXE estimator. Using an illustration, we show the effectiveness of pooling with an epidemiologic study, which tests an interaction for fiber and paraoxonase on anovulation. Through simulation, we show that taking 12 pooled measurements from 1000 individuals achieves more power than individually genotyping 500 individuals. Our findings suggest that strategic pooling should be considered when an investigator designs a pilot study to test for a GXE. Published 2012. This article is a US Government work and is in the public domain in the USA.
C1 [Danaher, M. R.; Schisterman, E. F.; Roy, A.; Albert, P. S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, Rockville, MD USA.
[Danaher, M. R.] Univ Maryland Baltimore Cty, Baltimore, MD 21228 USA.
RP Schisterman, EF (reprint author), NICHD, Div Epidemiol Stat & Prevent Res, NIH, 6100 Execut Blvd,Rm 7B03, Rockville, MD 20852 USA.
EM schistee@mail.nih.gov
OI Schisterman, Enrique/0000-0003-3757-641X
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health; Long-Range Research
Initiative of the American Chemistry Council
FX This research was supported partially by the Intramural Research Program
of the Eunice Kennedy Shriver National Institute of Child Health and
Human Development, National Institutes of Health and by the Long-Range
Research Initiative of the American Chemistry Council.
NR 26
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U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD NOV 20
PY 2012
VL 31
IS 26
BP 3241
EP 3252
DI 10.1002/sim.5357
PG 12
WC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Medicine, Research &
Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Research & Experimental
Medicine; Mathematics
GA 019NA
UT WOS:000309745400012
PM 22859290
ER
PT J
AU Agarwal, S
Nettleton, JA
de Roer, I
Ix, JH
Siscovick, D
Eng, J
Bild, D
Burke, GL
Herrington, DM
AF Agarwal, Subhashish
Nettleton, Jennifer A.
de Roer, Ian
Ix, Joachim H.
Siscovick, David
Eng, John
Bild, Diane
Burke, Gregory L.
Herrington, David M.
TI The Association of Calcium Supplementation and Incident Cardiovascular
Events: Multi-Ethnic Study of Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
DE Nutrition; Cardiovascular disease prevention; Population science
C1 [Agarwal, Subhashish] Oakwood Hosp, Med Cntr, Dearborn, MI USA.
[Nettleton, Jennifer A.] Univ Texas Houston, Sch Publ Hlth, Div Epidemiol Human Genet & Environm Sci, Houston, TX USA.
[de Roer, Ian] Univ Washington, Dept Nephrol, Seattle, WA 98195 USA.
[Ix, Joachim H.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Ix, Joachim H.] San Diego Vet Affairs Healthcare Syst, San Diego, CA USA.
[Siscovick, David] Univ Washington, Dept Epidemiol, Cardiovasc Hlth Rsch Unit, Seattle, WA 98195 USA.
[Eng, John] Johns Hopkins Univ, Baltimore, MD USA.
[Bild, Diane] NHLBI, Prevent & Populat Sci Program, Bethesda, MD 20892 USA.
[Burke, Gregory L.] Wake Forest Univ Hlth Sci, Dept Publ Hlth Sci, Winston Salem, NC USA.
[Herrington, David M.] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 9231
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885000058
ER
PT J
AU Ahmet, I
Tae, HJ
Brines, M
Cerami, A
Lakatta, EG
Talan, M
AF Ahmet, Ismayil
Tae, Hyun-Jin
Brines, Michael
Cerami, Anthony
Lakatta, Edward G.
Talan, Mark
TI Helix B Surface Peptide, a Small Non-erythropoictic Molecule Based on
the Erythropoietin Structure, Effectively Ameliorates the Progression of
Chronic Heart Failure in the Rat Post Myocardial Infarction Model
SO CIRCULATION
LA English
DT Meeting Abstract
DE Heart failure; Pharmacology; Infarction
C1 [Ahmet, Ismayil; Tae, Hyun-Jin; Lakatta, Edward G.; Talan, Mark] NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA.
[Brines, Michael] Araim Pharmaceut, Ossining, NY USA.
[Cerami, Anthony] Araim Pharmaceut Inc, Ossining, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 9927
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885000258
ER
PT J
AU Bild, DE
McClelland, R
Kaufman, J
Blumenthal, R
Burke, G
Carr, JJ
Post, W
Register, T
Shea, S
Szklo, M
Szklo, M
AF Bild, Diane E.
McClelland, Robyn
Kaufman, Joel
Blumenthal, Roger
Burke, Gregory
Carr, J. Jeffrey
Post, Wendy
Register, Thomas
Shea, Steven
Szklo, Moyses
Szklo, Moyses
TI Ten-year Trends in Coronary Calcification in Individuals Without
Clinical Cardiovascular Disease in the Multi-Ethnic Study of
Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Subclinical atherosclerosis; Risk factors
C1 [Bild, Diane E.] NHLBI, NIH, Bethesda, MD 20892 USA.
[McClelland, Robyn] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Kaufman, Joel] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Blumenthal, Roger] Johns Hopkins Univ, Sch Med, Dept Med Cardiol, Baltimore, MD USA.
[Burke, Gregory] Wake Forest Univ, Dept Publ Hlth Sci, Winston Salem, NC 27109 USA.
[Carr, J. Jeffrey] Wake Forest Univ, Dept Radiol, Winston Salem, NC 27109 USA.
[Post, Wendy] Johns Hopkins Univ, Dept Cardiol, Baltimore, MD USA.
[Register, Thomas] Wake Forest Univ, Dept Pathol, Winston Salem, NC 27109 USA.
[Shea, Steven] Columbia Univ, Div Gen Internal Med, New York, NY USA.
[Szklo, Moyses; Szklo, Moyses] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA.
RI Carr, John/A-1938-2012
OI Carr, John/0000-0002-4398-8237
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 14442
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885004214
ER
PT J
AU Cater, GM
Yang, E
Sibley, CT
Nacif, MS
Rosen, B
Balling, KD
May, HT
Anderson, JL
Lappe, DL
Lima, JA
Bluemke, DA
Muhlestein, JB
AF Cater, George M.
Yang, Eunice
Sibley, Christopher T.
Nacif, Marcelo S.
Rosen, Boaz
Balling, Kyle D.
May, Heidi T.
Anderson, Jeffery L.
Lappe, Donald L.
Lima, Joao A.
Bluemke, David A.
Muhlestein, Joseph B.
TI Diabetes Severity is Associated with High Risk Plaque by Coronary CT
Angiography: The FACTOR-64 Trial
SO CIRCULATION
LA English
DT Meeting Abstract
DE Angiography; Computed tomography; Plaque; Type 2 Diabetes; Risk factors
C1 [Cater, George M.] Cleveland Clin, Lerner Coll Med, Cleveland, OH 44106 USA.
[Yang, Eunice] Johns Hopkins Univ, Coll Med, Baltimore, MD USA.
[Sibley, Christopher T.; Nacif, Marcelo S.; Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
[Rosen, Boaz] Harbor Hosp, Baltimore, MD USA.
[Balling, Kyle D.; May, Heidi T.; Anderson, Jeffery L.; Lappe, Donald L.; Muhlestein, Joseph B.] Intermt Med Cntr, Cardiovasc Dept, Murray, UT USA.
[Lima, Joao A.] Johns Hopkins Univ, Inst Heart & Vasc, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 13426
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885003224
ER
PT J
AU Chahal, H
Bluemke, DA
McClelland, R
Liu, K
Balfour, PC
Herrington, D
Shea, SI
Burke, G
Post, W
Shi, PB
Olson, J
Watson, KE
Folsom, AR
Lima, JA
AF Chahal, Harjit
Bluemke, David A.
McClelland, Robyn
Liu, Kiang
Balfour, Pelbreton C.
Herrington, David
Shea, Steven I.
Burke, Gregory
Post, Wendy
Shi, PeiBei
Olson, Jean
Watson, Karol E.
Folsom, Aaron R.
Lima, Joao A.
TI Traditional and Novel Risk Factors Can Estimate Five Year Risk of
Developing Heart Failure: Results From the Multi-ethnic Study of
Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Heart failure; Risk factors; Epidemiology; Prevention; Biomarkers
C1 [Chahal, Harjit; Post, Wendy; Lima, Joao A.] Johns Hopkins Univ, Baltimore, MD USA.
[Bluemke, David A.] NIH, Clin Cntr, Radiol & Imaging Sci, Bethesda, MD 20892 USA.
[McClelland, Robyn] Univ Washington, Collaborat Hlth Studies Coordinating Cntr, Seattle, WA 98195 USA.
[Liu, Kiang] Northwestern Univ, Sch Med, Dept Prevent Med, Chicago, IL USA.
[Balfour, Pelbreton C.] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Herrington, David] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
[Shea, Steven I.] Columbia Univ, New York, NY USA.
[Burke, Gregory] Wake Forest Univ Hlth Sci, Dept Publ Hlth Sci, Winston Salem, NC USA.
[Shi, PeiBei] NIH, Bethesda, MD 20892 USA.
[Olson, Jean] NIH, Div Epidemiol & Clin Applicat, Bethesda, MD 20892 USA.
[Watson, Karol E.] Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA.
[Folsom, Aaron R.] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 11145
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885001205
ER
PT J
AU Chen, MY
Bandettini, WP
Shanbhag, S
Hsu, LY
Arai, AE
AF Chen, Marcus Y.
Bandettini, W. P.
Shanbhag, Sujata
Hsu, Li-Yueh
Arai, Andrew E.
TI Cost effectiveness of Coronary CTA or Vasodilator Stress Cardiac MRI for
Determination of Invasive Angiography Following Equivocal Nuclear SPECT
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac CT; Cardiac MRI; Cost-effectiveness; Coronary artery disease;
Cardiovascular imaging
C1 [Chen, Marcus Y.; Bandettini, W. P.; Shanbhag, Sujata; Hsu, Li-Yueh; Arai, Andrew E.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 17902
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885007329
ER
PT J
AU Cheng, SS
Gupta, DK
Shah, AM
Sharrett, AR
Skali, H
Takeuchi, M
Clagett, B
Ni, HY
Solomon, SD
AF Cheng, Susan
Gupta, Deepak K.
Shah, Amil M.
Sharrett, A. Richey
Skali, Hicham
Takeuchi, Madoka
Clagett, Brian
Ni, Hanyi
Solomon, Sott D.
TI Relation of Blood Pressure Indices with Differential Risk for
Cardiovascular Events: The Atherosclerosis Risk in Communities Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Blood pressure; Epidemiology
C1 [Cheng, Susan; Gupta, Deepak K.; Shah, Amil M.; Skali, Hicham; Takeuchi, Madoka; Clagett, Brian; Solomon, Sott D.] Brigham & Womens Hosp, Cardiovasc Div, Cambridge, MA USA.
[Sharrett, A. Richey] Johns Hopkins Sch Publ Hlth, Baltimore, MD USA.
[Ni, Hanyi] NHLBI, Epidemiol Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 15476
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885005210
ER
PT J
AU Desai, CS
Ning, HY
Liu, K
Reis, J
Gidding, SS
Lima, JC
Lloyd-Jones, DM
AF Desai, Chintan S.
Ning, Hongyan
Liu, Kiang
Reis, Jared
Gidding, Samuel S.
Lima, Joao C.
Lloyd-Jones, Donald M.
TI Association of Cardiovascular Health in Young Adulthood with Left
Ventricular Structure and Function Later in Life: The Coronary Artery
Risk Development in Young Adults (Cardia) Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Echocardiography; 2020 Goals; Risk factors
C1 [Desai, Chintan S.; Ning, Hongyan; Liu, Kiang; Lloyd-Jones, Donald M.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Reis, Jared] NHLBI, Bethesda, MD 20892 USA.
[Gidding, Samuel S.] Nemours Cardiac Cntr, Wilmington, DE USA.
[Lima, Joao C.] Johns Hopkins Univ, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 16640
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885006243
ER
PT J
AU Donekal, S
Liu, YC
Liu, CY
Venkatesh, BA
Yoneyama, K
Wu, CO
Nacif, M
Gomes, AS
Hundley, G
Bluemke, DA
Lima, JA
AF Donekal, Sirisha
Liu, Yuan Chano
Liu, Chia Ying
Venkatesh, Bharath Ambale
Yoneyama, Kihei
wu, Colin O.
Nacif, Marcelo
Gomes, Antoinette S.
Hundley, Gregory
Bluemke, David A.
Lima, Joao A.
TI The Relationship Between Interstitial Fibrosis by T1 Mapping and
Regional Myocardial Function by Tagging: The MESA Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Fibrosis; Myocardial contraction; Myocardial torsion and recoil;
Magnetic resonance imaging; Hypertrophy
C1 [Donekal, Sirisha; Liu, Yuan Chano; Liu, Chia Ying; Venkatesh, Bharath Ambale; Yoneyama, Kihei; Lima, Joao A.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[wu, Colin O.; Nacif, Marcelo] NHLBI, Bethesda, MD 20892 USA.
[Gomes, Antoinette S.] Univ Calif Los Angeles, Sch Med, Bethesda, MD USA.
[Hundley, Gregory] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
[Bluemke, David A.] NIH, Clin Cntr, Bethesda, MD USA.
RI Ambale Venkatesh, Bharath/F-4941-2016
OI Ambale Venkatesh, Bharath/0000-0002-2330-2373
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 11168
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885001209
ER
PT J
AU Dracup, K
Moser, D
Pelter, M
Nesbitt, T
Southard, J
Paul, SM
Biddle, MJ
Robinson, S
Loranger, D
Cooper, LS
AF Dracup, Kathleen
Moser, Debra
Pelter, Michele
Nesbitt, Thomas
Southard, Jeffrey
Paul, Steven M.
Biddle, Martha J.
Robinson, Susan
Loranger, Denise
Cooper, Lawton S.
TI A Focused Heart Failure Self-Care Intervention Reduces Cardiac Deaths in
Rural Patients
SO CIRCULATION
LA English
DT Meeting Abstract
DE Heart failure
C1 [Dracup, Kathleen; Paul, Steven M.; Robinson, Susan] UCSF, San Francisco, CA USA.
[Moser, Debra; Biddle, Martha J.] Univ Kentucky, Lexington, KY USA.
[Pelter, Michele] Univ Nevada, Reno, NV 89557 USA.
[Nesbitt, Thomas] Univ Calif Davis, Sacramento, CA USA.
[Southard, Jeffrey] Univ Calif Davis, San Francisco, CA USA.
[Loranger, Denise] UCSF, Reno, NV USA.
[Cooper, Lawton S.] UCSF, NHLBI, Bethseda, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 10687
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885001019
ER
PT J
AU Duprez, D
Jacobs, DR
Brumback, L
Peraita, CA
Steffen, LM
Alonso, A
Sibley, CT
Heckbert, SR
Kronmal, R
AF Duprez, Daniel
Jacobs, David R.
Brumback, Lyndia
Peraita, Carmen A.
Steffen, Lyn M.
Alonso, Alvaro
Sibley, Christopher T.
Heckbert, Susan R.
Kronmal, Richard
TI Diastolic Pulse Wave Analysis in the Prediction of Incident Atrial
Fibrillation in The Multi-ethnic Study Of Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Atrial fibrillation; Blood pressure; Cardiovascular disease prevention;
Risk factors
C1 [Duprez, Daniel] Univ Minnesota, Div Cardiovasc, Minneapolis, MN 55455 USA.
[Jacobs, David R.; Steffen, Lyn M.; Alonso, Alvaro] Univ Minnesota, Minneapolis, MN USA.
[Brumback, Lyndia; Kronmal, Richard] Univ Washington, Seattle, WA 98195 USA.
[Peraita, Carmen A.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Sibley, Christopher T.] NIH, Bethesda, MD 20892 USA.
[Heckbert, Susan R.] Univ Washington, Cardiovasc Hlth Rsch Unit, Seattle, WA 98195 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 12133
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885002140
ER
PT J
AU Ebong, IA
Goff, DC
Rodriguez, CJ
Chen, HY
Sibley, CT
Bertoni, AG
AF Ebong, Imo A.
Goff, David C.
Rodriguez, Carlos J.
Chen, Haiyng
Sibley, Christopher T.
Bertoni, Alain G.
TI Association of Lipids with Incident Heart Failure among Adults with and
Without Diabetes: The Multi-Ethnic Study of Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Lipids; Heart failure
C1 [Ebong, Imo A.; Rodriguez, Carlos J.; Chen, Haiyng; Bertoni, Alain G.] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Goff, David C.] Colorado Sch Publ Hlth, Aurora, CO USA.
[Sibley, Christopher T.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 11065
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885001173
ER
PT J
AU Gencer, B
Butler, J
Bauer, DC
Auer, R
Kalogeropoulos, A
Maroues-Vidal, P
Applegate, WB
Satterfield, S
Vittinghoff, E
Harris, T
Newman, A
Rodondi, N
AF Gencer, Baris
Butler, Javed
Bauer, Douglas C.
Auer, Reto
Kalogeropoulos, Andreas
Maroues-Vidal, Pedro
Applegate, William B.
Satterfield, Suzanne
Vittinghoff, Eric
Harris, Tamara
Newman, Anne
Rodondi, Nicolas
TI Association of ECG Abnormalities and Incident Heart Failure Events
SO CIRCULATION
LA English
DT Meeting Abstract
DE Heart failure; Electrocardiography; Epidemiologic methods
C1 [Gencer, Baris] Univ Hosp Geneva, Geneva, Switzerland.
[Butler, Javed; Kalogeropoulos, Andreas] Emory Clin, Cardiovas Rsch Inst, Div Cardiol, Atlanta, GA 30322 USA.
[Bauer, Douglas C.] Dept Med, San Francisco, CA USA.
[Auer, Reto; Vittinghoff, Eric] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Maroues-Vidal, Pedro] Clin Rsch Cntr, Inst Social & Prevent Med, Lausanne, Switzerland.
[Applegate, William B.] Wake Forest Univ, Baptist Med Ctr, Winston Salem, NC 27109 USA.
[Satterfield, Suzanne] Univ Tennessee, Hlth Sci Ctr, Dept Prevent Med, Memphis, TN USA.
[Harris, Tamara] NIH, Geriatr Epidemiol Sect, Bethesda, MD 20892 USA.
[Newman, Anne] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
[Rodondi, Nicolas] Univ Hosp Bern, Dept Gen Internal Med, CH-3010 Bern, Switzerland.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 14987
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885005023
ER
PT J
AU Gjesdal, O
Mewton, N
Yoneyama, K
Wu, C
Jacobs, D
Sydney, S
Lewis, CE
Liu, K
Bluemke, DA
Lima, JA
AF Gjesdal, Ola
Mewton, Nathan
Yoneyama, Kihei
Wu, Colin
Jacobs, David
Sydney, Stephen
Lewis, Cora E.
Liu, Kiang
Bluemke, David A.
Lima, Joao A.
TI Dose Response Effect of Cigarette Smoking on Cardiac Function and Heart
Failure in the Multi-Ethnic Study of Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac MRI; Myocardial contraction; Population science; Heart failure;
Smoking
C1 [Gjesdal, Ola; Mewton, Nathan; Yoneyama, Kihei; Lima, Joao A.] Johns Hopkins Univ, Baltimore, MD USA.
[Wu, Colin] NHLBI, Bethesda, MD 20892 USA.
[Jacobs, David] Univ Minnesota, Sch Publ Hlth, Minneapolis, MN USA.
[Sydney, Stephen] Kaiser Permanente, Div Rsch, Oakland, CA USA.
[Lewis, Cora E.] Univ Alabama Birmingham, Div Prevent Med, Birmingham, AL USA.
[Liu, Kiang] Northwestern Univ, Feinberg Cardiovasc Rsch Inst, Chicago, IL 60611 USA.
[Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 14447
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885004217
ER
PT J
AU Goldberg, CS
Lu, MM
Mahle, WT
Gaynor, JW
Williams, I
Mussatto, KA
Ohye, RG
Frank, D
Graham, EM
Jacobs, JP
Krawczeski, CD
Ambert, LI
Lewis, A
Pemberton, VL
Sananes, R
Sood, E
Wechsler, S
Newburger, JW
AF Goldberg, Caren S.
Lu, Minmin
Mahle, William T.
Gaynor, J. W.
Williams, Ismee
Mussatto, Kathleen A.
Ohye, Richard G.
Frank, Deborah
Graham, Eric M.
Jacobs, Jeffrey P.
Krawczeski, Catherine D.
Ambert, Linda I.
Lewis, Alan
Pemberton, Victoria L.
Sananes, Renee
Sood, Erica
Wechsler, Stephanie
Newburger, Jane W.
CA Pediat Heart Network Investigators
TI Factors Associated with Impaired Neurodevelopment at 3 Years of Age in
Children with Single Right Ventricle Lesions
SO CIRCULATION
LA English
DT Meeting Abstract
DE Hypoplastic left heart; Pediatric cardiology
C1 [Goldberg, Caren S.] Univ Michigan, Dept Pediat, Ann Arbor, MI 48109 USA.
[Lu, Minmin] New England Res Inst, Boston, MA USA.
[Mahle, William T.] Sibley Heart Cntr, Atlanta, GA USA.
[Gaynor, J. W.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Williams, Ismee] Columbia Univ, Dept Pediat, Med Ctr, New York, NY 10027 USA.
[Mussatto, Kathleen A.] Childrens Hosp Wisconsin, Milwaukee, WI 53201 USA.
[Ohye, Richard G.] Univ Michigan, Dept Cardiac Surg, Ann Arbor, MI 48109 USA.
[Frank, Deborah] Primary Childrens Med Ctr, Dept Pediat, Salt Lake City, UT USA.
[Graham, Eric M.] Med Univ S Carolina, Dept Pediat, Charleston, SC 29425 USA.
[Jacobs, Jeffrey P.] Cardiac Surg Associates, Congenital Heart Inst Florida, St Petersburg, FL USA.
[Krawczeski, Catherine D.] Cincinnati Childrens Hosp, Div Cardiol, Cincinnati, OH USA.
[Ambert, Linda I.] Primary Childrens Med Ctr, Salt Lake City, UT 84103 USA.
[Lewis, Alan] Childrens Hosp Los Angeles, Div Cardiol, Los Angeles, CA 90027 USA.
[Pemberton, Victoria L.] NHLBI, Bethesda, MD 20892 USA.
[Sananes, Renee] Hosp Sick Children, Div Cardiol, Toronto, ON M5G 1X8, Canada.
[Sood, Erica] Nemours Al duPont Hosp Children, Nemours Cardiac Cntr, Wilmington, DE USA.
[Wechsler, Stephanie] Duke Univ, Med Ctr, Dept Pediat, Durham, NC USA.
[Newburger, Jane W.] Childrens Hosp, Dept Cardiol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 13230
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885003144
ER
PT J
AU Guenther, F
Kaufmann, BA
Klibanov, AL
Heidt, T
Kramer, M
Khanicheh, E
Ferrante, EA
Neudorfer, I
Yasuhiro, K
Peter, K
Bode, C
von zur Muhlent, C
AF Guenther, Felix
Kaufmann, Beat A.
Klibanov, Alexander L.
Heidt, Timo
Kramer, Mara
Khanicheh, Elham
Ferrante, Elisa A.
Neudorfer, Irene
Yasuhiro, Katagiri
Peter, Karlheinz
Bode, Christoph
von zur Muhlent, Constantin
TI Dual Microbubble Targeting Improves in vitro Capture Efficiency of
Ultrasound Micro-Bubbles Targeted to Selectins and Activated Platelets
Although not Providing Additional Signal Effect for in vivo Imaging of
Arterial Thrombosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Ultrasound; Molecular; Imaging agents; Cardiovascular imaging;
Arteriosclerosis
C1 [Guenther, Felix; Heidt, Timo; Kramer, Mara; Neudorfer, Irene; Bode, Christoph; von zur Muhlent, Constantin] Univ Heart Cntr, Freiburg, Germany.
[Kaufmann, Beat A.; Khanicheh, Elham] Univ Basel Hosp, CH-4031 Basel, Switzerland.
[Klibanov, Alexander L.] Univ Virginia, Div Cardiovasc Med, Charlottesville, VA USA.
[Ferrante, Elisa A.] Univ Virginia, Dept Biomed Engn, Charlottesville, VA USA.
[Yasuhiro, Katagiri] NIH, Dev Neurobiol Sect, Bethesda, MD 20892 USA.
[Peter, Karlheinz] Baker IDI, Heart & Diabet Inst, Melbourne, Vic, Australia.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 13226
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885003142
ER
PT J
AU Gulati, A
Krishnathasan, K
Hsu, LY
Ali, A
Ismail, T
Ferreira, P
Ismail, N
Goncalves, C
Davendralingam, N
Wage, R
Roughton, M
Gatehouse, P
Jabbour, A
Pennell, DJ
Arai, AE
Prasad, S
AF Gulati, Ankur
Krishnathasan, Kaushiga
Hsu, Li-Yueh
Ali, Aamir
Ismail, Tevfik
Ferreira, Pedro
Ismail, Nizar
Goncalves, Carla
Davendralingam, Natasha
Wage, Rick
Roughton, Michael
Gatehouse, Peter
Jabbour, Andrew
Pennell, Dudley J.
Arai, Andrew E.
Prasad, Sanjay
TI Absolute Hyperemic Myocardial Blood Flow is Impaired in Non-Ischemic
Dilated Cardiomyopathy and is Related to the Severity of Left
Ventricular Systolic Dysfunction
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiomyopathy; Cardiac MRI; Perfusion imaging; Blood flow; Ventricular
function
C1 [Gulati, Ankur] Royal Brompton Hosp, London SW3 6LY, England.
[Krishnathasan, Kaushiga; Ali, Aamir; Ismail, Tevfik; Ferreira, Pedro; Ismail, Nizar; Goncalves, Carla; Davendralingam, Natasha; Wage, Rick; Roughton, Michael; Gatehouse, Peter; Jabbour, Andrew; Pennell, Dudley J.; Prasad, Sanjay] Royal Brompton Hosp, CMR Dept, London SW3 6LY, England.
[Hsu, Li-Yueh; Arai, Andrew E.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 10654
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885001006
ER
PT J
AU Guvton, JR
Slee, AE
Anderson, T
Fleg, JL
Goldberg, RB
Kashyap, ML
Marcovina, SM
Nash, SD
O'Brien, KD
Weintraub, W
Xu, P
Zhao, XQ
Boden, WE
AF Guvton, John R.
Slee, April E.
Anderson, Todd
Fleg, Jerome L.
Goldberg, Ronald B.
Kashyap, Moti L.
Marcovina, Santica M.
Nash, Stephen D.
O'Brien, Kevin D.
Weintraub, William
Xu, Ping
Zhao, Xue-Qiao
Boden, William E.
TI Relation of Lipoprotein Levels to Cardiovascular Events in the
Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High
Triglyceride and Impact on Global Health Outcomes (AIM-HIGH) Trial
SO CIRCULATION
LA English
DT Meeting Abstract
DE Coronary heart disease; Lipoproteins; Cholesterol-lowering drugs;
Clinical trials
C1 [Guvton, John R.] Duke Univ, Med Cntr, Durham, NC USA.
[Slee, April E.; Xu, Ping] Axio Rsch, Biostat, Seattle, WA USA.
[Anderson, Todd] Univ Calgary, Calgary, AB, Canada.
[Fleg, Jerome L.] NHLBI, Div Cardiovasc Dis, Bethesda, MD 20892 USA.
[Goldberg, Ronald B.] Univ Miami, Miller Sch Med, Hollywood, FL USA.
[Kashyap, Moti L.] Univ Calif Irvine, Irvine, CA USA.
[Marcovina, Santica M.] Univ Washington, Seattle, WA 98195 USA.
[Nash, Stephen D.] SUNY Hlth Sci Cntr Syracuse, Syracuse, NY USA.
[O'Brien, Kevin D.] Univ Washington, Med Div Cardiol, Seattle, WA 98195 USA.
[Weintraub, William] Cntr Heart & Vasc Hlth, Newark, DE USA.
[Zhao, Xue-Qiao] Univ Washington, Sch Med, Seattle, WA USA.
[Boden, William E.] Samuel S Stratton VA Med Cntr, Albany, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 14501
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885004238
ER
PT J
AU Habibi, M
Chahal, H
Opdahl, A
Helle-Valle, TM
Gjesdal, O
Heckbert, SR
McClelland, R
Wu, CO
Shea, S
Hundley, WG
Bluemke, DA
Lima, JA
AF Habibi, Mohammadali
Chahal, Harjit
Opdahl, Anders
Helle-Valle, Thomas M.
Gjesdal, Ola
Heckbert, Susan R.
McClelland, Robyn
Wu, Colin O.
Shea, Steven
Hundley, W. Gregory
Bluemke, David A.
Lima, Joao A.
TI Left Atrial Function and Incident Heart Failure: Results front The
Multi-Ethnic Study of Atherosclerosis(MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
DE Atrial function; Heart failure Magnetic resonance imaging; Risk factors
C1 [Habibi, Mohammadali; Chahal, Harjit; Opdahl, Anders; Helle-Valle, Thomas M.; Gjesdal, Ola; Lima, Joao A.] Johns Hopkins Univ, Baltimore, MD USA.
[Heckbert, Susan R.; McClelland, Robyn] Univ Washington, Seattle, WA 98195 USA.
[Wu, Colin O.] NHLBI, Off Biostat Rsch, Bethesda, MD 20892 USA.
[Shea, Steven] Columbia Univ, New York, NY USA.
[Hundley, W. Gregory] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 13569
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885003294
ER
PT J
AU Hamad, YA
Armstrong, AC
Kishi, S
Gidding, SS
Jacobs, DR
Sidney, S
Lewis, CE
Cook, NL
Liu, KJ
Lima, J
AF Hamad, Yasir A.
Armstrong, Anderson C.
Kishi, Satoru
Gidding, Samuel S.
Jacobs, David R.
Sidney, Stephen
Lewis, Cora E.
Cook, Nakela L.
Liu, Kiang J.
Lima, Joao
TI Smoking at Age 18 to 30 is Associated with Diastolic Function Over a
25-Year Follow-Up Period: The CARDIA Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Smoking; Epidemiology
C1 [Hamad, Yasir A.; Armstrong, Anderson C.; Kishi, Satoru; Lima, Joao] Johns Hopkins, Cardiol, Baltimore, MD USA.
[Gidding, Samuel S.] Nemours Cardiac Cntr, Div Pediat Cardiol, Wilmington, DE USA.
[Jacobs, David R.] Univ Minnesota, Minneapolis, MN USA.
[Sidney, Stephen] Kaiser Permanente, Phys Act, Obes, Illicit Drugs, Oakland, CA USA.
[Lewis, Cora E.] Univ Alabama Birmingham, Birmingham, AL USA.
[Cook, Nakela L.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Liu, Kiang J.] Northwestern Univ, Chicago, IL 60611 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 16927
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885006331
ER
PT J
AU He, J
Yang, W
Anderson, A
Dries, D
Feldman, H
Kallem, R
Kanthety, R
Kusek, J
Mazurick, C
Ojo, A
Raj, D
Rahman, M
Ricardo, A
Shlipak, M
Soliman, E
Wolf, M
Hamm, L
AF He, Jiang
Yang, Wei
Anderson, Amanda
Dries, Daniel
Feldman, Harold
Kallem, RadhaKrishna
Kanthety, Radhika
Kusek, John
Mazurick, Carissa
Ojo, Akinlolu
Raj, Dominic
Rahman, Mahboob
Ricardo, Ana
Shlipak, Michael
Soliman, Elsayed
Wolf, Myles
Hamm, Lee
TI Risk Factors for Congestive Heart Failure in Patients with Chronic
Kidney Disease: the CRIC Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Heart failure; Kidney; Risk factors
C1 [He, Jiang] Tulane Univ, Dept Epidemiol, New Orleans, LA 70118 USA.
[Yang, Wei; Anderson, Amanda; Feldman, Harold; Mazurick, Carissa] Univ Penn, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA.
[Dries, Daniel; Kallem, RadhaKrishna] Univ Penn, Dept Med, Philadelphia, PA 19104 USA.
[Kanthety, Radhika; Rahman, Mahboob] Case Western Reserve Univ, Dept Med, Cleveland, OH 44106 USA.
[Kusek, John] NIDDK, NIH, Bethesda, MD 20892 USA.
[Ojo, Akinlolu] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Raj, Dominic] George Washington Univ, Dept Med, Washington, DC USA.
[Ricardo, Ana] Univ Illinois, Dept Med, Chicago, IL USA.
[Shlipak, Michael] UCSF, Dept Med, San Francisco, CA USA.
[Soliman, Elsayed] Wake Forest Univ, Dept Epidemiol & Prevent, Winston Salem, NC 27109 USA.
[Wolf, Myles] Univ Miami, Dept Med, Miami, LA USA.
[Hamm, Lee] Tulane Univ, Dept Med, New Orleans, LA 70118 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 11651
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885001379
ER
PT J
AU Huan, TX
Zhang, B
Wang, Z
Joehanes, R
Zhu, J
Johnson, AD
Ying, SX
Munson, PJ
Raghavachari, N
Wang, R
Liu, PC
Courchesne, P
Assimes, TL
McPherson, R
Samani, N
Schunkert, H
O'Donnell, CJ
Derry, J
Yang, X
Levy, D
AF Huan, Tianxiao
Zhang, Bin
Wang, Zhi
Joehanes, Roby
Zhu, Jun
Johnson, Andrew D.
Ying, Saixia
Munson, Peter J.
Raghavachari, Nalini
Wang, Richard
Liu, Poching
Courchesne, Paul
Assimes, Themistocles L.
McPherson, Ruth
Samani, Nilesh
Schunkert, Heribert
O'Donnell, Christopher J.
Derry, Jonathan
Yang, Xia
Levy, Daniel
CA Coronary ARteryDIs Genome Wide
TI Identification of Disrupted Network Modules and Key Regulators of
Coronary Artery Disease via Integration of Blood Gene Expression
Profiling and Network Analysis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Coronary artery disease; Biomarkers; Gene expression; Systems biology;
Genome-wide association studies (GWAS)
C1 [Huan, Tianxiao; Joehanes, Roby; Johnson, Andrew D.; Courchesne, Paul; O'Donnell, Christopher J.; Levy, Daniel] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Zhang, Bin; Zhu, Jun] Mt Sinai Sch Med, Inst Genom & Multiscale Biol, New York, NY USA.
[Wang, Zhi; Derry, Jonathan] Sage Bionetworks, Seattle, WA USA.
[Ying, Saixia; Munson, Peter J.] NIH, CIT, Bethesda, MA USA.
[Raghavachari, Nalini; Wang, Richard; Liu, Poching] NHLBI, Genom Core Facil, Genet & Dev Biol Cntr, Bethesda, MD 20892 USA.
[Assimes, Themistocles L.] Stanford Univ, Framingham Heart Study, Stanford, CA 94305 USA.
[McPherson, Ruth] Univ Ottawa, Inst Heart, Div Cardiol, Ottawa, ON, Canada.
[Samani, Nilesh] Univ Leicester, Dept Cardiovasc Sci, Leicester, Leics, England.
[Schunkert, Heribert] Med Univ Lubeck, Med Klin B, D-23538 Lubeck, Germany.
[Yang, Xia] Univ Calif Los Angeles, Framingham Heart Study, Los Angeles, CA USA.
RI Johnson, Andrew/G-6520-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 16106
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885006014
ER
PT J
AU Idris, AH
Guffey, D
Pepe, PE
Brown, SP
Aufderheide, TP
Brooks, SC
Callaway, CW
Christenson, J
Davis, DP
Daya, MR
Gray, R
Kudenchuk, PJ
Larsen, J
Lin, S
Menegazzi, JJ
Sheehan, K
Sopko, G
Stiell, IG
Nichol, G
AF Idris, Ahamed H.
Guffey, Danielle
Pepe, Paul E.
Brown, Siobhan P.
Aufderheide, Tom P.
Brooks, Steven C.
Callaway, Clifton W.
Christenson, Jim
Davis, Daniel P.
Daya, Mohamud R.
Gray, Randal
Kudenchuk, Peter J.
Larsen, Jonathan
Lin, Steven
Menegazzi, James J.
Sheehan, Kellie
Sopko, George
Stiell, Ian G.
Nichol, Graham
CA ROC Investigators
TI Chest Compression Rates Between 100 and 120 per Minute are Independently
Associated with Increased Adult Survival Following Out-of-Hospital
Cardiac Arrest
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiopulmonary resuscitation; Cardiac arrest; Emergency care;
Guidelines; Health services research
C1 [Idris, Ahamed H.; Pepe, Paul E.] UT Southwestern Med Cntr, Dallas, TX USA.
[Guffey, Danielle; Brown, Siobhan P.; Sheehan, Kellie; Nichol, Graham] Univ Washington, Clin Trials Cntr, Seattle, WA 98195 USA.
[Aufderheide, Tom P.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Brooks, Steven C.] Queens Univ, Toronto, ON, Canada.
[Callaway, Clifton W.; Menegazzi, James J.] Univ Pittsburgh, Pittsburgh, PA USA.
[Christenson, Jim] Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
[Davis, Daniel P.] UCSD Med Cntr, San Diego, CA USA.
[Daya, Mohamud R.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Gray, Randal] Univ Alabama Birmingham, Birmingham, AL USA.
[Kudenchuk, Peter J.] Univ Washington, Seattle, WA 98195 USA.
[Larsen, Jonathan] Seattle Fire Dept, Seattle Fire Dept Training Div, Seattle, WA USA.
[Lin, Steven] St Michaels Hosp, Toronto, ON M5B 1W8, Canada.
[Sopko, George] NIH, Heart Failure & Arrhythmia Branch, Bethesda, MD 20892 USA.
[Stiell, Ian G.] Univ Ottawa, Ottawa, ON, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 16132
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885006027
ER
PT J
AU Ismail, TF
Hsu, LY
Greve, A
Goncalves, C
Hewins, B
Ferrera, P
Jabbour, A
Gulati, A
Wage, R
Gatehouse, P
Firmin, D
Pennell, D
Arai, A
Prasad, S
AF Ismail, Tevfik F.
Hsu, Li-Yueh
Greve, Anders
Goncalves, Carla
Hewins, Benjamin
Ferrera, Pedro
Jabbour, Andrew
Gulati, Ankur
Wage, Ricardo
Gatehouse, Peter
Firmin, David
Pennell, Dudley
Arai, Andrew
Prasad, Sanjay
TI Novel Evidence of the Coronary Microvascular Steal Phenomenon in
Hypertrophic Cardiomyopathy - A Quantitative Stress Perfusion
Cardiovascular Magnetic Resonance Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Perfusion imaging; Magnetic resonance imaging; Hypertrophic
cardiomyopathy; Cardiac hypertrophy; Cardiac MRI
C1 [Ismail, Tevfik F.; Goncalves, Carla; Hewins, Benjamin; Ferrera, Pedro; Jabbour, Andrew; Gulati, Ankur; Wage, Ricardo; Gatehouse, Peter; Firmin, David; Pennell, Dudley; Prasad, Sanjay] Royal Brompton Hosp, CMR Unit, London SW3 6LY, England.
[Hsu, Li-Yueh; Greve, Anders; Arai, Andrew] NHLBI, Cardiovasc & Pulm Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 17333
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885007067
ER
PT J
AU Kalogeropoulos, A
Georgiopoulou, V
Murphv, R
Newman, AB
Bauer, DC
Harris, T
Applegate, WB
Kritchevsky, SB
Butler, J
AF Kalogeropoulos, Andreas
Georgiopoulou, Vasiliki
Murphv, Rachel
Newman, Anne B.
Bauer, Douglas C.
Harris, Tamara
Applegate, William B.
Kritchevsky, Stephen B.
Butler, Javed
TI Dietary Sodium Intake and 10-Year Mortality in Older Adults: The Health,
Aging, and Body Composition (Health ABC) Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Sodium; Elderly; Prognosis
C1 [Kalogeropoulos, Andreas; Georgiopoulou, Vasiliki; Butler, Javed] Emory Univ, Atlanta, GA 30322 USA.
[Murphv, Rachel; Harris, Tamara] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
[Newman, Anne B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Bauer, Douglas C.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Applegate, William B.; Kritchevsky, Stephen B.] Wake Forest Univ, Winston Salem, NC 27109 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 17602
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885007192
ER
PT J
AU Kalyani, RR
Lazo, M
Turkbey, E
Chevalier, K
Brancati, F
Ouyang, P
Becker, D
Vaidya, D
AF Kalyani, Rita R.
Lazo, Mariana
Turkbey, Evrim
Chevalier, Karinne
Brancati, Frederick
Ouyang, Pamela
Becker, Diane
Vaidya, Dhananjay
TI Gender Differences in the Association of Diabetes with Incident Coronary
Heart Disease in Two Populations
SO CIRCULATION
LA English
DT Meeting Abstract
DE Coronary heart disease; Epidemiology; Disparities; Insulin resistance
C1 [Kalyani, Rita R.] Johns Hopkins Univ Hosp, Div Endocrinol, Baltimore, MD 21287 USA.
[Lazo, Mariana; Chevalier, Karinne; Brancati, Frederick; Becker, Diane; Vaidya, Dhananjay] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[Turkbey, Evrim] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Ouyang, Pamela] Johns Hopkins Bayview, Internal Med, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 14149
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885004085
ER
PT J
AU Khan, H
Kalogeropoulos, A
Georgiopoulou, V
Newman, AB
Shlipak, M
Garcia, M
Harris, TB
Kritchevsky, S
Butler, J
AF Khan, Hassan
Kalogeropoulos, Andreas
Georgiopoulou, Vasiliki
Newman, Anne B.
Shlipak, Michael
Garcia, Melissa
Harris, Tamara B.
Kritchevsky, Stephen
Butler, Javed
TI Cellular Aging as Reflected by Leukocyte Telomere Length and Incident
Heart Failure Risk in Older Adults
SO CIRCULATION
LA English
DT Meeting Abstract
DE Elderly; Heart failure; Gene expression; Risk factors
C1 [Khan, Hassan; Kalogeropoulos, Andreas; Georgiopoulou, Vasiliki; Butler, Javed] Emory Univ, Atlanta, GA 30322 USA.
[Newman, Anne B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Shlipak, Michael] Univ Calif San Francisco, San Francisco, GA USA.
[Garcia, Melissa; Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
[Kritchevsky, Stephen] Wake Forest Univ, Winston Salem, NC 27109 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 17709
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885007242
ER
PT J
AU Kizer, JR
Benkeser, D
Arnold, AM
Ix, JH
Mukamal, KJ
Djousse, L
Tracy, RP
Siscovick, DS
Zieman, SJ
AF Kizer, Jorge R.
Benkeser, David
Arnold, Alice M.
Ix, Joachim H.
Mukamal, Kenneth J.
Djousse, Luc
Tracy, Russell P.
Siscovick, David S.
Zieman, Susan J.
TI Advanced Glycation Endproduct Carboxymethyl-Lysine and Risk of
Cardiovascular Disease in Older Adults
SO CIRCULATION
LA English
DT Meeting Abstract
DE Biomarkers; Aging; Cardiovascular disease
C1 [Kizer, Jorge R.] Weill Cornell Med Coll, New York, NY USA.
[Benkeser, David; Arnold, Alice M.] Univ Washington, Seattle, WA 98195 USA.
[Ix, Joachim H.] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Mukamal, Kenneth J.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Djousse, Luc] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Tracy, Russell P.] Univ Vermont, Colchester, VT USA.
[Siscovick, David S.] Univ Washington, Seattle, WA 98195 USA.
[Zieman, Susan J.] NIA, Div Geriatr & Clin Gerontol, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 11110
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885001190
ER
PT J
AU Koh, K
Quon, M
Han, S
AF Koh, Kwang
Quon, Michael
Han, Seung
TI Pravastatin Combined with Valsartan Shows Additive Beneficial Vascular
Effects in Patients with Hypercholesterolemia
SO CIRCULATION
LA English
DT Meeting Abstract
DE Arteriosclerosis; Endothelial function
C1 [Koh, Kwang; Han, Seung] Gachon Univ, Inchon, South Korea.
[Quon, Michael] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 14163
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885004094
ER
PT J
AU Liu, CY
Liu, YC
Wu, CL
Armstrong, A
Volpe, GJ
van der Geest, RI
Liu, M
Hundley, WG
Gomes, A
Liu, ST
Nacif, M
Bluemke, DA
Lima, JAC
AF Liu, Chia-Ying
Liu, Yuan Chang
Wu, Colin
Armstrong, Anderson
Volpe, Gustavo J.
van der Geest, Rob I.
Liu, Mei
Hundley, William G.
Gomes, Antoinette
Liu, Songtao
Nacif, Marcelo
Bluemke, David A.
Lima, Joao A. C.
TI Age is Related to Interstitial Myocardial Fibrosis in Asymptomatic
Adults: Magnetic Resonance T-1 Mapping in the Multi-ethnic Study of
Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac MRI; Fibrosis; Biomarkers
C1 [Liu, Chia-Ying; Liu, Yuan Chang] Johns Hopkins Univ, Dept Radiol, Baltimore, MD USA.
[Wu, Colin] NHLBI, Off Biostat, Bethesda, MD 20892 USA.
[Armstrong, Anderson; Volpe, Gustavo J.; Lima, Joao A. C.] Johns Hopkins Univ Hosp, Dept Med, Div Cardiol, Baltimore, MD 21287 USA.
[van der Geest, Rob I.] Leiden Univ, Med Cntr, Dept Radiol, Leiden, Netherlands.
[Liu, Mei] Wake Forest Univ Hlth Sci, Dept Epidemiology& Prevent, Winston Salem, NC USA.
[Hundley, William G.] Wake Forest Univ, Sch Med, Baltimore, NC USA.
[Gomes, Antoinette] Univ Calif Los Angeles, Dept Radiol, Los Angeles, CA USA.
[Liu, Songtao; Nacif, Marcelo; Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
RI Armstrong, Anderson/G-8407-2012
OI Armstrong, Anderson/0000-0003-3161-8922
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 10747
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885001043
ER
PT J
AU Liu, JK
Hickson, DA
Hairston, KG
Taylor, HA
Fox, CS
AF Liu, Jiankang
Hickson, DeMarc A.
Hairston, Kristen G.
Taylor, Herman A.
Fox, Caroline S.
TI Abdominal Visceral Adiposity, Fatty Liver and
Renin-Angiotensin-Aldosterone System: The Jackson Heart Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Obesity; Adipose; Aldosterone
C1 [Liu, Jiankang; Taylor, Herman A.] Univ Mississippi, Med Ctr, Jackson, MS 39216 USA.
[Hickson, DeMarc A.] Jackson State Univ, Jackson Heart Study, Jackson, MS USA.
[Hairston, Kristen G.] Wake Forest Baptist Hlth, Internal Med, Winston Salem, NC USA.
[Fox, Caroline S.] NHLBI, Cntr Populat Studies, Framingham, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 15531
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885005227
ER
PT J
AU Maatz, H
Monti, J
Goesele, C
Breiderhoff, T
Pravenec, M
Willnow, T
Sack, M
Hubner, N
AF Maatz, Henrike
Monti, Jan
Goesele, Claudia
Breiderhoff, Tilmann
Pravenec, Michal
Willnow, Thomas
Sack, Michael
Hubner, Norbert
TI MrpL48 is Associated with Impaired Mitochondrial Function and Blood
Pressure Regulation in Genetic Hypertension
SO CIRCULATION
LA English
DT Meeting Abstract
DE Hypertension; Mitochondria; Gene expression; Molecular biology
C1 [Maatz, Henrike; Monti, Jan; Goesele, Claudia; Breiderhoff, Tilmann; Willnow, Thomas; Hubner, Norbert] Max Delbruck Cntr Berlin, Berlin, Germany.
[Pravenec, Michal] Inst Physiol ASCR, Inst Physiol, Prague, Czech Republic.
[Sack, Michael] NHLBI, Div Intramural Rsch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 18962
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885008322
ER
PT J
AU Manavski, Y
Manavski, Y
Bennewitz, K
Tang, ZS
Zhang, F
Sakurai, A
Gutkind, SJ
Li, XR
Kroll, J
Dimmeler, S
Chavakis, E
AF Manavski, Yosif
Carmona, Guillaume
Bennewitz, Katrin
Tang, Zhongshu
Zhang, Fan
Sakurai, Atsuko
Gutkind, Silvio J.
Li, Xuri
Kroll, Jens
Dimmeler, Stefanie
Chavakis, Emmanouil
TI Brag2, An Arf6 Gef, Regulates Integrin-dependent Adhesion in Endothelial
Cells and is Involved in Angiogenesis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Angiogenesis; Extracellular matrix; Signal transduction
C1 [Manavski, Yosif] Goethe Univ Frankfurt, Inst Cardiovasc Regenerat, D-60054 Frankfurt, Germany.
[Carmona, Guillaume] MIT, David H Koch Inst Integrat Canc Rsch, Cambridge, MA 02139 USA.
[Bennewitz, Katrin; Kroll, Jens] Heidelberg Univ, Fac Med, Cntr Biomed & Med Technol Mannheim CBTM, Mannheim, Germany.
[Tang, Zhongshu; Zhang, Fan; Li, Xuri] NEI, NIH, Rockville, MD USA.
[Sakurai, Atsuko; Gutkind, Silvio J.] Natl Inst Dent & Craniofacial Rsch, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD USA.
[Dimmeler, Stefanie] Goethe Univ Frankfurt, Inst Cardiovasc Regenerat, D-60054 Frankfurt, Germany.
[Chavakis, Emmanouil] Goethe Univ Frankfurt, Dept Internal Med 3, D-60054 Frankfurt, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 19123
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885008380
ER
PT J
AU Marti, CN
Khan, H
Kalogeropoulos, AP
Georgiopoulou, VV
Mann, DL
Bibbins-Domingo, K
Koster, A
Newman, AB
Harris, T
Kritchevsky, SB
Butler, J
AF Marti, Catherine N.
Khan, Hassan
Kalogeropoulos, Andreas P.
Georgiopoulou, Vasiliki V.
Mann, Douglas L.
Bibbins-Domingo, Kristen
Koster, Annemarie
Newman, Anne B.
Harris, Tamara
Kritchevsky, Stephen B.
Butler, Javed
TI Soluble Tumor Necrosis Factor Receptors and Heart Failure Risk in Older
Adults: The Health, Aging, and Body Composition Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Heart failure; Biomarkers; Elderly
C1 [Marti, Catherine N.; Khan, Hassan; Kalogeropoulos, Andreas P.; Georgiopoulou, Vasiliki V.; Butler, Javed] Emory Univ, Sch Med, Atlanta, GA USA.
[Mann, Douglas L.] Washington Univ, St Louis, MO USA.
[Bibbins-Domingo, Kristen] UCSF, San Francisco, CA USA.
[Koster, Annemarie] NIH, Bethesda, MD 20892 USA.
[Newman, Anne B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Harris, Tamara] NIH, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Kritchevsky, Stephen B.] Wake Forest, Cardiol, Winston Salem, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 11673
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885001385
ER
PT J
AU McCulloch, MA
Gidding, S
Canas, JA
Ross, J
Hossain, J
Caulfield, M
Sikes, K
Sibley, C
De Cesare, A
Mauras, N
AF McCulloch, Michael A.
Gidding, Samuel
Canas, J. Atilio
Ross, Judith
Hossain, Jobayer
Caulfield, Michael
Sikes, Kaitlin
Sibley, Christopher
De Cesare, Alain
Mauras, Nelly
TI Aortic Distensibility, Assessed by MRI, is Decreased in Adolescents with
Type Diabetes Mellitus and Elevated LDL-C
SO CIRCULATION
LA English
DT Meeting Abstract
DE Arteriosclerosis; Type 1 Diabetes; Magnetic resonance imaging; Children
C1 [McCulloch, Michael A.; Gidding, Samuel] Alfred I duPont Hosp Children, Nemours Cardiac Cntr, Wilmington, DE USA.
[Canas, J. Atilio; Sikes, Kaitlin; Mauras, Nelly] Nemours Childrens Clin, Jacksonville, FL USA.
[Ross, Judith] Thomas Jefferson Univ, Jefferson Med Coll, Endocrinol TJU, Philadelphia, PA 19107 USA.
[Hossain, Jobayer] Alfred I duPont Hosp Children, Biostat Dept, Wilmington, DE USA.
[Caulfield, Michael] Quest Diagnost Nichols Inst, San Juan Capistrano, CA USA.
[Sibley, Christopher] NIH, Clin Cntr, Bethesda, MD 20892 USA.
[De Cesare, Alain] UMR S 678 UPMC Inserm, Paris, France.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 13620
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885003316
ER
PT J
AU Mehta, NN
Matthews, G
Krishnamoorthy, P
Budoff, M
Chen, J
Glenn, M
Go, A
He, J
Kanetsky, PA
Master, S
Rader, DJ
Raj, D
Shah, R
Schreiber, M
Fischer, MI
Townsend, R
Kusek, J
Feldman, H
Foulkes, A
Reilly, MP
AF Mehta, Nehal N.
Matthews, Gregory
Krishnamoorthy, Parasuram
Budoff, Matthew
Chen, Jing
Glenn, Melanie
Go, Alan
He, Jiang
Kanetsky, Peter A.
Master, Stephen
Rader, Daniel J.
Raj, Dominic
Shah, Rachana
Schreiber, Martv
Fischer, Michael I.
Townsend, Ray
Kusek, John
Feldman, Harvey
Foulkes, Andrea
Reilly, Muredach P.
TI Higher Plasma CXCL12 Levels Predict Incident Cardiovascular Disease
Events: Findings from the Chronic Renal Insufficiency Cohort Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Genomics; Chemokines; Myocardial infarction; Outcomes
C1 [Mehta, Nehal N.; Krishnamoorthy, Parasuram; Glenn, Melanie; Kanetsky, Peter A.; Master, Stephen; Rader, Daniel J.; Shah, Rachana; Townsend, Ray; Feldman, Harvey; Reilly, Muredach P.] Univ Penn, Philadelphia, PA 19104 USA.
[Matthews, Gregory; Foulkes, Andrea] Univ Massachusetts, Amherst, MA 01003 USA.
[Budoff, Matthew] Los Angeles Bio Med Rsch Inst, Torrance, CA USA.
[Chen, Jing; He, Jiang] Tulane Med Cntr, New Orleans, LA USA.
[Go, Alan] Kaiser, Cardiovasc Med, Oakland, CA USA.
[Raj, Dominic] George Washington Univ, Washington, DC USA.
[Schreiber, Martv] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Fischer, Michael I.] Univ Penn, Chicago, IL USA.
[Kusek, John] Natl Inst Diabet & Digest & Kidney Dis, Bethesda, 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
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 13352
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885003199
ER
PT J
AU Mentz, RJ
Bittner, V
Starr, AZ
Fleg, JL
Moe, G
Swank, AM
Fitz-Gerald, M
Nigam, A
Kao, A
Onwuanyi, A
Kraus, WE
Whellan, DJ
Ellis, SJ
O'Connor, CM
AF Mentz, Robert J.
Bittner, Vera
Starr, Aijing Z.
Fleg, Jerome L.
Moe, Gordon
Swank, Ann M.
Fitz-Gerald, Meredith
Nigam, Anil
Kao, Andrew
Onwuanyi, Anekwe
Kraus, William E.
Whellan, David J.
Ellis, Stephen J.
O'Connor, Christopher M.
TI Race, Exercise Training and Outcomes in Chronic Heart Failure
SO CIRCULATION
LA English
DT Meeting Abstract
DE Heart failure; Exercise tests; Outcomes; Health and fitness
C1 [Mentz, Robert J.; Kraus, William E.; O'Connor, Christopher M.] Duke Univ Med Cntr, Durham, NC USA.
[Bittner, Vera; Fitz-Gerald, Meredith] Univ Alabama Birmingham, Birmingham, AL USA.
[Starr, Aijing Z.; Ellis, Stephen J.] Duke Clin Rsch Inst, Durham, NC USA.
[Fleg, Jerome L.] NHLBI, Bethesda, MD 20892 USA.
[Moe, Gordon] St Michaels Hosp, Toronto, ON M5B 1W8, Canada.
[Swank, Ann M.] Univ Louisville, Louisville, KY 40292 USA.
[Nigam, Anil] Montreal Heart Inst, Montreal, PQ H1T 1C8, Canada.
[Nigam, Anil] Univ Montreal, Montreal, PQ, Canada.
[Kao, Andrew] St Lukes Hosp, Kansas City, MO USA.
[Onwuanyi, Anekwe] Morehouse Sch Med, Atlanta, GA 30310 USA.
[Whellan, David J.] Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 13253
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885003155
ER
PT J
AU Meyer, ML
Love, SA
Sorlie, PD
Rosamond, WD
Antini, C
Metcalf, PA
Simmons, S
Suchindran, CM
Heiss, G
AF Meyer, Michelle L.
Love, Shelly-Ann
Sorlie, Paul D.
Rosamond, Wayne D.
Antini, Carmen
Metcalf, Patricia A.
Simmons, Shakia
Suchindran, Chirayath M.
Heiss, Gerardo
TI Calibration of Heart Failure as the Cause of Death: The ARIC Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Heart failure; Epidemiologic methods; Cardiovascular disease;
Epidemiology
C1 [Meyer, Michelle L.; Love, Shelly-Ann; Rosamond, Wayne D.; Simmons, Shakia; Heiss, Gerardo] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Sorlie, Paul D.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Antini, Carmen] Univ Chile, Dept Epidemiol, Sch Publ Hlth, Santiago, Chile.
[Metcalf, Patricia A.] Univ Auckland, Dept Stat, Auckland 1142, New Zealand.
[Suchindran, Chirayath M.] Univ N Carolina, Dept Biostat, Chapel Hill, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 17464
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885007123
ER
PT J
AU Nacif, M
Turkbey, E
Rizzi, P
McClelland, R
Bild, D
Liu, CY
Barr, RG
Shea, S
Burke, G
Budoff, M
Folsom, AR
Post, WS
Eng, J
Lima, JA
Bluemke, DA
AF Nacif, Marcelo
Turkbey, Evrim
Rizzi, Patricia
McClelland, Robyn
Bild, Diane
Liu, Chia-Ying
Barr, R. Graham
Shea, Steven
Burke, Gregory
Budoff, Matthew
Folsom, Aaron R.
Post, Wendy S.
Eng, John
Lima, Joao A.
Bluemke, David A.
TI Prevalence and Determinants of Myocardial Scar by Late Gadolinium
Enhancement CMR: The Multi-Ethnic Study of Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac MRI; Heart failure; Longitudinal studies; Risk factors
C1 [Nacif, Marcelo; Turkbey, Evrim; Bluemke, David A.] NIH, Clin Cntr, Bethesda, MD 20892 USA.
[Rizzi, Patricia; Post, Wendy S.; Lima, Joao A.] Johns Hopkins Univ, Div Cardiol, Baltimore, MD USA.
[McClelland, Robyn] Univ Washington, Collaborat Hlth Studies Coordinating Cntr, Seattle, WA 98195 USA.
[Bild, Diane] NHLBI, Prevent & Populat Sci Program, Bethesda, MD 20892 USA.
[Liu, Chia-Ying; Eng, John] Johns Hopkins Univ, Dept Radiol, Baltimore, MD USA.
[Barr, R. Graham; Shea, Steven] Columbia Univ, New York, NY USA.
[Burke, Gregory] Wake Forest Univ Hlth Sci, Dept Publ Hlth Sci, Winston Salem, NC USA.
[Budoff, Matthew] Harbor UCLA Med Cntr, Los Angeles Biomed Rsch Inst, Div Cardiol, Torrance, CA USA.
[Folsom, Aaron R.] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 11292
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885001258
ER
PT J
AU Nambi, V
Liu, XX
Chambless, L
De Lemos, JA
Agarwal, S
Virani, SS
Aguilar, D
Srinivas, P
Deswal, A
Mosley, T
Boerwinkle, E
Hoogeveen, RC
Coresh, J
Folsom, AR
Heiss, G
Ballantyne, CM
AF Nambi, Vijay
Liu, Xiaoxi
Chambless, Lloyd
De Lemos, James A.
Agarwal, Sunil
Virani, Salim S.
Aguilar, David
Srinivas, Pothur
Deswal, Anita
Mosley, Thomas
Boerwinkle, Eric
Hoogeveen, Ron C.
Coresh, Joe
Folsom, Aaron R.
Heiss, Gerardo
Ballantyne, Christie M.
TI High Sensitivity Troponin T and NT-proBNP in Heart Failure Risk
Prediction: an Analysis from the Atherosclerosis Risk in Communities
(ARIC) Sudy
SO CIRCULATION
LA English
DT Meeting Abstract
DE Biomarkers; Heart failure; Troponin; Risk factors
C1 [Nambi, Vijay] Baylor Coll Med, Pearland, TX USA.
[Liu, Xiaoxi; Chambless, Lloyd; Agarwal, Sunil; Heiss, Gerardo] Univ N Carolina, Chapel Hill, NC USA.
[De Lemos, James A.] Univ Texas Southwestern Med Cntr, Dallas, TX USA.
[Virani, Salim S.; Deswal, Anita] Michael E Debakey Vet Affairs Hosp, Baylor Coll Med, Houston, TX USA.
[Aguilar, David; Hoogeveen, Ron C.; Ballantyne, Christie M.] Baylor Coll Med, Houston, TX 77030 USA.
[Srinivas, Pothur] NIH, Prote Ctr, Bethesda, MD 20892 USA.
[Mosley, Thomas] Univ Mississippi, Med Cntr, Jackson, MS 39216 USA.
[Boerwinkle, Eric] Univ Texas Houston, Sch Publ Hlth, Houston, TX USA.
[Coresh, Joe] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Folsom, Aaron R.] Univ Minnesota, Minneapolis, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 14209
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885004106
ER
PT J
AU Nasir, K
Blaha, MJ
Budoff, MJ
Blankstien, R
Agatston, AS
Sibley, CT
Shaw, LJ
Blumenthal, RS
Krumholz, H
AF Nasir, Khurram
Blaha, Michael J.
Budoff, Matthew J.
Blankstien, Ron
Agatston, Arthur S.
Sibley, Christopher T.
Shaw, Leslee J.
Blumenthal, Roger S.
Krumholz, Harlan
TI Eligibility for Lipid Lowering Therapy, Coronary Artery Calcification,
and CHD Events - National Implications for the Appropriate Use of
Preventive Pharmacotherapy: Multi-Ethnic Study of Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
DE Outcomes; Statins; Health services research; Calcification; Guidelines
C1 [Nasir, Khurram; Agatston, Arthur S.] Baptist Hlth South Florida, Prevent & Wellness, Coral Gables, FL USA.
[Blaha, Michael J.; Blumenthal, Roger S.] Johns Hopkins Univ, Sch Med, Ciccarone Prevent Cardiol Cntr, Baltimore, MD USA.
[Budoff, Matthew J.] Los Angeles Biomed Rsch Inst, Torrance, CA USA.
[Blankstien, Ron] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Sibley, Christopher T.] NIH, Clin Res Unit, Bethesda, MD 20892 USA.
[Shaw, Leslee J.] Emory Univ, Sch Med, Emory Clin Cardiovasc Rsch Inst, Atlanta, GA USA.
[Krumholz, Harlan] Yale Univ, Yale New Haven Hosp Cntr Outcomes Rsch & Evaluat, New Haven, CT USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 16758
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885006271
ER
PT J
AU Newburger, JW
Sleeper, LA
Pearson, GD
Mahle, WT
Dunbar-Masterson, C
Mital, S
Williams, I
Atz, AM
Ghanavem, N
Goldberg, C
Jacobs, J
Krawczeski, CD
Lewis, A
Pasquali, S
Pizarro, C
Gruber, PJ
Khaikin, S
Gaynor, JW
Ohye, R
AF Newburger, Jane W.
Sleeper, Lynn A.
Pearson, Gail D.
Mahle, William T.
Dunbar-Masterson, Carolyn
Mital, Seema
Williams, Ismee
Atz, Andrew M.
Ghanavem, Nancy
Goldberg, Caren
Jacobs, Jeff
Krawczeski, Catherine D.
Lewis, Alan
Pasquali, Sara
Pizarro, Christian
Gruber, Peter J.
Khaikin, Svetlana
Gaynor, J. W.
Ohye, Richard
CA Pediat Heart Network Investigators
TI Transplant-Free Survival, Catheter Interventions, and Events at 3 Years
in the Single Ventricle Reconstruction Trial
SO CIRCULATION
LA English
DT Meeting Abstract
DE Congenital heart disease; Children; Congenital heart surgery; Pediatric
cardiology
C1 [Newburger, Jane W.; Dunbar-Masterson, Carolyn] Boston Childrens Hosp, Boston, MA USA.
[Sleeper, Lynn A.] New England Rsch Inst, Watertown, MA USA.
[Pearson, Gail D.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Mahle, William T.] Emory Univ, Sch Med, Sibley Heart Cntr, Atlanta, GA USA.
[Mital, Seema] Hosp Sick Children, Div Pediat Cardiol, Toronto, ON M5G 1X8, Canada.
[Williams, Ismee] Columbia Univ, Med Cntr, New York, NY USA.
[Atz, Andrew M.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Ghanavem, Nancy] Childrens Hosp Wisconsin, Milwaukee, WI 53201 USA.
[Goldberg, Caren; Ohye, Richard] Univ Michigan Hlth Syst, Ann Arbor, MI USA.
[Jacobs, Jeff] Congenital Heart Inst Florida, Cardiac Surg Associates, St Petersburg, FL USA.
[Krawczeski, Catherine D.] Cincinnati Childrens Hosp, Cincinnati, OH USA.
[Lewis, Alan] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Pasquali, Sara] Duke Clin Rsch Inst, Durham, NC USA.
[Pizarro, Christian] Alfred I duPont Hosp Children, Nemours Cardiac Cntr, Wilmington, DE USA.
[Gruber, Peter J.] Primary Childrens Med Cntr, Salt Lake City, UT USA.
[Khaikin, Svetlana] Hosp Sick Children, Cardiovasc Clin Rsch Unit, Toronto, ON M5G 1X8, Canada.
[Gaynor, J. W.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 11328
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885001264
ER
PT J
AU Nguyen, KL
Bandettini, WP
Shanbhag, S
Leung, SW
Wilson, JR
Arai, AE
AF Nguyen, Kim-L
Bandettini, W. P.
Shanbhag, Sujata
Leung, Steve W.
Wilson, Joel R.
Arai, Andrew E.
TI Safety and Tolerability of Regadenoson Stress CMR
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac MRI; Perfusion imaging; Coronary artery disease; Myocardial
perfusion; Vasodilator agents
C1 [Nguyen, Kim-L; Bandettini, W. P.; Shanbhag, Sujata; Leung, Steve W.; Wilson, Joel R.; Arai, Andrew E.] NHLBI, Cardiovasc & Pulm Branch, 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 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 17636
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885007212
ER
PT J
AU Olivier, L
Baba, R
Bandettini, WP
Bakalov, V
Sachdev, V
Rosing, D
Bondy, C
Arai, A
AF Olivier, Laura
Baba, Ridhwan
Bandettini, W. P.
Bakalov, Vladimir
Sachdev, Vandana
Rosing, Douglas
Bondy, Carolyn
Arai, Andrew
TI Bicuspid and 'Partially Fused' Aortic Valves are Common and Associated
with Aortic Dilation Across Age Groups in Turner Syndrome
SO CIRCULATION
LA English
DT Meeting Abstract
DE Aortic valve; Aorta; Cardiac MRI; Congenital heart disease; Aortic
diseases
C1 [Olivier, Laura; Bandettini, W. P.; Sachdev, Vandana; Rosing, Douglas; Arai, Andrew] NHLBI, NIH, Bethesda, MD 20892 USA.
[Baba, Ridhwan; Bakalov, Vladimir; Bondy, Carolyn] NICHHD, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 10685
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885001018
ER
PT J
AU Povsic, TJ
Rao, SV
Najjar, SS
Melton, LG
Prather, K
Zhou, JY
Adams, SD
Zavodni, KL
Kelly, F
Hasselblad, V
Heitner, JF
Raman, SV
Barsness, GW
Patel, MR
Kim, RJ
Lakatta, EG
Harrington, RA
AF Povsic, Thomas J.
Rao, Sunil V.
Najjar, Samer S.
Melton, Laura G.
Prather, Kristi
Zhou, Jiying
Adams, Stacie D.
Zavodni, Katherine L.
Kelly, Francine
Hasselblad, Vic
Heitner, John F.
Raman, Subha V.
Barsness, Gregory W.
Patel, Manesh R.
Kim, Raymond J.
Lakatta, Edward G.
Harrington, Robert A.
TI EPC Mobilization After Erythropoietin Treatment in Acute St-elevation
Myocardial Infarction: The Reveal EPC Substudy
SO CIRCULATION
LA English
DT Meeting Abstract
DE Endothelial progenitor cell; Reperfusion injury; Myocardial infarction,
STEMI; Infarct size; Regenerative medicine stem cells
C1 [Povsic, Thomas J.; Rao, Sunil V.; Melton, Laura G.; Prather, Kristi; Zhou, Jiying; Hasselblad, Vic; Patel, Manesh R.] Duke Clin Rsch Inst, Durham, NC USA.
[Najjar, Samer S.] MedStar Hlth Rsch Inst, Hyattsville, MD USA.
[Adams, Stacie D.; Zavodni, Katherine L.; Kelly, Francine; Kim, Raymond J.] Duke Univ, Med Ctr, Durham, NC USA.
[Heitner, John F.] New York Methoodist Hosp, Brooklyn, NY USA.
[Raman, Subha V.] Ohio State Univ, Columbus, OH 43210 USA.
[Barsness, Gregory W.] Mayo Clin, Rochester, MN USA.
[Lakatta, Edward G.] NIA, Intramural Program, Baltimore, MD 21224 USA.
[Harrington, Robert A.] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 11778
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885002002
ER
PT J
AU Rastegar, N
Burt, JR
Coronal-Villalobos, CP
Te Riele, AS
James, C
Murray, B
Calkins, H
Tandri, H
Bhonsale, A
Bluemke, D
Zimmerman, SL
Kamel, IR
AF Rastegar, Neda
Burt, Jeremy R.
Coronal-Villalobos, Celia P.
Te Riele, Anneline S.
James, Cynthia
Murray, Brittney
Calkins, Hugh
Tandri, Harikrishna
Bhonsale, Aditya
Bluemke, David
Zimmerman, Stefan L.
Kamel, Ihab R.
TI Spectrum of Imaging Findings on Cardiac MR in Subjects with an
Arrythmogenic Right Ventricular Cardiomyopathy-Associated Gene Mutation
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiomyopathy; Cardiac MRI; Epidemiology; Magnetic resonance imaging
C1 [Rastegar, Neda; Burt, Jeremy R.; Coronal-Villalobos, Celia P.] Johns Hopkins Sch Med, Radiol Cardiac MRI Div, Baltimore, MD USA.
[Te Riele, Anneline S.; Bhonsale, Aditya] Johns Hopkins Sch Med, Baltimore, MD USA.
[James, Cynthia; Murray, Brittney; Calkins, Hugh; Tandri, Harikrishna] Johns Hopkins Sch Med, SOM DOM Cardiol, Baltimore, MD USA.
[Bluemke, David] NIH, Radiol Cardiac MRI Div, Baltimore, MD USA.
[Zimmerman, Stefan L.; Kamel, Ihab R.] Johns Hopkins Sch Med, SOM Rad Diagnost Imaging, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 16086
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885006005
ER
PT J
AU Rizzi, PB
Nacif, MS
Ricketts, EP
Liu, CY
Gomes, AS
Hundley, G
Prince, MR
Carr, J
McClelland, R
Liu, K
Eng, J
Johnson, C
Winslow, RL
Bluemke, DA
Lima, JA
AF Rizzi, Patricia B.
Nacif, Marcelo S.
Ricketts, Erin P.
Liu, Chia-Ying
Gomes, Antoinette S.
Hundley, Gregory
Prince, Martin R.
Carr, James
McClelland, Robyn
Liu, Kiang
Eng, John
Johnson, Craig
Winslow, Raimond L.
Bluemke, David A.
Lima, Joao A.
TI Variations in T1 Mapping and LV Functional Parameters in a Multi-Center
Study: The Multi-Ethnic Study of Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
DE Magnetic resonance imaging; Quality assessment; Fibrosis; Ejection
fraction
C1 [Rizzi, Patricia B.; Ricketts, Erin P.; Eng, John; Lima, Joao A.] Johns Hopkins Univ, Baltimore, MD USA.
[Nacif, Marcelo S.] NIH, Bethesda, MD 20892 USA.
[Liu, Chia-Ying] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[Gomes, Antoinette S.] Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA.
[Hundley, Gregory] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
[Prince, Martin R.] Cornell Univ, Cornell MRI, New York, NY 10021 USA.
[Prince, Martin R.] Columbia Univ, New York, NY USA.
[Carr, James; Liu, Kiang] Northwestern Univ, Sch Med, Chicago, IL USA.
[McClelland, Robyn; Johnson, Craig] Univ Washington, Collaborat Hlth Studies Coordinating Cntr, Seattle, WA 98195 USA.
[Winslow, Raimond L.] Johns Hopkins Univ, Inst Computat Med, Baltimore, MD USA.
[Bluemke, David A.] NIH, Clin Cntr, Bethesda, MD 20892 USA.
RI Prince, Martin/S-6850-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 15467
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885005205
ER
PT J
AU Robinson, S
Pelter, MM
Nesbitt, T
Moser, D
Paul, SM
Cooper, LS
Dracup, K
AF Robinson, Susan
Pelter, Michele M.
Nesbitt, Thomas
Moser, Debra
Paul, Steve M.
Cooper, Lawton S.
Dracup, Kathleen
TI Relationship Between Poor Health Literacy and Heart Failure Readmissions
SO CIRCULATION
LA English
DT Meeting Abstract
DE Heart failure
C1 [Robinson, Susan; Paul, Steve M.; Dracup, Kathleen] UCSF, San Francisco, CA USA.
[Pelter, Michele M.] Univ Nevada, Reno, NV 89557 USA.
[Nesbitt, Thomas] Univ Calif Davis, Sacramento, CA USA.
[Moser, Debra] Univ Kentucky, Lexington, KY USA.
[Cooper, Lawton S.] NHLBI, Clin Applicat & Prevent Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 10658
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885001008
ER
PT J
AU Sasaki, T
Sasaki, T
Miller, CF
Hansford, R
Zviman, MM
Marine, JE
Spragg, D
Cheng, A
Tandri, H
Sinha, S
Kolandaivelu, A
Zimmerman, SL
Bluemke, DA
Tomaselli, GF
Berger, RD
Halperin, HR
Calkins, H
Nazarian, S
AF Sasaki, Takeshi
Sasaki, Takeshi
Miller, Christopher F.
Hansford, Rozann
Zviman, Menekhem M.
Marine, Joseph E.
Spragg, David
Cheng, Alan
Tandri, Harikrishna
Sinha, Sunil
Kolandaivelu, Aravindan
Zimmerman, Stefan L.
Bluemke, David A.
Tomaselli, Gordon F.
Berger, Ronald D.
Halperin, Henry R.
Calkins, Hugh
Nazarian, Saman
TI Association of Electrogram Features and Critical Reentrant Ventricular
Tachycardia Sites with Nonischemic Scar on Late Gadolinium Enhanced
Cardiac Magnetic Resonance
SO CIRCULATION
LA English
DT Meeting Abstract
DE Ventricular arrhythmia; Cardiac MRI; Cardiomyopathy; Electrophysiology
C1 [Sasaki, Takeshi; Sasaki, Takeshi; Miller, Christopher F.; Hansford, Rozann; Zviman, Menekhem M.; Marine, Joseph E.; Spragg, David; Cheng, Alan; Tandri, Harikrishna; Sinha, Sunil; Kolandaivelu, Aravindan; Zimmerman, Stefan L.; Tomaselli, Gordon F.; Berger, Ronald D.; Halperin, Henry R.; Calkins, Hugh; Nazarian, Saman] Johns Hopkins Univ, Baltimore, MD USA.
[Bluemke, David A.] Natl Inst Biomed Imaging & Bioengn, Bethesda, 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
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 9628
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885000172
ER
PT J
AU Schwartz, SM
Lu, MM
Ohye, RG
Hill, KD
Atz, AM
Naim, M
Williams, I
Goldberg, C
Lewis, A
Pigula, F
Manning, P
Pizarro, C
Chai, P
Burch, P
Dunbar-Masterson, C
Kaltman, J
Kanter, K
Sleeper, LA
Schonbeck, J
Ghanayem, N
AF Schwartz, Steven M.
Lu, Minmin
Ohye, Richard G.
Hill, Kevin D.
Atz, Andrew M.
Naim, Maryam
Williams, Ismee
Goldberg, Caren
Lewis, Alan
Pigula, Frank
Manning, Peter
Pizarro, Christian
Chai, Paul
Burch, Phillin
Dunbar-Masterson, Carolyn
Kaltman, Jonathan
Kanter, Kirk
Sleeper, Lynn A.
Schonbeck, Julie
Ghanayem, Nancy
CA Pediat Heart Network Investigators
TI Risk Factors for Prolonged Length of Stay Following Stage II procedure
in the Single Ventricle Reconstruction Trial
SO CIRCULATION
LA English
DT Meeting Abstract
DE Congenital heart surgery; Single ventricle; Hypoplastic left heart;
NHLBI; Pediatric cardiology
C1 [Schwartz, Steven M.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Lu, Minmin; Sleeper, Lynn A.; Schonbeck, Julie] New England Res Inst, Cntr Stat Anal & Rsch, Watertown, MA 02172 USA.
[Ohye, Richard G.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Hill, Kevin D.] Duke Univ, Fayetteville, NC USA.
[Atz, Andrew M.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Naim, Maryam] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Williams, Ismee] Columbia Univ, New York, NY USA.
[Goldberg, Caren] Univ Michigan, Ann Arbor, MI 48109 USA.
[Lewis, Alan] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Pigula, Frank; Dunbar-Masterson, Carolyn] Childrens Hosp, Boston, MA 02115 USA.
[Manning, Peter] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
[Pizarro, Christian] Alfred I duPont Hosp Children, Wilmington, DE USA.
[Chai, Paul] All Childrens Hosp, Tampa, FL USA.
[Burch, Phillin] Primary Childrens Med Ctr, Salt Lake City, UT 84103 USA.
[Kaltman, Jonathan] NHLBI, NIH, Bethesda, MD 20892 USA.
[Kanter, Kirk] Emory Univ, Atlanta, GA 30322 USA.
[Ghanayem, Nancy] Childrens Hosp Wisconsin, Milwaukee, WI 53201 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 16568
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885006213
ER
PT J
AU Sinner, MF
Krijthe, B
Aspelund, T
Stepas, K
Pencina, M
Moser, C
Sootodehnia, N
Fontes, J
Janssens, C
Kronmal, R
Magnani, J
Witteman, J
Chamberlain, A
Lubitz, S
Schnabel, R
Vasan, R
Wang, T
Agarwal, S
McManus, D
Ellinor, P
Larson, M
Burke, G
Launer, L
Hofman, A
Levy, D
Gottdiener, J
Kaab, S
Couper, D
Harris, T
Soliman, E
Stricker, B
Gudnason, V
Heckbert, S
Benjamin, E
Alonso, A
AF Sinner, Moritz F.
Krijthe, Bouwe
Aspelund, Thor
Stepas, Katherine
Pencina, Michael
Moser, Carlee
Sootodehnia, Nona
Fontes, Joao
Janssens, Cecile
Kronmal, Richard
Magnani, Jared
Witteman, Jacqueline
Chamberlain, Alanna
Lubitz, Steven
Schnabel, Renate
Vasan, Ramachandran
Wang, Thomas
Agarwal, Sunil
McManus, David
Ellinor, Patrick
Larson, Martin
Burke, Gregory
Launer, Leonore
Hofman, Albert
Levy, Daniel
Gottdiener, John
Kaeaeb, Stefan
Couper, David
Harris, Tamara
Soliman, Elsayed
Stricker, Bruno
Gudnason, Vilmundur
Heckbert, Susan
Benjamin, Emelia
Alonso, Alvaro
TI B-Type-Natriuretic Peptide and C-Reactive Protein in the Prediction of
Atrial Fibrillation Risk: The CHARGE-AF Consortium
SO CIRCULATION
LA English
DT Meeting Abstract
DE Atrial fibrillation; Risk factors; Biomarkers; Natriuretic peptide;
Epidemiology
C1 [Sinner, Moritz F.; Lubitz, Steven; Ellinor, Patrick] Massachusetts Gen Hosp, Cardiovasc Rsch Cntr, Charlestown, MA USA.
[Krijthe, Bouwe; Janssens, Cecile; Witteman, Jacqueline; Hofman, Albert; Stricker, Bruno] Erasmus Med Cntr, Dept Epidemiolgy, Rotterdam, Netherlands.
[Aspelund, Thor; Gudnason, Vilmundur] Iceland Heart Assoc, Rsch Inst, Kopavogur, Iceland.
[Stepas, Katherine; Pencina, Michael; Moser, Carlee] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Sootodehnia, Nona] Univ Washington, Div Cardiol, Seattle, WA 98195 USA.
[Fontes, Joao; Magnani, Jared; Vasan, Ramachandran; Larson, Martin; Levy, Daniel; Benjamin, Emelia] Boston Univ, Framingham Heart study, Framingham, MA USA.
[Kronmal, Richard] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Chamberlain, Alanna] Mayo Clini, Dept Hlth Sci Rsch, Rochester, MN USA.
[Schnabel, Renate] Univ Heart Cntr, Dept Gen & Intervent Cardiol, Hamburg, Germany.
[Wang, Thomas] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Agarwal, Sunil] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[McManus, David] Univ Massachusetts, Dept Med, Worcester, MA 01605 USA.
[Burke, Gregory] Wake Forest Sch Med, Div Publ Hlth Sci, Winston Salem, NC USA.
[Launer, Leonore; Harris, Tamara] NIA, Lab Epidemiol, Bethesda, MD 20892 USA.
[Gottdiener, John] Univ Maryland, Med Ctr, Div Cardiol, Baltimore, MD 21201 USA.
[Kaeaeb, Stefan] Univ Hosp Munich, Dept Med 1, Munich, Germany.
[Couper, David] Univ N Carolina, Dept Biostat, Chapel Hill, NC USA.
[Soliman, Elsayed] Wake Forest Sch Med, Dept Epidemiol, Winston Salem, NC USA.
[Heckbert, Susan] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Alonso, Alvaro] Univ Minnesota, Div Epidemiol, Minneapolis, MN 55455 USA.
RI Gudnason, Vilmundur/K-6885-2015; Aspelund, Thor/C-5983-2008
OI Gudnason, Vilmundur/0000-0001-5696-0084; Aspelund,
Thor/0000-0002-7998-5433
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 12621
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885002323
ER
PT J
AU Sundaresan, NR
Vasudevan, P
Lei, Z
Kim, G
Sadhana, S
Ravindra, PV
Pillai, V
Jeevananadam, V
Gupta, M
Mostoslavsky, R
Gupta, MP
AF Sundaresan, Nagalingam Ravi
Vasudevan, Prabhakaran
Lei, Zhong
Kim, Gene
Sadhana, Samant
Ravindra, P. V.
Pillai, Vinodkumar
Jeevananadam, Valluvan
Gupta, Madhu
Mostoslavsky, Raul
Gupta, Mahesh P.
TI Novel players in Hypertrophy
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac hypertrophy
C1 [Sundaresan, Nagalingam Ravi; Vasudevan, Prabhakaran; Sadhana, Samant; Pillai, Vinodkumar; Jeevananadam, Valluvan; Gupta, Mahesh P.] Univ Chicago, Chicago, IL 60637 USA.
[Lei, Zhong; Mostoslavsky, Raul] Harvard Univ, Sch Med, Boston, MA USA.
[Kim, Gene] Univ Chicago, Dept Med 4, Chicago, IL 60637 USA.
[Ravindra, P. V.] NCI, Ctr Canc, Chicago, IL USA.
[Gupta, Madhu] Univ Illinois, Dept Physiol & Biophys, Chicago, IL 60680 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885005325
ER
PT J
AU Taylor, DA
Perin, EC
Willerson, JT
Pepine, CJ
Henry, TD
Ellis, SG
Zhao, DX
Bolli, R
Byrne, BJ
Traverse, JH
Penn, MS
Hatzopoulos, AK
Carlson, MA
Wise, E
Lai, DJ
Baraniuk, S
Cabreira-Hansen, MG
Smith, D
Moye, LA
Skarlatos, SI
Simari, RD
Cogle, CR
AF Taylor, Doris A.
Perin, Emerson C.
Willerson, James T.
Pepine, Carl J.
Henry, Timothy D.
Ellis, Stephen G.
Zhao, David X.
Bolli, Roberto
Byrne, Barry J.
Traverse, Jay H.
Penn, Marc S.
Hatzopoulos, Antonis K.
Carlson, Marjorie A.
Wise, Elizabeth
Lai, Dejian
Baraniuk, Sarah
Cabreira-Hansen, Maria G.
Smith, Deirdre
Moye, Lemuel A.
Skarlatos, Sonia I.
Simari, Robert D.
Cogle, Christopher R.
TI Improved Myocardial Function in Patients with Chronic Ischemic Heart
Disease Treated with Transendocardial Delivery of Bone Marrow
Mononuclear Cells Depends Upon Input Cell Phenotype and Function
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac injection; Cells; Heart failure; Clinical trials; Ejection
fraction
C1 [Taylor, Doris A.; Perin, Emerson C.; Willerson, James T.; Cabreira-Hansen, Maria G.; Smith, Deirdre] St Lukes Episcopal Hosp, Texas Heart Inst, Houston, TX USA.
[Pepine, Carl J.] Univ Florida, Coll Med, Houston, TX USA.
[Henry, Timothy D.] Univ Minnesota, Sch Med, Minneapolis Heart Inst Fdn, Minneapolis, MN 55455 USA.
[Ellis, Stephen G.] Cleveland Clin, Cleveland, OH 44106 USA.
[Zhao, David X.; Hatzopoulos, Antonis K.] Vanderbilt Univ, Sch Med, Nashville, TN 37212 USA.
[Bolli, Roberto] Univ Louisville, Inst Mol Cardiol, Louisville, KY 40292 USA.
[Byrne, Barry J.; Wise, Elizabeth; Cogle, Christopher R.] Univ Florida, Coll Med, Gainesville, FL USA.
[Traverse, Jay H.] Univ Minnesota, Sch Med, Minneapolis Heart Inst Fdn Abbott, Minneapolis, MN 55455 USA.
[Penn, Marc S.] Summa Cardiovasc Inst, Rootstown, OH USA.
[Carlson, Marjorie A.] Univ Minnesota, Sch Med, Cntr Cardiovasc Repair, Minneapolis, MN 55455 USA.
[Lai, Dejian; Baraniuk, Sarah; Moye, Lemuel A.] Univ Texas Houston, Sch Publ Hlth, Houston, TX USA.
[Skarlatos, Sonia I.] NHLBI, Bethesda, MD 20892 USA.
[Simari, Robert D.] Mayo Clin, Rochester, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 16354
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885006119
ER
PT J
AU Trivedi, D
Loftin, C
Langenbach, R
AF Trivedi, Darshini
Loftin, Charles
Langenbach, Robert
TI The Deficiency of beta-Arrestin 2 Attenuates Abdominal Aortic Aneurysm
Formation in Mice
SO CIRCULATION
LA English
DT Meeting Abstract
DE Abdominal aortic aneurysm
C1 [Trivedi, Darshini; Langenbach, Robert] NIEHS, Lab Toxicol & Pharmacol, Durham, NC USA.
[Loftin, Charles] Univ Kentucky, Dept Pharmaceut Sci, Lexington, KY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 19684
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885009168
ER
PT J
AU Truong, QA
Hayden, D
Woodard, PK
Kirby, R
Chou, ET
Wiviott, SD
Fleg, JL
Schoenfeld, DA
Udelson, JE
Hoffmann, U
AF Truong, Quynh A.
Hayden, Douglas
Woodard, Pamela K.
Kirby, Ruth
Chou, Eric T.
Wiviott, Stephen D.
Fleg, Jerome L.
Schoenfeld, David A.
Udelson, James E.
Hoffmann, Udo
TI Women Benefit Most from Early CCTA Compared to Standard ED Evaluation
for Acute Chest Pain: The ROMICAT II Trial
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac CT; Emergency care; Comparative effectiveness; Clinical trials;
Cardiovascular imaging
C1 [Truong, Quynh A.; Hoffmann, Udo] Massachusetts Gen Hosp, Cardiac MR PET CT Program, Div Cardiol, Boston, MA 02114 USA.
[Truong, Quynh A.; Hoffmann, Udo] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Hayden, Douglas; Schoenfeld, David A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Woodard, Pamela K.] Washington Univ, Sch Med, Edward Mallinckrodt Inst Radiol, St Louis, MO 63110 USA.
[Kirby, Ruth; Fleg, Jerome L.] NHLBI, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
[Chou, Eric T.] Kaiser Permanente Fontana Med Cntr, Fontana, CA USA.
[Wiviott, Stephen D.] Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA.
[Udelson, James E.] Tufts Med Cntr, Cardiol & CardioVasc Cntr, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 12596
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885002314
ER
PT J
AU Turkbey, EB
Backlund, JYC
Cleary, PA
Nacif, MS
Gai, N
van der Geest, RJ
Armstrong, A
Volpe, GJ
Nazarian, S
Lachin, JM
Lima, JA
Bluemke, DA
AF Turkbey, Evrim B.
Backlund, Jye-Yu C.
Cleary, Patricia A.
Nacif, Marcelo S.
Gai, Neville
van der Geest, Rob J.
Armstrong, Anderson
Volpe, Gustavo J.
Nazarian, Saman
Lachin, John M.
Lima, Joao A.
Bluemke, David A.
CA DCCT EDIC Rsch Grp
TI Myocardial Structural Remodeling and Tissue Composition by Cardiac
Magnetic Resonance (CMR) in Relation to Metabolic Syndrome in Type 1
Diabetes: The DCCT/EDIC Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Type 1 Diabetes; Magnetic resonance Imaging; Metabolic syndromie;
Ventricular remodeling
C1 [Turkbey, Evrim B.] NIH, North Bethesda, MD USA.
[Backlund, Jye-Yu C.; Cleary, Patricia A.; Lachin, John M.] George Washington Univ, Ctr Biostat, Rockville, MD USA.
[Nacif, Marcelo S.; Gai, Neville; Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
[van der Geest, Rob J.] Leiden Univ, Div Image Proc, Leiden, Netherlands.
[Armstrong, Anderson; Volpe, Gustavo J.; Nazarian, Saman; Lima, Joao A.] Johns Hopkins Univ, Baltimore, MD USA.
RI Armstrong, Anderson/G-8407-2012; van der Geest, Rob/J-8193-2015
OI Armstrong, Anderson/0000-0003-3161-8922; van der Geest,
Rob/0000-0002-9084-5597
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 16435
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885006149
ER
PT J
AU Vaidya, D
Bennett, WL
Sibley, CT
Polak, JF
Herrington, DM
Ouyang, P
AF Vaidya, Dhananjay
Bennett, Wendy L.
Sibley, Christopher T.
Polak, Joseph F.
Herrington, David M.
Ouyang, Pamela
TI Ever-pregnant Women Have Less Distensible Carotid Arteries Than
Never-pregnant Women: Multi-Ethnic Study of Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
DE Arteries; Ultrasound; Pregnancy
C1 [Vaidya, Dhananjay; Bennett, Wendy L.; Ouyang, Pamela] Johns Hopkins Univ, Baltimore, MD USA.
[Sibley, Christopher T.] NIH, Clin Cntr, Bethesda, MD 20892 USA.
[Polak, Joseph F.] Tufts Univ Sch Med, Boston, MA USA.
[Herrington, David M.] Wake Forest Univ, Winston Salem, NC 27109 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 10126
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885000312
ER
PT J
AU Van Hee, VC
Chan, SH
Szpiro, AA
Oron, AP
DeRoo, LA
London, SJ
Kaufman, JD
Sandler, DP
AF Van Hee, Victor C.
Chan, Stephanie H.
Szpiro, Adam A.
Oron, Assaf P.
DeRoo, Lisa A.
London, Stephanie J.
Kaufman, Joel D.
Sandler, Dale P.
TI Long Term Air Pollution Exposure and Blood Pressure in the Sister Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Air pollution; Blood pressure; Epidemiology; Risk factors; Prevention
C1 [Van Hee, Victor C.; Chan, Stephanie H.; Szpiro, Adam A.; Oron, Assaf P.; Kaufman, Joel D.] Univ Washington, Seattle, WA 98195 USA.
[DeRoo, Lisa A.; Sandler, Dale P.] NIEHS, Chron Dis Epidemiol Grp, Rsch Triangle Pk, NC USA.
[London, Stephanie J.] NIEHS, Genet Environm & Resp Dis Grp, Rsch Triangle Pk, NC USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 15418
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885005193
ER
PT J
AU Venkatesan, B
Valente, AJ
Siebenlist, U
Chandrasekar, B
AF Venkatesan, Balachandar
Valente, Anthony J.
Siebenlist, Ulrich
Chandrasekar, Bysani
TI CIKS (Act1 Or TRAF3IP2) is Critical in High Glucose-induced Endothelial
Dysfunction
SO CIRCULATION
LA English
DT Meeting Abstract
DE Endothelin; Inflammation; Adherence; Oxidative stress; Arteriosclerosis
C1 [Venkatesan, Balachandar] Madras Diabet Rsch Fdn, Siruseri, India.
[Valente, Anthony J.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 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 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 9690
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885000189
ER
PT J
AU Venkatesh, BA
Armstrong, A
Liu, CY
Donekal, S
Yoneyama, K
Wu, C
Gomes, AS
Hundley, GW
Bluemke, DA
Lima, JA
AF Venkatesh, Bharath Ambale
Armstrong, Anderson
Liu, Chia-Ying
Donekal, Sirisha
Yoneyama, Kihei
Wu, Colin
Gomes, Antoinette S.
Hundley, Gregory W.
Bluemke, David A.
Lima, Joao A.
TI Strain Relaxation Index Predicts Heart Failure and Atrial Fibrillation
Over a 10 Year Follow-Up Period: The Multi-Ethnic Study of
Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Diastolic function; Magnetic resonance imaging; Cardiac imaging; Heart
failure; Ventricular function
C1 [Venkatesh, Bharath Ambale; Liu, Chia-Ying; Lima, Joao A.] Johns Hopkins Univ, Baltimore, MD USA.
[Armstrong, Anderson; Donekal, Sirisha; Yoneyama, Kihei] Johns Hopkins Univ, Div Cardiovasc Imaging, Baltimore, MD USA.
[Wu, Colin] NHLBI, Rockledge Cntr 2, OD, NIH, Bethesda, MD 20892 USA.
[Gomes, Antoinette S.] Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA.
[Hundley, Gregory W.] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
[Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
RI Armstrong, Anderson/G-8407-2012; Ambale Venkatesh, Bharath/F-4941-2016
OI Armstrong, Anderson/0000-0003-3161-8922; Ambale Venkatesh,
Bharath/0000-0002-2330-2373
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 14547
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885004260
ER
PT J
AU Vinogradova, TM
Lyashkov, AE
Li, Y
Lukyanenko, Y
Lakatta, EG
AF Vinogradova, Tatiana M.
Lyashkov, Alexey E.
Li, Yue
Lukyanenko, Yevgeniya
Lakatta, Edward G.
TI Synergism of PDE3 and PDE4 Activity Regulates cAMP-Mediated
PKA-Dependent Local Ca2+ Releases to Modulate Basal Spontaneous Firing
of Cardiac Pacemaker Cells
SO CIRCULATION
LA English
DT Meeting Abstract
DE Sinoatrial node; Calcium; Phospholamban; Electrophysiology; Pacemakers
C1 [Vinogradova, Tatiana M.; Lyashkov, Alexey E.; Li, Yue; Lukyanenko, Yevgeniya; Lakatta, Edward G.] NIA, NIH, Baltimore, MD 21224 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 13555
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885003286
ER
PT J
AU Volpe, GJ
Nacif, MS
Liu, YC
Turkbey, EB
Rizzi, PB
Lederer, DJ
Barr, RG
Polak, JF
Wu, C
Liu, CY
Bluemke, DA
Lima, JA
AF Volpe, Gustavo J.
Nacif, Marcelo S.
Liu, Yuan Chang
Turkbey, Evrim B.
Rizzi, Patricia B.
Lederer, David J.
Barr, R. Graham
Polak, Joseph F.
Wu, Colin
Liu, Chia-Ying
Bluemke, David A.
Lima, Joao A.
TI Factors Associated with Interstitial Fibrosis by CMR T1 Mapping After 10
Years: The Multi-Ethnic Study of Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
DE Fibrosis; Magnetic resonance imaging; Risk factors; Smoking
C1 [Volpe, Gustavo J.; Liu, Yuan Chang; Liu, Chia-Ying; Lima, Joao A.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[Nacif, Marcelo S.] NIH, Bethesda, MD 20892 USA.
[Turkbey, Evrim B.] NIH, Radiol & Imaging Sci RAD & IS, Bethesda, MD 20892 USA.
[Rizzi, Patricia B.] Johns Hopkins Univ Hosp, Dvis Cardiol, Baltimore, MD 21287 USA.
[Lederer, David J.] Columbia Univ, Coll Phys & Surg, New York, NY USA.
[Barr, R. Graham] Columbia Univ, New York, NY USA.
[Polak, Joseph F.] Tufts Med Cntr, Ultrasound Reading Cntr, Boston, MA USA.
[Wu, Colin] NHLBI, Rockledge Cntr 2, NIH, OD, Bethesda, MD 20892 USA.
[Bluemke, David A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 17372
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885007090
ER
PT J
AU Wong, TC
Piehler, K
Klock, AM
Kang, IA
Kadakkal, A
Kellman, P
Schwartzman, DS
Mulukutla, SR
Simon, MA
Schelbert, EB
AF Wong, Timothy C.
Piehler, Kayla
Klock, Amanda M.
Kang, Ian A.
Kadakkal, Ajay
Kellman, Peter
Schwartzman, David S.
Mulukutla, Suresh R.
Simon, Marc A.
Schelbert, Erik B.
TI Myocardial Fibrosis Quantified by Cardiovascular Magnetic Resonance is
Associated with Diabetes and Predicts Mortality
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac MRI; Fibrosis; Outcomes; Diastole
C1 [Wong, Timothy C.; Piehler, Kayla; Klock, Amanda M.; Kang, Ian A.; Kadakkal, Ajay; Schwartzman, David S.; Mulukutla, Suresh R.; Simon, Marc A.; Schelbert, Erik B.] Univ Pittsburgh, Sch Med, Dept Med, Pittsburgh, PA 15213 USA.
[Kellman, Peter] NHLBI, Med Imaging Sect, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 16452
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885006158
ER
PT J
AU Xie, A
Kapoor, N
Liu, H
Bare, D
Gu, LZ
Boheler, KR
Banach, K
Dudley, SC
AF Xie, An
Kapoor, Nidhi
Liu, Hong
Bare, Dan
Gu, Lianzhi
Boheler, Kenneth R.
Banach, Kathrin
Dudley, Samuel C.
TI A Role for Mitochondria in Triggered Activity from Cardiomyocytes with
Reduced Sarcoplasmic Reticulum Calcium Release
SO CIRCULATION
LA English
DT Meeting Abstract
DE Arrhythmias treatment of; Mitochondria; Calcium
C1 [Xie, An; Liu, Hong; Bare, Dan; Gu, Lianzhi; Banach, Kathrin; Dudley, Samuel C.] Univ Illinois, Chicago, IL USA.
[Kapoor, Nidhi] Cedars Sinai Med Ctr, Inst Heart, Los Angeles, CA 90048 USA.
[Boheler, Kenneth R.] NIA, Mol Cardiol & Stem Cell Unit, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 19255
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885009001
ER
PT J
AU Yang, E
Nacif, MS
Liu, CY
Donekal, S
Venkatesh, BA
Prince, MR
Lima, JA
Bluemke, DA
AF Yang, Eunice
Nacif, Marcelo S.
Liu, Chia-Ying
Donekal, Sirisha
Venkatesh, Bharath A.
Prince, Martin R.
Lima, Joao A.
Bluemke, David A.
TI Assessment of Myocardial Wall Thickness and T1 Mapping is Highly
Reproducible in Multi-Center Trials: The Multi-Ethnic Study of
Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
DE Muscle, cardiac - see Myocardium; Strain rate; Magnetic resonance
imaging
C1 [Yang, Eunice; Nacif, Marcelo S.; Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
[Liu, Chia-Ying; Donekal, Sirisha; Venkatesh, Bharath A.; Lima, Joao A.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[Prince, Martin R.] Weill Cornell Med Coll, New York, NY USA.
RI Ambale Venkatesh, Bharath/F-4941-2016; Prince, Martin/S-6850-2016
OI Ambale Venkatesh, Bharath/0000-0002-2330-2373;
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 14728
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885004337
ER
PT J
AU Yeboah, J
Carr, JJ
Terry, JG
Ding, JZ
Zeb, I
Liu, ST
Nasir, K
Post, W
Blumenthal, RS
Budoff, M
AF Yeboah, Joseph
Carr, Jeffery J.
Terry, James G.
Ding, Jingzhong
Zeb, Irfan
Liu, Songtao
Nasir, Khurram
Post, Wendy
Blumenthal, Roger S.
Budoff, Mathew
TI Computed Tomography Derived Cardiovascular Risk Markers, Incident
Cardiovascular Events and All- Cause Mortality In Adults Free of
Clinical Cardiovascular Disease. The Multi Ethnic Study of
Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac CT; Risk factors; Cardiovascular disease; Calcification;
Valvular heart disease
C1 [Yeboah, Joseph; Carr, Jeffery J.; Terry, James G.; Ding, Jingzhong] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Zeb, Irfan] Los Angeles Biomed Rsch Inst, Torrance, CA USA.
[Liu, Songtao] NIH, Bethesda, MD 20892 USA.
[Nasir, Khurram; Post, Wendy; Blumenthal, Roger S.] Johns Hopkins Univ, Baltimore, MD USA.
[Budoff, Mathew] Los Angeles Biomed Rsch Inst, Torrance, CA 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
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 20
PY 2012
VL 126
IS 21
SU S
MA 9536
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V31LL
UT WOS:000208885000148
ER
PT J
AU Scheidweiler, KB
Desrosiers, NA
Huestis, MA
AF Scheidweiler, Karl B.
Desrosiers, Nathalie A.
Huestis, Marilyn A.
TI Simultaneous quantification of free and glucuronidated cannabinoids in
human urine by liquid chromatography tandem mass spectrometry
SO CLINICA CHIMICA ACTA
LA English
DT Article
DE Cannabinoids; Cannabinoid glucuronides; Urine; Metabolites; Analytical
method; LCMSMS
ID SOLID-PHASE EXTRACTION; GAS-CHROMATOGRAPHY; GC-MS;
11-NOR-DELTA(9)-TETRAHYDROCANNABINOL-9-CARBOXYLIC ACID; WHOLE-BLOOD;
TETRAHYDROCANNABINOL GLUCURONIDE; AUTOMATED EXTRACTION; PLASMA;
METABOLITES; STABILITY
AB Background: cannabis is the most commonly abused drug of abuse and is commonly quantified during urine drug testing. We are conducting a controlled drug administration study investigating efficacy of urinary cannabinoid glucuronide metabolites for documenting recency of cannabis intake and for determining stability of urinary cannabinoids.
Methods: A liquid chromatography tandem mass spectrometry method was developed and validated quantifying Delta 9-tetrahydrocannabinol (THC), 11-hydroxy-THC (11-OH-THC), 11-nor-9-carboxy-THC (THCCOOH), cannabidiol, cannabinol, THC-glucuronide and THCCOOH-glucuronide in 0.5 ml human urine via supported-liquid extraction. Chromatography was performed on an Ultra Biphenyl column with a gradient of 10 mmol/l ammonium acetate, pH 6.15 and 15% methanol in acetonitrile at 0.4 ml/min. Analytes were monitored by positive and negative mode electrospray ionization and multiple reaction monitoring mass spectrometry.
Results: Linear ranges were 0.5-50 ng/ml for THC-glucuronide, 1-100 ng/ml for THCCOOH, 11-OH-THC and cannabidiol, 2-100 ng/ml for THC and cannabinol, and 5-500 ng/ml for THCCOOH-glucuronide (R-2 > 0.99). Mean extraction efficiencies were 34-73% with analytical recovery (bias) 80.5-118.0% and total imprecision 3.0-10.2% coefficient of variation.
Conclusion: This method simultaneously quantifies urinary cannabinoids and phase II glucuronide metabolites, and enables evaluation of urinary cannabinoid glucuronides for documenting recency of cannabis intake and cannabinoid stability. The assay is applicable for routine urine cannabinoid testing. Published by Elsevier B.V.
C1 [Huestis, Marilyn A.] NIDA, IRP, NIH, Biomed Res Ctr, Baltimore, MD 21224 USA.
RP Huestis, MA (reprint author), NIDA, IRP, NIH, Biomed Res Ctr, 251 Bayview Blvd,Suite 200 Room 05A-721, Baltimore, MD 21224 USA.
EM mhuestis@intra.nida.nih.gov
FU National Institute on Drug Abuse, National Institutes of Health
FX The authors recognize David M. Schwope's technical advice during method
development. This research was supported by the Intramural Research
Program of the National Institute on Drug Abuse, National Institutes of
Health.
NR 40
TC 29
Z9 29
U1 7
U2 38
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0009-8981
J9 CLIN CHIM ACTA
JI Clin. Chim. Acta
PD NOV 20
PY 2012
VL 413
IS 23-24
BP 1839
EP 1847
DI 10.1016/j.cca.2012.06.034
PG 9
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 006UN
UT WOS:000308844700007
PM 22771478
ER
PT J
AU Zheng, X
Vittar, NBR
Gai, XH
Fernandez-Barrena, MG
Moser, CD
Hu, CL
Almada, LL
McCleary-Wheeler, AL
Elsawa, SF
Vrabel, AM
Shire, AM
Comba, A
Thorgeirsson, SS
Kim, Y
Liu, QG
Fernandez-Zapico, ME
Roberts, LR
AF Zheng, Xin
Vittar, Natalia B. Rumie
Gai, Xiaohong
Fernandez-Barrena, Maite G.
Moser, Catherine D.
Hu, Chunling
Almada, Luciana L.
McCleary-Wheeler, Angela L.
Elsawa, Sherine F.
Vrabel, Anne M.
Shire, Abdirashid M.
Comba, Andrea
Thorgeirsson, Snorri S.
Kim, Youngsoo
Liu, Qingguang
Fernandez-Zapico, Martin E.
Roberts, Lewis R.
TI The Transcription Factor GLI1 Mediates TGF beta 1 Driven EMT in
Hepatocellular Carcinoma via a SNAI1-Dependent Mechanism
SO PLOS ONE
LA English
DT Article
ID EPITHELIAL-MESENCHYMAL TRANSITION; E-CADHERIN; SONIC HEDGEHOG;
RISK-FACTORS; CELLS; BETA; METASTASIS; RECURRENCE; CANCER; SNAIL
AB The role of the epithelial-to-mesenchymal transition (EMT) during hepatocellular carcinoma (HCC) progression is well established, however the regulatory mechanisms modulating this phenomenon remain unclear. Here, we demonstrate that transcription factor glioma-associated oncogene 1 (GLI1) modulates EMT through direct up-regulation of SNAI1 and serves as a downstream effector of the transforming growth factor-beta 1 (TGF beta 1) pathway, a well-known regulator of EMT in cancer cells. Overexpression of GLI1 increased proliferation, viability, migration, invasion, and colony formation by HCC cells. Conversely, GLI1 knockdown led to a decrease in all the above-mentioned cancer-associated phenotypes in HCC cells. Further analysis of GLI1 regulated cellular functions showed that this transcription factor is able to induce EMT and identified SNAI1 as a transcriptional target of GLI1 mediating this cellular effect in HCC cells. Moreover, we demonstrated that an intact GLI1-SNAI1 axis is required by TGF beta 1 to induce EMT in these cells. Together, these findings define a novel cellular mechanism regulated by GLI1, which controls the growth and EMT phenotype in HCC.
C1 [Zheng, Xin; Vittar, Natalia B. Rumie; Gai, Xiaohong; Fernandez-Barrena, Maite G.; Moser, Catherine D.; Hu, Chunling; Almada, Luciana L.; McCleary-Wheeler, Angela L.; Vrabel, Anne M.; Shire, Abdirashid M.; Comba, Andrea; Fernandez-Zapico, Martin E.; Roberts, Lewis R.] Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN 55905 USA.
[Zheng, Xin; Gai, Xiaohong; Liu, Qingguang] Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Hepatobiliary Surg, Xian 710049, Shaanxi, Peoples R China.
[Zheng, Xin; Vittar, Natalia B. Rumie; Gai, Xiaohong; Fernandez-Barrena, Maite G.; Moser, Catherine D.; Hu, Chunling; Almada, Luciana L.; McCleary-Wheeler, Angela L.; Elsawa, Sherine F.; Vrabel, Anne M.; Shire, Abdirashid M.; Comba, Andrea; Fernandez-Zapico, Martin E.; Roberts, Lewis R.] Mayo Clin, Ctr Canc, Rochester, MN USA.
[Vittar, Natalia B. Rumie; Fernandez-Barrena, Maite G.; Almada, Luciana L.; McCleary-Wheeler, Angela L.; Elsawa, Sherine F.; Vrabel, Anne M.; Comba, Andrea; Fernandez-Zapico, Martin E.] Mayo Clin, Schulze Ctr Novel Therapeut, Rochester, MN USA.
[Elsawa, Sherine F.] No Illinois Univ, Dept Biol Sci, De Kalb, IL USA.
[Thorgeirsson, Snorri S.] NCI, Expt Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Kim, Youngsoo] Isis Pharmaceut Inc, Carlsbad, CA USA.
RP Roberts, LR (reprint author), Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN 55905 USA.
EM roberts.lewis@mayo.edu
RI GARCIA FERNANDEZ DE BARRENA, MAITE/J-8040-2014
OI GARCIA FERNANDEZ DE BARRENA, MAITE/0000-0003-0375-6236
FU National Institutes of Health [CA100882, CA128633, CA165076]; Mayo
Clinic Center for Cell Signaling in Gastroenterology [NIDDK
P30DK084567]; Mayo Clinic Cancer Center [CA15083]; Mayo Clinic Center
for Translational Science Activities (NIH/NCRR CTSA) [KL2 RR024151];
American Gastroenterological Association Foundation for Digestive Health
and Nutrition Bridgin Grant
FX This work was supported by National Institutes of Health Grants CA100882
and CA128633 (to LRR) and CA165076 (to LRR and MEFZ); the Mayo Clinic
Center for Cell Signaling in Gastroenterology (NIDDK P30DK084567) (to
MEFZ); the Mayo Clinic Cancer Center (CA15083), the Mayo Clinic Center
for Translational Science Activities (NIH/NCRR CTSA Grant Number KL2
RR024151), and an American Gastroenterological Association Foundation
for Digestive Health and Nutrition Bridging Grant (to LRR). Its contents
are solely the responsibility of the authors and do not necessarily
represent the official views of the 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 40
TC 35
Z9 39
U1 0
U2 19
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 19
PY 2012
VL 7
IS 11
AR e49581
DI 10.1371/journal.pone.0049581
PG 13
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 040PB
UT WOS:000311333800040
PM 23185371
ER
PT J
AU Zhang, L
Orban, M
Lorenz, M
Barocke, V
Braun, D
Urtz, N
Schulz, C
von Bruhl, ML
Tirniceriu, A
Gaertner, F
Proia, RL
Graf, T
Bolz, SS
Montanez, E
Prinz, M
Muller, A
von Baumgarten, L
Billich, A
Sixt, M
Fassler, R
von Andrian, UH
Junt, T
Massberg, S
AF Zhang, Lin
Orban, Martin
Lorenz, Michael
Barocke, Verena
Braun, Daniel
Urtz, Nicole
Schulz, Christian
von Bruehl, Marie-Luise
Tirniceriu, Anca
Gaertner, Florian
Proia, Richard L.
Graf, Thomas
Bolz, Steffen-Sebastian
Montanez, Eloi
Prinz, Marco
Mueller, Alexandra
von Baumgarten, Louisa
Billich, Andreas
Sixt, Michael
Faessler, Reinhard
von Andrian, Ulrich H.
Junt, Tobias
Massberg, Steffen
TI A novel role of sphingosine 1-phosphate receptor S1pr1 in mouse
thrombopoiesis
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID DEMARCATION MEMBRANE SYSTEM; PROTEIN-COUPLED RECEPTOR; HEMATOPOIETIC
STEM-CELL; IN-VIVO; PLATELET PRODUCTION; LYMPHOCYTE EGRESS;
BLOOD-PLATELETS; RETICULATED PLATELETS; HUMAN MEGAKARYOCYTES; VASCULAR
MATURATION
AB Millions of platelets are produced each hour by bone marrow (BM) megakaryocytes (MKs). MKs extend transendothelial proplatelet (PP) extensions into BM sinusoids and shed new platelets into the blood. The mechanisms that control platelet generation remain incompletely understood. Using conditional mutants and intravital multiphoton microscopy, we show here that the lipid mediator sphingosine 1-phosphate (S1P) serves as a critical directional cue guiding the elongation of megakaryocytic PP extensions from the interstitium into BM sinusoids and triggering the subsequent shedding of PPs into the blood. Correspondingly, mice lacking the S1P receptor S1pr1 develop severe thrombocytopenia caused by both formation of aberrant extravascular PPs and defective intravascular PP shedding. In contrast, activation of S1pr1 signaling leads to the prompt release of new platelets into the circulating blood. Collectively, our findings uncover a novel function of the S1P-S1pr1 axis as master regulator of efficient thrombopoiesis and might raise new therapeutic options for patients with thrombocytopenia.
C1 [Zhang, Lin; Orban, Martin; Lorenz, Michael; Barocke, Verena; Braun, Daniel; Urtz, Nicole; Schulz, Christian; von Bruehl, Marie-Luise; Tirniceriu, Anca; Gaertner, Florian; Massberg, Steffen] Univ Munich, Klinikum Univ, Med Klin & Poliklin 1, D-81337 Munich, Germany.
[von Baumgarten, Louisa] Univ Munich, Klinikum Univ, Neurol Klin, D-81337 Munich, Germany.
[Zhang, Lin; Orban, Martin; Lorenz, Michael; Barocke, Verena; Braun, Daniel; Urtz, Nicole; Schulz, Christian; von Bruehl, Marie-Luise; Tirniceriu, Anca; Gaertner, Florian; Massberg, Steffen] Tech Univ Munich, Deutsch Herzzentrum Munchen, D-80636 Munich, Germany.
[Proia, Richard L.] NIDDK, Genet Dev & Dis Branch, NIH, Bethesda, MD 20892 USA.
[Graf, Thomas] Ctr Genom Regulat, Barcelona 08003, Spain.
[Graf, Thomas] Catalan Inst Res & Adv Studies ICREA, Barcelona 08010, Spain.
[Bolz, Steffen-Sebastian] Univ Toronto, Dept Physiol, Toronto, ON M5S 1A8, Canada.
[Montanez, Eloi; Sixt, Michael; Faessler, Reinhard] Max Planck Inst Biochem, D-82152 Martinsried, Germany.
[Prinz, Marco; Mueller, Alexandra] Univ Freiburg Klinikum, Inst Pathol, Abt Neuropathol, D-79106 Freiburg, Germany.
[Prinz, Marco] Univ Freiburg, BIOSS Ctr Biol Signalling, D-79108 Freiburg, Germany.
[Billich, Andreas; Junt, Tobias] Novartis Inst BioMed Res, CH-4002 Basel, Switzerland.
[von Andrian, Ulrich H.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Massberg, Steffen] German Cardiovasc Res Ctr, Munich Heart Alliance, D-80802 Munich, Germany.
RP Massberg, S (reprint author), Univ Munich, Klinikum Univ, Med Klin & Poliklin 1, D-81337 Munich, Germany.
EM steffen.massberg@med.uni-muenchen.de
RI Schulz, Christian/J-8545-2012; von Andrian, Ulrich/A-5775-2008; Graf,
Thomas/B-4252-2015
OI Schulz, Christian/0000-0003-3878-7833; Sixt,
Michael/0000-0002-6620-9179; Graf, Thomas/0000-0003-2774-4117
FU Deutsche Forschungsgemeinschaft; Intramural Research Program of the
National Institutes of Health, National Institute of Diabetes and
Digestive and Kidney Diseases
FX This study was supported by the Deutsche Forschungsgemeinschaft and by
the Intramural Research Program of the National Institutes of Health,
National Institute of Diabetes and Digestive and Kidney Diseases.
NR 52
TC 46
Z9 47
U1 1
U2 8
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 19
PY 2012
VL 209
IS 12
BP 2165
EP 2181
DI 10.1084/jem.20121090
PG 17
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 040BY
UT WOS:000311295600005
PM 23148237
ER
PT J
AU Snow, AL
Xiao, WM
Stinson, JR
Lu, W
Chaigne-Delalande, B
Zheng, LX
Pittaluga, S
Matthews, HF
Schmitz, R
Jhavar, S
Kuchen, S
Kardava, L
Wang, W
Lamborn, IT
Jing, HE
Raffeld, M
Moir, S
Fleisher, TA
Staudt, LM
Su, HC
Lenardo, MJ
AF Snow, Andrew L.
Xiao, Wenming
Stinson, Jeffrey R.
Lu, Wei
Chaigne-Delalande, Benjamin
Zheng, Lixin
Pittaluga, Stefania
Matthews, Helen F.
Schmitz, Roland
Jhavar, Sameer
Kuchen, Stefan
Kardava, Lela
Wang, Wei
Lamborn, Ian T.
Jing, Huie
Raffeld, Mark
Moir, Susan
Fleisher, Thomas A.
Staudt, Louis M.
Su, Helen C.
Lenardo, Michael J.
TI Congenital B cell lymphocytosis explained by novel germline CARD11
mutations
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID NF-KAPPA-B; TRANSCRIPTION FACTORS; HEALTHY-CHILDREN; LYMPHOMA;
ACTIVATION; RECEPTOR; CARMA1; PROLIFERATION; PATHOGENESIS; COMPARTMENT
AB Nuclear factor-kappa B (NF-kappa B) controls genes involved in normal lymphocyte functions, but constitutive NF-kappa B activation is often associated with B cell malignancy. Using high-throughput whole transcriptome sequencing, we investigated a unique family with hereditary polyclonal B cell lymphocytosis. We found a novel germline heterozygous missense mutation (E127G) in affected patients in the gene encoding CARD11, a scaffolding protein required for antigen receptor (AgR)-induced NF-kappa B activation in both B and T lymphocytes. We subsequently identified a second germline mutation (G116S) in an unrelated, phenotypically similar patient, confirming mutations in CARD11 drive disease. Like somatic, gain-of-function CARD11 mutations described in B cell lymphoma, these germline CARD11 mutants spontaneously aggregate and drive constitutive NF-kappa B activation. However, these CARD11 mutants rendered patient T cells less responsive to AgR-induced activation. By reexamining this rare genetic disorder first reported four decades ago, our findings provide new insight into why activating CARD11 mutations may induce B cell expansion and preferentially predispose to B cell malignancy without dramatically perturbing T cell homeostasis.
C1 [Snow, Andrew L.; Lu, Wei; Chaigne-Delalande, Benjamin; Zheng, Lixin; Matthews, Helen F.; Lenardo, Michael J.] NIAID, Lymphocyte Mol Genet Unit, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Kardava, Lela; Wang, Wei; Moir, Susan] NIAID, Immunopathogenesis Sect, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Lamborn, Ian T.; Jing, Huie; Su, Helen C.] NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA.
[Snow, Andrew L.; Stinson, Jeffrey R.] Uniformed Serv Univ Hlth Sci, Dept Pharmacol, Bethesda, MD 20814 USA.
[Xiao, Wenming] NIH, Bioinformat & Mol Anal Sect, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
[Pittaluga, Stefania; Raffeld, Mark] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Schmitz, Roland; Jhavar, Sameer; Staudt, Louis M.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Kuchen, Stefan] NIAMSD, Genom & Immun Sect, NIH, Bethesda, MD 20892 USA.
[Fleisher, Thomas A.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Snow, AL (reprint author), NIAID, Lymphocyte Mol Genet Unit, Immunol Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM andrew.snow@usuhs.edu; lenardo@nih.gov
RI Su, Helen/H-9541-2015;
OI Su, Helen/0000-0002-5582-9110; Kuchen, Stefan/0000-0003-4899-8132; Snow,
Andrew/0000-0002-8728-6691
FU National Institutes of Health; National Institute of Allergy and
Infectious Diseases; National Cancer Institute; Uniformed Services
University of Health Sciences
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, the National Institute of Allergy and
Infectious Diseases, and the National Cancer Institute and an intramural
grant from Uniformed Services University of the Health Sciences (to A.L.
Snow and J.R. Stinson).
NR 38
TC 41
Z9 44
U1 0
U2 8
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 19
PY 2012
VL 209
IS 12
BP 2247
EP 2261
DI 10.1084/jem.20120831
PG 15
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 040BY
UT WOS:000311295600010
PM 23129749
ER
PT J
AU McCaughtry, TM
Etzensperger, R
Alag, A
Tai, XG
Kurtulus, S
Park, JH
Grinberg, A
Love, P
Feigenbaum, L
Erman, B
Singer, A
AF McCaughtry, Tom M.
Etzensperger, Ruth
Alag, Amala
Tai, Xuguang
Kurtulus, Sema
Park, Jung-Hyun
Grinberg, Alex
Love, Paul
Feigenbaum, Lionel
Erman, Batu
Singer, Alfred
TI Conditional deletion of cytokine receptor chains reveals that IL-7 and
IL-15 specify CD8 cytotoxic lineage fate in the thymus
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID T-CELL DEVELOPMENT; DOUBLE-POSITIVE THYMOCYTES; INTERLEUKIN-7 RECEPTOR;
STROMAL LYMPHOPOIETIN; TRANSCRIPTION FACTOR; DEFICIENT MICE; GAMMA
CHAIN; LYMPHOID DEVELOPMENT; NEGATIVE SELECTION; RUNX PROTEINS
AB The thymus generates T cells with diverse specificities and functions. To assess the contribution of cytokine receptors to the differentiation of T cell subsets in the thymus, we constructed conditional knockout mice in which IL-7R alpha or common cytokine receptor gamma chain (gamma(c)) genes were deleted in thymocytes just before positive selection. We found that gamma(c) expression was required to signal the differentiation of MHC class I (MHC-I)-specific thymocytes into CD8(+) cytotoxic lineage T cells and into invariant natural killer T cells but did not signal the differentiation of MHC class II (MHC-II)-specific thymocytes into CD4(+) T cells, even into regulatory Foxp3(+)CD4(+) T cells which require gamma(c) signals for survival. Importantly, IL-7 and IL-15 were identified as the cytokines responsible for CD8(+) cytotoxic T cell lineage specification in vivo. Additionally, we found that small numbers of aberrant CD8(+) T cells expressing Runx3d could arise without gamma(c) signaling, but these cells were developmentally arrested before expressing cytotoxic lineage genes. Thus, gamma(c)-transduced cytokine signals are required for cytotoxic lineage specification in the thymus and for inducing the differentiation of MHC-I-selected thymocytes into functionally mature T cells.
C1 [McCaughtry, Tom M.; Etzensperger, Ruth; Alag, Amala; Tai, Xuguang; Park, Jung-Hyun; Singer, Alfred] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Kurtulus, Sema; Erman, Batu] Sabanci Univ, Fac Engn & Nat Sci, Biol Sci & Bioengn Program, TR-34956 Istanbul, Turkey.
[Grinberg, Alex; Love, Paul] NICHHD, Lab Mammalian Genes & Dev, Bethesda, MD 20892 USA.
[Feigenbaum, Lionel] NCI, SAIC Frederick, Canc Res & Dev Ctr, Frederick, MD 21702 USA.
RP Singer, A (reprint author), NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
EM singera@nih.gov
RI Park, Jung Hyun /B-5712-2015
OI Park, Jung Hyun /0000-0002-9547-9055
FU National Institutes of Health, National Cancer Institute, Center for
Cancer Research
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research.
NR 49
TC 29
Z9 29
U1 0
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 19
PY 2012
VL 209
IS 12
BP 2263
EP 2276
DI 10.1084/jem.20121505
PG 14
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 040BY
UT WOS:000311295600011
PM 23109710
ER
PT J
AU Siao, CJ
Lorentz, CU
Kermani, P
Marinic, T
Carter, J
McGrath, K
Padow, VA
Mark, W
Falcone, DJ
Cohen-Gould, L
Parrish, DC
Habecker, BA
Nykjaer, A
Ellenson, LH
Tessarollo, L
Hempstead, BL
AF Siao, Chia-Jen
Lorentz, Christina U.
Kermani, Pouneh
Marinic, Tina
Carter, John
McGrath, Kelly
Padow, Victoria A.
Mark, Willie
Falcone, Domenick J.
Cohen-Gould, Leona
Parrish, Diana C.
Habecker, Beth A.
Nykjaer, Anders
Ellenson, Lora H.
Tessarollo, Lino
Hempstead, Barbara L.
TI ProNGF, a cytokine induced after myocardial infarction in humans,
targets pericytes to promote microvascular damage and activation
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID NERVE GROWTH-FACTOR; P75 NEUROTROPHIN RECEPTOR; SMOOTH-MUSCLE-CELLS;
BLOOD-VESSEL FORMATION; THERAPEUTIC INTERVENTION; SYMPATHETIC NEURONS;
DEFICIENT MICE; TGF-BETA; PDGF-B; SURVIVAL
AB Treatment of acute cardiac ischemia focuses on reestablishment of blood flow in coronary arteries. However, impaired microvascular perfusion damages peri-infarct tissue, despite arterial patency. Identification of cytokines that induce microvascular dysfunction would provide new targets to limit microvascular damage. Pro-nerve growth factor (NGF), the precursor of NGF, is a well characterized cytokine in the brain induced by injury. ProNGF activates p75 neurotrophin receptor (p75(NTR)) and sortilin receptors to mediate proapoptotic responses. We describe induction of proNGF by cardiomyocytes, and p75(NTR) in human arterioles after fatal myocardial infarction, but not with unrelated pathologies. After mouse cardiac ischemia-reperfusion (I-R) injury, rapid up-regulation of proNGF by cardiomyocytes and p75(NTR) by microvascular pericytes is observed. To identify proNGF actions, we generated a mouse expressing a mutant Ngf allele with impaired processing of proNGF to mature NGF. The proNGF-expressing mouse exhibits cardiac microvascular endothelial activation, a decrease in pericyte process length, and increased vascular permeability, leading to lethal cardiomyopathy in adulthood. Deletion of p75(NTR) in proNGF-expressing mice rescues the phenotype, confirming the importance of p75(NTR)-expressing pericytes in the development of microvascular injury. Furthermore, deficiency in p75(NTR) limits infarct size after I-R. These studies identify novel, nonneuronal actions for proNGF and suggest that proNGF represents a new target to limit microvascular dysfunction.
C1 [Siao, Chia-Jen; Lorentz, Christina U.; Kermani, Pouneh; Marinic, Tina; McGrath, Kelly; Padow, Victoria A.; Hempstead, Barbara L.] Weill Cornell Med Coll, Div Hematol Med Oncol, New York, NY 10065 USA.
[Carter, John] Weill Cornell Med Coll, Div Cardiovasc Pathophysiol, Dept Med, New York, NY 10065 USA.
[Cohen-Gould, Leona] Weill Cornell Med Coll, Dept Biochem, New York, NY 10065 USA.
[Cohen-Gould, Leona] Weill Cornell Med Coll, Dept Cell & Dev Biol, New York, NY 10065 USA.
[Falcone, Domenick J.; Ellenson, Lora H.] Weill Cornell Med Coll, Dept Pathol, New York, NY 10065 USA.
[Parrish, Diana C.; Habecker, Beth A.] Oregon Hlth & Sci Univ, Dept Physiol & Pharmacol, Portland, OR 97239 USA.
[Mark, Willie] Sloan Kettering Inst, Dev Biol Program, New York, NY 10065 USA.
[Nykjaer, Anders] Univ Aarhus, Dept Med Biochem, DK-8000 Aarhus, Denmark.
[Tessarollo, Lino] NCI, Mouse Canc Genet Program, Ctr Canc Res, NIH, Bethesda, MD 21702 USA.
RP Hempstead, BL (reprint author), Weill Cornell Med Coll, Div Hematol Med Oncol, New York, NY 10065 USA.
EM blhempst@med.cornell.edu
OI Nykjaer, Anders/0000-0001-6422-6736; Habecker, Beth/0000-0002-4658-8730
FU National Institutes of Health [HL046403, NS030687]; NIH [HL093056]
FX This work was supported by National Institutes of Health (HL046403 and
NS030687) to B. L. Hempstead and by NIH HL093056 to B.A. Habecker.
NR 60
TC 18
Z9 18
U1 1
U2 11
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 19
PY 2012
VL 209
IS 12
BP 2291
EP 2305
DI 10.1084/jem.20111749
PG 15
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 040BY
UT WOS:000311295600013
PM 23091165
ER
PT J
AU Kim, S
Kim, W
Wei, CH
Lu, ZY
Wilbur, WJ
AF Kim, Sun
Kim, Won
Wei, Chih-Hsuan
Lu, Zhiyong
Wilbur, W. John
TI Prioritizing PubMed articles for the Comparative Toxicogenomic Database
utilizing semantic information
SO DATABASE-THE JOURNAL OF BIOLOGICAL DATABASES AND CURATION
LA English
DT Article
ID NAMED ENTITY RECOGNITION; BIOMEDICAL LITERATURE; FEATURES
AB The Comparative Toxicogenomics Database (CTD) contains manually curated literature that describes chemical-gene interactions, chemical-disease relationships and gene-disease relationships. Finding articles containing this information is the first and an important step to assist manual curation efficiency. However, the complex nature of named entities and their relationships make it challenging to choose relevant articles. In this article, we introduce a machine learning framework for prioritizing CTD-relevant articles based on our prior system for the protein-protein interaction article classification task in BioCreative III. To address new challenges in the CTD task, we explore a new entity identification method for genes, chemicals and diseases. In addition, latent topics are analyzed and used as a feature type to overcome the small size of the training set. Applied to the BioCreative 2012 Triage dataset, our method achieved 0.8030 mean average precision (MAP) in the official runs, resulting in the top MAP system among participants. Integrated with PubTator, a Web interface for annotating biomedical literature, the proposed system also received a positive review from the CTD curation
C1 [Kim, Sun; Kim, Won; Wei, Chih-Hsuan; Lu, Zhiyong; Wilbur, W. John] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Wilbur, WJ (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
EM wilbur@ncbi.nlm.nih.gov
FU Intramural Research Program of the National Institutes of Health,
National Library of Medicine
FX Funding for open access charge: The Intramural Research Program of the
National Institutes of Health, National Library of Medicine.
NR 32
TC 4
Z9 4
U1 1
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1758-0463
J9 DATABASE-OXFORD
JI Database
PD NOV 17
PY 2012
AR bas042
DI 10.1093/database/bas042
PG 7
WC Mathematical & Computational Biology
SC Mathematical & Computational Biology
GA 106AF
UT WOS:000316113100004
ER
PT J
AU Lu, ZY
Hirschman, L
AF Lu, Zhiyong
Hirschman, Lynette
TI Biocuration workflows and text mining: overview of the BioCreative 2012
Workshop Track II
SO DATABASE-THE JOURNAL OF BIOLOGICAL DATABASES AND CURATION
LA English
DT Article
ID GENE NORMALIZATION; TASK; ANNOTATION; ONTOLOGY; BIOLOGY; EXTRACTION;
CURATION; DATABASE
AB Manual curation of data from the biomedical literature is a rate- limiting factor for many expert curated databases. Despite the continuing advances in biomedical text mining and the pressing needs of biocurators for better tools, few existing text- mining tools have been successfully integrated into production literature curation systems such as those used by the expert curated databases. To close this gap and better understand all aspects of literature curation, we invited submissions of written descriptions of curation workflows from expert curated databases for the BioCreative 2012 Workshop Track II. We received seven qualified contributions, primarily from model organism databases. Based on these descriptions, we identified commonalities and differences across the workflows, the common ontologies and controlled vocabularies used and the current and desired uses of text mining for biocuration. Compared to a survey done in 2009, our 2012 results show that many more databases are now using text mining in parts of their curation workflows. In addition, the workshop participants identified text- mining aids for finding gene names and symbols (gene indexing), prioritization of documents for curation (document triage) and ontology concept assignment as those most desired by the biocurators.
Database URL: http://www. biocreative. org/tasks/bc- workshop- 2012/workflow/
C1 [Lu, Zhiyong] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
[Hirschman, Lynette] Mitre Corp, Bedford, MA 01730 USA.
RP Hirschman, L (reprint author), Mitre Corp, 202 Burlington Rd, Bedford, MA 01730 USA.
EM lynette@mitre.org
FU US National Science Foundation [DBI-0850319]; NIH Intramural Research
Program, National Library of Medicine, National Institutes of Health;
MITRE Corporation
FX The US National Science Foundation Grant [DBI-0850319 (to L.H.)]; the
NIH Intramural Research Program, National Library of Medicine, National
Institutes of Health (to Z.L.). Funding for open access charge: The
MITRE Corporation.
NR 30
TC 18
Z9 18
U1 0
U2 6
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1758-0463
J9 DATABASE-OXFORD
JI Database
PD NOV 17
PY 2012
AR bas043
DI 10.1093/database/bas043
PG 6
WC Mathematical & Computational Biology
SC Mathematical & Computational Biology
GA 106AF
UT WOS:000316113100005
ER
PT J
AU Wei, CH
Harris, BR
Li, DH
Berardini, TZ
Huala, E
Kao, HY
Lu, ZY
AF Wei, Chih-Hsuan
Harris, Bethany R.
Li, Donghui
Berardini, Tanya Z.
Huala, Eva
Kao, Hung-Yu
Lu, Zhiyong
TI Accelerating literature curation with text-mining tools: a case study of
using PubTator to curate genes in PubMed abstracts
SO DATABASE-THE JOURNAL OF BIOLOGICAL DATABASES AND CURATION
LA English
DT Article
ID ANNOTATION
AB Today's biomedical research has become heavily dependent on access to the biological knowledge encoded in expert curated biological databases. As the volume of biological literature grows rapidly, it becomes increasingly difficult for biocurators to keep up with the literature because manual curation is an expensive and time-consuming endeavour. Past research has suggested that computer-assisted curation can improve efficiency, but few text-mining systems have been formally evaluated in this regard. Through participation in the interactive text-mining track of the BioCreative 2012 workshop, we developed PubTator, a PubMed-like system that assists with two specific human curation tasks: document triage and bioconcept annotation. On the basis of evaluation results from two external user groups, we find that the accuracy of PubTator-assisted curation is comparable with that of manual curation and that PubTator can significantly increase human curatorial speed. These encouraging findings warrant further investigation with a larger number of publications to be annotated.
Database URL: http://www.ncbi.nlm.nih.gov/CBBresearch/Lu/Demo/PubTator/
C1 [Wei, Chih-Hsuan; Harris, Bethany R.; Lu, Zhiyong] Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
[Wei, Chih-Hsuan; Kao, Hung-Yu] Natl Cheng Kung Univ, Dept Comp Sci & Informat Engn, Tainan 70101, Taiwan.
[Berardini, Tanya Z.; Huala, Eva] Carnegie Inst Sci, Dept Plant Biol, Stanford, CA 94305 USA.
RP Lu, ZY (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, 8600 Rockville Pike, Bethesda, MD 20894 USA.
EM zhiyong.lu@nih.gov
OI Huala, Eva/0000-0003-4631-7241
FU NIH, National Library of Medicine; National Science Foundation
[DBI-0850219]; TAIR sponsors
FX Intramural Research Program of the NIH, National Library of Medicine (to
C.W. and Z.L.); National Library of Medicine and administered by the Oak
Ridge Institute for Science and Education (to B.H.); National Science
Foundation (DBI-0850219 to TAIR); TAIR sponsors (http://www. arabi
dopsis. org/doc/about/tair_ sponsors/413). Funding for open access
charge: National Institutes of Health, National Library of Medicine.
NR 24
TC 25
Z9 25
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1758-0463
J9 DATABASE-OXFORD
JI Database
PD NOV 17
PY 2012
AR bas041
DI 10.1093/database/bas041
PG 6
WC Mathematical & Computational Biology
SC Mathematical & Computational Biology
GA 106AF
UT WOS:000316113100003
ER
PT J
AU Pearce, MS
Salotti, JA
Little, MP
McHugh, K
Lee, C
Kim, KP
Howe, NL
Ronckers, CM
Rajaraman, P
Craft, AW
Parker, L
de Gonzalez, AB
AF Pearce, Mark S.
Salotti, Jane A.
Little, Mark P.
McHugh, Kieran
Lee, Choonsik
Kim, Kwang Pyo
Howe, Nicola L.
Ronckers, Cecile M.
Rajaraman, Preetha
Craft, Alan W.
Parker, Louise
de Gonzalez, Amy Berrington
TI CT scans in childhood and risk of leukaemia and brain tumours reply
SO LANCET
LA English
DT Letter
ID CHILDREN
C1 [Pearce, Mark S.; Salotti, Jane A.; Howe, Nicola L.] Newcastle Univ, Royal Victoria Infirm, Inst Hlth & Soc, Sir James Spence Inst, Newcastle Upon Tyne NE1 4LP, Tyne & Wear, England.
[Little, Mark P.; Lee, Choonsik; Ronckers, Cecile M.; Rajaraman, Preetha; de Gonzalez, Amy Berrington] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[McHugh, Kieran] Great Ormond St Hosp Sick Children, London WC1N 3JH, England.
[Kim, Kwang Pyo] Kyung Hee Univ, Dept Nucl Engn, Gyeongi Do, South Korea.
[Ronckers, Cecile M.] Dutch Childhood Oncol Grp Longterm Effects Childh, The Hague, Netherlands.
[Craft, Alan W.] Newcastle Univ, Royal Victoria Infirm, No Inst Canc Res, Sir James Spence Inst, Newcastle Upon Tyne NE1 4LP, Tyne & Wear, England.
[Parker, Louise] Dalhousie Univ, Dept Med, Halifax, NS, Canada.
[Parker, Louise] Dalhousie Univ, Dept Paediat, Populat Canc Res Program, Halifax, NS, Canada.
RP Pearce, MS (reprint author), Newcastle Univ, Royal Victoria Infirm, Inst Hlth & Soc, Sir James Spence Inst, Newcastle Upon Tyne NE1 4LP, Tyne & Wear, England.
EM mark.pearce@ncl.ac.uk
NR 5
TC 3
Z9 3
U1 1
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0140-6736
J9 LANCET
JI Lancet
PD NOV 17
PY 2012
VL 380
IS 9855
BP 1736
EP 1737
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 038CV
UT WOS:000311153700022
ER
PT J
AU Aalbers, AM
Calado, RT
Young, NS
Zwaan, CM
Wu, CO
Kajigaya, S
Coenen, EA
Baruchel, A
Geleijns, K
de Haas, V
Kaspers, GJL
Kuijpers, TW
Reinhardt, D
Trka, J
Zimmermann, M
Pieters, R
van der Velden, VHJ
Eibrink, MMV
AF Aalbers, Anna M.
Calado, Rodrigo T.
Young, Neal S.
Zwaan, Christian M.
Wu, Colin O.
Kajigaya, Sachiko
Coenen, Eva A.
Baruchel, Andre
Geleijns, Karin
de Haas, Valerie
Kaspers, Gertjan J. L.
Kuijpers, Taco W.
Reinhardt, Dirk
Trka, Jan
Zimmermann, Martin
Pieters, Rob
van der Velden, Vincent H. J.
Eibrink, Marry M. van den Heuvel
TI Telomere Length and Telomerase Complex Mutations in Pediatric Acute
Myeloid Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Aalbers, Anna M.; Young, Neal S.; Wu, Colin O.; Kajigaya, Sachiko] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Calado, Rodrigo T.] Univ Sao Paulo, Dept Internal Med, BR-14049 Ribeirao Preto, Brazil.
[Zwaan, Christian M.; Coenen, Eva A.; Pieters, Rob; Eibrink, Marry M. van den Heuvel] Erasmus MC Sophia Childrens Hosp, Dept Pediat Oncol Hematol, Rotterdam, Netherlands.
[Baruchel, Andre] Hop Robert Debre, Dept Pediat Hematol, F-75019 Paris, France.
[Geleijns, Karin; van der Velden, Vincent H. J.] Erasmus MC, Dept Immunol, Rotterdam, Netherlands.
[de Haas, Valerie] Dutch Childhood Oncol Grp, The Hague, Netherlands.
[Kaspers, Gertjan J. L.] Vrije Univ Amsterdam, Dept Pediat Oncol Hematol, Med Ctr, Amsterdam, Netherlands.
[Kuijpers, Taco W.] Emma Childrens Hosp, Dept Pediat Hematol Immunol & Infect Dis, Acad Med Ctr, Amsterdam, Netherlands.
[Reinhardt, Dirk; Zimmermann, Martin] Hannover Med Sch, AML BFM Study Grp, Hannover, Germany.
[Trka, Jan] Charles Univ Prague, Dept Pediat Hematol & Oncol, Prague, Czech Republic.
RI Calado, Rodrigo/G-2619-2011
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1482
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838905151
ER
PT J
AU Aka, P
Vila, M
Jariwala, A
Nkrumah, F
Emmanuel, B
Yagi, M
Palacpac, N
Periago, M
Neequaye, J
Kiruthu, C
Tougan, T
Levine, P
Biggar, R
Pfeiffer, RM
Horii, T
Bhatia, K
Bethony, J
Mbulaiteye, S
AF Aka, Peter
Vila, Maria
Jariwala, Amar
Nkrumah, Francis
Emmanuel, Benjamin
Yagi, Masanory
Palacpac, Nirianne
Periago, Maria
Neequaye, Janet
Kiruthu, Christine
Tougan, Takahiro
Levine, Paul
Biggar, Robert
Pfeiffer, Ruth M.
Horii, Toshihiro
Bhatia, Kishor
Bethony, Jeffrey
Mbulaiteye, Sam
TI Risk of Burkitt Lymphoma Correlates with Breadth and Strength of
Antibody Response to Plasmodium Falciparum Malaria Stage-Specific
Antigens
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Aka, Peter; Emmanuel, Benjamin; Bhatia, Kishor; Mbulaiteye, Sam] NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD USA.
[Vila, Maria; Jariwala, Amar; Periago, Maria; Kiruthu, Christine; Levine, Paul; Bethony, Jeffrey] George Washington Univ, Washington, DC USA.
[Nkrumah, Francis] Noguchi Mem Inst, Accra, Ghana.
[Yagi, Masanory; Palacpac, Nirianne; Tougan, Takahiro; Horii, Toshihiro] Osaka Univ, Suita, Osaka 565, Japan.
[Neequaye, Janet] Korle Bu Univ, Korle, Ghana.
[Biggar, Robert] Queensland Univ Technol, Brisbane, Qld 4001, Australia.
[Pfeiffer, Ruth M.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
RI Periago, Maria/H-1054-2013
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900050
ER
PT J
AU Akrawinthawong, K
Piknova, B
Sibmooh, N
Fucharoen, S
Schechter, AN
AF Akrawinthawong, Krittapoom
Piknova, Barbora
Sibmooh, Nathawut
Fucharoen, Suthat
Schechter, Alan N.
TI Nitrite Inhibits Platelet Reactivity in Presence of Deoxygenated Red
Blood Cells As Measured by Flow Cytometry
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Akrawinthawong, Krittapoom; Piknova, Barbora; Schechter, Alan N.] NIDDKD, Mol Med Branch, NIH, Bethesda, MD 20892 USA.
[Sibmooh, Nathawut] Mahidol Univ, Fac Sci, Dept Pharmacol, Bangkok 10400, Thailand.
[Fucharoen, Suthat] Mahidol Univ, Thalassemia Res Ctr, Inst Sci & Technol Res & Dev, Nakhon Pathom, Thailand.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 5146
PG 1
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049605442
ER
PT J
AU Alter, BP
Giri, N
Pan, YJ
Quint, W
de Koning, M
Schiffman, M
Pinto, L
AF Alter, Blanche P.
Giri, Neelam
Pan, Yuanji
Quint, Wim
de Koning, Maurits
Schiffman, Mark
Pinto, Ligia
TI The HPV Status of Patients with Fanconi Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Alter, Blanche P.; Giri, Neelam; Schiffman, Mark] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Quint, Wim; de Koning, Maurits] DDL Diagnost Lab, Rijswijk, Netherlands.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2362
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049601099
ER
PT J
AU Alter, BP
Giri, N
Calvo, KR
Maric, I
Arthur, DC
Hickstein, DD
Hastings, CA
Lee, MA
Hsu, A
Holland, SM
AF Alter, Blanche P.
Giri, Neelam
Calvo, Katherine R.
Maric, Irina
Arthur, Diane C.
Hickstein, Dennis D.
Hastings, Caroline A.
Lee, Michelle A.
Hsu, Amy
Holland, Steven M.
TI Clinically Silent Carriers in Families with Myelodysplastic Syndrome Due
to GATA2 Mutations
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Alter, Blanche P.; Giri, Neelam] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Calvo, Katherine R.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Maric, Irina] NIH, Hematol Sect, Dept Lab, CCR, Bethesda, MD 20892 USA.
[Arthur, Diane C.] NCI, Pathol Lab, NIH, CCR, Bethesda, MD 20892 USA.
[Hickstein, Dennis D.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Hastings, Caroline A.] Childrens Hosp & Res Ctr Oakland, Oakland, CA USA.
[Lee, Michelle A.] Dana Farber Canc Inst, Brookline, MA USA.
[Hsu, Amy] NIH, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
[Holland, Steven M.] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
RI Calvo, Katherine/A-8109-2009
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1264
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838902302
ER
PT J
AU Arons, E
Roth, L
Adams, S
Sapolsky, J
Pastan, I
Kreitman, RJ
AF Arons, Evgeny
Roth, Laura
Adams, Sharon
Sapolsky, Jeffery
Pastan, Ira
Kreitman, Robert J.
TI The HLA-DRB1*11 Antigen Is Preferentially Expressed in Hairy Cell
Leukemia, Particularly in Patients Who Had Hemolytic Uremic Syndrome
with Recombinant Immunotoxin BL22
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Arons, Evgeny; Roth, Laura; Sapolsky, Jeffery; Pastan, Ira; Kreitman, Robert J.] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Adams, Sharon] NIH, Dept Transfus Med, HLA Lab, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2488
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049602193
ER
PT J
AU Ayyappan, S
Drawz, P
Nouraie, M
Hildesheim, ME
Zhang, YZ
Gordeuk, VR
Hostetter, TH
Gladwin, MT
Little, JA
AF Ayyappan, Sabarish
Drawz, Paul
Nouraie, Mehdi
Hildesheim, Mariana E.
Zhang, Yingze
Gordeuk, Victor R.
Hostetter, Thomas H.
Gladwin, Mark T.
Little, Jane A.
TI Renal Disease in Sickle Cell: Clinically Varied and Associated with
Increased Mortality
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Ayyappan, Sabarish; Little, Jane A.] Case Western Reserve Univ, Univ Hosp Seidman Canc Ctr, Cleveland, OH 44106 USA.
[Drawz, Paul] Univ Minnesota, Div Renal Dis & Hypertens, Minneapolis, MN USA.
[Nouraie, Mehdi] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
[Hildesheim, Mariana E.] NIH, Dept Crit Care Med, Bethesda, MD 20892 USA.
[Gordeuk, Victor R.] Univ Illinois, Dept Med, Sect Hematol Oncol, Ctr Comprehens Sickle Cell, Chicago, IL USA.
[Hostetter, Thomas H.] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Gladwin, Mark T.] Univ Pittsburgh, Med Ctr, Div Pulm Allergy & Crit Care Med, Pittsburgh, PA USA.
NR 0
TC 1
Z9 1
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 90
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900075
ER
PT J
AU Baird, K
Fry, TJ
Merchant, M
Richards, K
Delbrook, C
Wayne, AS
Mackall, CL
AF Baird, Kristin
Fry, Terry J.
Merchant, Melinda
Richards, Kelly
Delbrook, Cynthia
Wayne, Alan S.
Mackall, Crystal L.
TI Early Clinical Experience of aAPC Activated NK-DLI Following Allogeneic
PBSCT in Pediatric Solid Tumor Patients.
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Baird, Kristin; Fry, Terry J.; Merchant, Melinda; Richards, Kelly; Delbrook, Cynthia; Wayne, Alan S.; Mackall, Crystal L.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3013
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049601250
ER
PT J
AU Barta, SK
Xue, XN
Wang, D
Tamari, R
Lee, JY
Mounier, N
Kaplan, LD
Ribera, JM
Spina, M
Tirelli, U
Weiss, R
Galicier, L
Boue, F
Wilson, WH
Wyen, C
Oriol, A
Navarro, JT
Dunleavy, K
Little, RF
Ratner, L
Garcia, O
Morgades, M
Oksenhendler, E
Remick, S
Sparano, JA
AF Barta, Stefan K.
Xue, Xiaonan
Wang, Dan
Tamari, Roni
Lee, Jeannette Y.
Mounier, Nicolas
Kaplan, Lawrence D.
Ribera, Josep-Maria
Spina, Michele
Tirelli, Umberto
Weiss, Rudolf
Galicier, Lionel
Boue, Francois
Wilson, Wyndham H.
Wyen, Christoph
Oriol, Albert
Navarro, Jose-Tomas
Dunleavy, Kieron
Little, Richard F.
Ratner, Lee
Garcia, Olga
Morgades, Mireia
Oksenhendler, Eric
Remick, Scot
Sparano, Joseph A.
TI A Pooled Analysis of 1,546 Patients with HIV-Associated Lymphoma:
Assessment of Lymphoma-, HIV-, and Treatment-Specific Factors On
Clinical Outcomes
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Barta, Stefan K.] Montefiore Med Ctr, Albert Einstein Canc Ctr, Dept Oncol, Bronx, NY 10467 USA.
[Xue, Xiaonan] Albert Einstein Coll Med, Div Biostat, Bronx, NY 10467 USA.
[Wang, Dan] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA.
[Tamari, Roni] Dept Med, New York, NY USA.
[Lee, Jeannette Y.] Univ Arkansas Med Sci, Dept Biostat, Little Rock, AR 72205 USA.
[Mounier, Nicolas] Hop Archet, Serv Hematol, Nice, France.
[Kaplan, Lawrence D.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Ribera, Josep-Maria] Univ Autonoma Barcelona, Hosp Germans Trias & Pujol, IJC ICO Badalona, Badalona, Spain.
[Spina, Michele] Natl Canc Inst, Div Med Oncol A, Aviano, Italy.
[Tirelli, Umberto] Ctr Riferimento Oncol, Div Med Oncol A, I-33081 Aviano, Italy.
[Weiss, Rudolf] Gemeinschaftspraxis Haematol & Onkol, Bremen, Germany.
[Galicier, Lionel] Hop St Louis, AP HP, Paris, France.
[Galicier, Lionel] Univ Paris Diderot, Sorbonne Paris Cite, Paris, France.
[Boue, Francois] Hop Antoine Beclere, Clamart, France.
[Wilson, Wyndham H.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
[Wyen, Christoph] Univ Cologne, D-50931 Cologne, Germany.
[Oriol, Albert] Spanish Soc Hematol, PETHEMA Grp, Badalona, Spain.
[Dunleavy, Kieron] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Little, Richard F.] NCI, HIV AIDS Malignancy Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Ratner, Lee] Washington Univ, St Louis, MO USA.
[Garcia, Olga] Univ Autonoma Barcelona, Hosp Germans Trias & Pujol, IJC, Badalona, Spain.
[Morgades, Mireia] Hosp Badalona Germans Trias & Pujol, Josep Carreras Leukemia Res Inst, Dept Clin Hematol, ICO, Paris, France.
[Oksenhendler, Eric] CHU St Louis, Paris, France.
[Remick, Scot] W Virginia Univ, Dept Med, Hematol Oncol Sect, Morgantown, WV 26506 USA.
RI Barta, Stefan/D-9554-2013
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3682
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049600236
ER
PT J
AU Barta, SK
Xue, XN
Wang, D
Lee, JY
Kaplan, LD
Ribera, JM
Oriol, A
Garcia, O
Morgades, M
Spina, M
Tirelli, U
Boue, F
Wilson, WH
Wyen, C
Dunleavy, K
Sparano, JA
AF Barta, Stefan K.
Xue, Xiaonan
Wang, Dan
Lee, Jeannette Y.
Kaplan, Lawrence D.
Ribera, Josep-Maria
Oriol, Albert
Garcia, Olga
Morgades, Mireia
Spina, Michele
Tirelli, Umberto
Boue, Francois
Wilson, Wyndham H.
Wyen, Christoph
Dunleavy, Kieron
Sparano, Joseph A.
TI ARL-IPI - A New Prognostic Score for AIDS-Related Lymphomas in the
Rituximab Era
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Barta, Stefan K.] Montefiore Med Ctr, Albert Einstein Canc Ctr, Dept Oncol, Bronx, NY 10467 USA.
[Xue, Xiaonan] Albert Einstein Coll Med, Div Biostat, Bronx, NY 10467 USA.
[Wang, Dan] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA.
[Lee, Jeannette Y.] Univ Arkansas Med Sci, Dept Biostat, Little Rock, AR 72205 USA.
[Kaplan, Lawrence D.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Ribera, Josep-Maria] Univ Autonoma Barcelona, Hosp Germans Trias & Pujol, IJC ICO Badalona, Badalona, Spain.
[Oriol, Albert] Spanish Soc Hematol, PETHEMA Grp, Badalona, Spain.
[Garcia, Olga] Univ Autonoma Barcelona, Hosp Germans Trias & Pujol, IJC, Badalona, Spain.
[Morgades, Mireia] Hosp Badalona Germans Trias & Pujol, Inst Catala Oncol, Aviano, Italy.
[Spina, Michele] Natl Canc Inst, Div Med Oncol A, Aviano, Italy.
[Tirelli, Umberto] Ctr Riferimento Oncol, Div Med Oncol A, I-33081 Aviano, Italy.
[Boue, Francois] Hop Antoine Beclere, Clamart, France.
[Wilson, Wyndham H.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
[Wyen, Christoph] Univ Cologne, D-50931 Cologne, Germany.
[Dunleavy, Kieron] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
RI Barta, Stefan/D-9554-2013
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1564
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838906274
ER
PT J
AU Bat, T
Leitman, SF
Calvo, KR
Chauvet, D
Dunbar, CE
AF Bat, Taha
Leitman, Susan F.
Calvo, Katherine R.
Chauvet, Donna
Dunbar, Cynthia E.
TI Measurement of the Absolute Immature Platelet Number Reflects Marrow
Production and Is Not Impacted by Platelet Transfusion
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Bat, Taha; Dunbar, Cynthia E.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Leitman, Susan F.] NIH, Dept Transfus Med, Bethesda, MD 20892 USA.
[Calvo, Katherine R.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3425
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604102
ER
PT J
AU Bennardo, S
Iacovelli, S
Gobessi, S
Suljagic, M
Bilbao, D
Eckl-Dorna, J
Wang, HS
Cornall, RJ
Clarke, SH
Croce, CM
Efremov, DG
AF Bennardo, Sara
Iacovelli, Stefano
Gobessi, Stefania
Suljagic, Mirza
Bilbao, Daniel
Eckl-Dorna, Julia
Wang, Hongsheng
Cornall, Richard J.
Clarke, Stephen H.
Croce, Carlo M.
Efremov, Dimitar G.
TI The Nature of the Antigen Determines Leukemia Development and Behavior
in the E mu-TCL1 Transgenic Mouse Model of CLL
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Bennardo, Sara; Iacovelli, Stefano; Gobessi, Stefania; Suljagic, Mirza; Efremov, Dimitar G.] Int Ctr Genet Engn & Biotechnol, Rome, Italy.
[Bilbao, Daniel] European Mol Biol Lab, Rome, Italy.
[Eckl-Dorna, Julia] Med Univ Vienna, Dept Otorlinolaryngol, Vienna, Austria.
[Wang, Hongsheng] NIAID, Immunopathol Lab, NIH, Rockville, MD USA.
[Cornall, Richard J.] Univ Oxford, Nuffield Dept Clin Med, Oxford, England.
[Clarke, Stephen H.] Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC USA.
[Croce, Carlo M.] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 181
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900276
ER
PT J
AU Bergsagel, PL
Affer, M
Glebov, OK
Chen, WDD
Keats, JJ
Brents, LA
Chesi, M
Van Wier, S
Badar, SK
Fonseca, R
Kuehl, WM
AF Bergsagel, P. Leif
Affer, Maurizio
Glebov, Oleg K.
Chen, Wei-Dong D.
Keats, Jonathan J.
Brents, Leslie A.
Chesi, Marta
Van Wier, Scott
Badar, Sandra K.
Fonseca, Rafael
Kuehl, W. Michael
TI Promiscuous Cryptic Rearrangements of the MYC Locus Cis-Dysregulate MYC
Expression and Are Present in the Majority of Patients with Hyperdiploid
Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Bergsagel, P. Leif; Affer, Maurizio; Chesi, Marta; Van Wier, Scott; Badar, Sandra K.; Fonseca, Rafael] Mayo Clin Arizona, Div Hematol Oncol, Scottsdale, AZ USA.
[Glebov, Oleg K.; Chen, Wei-Dong D.; Brents, Leslie A.; Kuehl, W. Michael] NCI, Canc Genet Branch, Bethesda, MD 20892 USA.
[Keats, Jonathan J.] Translat Genom Res Inst, Phoenix, AZ USA.
RI CHEN, WEI-DONG/F-4521-2014
OI CHEN, WEI-DONG/0000-0003-2264-5515
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 724
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900235
ER
PT J
AU Blimark, C
Mellqvist, UH
Landgren, O
Bjorkholm, M
Hultcrantz, ML
Kjellander, C
Turesson, I
Holmberg, E
Kristinsson, SY
AF Blimark, Cecilie
Mellqvist, Ulf-Henrik
Landgren, Ola
Bjorkholm, Magnus
Hultcrantz, Malin L.
Kjellander, Christian
Turesson, Ingemar
Holmberg, Erik
Kristinsson, Sigurdur Y.
TI Multiple Myeloma and Infections: A Population-Based Study Based On 9,610
Multiple Myeloma Patients
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Blimark, Cecilie] Sahlgrens Univ Hosp, Dept Hematol, Gothenburg, Sweden.
[Landgren, Ola] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Bjorkholm, Magnus; Hultcrantz, Malin L.; Kjellander, Christian; Kristinsson, Sigurdur Y.] Karolinska Univ Hosp, Div Hematol, Dept Med, Stockholm, Sweden.
[Bjorkholm, Magnus; Hultcrantz, Malin L.; Kjellander, Christian; Kristinsson, Sigurdur Y.] Karolinska Inst, Stockholm, Sweden.
[Turesson, Ingemar] Skane Univ Hosp Malmo, Malmo, Sweden.
[Holmberg, Erik] Univ Gothenburg, Sahlgrenska Acad, Dept Oncol, Inst Clin Sci, Gothenburg, Sweden.
RI Kristinsson, Sigurdur /M-2910-2015
OI Kristinsson, Sigurdur /0000-0002-4964-7476
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 945
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838902016
ER
PT J
AU Blimark, C
Mellqvist, UH
Landgren, O
Bjorkholm, M
Hultcrantz, ML
Kjellander, C
Turesson, I
Holmberg, E
Kristinsson, SY
AF Blimark, Cecilie
Mellqvist, Ulf-Henrik
Landgren, Ola
Bjorkholm, Magnus
Hultcrantz, Malin L.
Kjellander, Christian
Turesson, Ingemar
Holmberg, Erik
Kristinsson, Sigurdur Y.
TI Multiple Myeloma and Infections: A Population-Based Study Based On 9,610
Multiple Myeloma Patients
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Blimark, Cecilie] Sahlgrens Univ Hosp, Dept Hematol, Gothenburg, Sweden.
[Landgren, Ola] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Bjorkholm, Magnus; Hultcrantz, Malin L.; Kjellander, Christian; Kristinsson, Sigurdur Y.] Karolinska Univ Hosp, Dept Med, Div Hematol, Stockholm, Sweden.
[Bjorkholm, Magnus; Hultcrantz, Malin L.; Kjellander, Christian; Kristinsson, Sigurdur Y.] Karolinska Inst, Stockholm, Sweden.
[Turesson, Ingemar] Skane Univ Hosp Malmo, Malmo, Sweden.
[Holmberg, Erik] Univ Gothenburg, Dept Oncol, Inst Clin Sci, Sahlgrenska Acad, Gothenburg, Sweden.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 945
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838901192
ER
PT J
AU Bolouri, H
Ries, RE
Ramamurthy, R
Alonzo, TA
Auvil, JMG
Davidsen, TM
Gesuwan, P
Gamis, AS
Smith, MA
Gerhard, DS
Arceci, RJ
Meshinchi, S
AF Bolouri, Hamid
Ries, Rhonda E.
Ramamurthy, Ranjani
Alonzo, Todd A.
Auvil, Jaime M. Guidry
Davidsen, Tanja M.
Gesuwan, Patee
Gamis, Alan S.
Smith, Malcolm A.
Gerhard, Daniela S.
Arceci, Robert J.
Meshinchi, Soheil
TI Integrative Network Analysis of Pediatric AML Whole Genomes, cDNA
Expression and Clinical Data Elements Reveals Shared As Well As t(8;21),
Inv16 and MLL Specific Pathways; A Report From COG/NCI Target AML
Initiative
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Bolouri, Hamid] Fred Hutchinson Canc Res Ctr, Human Biol Div, Seattle, WA 98104 USA.
[Ries, Rhonda E.; Meshinchi, Soheil] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
[Ramamurthy, Ranjani] Univ Washington, Sch Med, Seattle, WA USA.
[Alonzo, Todd A.] Univ So Calif, Los Angeles, CA USA.
[Auvil, Jaime M. Guidry; Davidsen, Tanja M.; Gesuwan, Patee; Gerhard, Daniela S.] NCI, Off Canc Genom, Bethesda, MD 20892 USA.
[Gamis, Alan S.] Childrens Mercy Hosp & Clin, Kansas City, MO USA.
[Smith, Malcolm A.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Arceci, Robert J.] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3519
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838906138
ER
PT J
AU Bouska, A
McKeithan, T
Deffenbacher, KE
Lachel, C
Wright, GW
Iqbal, J
Smith, LM
Liu, ZF
Kucuk, C
Bertoni, F
Rinaldi, A
Fitzgibbon, J
Fu, K
Weisenburger, DD
Greiner, TC
Gascoyne, RD
Rosenwald, A
Campo, E
Rimsza, LM
Delabie, J
Jaffe, ES
Staudt, LM
Chan, WC
AF Bouska, Alyssa
McKeithan, Timothy
Deffenbacher, Karen E.
Lachel, Cynthia
Wright, George W.
Iqbal, Javeed
Smith, Lynette M.
Liu, Zhongfeng
Kucuk, Can
Bertoni, Francesco
Rinaldi, Andrea
Fitzgibbon, Jude
Fu, Kai
Weisenburger, Dennis D.
Greiner, Timothy C.
Gascoyne, Randy D.
Rosenwald, Andreas
Campo, Elias
Rimsza, Lisa M.
Delabie, Jan
Jaffe, Elaine S.
Staudt, Louis M.
Chan, Wing-Chung
TI Genetic Abnormalities in Follicular Lymphoma and Transformed Follicular
Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Wright, George W.] NCI, Biometr Res Branch, DCTD, Bethesda, MD 20892 USA.
[Smith, Lynette M.] Univ Nebraska Med Ctr, COPH Biostat, Omaha, NE USA.
[Bertoni, Francesco; Rinaldi, Andrea] Oncol Inst So Switzerland IOSI, Lymphoma Unit, Bellinzona, Switzerland.
[Rinaldi, Andrea] Oncol Inst So Switzerland IOSI, Expt Oncol Lab, Bellinzona, Switzerland.
[Fitzgibbon, Jude] Queen Mary Univ London, Barts Canc Inst, Ctr Haematooncol, London, England.
[Gascoyne, Randy D.] BC Canc Agcy, Ctr Lymphoid Canc, Dept Pathol, Vancouver, BC, Canada.
[Rosenwald, Andreas] Univ Wurzburg, D-97070 Wurzburg, Germany.
[Campo, Elias] Hosp Clin Barcelona, Hematopathol Unit, Barcelona, Spain.
[Rimsza, Lisa M.] Univ Arizona, Tucson, AZ USA.
[Delabie, Jan] Univ Oslo, Dept Pathol, Norwegian Radium Hosp, Oslo, Norway.
[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 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2648
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049602234
ER
PT J
AU Bouska, A
McKeithan, T
Deffenbacher, KE
Lachel, C
Wright, GW
Iqbal, J
Smith, LM
Liu, ZF
Kucuk, C
Bertoni, F
Rinaldi, A
Fitzgibbon, J
Fu, K
Weisenburger, DD
Greiner, TC
Gascoyne, RD
Rosenwald, A
Campo, E
Rimsza, LM
Delabie, J
Jaffe, ES
Staudt, LM
Chan, WC
AF Bouska, Alyssa
McKeithan, Timothy
Deffenbacher, Karen E.
Lachel, Cynthia
Wright, George W.
Iqbal, Javeed
Smith, Lynette M.
Liu, Zhongfeng
Kucuk, Can
Bertoni, Francesco
Rinaldi, Andrea
Fitzgibbon, Jude
Fu, Kai
Weisenburger, Dennis D.
Greiner, Timothy C.
Gascoyne, Randy D.
Rosenwald, Andreas
Campo, Elias
Rimsza, Lisa M.
Delabie, Jan
Jaffe, Elaine S.
Staudt, Louis M.
Chan, Wing-Chung
TI Genetic Abnormalities in Follicular Lymphoma and Transformed Follicular
Lymphoma.
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Wright, George W.] NCI, Biometr Res Branch, DCTD, Bethesda, MD 20892 USA.
[Smith, Lynette M.] Univ Nebraska Med Ctr, COPH Biostat, Omaha, NE USA.
[Bertoni, Francesco; Rinaldi, Andrea] Oncol Inst So Switzerland IOSI, Lymphoma Unit, Bellinzona, Switzerland.
[Rinaldi, Andrea] Oncol Inst So Switzerland IOSI, Expt Oncol Lab, Bellinzona, Switzerland.
[Fitzgibbon, Jude] Queen Mary Univ London, Barts Canc Inst, Ctr Haematooncol, London, England.
[Gascoyne, Randy D.] BC Canc Agcy Ctr Lymphoid Canc, Dept Pathol, Vancouver, BC, Canada.
[Rosenwald, Andreas] Univ Wurzburg, D-97070 Wurzburg, Germany.
[Campo, Elias] Hosp Clin Barcelona, Hematopathol Unit, Barcelona, Spain.
[Rimsza, Lisa M.] Univ Arizona, Tucson, AZ USA.
[Delabie, Jan] Univ Oslo, Norwegian Radium Hosp, Dept Pathol, Oslo, Norway.
[Staudt, Louis M.] NCI, Metab 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 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2648
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838903145
ER
PT J
AU Bryant, BJ
Yau, YY
Arceo, SM
Hopkins, JA
Leitman, SF
AF Bryant, Barbara J.
Yau, Yu Ying
Arceo, Sarah M.
Hopkins, Julie A.
Leitman, Susan F.
TI Ascertainment of Iron Depletion and Deficiency in Blood Donors Through
Screening Questions for Pica and Restless Legs Syndrome
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Bryant, Barbara J.] Univ Texas Med Branch, Galveston, TX USA.
[Yau, Yu Ying; Arceo, Sarah M.; Hopkins, Julie A.; 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 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2283
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049600077
ER
PT J
AU Carpenter, RO
Evbuomwan, MO
Pittaluga, S
Rose, JJ
Raffeld, M
Yang, SC
Gress, RE
Hakim, FT
Kochenderfer, JN
AF Carpenter, Robert O.
Evbuomwan, Moses O.
Pittaluga, Stefania
Rose, Jeremy J.
Raffeld, Mark
Yang, Shicheng
Gress, Ronald E.
Hakim, Frances T.
Kochenderfer, James N.
TI B-Cell Maturation Antigen Is a Promising Target for Genetically-Modified
T-Cell Therapy of Multiple Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Carpenter, Robert O.] NCI, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA.
[Raffeld, Mark] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Yang, Shicheng] Duke Univ, Dept Surg, Div Neurosurg, Durham, NC USA.
[Hakim, Frances T.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 937
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838902024
ER
PT J
AU Carpenter, RO
Evbuomwan, MO
Pittaluga, S
Rose, JJ
Raffeld, M
Yang, SC
Gress, RE
Hakim, FT
Kochenderfer, JN
AF Carpenter, Robert O.
Evbuomwan, Moses O.
Pittaluga, Stefania
Rose, Jeremy J.
Raffeld, Mark
Yang, Shicheng
Gress, Ronald E.
Hakim, Frances T.
Kochenderfer, James N.
TI B-Cell Maturation Antigen Is a Promising Target for Genetically-Modified
T-Cell Therapy of Multiple Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Rose, Jeremy J.; Gress, Ronald E.; Kochenderfer, James N.] NCI, ETIB, Bethesda, MD 20892 USA.
[Raffeld, Mark] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Yang, Shicheng] Duke Univ, Div Neurosurg, Dept Surg, Durham, NC USA.
[Hakim, Frances T.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 937
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838901200
ER
PT J
AU Chen, JC
Dent, JJ
Desierto, MJ
Bryant, MA
Sheppard, N
Feng, XM
Young, NS
AF Chen, Jichun
Dent, James J.
Desierto, Marie J.
Bryant, Mark A.
Sheppard, Nolan
Feng, Xingmin
Young, Neal S.
TI Hematological Abnormalities in Aged Telomerase RNA Component Deficient
Mice Are Associated with Intestinal Epithelial Degeneration and Bone
Marrow Stromal Dysfunction
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Chen, Jichun; Dent, James J.; Desierto, Marie J.; Sheppard, Nolan; Feng, Xingmin; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Bryant, Mark A.] NIH, Off Res Serv, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1244
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838902322
ER
PT J
AU Chen, ZS
Geng, HM
Buchner, M
Klemm, L
Hemati, K
Shojaee, S
Tak, MW
Coligan, JE
Carroll, WL
Willman, CL
Muschen, M
AF Chen, Zhengshan
Geng, Huimin
Buchner, Maike
Klemm, Lars
Hemati, Kaveh
Shojaee, Seyedmehdi
Tak, Mak W.
Coligan, John E.
Carroll, William L.
Willman, Cheryl L.
Muschen, Markus
TI ITIM-Containing Inhibitory Receptors Are Required to Balance Oncogenic
Signaling Strength in Ph+ ALL
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Chen, Zhengshan; Geng, Huimin; Buchner, Maike; Klemm, Lars; Hemati, Kaveh; Shojaee, Seyedmehdi; Muschen, Markus] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA.
[Tak, Mak W.] Ontario Canc Inst, Campbell Family Inst Breast Canc Res, Toronto, ON M4X 1K9, Canada.
[Coligan, John E.] NIH, Receptor Cell Biol Sect, Rockville, MD USA.
[Carroll, William L.] NYU, Inst Canc, New York, NY USA.
[Willman, Cheryl L.] Univ New Mexico, Ctr Canc, Albuquerque, NM 87131 USA.
RI Chen, Zhengshan/J-7499-2014
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 291
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838901155
ER
PT J
AU Cherkasova, E
Weisman, Q
Kajigaya, S
Takahashi, Y
Reger, RN
Harashima, N
AF Cherkasova, Elena
Weisman, Quinn
Kajigaya, Sachiko
Takahashi, Yoshiyuki
Reger, Robert N.
Harashima, Nanae
TI Identification of a Human Endogenous Retrovirus Type-E (HERV-E) Envelope
with Selective Expression in Clear Cell Kidney Cancer That Is
Immunogenic in Vitro.
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Cherkasova, Elena; Kajigaya, Sachiko; Reger, Robert N.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Takahashi, Yoshiyuki] Nagoya Univ, Dept Pediat, Grad Sch Med, Nagoya, Aichi 4648601, Japan.
[Harashima, Nanae] Shimane Univ, Fac Med, Matsue, Shimane, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3015
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049601248
ER
PT J
AU Chien, CD
Hicks, ED
Su, PP
Qin, HY
Fry, TJ
AF Chien, Christopher D.
Hicks, Elizabeth D.
Su, Paul P.
Qin, Haiying
Fry, Terry J.
TI Precursor B Cell Acute Lymphoblastic Leukemia Induces Pro-Leukemic
Changes in the Bone Marrow Microenvironment That Contribute to
Therapeutic Resistance
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Chien, Christopher D.; 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 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1466
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838905167
ER
PT J
AU Connelly, JP
Horwitz, MS
Liu, PP
AF Connelly, Jon P.
Horwitz, Marshall S.
Liu, Pu Paul
TI Towards Cell Therapy for FPD/AML with Patient-Specific IPS Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Connelly, Jon P.; Liu, Pu Paul] NHGRI, GMBB, ODS, NIH, Bethesda, MD 20892 USA.
[Horwitz, Marshall S.] Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98195 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4677
PG 1
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049606108
ER
PT J
AU Cooley, S
Verneris, MR
Curtsinger, J
McKenna, D
Weisdorf, DJ
Blazar, BR
Waldmann, TA
Miller, JS
AF Cooley, Sarah
Verneris, Michael R.
Curtsinger, Julie
McKenna, David
Weisdorf, Daniel J.
Blazar, Bruce R.
Waldmann, Thomas A.
Miller, Jeffrey S.
TI Recombinant Human IL-15 Promotes in Vivo Expansion of Adoptively
Transferred NK Cells in a First-in-Human Phase I Dose Escalation Study
in Patients with AML
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Verneris, Michael R.; Blazar, Bruce R.] Univ Minnesota, Dept Pediat, Div Blood & Marrow Transplantat, Minneapolis, MN 55455 USA.
[Curtsinger, Julie] Univ Minnesota, Masonic Canc Res Ctr, Minneapolis, MN USA.
[McKenna, David] Univ Minnesota, St Paul, MN 55108 USA.
[Waldmann, Thomas A.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
[Miller, Jeffrey S.] Univ Minnesota, Dept Med, Div Hematol Oncol & Transplantat, Minneapolis, MN 55455 USA.
NR 0
TC 3
Z9 3
U1 1
U2 5
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 894
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900365
ER
PT J
AU Cozen, W
Yu, GQ
Gail, M
Nathwani, BN
Hwang, AE
Hamilton, AS
Mack, TM
Goedert, JJ
AF Cozen, Wendy
Yu, Guoqin
Gail, Mitchell
Nathwani, Bharat N.
Hwang, Amie E.
Hamilton, Ann S.
Mack, Thomas M.
Goedert, James J.
TI Fecal Microbiota Diversity in Survivors of Adolescent/Young Adult
Hodgkin Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Yu, Guoqin] NCI, Div Canc Epidemiol & Genet, Infect & Immunol Branch, NIH, Rockville, MD USA.
[Nathwani, Bharat N.] Cedars Sinai Med Ctr, Dept Pathol, Los Angeles, CA 90048 USA.
[Hwang, Amie E.] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
[Hamilton, Ann S.; Mack, Thomas M.] Univ So Calif, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1533
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838906243
ER
PT J
AU Cuellar-Rodriguez, J
Gea-Banacloche, J
Hsu, AP
Zerbe, C
Freeman, A
Olivier, KN
Calvo, KR
Fry, TJ
Holland, SM
Hickstein, DD
AF Cuellar-Rodriguez, Jennifer
Gea-Banacloche, Juan
Hsu, Amy P.
Zerbe, Christa
Freeman, Alexandra
Olivier, Kenneth N.
Calvo, Katherine R.
Fry, Terry J.
Holland, Steven M.
Hickstein, Dennis D.
TI Allogeneic Hematopoietic Stem Cell Transplant Reverses the Phenotype of
GATA2 Deficiency.
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Cuellar-Rodriguez, Jennifer; Hsu, Amy P.; Zerbe, Christa; Freeman, Alexandra; Olivier, Kenneth N.; Holland, Steven M.] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
[Calvo, Katherine R.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Fry, Terry J.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Hickstein, Dennis D.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
RI Calvo, Katherine/A-8109-2009
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3091
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049601172
ER
PT J
AU de Vasconcellos, JF
Lee, YT
Yuan, J
Byrnes, C
Noh, SJ
Meier, ER
Kim, KS
Rabel, A
Muljo, SA
Miller, JL
AF de Vasconcellos, Jaira F.
Lee, Y. Terry
Yuan, Joan
Byrnes, Colleen
Noh, Seung-Jae
Meier, Emily R.
Kim, Ki Soon
Rabel, Antoinette
Muljo, Stefan A.
Miller, Jeffery L.
TI Lin28B Increases Fetal Hemoglobin and Regulates BCL11A Expression in
Human Erythroid Tissues
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [de Vasconcellos, Jaira F.; Lee, Y. Terry; Byrnes, Colleen; Noh, Seung-Jae; Meier, Emily R.; Kim, Ki Soon; Rabel, Antoinette; Miller, Jeffery L.] NIDDK, Mol Genom & Therapeut Sect, Mol Med Branch, NIH, Bethesda, MD USA.
[Yuan, Joan; Muljo, Stefan A.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RI yuan, joan/A-8185-2013; Muljo, Stefan/F-5671-2015
OI yuan, joan/0000-0001-9129-8356; Muljo, Stefan/0000-0003-1013-446X
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 827
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838901037
ER
PT J
AU Delaney, KM
Gorbach, A
Malik, N
Maivelett, J
Hon, YY
Xu, DH
Novelli, EM
Lanzkron, S
Taylor, JG
Kato, GJ
Minniti, CP
AF Delaney, Kara M.
Gorbach, Alexander
Malik, Nitin
Maivelett, Jordan
Hon, Yuen Yi
Xu, Dihua
Novelli, Enrico M.
Lanzkron, Sophia
Taylor, James G.
Kato, Gregory J.
Minniti, Caterina P.
TI Blood Flow Is Increased in Wounds and Peri-Wound Area by Laser Speckle
Contrast Imaging and Infrared Thermography in Adults with Sickle Cell
Leg Ulcers
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Delaney, Kara M.; Taylor, James G.; Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Gorbach, Alexander; Malik, Nitin; Maivelett, Jordan] Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD USA.
[Hon, Yuen Yi] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Novelli, Enrico M.] Univ Pittsburgh, Dept Med, Div Hem Onc, Pittsburgh, PA USA.
[Lanzkron, Sophia] Johns Hopkins Sch Med, Baltimore, MD 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 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1009
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049602062
ER
PT J
AU Desmond, RG
Bat, T
Kamenyeva, O
Mizukawa, B
Mulloy, JC
Larochelle, A
Dunbar, CE
AF Desmond, Ronan G.
Bat, Taha
Kamenyeva, Olena
Mizukawa, Benjamin
Mulloy, James C.
Larochelle, Andre
Dunbar, Cynthia E.
TI Leukemic and Hematopoietic Stem Cells Compete for the Same Functional
Marrow Niche in a MLL-AF9 Murine Leukemia Model
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Desmond, Ronan G.; Bat, Taha; Larochelle, Andre; Dunbar, Cynthia E.] NHLBI, Bethesda, MD 20892 USA.
[Mizukawa, Benjamin] Cincinnati Childrens Hosp Med Ctr, Div Oncol, Canc & Blood Dis Inst, Cincinnati, OH USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4897
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604345
ER
PT J
AU Dumitriu, B
Ueda, Y
Kajigaya, S
Townsley, DM
Young, NS
AF Dumitriu, Bogdan
Ueda, Yasutaka
Kajigaya, Sachiko
Townsley, Danielle M.
Young, Neal S.
TI Very Short Telomeres of Peripheral Blood Leukocytes Precede Clinical
Progression to Myelodysplasia with Monosomy 7 in Aplastic Anemia
Patients
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Kajigaya, Sachiko; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1265
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838902301
ER
PT J
AU Dunleavy, K
Grant, C
Hessler, J
Miller, BW
Steinberg, SM
Pittaluga, S
Roschewski, M
Jaffe, ES
Wiestner, A
Wilson, WH
AF Dunleavy, Kieron
Grant, Cliona
Hessler, Julieanne
Miller, Barry W.
Steinberg, Seth M.
Pittaluga, Stefania
Roschewski, Mark
Jaffe, Elaine S.
Wiestner, Adrian
Wilson, Wyndham H.
TI Bortezomib plus DA-EPOCH-R Induction Therapy Followed by Maintenance
Bortezomib Versus Observation in Newly Diagnosed Mantle Cell Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Dunleavy, Kieron; Grant, Cliona; Hessler, Julieanne; Miller, Barry W.; Roschewski, Mark] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, Rockville, MD USA.
[Pittaluga, Stefania; Jaffe, Elaine S.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
[Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Wilson, Wyndham H.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
RI Jaffe, Elaine/G-8984-2014
OI Jaffe, Elaine/0000-0003-4632-0301
NR 0
TC 3
Z9 3
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3672
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049600246
ER
PT J
AU Duvic, M
Pinter-Brown, L
Foss, F
Sokol, L
Jorgensen, J
Ni, X
Challagundla, P
Goswami, M
Dwyer, K
Mohamed, N
Kim, YH
AF Duvic, Madeleine
Pinter-Brown, Lauren
Foss, Francine
Sokol, Lubomir
Jorgensen, Jeffrey
Ni, Xiao
Challagundla, Pramoda
Goswami, Meghali
Dwyer, Karen
Mohamed, Nehal
Kim, Youn H.
TI Correlation of Target Molecule Expression and Overall Response in
Refractory Cutaneous T-Cell Lymphoma Patients Dosed with Mogamulizumab
(KW-0761), a Monoclonal Antibody Directed Against CC Chemokine Receptor
Type 4 (CCR4)
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Pinter-Brown, Lauren] Univ Calif Los Angeles, Los Angeles, CA USA.
[Foss, Francine] Yale Canc Ctr, New Haven, CT USA.
[Sokol, Lubomir] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Jorgensen, Jeffrey] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Houston, TX 77030 USA.
[Ni, Xiao] Univ Texas MD Anderson Canc Ctr, Dept Dermatol, Houston, TX 77030 USA.
[Goswami, Meghali] NHLBI, NIH, Bethesda, MD 20892 USA.
[Dwyer, Karen; Mohamed, Nehal] Kyowa Hakko Kirin Pharma Inc, Kyowa, NJ USA.
[Kim, Youn H.] Stanford Univ, Stanford, CA 94305 USA.
NR 0
TC 1
Z9 1
U1 0
U2 5
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3697
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049600221
ER
PT J
AU Evans, ME
Tisdale, JF
Uchida, N
AF Evans, Molly E.
Tisdale, John F.
Uchida, Naoya
TI Lentiviral Transduction Efficiency for Human CD34+Cells Is Affected by
TRIM5 alpha Expression and Cell Proliferation
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Evans, Molly E.; Tisdale, John F.; Uchida, Naoya] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4220
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838906213
ER
PT J
AU Farooqui, M
Lozier, JN
Valdez, J
Saba, N
Wells, A
Soto, S
Liu, DL
Aue, G
Wiestner, A
AF Farooqui, Mohammed
Lozier, Jay Nelson
Valdez, Janet
Saba, Nakhle
Wells, Ajunae
Soto, Susan
Liu, Delong
Aue, Georg
Wiestner, Adrian
TI Ibrutinib (PCI 32765) Rapidly Improves Platelet Counts in Chronic
Lymphocytic Leukemia/Small Lymphocytic Lymphoma (CLL/SLL) Patients and
Has Minimal Effects On Platelet Aggregation
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Farooqui, Mohammed; Valdez, Janet; Saba, Nakhle; Wells, Ajunae; Soto, Susan; Liu, Delong; Aue, Georg; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Lozier, Jay Nelson] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 6
Z9 6
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1789
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049602088
ER
PT J
AU Farooqui, M
Aue, G
Valdez, J
Saba, N
Herman, SEM
Lipsky, A
Bojanowski, L
Wells, A
Soto, S
Liu, DL
Wiestner, A
AF Farooqui, Mohammed
Aue, Georg
Valdez, Janet
Saba, Nakhle
Herman, Sarah E. M.
Lipsky, Andrew
Bojanowski, Leodayan
Wells, Ajunae
Soto, Susan
Liu, Delong
Wiestner, Adrian
TI Rapid Decrease in Overall Tumor Burden On Ibrutinib (PCI-32765) in CLL
Despite Transient Increase in ALC Indicates a Significant Degree of
Treatment Induced Cell Death
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Farooqui, Mohammed; Aue, Georg; Valdez, Janet; Saba, Nakhle; Herman, Sarah E. M.; Lipsky, Andrew; Bojanowski, Leodayan; Wells, Ajunae; Soto, Susan; Liu, Delong; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 4
Z9 5
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2899
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838905340
ER
PT J
AU Felices, M
Lenvik, T
Ankarlo, D
Curtsinger, J
Tolar, J
Blazar, BR
Anderson, S
Miller, JS
AF Felices, Martin
Lenvik, Todd
Ankarlo, Dave
Curtsinger, Julie
Tolar, Jakub
Blazar, Bruce R.
Anderson, Stephen
Miller, Jeffrey S.
TI Education and Cytokine Receptor Balance Play a Critical Role in Long
Term Survival of the Most Differentiated Natural Killer (NK) Cells.
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Curtsinger, Julie] Univ Minnesota, Masonic Canc Res Ctr, Minneapolis, MN USA.
[Tolar, Jakub] Univ Minnesota, Dept Pediat, Div Blood & Marrow Transplantat, Masonic Canc Ctr, Minneapolis, MN 55455 USA.
[Anderson, Stephen] NCI, Frederick, MD 21701 USA.
[Miller, Jeffrey S.] Univ Minnesota, Dept Med, Div Hematol Oncol & Transplantat, Minneapolis, MN 55455 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2148
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838905288
ER
PT J
AU Fisher, R
Henson, A
Quarello, P
Aspesi, A
Farrar, JE
Arceci, RJ
Bodine, DM
Dianzani, I
Lipton, JM
Ramenghi, U
Vlachos, A
Ellis, SR
AF Fisher, Ross
Henson, Adrianna
Quarello, Paola
Aspesi, Anna
Farrar, Jason E.
Arceci, Robert J.
Bodine, David M.
Dianzani, Irma
Lipton, Jeffrey M.
Ramenghi, Ugo
Vlachos, Adrianna
Ellis, Steven R.
TI Insights Into Diagnosis and Etiology of Diamond Blackfan Anemia by
Analysis of Pre-rRNA Processing
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Fisher, Ross] Loma Linda Univ, San Bernardino, CA USA.
[Henson, Adrianna; Ellis, Steven R.] Univ Louisville, Sch Med, Dept Biochem & Mol Biol, Louisville, KY 40292 USA.
[Quarello, Paola] Regina Margherita Childrens Hosp, Turin, Italy.
[Aspesi, Anna] Univ Piemonte Orientale, Novara, Italy.
[Farrar, Jason E.] Johns Hopkins Univ, Dept Oncol, Div Pediat Oncol, Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
[Arceci, Robert J.] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Bodine, David M.] NHGRI, Genet & Mol Biol Branch, Bethesda, MD 20892 USA.
[Dianzani, Irma] Univ Piemonte Orientale, Dept Med Sci, Novara, Italy.
[Lipton, Jeffrey M.] Hofstra Univ, Steven & Alexandra Cohen Childrens Med Ctr, Div Hematol Oncol & Stem Cell Transplantat, Feinstein Inst Med Res,Sch Med, New Hyde Pk, NY USA.
[Ramenghi, Ugo] Univ Turin, Dept Pediat, I-10124 Turin, Italy.
[Vlachos, Adrianna] Hofstra N Shore LIJ Sch Med, Feinstein Inst Med Res, Steven & Alexandra Cohen Childrens Med Ctr, New Hyde Pk, NY USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3476
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604051
ER
PT J
AU Fitzhugh, C
Allen, D
Coles, W
Seamon, C
Zhao, XC
Darbari, D
Wilson, J
Quinn, M
Hsieh, M
Kato, GJ
Taylor, JG
AF Fitzhugh, Courtney
Allen, Darlene
Coles, Wynona
Seamon, Cassie
Zhao, Xiongce
Darbari, Deepika
Wilson, Jonathan
Quinn, Meghan
Hsieh, Matthew
Kato, Gregory J.
Taylor, James G.
TI Etiology of and Associations with Early Death in Adult Patients with
Sickle Cell Disease At a Single Referral Institution
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Fitzhugh, Courtney; Coles, Wynona; Hsieh, Matthew] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
[Allen, Darlene; Seamon, Cassie; Darbari, Deepika; Wilson, Jonathan; Quinn, Meghan; Kato, Gregory J.; Taylor, James G.] NHLBI, HB, NIH, Bethesda, MD 20892 USA.
[Zhao, Xiongce] NIDDK, NIH, Bethesda, MD USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 1
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2117
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838905319
ER
PT J
AU Gerrie, AS
White, S
Harvey, KL
Gill, R
Toze, CL
AF Gerrie, Alina S.
White, Siobhan
Harvey, Katherine L.
Gill, Ritu
Toze, Cynthia L.
TI Effect of Physical Activity (PA) Interventions On Health-Related Quality
of Life (HRQoL) Post Hematopoietic Stem Cell Transplantation (HSCT): A
Systematic Review and Meta-Analysis
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Gerrie, Alina S.; Toze, Cynthia L.] Univ British Columbia, British Columbia Canc Agcy, Leukemia & Bone Marrow Transplantat Program BC, Vancouver, BC V5Z 1M9, Canada.
[White, Siobhan] NCI, Washington, DC USA.
[Harvey, Katherine L.] Yale Univ, Sch Med, New Haven, CT USA.
[Harvey, Katherine L.] Yale Canc Ctr, New Haven, CT USA.
[Gill, Ritu] Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 2
U2 5
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1968
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838903023
ER
PT J
AU Giri, N
Matsui, K
Alter, BP
Savage, SA
Pan, YJ
Pinto, L
AF Giri, Neelam
Matsui, Ken
Alter, Blanche P.
Savage, Sharon A.
Pan, Yuanji
Pinto, Ligia
TI Bone Marrow Cellular Composition and Inflammatory Cytokine Expression in
Patients with Inherited Bone Marrow Failure Syndromes
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
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.
[Matsui, Ken; Pan, Yuanji; Pinto, Ligia] NCI, Human Papilloma Virus Immunol Lab, Frederick, MD 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 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4401
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049605123
ER
PT J
AU Grant, C
Dunleavy, K
Hessler, J
Steinberg, SM
Pittaluga, S
Jaffe, ES
Wilson, WH
AF Grant, Cliona
Dunleavy, Kieron
Hessler, Julieanne
Steinberg, Seth M.
Pittaluga, Stefania
Jaffe, Elaine S.
Wilson, Wyndham H.
TI A Phase II Trial of Alemtuzumab (Campath) with DA-EPOCH-R in Relapsed or
Refractory Diffuse Large B-Cell Lymphoma and Hodgkin Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Grant, Cliona; Dunleavy, Kieron; Hessler, Julieanne] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, Rockville, MD USA.
[Pittaluga, Stefania; Jaffe, Elaine S.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
[Wilson, Wyndham H.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
RI Jaffe, Elaine/G-8984-2014
OI Jaffe, Elaine/0000-0003-4632-0301
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3709
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049600209
ER
PT J
AU Grkovic, L
Pulanic, D
Steinberg, SM
Williams, KM
Baird, K
Mitchell, SA
Cowen, EW
Datiles, MB
Bassim, CW
Galen, J
Comis, L
Avila, DN
Taylor, TN
Zhang, D
Cole, K
Fowler, DH
Hakim, FT
Gress, RE
Pavletic, SZ
AF Grkovic, Lana
Pulanic, Drazen
Steinberg, Seth M.
Williams, Kirsten M.
Baird, Kristin
Mitchell, Sandra A.
Cowen, Edward W.
Datiles, Manuel B., III
Bassim, Carol W.
Galen, Joe
Comis, Leora
Avila, Daniele N.
Taylor, Tiffani N.
Zhang, Dan
Cole, Kristen
Fowler, Dan H.
Hakim, Frances T.
Gress, Ronald E.
Pavletic, Steven Z.
TI Chronic Graft-Versus-Host Disease (cGVHD) Patients with Bronchiolitis
Obliterans Syndrome (BOS) Have Worse Clinical Manifestations and
Severity of cGVHD with More Impairment in Self-Assessed Physical and
Mental Health than cGVHD Patients without BOS
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Grkovic, Lana; Pulanic, Drazen] Clin Hosp Ctr Zagreb, Dept Hematol, Zagreb, Croatia.
[Williams, Kirsten M.; Avila, Daniele N.; Taylor, Tiffani N.; Cole, Kristen; Fowler, Dan H.; Hakim, Frances T.; Gress, Ronald E.; Pavletic, Steven Z.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Baird, Kristin] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Mitchell, Sandra A.] NCI, Div Canc Control & Populat Sci, 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.
[Bassim, Carol W.] Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD USA.
[Galen, Joe; Comis, Leora] NIH, Dept Rehabil Med, Ctr Clin, Bethesda, MD 20892 USA.
[Zhang, Dan] NCI, Biostat & Data Management Sect, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 2
U2 5
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1939
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838903052
ER
PT J
AU Halverson, D
Mossoba, ME
Steinberg, SM
Blacklock-Schuver, B
Hakim, FT
Kurlander, R
Gea-Banacloche, J
Sportes, C
Hardy, NM
Hickstein, DD
Pavletic, SZ
Khuu, H
Sabatino, M
Stroncek, D
Leitman, SF
Rowley, SD
Donato, ML
Goy, A
Korngold, R
Pecora, AL
Levine, BL
June, CH
Bishop, MR
Carini, C
Feldman, T
Mato, AR
Gress, RE
Fowler, DH
AF Halverson, David
Mossoba, Miriam E.
Steinberg, Seth M.
Blacklock-Schuver, Bazetta
Hakim, Frances T.
Kurlander, Roger
Gea-Banacloche, Juan
Sportes, Claude
Hardy, Nancy M.
Hickstein, Dennis D.
Pavletic, Steven Z.
Khuu, Hanh
Sabatino, Marianna
Stroncek, David
Leitman, Susan F.
Rowley, Scott D.
Donato, Michele L.
Goy, Andre
Korngold, Robert
Pecora, Andrew L.
Levine, Bruce L.
June, Carl H.
Bishop, Michael R.
Carini, Carol
Feldman, Tatyana
Mato, Anthony R.
Gress, Ronald E.
Fowler, Daniel H.
TI Pre-Emptive T-Rapa Cell DLI for Therapy of High-Risk Lymphoma After
Low-Intensity Allogeneic HCT
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Mossoba, Miriam E.] NCI, Expt Transplantat & Immunol Branch, NIH, Ctr Canc Res, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, Rockville, MD USA.
[Kurlander, Roger] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Khuu, Hanh; Sabatino, Marianna; Stroncek, David] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Rowley, Scott D.; Donato, Michele L.; Goy, Andre; Pecora, Andrew L.; Feldman, Tatyana; Mato, Anthony R.] Hackensack Univ Med Ctr, John Theurer Canc Ctr, Hackensack, NJ USA.
[Korngold, Robert] Hackensack Univ Med Ctr, Ctr Canc, Hackensack, NJ USA.
[Levine, Bruce L.] Univ Penn, Dept Pathol & Lab Med, Philadelphia, PA USA.
[June, Carl H.] Univ Penn, Perelman Sch Med, Philadelphia, PA USA.
[Bishop, Michael R.] Med Coll Wisocnson, Milwaukee, WI USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 471
PG 3
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838902189
ER
PT J
AU Halverson, D
Mossoba, ME
Steinberg, SM
Blacklock-Schuver, B
Hakim, FT
Kurlander, R
Gea-Banacloche, J
Sportes, C
Hardy, NM
Hickstein, DD
Pavletic, SZ
Khuu, H
Sabatino, M
Stroncek, D
Leitman, SF
Rowley, SD
Donato, ML
Goy, A
Korngold, R
Pecora, AL
Levine, BL
June, CH
Bishop, MR
Carini, C
Feldman, T
Mato, AR
Gress, RE
Fowler, DH
AF Halverson, David
Mossoba, Miriam E.
Steinberg, Seth M.
Blacklock-Schuver, Bazetta
Hakim, Frances T.
Kurlander, Roger
Gea-Banacloche, Juan
Sportes, Claude
Hardy, Nancy M.
Hickstein, Dennis D.
Pavletic, Steven Z.
Khuu, Hanh
Sabatino, Marianna
Stroncek, David
Leitman, Susan F.
Rowley, Scott D.
Donato, Michele L.
Goy, Andre
Korngold, Robert
Pecora, Andrew L.
Levine, Bruce L.
June, Carl H.
Bishop, Michael R.
Carini, Carol
Feldman, Tatyana
Mato, Anthony R.
Gress, Ronald E.
Fowler, Daniel H.
TI Pre-Emptive T-Rapa Cell DLI for Therapy of High-Risk Lymphoma After
Low-Intensity Allogeneic HCT
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Mossoba, Miriam E.] NCI, Expt Transplantat & Immunol Branch, NIH, Ctr Canc Res, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, Rockville, MD USA.
[Kurlander, Roger] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Khuu, Hanh; Sabatino, Marianna; Stroncek, David] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Rowley, Scott D.; Donato, Michele L.; Goy, Andre; Pecora, Andrew L.; Feldman, Tatyana; Mato, Anthony R.] Hackensack Univ, Med Ctr, John Theurer Canc Ctr, Hackensack, NJ USA.
[Levine, Bruce L.] Univ Penn, Dept Pathol & Lab Med, Philadelphia, PA USA.
[June, Carl H.] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Bishop, Michael R.] Med Coll Wisconsin, Milwaukee, WI USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 471
PG 3
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838901365
ER
PT J
AU He, S
Xie, F
Tong, Q
Mochizuki, K
Liu, YN
Lapinski, PE
Mineishi, S
Mani, RS
Marquez, VE
Chinnaiyan, AM
King, PD
Zhang, Y
AF He, Shan
Xie, Fang
Tong, Qing
Mochizuki, Kazuhiro
Liu, Yongnian
Lapinski, Philip E.
Mineishi, Shin
Mani, Ram Shankar
Marquez, Victor E.
Chinnaiyan, Arul M.
King, Philip D.
Zhang, Yi
TI Histone Methyltransferase Ezh2 Controls T-Cell Immunity by Regulating
Bioenergetic Metabolism
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [He, Shan; Xie, Fang; Tong, Qing; Mochizuki, Kazuhiro; Liu, Yongnian; Mineishi, Shin; Zhang, Yi] Univ Michigan, Sch Med, Dept Internal Med, Ann Arbor, MI USA.
[Lapinski, Philip E.; King, Philip D.] Univ Michigan, Dept Microbiol & Immunol, Ann Arbor, MI 48109 USA.
[Mani, Ram Shankar; Chinnaiyan, Arul M.] Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA.
[Marquez, Victor E.] NCI, Biol Chem Lab, Ctr Canc Res, NIH, Frederick, MD 21701 USA.
RI He, Shan/C-4989-2015
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 953
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838901184
ER
PT J
AU Helton, HL
Ries, RE
Alonzo, TA
Gerbing, RB
Trevino, LR
Farrar, J
Auvil, JMG
Davidsen, TM
Gesuwan, P
Muzny, DM
Gamis, AS
Franklin, J
Wheeler, DA
Smith, MA
Gerhard, DS
Arceci, RJ
Meshinchi, S
AF Helton, Heather L.
Ries, Rhonda E.
Alonzo, Todd A.
Gerbing, Robert B.
Trevino, Lisa R.
Farrar, Jason
Auvil, Jaime M. Guidry
Davidsen, Tanja M.
Gesuwan, Patee
Muzny, Donna M.
Gamis, Alan S.
Franklin, Janet
Wheeler, David A.
Smith, Malcolm A.
Gerhard, Daniela S.
Arceci, Robert J.
Meshinchi, Soheil
TI Clinically Significant Mutations, Deletions and Translocations Involving
ETV6 Identified by Whole Genome and Whole Exome Sequencing; Report From
NCI/COG Target AML Initiative
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Helton, Heather L.; Ries, Rhonda E.; Meshinchi, Soheil] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Alonzo, Todd A.] Univ So Calif, Los Angeles, CA USA.
[Gerbing, Robert B.] Childrens Oncol Grp, Arcadia, CA USA.
[Trevino, Lisa R.; Muzny, Donna M.; Wheeler, David A.] Baylor Coll Med, Human Genome Sequencing Ctr, Houston, TX 77030 USA.
[Farrar, Jason] Univ Arkansas Med Sci, Little Rock, AR 72205 USA.
[Auvil, Jaime M. Guidry; Davidsen, Tanja M.; Gesuwan, Patee; Smith, Malcolm A.; Gerhard, Daniela S.] NCI, Off Canc Genom, Bethesda, MD 20892 USA.
[Gamis, Alan S.] Childrens Mercy Hosp & Clin, Kansas City, MO USA.
[Franklin, Janet] Amgen Inc, Thousand Oaks, CA 91320 USA.
[Arceci, Robert J.] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 125
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900334
ER
PT J
AU Herman, SEM
Barr, PM
McAuley, EM
Liu, DL
Friedberg, JW
Wiestner, A
AF Herman, Sarah E. M.
Barr, Paul M.
McAuley, Erin M.
Liu, Delong
Friedberg, Jonathan W.
Wiestner, Adrian
TI Fostamatinib Inhibits BCR Signaling, and Reduces Tumor Cell Activation
and Proliferation in Patients with Relapsed Refractory Chronic
Lymphocytic Leukemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Herman, Sarah E. M.; McAuley, Erin M.; Liu, Delong; Wiestner, Adrian] NHLBI, NIH, Bethesda, MD 20892 USA.
[Barr, Paul M.; Friedberg, Jonathan W.] Univ Rochester, Med Ctr, Rochester, NY 14642 USA.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2882
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838905357
ER
PT J
AU Herman, SEM
Farooqui, M
Bezabhie, R
Aue, G
Wiestner, A
AF Herman, Sarah E. M.
Farooqui, Mohammed
Bezabhie, Rahel
Aue, Georg
Wiestner, Adrian
TI In Vivo Effects of Ibrutinib On BCR Signaling, Tumor Cell Activation and
Proliferation in Blood and Tissue-Resident Cells of Chronic Lymphocytic
Leukemia Patients
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Herman, Sarah E. M.; Farooqui, Mohammed; Bezabhie, Rahel; Aue, Georg; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 4
Z9 4
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 185
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900272
ER
PT J
AU HerndonMd, TM
Chen, SS
Gatmaitan, M
Emson, C
Valdez, J
Saba, N
Chiorazzi, N
Wiestner, A
AF HerndonMd, Thomas M.
Chen, Shih-Shih
Gatmaitan, Michelle
Emson, Claire
Valdez, Janet
Saba, Nakhle
Chiorazzi, Nicholas
Wiestner, Adrian
TI Direct in Vivo Evidence of Increased Chronic Lymphocytic Leukemia Cell
Proliferation in Lymph Nodes Compared to Bone Marrow and Peripheral
Blood
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [HerndonMd, Thomas M.; Valdez, Janet; Saba, Nakhle; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Chen, Shih-Shih; Chiorazzi, Nicholas] N Shore Long Isl Jewish Hlth Syst, Feinstein Inst Med Res, Manhasset, NY USA.
[Gatmaitan, Michelle; Emson, Claire] KineMed Inc, Emeryville, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 184
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900273
ER
PT J
AU Hillengass, J
Kilk, K
Listl, K
Hielscher, T
Neben, K
Hose, D
Ho, AD
Weber, MA
Landgren, O
Goldschmidt, H
AF Hillengass, Jens
Kilk, Kerstin
Listl, Karin
Hielscher, Thomas
Neben, Kai
Hose, Dirk
Ho, Anthony D.
Weber, Marc-Andre
Landgren, Ola
Goldschmidt, Hartmut
TI Appearance of Monoclonal Plasma Cell Diseases in Whole Body MRI in 544
Patients and Correlation with Parameters of Disease Activity
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Hielscher, Thomas] DKFZ, Heidelberg, Germany.
[Hose, Dirk; Ho, Anthony D.] Heidelberg Univ, Dept Internal Med 5, Heidelberg, Germany.
[Hose, Dirk] Heidelberg Univ, Natl Ctr Tumor Dis, Heidelberg, Germany.
[Landgren, Ola] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RI Weber, Marc-Andre/C-4452-2016
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4966
PG 1
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049605102
ER
PT J
AU Hillengass, J
Kilk, K
Listl, K
Hielscher, T
Neben, K
Hose, D
Weber, MA
Ho, AD
Goldschmidt, H
Landgren, O
AF Hillengass, Jens
Kilk, Kerstin
Listl, Karin
Hielscher, Thomas
Neben, Kai
Hose, Dirk
Weber, Marc-Andre
Ho, Anthony D.
Goldschmidt, Hartmut
Landgren, Ola
TI Over 30% of Smoldering Myeloma Patients Have Tumor Cell Bone Marrow
Infiltration Patterns Similar to Multiple Myeloma: A Large (n=544)
Clinical Study Using Whole-Body MRI
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Hielscher, Thomas] German Canc Res Ctr, Dept Biostat, Heidelberg, Germany.
[Hose, Dirk; Ho, Anthony D.] Heidelberg Univ, Dept Internal Med 5, Heidelberg, Germany.
[Hose, Dirk] Heidelberg Univ, Natl Ctr Tumor Dis, Heidelberg, Germany.
[Landgren, Ola] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RI Weber, Marc-Andre/C-4452-2016
NR 0
TC 1
Z9 1
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2911
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838905328
ER
PT J
AU Hultcrantz, ML
Pfeiffer, RM
Bjorkholm, M
Goldin, L
Turesson, I
Schulman, S
Landgren, O
Kristinsson, SY
AF Hultcrantz, Malin L.
Pfeiffer, Ruth M.
Bjorkholm, Magnus
Goldin, Lynn
Turesson, Ingemar
Schulman, Sam
Landgren, Ola
Kristinsson, Sigurdur Y.
TI Elevated Risk of Venous but Not Arterial Thrombosis in Waldenstrm's
Macroglobulinemia and Lymphoplasmacytic Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Hultcrantz, Malin L.; Bjorkholm, Magnus; Kristinsson, Sigurdur Y.] Karolinska Univ Hosp, Dept Med, Div Hematol, Stockholm, Sweden.
[Hultcrantz, Malin L.; Kristinsson, Sigurdur Y.] Karolinska Inst, Stockholm, Sweden.
[Pfeiffer, Ruth M.; Goldin, Lynn] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Turesson, Ingemar] Malmo Univ Hosp, Dept Med, Malmo, Sweden.
[Schulman, Sam] McMaster Univ, Dept Med, Hamilton, ON, Canada.
[Landgren, Ola] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RI Kristinsson, Sigurdur /M-2910-2015
OI Kristinsson, Sigurdur /0000-0002-4964-7476
NR 0
TC 2
Z9 2
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1603
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838906313
ER
PT J
AU Ikawa, Y
Uchiyama, T
Jagadeesh, GJ
Candotti, F
AF Ikawa, Yasuhiro
Uchiyama, Toru
Jagadeesh, Guridevi Jayashree
Candotti, Fabio
TI Analysis of Risk and Mechanism of Insertional Oncogenesis After Gene
Transfer Into Hematopoietic Progenitors with Integrating Viral Vectors
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
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 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2049
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049603246
ER
PT J
AU Ikeda, AK
Anaebere, TC
Malik, N
Antalek, MD
Seidel, ML
Seamon, C
Gorbach, A
Kato, GJ
Ackerman, HC
AF Ikeda, Allison K.
Anaebere, Tiffany C.
Malik, Nitin
Antalek, Matthew D.
Seidel, Miles L.
Seamon, Catherine
Gorbach, Alexander
Kato, Gregory J.
Ackerman, Hans C.
TI Laser Speckle Contrast Imaging Characterizes Delayed Reperfusion After
Transient Brachial Artery Occlusion in Patients with Sickle Cell Diseas
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Ikeda, Allison K.; Anaebere, Tiffany C.; Ackerman, Hans C.] NIAID, Lab Malaria & Vector Res, Rockville, MD USA.
[Malik, Nitin; Antalek, Matthew D.; Seidel, Miles L.; Gorbach, Alexander] Natl Inst Biomed Imaging & Bioengn, Bethesda, MD USA.
[Seamon, Catherine; Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, Hematol Branch, 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 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1080
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049601376
ER
PT J
AU Inamoto, Y
Chai, XY
Kurland, B
Weisdorf, DJ
Martin, PJ
Jacobsohn, D
Pidala, J
Palmer, J
Arai, S
Cutler, C
Jagasia, M
Flowers, MED
Arora, M
Pavletic, SZ
Vogelsang, GB
Lee, SJ
Carpenter, PA
AF Inamoto, Yoshihiro
Chai, Xiaoyu
Kurland, Brenda
Weisdorf, Daniel J.
Martin, Paul J.
Jacobsohn, David
Pidala, Joseph
Palmer, Jeanne
Arai, Sally
Cutler, Corey
Jagasia, Madan
Flowers, Mary E. D.
Arora, Mukta
Pavletic, Steven Z.
Vogelsang, Georgia B.
Lee, Stephanie J.
Carpenter, Paul A.
TI Recommended Tools for Joint Chronic Graft-Versus-Host Disease: Results
From the Chronic Gvhd Consortium
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Weisdorf, Daniel J.; Arora, Mukta] Univ Minnesota, Med Ctr, Minneapolis, MN 55455 USA.
[Martin, Paul J.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
[Jacobsohn, David] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Pidala, Joseph] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Palmer, Jeanne] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Arai, Sally] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
[Cutler, Corey] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Jagasia, Madan] Vanderbilt Univ, Med Ctr, Dept Med, Div Hematol Oncol, Nashville, TN USA.
[Pavletic, Steven Z.] NCI, Bethesda, MD 20892 USA.
[Vogelsang, Georgia B.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 464
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838901372
ER
PT J
AU Ito, S
Barrett, AJ
Larochelle, A
Hensel, NF
Keyvanfar, K
Melenhorst, JJ
AF Ito, Sawa
Barrett, A. John
Larochelle, Andre
Hensel, Nancy F.
Keyvanfar, Keyvan
Melenhorst, J. Joseph
TI Long Term Maintenance of Myeloid Leukemia Stem Cell-Like Populations
Cultured with Mesenchymal Stromal Cells (MSC)
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Ito, Sawa; Barrett, A. John; Larochelle, Andre; Hensel, Nancy F.; Keyvanfar, Keyvan; Melenhorst, J. Joseph] 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 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3546
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838906111
ER
PT J
AU Jain, NA
Koklanaris, EK
Chawla, K
Pophali, PA
Klotz, JK
Hourigan, CS
Savani, BN
Ito, S
Barrett, AJ
Battiwalla, M
AF Jain, Natasha A.
Koklanaris, Eleftheria K.
Chawla, Kamna
Pophali, Priyanka A.
Klotz, Jeffrey K.
Hourigan, Christopher S.
Savani, Bipin N.
Ito, Sawa
Barrett, A. John
Battiwalla, Minoo
TI Post-Transplant Pulmonary Function Abnormalities Normalize in Survivors
by the Second Decade After Allogeneic Stem Cell Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Jain, Natasha A.; Koklanaris, Eleftheria K.; Chawla, Kamna; Pophali, Priyanka A.; Klotz, Jeffrey K.; Hourigan, Christopher S.; Savani, Bipin N.; Ito, Sawa; Barrett, A. John; 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 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1967
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838903024
ER
PT J
AU Jiang, X
Huang, H
Li, ZJ
Li, YY
Wang, X
Gurbuxani, S
Chen, P
He, CJ
You, DW
Zhang, SD
Wang, JH
Arnovitz, S
Elkahloun, A
Price, C
Hong, GM
Ren, HM
Kunjamma, RB
Neilly, MB
Larson, RA
Le Beau, MM
Slany, RK
Liu, PP
Lu, J
Zhang, JW
He, C
Rowley, JD
Chen, JJ
AF Jiang, Xi
Huang, Hao
Li, Zejuan
Li, Yuanyuan
Wang, Xiao
Gurbuxani, Sandeep
Chen, Ping
He, Chunjiang
You, Dewen
Zhang, Shuodan
Wang, Jinhua
Arnovitz, Stephen
Elkahloun, Abdel
Price, Colles
Hong, Gia-Ming
Ren, Haomin
Kunjamma, Rejani B.
Neilly, Mary Beth
Larson, Richard A.
Le Beau, Michelle M.
Slany, Robert K.
Liu, Paul P.
Lu, Jun
Zhang, Jiwang
He, Chuan
Rowley, Janet D.
Chen, Jianjun
TI Blockade of Mir-150 Maturation by MLL-Fusion/MYC/Lin-28 Is Required for
MLL-Associated Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Jiang, Xi; Huang, Hao; Li, Zejuan; Li, Yuanyuan; Chen, Ping; He, Chunjiang; Zhang, Shuodan; Wang, Jinhua; Arnovitz, Stephen; Price, Colles; Hong, Gia-Ming; Ren, Haomin; Kunjamma, Rejani B.; 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.
[Wang, Xiao; He, Chuan] Univ Chicago, Dept Chem, Chicago, IL 60637 USA.
[Wang, Xiao; He, Chuan] Univ Chicago, Inst Biophys Dynam, Chicago, IL 60637 USA.
[Gurbuxani, Sandeep] Univ Chicago, Dept Pathol, Chicago, IL 60637 USA.
[You, Dewen; Zhang, Jiwang] Loyola Univ, Med Ctr, Cardinal Bernardin Canc Ctr, Inst Oncol, Maywood, IL 60153 USA.
[Elkahloun, Abdel; Liu, Paul P.] NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
[Slany, Robert K.] Univ Erlangen Nurnberg, Dept Genet, D-91054 Erlangen, Germany.
[Lu, Jun] Yale Univ, Dept Genet, Yale Stem Cell Ctr, New Haven, CT USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3499
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604028
ER
PT J
AU Johnson, KD
Gao, X
Sanalkumar, R
Hsu, AP
Ryu, MJ
Wang, JY
Boyer, ME
Liu, YG
Calvo, KR
Keles, S
Zhang, J
Holland, SM
Bresnick, EH
AF Johnson, Kirby D.
Gao, Xin
Sanalkumar, Rajendran
Hsu, Amy P.
Ryu, Myung-Jeom
Wang, Jinyong
Boyer, Meghan E.
Liu, Yangang
Calvo, Katherine R.
Keles, Sunduz
Zhang, Jing
Holland, Steven M.
Bresnick, Emery H.
TI Genetic Determinants of the Definitive Hematopoietic Stem/Progenitor
Cell Compartment
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Johnson, Kirby D.; Gao, Xin; Sanalkumar, Rajendran; Boyer, Meghan E.; Bresnick, Emery H.] Univ Wisconsin, Sch Med & Publ Hlth, Dept Cell & Regenerat Biol, UW Carbone Canc Ctr, Madison, WI USA.
[Hsu, Amy P.; Holland, Steven M.] NIH, Hematol Sect, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Ryu, Myung-Jeom; Wang, Jinyong; Zhang, Jing] Univ Wisconsin, McArdle Lab Canc Res, Madison, WI 53706 USA.
[Keles, Sunduz] Univ Wisconsin, Sch Med & Publ Hlth, Dept Biostat, Madison, WI USA.
[Keles, Sunduz] Univ Wisconsin, Sch Med & Publ Hlth, Dept Med Informat & Stat, Madison, WI USA.
RI Calvo, Katherine/A-8109-2009
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1226
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838902340
ER
PT J
AU Kang, YY
Patel, B
Cui, KR
Zhao, KJ
Qiu, Y
Huang, SM
AF Kang, Yuanyuan
Patel, Bhavita
Cui, Kairong
Zhao, Keji
Qiu, Yi
Huang, Suming
TI A T-Cell Specific Element Activates the TAL1 Oncogene Via an
Interchromosomal Interaction During Leukemogenesis
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Zhao, Keji] NHLBI, NIH, Bethesda, MD 20892 USA.
[Huang, Suming] Univ Florida, Coll Med, Shands Canc Ctr, Gainesville, FL USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3507
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604020
ER
PT J
AU Khincha, P
Wentzensen, I
Giri, N
Alter, BP
Savage, SA
AF Khincha, Payal
Wentzensen, Ingrid
Giri, Neelam
Alter, Blanche P.
Savage, Sharon A.
TI Response to Androgen Therapy and Side Effects in Patients with
Dyskeratosis Congenita
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Khincha, Payal; Giri, Neelam; Alter, Blanche P.; Savage, Sharon A.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Wentzensen, Ingrid] Johns Hopkins Univ, Inst Med Genet, Baltimore, MD USA.
RI Savage, Sharon/B-9747-2015
OI Savage, Sharon/0000-0001-6006-0740
NR 0
TC 1
Z9 1
U1 1
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2361
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049601100
ER
PT J
AU Kim, KS
Byrnes, C
Lee, YT
de Vasconcellos, JF
Noh, SJ
Miller, JL
AF Kim, Ki Soon
Byrnes, Colleen
Lee, Y. Terry
de Vasconcellos, Jaira F.
Noh, Seung-Jae
Miller, Jeffery L.
TI Mitochondria Superoxide Is an Early Trigger of Apoptosis in an Ex Vivo
Model of Human Beta Thalassemia
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Kim, Ki Soon; Byrnes, Colleen; Lee, Y. Terry; de Vasconcellos, Jaira F.; Noh, Seung-Jae; 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 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2131
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838905305
ER
PT J
AU Nguyen, KL
Alam, S
Tian, X
Leung, SW
Seamon, C
Minniti, C
Taylor, JG
Sachdev, V
Arai, AE
Kato, GJ
AF Kim-Lien Nguyen
Alam, Shoaib
Tian, Xian
Leung, Steve W.
Seamon, Catherine
Minniti, Caterina
Taylor, James G.
Sachdev, Vandana
Arai, Andrew E.
Kato, Gregory J.
TI Increased Transpulmonary Gradient Predicts Functional Class, Mortality,
and RV Dysfunction by MRI in Patients with Sickle Cell Associated
Pulmonary Hypertension
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Kim-Lien Nguyen; Alam, Shoaib; Leung, Steve W.; Sachdev, Vandana; Arai, Andrew E.] NHLBI, Cardiovasc & Pulm Branch, Bethesda, MD 20892 USA.
[Tian, Xian] NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
[Seamon, Catherine; Minniti, Caterina; Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, Hematol Branch, Bethesda, MD 20892 USA.
[Taylor, James G.] NHLBI, Genom Med Sect, Hematol Branch, Bethesda, MD 20892 USA.
RI Leung, Steve/E-5624-2011; Kato, Gregory/I-7615-2014
OI Leung, Steve/0000-0003-2832-2258; Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 89
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900076
ER
PT J
AU Korde, N
Liu, QY
Kwok, M
Manasanch, EE
Simakova, O
Mailankody, S
Roschewski, M
Zingone, A
Costello, R
Zuchlinski, D
Mulquin, M
Calvo, KR
Braylan, RC
Maric, I
Landgren, O
AF Korde, Neha
Liu, Qing Yan
Kwok, Mary
Manasanch, Elisabet E.
Simakova, Olga
Mailankody, Sham
Roschewski, Mark
Zingone, Adriana
Costello, Rene
Zuchlinski, Diamond
Mulquin, Marcia
Calvo, Katherine R.
Braylan, Raul C.
Maric, Irina
Landgren, Ola
TI Early Myelodysplastic Changes Present in Substantial Proportion of
Monoclonal Gammopathy of Unknown Significance (MGUS) and Smoldering
Multiple Myeloma (SMM) Patients
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Liu, Qing Yan] NIH, Hematol Sect, DLM, CC, Bethesda, MD 20892 USA.
[Manasanch, Elisabet E.; Zingone, Adriana; Landgren, Ola] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Roschewski, Mark] NCI, Multiple Myeloma Sect, Metab Branch, NIH, Bethesda, MD 20892 USA.
[Braylan, Raul C.; Maric, Irina] NIH, Hematol Sect, Dept Lab Med, CCR, Bethesda, MD 20892 USA.
RI Calvo, Katherine/A-8109-2009
NR 0
TC 2
Z9 2
U1 1
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1805
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049602072
ER
PT J
AU Korde, N
Zingone, A
Kwok, M
Manasanch, EE
Costello, R
Zuchlinski, D
Mulquin, M
Maric, I
Calvo, KR
Braylan, RC
Yuan, C
Tembhare, PR
Stetler-Stevenson, M
Arthur, DC
Raffeld, M
Xi, LQ
Choyke, P
Kurdziel, K
Lindenberg, L
Steinberg, SM
Roschewski, M
Landgren, O
AF Korde, Neha
Zingone, Adriana
Kwok, Mary
Manasanch, Elisabet E.
Costello, Rene
Zuchlinski, Diamond
Mulquin, Marcia
Maric, Irina
Calvo, Katherine R.
Braylan, Raul C.
Yuan, Constance
Tembhare, Prashant Ramesh
Stetler-Stevenson, Maryalice
Arthur, Diane C.
Raffeld, Mark
Xi, Liqiang
Choyke, Peter
Kurdziel, Karen
Lindenberg, Liza
Steinberg, Seth M.
Roschewski, Mark
Landgren, Ola
TI Phase II Clinical and Correlative Study of Carfilzomib, Lenalidomide,
and Dexamethasone (CRd) in Newly Diagnosed Multiple Myeloma (MM)
Patients
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Manasanch, Elisabet E.; Landgren, Ola] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Maric, Irina; Braylan, Raul C.] NIH, Hematol Sect, Dept Lab Med, CCR, Bethesda, MD 20892 USA.
[Calvo, Katherine R.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Yuan, Constance; Tembhare, Prashant Ramesh; Stetler-Stevenson, Maryalice] NCI, Flow Cytometry Unit, Pathol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Arthur, Diane C.] NCI, Pathol Lab, NIH, CCR, Bethesda, MD 20892 USA.
[Raffeld, Mark; Xi, Liqiang] NCI, Mol Diagnost Core Lab, NIH, CCR, Bethesda, MD 20892 USA.
[Choyke, Peter; Kurdziel, Karen; Lindenberg, Liza] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, Rockville, MD USA.
[Roschewski, Mark] NCI, Multiple Myeloma Sect, Metab Branch, NIH, Bethesda, MD 20892 USA.
RI Calvo, Katherine/A-8109-2009
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 732
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900227
ER
PT J
AU Kreitman, RJ
Arons, E
Jeffrey, S
Roth, L
Zhou, H
Stetler-Stevenson, M
Wilson, WH
Raffeld, M
FitzGerald, DJP
Fei, J
Ibrahim, R
Pastan, I
AF Kreitman, Robert J.
Arons, Evgeny
Jeffrey, Sapolsky
Roth, Laura
Zhou, Hong
Stetler-Stevenson, Maryalice
Wilson, Wyndham H.
Raffeld, Mark
FitzGerald, David J. P.
Fei, Ji
Ibrahim, Ramy
Pastan, Ira
TI Resolution of Hairy Cell Leukemia Minimal Residual Disease by Both BRAF
and Clone-Specific Real-Time Quantitative PCR (RQ-PCR) After Treatment
with Moxetumomab Pasudotox
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Kreitman, Robert J.; Arons, Evgeny; Jeffrey, Sapolsky; Roth, Laura; Zhou, Hong; FitzGerald, David J. P.; Pastan, Ira] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Stetler-Stevenson, Maryalice; Raffeld, Mark] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Wilson, Wyndham H.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
[Fei, Ji; Ibrahim, Ramy] MedImmune LLC, Gaithersburg, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2896
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838905343
ER
PT J
AU Lanasa, MC
Allgood, SD
Goldin, LR
Brander, DM
McMaster, ML
AF Lanasa, Mark C.
Allgood, Sallie D.
Goldin, Lynn R.
Brander, Danielle M.
McMaster, Mary L.
TI Circulating B Cell Clones in Familial Waldenstrom Macroglobulinemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Lanasa, Mark C.; Allgood, Sallie D.] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
[Goldin, Lynn R.; McMaster, Mary L.] NCI, Genet Epidemiol Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2703
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838903090
ER
PT J
AU Lancet, JE
Feldman, E
Foster, MC
Gojo, I
Odenike, O
Komrokji, RS
Strair, R
Kaufmann, SH
Knoblauch, R
Karkera, JD
Wright, JJ
Karp, JE
AF Lancet, Jeffrey E.
Feldman, Eric
Foster, Matthew C.
Gojo, Ivana
Odenike, Olatoyosi
Komrokji, Rami S.
Strair, Roger
Kaufmann, Scott H.
Knoblauch, Roland
Karkera, J. D.
Wright, John J.
Karp, Judith E.
TI Phase 2 Trial of the Farnesyltransferase Inhibitor Tipifarnib in
Previously Untreated Older Adults with AML and Baseline Presence of a
Specific 2-Gene Expression Signature Ratio
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Lancet, Jeffrey E.; Komrokji, Rami S.] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Feldman, Eric] Weill Cornell Med Coll, New York, NY USA.
[Foster, Matthew C.] Lineberger Canc Ctr, Chapel Hill, NC USA.
[Gojo, Ivana] Johns Hopkins Univ, Kimmel Canc Ctr, Baltimore, MD 21218 USA.
[Odenike, Olatoyosi] Univ Chicago, Dept Med, Hematol Oncol Sect, Chicago, IL 60637 USA.
[Strair, Roger] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Canc Inst New Jersey, Div Hematol, New Brunswick, NJ USA.
[Kaufmann, Scott H.] Mayo Clin, Dept Mol Pharmacol & Expt Therapeut, Rochester, MN USA.
[Knoblauch, Roland; Karkera, J. D.] Janssen, Res & Dev, Raritan, NJ USA.
[Wright, John J.] NCI, Bethesda, MD 20892 USA.
[Karp, Judith E.] Sidney Kimmel Comprehens Canc Ctr John Hopkins, Div Hematol Malignancies, Dept Oncol, Baltimore, MD USA.
NR 0
TC 1
Z9 2
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1508
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838906218
ER
PT J
AU Lederman, HM
Connolly, MA
Kalpatthi, R
Ware, RE
Wang, WC
Luchtman-Jones, L
Waclawiw, M
Goldsmith, JC
Casella, JF
AF Lederman, Howard M.
Connolly, Margaret A.
Kalpatthi, Ram
Ware, Russell E.
Wang, Winfred C.
Luchtman-Jones, Lori
Waclawiw, Myron
Goldsmith, Jonathan C.
Casella, James F.
TI Effects of Hydroxyurea (HU) On Lymphocyte Subsets and the Immune
Response to Pneumococcal, Measles, Mumps and Rubella Vaccination in the
Pediatric Hydroxyurea Phase III Clinical Trial - BABY HUG -
(ClinicalTrials.gov Identifier: NCT00006400)
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Lederman, Howard M.; Casella, James F.] Johns Hopkins Univ, Sch Med, Div Immunol, Baltimore, MD USA.
[Connolly, Margaret A.] C TASC, Owings Mills, MD USA.
[Kalpatthi, Ram] Childrens Mercy Hosp, Kansas City, MO 64108 USA.
[Ware, Russell E.] Baylor Coll Med, Houston, TX 77030 USA.
[Wang, Winfred C.] St Jude Childrens Res Hosp, Dept Hematol, Memphis, TN 38105 USA.
[Luchtman-Jones, Lori] Childrens Natl Med Ctr, Washington, DC USA.
[Goldsmith, Jonathan C.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 243
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838901107
ER
PT J
AU Li, ZJ
Zhang, ZY
Li, YY
Arnovitz, S
Chen, P
Huang, H
Jiang, X
Hong, GM
He, CJ
Wang, CZ
Elkahloun, A
Valk, PJM
Dohner, K
Neilly, MB
Bullinger, L
Delwel, R
Lowenberg, B
Liu, PP
Morgan, R
Rowley, JD
Yuan, CS
Chen, JJ
AF Li, Zejuan
Zhang, Zhiyu
Li, Yuanyuan
Arnovitz, Stephen
Chen, Ping
Huang, Hao
Jiang, Xi
Hong, Gia-Ming
He, Chunjiang
Wang, Chong-Zhi
Elkahloun, Abdel
Valk, Peter J. M.
Dohner, Konstanze
Neilly, Mary Beth
Bullinger, Lars
Delwel, Ruud
Lowenberg, Bob
Liu, Pu Paul
Morgan, Richard
Rowley, Janet D.
Yuan, Chun-Su
Chen, Jianjun
TI The HOXA/PBX3 Pathway Is an Attractive Therapeutic Target in
MLL-Rearranged Acute Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Li, Zejuan; Li, Yuanyuan; Arnovitz, Stephen; Chen, Ping; Huang, Hao; Jiang, Xi; Hong, Gia-Ming; He, Chunjiang; Neilly, Mary Beth; Rowley, Janet D.; Chen, Jianjun] Univ Chicago, Dept Med, Hematol Oncol Sect, Chicago, IL 60637 USA.
[Zhang, Zhiyu] Univ Chicago, Dept Anesthesia & Crit Care, Chicgao, IL USA.
[Wang, Chong-Zhi; Yuan, Chun-Su] Univ Chicago, Dept Anesthesia & Crit Care, Chicago, IL 60637 USA.
[Valk, Peter J. M.; Lowenberg, Bob] Erasmus Univ, Med Ctr, Dept Hematol, Rotterdam, Netherlands.
[Dohner, Konstanze] Univ Hosp Ulm, Dept Internal Med 3, Ulm, Germany.
[Bullinger, Lars] Univ Ulm, Dept Internal Med 3, D-89069 Ulm, Germany.
[Delwel, Ruud] Univ Med Ctr Rotterdam, Erasmus MC, Dept Hem, Rotterdam, Netherlands.
[Liu, Pu Paul] NHGRI, GMBB, ODS, NIH, Bethesda, MD 20892 USA.
[Morgan, Richard] Univ Surrey, Guildford GU2 5XH, Surrey, England.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3522
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838906135
ER
PT J
AU Lim, KH
Romero, DL
Chaudhary, D
Robinson, SD
Staudt, LM
AF Lim, Kian-Huat
Romero, Donna L.
Chaudhary, Divya
Robinson, Shaughnessy D.
Staudt, Louis M.
TI IRAK4 Kinase As A Novel Therapeutic Target in the ABC Subtype of Diffuse
Large B Cell Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Lim, Kian-Huat] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Romero, Donna L.; Chaudhary, Divya] Nimbus Discovery Inc, Cambridge, MA USA.
[Robinson, Shaughnessy D.] Schrodinger Inc, New York, NY USA.
[Staudt, Louis M.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 62
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900102
ER
PT J
AU Loaiza-Bonilla, A
Artz, A
Salerno, F
Leng, SX
Yeh, SS
Biedenbender, R
Gravenstein, S
Loera, J
Geloo, ZS
Ershler, WB
AF Loaiza-Bonilla, Arturo
Artz, Andrew
Salerno, Francis
Leng, Sean X.
Yeh, Shing-Shing
Biedenbender, Rex
Gravenstein, Stefan
Loera, Jose
Geloo, Zeba Shaheen
Ershler, William B.
TI Correction of Anemia in the Frail Elderly (CAFE): Results of a
Randomized, Double-Blind, Placebo-Controlled Study with Darbepoetin Alfa
in Elderly Patients with Chronic Unexplained Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Loaiza-Bonilla, Arturo] Univ Miami, Miller Sch Med, Div Hematol & Oncol, Dept Med, Miami, FL 33136 USA.
[Artz, Andrew] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
[Salerno, Francis] Lehigh Valley Hosp, Div Geriatr, Dept Med, Allentown, PA USA.
[Leng, Sean X.] Johns Hopkins Univ, Dept Med, Div Geriatr, Baltimore, MD USA.
[Yeh, Shing-Shing] Vet Affairs Med Ctr, Div Geriatr, Dept Med, Northport, NY USA.
[Biedenbender, Rex; Gravenstein, Stefan] Eastern Virginia Med Sch, Glennan Ctr Geriatr & Gerontol, Norfolk, VA 23501 USA.
[Loera, Jose] Vet Affairs & Scott & White, Div Geriatr, Temple, TX USA.
[Geloo, Zeba Shaheen] Inst Adv Studies Aging & Geriatr Med IASIA, Gaithersburg, MD USA.
[Ershler, William B.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 5153
PG 1
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049605435
ER
PT J
AU Lorenzo, FR
Zhuang, ZP
Yang, CZ
Fui, MNT
Vankayalapati, H
Pacak, K
Prchal, JT
AF Lorenzo, Felipe R.
Zhuang, Zhengping
Yang, Chunzhang
Fui, Mark Ng Tang
Vankayalapati, Hariprasad
Pacak, Karel
Prchal, Josef T.
TI Three Novel EPAS1/HIF2A Somatic and Germline mutations Associated with
Polycythemia and Pheochromocytoma/Paraganglioma
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Lorenzo, Felipe R.; Prchal, Josef T.] Univ Utah, Div Hematol, Salt Lake City, UT USA.
[Yang, Chunzhang; Fui, Mark Ng Tang; Pacak, Karel] NIH, Bethesda, MD 20892 USA.
[Fui, Mark Ng Tang] Univ Melbourne, Dept Endocrinol, Heidelberg, Vic, Australia.
[Vankayalapati, Hariprasad] Univ Utah, Ctr Invest Therapeut, Salt Lake City, UT USA.
[Vankayalapati, Hariprasad] Huntsman Canc Inst, Salt Lake City, UT USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2080
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049603215
ER
PT J
AU Lozier, JN
Nghiem, K
Lee, M
Hodsdon, B
Joe, G
Weitzel, RP
Tisdale, JF
Hsieh, M
AF Lozier, Jay N.
Nghiem, Khanh
Lee, Martin
Hodsdon, Bonnie
Joe, Galen
Weitzel, R. Patrick
Tisdale, John F.
Hsieh, Matthew
TI Acquired Hemophilia A in an African-American Male After Stem Cell
Transplant for Sickle Cell Disease: Successful Treatment with
Recombinant Porcine Factor VIII (OBI-1) and Tolerance Induction with
Rituximab and Prednisone
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Lozier, Jay N.; Nghiem, Khanh] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Lee, Martin] Inspirat Biopharmaceut Inc, E Cambridge, MA USA.
[Hodsdon, Bonnie; Joe, Galen] NIH, Dept Rehabil Med, Ctr Clin, Bethesda, MD 20892 USA.
[Weitzel, R. Patrick] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
[Tisdale, John F.; Hsieh, Matthew] NHLBI, Mol & Clin Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4631
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049606087
ER
PT J
AU Mamcarz, EK
Berg, M
Peled, T
Frei, GM
Reger, R
Tian, X
Childs, R
AF Mamcarz, Ewelina K.
Berg, Maria
Peled, Tony
Frei, Gabi M.
Reger, Robert
Tian, Xin
Childs, Richard
TI Nicotinamide (NAM) Increases Surface Expression of CD62L On in Vitro
Expanded NK Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Mamcarz, Ewelina K.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Berg, Maria; Reger, Robert; Childs, Richard] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Peled, Tony; Frei, Gabi M.] Gamida Cell, Jerusalem, Israel.
[Tian, Xin] NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4355
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049605167
ER
PT J
AU Masters, SL
Gerlic, M
Metcalf, D
Preston, SP
Pellegrini, M
O'Donnell, JA
McArthur, K
Baldwin, TM
Chevrier, S
Nowell, CJ
Cengia, LH
Henley, KJ
Collinge, JE
Kastner, DL
Feigenbaum, L
Hilton, DJ
Alexander, WS
Croker, BA
Kile, BT
AF Masters, Seth L.
Gerlic, Mordechay
Metcalf, Donald
Preston, Simon P.
Pellegrini, Marc
O'Donnell, Joanne A.
McArthur, Kate
Baldwin, Tracey M.
Chevrier, Stephane
Nowell, Cameron J.
Cengia, Louise H.
Henley, Katya J.
Collinge, Janelle E.
Kastner, Daniel L.
Feigenbaum, Lionel
Hilton, Douglas J.
Alexander, Warren S.
Croker, Ben A.
Kile, Benjamin T.
TI Activation of the NLRP1 Inflammasome Induces the Pyroptotic Death of
Hematopoietic Progenitor Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Masters, Seth L.; Gerlic, Mordechay; Metcalf, Donald; Preston, Simon P.; Pellegrini, Marc; O'Donnell, Joanne A.; McArthur, Kate; Baldwin, Tracey M.; Chevrier, Stephane; Cengia, Louise H.; Henley, Katya J.; Collinge, Janelle E.; Hilton, Douglas J.; Alexander, Warren S.; Croker, Ben A.; Kile, Benjamin T.] Royal Melbourne Hosp, Walter & Eliza Hall Inst Med Res, Parkville, Vic 3050, Australia.
[Nowell, Cameron J.] Ludwig Inst Canc Res, Ctr Adv Microscopy, Parkville, Vic, Australia.
[Kastner, Daniel L.] NIAMSD, Bethesda, MD 20892 USA.
[Feigenbaum, Lionel] NCI, Frederick, MD 21701 USA.
RI Hilton, Douglas/C-7250-2013; Pellegrini, Marc/F-7670-2014
OI Hilton, Douglas/0000-0002-7698-2392;
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1213
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838902353
ER
PT J
AU McDonnell, SRP
Hwang, SR
Basrur, V
Conlon, K
Fermin, D
Murga-Zamalloa, C
Rolland, DCM
Thomas, CJ
Elenitoba-Johnson, KSJ
Lim, MS
AF McDonnell, Scott R. P.
Hwang, Steven R.
Basrur, Venkatesha
Conlon, Kevin
Fermin, Damian
Murga-Zamalloa, Carlos
Rolland, Delphine C. M.
Thomas, Craig J.
Elenitoba-Johnson, Kojo S. J.
Lim, Megan S.
TI Phosphorylation of PKM2 by NPM-ALK Regulates a Metabolic Shift and
Increased Oncogenic Potential
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Thomas, Craig J.] NIH Chem Genom Ctr, Bethesda, MD 20892 USA.
[Lim, Megan S.] Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 896
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900363
ER
PT J
AU Meier, ER
Wright, EC
Luban, NLC
Miller, JL
AF Meier, Emily Riehm
Wright, Elizabeth C.
Luban, Naomi L. C.
Miller, Jeffery L.
TI Risk Stratification in Pediatric Sickle Cell Disease Using Absolute
Reticulocyte Counts
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Meier, Emily Riehm; Miller, Jeffery L.] NIDDKD, Mol Genom & Therapeut Sect, Mol Med Branch, NIH, Bethesda, MD 20892 USA.
[Wright, Elizabeth C.] NIDDKD, Off Director, NIH, Bethesda, MD 20892 USA.
[Luban, Naomi L. C.] Childrens Natl Med Ctr, Ctr Canc & Blood Disorders, Washington, DC 20010 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1014
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049602057
ER
PT J
AU Mendelsohn, LG
Pedoeim, L
van Beers, EJ
Saiyed, R
Nichols, JS
Wang, XD
Kato, GJ
AF Mendelsohn, Laurel G.
Pedoeim, Leah
van Beers, Eduard J.
Saiyed, Rehan
Nichols, James S.
Wang, Xunde
Kato, Gregory J.
TI Effect of Aes-103 Anti-Sickling Agent On Oxygen Affinity and Stability
of Red Blood Cells From Patients with Sickle Cell Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Mendelsohn, Laurel G.; Pedoeim, Leah; van Beers, Eduard J.; Saiyed, Rehan; Nichols, James S.; Wang, Xunde; Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, Hematol Branch, Bethesda, MD USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 1
Z9 1
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 85
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900080
ER
PT J
AU Meshinchi, S
Ries, RE
Trevino, LR
Hampton, OA
Alonzo, T
Farrar, JE
Auvil, JMG
Davidsen, TM
Gesuwan, P
Muzny, DM
Gamis, AS
Helton, HL
Wheeler, DA
Smith, MA
Gerhard, DS
Arceci, RJ
AF Meshinchi, Soheil
Ries, Rhonda E.
Trevino, Lisa R.
Hampton, Oliver A.
Alonzo, Todd
Farrar, Jason E.
Auvil, Jaime M. Guidry
Davidsen, Tanja M.
Gesuwan, Patee
Muzny, Donna M.
Gamis, Alan S.
Helton, Heather L.
Wheeler, David A.
Smith, Malcolm A.
Gerhard, Daniela S.
Arceci, Robert J.
TI Identification of Novel Somatic Mutations, Regions of Recurrent Loss of
Heterozygosity (LOH) and Significant Clonal Evolution From Diagnosis to
Relapse in Childhood AML Determined by Exome Capture Sequencing - an
NCI/COG Target AML Study
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Meshinchi, Soheil; Ries, Rhonda E.; Helton, Heather L.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
[Trevino, Lisa R.; Hampton, Oliver A.; Muzny, Donna M.; Wheeler, David A.] Baylor Coll Med, Human Genome Sequencing Ctr, Houston, TX 77030 USA.
[Alonzo, Todd] Childrens Oncol Grp, Arcadia, CA USA.
[Farrar, Jason E.] Univ Arkansas Med Sci, Little Rock, AR 72205 USA.
[Auvil, Jaime M. Guidry; Davidsen, Tanja M.; Gesuwan, Patee; Gerhard, Daniela S.] NCI, Off Canc Genom, Bethesda, MD 20892 USA.
[Gamis, Alan S.] Childrens Mercy Hosp & Clin, Kansas City, MO USA.
[Smith, Malcolm A.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Arceci, Robert J.] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 123
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900335
ER
PT J
AU Milton, JN
Rooks, H
Drasar, E
McCabe, EL
Baldwin, CT
Melista, E
Gordeuk, VR
Nouraie, M
Kato, GJ
Minniti, C
Taylor, JG
Campbell, A
Luchtman-Jones, L
Rana, SR
Castro, OL
Zhang, YZ
Thein, SL
Gladwin, MT
Sebastiani, P
Steinberg, MH
AF Milton, Jacqueline N.
Rooks, Helen
Drasar, Emma
McCabe, Elizabeth L.
Baldwin, Clinton T.
Melista, Efthymia
Gordeuk, Victor R.
Nouraie, Mehdi
Kato, Gregory J.
Minniti, Caterina
Taylor, James G.
Campbell, Andrew
Luchtman-Jones, Lori
Rana, Sohail R.
Castro, Oswaldo L.
Zhang, Yingze
Thein, Swee Lay
Gladwin, Mark T.
Sebastiani, Paola
Steinberg, Martin H.
TI Genetic Determinants of Hemolysis in Sickle Cell Anemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Drasar, Emma] Kings Coll London, Sch Med, London SE5 9NU, England.
[Baldwin, Clinton T.; Steinberg, Martin H.] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Gordeuk, Victor R.; Castro, Oswaldo L.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
[Minniti, Caterina] NHLBI, Sickle Cell Vasc Dis Sect, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Taylor, James G.] NHLBI, Sickle Cell Vasc Dis Sect, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Campbell, Andrew] Univ Michigan, Ann Arbor, MI 48109 USA.
[Luchtman-Jones, Lori] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Zhang, Yingze; Gladwin, Mark T.] Univ Pittsburgh, Div Pulm Allergy & Crit Care Med, Pittsburgh, PA USA.
[Thein, Swee Lay] Kings Coll London, Sch Med, Kings Coll Hosp Haematol Med, London SE5 9NU, England.
[Sebastiani, Paola] Boston Univ, Dept Biostat, Sch Publ Hlth, Boston, MA 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 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2104
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049603191
ER
PT J
AU Minniti, CP
Hon, YY
Gorbach, A
Delaney, KM
Xu, DH
Malik, N
Maivelett, J
Novelli, EM
Lanzkron, S
Kato, GJ
AF Minniti, Caterina P.
Hon, Yuen Yi
Gorbach, Alexander
Delaney, Kara M.
Xu, Dihua
Malik, Nitin
Maivelett, Jordan
Novelli, Enrico M.
Lanzkron, Sophia
Kato, Gregory J.
TI A Phase 1, Dose-Escalation Study of Topical Sodium Nitrite in Patients
with Sickle Cell Anemia and Leg Ulcers
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Delaney, Kara M.; Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Hon, Yuen Yi] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Gorbach, Alexander; Malik, Nitin; Maivelett, Jordan] Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD USA.
[Novelli, Enrico M.] Univ Pittsburgh, Vasc Med Inst, Pittsburgh, PA USA.
[Lanzkron, Sophia] Johns Hopkins Sch Med, Dept Med, Baltimore, MD 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 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 86
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900079
ER
PT J
AU Miyazaki, T
Kim, YS
Yoon, JH
Wang, HS
Morse, HC
AF Miyazaki, Takuya
Kim, Yong-Soo
Yoon, Jeong-Heon
Wang, Hongsheng
Morse, Herbert C., III
TI The 3 '-5 ' Exonuclease, TREX1, Interacts with Poly(ADP-ribose)
Polymerase-1 (PARP1) in Response to DNA Damage
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Miyazaki, Takuya; Kim, Yong-Soo; Yoon, Jeong-Heon; Wang, Hongsheng; Morse, Herbert C., III] NIAID, Virol & Cellular Immunol Sect, Immunogenet Lab, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1046
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049602027
ER
PT J
AU Morris, CR
Kim, HY
Wood, JC
Trachtenberg, F
Klings, ES
Porter, JB
Sweeters, N
Olivieri, NF
Kwiatkowski, JL
Singer, ST
Taher, AT
Neufeld, EJ
Thompson, AA
Sachdev, V
Larkin, SK
Suh, JH
Kuypers, FA
Vichinsky, E
AF Morris, Claudia R.
Kim, Hae-Young
Wood, John C.
Trachtenberg, Felicia
Klings, Elizabeth S.
Porter, John B.
Sweeters, Nancy
Olivieri, Nancy F.
Kwiatkowski, Janet L.
Singer, Sylvia Titi
Taher, Ali T.
Neufeld, Ellis J.
Thompson, Alexis A.
Sachdev, Vandana
Larkin, Sandra K.
Suh, Jung H.
Kuypers, Frans A.
Vichinsky, Elliott
TI Sildenafil Therapy in Patients with Thalassemia and an Elevated
Tricuspid Regurgitant Jet Velocity (TRV) On Doppler Echocardiography At
Risk for Pulmonary Hypertension: Report From the Thalassemia Clinical
Research Network
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Morris, Claudia R.] Emory Univ, Sch Med, Atlanta, GA USA.
[Kim, Hae-Young; Trachtenberg, Felicia] New England Res Inst, Watertown, MA 02172 USA.
[Wood, John C.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Klings, Elizabeth S.] Boston Univ, Sch Med, Ctr Pulm, Boston, MA 02118 USA.
[Porter, John B.] UCL, London, England.
[Sweeters, Nancy; Singer, Sylvia Titi; Vichinsky, Elliott] Childrens Hosp & Res Ctr Oakland, Oakland, CA USA.
[Olivieri, Nancy F.] Univ Toronto, Univ Hlth Network, Toronto, ON, Canada.
[Kwiatkowski, Janet L.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Taher, Ali T.] Amer Univ Beirut, Beirut, Lebanon.
[Neufeld, Ellis J.] Boston Childrens Hosp, Dana Farber Canc Inst, Boston, MA USA.
[Thompson, Alexis A.] Childrens Mem Hosp, Chicago, IL 60614 USA.
[Sachdev, Vandana] NHLBI, Cardiovasc & Pulm Med Branch, NIH, Bethesda, MD 20892 USA.
[Suh, Jung H.] Childrens Hosp Oakland, Res Inst, Nutr & Metab Ctr, Oakland, CA 94609 USA.
NR 0
TC 2
Z9 2
U1 1
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1023
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049602048
ER
PT J
AU Muller, TA
Dechow, R
Istyanffy, R
Hennighausen, L
Peschel, C
Duyster, J
AF Mueller, Tony Andreas
Dechow, Rebekka
Istyanffy, Rouzanna
Hennighausen, Lothar
Peschel, Christian
Duyster, Justus
TI The Role of STAT5 in FLT3-Mediated Leukemogenesis
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Mueller, Tony Andreas; Dechow, Rebekka; Istyanffy, Rouzanna; Peschel, Christian; Duyster, Justus] Tech Univ Munich, Klinikum Rechts Isar, Dept Internal Med 3, D-80290 Munich, Germany.
[Hennighausen, Lothar] NIDDK, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 771
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900188
ER
PT J
AU Nash, RA
Hutton, GJ
Racke, MK
Popat, UR
Devine, SM
Georges, GE
Griffith, LM
Muraro, PA
Openshaw, H
Sayre, PH
Stuve, O
Arnold, DL
Spychala, M
Lim, N
Malhotra, S
Phippard, D
Wundes, A
Kraft, GH
Bowen, JD
AF Nash, Richard A.
Hutton, George J.
Racke, Michael K.
Popat, Uday R.
Devine, Steven M.
Georges, George E.
Griffith, Linda M.
Muraro, Paolo A.
Openshaw, Harry
Sayre, Peter H.
Stuve, Olaf
Arnold, Douglas L.
Spychala, Meagan
Lim, Noha
Malhotra, Sachin
Phippard, Deborah
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: 2-Year Follow-up Results of the HALT MS Clinical Trial
(Immune Tolerance Network: ITN033AI)
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Nash, Richard A.] Colorado Blood Canc Inst, Denver, CO USA.
[Hutton, George J.] Baylor Coll Med, Houston, TX 77030 USA.
[Racke, Michael K.; Devine, Steven M.] Ohio State Univ, Columbus, OH 43210 USA.
[Popat, Uday R.] Univ Texas MD Anderson Canc Ctr, Dept Stem Cell Transplantat & Cellular Therapy, Houston, TX 77030 USA.
[Georges, George E.] Fred Hutchinson Canc Res Ctr, Transplantat Biol Program, Seattle, WA 98104 USA.
[Griffith, Linda M.] NIAID, Div Allergy Immunol & Transplantat, NIH, Bethesda, MD 20892 USA.
[Muraro, Paolo A.] Univ London Imperial Coll Sci Technol & Med, Div Neurosci & Mental Hlth, London SW7 2AZ, England.
[Stuve, Olaf] Univ Texas SW, Sch Med, Dallas, TX USA.
[Arnold, Douglas L.] McGill Univ, Montreal, PQ H3A 2T5, Canada.
[Malhotra, Sachin] Harvard Univ, Cambridge, MA 02138 USA.
[Wundes, Annette; Kraft, George H.] Univ Washington, Seattle, WA 98195 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 962
PG 3
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838901175
ER
PT J
AU Natarajan, K
Bhullar, J
Shukla, S
Burcu, M
Ambudkar, SV
Baer, MR
AF Natarajan, Karthika
Bhullar, Jasjeet
Shukla, Suneet
Burcu, Mehmet
Ambudkar, Suresh V.
Baer, Maria R.
TI The Pim Kinase Inhibitor SGI-1776 Chemosensitizes Multidrug Resistant
Cells by Both Inhibiting Drug Transport by ABCB1 and ABCG2 and
Decreasing ABCB1 and ABCG2 Surface Expression On Cells That Overexpress
Pim-1
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Natarajan, Karthika; Bhullar, Jasjeet; Burcu, Mehmet; Baer, Maria R.] Univ Maryland, Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
[Shukla, Suneet; Ambudkar, Suresh V.] NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2462
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049602219
ER
PT J
AU Nayar, U
Akar, G
Shoemaker, RH
Sei, S
Cesarman, E
AF Nayar, Utthara
Akar, Gunkut
Shoemaker, Robert H.
Sei, Shizuko
Cesarman, Ethel
TI Identification of a Novel Inhibitor That Selectively Targets NF-kappa B
Activity in KSHV-Infected Lymphoma Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Nayar, Utthara; Akar, Gunkut] Weill Cornell Med Coll, New York, NY USA.
[Shoemaker, Robert H.] NCI, Div Canc Treatment & Diag, Frederick, MD 21701 USA.
[Sei, Shizuko] NCI Frederick, Frederick, MD USA.
[Cesarman, Ethel] Cornell Univ, Weill Med Coll, New York, NY 10021 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 160
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900297
ER
PT J
AU Ochs, M
Farrar, J
Considine, M
Ries, RE
Trevino, LR
Alonzo, TA
Guidry-Auvil, J
Davidsen, TM
Gesuwan, P
Muzny, DM
Gamis, AS
Wheeler, DA
Helton, HL
Smith, MA
Gerhard, DS
Meshinchi, S
Arceci, RJ
AF Ochs, Michael
Farrar, Jason
Considine, Michael
Ries, Rhonda E.
Trevino, Lisa R.
Alonzo, Todd A.
Guidry-Auvil, Jaime
Davidsen, Tanja M.
Gesuwan, Patee
Muzny, Donna M.
Gamis, Alan S.
Wheeler, David A.
Helton, Heather L.
Smith, Malcolm A.
Gerhard, Daniela S.
Meshinchi, Soheil
Arceci, Robert J.
TI Genome Wide Promoter Methylation Patterns Predict AML Subtype Outcomes
and Identify Novel Pathways Characterizing Diagnostic and Relapsed
Disease in Children
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Ochs, Michael; Considine, Michael] Kimmel Comprehens Canc Ctr Johns Hopkins, Baltimore, MD USA.
[Farrar, Jason] Univ Arkansas Med Sci, Little Rock, AR 72205 USA.
[Ries, Rhonda E.; Helton, Heather L.; Meshinchi, Soheil] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
[Trevino, Lisa R.; Muzny, Donna M.; Wheeler, David A.] Baylor Coll Med, Human Genome Sequencing Ctr, Houston, TX 77030 USA.
[Alonzo, Todd A.] Childrens Oncol Grp, Arcadia, CA USA.
[Guidry-Auvil, Jaime] NIH, Off Canc Genom, Bethesda, MD 20892 USA.
[Davidsen, Tanja M.; Gesuwan, Patee; Smith, Malcolm A.; Gerhard, Daniela S.] NCI, Off Canc Genom, Bethesda, MD 20892 USA.
[Gamis, Alan S.] Childrens Mercy Hosp & Clin, Kansas City, MO USA.
[Arceci, Robert J.] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1287
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838902279
ER
PT J
AU Onozawa, M
Kim, H
Gough, SM
Lin, YW
Cui, YZ
Beachy, SH
Mackall, CL
Aplan, P
AF Onozawa, Masahiro
Kim, Hyunkyung
Gough, Sheryl M.
Lin, Yingwei
Cui, Yongzhi
Beachy, Sarah H.
Mackall, Crystal L.
Aplan, Peter
TI Illegitimate V(D)J Recombination Involving Notch1 and Bcl11b in
Precursor T-Cell Lymphoblastic Leukemia/Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Onozawa, Masahiro; Kim, Hyunkyung; Gough, Sheryl M.; Beachy, Sarah H.; Aplan, Peter] NCI, Genet Branch, NIH, Bethesda, MD 20892 USA.
[Lin, Yingwei] Date Red Cross Hosp, Date, Japan.
[Cui, Yongzhi; Mackall, Crystal L.] NCI, Pediat Oncol Branch, Ctr Canc Res, 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 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1323
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049603168
ER
PT J
AU Onozawa, M
Varga, T
Kim, YJ
Zhang, ZH
Aplan, P
AF Onozawa, Masahiro
Varga, Tamas
Kim, Yoo Jung
Zhang, Zhenhua
Aplan, Peter
TI Repair of DNA Double Strand Breaks by RNA/DNA Patches in U937 Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Onozawa, Masahiro; Varga, Tamas; Kim, Yoo Jung; Zhang, Zhenhua; 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 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2375
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049601086
ER
PT J
AU Pantin, JM
Hoyt, RF
Aras, O
Chen, MY
Sato, N
Choyke, P
Childs, R
AF Pantin, Jeremy M.
Hoyt, Robert F., Jr.
Aras, Omer
Chen, Marcus Y.
Sato, Noriko
Choyke, Peter
Childs, Richard
TI Optimization of an Intra-Bone Hematopoietic Stem Cell Delivery Technique
in a Swine Model
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Pantin, Jeremy M.] Georgia Hlth Sci Univ, Dept Med Hematol & Oncol, Augusta, GA USA.
[Hoyt, Robert F., Jr.] NHLBI, LAMS, NIH, Bethesda, MD 20892 USA.
[Aras, Omer; Sato, Noriko; Choyke, Peter] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Chen, Marcus Y.] NHLBI, Cardiol Branch, NIH, Bethesda, MD 20892 USA.
[Childs, Richard] 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 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2990
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049600182
ER
PT J
AU Paralkar, VR
Mishra, T
Luan, J
Yao, Y
Konuthula, N
Bodine, DM
Hardison, RC
Weiss, MJ
AF Paralkar, Vikram R.
Mishra, Tejaswini
Luan, Jing
Yao, Yu
Konuthula, Neeraja
Bodine, David M.
Hardison, Ross C.
Weiss, Mitchell J.
TI Long Noncoding RNAs in Erythropoiesis and Megakaryopoiesis.
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Paralkar, Vikram R.] Univ Penn, Div Hematol Oncol, Philadelphia, PA 19104 USA.
[Mishra, Tejaswini; Hardison, Ross C.] Penn State Univ, Dept Biochem & Mol Biol, University Pk, PA 16802 USA.
[Luan, Jing; Yao, Yu; Konuthula, Neeraja; Weiss, Mitchell J.] Childrens Hosp Philadelphia, Div Hematol, Philadelphia, PA 19104 USA.
[Bodine, David M.] NHGRI, Genet & Mol Biol Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2331
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049601129
ER
PT J
AU Park, JW
Piknova, B
Nghiem, K
Lozier, JN
Schechter, AN
AF Park, Ji-Won
Piknova, Barbora
Nghiem, Khanh
Lozier, Jay N.
Schechter, Alan N.
TI Thrombelastographic Demonstration of Nitrite Inhibition of Platelet
Function
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Park, Ji-Won; Piknova, Barbora; Schechter, Alan N.] NIDDKD, Mol Med Branch, NIH, Bethesda, MD 20892 USA.
[Nghiem, Khanh; Lozier, Jay N.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 5148
PG 1
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049605440
ER
PT J
AU Patel, B
Deng, CW
Litt, M
Riberio, MS
Cui, KR
Kang, YY
Qiu, Y
Zhao, KJ
Huang, SM
AF Patel, Bhavita
Deng, Changwang
Litt, Michael
Riberio, Mariana St Just
Cui, Kairong
Kang, Yuanyuan
Qiu, Yi
Zhao, Keji
Huang, Suming
TI CTCF Mediated Enhancer and Promoter Interaction Regulates Differential
Expression of TAL1 Oncogene in Normal and Malignant Hematopoiesis
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Litt, Michael] Ball State Univ, Muncie, IN 47306 USA.
[Zhao, Keji] NHLBI, NIH, Bethesda, MD 20892 USA.
[Huang, Suming] Univ Florida, Coll Med, Shands Canc Ctr Biochem & Mol Biol, Gainesville, FL USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 281
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838901145
ER
PT J
AU Pawelczyk, E
Degheidy, HA
Branchaw, AL
Holmbeck, K
Bauer, SR
AF Pawelczyk, Edyta
Degheidy, Heba A.
Branchaw, Allison L.
Holmbeck, Kenn
Bauer, Steven R.
TI Dlk-1 Regulates B Cell Development Through Altered Bone Marrow Stromal
Microenvironment, Not by Affecting Hematopoitic Stem/Progenitor Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Pawelczyk, Edyta; Branchaw, Allison L.; Bauer, Steven R.] US FDA, CBER, Bethesda, MD 20014 USA.
[Degheidy, Heba A.] US FDA, CDRH, OSEL, DB, Silver Spring, MD USA.
[Holmbeck, Kenn] NIDCR, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3465
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604062
ER
PT J
AU Perkins, K
Davis, J
Price, S
Niemela, J
Huber, AR
Wall, DA
Pittaluga, S
Fleisher, TA
Rao, VK
AF Perkins, Katie
Davis, Joie
Price, Susan
Niemela, Julie
Huber, Andreas R.
Wall, Donna A.
Pittaluga, Stefania
Fleisher, Thomas A.
Rao, V. Koneti
TI Expanding Spectrum of Malignancies in ALPS: A Cancer Predisposing
Syndrome?.
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Perkins, Katie; Davis, Joie; Price, Susan; Rao, V. Koneti] NIAID, ALPS Unit, LCID, NIH, Bethesda, MD 20892 USA.
[Niemela, Julie; Fleisher, Thomas A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Wall, Donna A.] Univ Manitoba, Winnipeg, MB, Canada.
[Pittaluga, Stefania] NCI, Pathol Lab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2149
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838905287
ER
PT J
AU Pidala, J
Wang, T
Haagenson, MD
Spellman, S
Askar, M
Battiwalla, M
Baxter-Lowe, LA
Bitan, M
Fernandez-Vina, M
Gandhi, M
Jakubowski, AA
Maiers, M
Marino, SR
Marsh, SGE
Oudshoorn, M
Palmer, J
Prasad, VK
Reddy, V
Ringden, O
Saber, W
Santarone, S
Schultz, KR
Setterholm, M
Trachtenberg, E
Turner, V
Woolfrey, A
Lee, SJ
Anasetti, C
AF Pidala, Joseph
Wang, Tao
Haagenson, Michael D.
Spellman, Stephen
Askar, Medhat
Battiwalla, Minoo
Baxter-Lowe, Lee Ann
Bitan, Menachem
Fernandez-Vina, Marcelo
Gandhi, Manish
Jakubowski, Ann A.
Maiers, Martin
Marino, Susana R.
Marsh, Steven G. E.
Oudshoorn, Machteld
Palmer, Jeanne
Prasad, Vinod K.
Reddy, Vijay
Ringden, Olle
Saber, Wael
Santarone, Stella
Schultz, Kirk R.
Setterholm, Michelle
Trachtenberg, Elizabeth
Turner, Vicky
Woolfrey, Ann
Lee, Stephanie J.
Anasetti, Claudio
TI Amino Acid Substitution At Peptide-Binding Pockets of HLA Class I
Molecules Adversely Impacts Hematopoietic Cell Transplantation Outcomes
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Pidala, Joseph] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Wang, Tao] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Haagenson, Michael D.] CIBMTR Minneapolis, Minneapolis, MN USA.
[Spellman, Stephen] Ctr Int Blood & Marrow Transplant Res, Minneapolis, MN USA.
[Askar, Medhat] Cleveland Clin, Allogen Labs, Cleveland, OH 44106 USA.
[Battiwalla, Minoo] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Baxter-Lowe, Lee Ann] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Bitan, Menachem] Tel Aviv Univ, Tel Aviv Sourasky Med Ctr, IL-69978 Tel Aviv, Israel.
[Fernandez-Vina, Marcelo] Univ Texas MD Anderson Canc Ctr, Dept Stem Cell Transplantat & Cellular Therapy, Houston, TX 77030 USA.
[Gandhi, Manish] Mayo Clin, Rochester, MN USA.
[Jakubowski, Ann A.] Mem Sloan Kettering Canc Ctr, Dept Med Adult Allogene Bone Marrow Transplantat, New York, NY 10021 USA.
[Maiers, Martin; Setterholm, Michelle] Natl Marrow Donor Program, Minneapolis, MN USA.
[Marino, Susana R.] Univ Chicago, Chicago, IL 60637 USA.
[Marsh, Steven G. E.] Anthony Nolan Res Inst, HLA Informat Grp, London, England.
[Oudshoorn, Machteld] Europdonor Fdn, Leiden, Netherlands.
[Palmer, Jeanne] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Prasad, Vinod K.] Duke Univ, Med Ctr, Durham, NC USA.
[Reddy, Vijay] Florida Ctr Cellular Therapy, Orlando, FL USA.
[Ringden, Olle] Karolinska Univ, Huddinge Hosp, Ctr Allogene Stem Cell Transplantat, Stockholm, Sweden.
[Saber, Wael] Med Coll Wisconsin CIBMTR, Milwaukee, WI USA.
[Santarone, Stella] Spirito Santo Hosp, Hematol Bone Marrow Transplant Ctr, Pescara, Italy.
[Schultz, Kirk R.] British Columbia Childrens Hosp, Div Pediat Hem Onc BMT, Vancouver, BC V6H 3V4, Canada.
[Trachtenberg, Elizabeth] Childrens Hosp Oakland, Res Inst, Oakland, CA 94609 USA.
[Turner, Vicky] St Jude Childrens Res Hosp, HLA Lab, Memphis, TN 38105 USA.
[Woolfrey, Ann] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Anasetti, Claudio] H Lee Moffitt Canc Ctr & Res Inst, Dept Immunol, Tampa, FL USA.
[Anasetti, Claudio] H Lee Moffitt Canc Ctr & Res Inst, Dept Blood & Marrow Transplantat, Tampa, FL USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 467
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838901369
ER
PT J
AU Porter, JB
Walter, PB
Neumayr, LD
Evans, P
Weyhmiller, MG
Harmatz, P
Wood, JC
Miller, JL
Weiss, G
Yuan, Q
Wang, ZYJ
Grosse, R
Schoennagel, BP
Meerpohl, J
Fischer, R
Vichinsky, E
AF Porter, John B.
Walter, Patrick B.
Neumayr, Lynne D.
Evans, Patricia
Weyhmiller, Marcela G.
Harmatz, Paul
Wood, John C.
Miller, Jeffery L.
Weiss, Guenter
Yuan, Qing
Wang, Zhiyue J.
Grosse, Regine
Schoennagel, Bjoern P.
Meerpohl, Joerg
Fischer, Roland
Vichinsky, Elliott
TI Iron Trafficking and Distribution in Transfusional Overload: Insights
From Comparing Diamond Blackfan Anemia with Sickle Cell Disease and
Thalassemia
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Porter, John B.; Evans, Patricia] UCL, London, England.
[Walter, Patrick B.; Neumayr, Lynne D.; Weyhmiller, Marcela G.; Harmatz, Paul; Vichinsky, Elliott] Childrens Hosp & Res Ctr Oakland, Oakland, CA USA.
[Wood, John C.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Miller, Jeffery L.] NIDDK, Mol Genom & Therapeut Sect, Mol Med Branch, NIH, Bethesda, MD USA.
[Weiss, Guenter] Med Univ Innsbruck, A-6020 Innsbruck, Austria.
[Yuan, Qing; Wang, Zhiyue J.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Grosse, Regine; Schoennagel, Bjoern P.; Fischer, Roland] Univ Hosp Hamburg Eppendorf, Hamburg, Germany.
[Meerpohl, Joerg] Univ Med Ctr Freiburg, German Cochrane Ctr, Freiburg, Germany.
RI Meerpohl, Joerg/J-4224-2013; Wang, Zhiyue/L-3851-2014
OI Meerpohl, Joerg/0000-0002-1333-5403; Wang, Zhiyue/0000-0002-5649-2900
NR 0
TC 1
Z9 1
U1 1
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 995
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049600310
ER
PT J
AU Rao, VK
Oliveira, JB
Niemela, J
Davis, J
Price, S
Kuehn, H
Calvo, KR
Pittaluga, S
Werner, EJ
Lee, J
Barbour, M
Natter, M
Loh, ML
Fleisher, TA
AF Rao, V. Koneti
Oliveira, Joao Bosco
Niemela, Julie
Davis, Joie
Price, Susan
Kuehn, Hyesun
Calvo, Katherine R.
Pittaluga, Stefania
Werner, Eric J.
Lee, Joohee
Barbour, Mustafa
Natter, Marc
Loh, Mignon L.
Fleisher, Thomas A.
TI Clinical Spectrum of RAS-Associated Autoimmune Leukoproliferative
Disorder (RALD): A Distinct Clinical Entity Mimicking Juvenile
Myelomonocytioc Leukemia (JMML) or Chronic Myelomonocytic Leukemia
(CMML)
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Rao, V. Koneti; Davis, Joie; Price, Susan; Lee, Joohee] NIAID, ALPS Unit, LCID, NIH, Bethesda, MD 20892 USA.
[Calvo, Katherine R.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Pittaluga, Stefania] NCI, Pathol Lab, Bethesda, MD 20892 USA.
[Werner, Eric J.] Childrens Hosp, Kings Daughters, Norfolk, VA USA.
[Barbour, Mustafa] Sanford Childrens Hosp, Sioux Falls, SD USA.
[Natter, Marc] Tufts Med Ctr, Floating Hosp Children, Boston, MA USA.
[Loh, Mignon L.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RI Calvo, Katherine/A-8109-2009
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1033
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049602038
ER
PT J
AU Rissone, A
Jagadeesh, J
Karen, S
Bishop, K
Blake, T
Sood, RB
Candotti, F
AF Rissone, Alberto
Jagadeesh, Jaya
Karen, Simon
Bishop, Kevin
Blake, Trevor
Sood, Raman B.
Candotti, Fabio
TI Adenylate Kinase 2 Regulates Zebrafish Primitive and Definitive
Hematopoiesis
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Rissone, Alberto; Candotti, Fabio] NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
[Bishop, Kevin; Blake, Trevor; Sood, Raman B.] NHGRI, Oncogenesis & Dev Sect, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1208
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838902358
ER
PT J
AU Roschewski, M
Farooqui, M
Aue, G
Mo, CC
Valdez, J
Soto, S
Perez-Galan, P
Wilhelm, F
Wiestner, A
AF Roschewski, Mark
Farooqui, Mohammed
Aue, Georg
Mo, Clifton C.
Valdez, Janet
Soto, Susan
Perez-Galan, Patricia
Wilhelm, Francois
Wiestner, Adrian
TI Phase I Study of On 01910.Na (rigosertib), a Multikinase PI3K Inhibitor
in Relapsed/Refractory B-Cell Malignancies
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Roschewski, Mark] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
[Farooqui, Mohammed; Aue, Georg; Mo, Clifton C.; Valdez, Janet; Soto, Susan; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Perez-Galan, Patricia] IDIAPS, Barcelona, Spain.
[Wilhelm, Francois] Onconova Therapeut Inc, Newtown, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1803
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049602074
ER
PT J
AU Roulland, S
Sungalee, JS
Morgado, E
Mamessier, E
Gregoire, E
Monvoisin, C
Menard, C
Navarro, JM
Eberle, FC
Ruminy, P
Jaffe, ES
Schiff, C
Hardwigsen, J
Tarte, K
Nadel, B
AF Roulland, Sandrine
Sungalee, Jocelyne Stephanie
Morgado, Ester
Mamessier, Emilie
Gregoire, Emilie
Monvoisin, Celine
Menard, Cedric
Navarro, Jean-Marc
Eberle, Franziska C.
Ruminy, Philippe
Jaffe, Elaine S.
Schiff, Claudine
Hardwigsen, Jean
Tarte, Karin
Nadel, Bertrand
TI Iterative Germinal Center Re-Entries of Memory B-Cells with t(14;18)
Translocation and Early Steps of Follicular Lymphoma Progression
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Roulland, Sandrine; Sungalee, Jocelyne Stephanie; Morgado, Ester; Mamessier, Emilie; Navarro, Jean-Marc; Schiff, Claudine; Nadel, Bertrand] Univ Aix Marseille 2, Ctr Immunol Marseille Luminy, INSERM, U1104, Marseille, France.
[Gregoire, Emilie; Hardwigsen, Jean] Hop Conception, AP HM, Serv Chirurg Digest & Transplantat Hepat, Marseille, France.
[Eberle, Franziska C.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
[Jaffe, Elaine S.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Tarte, Karin] Fac Med, INSERM, U917, Rennes, France.
RI Nadel, Bertrand/J-2197-2014; Jaffe, Elaine/G-8984-2014
OI Jaffe, Elaine/0000-0003-4632-0301
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 150
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900309
ER
PT J
AU Saba, N
Shen, M
Gias, M
Farooqui, M
Austin, C
Farooqui, M
Austin, C
Schorno, K
Weir, S
Bhalla, K
Wiestner, A
AF Saba, Nakhle
Shen, Min
Gias, Mondana
Farooqui, Mohammed
Austin, Christopher
Farooqui, Mohammed
Austin, Christopher
Schorno, Kevin
Weir, Scott
Bhalla, Kapil
Wiestner, Adrian
TI The Gold Compound Auranofin Induces Oxidative Stress and Apoptosis in
Primary CLL Cells Independent of Classic Prognostic Markers and the
Protective Effect of the Tissue Microenvironment
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Saba, Nakhle] Tulane Univ, Dept Hematol & Med Oncol, New Orleans, LA 70118 USA.
[Shen, Min; Austin, Christopher] NIH, Natl Ctr Adv Translat Sci, Bethesda, MD 20892 USA.
[Gias, Mondana; Farooqui, Mohammed; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Schorno, Kevin; Weir, Scott; Bhalla, Kapil] Univ Kansas, Inst Adv Med Innovat, Kansas City, KS USA.
NR 0
TC 1
Z9 1
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 865
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900393
ER
PT J
AU Salit, RB
Hakim, FT
Bishop, MR
Friedman, TM
Korngold, R
Goldgirsh, K
Memon, S
Steinberg, SM
Liewehr, D
Peaceman, D
Wilder, J
Bryant, K
Fowler, DH
Gea-Banacloche, J
Gress, RE
Pavletic, SZ
AF Salit, Rachel B.
Hakim, Frances T.
Bishop, Michael R.
Friedman, Thea M.
Korngold, Robert
Goldgirsh, Kira
Memon, Sarfraz
Steinberg, Seth M.
Liewehr, David
Peaceman, Daniel
Wilder, Jennifer
Bryant, Kelly
Fowler, Daniel H.
Gea-Banacloche, Juan
Gress, Ronald E.
Pavletic, Steven Z.
TI Influence of Graft Versus-Host Disease Prophylaxis Regimen On T-Cell
Repertoire Diversity Following Reduced-Intensity HLA-Matched Unrelated
Donor Allogeneic Hematopoietic Stem Cell Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Salit, Rachel B.; Hakim, Frances T.; Memon, Sarfraz; Peaceman, Daniel; Bryant, Kelly; Fowler, Daniel H.; Gea-Banacloche, Juan; Gress, Ronald E.; Pavletic, Steven Z.] NCI, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA.
[Bishop, Michael R.] Med Coll Wisconsin, Ctr Clin Canc, Milwaukee, WI 53226 USA.
[Friedman, Thea M.; Korngold, Robert; Goldgirsh, Kira] Hackensack Univ, Ctr Canc, Med Ctr, Hackensack, NJ USA.
[Steinberg, Seth M.; Liewehr, David] NCI, Biostat & Data Management Sect, Rockville, MD USA.
[Wilder, Jennifer] SAIC, Clin Res Directorate, CMRP, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3054
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049601209
ER
PT J
AU Sanda, T
Tyner, JW
Gutierrez, A
Ngo, VN
Glover, JM
Chang, BH
Yost, AJ
Weng, AP
Ma, WX
Tatarek, J
Fleischman, AG
Ahn, Y
Yang, YD
Zhou, WJ
Neuberg, DS
Moriggl, R
Muller, M
Kelliher, M
Jamieson, C
Gray, NS
Staudt, LM
Druker, BJ
Look, T
AF Sanda, Takaomi
Tyner, Jeffrey W.
Gutierrez, Alejandro
Ngo, Vu N.
Glover, Jason M.
Chang, Bill H.
Yost, Arla J.
Weng, Andrew P.
Ma, Wenxue
Tatarek, Jessica
Fleischman, Angela G.
Ahn, Yebin
Yang, Yandan
Zhou, Wenjun
Neuberg, Donna S.
Moriggl, Richard
Mueller, Mathias
Kelliher, Michelle
Jamieson, Catriona
Gray, Nathanael S.
Staudt, Louis M.
Druker, Brian J.
Look, Thomas
TI TYK2-STAT1 Pathway Positively Regulates BCL2 Gene Expression in T-Cell
Acute Lymphoblastic Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Tyner, Jeffrey W.; Glover, Jason M.; Chang, Bill H.; Fleischman, Angela G.; Druker, Brian J.] Oregon Hlth & Sci Univ, Knight Canc Inst, Portland, OR 97201 USA.
[Ngo, Vu N.] City Hope Natl Med Ctr, Div Hematopoiet Stem Cell & Leukemia Res, Duarte, CA USA.
[Yost, Arla J.] BC Canc Agcy, Terry Fox Lab, Vancouver, BC, Canada.
[Weng, Andrew P.] British Columbia Canc Agcy, Terry Fox Lab, Vancouver, BC V5Z 1L3, Canada.
[Ma, Wenxue] Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA.
[Tatarek, Jessica] UMass Med Sch, Worcester, MA USA.
[Zhou, Wenjun] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
[Neuberg, Donna S.] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Moriggl, Richard] Ludwig Boltzmann Inst Canc Res, Vienna, Austria.
[Mueller, Mathias] Univ Vet Med Vienna, Dept Biomed Sci, Vienna, Austria.
[Kelliher, Michelle] Univ Massachusetts, Sch Med, Worcester, MA USA.
[Staudt, Louis M.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
RI Weng, Andrew/I-5015-2014
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1470
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838905163
ER
PT J
AU Sato, K
Feng, XM
Chen, JC
Desierto, MJ
Keyvanfar, K
Malide, D
Kajigaya, S
Young, NS
AF Sato, Kazuya
Feng, Xingmin
Chen, Jichun
Desierto, Marie J.
Keyvanfar, Keyvan
Malide, Daniela
Kajigaya, Sachiko
Young, Neal S.
TI Adipocytes and Aplastic Anemia: Peroxisome Proliferator-Activated
Receptor-gamma (PPAR-gamma) Antagonists Attenuate Bone Marrow Failure in
an Aplastic Anemia Mouse Model but Not in Radiation Marrow Destruction
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Sato, Kazuya; Feng, Xingmin; Chen, Jichun; Desierto, Marie J.; Keyvanfar, Keyvan; Kajigaya, Sachiko; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Malide, Daniela] NHLBI, Light Microscopy Core Facil, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3483
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604044
ER
PT J
AU Scheinberg, P
Townsley, DM
Dumitriu, B
Rios, O
Weinstein, B
Battiwalla, M
Childs, R
Dunbar, CE
Barrett, AJ
Wu, CO
Young, NS
AF Scheinberg, Phillip
Townsley, Danielle M.
Dumitriu, Bogdan
Rios, Olga
Weinstein, Barbara
Battiwalla, Minoo
Childs, Richard
Dunbar, Cynthia E.
Barrett, A. John
Wu, Colin O.
Young, Neal S.
TI Even "Moderate" Dose Cyclophosphamide for Severe Aplastic Anemia Is
Associated with Significant Toxicities and Does Not Prevent Relapse and
Clonal Evolution
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Scheinberg, Phillip; Townsley, Danielle M.; Dumitriu, Bogdan; Rios, Olga; Weinstein, Barbara; Battiwalla, Minoo; Childs, Richard; Dunbar, Cynthia E.; Barrett, A. John; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Wu, Colin O.] NHLBI, Off Biostat Reserach, NIH, Bethesda, MD 20892 USA.
NR 0
TC 3
Z9 3
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1259
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838902307
ER
PT J
AU Shaffer, BC
Tremblay, C
Peaceman, D
Hsu, J
Steinberg, SM
Uribe, M
Adams, S
Flegel, WA
Pavletic, SZ
AF Shaffer, Brian C.
Tremblay, Christine
Peaceman, Daniel
Hsu, Jennifer
Steinberg, Seth M.
Uribe, Marcela
Adams, Sharon
Flegel, Willy A.
Pavletic, Steven Z.
TI Minor Histocompatibility Antigen Mismatch and Incidence of Graft Versus
Host Disease, Event-Free, and Overall Survival in Patients Undergoing
Unrelated Donor Allogeneic Hematopoietic Cell Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Shaffer, Brian C.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Tremblay, Christine; Uribe, Marcela; Adams, Sharon; Flegel, Willy A.] NIH, Dept Transfus Med, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, Rockville, MD USA.
[Pavletic, Steven Z.] NCI, Expt Transplantat & Immunol Branch, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4201
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604129
ER
PT J
AU Shaffer, BC
Leitner, J
Wiestner, A
Bishop, MR
Pavletic, SZ
Gress, RE
Steinberger, P
Baskar, S
Rader, C
AF Shaffer, Brian C.
Leitner, Judith
Wiestner, Adrian
Bishop, Michael R.
Pavletic, Steven Z.
Gress, Ronald E.
Steinberger, Peter
Baskar, Sivasubramanian
Rader, Christoph
TI Generation of a Platform for Identification of CLL Specific Cell Surface
Proteins Targeted by Anti-Tumor Antibodies in Patient Sera After
Allogeneic Hematopoietic Cell Transplantion
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Shaffer, Brian C.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Leitner, Judith; Steinberger, Peter] Med Univ Vienna, Inst Immunol, Vienna, Austria.
[Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Bishop, Michael R.] Med Coll Wisconsin, Ctr Clin Canc, Milwaukee, WI 53226 USA.
[Pavletic, Steven Z.; Gress, Ronald E.; Baskar, Sivasubramanian] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Rader, Christoph] Scripps Res Inst, Dept Canc Biol, Jupiter, FL USA.
[Rader, Christoph] Scripps Res Inst, Dept Mol Therapeut, Jupiter, FL USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1349
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049603142
ER
PT J
AU Shah, NN
Borowitz, MJ
Robey, N
Gamper, C
Symons, HJ
Loeb, D
Wayne, AS
Chen, AR
AF Shah, Nirali N.
Borowitz, Michael J.
Robey, Nancy
Gamper, Christopher
Symons, Heather J.
Loeb, David
Wayne, Alan S.
Chen, Allen R.
TI Outcomes of Children with Hematologic Malignancies Who Relapse After
Allogeneic Hematopoietic Cell Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Shah, Nirali N.; Wayne, Alan S.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Borowitz, Michael J.] Johns Hopkins Univ, Dept Pathol, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4205
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604125
ER
PT J
AU Shah, NN
Borowitz, MJ
Steinberg, SM
Lefell, M
Robey, N
Gamper, C
Symons, HJ
Loeb, D
Wayne, AS
Chen, AR
AF Shah, Nirali N.
Borowitz, Michael J.
Steinberg, Seth M.
Lefell, Mary
Robey, Nancy
Gamper, Christopher
Symons, Heather J.
Loeb, David
Wayne, Alan S.
Chen, Allen R.
TI Factors Predictive of Relapse of Hematologic Malignancies in Pediatric
Patients Post Allogeneic Hematopoietic Cell Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Shah, Nirali N.; Wayne, Alan S.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Borowitz, Michael J.; Robey, Nancy; Gamper, Christopher; Symons, Heather J.; Loeb, David; Chen, Allen R.] Johns Hopkins Univ, Baltimore, MD USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, Rockville, MD USA.
[Lefell, Mary] Johns Hopkins Univ Hosp, DOM Immunogenet, Baltimore, MD 21287 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4206
PG 3
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604124
ER
PT J
AU Shah, NN
Merchant, M
Cole, D
Richards, K
Delbrook, C
Widemann, BC
Wayne, AS
AF Shah, Nirali N.
Merchant, Melinda
Cole, Diane
Richards, Kelly
Delbrook, Cindy
Widemann, Brigitte C.
Wayne, Alan S.
TI Vincristine Sulfate Liposomes Injection (VSLI, Marqibo): Interim Results
From a Phase I Study in Children and Adolescents with Refractory Cancer
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Shah, Nirali N.; Merchant, Melinda; Cole, Diane; Richards, Kelly; Delbrook, Cindy; Widemann, Brigitte C.; Wayne, Alan S.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1497
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838905136
ER
PT J
AU Shand, JC
Kanu, A
Fry, TJ
AF Shand, Jessica C.
Kanu, Alieu
Fry, Terry J.
TI CD8 Suppressor Cells Can Be Induced by Pre-B Acute Lymphoblastic
Leukemia As a Potential Mechanism of Immune Escape
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Kanu, Alieu] George Washington Univ, Sch Publ Hlth, Washington, DC USA.
[Fry, Terry J.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4797
PG 1
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604291
ER
PT J
AU Shand, JC
Capitini, CM
Qin, HY
Nasholm, N
Fry, TJ
AF Shand, Jessica C.
Capitini, Christian M.
Qin, Haiying
Nasholm, Nicole
Fry, Terry J.
TI Tissue Distribution of a Minor Antigen, but Not PD-1 Expression,
Predicts the Antileukemia Efficacy of Adoptively Transferred,
Antigen-Specific T-Cells in a Preclinical Model of Allogeneic Transplant
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
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 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 456
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838902204
ER
PT J
AU Shand, JC
Capitini, CM
Qin, HY
Nasholm, N
Fry, TJ
AF Shand, Jessica C.
Capitini, Christian M.
Qin, Haiying
Nasholm, Nicole
Fry, Terry J.
TI Tissue Distribution of a Minor Antigen, but Not PD-1 Expression,
Predicts the Antileukemia Efficacy of Adoptively Transferred,
Antigen-Specific T-Cells in a Preclinical Model of Allogeneic Transplant
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
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 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 456
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838902004
ER
PT J
AU Sivina, M
Kreitman, RJ
Arons, E
Buggy, JJ
Ravandi, F
Burger, JA
AF Sivina, Mariela
Kreitman, Robert J.
Arons, Evgeny
Buggy, Joseph J.
Ravandi, Farhad
Burger, Jan A.
TI Bruton's Tyrosine Kinase (BTK) Inhibitor Ibrutinib (PCI-32765) Blocks
Hairy Cell Leukemia (HCL) Survival, Proliferation, and BCR Signaling: A
New Therapeutic Approach for HCL
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Sivina, Mariela; Ravandi, Farhad; Burger, Jan A.] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Houston, TX 77030 USA.
[Kreitman, Robert J.; Arons, Evgeny] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Buggy, Joseph J.] Pharmacyclics Inc, Sunnyvale, CA USA.
RI Jones, Jeffrey/E-9827-2013
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 1802
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049602075
ER
PT J
AU Smith, MA
Carol, H
Evans, K
Richmond, J
Kang, M
Reynolds, CP
Chunduru, S
Graham, MA
Geier, B
Kurmasheva, R
Houghton, PJ
Lock, RB
AF Smith, Malcolm A.
Carol, Hernan
Evans, Kathryn
Richmond, Jennifer
Kang, Min
Reynolds, C. Patrick
Chunduru, Srinivas
Graham, Martin A.
Geier, Brian
Kurmasheva, Raushan
Houghton, Peter J.
Lock, Richard B.
TI Birinapant (TL32711), a Small Molecule Smac Mimetic, Induces Regressions
in Childhood Acute Lymphoblastic Leukemia (ALL) Xenografts That Express
TNF alpha and Synergizes with TNF alpha in Vitro - A Report From the
Pediatric Preclinical Testing Program (PPTP)
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Smith, Malcolm A.] NCI, Off Canc Genom, Bethesda, MD 20892 USA.
[Carol, Hernan; Evans, Kathryn; Richmond, Jennifer; Lock, Richard B.] Univ New S Wales, Childrens Canc Inst Australia Med Res, Sydney, NSW, Australia.
[Kang, Min; Reynolds, C. Patrick] Texas Tech Univ, Hlth Sci Ctr, Lubbock, TX 79409 USA.
[Chunduru, Srinivas; Graham, Martin A.] TetraLogic Pharmaceut, Malvern, PA USA.
[Geier, Brian; Kurmasheva, Raushan; Houghton, Peter J.] Nationwide Childrens Hosp, Columbus, OH USA.
RI Carol, Hernan/F-5750-2013; Lock, Richard/G-4253-2013
OI Carol, Hernan/0000-0002-9443-8032;
NR 0
TC 0
Z9 0
U1 0
U2 6
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3565
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838906092
ER
PT J
AU Spyridonidis, A
Muranski, P
Kerkar, S
Tanimoto, K
Hensel, NF
Melenhorst, JJ
Barrett, AJ
AF Spyridonidis, Alexandros
Muranski, Pawel
Kerkar, Sid
Tanimoto, Kazushi
Hensel, Nancy F.
Melenhorst, J. Joseph
Barrett, A. John
TI Improved Strategy for Rapid Generation of Quadrivirus-Specific CD8+and
CD4+Cytotoxic T Lymphocytes (CTLs) for Adoptive Transfer After Stem Cell
Transplantation (SCT)
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Kerkar, Sid; Tanimoto, Kazushi; Hensel, Nancy F.; Melenhorst, J. Joseph; Barrett, A. John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4121
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604207
ER
PT J
AU St Louis, J
Kruse-Jarres, R
Greist, A
Shapiro, AD
Smith, H
Drebes, AB
Lozier, JN
Gomperts, ED
AF St Louis, Jean
Kruse-Jarres, Rebecca
Greist, Anne
Shapiro, Amy D.
Smith, Hedy
Drebes, Anja B.
Lozier, Jay N.
Gomperts, Edward D.
TI Recombinant B-Domain Deleted Porcine Factor VIII (OBI-1) Safety and
Efficacy in the Treatment of Acquired Hemophilia A: Interim Results
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [St Louis, Jean] Hop Maison Neuve Rosemont, Dept Hematol, Montreal, PQ H1T 2M4, Canada.
[Kruse-Jarres, Rebecca] Tulane Univ, Sch Med, New Orleans, LA 70112 USA.
[Greist, Anne; Shapiro, Amy D.] Indiana Hemophilia & Thrombosis Ctr, Indianapolis, IN USA.
[Smith, Hedy] Tufts Med Ctr, Dept Hematol Oncol, Boston, MA USA.
[Drebes, Anja B.] Royal Free NHS Trust, Thrombosis Unit, London, England.
[Drebes, Anja B.] Royal Free NHS Trust, Katharine Dormandy Haemophilia Ctr, London, England.
[Lozier, Jay N.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Gomperts, Edward D.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2224
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049600018
ER
PT J
AU Staudt, LM
AF Staudt, Louis M.
TI Chronic Active B-Cell Receptor Signaling in Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Staudt, Louis M.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 26
PG 1
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900002
ER
PT J
AU Suryani, S
Sia, KCS
Bracken, L
Carol, H
Evans, K
Kurmasheva, R
Houghton, PJ
Smith, MA
Lock, RB
AF Suryani, Santi
Sia, Keith C. S.
Bracken, Lauryn
Carol, Hernan
Evans, Kathryn
Kurmasheva, Raushan
Houghton, Peter J.
Smith, Malcolm A.
Lock, Richard B.
TI Dual Inhibition of JAK/STAT and MAPK Pathways Results in Synergistic
Cell Killing of JAK-Mutated Pediatric Acute Lymphoblastic Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Suryani, Santi; Sia, Keith C. S.; Bracken, Lauryn; Carol, Hernan; Evans, Kathryn; Lock, Richard B.] Univ New S Wales, Childrens Canc Inst Australia Med Res, Sydney, NSW, Australia.
[Kurmasheva, Raushan; Houghton, Peter J.] Nationwide Childrens Hosp, Columbus, OH USA.
[Smith, Malcolm A.] NCI, Ctep, Cib, NIH, Bethesda, MD 20892 USA.
RI Carol, Hernan/F-5750-2013; Lock, Richard/G-4253-2013
OI Carol, Hernan/0000-0002-9443-8032;
NR 0
TC 2
Z9 2
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3562
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838906095
ER
PT J
AU Tanimoto, K
Muranski, P
Hensel, NF
Keyvanfar, K
Fujiwara, H
Barrett, AJ
Melenhorst, JJ
AF Tanimoto, Kazushi
Muranski, Pawel
Hensel, Nancy F.
Keyvanfar, Keyvan
Fujiwara, Hiroshi
Barrett, A. John
Melenhorst, J. Joseph
TI Abrogation of Myeloid Derived Suppressor Cell-Like Inhibitory Activity
of K562 Restores Antigen Presenting Cell Functions
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Tanimoto, Kazushi; Muranski, Pawel; Hensel, Nancy F.; Keyvanfar, Keyvan; Barrett, A. John; Melenhorst, J. Joseph] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Fujiwara, Hiroshi] Ehime Univ, Grad Sch Med, Toon, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4118
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604210
ER
PT J
AU Tembhare, PR
Yuan, C
Korde, N
Manasanch, EE
Kwok, M
Roschewski, M
Maric, I
Calvo, KR
Mulquin, M
Zuchlinski, D
Landgren, O
Stetler-Stevenson, M
AF Tembhare, Prashant Ramesh
Yuan, Constance
Korde, Neha
Manasanch, Elisabet E.
Kwok, Mary
Roschewski, Mark
Maric, Irina
Calvo, Katherine R.
Mulquin, Marcia
Zuchlinski, Diamond
Landgren, Ola
Stetler-Stevenson, Maryalice
TI Peripheral Blood Involvement with Minimal Disease Is Common in Multiple
Myeloma but Not in Smoldering Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
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; Kwok, Mary; Mulquin, Marcia; Zuchlinski, Diamond] NCI, Multiple Myeloma Sect, NIH, Bethesda, MD 20892 USA.
NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Manasanch, Elisabet E.] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Roschewski, Mark; Landgren, Ola] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
[Maric, Irina; Calvo, Katherine R.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
RI Calvo, Katherine/A-8109-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4994
PG 1
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049605042
ER
PT J
AU Townsley, DM
Hsu, A
Dumitriu, B
Holland, SM
Young, NS
AF Townsley, Danielle M.
Hsu, Amy
Dumitriu, Bogdan
Holland, Steven M.
Young, Neal S.
TI Regulatory Mutations in GATA2 Associated with Aplastic Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Townsley, Danielle M.; Dumitriu, Bogdan; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Hsu, Amy] NIH, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
[Holland, Steven M.] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3488
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604039
ER
PT J
AU Townsley, DM
Dumitriu, B
Kajigaya, S
Calado, RT
Scheinberg, P
Young, NS
AF Townsley, Danielle M.
Dumitriu, Bogdan
Kajigaya, Sachiko
Calado, Rodrigo T.
Scheinberg, Phillip
Young, Neal S.
TI Clinical and Genetic Heterogeneity of Telomere Diseases
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Townsley, Danielle M.; Dumitriu, Bogdan; Kajigaya, Sachiko; Scheinberg, Phillip; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Calado, Rodrigo T.] Univ Sao Paulo, Dept Internal Med, BR-14049 Ribeirao Preto, Brazil.
RI Calado, Rodrigo/G-2619-2011
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2373
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049601088
ER
PT J
AU Ueda, K
Yoshimi, A
Nakagawa, M
Nishikawa, S
Marquez, VE
Kumano, K
Kurokawa, M
AF Ueda, Koki
Yoshimi, Akihide
Nakagawa, Masahiro
Nishikawa, Satoshi
Marquez, Victor E.
Kumano, Keiki
Kurokawa, Mineo
TI Inhibition of EZH2 Depletes MLL Fusion Leukemia Stem Cells Through
Restoration of p16 Expression
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Ueda, Koki; Nakagawa, Masahiro; Nishikawa, Satoshi; Kumano, Keiki] Univ Tokyo, Tokyo, Japan.
[Yoshimi, Akihide; Kurokawa, Mineo] Tokyo Univ Hosp, Dept Cell Therapy & Transplantat, Tokyo 113, Japan.
[Marquez, Victor E.] NCI, Biol Chem Lab, Ctr Canc Res, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3510
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604017
ER
PT J
AU Uldrick, TS
Polizzotto, MN
Filie, A
Aleman, K
Wyvill, KM
Little, RF
Steinberg, SM
Jaffe, ES
Whitby, D
Pittaluga, S
Yarchoan, R
AF Uldrick, Thomas S.
Polizzotto, Mark N.
Filie, Armando
Aleman, Karen
Wyvill, Kathleen M.
Little, Richard F.
Steinberg, Seth M.
Jaffe, Elaine S.
Whitby, Denise
Pittaluga, Stefania
Yarchoan, Robert
TI Clinical, Immunologic, and Virologic Findings in Kaposi Sarcoma
Herpesvirus (KSHV)-Associated Lymphomas Suggest KSHV-Associated
Inflammatory Syndromes Contribute to Symptoms and Disease Pathogenesis.
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Uldrick, Thomas S.; Polizzotto, Mark N.; Aleman, Karen; Wyvill, Kathleen M.; Little, Richard F.; Yarchoan, Robert] NCI, HIV AIDS Malignancy Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Filie, Armando; Jaffe, Elaine S.; Pittaluga, Stefania] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, Rockville, MD USA.
[Whitby, Denise] NCI, Viral Oncol Sect, AIDS & Canc Virus Program, SAIC Frederick, Frederick, MD 21701 USA.
RI Jaffe, Elaine/G-8984-2014
OI Jaffe, Elaine/0000-0003-4632-0301
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2708
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838903085
ER
PT J
AU van Beers, EJ
Samsel, L
Mendelsohn, LG
Saiyed, R
Nichols, JS
McCoy, JP
Kato, GJ
AF van Beers, Eduard J.
Samsel, Leigh
Mendelsohn, Laurel G.
Saiyed, Rehan
Nichols, James S.
McCoy, J. Philip, Jr.
Kato, Gregory J.
TI Imaging Flow Cytometry for Fully Automated Quantification of Percentage
of Sickled Cells in Sickle Cell Anemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [van Beers, Eduard J.; Mendelsohn, Laurel G.; Saiyed, Rehan; Nichols, James S.; Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, Hematol Branch, Bethesda, MD 20892 USA.
[Samsel, Leigh] NHLBI, Flow Cytometry Core Facil, NIH, Bethesda, MD 20892 USA.
[McCoy, J. Philip, Jr.] NHLBI, Flow Cytometry Core, NIH, Bethesda, MD 20892 USA.
RI Kato, Gregory/I-7615-2014; van Beers, Eduard/I-3561-2012
OI Kato, Gregory/0000-0003-4465-3217; van Beers, Eduard/0000-0002-3934-7189
NR 0
TC 1
Z9 1
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2105
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049603190
ER
PT J
AU van Beers, EJ
Yang, YQ
Yuditskaya, S
Raghavachari, N
Kato, GJ
AF van Beers, Eduard J.
Yang, Yanqin
Yuditskaya, Susan
Raghavachari, Nalini
Kato, Gregory J.
TI Turnover of Heme-Bound Iron Is Associated with Activation of TLR4 and
Chemokine Receptor Pathways in the Peripheral Blood Mononuclear Cell
Transcriptome in Sickle Cell Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [van Beers, Eduard J.] Univ Amsterdam, Acad Med Ctr, Dept Hematol, NL-1105 AZ Amsterdam, Netherlands.
[Yang, Yanqin] NHLBI, Genom Core Facil, Bethesda, MD 20892 USA.
[Yuditskaya, Susan; Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, Hematol Branch, Bethesda, MD 20892 USA.
[Raghavachari, Nalini] NHLBI, Genet & Dev Biol Ctr, 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 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 819
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838901045
ER
PT J
AU Wang, DP
Yu, Y
Semple, KM
Haarberg, KMK
Fu, JN
Kaosaard, K
Anasetti, C
Srinivas, N
Gabrilovich, D
Yu, XZ
AF Wang, Dapeng
Yu, Yu
Semple, Kenrick M.
Haarberg, Kelley M. K.
Fu, Jianing
Kaosaard, Kane
Anasetti, Claudio
Srinivas, Nagaraj
Gabrilovich, Dmitry
Yu, Xue-Zhong
TI Dynamic Changes and Impact of Myeloid Derived Suppressor Cells in
Allogeneic Bone Marrow Transplantation in Mice
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Semple, Kenrick M.] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Haarberg, Kelley M. K.; Anasetti, Claudio; Yu, Xue-Zhong] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Dept Immunol, Tampa, FL 33612 USA.
[Haarberg, Kelley M. K.; Anasetti, Claudio; Yu, Xue-Zhong] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Dept Blood & Marrow Transplantat, Tampa, FL 33612 USA.
[Fu, Jianing] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
RI Fu, Jianing/F-4031-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2999
PG 1
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049600190
ER
PT J
AU Wang, WX
Corrigan-Cummins, M
Vinh, DC
Hsu, AP
Hickstein, DD
Holland, SM
Calvo, KR
AF Wang, Weixin
Corrigan-Cummins, Meghan
Vinh, Donald C.
Hsu, Amy P.
Hickstein, Dennis D.
Holland, Steven M.
Calvo, Katherine R.
TI MCL-1 and Mir-181c in GATA2 Mutation Associated Monomac and Familial
Myelodysplastic Syndrome
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Wang, Weixin; Corrigan-Cummins, Meghan; Calvo, Katherine R.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Vinh, Donald C.] McGill Univ, Dept Med, Ctr Hlth, Montreal, PQ, Canada.
[Hsu, Amy P.; Holland, Steven M.] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
[Hickstein, Dennis D.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
RI Calvo, Katherine/A-8109-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 3807
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049601258
ER
PT J
AU Weed, J
Keyvanfar, K
Swamy, P
Kajigaya, S
Calado, RT
Young, NS
AF Weed, Jason
Keyvanfar, Keyvan
Swamy, Prashanth
Kajigaya, Sachiko
Calado, Rodrigo T.
Young, Neal S.
TI Interphase Chromosome Flow-FISH
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Keyvanfar, Keyvan; Kajigaya, Sachiko; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Calado, Rodrigo T.] Univ Sao Paulo, Dept Internal Med, BR-14049 Ribeirao Preto, Brazil.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4925
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604319
ER
PT J
AU Weitzel, RP
Biancotto, A
Fitzhugh, CD
McCoy, JP
Hsieh, M
Tisdale, JF
AF Weitzel, R. Patrick
Biancotto, Angelique
Fitzhugh, Courtney D.
McCoy, J. Philip
Hsieh, Matthew
Tisdale, John F.
TI Characterization of Early Lymphocytes Emerging After Nonmyeloablative
Conditioning and Hematopoietic Stem Cell Transplant Supported with
Sirolimus
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Weitzel, R. Patrick; Fitzhugh, Courtney D.; Hsieh, Matthew; Tisdale, John F.] NHLBI, Mol & Clin Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Biancotto, Angelique; McCoy, J. Philip] NIH, Ctr Human Immunol, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4150
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049604178
ER
PT J
AU West, RR
Hsu, A
Calvo, KR
Cuellar-Rodriguez, J
Holland, SM
Hickstein, DD
AF West, Robert R.
Hsu, Amy
Calvo, Katherine R.
Cuellar-Rodriguez, Jennifer
Holland, Steven M.
Hickstein, Dennis D.
TI ASXL1 mutations in GATA2-Deficiency Correlate with Leukemic
Transformation
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [West, Robert R.] NIH, ETIB, Bethesda, MD 20892 USA.
[Hsu, Amy] NIH, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
[Calvo, Katherine R.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Cuellar-Rodriguez, Jennifer; Holland, Steven M.] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
[Hickstein, Dennis D.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
RI Calvo, Katherine/A-8109-2009
NR 0
TC 0
Z9 0
U1 1
U2 10
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 405
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838902255
ER
PT J
AU Wu, CF
Hong, SG
Jares, A
Guo, V
Winkler, T
Dunbar, CE
AF Wu, Chuanfeng
Hong, So Gun
Jares, Alexander
Guo, Vicky
Winkler, Thomas
Dunbar, Cynthia E.
TI Development of an Inducible Caspase-9 Safety Switch for Pluripotent Stem
Cell Based Therapies
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Wu, Chuanfeng; Hong, So Gun; Jares, Alexander; Guo, Vicky; Winkler, Thomas; Dunbar, Cynthia E.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 2047
PG 2
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049603248
ER
PT J
AU Xu, BY
Zhi, N
Hu, GQ
Wan, ZH
Kajigaya, S
Zhao, KJ
Mao, Q
Young, NS
AF Xu, Baoyan
Zhi, Ning
Hu, Gangqing
Wan, Zhihong
Kajigaya, Sachiko
Zhao, Keji
Mao, Qing
Young, Neal S.
TI Identification and Characterization of a Novel Parvovirus-Like Virus in
Seronegative Hepatitis Patients by Next Generation Sequencing
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Hu, Gangqing] NIH, Syst Biol Ctr, Bethesda, MD 20892 USA.
[Kajigaya, Sachiko; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Mao, Qing] Third Mil Med Univ, Inst Infect Dis, Chongqing, Peoples R China.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 273
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838901137
ER
PT J
AU Yang, JJ
Xu, H
Yang, WJ
Perez-Andreu, V
Dmidas, M
Fan, YP
Cheng, C
Pei, DQ
Scheet, P
Burchard, EG
Eng, C
Huntsman, S
Torgerson, DG
Dean, M
Winick, N
Martin, PL
Camitta, B
Bowman, WP
Willman, CL
Carroll, WL
Mullighan, CG
Bhojwani, D
Hunger, SP
Pui, CH
Evans, WE
Belling, MV
Loh, ML
AF Yang, Jun J.
Xu, Heng
Yang, Wenjian
Perez-Andreu, Virginia
Dmidas, Meenakshi
Fan, Yiping
Cheng, Cheng
Pei, Deqing
Scheet, Paul
Burchard, Esteban Gonzalez
Eng, Celeste
Huntsman, Scott
Torgerson, Dara G.
Dean, Michael
Winick, Naomi
Martin, Paul L.
Camitta, Bruce
Bowman, W. Paul
Willman, Cheryl L.
Carroll, William L.
Mullighan, Charles G.
Bhojwani, Deepa
Hunger, Stephen P.
Pui, Ching-Hon
Evans, William E.
Belling, Mary V.
Loh, Mignon L.
TI Genome-Wide Association Study Identifies a Novel Susceptibility Locus At
10p12.31-12.2 for Childhood Acute Lymphoblastic Leukemia in Ethinically
Diverse Populations
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Yang, Jun J.; Xu, Heng; Yang, Wenjian; Perez-Andreu, Virginia; Evans, William E.; Belling, Mary V.] St Jude Childrens Res Hosp, Dept Pharmaceut Sci, Memphis, TN 38105 USA.
[Dmidas, Meenakshi] Univ Florida, Dept Epidemiol & Hlth Policy Res Med, Gainesville, FL USA.
[Fan, Yiping] St Jude Childrens Res Hosp, Hartwell Ctr Bioinformat & Biotechnol, Memphis, TN 38105 USA.
[Cheng, Cheng; Pei, Deqing] St Jude Childrens Res Hosp, Dept Biostat, Memphis, TN 38105 USA.
[Scheet, Paul] Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX USA.
[Burchard, Esteban Gonzalez; Eng, Celeste; Huntsman, Scott; Torgerson, Dara G.] Univ Calif San Francisco, Dept Bioengn & Therapeut Sci & Med, San Francisco, CA 94143 USA.
[Dean, Michael] NCI, Expt Immunol Lab, Bethesda, MD 20892 USA.
[Winick, Naomi] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Martin, Paul L.] Duke Univ, Durham, NC USA.
[Camitta, Bruce] Med Coll Wisconsin, Wauwatosa, WI USA.
[Bowman, W. Paul] Cook Childrens Med Ctr, Ft Worth, TX USA.
[Willman, Cheryl L.] Univ New Mexico, Ctr Canc, Albuquerque, NM 87131 USA.
[Carroll, William L.] NYU, Inst Canc, New York, NY USA.
[Mullighan, Charles G.] St Jude Childrens Res Hosp, Dept Pathol, Memphis, TN 38105 USA.
[Hunger, Stephen P.] Univ Colorado, Sch Med, Aurora, CO USA.
[Hunger, Stephen P.] Childrens Hosp, Aurora, CO USA.
[Loh, Mignon L.] Univ Calif San Francisco, Dept Pediat, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 877
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900381
ER
PT J
AU Yu, WM
Liu, X
Shen, JH
Jovanovic, O
Pohl, EE
Gerson, SL
Finkel, T
Broxmeyer, HE
Qu, CK
AF Yu, Wen-Mei
Liu, Xia
Shen, Jinhua
Jovanovic, Olga
Pohl, Elena E.
Gerson, Stanton L.
Finkel, Toren
Broxmeyer, Hal E.
Qu, Cheng-Kui
TI Disruption of Mitochondrial Phosphatase Ptpmt1 Induces Bioenergetic
Stress and Differentiation Block in Hematopoietic Stem Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Yu, Wen-Mei; Liu, Xia; Shen, Jinhua; Gerson, Stanton L.; Qu, Cheng-Kui] Case Western Reserve Univ, Dept Med, Ctr Stem Cell & Regenerat Med, Div Hematol & Oncol,Case Comprehens Canc Ctr, Cleveland, OH 44106 USA.
[Jovanovic, Olga; Pohl, Elena E.] Univ Vet Med, Dept Mol Physiol & Biophys, Vienna, Austria.
[Finkel, Toren] NHLBI, Ctr Mol Med, NIH, Bethesda, MD 20892 USA.
[Broxmeyer, Hal E.] Indiana Univ Sch Med, Dept Microbiol & Immunol, Indianapolis, IN USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 857
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838901007
ER
PT J
AU Zeidner, JF
Gerber, JM
Blackford, A
Litzow, M
Foster, MC
Morris, LE
Gojo, I
Lancet, JE
Bose, P
Tibes, R
Strickland, SA
Greer, JM
Drye, M
Meads, K
Doyle, A
Little, RF
Wright, JJ
Karp, JE
AF Zeidner, Joshua F.
Gerber, Jonathan M.
Blackford, Amanda
Litzow, Mark
Foster, Matthew C.
Morris, Lawrence E., Jr.
Gojo, Ivana
Lancet, Jeffrey E.
Bose, Prithviraj
Tibes, Raoul
Strickland, Stephen A.
Greer, Jacqueline M.
Drye, Michelle
Meads, Kevin
Doyle, Austin
Little, Richard F.
Wright, John J.
Karp, Judith E.
TI Randomized Phase II Trial of Timed-Sequential Therapy (TST) with
Flavopiridol (Alvocidib), Ara-C and Mitoxantrone (FLAM) Versus "7+3" for
Adults Ages 70 Years and Under with Newly Diagnosed Acute Myeloid
Leukemia (AML)
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Zeidner, Joshua F.; Greer, Jacqueline M.; Drye, Michelle; Meads, Kevin; Karp, Judith E.] Johns Hopkins Univ Hosp, Sidney Kimnrl Comprehens Canc Ctr, Baltimore, MD 21205 USA.
[Gerber, Jonathan M.] Johns Hopkins Univ, Sch Med, Dept Med, Div Hematol, Baltimore, MD 21205 USA.
[Blackford, Amanda] Sidney Kimmel Comprehens Canc Ctr John Hopkins, Div Biostat, Dept Oncol, Baltimore, MD USA.
[Litzow, Mark] Mayo Clin, Rochester, MN USA.
[Foster, Matthew C.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Morris, Lawrence E., Jr.] Northside Hosp, Blood & Marrow Transplant Program, Atlanta, GA USA.
[Gojo, Ivana] Univ Maryland, Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
[Lancet, Jeffrey E.] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
[Bose, Prithviraj] Virginia Commonwealth Univ, Massey Canc Ctr, Richmond, VA USA.
[Tibes, Raoul] Mayo Clin Arizona, Scottsdale, AZ USA.
[Strickland, Stephen A.] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Doyle, Austin; Little, Richard F.; Wright, John J.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 47
PG 2
WC Hematology
SC Hematology
GA 074UG
UT WOS:000313838900117
ER
PT J
AU Zhao, XH
Lwin, T
Zhang, XW
Huang, A
Wang, J
Marquez, VE
Chen-Kiang, S
Bradner, JE
Dalton, WS
Sotomayor, EM
Tao, JG
AF Zhao, Xiaohong
Lwin, Tint
Zhang, Xinwei
Huang, Andy
Wang, Jian
Marquez, Victor E.
Chen-Kiang, Selina
Bradner, James E.
Dalton, William S.
Sotomayor, Eduardo M.
Tao, Jianguo
TI Silencing c-Myc Using Myc Inhibitor JQ1 and EZH2 Inhibitor DZNep Blocks
Converging Survival Signals in Aggressive B-Cell Lymphomas
SO BLOOD
LA English
DT Meeting Abstract
CT 54th Annual Meeting and Exposition of the American-Society-of-Hematology
(ASH)
CY DEC 08-11, 2012
CL Atlanta, GA
SP Amer Soc Hematol (ASH)
C1 [Zhao, Xiaohong] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Tao, Jianguo] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Dept Pathol, Tampa, FL 33612 USA.
[Zhang, Xinwei] Tianjin Med Univ, Canc Inst & Hosp, Dept Biotherapy, Tianjin, Peoples R China.
[Huang, Andy; Wang, Jian] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Marquez, Victor E.] NCI, Frederick, MD 21701 USA.
[Chen-Kiang, Selina] Weill Cornell Med Coll, New York, NY USA.
[Bradner, James E.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Dalton, William S.] Univ S Florida, H Lee Moffitt Canc Ctr & Res Inst, Dept Interdisciplinary Oncol, Tampa, FL USA.
[Dalton, William S.] Univ S Florida, H Lee Moffitt Canc Ctr & Res Inst, Expt Therapeut Program, Tampa, FL USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2012
VL 120
IS 21
MA 4618
PG 1
WC Hematology
SC Hematology
GA 077SZ
UT WOS:000314049606049
ER
PT J
AU Raran-Kurussi, S
Waugh, DS
AF Raran-Kurussi, Sreejith
Waugh, David S.
TI The Ability to Enhance the Solubility of Its Fusion Partners Is an
Intrinsic Property of Maltose-Binding Protein but Their Folding Is
Either Spontaneous or Chaperone-Mediated
SO PLOS ONE
LA English
DT Article
ID ESCHERICHIA-COLI STRAIN; ETCH VIRUS PROTEASE; HPV E6 ONCOPROTEIN;
IN-VIVO; DIHYDROFOLATE-REDUCTASE; RECOMBINANT PROTEINS; MOLECULAR
CHAPERONE; DISULFIDE BONDS; HIGH-AFFINITY; PURIFICATION
AB Escherichia coli maltose binding protein (MBP) is commonly used to promote the solubility of its fusion partners. To investigate the mechanism of solubility enhancement by MBP, we compared the properties of MBP fusion proteins refolded in vitro with those of the corresponding fusion proteins purified under native conditions. We fused five aggregation-prone passenger proteins to 3 different N-terminal tags: His(6)-MBP, His(6)-GST and His(6). After purifying the 15 fusion proteins under denaturing conditions and refolding them by rapid dilution, we recovered far more of the soluble MBP fusion proteins than their GST- or His-tagged counterparts. Hence, we can reproduce the solubilizing activity of MBP in a simple in vitro system, indicating that no additional factors are required to mediate this effect. We assayed both the soluble fusion proteins and their TEV protease digestion products (i.e., with the N-terminal tag removed) for biological activity. Little or no activity was detected for some fusion proteins whereas others were quite active. When the MBP fusions proteins were purified from E. coli under native conditions they were all substantially active. These results indicate that the ability of MBP to promote the solubility of its fusion partners in vitro sometimes, but not always, results in their proper folding. We show that the folding of some passenger proteins is mediated by endogenous chaperones in vivo. Hence, MBP serves as a passive participant in the folding process; passenger proteins either fold spontaneously or with the assistance of chaperones.
C1 [Raran-Kurussi, Sreejith; Waugh, David S.] Frederick Natl Lab Canc Res, Ctr Canc Res, Prot Engn Sect, Macromol Crystallog Lab, Frederick, MD USA.
RP Waugh, DS (reprint author), Frederick Natl Lab Canc Res, Ctr Canc Res, Prot Engn Sect, Macromol Crystallog Lab, Frederick, MD USA.
EM waughd@mail.nih.gov
FU Center for Cancer Research, National Cancer Institute; Frederick
National Laboratory for Cancer Research; National Institutes of Health
FX This work was funded by the intramural research program of the Center
for Cancer Research, National Cancer Institute, Frederick National
Laboratory for Cancer Research, 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 47
TC 27
Z9 28
U1 0
U2 14
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 16
PY 2012
VL 7
IS 11
AR e49589
DI 10.1371/journal.pone.0049589
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 048BN
UT WOS:000311885300055
PM 23166722
ER
PT J
AU Yu, SY
Zhou, XY
Steinke, FC
Liu, CY
Chen, SC
Zagorodna, O
Jing, XF
Yokota, Y
Meyerholz, DK
Mullighan, CG
Knudson, CM
Zhao, DM
Xue, HH
AF Yu, Shuyang
Zhou, Xinyuan
Steinke, Farrah C.
Liu, Chengyu
Chen, Shann-Ching
Zagorodna, Oksana
Jing, Xuefang
Yokota, Yoshifumi
Meyerholz, David K.
Mullighan, Charles G.
Knudson, C. Michael
Zhao, Dong-Mei
Xue, Hai-Hui
TI The TCF-1 and LEF-1 Transcription Factors Have Cooperative and Opposing
Roles in T Cell Development and Malignancy
SO IMMUNITY
LA English
DT Article
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; WNT SIGNALING PATHWAY; MOLECULAR
PATHOGENESIS; NOTCH1 MUTATIONS; CANCER; DIFFERENTIATION; TRANSFORMATION;
EXPRESSION; SURVIVAL; SPECIFICATION
AB The TCF-1 and LEF-1 transcription factors are known to play critical roles in normal thymocyte development. Unexpectedly, we found that TCF-1-deficient (Tcf7(-/-)) mice developed aggressive T cell malignancy, resembling human T cell acute lymphoblastic leukemia (T-ALL). LEF-1 was aberrantly up-regulated in premalignant Tcf7(-/-) early thymocytes and lymphoma cells. We further demonstrated that TCF-1 directly repressed LEF-1 expression in early thymocytes and that conditional inactivation of Lef1 greatly delayed or prevented T cell malignancy in Tcf7(-/-) mice. In human T-ALLs, an early thymic progenitor (ETP) subtype was associated with diminished TCF7 expression, and two of the ETP-ALL cases harbored TCF7 gene deletions. We also showed that TCF-1 and LEF-1 were dispensable for T cell lineage commitment but instead were required for early thymocytes to mature beyond the CD4(-)CD8(-) stage. TCF-1 thus has dual roles, i.e., acting cooperatively with LEF-1 to promote thymocyte maturation while restraining LEF-1 expression to prevent malignant transformation of developing thymocytes.
C1 [Yu, Shuyang; Zhou, Xinyuan; Steinke, Farrah C.; Jing, Xuefang; Zhao, Dong-Mei; Xue, Hai-Hui] Univ Iowa, Dept Microbiol, Carver Coll Med, Iowa City, IA 52242 USA.
[Zagorodna, Oksana; Meyerholz, David K.; Knudson, C. Michael] Univ Iowa, Dept Pathol, Carver Coll Med, Iowa City, IA 52242 USA.
[Zhao, Dong-Mei] Univ Iowa, Dept Internal Med, Carver Coll Med, Iowa City, IA 52242 USA.
[Xue, Hai-Hui] Univ Iowa, Interdisciplinary Immunol Grad Program, Carver Coll Med, Iowa City, IA 52242 USA.
[Liu, Chengyu] NHLBI, Transgen Core Facil, NIH, Bethesda, MD 20892 USA.
[Chen, Shann-Ching; Mullighan, Charles G.] St Jude Childrens Res Hosp, Dept Pathol, Memphis, TN 38105 USA.
[Yokota, Yoshifumi] Univ Fukui, Sch Med, Dept Biochem & Bioinformat Sci, Div Mol Genet, Fukui 9101193, Japan.
RP Zhao, DM (reprint author), Univ Iowa, Dept Microbiol, Carver Coll Med, Iowa City, IA 52242 USA.
EM dong-mei-zhao@uiowa.edu; hai-hui-xue@uiowa.edu
OI Mullighan, Charles/0000-0002-1871-1850
FU American Cancer Society [RSG-11-161-01-MPC]; NIH [HL095540, AI080966]
FX We thank H. Clevers for permission to use the Tcf7-/- mice,
D.L. Court and N.G. Copland (NCI) for providing all the recombineering
reagents, F. McCormick (UCSF) for WT and mutant beta-catenin constructs,
W.S. Pear (UPenn) for the ICN and DN-MAML constructs, D.G. Tenen
(Harvard) for the self-inactivating retroviral reporter construct, and
J.C. Zuniga-Pflucker (Sunnybrook Research Institute, Canada) for the
OP9-DL1 cells. We thank J. Harty and A. Dupuy for critical reading of
the manuscript, G. Hauser and T. Bair (DNA Facility) for performing
microarray analysis and assistance with the data analysis, H. Vignes and
G. Rasmussen (Flow Cytometry Facility) for cell sorting, and S. Martin
for cell cycle analysis. This study is supported by grants from the
American Cancer Society (RSG-11-161-01-MPC to H.-H.X.) and the NIH
(HL095540 and AI080966 to H.-H.X.).
NR 44
TC 54
Z9 55
U1 3
U2 12
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD NOV 16
PY 2012
VL 37
IS 5
BP 813
EP 826
DI 10.1016/j.immuni.2012.08.009
PG 14
WC Immunology
SC Immunology
GA 042GP
UT WOS:000311460000009
PM 23103132
ER
PT J
AU Jones, JL
Esber, GR
McDannald, MA
Gruber, AJ
Hernandez, A
Mirenzi, A
Schoenbaum, G
AF Jones, Joshua L.
Esber, Guillem R.
McDannald, Michael A.
Gruber, Aaron J.
Hernandez, Alex
Mirenzi, Aaron
Schoenbaum, Geoffrey
TI Orbitofrontal Cortex Supports Behavior and Learning Using Inferred But
Not Cached Values
SO SCIENCE
LA English
DT Article
ID VENTROMEDIAL PREFRONTAL CORTEX; VENTRAL STRIATUM; REWARD VALUE; LESIONS;
AMYGDALA; NEURONS; HUMANS; INACTIVATION; ASSOCIATIONS; DEVALUATION
AB Computational and learning theory models propose that behavioral control reflects value that is both cached (computed and stored during previous experience) and inferred (estimated on the fly on the basis of knowledge of the causal structure of the environment). The latter is thought to depend on the orbitofrontal cortex. Yet some accounts propose that the orbitofrontal cortex contributes to behavior by signaling "economic" value, regardless of the associative basis of the information. We found that the orbitofrontal cortex is critical for both value-based behavior and learning when value must be inferred but not when a cached value is sufficient. The orbitofrontal cortex is thus fundamental for accessing model-based representations of the environment to compute value rather than for signaling value per se.
C1 [Jones, Joshua L.; Hernandez, Alex; Schoenbaum, Geoffrey] Univ Maryland, Dept Anat & Neurobiol, Sch Med, Baltimore, MD 21201 USA.
[Esber, Guillem R.; McDannald, Michael A.; Mirenzi, Aaron; Schoenbaum, Geoffrey] NIDA, Behav Neurophysiol Res Sect, Cellular Neurobiol Res Branch, Intramural Res Program, Baltimore, MD 21201 USA.
[Gruber, Aaron J.] Univ Lethbridge, Dept Neurosci, Lethbridge, AB T1K 3M4, Canada.
RP Jones, JL (reprint author), Univ Maryland, Dept Anat & Neurobiol, Sch Med, 20 Penn St, Baltimore, MD 21201 USA.
EM josh.jones@nih.gov; geoffrey.schoenbaum@nih.gov
OI Hernandez, Alex/0000-0002-2267-4781
FU National Institute on Drug Abuse (NIDA), NIH [F32-031517]; NIDA
[R01-DA015718]; Natural Sciences and Engineering Research Council of
Canada; Intramural Research Program at NIDA
FX This work was supported by National Institute on Drug Abuse (NIDA), NIH,
F32-031517 to J.L.J., NIDA R01-DA015718 to G. S., funding from Natural
Sciences and Engineering Research Council of Canada to A.J.G., and by
the Intramural Research Program at NIDA. The opinions expressed in this
article are the authors' own and do not reflect the view of the NIH or
U.S. Department of Health and Human Services. The authors declare that
they have no conflicts of interest related to the data presented in this
manuscript.
NR 30
TC 60
Z9 61
U1 1
U2 25
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 16
PY 2012
VL 338
IS 6109
BP 953
EP 956
DI 10.1126/science.1227489
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 037DY
UT WOS:000311083600045
PM 23162000
ER
PT J
AU Lopez, CM
Pelkey, KA
Chittajallu, R
Nakashiba, T
Toth, K
Tonegawa, S
McBain, CJ
AF Lopez, Carla M.
Pelkey, Kenneth A.
Chittajallu, Ramesh
Nakashiba, Toshiaki
Toth, Katalin
Tonegawa, Susumu
McBain, Chris J.
TI Competition from newborn granule cells does not drive axonal retraction
of silenced old granule cells in the adult hippocampus
SO FRONTIERS IN NEURAL CIRCUITS
LA English
DT Article
DE neurogenesis; mossy fibers; hippocampal; activity-dependent circuit
refinement; tetanus toxin; Moloney virus
ID SPATIAL-PATTERN SEPARATION; MOSSY FIBER SYNAPSES; IN-VIVO; SYNAPTIC
PLASTICITY; NEURAL ACTIVITY; DENTATE GYRUS; NEURONS BORN; NEUROGENESIS;
ZINC; LOCALIZATION
AB In the developing nervous system synaptic refinement, typified by the neuromuscular junction where supernumerary connections are eliminated by axon retraction leaving the postsynaptic target innervated by a single dominant input, critically regulates neuronal circuit formation. Whether such competition-based pruning continues in established circuits of mature animals remains unknown. This question is particularly relevant in the context of adult neurogenesis where newborn cells must integrate into preexisting circuits, and thus, potentially compete with functionally mature synapses to gain access to their postsynaptic targets. The hippocampus plays an important role in memory formation/retrieval and the dentate gyrus (DG) subfield exhibits continued neurogenesis into adulthood. Therefore, this region contains both mature granule cells (old GCs) and immature recently born GCs that are generated throughout adult life (young GCs), providing a neurogenic niche model to examine the role of competition in synaptic refinement. Recent work from an independent group in developing animals indicated that embryonically/early postnatal generated GCs placed at a competitive disadvantage by selective expression of tetanus toxin (TeTX) to prevent synaptic release rapidly retracted their axons, and that this retraction was driven by competition from newborn GCs lacking TeTX. In contrast, following 3-6 months of selective TeTX expression in old GCs of adult mice we did not observe any evidence of axon retraction. Indeed ultrastructural analyses indicated that the terminals of silenced GCs even maintained synaptic contact with their postsynaptic targets. Furthermore, we did not detect any significant differences in the electrophysiological properties between old GCs in control and TeTX conditions. Thus, our data demonstrate a remarkable stability in the face of a relatively prolonged period of altered synaptic competition between two populations of neurons within the adult brain.
C1 [Lopez, Carla M.; Pelkey, Kenneth A.; Chittajallu, Ramesh; McBain, Chris J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Dev Neurobiol, NIH, Bethesda, MD USA.
[Nakashiba, Toshiaki; Tonegawa, Susumu] MIT, RIKEN MIT Ctr Neural Circuit Genet, Cambridge, MA 02139 USA.
[Nakashiba, Toshiaki; Tonegawa, Susumu] MIT, Picower Inst Learning & Memory, Cambridge, MA 02139 USA.
[Toth, Katalin] Univ Laval, Quebec Mental Hlth Inst, Dept Psychiat & Neurosci, Quebec City, PQ, Canada.
RP Pelkey, KA (reprint author), Porter Neurosci Res Ctr, 35 Lincoln Dr,MSC 3715, Bethesda, MD 20892 USA.
EM pelkeyk2@mail.nih.gov
FU Howard Hughes Medical Institute; Otsuka Maryland Research Institute;
Picower Foundation; NIH [R01-MH078821, P50-MH58880]; NICHD; CIHR grant
[MOP 81142]
FX We thank Daniel Abebe, Xiaoqing Yuan, Modesto R. Peralta III, and
Philippe Lemieux for providing expert technical assistance as well as
Jennie Z. Young for critical reading. RGS14 anti-body was generously
provided by Dr. John Helper. This work was supported by the Howard
Hughes Medical Institute, Otsuka Maryland Research Institute, the
Picower Foundation, and NIH grants R01-MH078821 and P50-MH58880 to
Susumu Tonegawa; NICHD intramural funding to Chris J. McBain; and CIHR
grant MOP 81142 to Katalin Toth.
NR 40
TC 4
Z9 4
U1 0
U2 12
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5110
J9 FRONT NEURAL CIRCUIT
JI Front. Neural Circuits
PD NOV 16
PY 2012
VL 6
AR 85
DI 10.3389/fncir.2012.00085
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 037SU
UT WOS:000311127600003
PM 23162435
ER
PT J
AU Okano, J
Levy, C
Lichti, U
Sun, HW
Yuspa, SH
Sakai, Y
Morasso, MI
AF Okano, Junko
Levy, Clara
Lichti, Ulrike
Sun, Hong-Wei
Yuspa, Stuart H.
Sakai, Yasuo
Morasso, Maria I.
TI Cutaneous Retinoic Acid Levels Determine Hair Follicle Development and
Downgrowth
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID BETA-CATENIN ACTIVITY; DERMAL PAPILLA CELLS; GENE-EXPRESSION; SEBACEOUS
GLAND; THYROID-HORMONE; SONIC HEDGEHOG; KERATIN GENE; RNA-SEQ;
DIFFERENTIATION; GROWTH
AB Retinoic acid (RA) is essential during embryogenesis and for tissue homeostasis, whereas excess RA is well known as a teratogen. In humans, excess RA is associated with hair loss. In the present study, we demonstrate that specific levels of RA, regulated by Cyp26b1, one of the RA-degrading enzymes, are required for hair follicle (hf) morphogenesis. Mice with embryonic ablation of Cyp26b1 (Cyp26b1(-/-)) have excessive endogenous RA, resulting in arrest of hf growth at the hair germ stage. The altered hf development is rescued by grafting the mutant skin on immunodeficient mice. Our results show that normalization of RA levels is associated with reinitiation of hf development. Conditional deficiency of Cyp26b1 in the dermis (En1Cre; Cyp26b1f/-) results in decreased hair follicle density and specific effect on hair type, indicating that RA levels also influence regulators of hair bending. Our results support the model of RA-dependent dermal signals regulating hf downgrowth and bending. To elucidate target gene pathways of RA, we performed microarray and RNA-Seq profiling of genes differentially expressed in Cyp26b1(-/-) skin and En1Cre; Cyp26b1f/- tissues. We show specific effects on the Wnt-catenin pathway and on members of the Runx, Fox, and Sox transcription factor families, indicating that RA modulates pathways and factors implicated in hf downgrowth and bending. Our results establish that proper RA distribution is essential for morphogenesis, development, and differentiation of hfs.
C1 [Okano, Junko; Levy, Clara; Morasso, Maria I.] NIAMS, Dev Skin Biol Sect, NIH, Bethesda, MD 20892 USA.
[Lichti, Ulrike; Yuspa, Stuart H.] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
[Sun, Hong-Wei] NIAMS, Biodata Min & Discovery Sect, NIH, Bethesda, MD 20892 USA.
[Sakai, Yasuo] Osaka Univ, Dept Plast Surg, Sch Med, Suita, Osaka 5650871, Japan.
RP Morasso, MI (reprint author), NIAMS, Dev Skin Biol Sect, NIH, 50 South Dr,Rm 1523, Bethesda, MD 20892 USA.
EM morassom@mail.nih.gov
FU National Institutes of Health grant from the Intramural Research Program
of the NIAMS
FX This work was supported by a National Institutes of Health grant from
the Intramural Research Program of the NIAMS.
NR 54
TC 5
Z9 5
U1 2
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 16
PY 2012
VL 287
IS 47
DI 10.1074/jbc.M112.397273
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 039GY
UT WOS:000311233800003
PM 23007396
ER
PT J
AU Plenge, P
Shi, L
Beuming, T
Te, J
Newman, AH
Weinstein, H
Gether, U
Loland, CJ
AF Plenge, Per
Shi, Lei
Beuming, Thijs
Te, Jerez
Newman, Amy Hauck
Weinstein, Harel
Gether, Ulrik
Loland, Claus J.
TI Steric Hindrance Mutagenesis in the Conserved Extracellular Vestibule
Impedes Allosteric Binding of Antidepressants to the Serotonin
Transporter
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID NEUROTRANSMITTER-SODIUM SYMPORTER; R-CITALOPRAM; DOPAMINE TRANSPORTER;
H-3 IMIPRAMINE; BACTERIAL HOMOLOG; 5-HT TRANSPORTER; S-CITALOPRAM; OPEN
STATES; IN-VITRO; SITE
AB The serotonin transporter (SERT) controls synaptic serotonin levels and is the primary target for antidepressants, including selective serotonin reuptake inhibitors (e.g. (S)-citalopram) and tricyclic antidepressants (e.g. clomipramine). In addition to a high affinity binding site, SERT possesses a low affinity allosteric site for antidepressants. Binding to the allosteric site impedes dissociation of antidepressants from the high affinity site, which may enhance antidepressant efficacy. Here we employ an induced fit docking/molecular dynamics protocol to identify the residues that may be involved in the allosteric binding in the extracellular vestibule located above the central substrate binding (S1) site. Indeed, mutagenesis of selected residues in the vestibule reduces the allosteric potency of (S)-citalopram and clomipramine. The identified site is further supported by the inhibitory effects of Zn2+ binding in an engineered site and the covalent attachment of benzocaine-methanethiosulfonate to a cysteine introduced in the extracellular vestibule. The data provide a mechanistic explanation for the allosteric action of antidepressants at SERT and suggest that the role of the vestibule is evolutionarily conserved among neurotransmitter: sodium symporter proteins as a binding pocket for small molecule ligands.
C1 [Shi, Lei; Te, Jerez; Weinstein, Harel] Cornell Univ, Weill Med Coll, Dept Physiol & Biophys, New York, NY 10021 USA.
[Shi, Lei; Weinstein, Harel] Cornell Univ, Weill Med Coll, Inst Computat Biomed, New York, NY 10021 USA.
[Plenge, Per; Gether, Ulrik; Loland, Claus J.] Univ Copenhagen, Fac Hlth & Med Sci, Dept Neurosci & Pharmacol, Mol Neuropharmacol Lab, DK-2200 Copenhagen, Denmark.
[Beuming, Thijs] Schrodinger Inc, New York, NY 10036 USA.
[Newman, Amy Hauck] NIDA, Med Chem Sect, Mol Targets & Medicat Discovery Branch, Intramural Res Program,Dept Hlth & Human Serv,NIH, Baltimore, MD 21224 USA.
RP Shi, L (reprint author), Cornell Univ, Weill Med Coll, Dept Physiol & Biophys, New York, NY 10021 USA.
EM les2007@med.cornell.edu; cllo@sund.ku.dk
RI Loland, Claus/E-5975-2014;
OI Loland, Claus/0000-0002-1773-1446; Gether, Ulrik/0000-0002-0020-3807
FU National Institutes of Health [DA12408, DA023694]; National Institutes
of Health, NIDA, Intramural Research Program; Danish Independent
Research Council-Sapere Aude; Danish Health Science Research Council;
Lundbeck Foundation; Novo Nordic Foundation; Maersk Foundation; BioSCART
center of excellence program; Lundbeck A/S
FX This work was supported, in whole or in part, by National Institutes of
Health Grants DA12408 (to U. G. and H. W.) and DA023694 (to L. S.) and
the National Institutes of Health, NIDA, Intramural Research Program (to
A. H. N.). This work was also supported in part by the Danish
Independent Research Council-Sapere Aude (to C. J. L.), the Danish
Health Science Research Council (to C. J. L. and U. G.), the Lundbeck
Foundation (to C. J. L. and U. G.), the Novo Nordic Foundation (to C. J.
L. and U. G.), the Maersk Foundation (to C. J. L.), the BioSCART center
of excellence program (to C. J. L. and U. G.), and Lundbeck A/S (to P.
P.).
NR 53
TC 35
Z9 36
U1 0
U2 6
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 16
PY 2012
VL 287
IS 47
DI 10.1074/jbc.M112.371765
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 039GY
UT WOS:000311233800004
PM 23007398
ER
PT J
AU Xu, M
Liu, K
Swaroop, M
Porter, FD
Sidhu, R
Finkes, S
Ory, DS
Marugan, JJ
Xiao, JB
Southall, N
Pavan, WJ
Davidson, C
Walkley, SU
Remaley, AT
Baxa, U
Sun, W
McKew, JC
Austin, CP
Zheng, W
AF Xu, Miao
Liu, Ke
Swaroop, Manju
Porter, Forbes D.
Sidhu, Rohini
Finkes, Sally
Ory, Daniel S.
Marugan, Juan J.
Xiao, Jingbo
Southall, Noel
Pavan, William J.
Davidson, Cristin
Walkley, Steven U.
Remaley, Alan T.
Baxa, Ulrich
Sun, Wei
McKew, John C.
Austin, Christopher P.
Zheng, Wei
TI delta-Tocopherol Reduces Lipid Accumulation in Niemann-Pick Type C1 and
Wolman Cholesterol Storage Disorders
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID LYSOSOMAL ACID LIPASE; ALPHA-TOCOPHEROL; VITAMIN-E; OMEGA-HYDROXYLASE;
DISEASE; EXOCYTOSIS; FIBROBLASTS; PLASMA; SUPPLEMENTATION; TOCOTRIENOLS
AB Niemann-Pick disease type C (NPC) and Wolman disease are two members of a family of storage disorders caused by mutations of genes encoding lysosomal proteins. Deficiency in function of either the NPC1 or NPC2 protein in NPC disease or lysosomal acid lipase in Wolman disease results in defective cellular cholesterol trafficking. Lysosomal accumulation of cholesterol and enlarged lysosomes are shared phenotypic characteristics of both NPC and Wolman cells. Utilizing a phenotypic screen of an approved drug collection, we found that delta-tocopherol effectively reduced lysosomal cholesterol accumulation, decreased lysosomal volume, increased cholesterol efflux, and alleviated pathological phenotypes in both NPC1 and Wolman fibroblasts. Reduction of these abnormalities may be mediated by a delta-tocopherol-induced intracellular Ca2+ response and subsequent enhancement of lysosomal exocytosis. Consistent with a general mechanism for reduction of lysosomal lipid accumulation, we also found that delta-tocopherol reduces pathological phenotypes in patient fibroblasts from other lysosomal storage diseases, including NPC2, Batten (ceroid lipofuscinosis, neuronal 2, CLN2), Fabry, Farber, Niemann-Pick disease type A, Sanfilippo type B (mucopolysaccharidosis type IIIB, MPSIIIB), and Tay-Sachs. Our data suggest that regulated exocytosis may represent a potential therapeutic target for reduction of lysosomal storage in this class of diseases.
C1 [Xu, Miao; Liu, Ke; Swaroop, Manju; Marugan, Juan J.; Xiao, Jingbo; Southall, Noel; Sun, Wei; McKew, John C.; Austin, Christopher P.; Zheng, Wei] NIH, Natl Ctr Adv Translat Sci, Bethesda, MD 20892 USA.
[Porter, Forbes D.] Eunice Kennedy Shriver NICHD, Program Dev Endocrinol & Genet, NIH, Bethesda, MD 20892 USA.
[Sidhu, Rohini; Finkes, Sally; Ory, Daniel S.] Washington Univ, Sch Med, Diabet Cardiovasc Dis Ctr, St Louis, MO 63110 USA.
[Pavan, William J.] NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA.
[Davidson, Cristin; Walkley, Steven U.] Albert Einstein Coll Med, Rose F Kennedy Ctr, Sidney Weisner Lab Genet Neurol Dis, Bronx, NY 10461 USA.
[Remaley, Alan T.] NHLBI, Lab Lipoprot Metab, NIH, Bethesda, MD 20892 USA.
[Xu, Miao] Zhejiang Univ, Sch Med, Sir Run Run Shaw Hosp, Hangzhou 310016, Zhejiang, Peoples R China.
[Baxa, Ulrich] NCI, Electron Microscopy Lab, NIH, Bethesda, MD 20892 USA.
RP Zheng, W (reprint author), NIH, Natl Ctr Adv Translat Sci, 9800 Med Ctr Dr,MSC 3370, Bethesda, MD 20892 USA.
EM wzheng@mail.nih.gov
RI Southall, Noel/H-8991-2012; Sidhu, Rohini/G-3547-2012; Zheng,
Wei/J-8889-2014; Davidson, Cristin/F-4889-2017
OI Southall, Noel/0000-0003-4500-880X; Zheng, Wei/0000-0003-1034-0757;
Davidson, Cristin/0000-0002-5508-8113
FU National Institutes of Health Intramural Research Program of the
National Center for Advancing Translational Sciences; Intramural
Research Program of the National Human Genome Research Institute;
Intramural Research Program of the Eunice Kennedy Shriver NICHD; NCI,
National Institutes of Health [HHSN26120080001E]; Ara Parseghian Medical
Research Foundation; National Institutes of Health [P60 DK020579]
FX This work was supported, in whole or in part, by the National Institutes
of Health Intramural Research Program of the National Center for
Advancing Translational Sciences, by the Intramural Research Program of
the National Human Genome Research Institute, by the Intramural Research
Program of the Eunice Kennedy Shriver NICHD, and by NCI, National
Institutes of Health, Contract HHSN26120080001E. This work was also
supported by a grant from the Ara Parseghian Medical Research
Foundation.; We thank Support of Accelerated Research for Niemann-Pick
Disease Type C (SOAR-NPC) for fostering a collaborative research
environment and stimulating discussion. Mass spectrometry analysis was
performed in the Washington University Metabolomics Facility, supported
by National Institutes of Health Grant P60 DK020579. We thank Dr.
Yiannis A. Ioannou (Mount Sinai School of Medicine) for technical
assistance with the exocytosis assays and Ferri Soheilian and Christina
Burks for assistance with electron microscopy.
NR 49
TC 39
Z9 40
U1 0
U2 11
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 16
PY 2012
VL 287
IS 47
DI 10.1074/jbc.M112.357707
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 039GY
UT WOS:000311233800007
PM 23035117
ER
PT J
AU Lee, S
Chang, J
Renvoise, B
Tipirneni, A
Yang, S
Blackstone, C
AF Lee, Seongju
Chang, Jaerak
Renvoise, Benoit
Tipirneni, Anita
Yang, Sarah
Blackstone, Craig
TI MITD1 is recruited to midbodies by ESCRT-III and participates in
cytokinesis
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID HEREDITARY SPASTIC PARAPLEGIA; AAA ATPASE VPS4; STRUCTURAL BASIS;
MEMBRANE DEFORMATION; PROTEIN IST1; MACHINERY; AUTOINHIBITION;
LOCALIZATION; RECOGNITION; ATLASTIN
AB Diverse cellular processes, including multivesicular body formation, cytokinesis, and viral budding, require the sequential functions of endosomal sorting complexes required for transport (ESCRTs) 0 to III. Of these multiprotein complexes, ESCRT-III in particular plays a key role in mediating membrane fission events by forming large, ring-like helical arrays. A number of proteins playing key effector roles, most notably the ATPase associated with diverse cellular activities protein VPS4, harbor present in microtubule-interacting and trafficking molecules (MIT) domains comprising asymmetric three-helical bundles, which interact with helical MIT-interacting motifs in ESCRT-III subunits. Here we assess comprehensively the ESCRT-III interactions of the MIT-domain family member MITD1 and identify strong interactions with charged multivesicular body protein 1B (CHMP1B), CHMP2A, and increased sodium tolerance-1 (IST1). We show that these ESCRT-III subunits are important for the recruitment of MITD1 to the midbody and that MITD1 participates in the abscission phase of cytokinesis. MITD1 also dimerizes through its C-terminal domain. Both types of interactions appear important for the role of MITD1 in negatively regulating the interaction of IST1 with VPS4. Because IST1 binding in turn regulates VPS4, MITD1 may function through downstream effects on the activity of VPS4, which plays a critical role in the processing and remodeling of ESCRT filaments in abscission.
C1 [Lee, Seongju; Chang, Jaerak; Renvoise, Benoit; Tipirneni, Anita; Yang, Sarah; Blackstone, Craig] Natl Inst Neurol Disorders & Stroke, Cell Biol Sect, Neurogenet Branch, NIH, Bethesda, MD 20892 USA.
RP Blackstone, C (reprint author), Natl Inst Neurol Disorders & Stroke, Cell Biol Sect, Neurogenet Branch, NIH, Bethesda, MD 20892 USA.
EM blackstc@ninds.nih.gov
FU Intramural Research Program of the National Institute of Neurological
Disorders and Stroke, National Institutes of Health; National Institutes
of Health Clinical Research Training Program
FX We thank J. Nagle and D. Kauffman (National Institute of Neurological
Disorders and Stroke DNA Sequencing Facility) for DNA sequencing. This
research was supported by the Intramural Research Program of the
National Institute of Neurological Disorders and Stroke, National
Institutes of Health, and the National Institutes of Health Clinical
Research Training Program (to A.T.).
NR 33
TC 14
Z9 16
U1 0
U2 7
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD NOV 15
PY 2012
VL 23
IS 22
BP 4347
EP 4361
DI 10.1091/mbc.E12-04-0292
PG 15
WC Cell Biology
SC Cell Biology
GA 082PP
UT WOS:000314404700002
PM 23015756
ER
PT J
AU Go, JT
Belisle, SE
Tchitchek, N
Tumpey, TM
Ma, WJ
Richt, JA
Safronetz, D
Feldmann, H
Katze, MG
AF Go, Jennifer T.
Belisle, Sarah E.
Tchitchek, Nicolas
Tumpey, Terrence M.
Ma, Wenjun
Richt, Juergen A.
Safronetz, David
Feldmann, Heinz
Katze, Michael G.
TI 2009 pandemic H1N1 influenza virus elicits similar clinical course but
differential host transcriptional response in mouse, macaque, and swine
infection models
SO BMC GENOMICS
LA English
DT Article
DE Pandemic; Influenza virus; Genomics; Inflammation; Lipid metabolism;
Glucocorticoid receptor; LXR/RXR
ID INNATE IMMUNE-RESPONSE; GENE-EXPRESSION; VITAMIN-D; A H1N1; IN-VITRO;
RECEPTOR; PIGS; MACROPHAGES; CIRCULATION; METABOLISM
AB Background: The 2009 pandemic H1N1 influenza virus emerged in swine and quickly became a major global health threat. In mouse, non human primate, and swine infection models, the pH1N1 virus efficiently replicates in the lung and induces pro-inflammatory host responses; however, whether similar or different cellular pathways were impacted by pH1N1 virus across independent infection models remains to be further defined. To address this we have performed a comparative transcriptomic analysis of acute phase responses to a single pH1N1 influenza virus, A/California/04/2009 (CA04), in the lung of mice, macaques and swine.
Results: Despite similarities in the clinical course, we observed differences in inflammatory molecules elicited, and the kinetics of their gene expression changes across all three species. We found genes associated with the retinoid X receptor (RXR) signaling pathway known to control pro-inflammatory and metabolic processes that were differentially regulated during infection in each species, though the heterodimeric RXR partner, pathway associated signaling molecules, and gene expression patterns varied among the three species.
Conclusions: By comparing transcriptional changes in the context of clinical and virological measures, we identified differences in the host transcriptional response to pH1N1 virus across independent models of acute infection. Antiviral resistance and the emergence of new influenza viruses have placed more focus on developing drugs that target the immune system. Underlying overt clinical disease are molecular events that suggest therapeutic targets identified in one host may not be appropriate in another.
C1 [Go, Jennifer T.; Belisle, Sarah E.; Tchitchek, Nicolas; Katze, Michael G.] Univ Washington, Dept Microbiol, Seattle, WA 98195 USA.
[Katze, Michael G.] Univ Washington, Washington Natl Primate Res Ctr, Seattle, WA 98195 USA.
[Ma, Wenjun; Richt, Juergen A.] Kansas State Univ, Dept Diagnost Med Pathobiol, Coll Vet Med, Manhattan, KS 66506 USA.
[Tumpey, Terrence M.] Ctr Dis Control & Prevent, Influenza Div, Atlanta, GA 30333 USA.
[Safronetz, David; Feldmann, Heinz] NIAID, Lab Virol, Div Intramural Res, NIH,Rocky Mt Labs, Hamilton, MT 59840 USA.
RP Go, JT (reprint author), Univ Washington, Dept Microbiol, Seattle, WA 98195 USA.
EM tisoncik@u.washington.edu
OI Tchitchek, Nicolas/0000-0003-3307-0446
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health, Department of Health and Human Services
[HHSN272200800060C, HHSN266200700005C]; Intramural research Program of
the NIAID, NIH
FX We thank Elizabeth Rosenzweig, Sara Kelly, and Jean Chang for microarray
technical support. We are grateful to Marcus Korth, Lynn Law, and Janine
Bryan for their critical review of the manuscript. This work was
supported by federal funds from the National Institute of Allergy and
Infectious Diseases, National Institutes of Health, Department of Health
and Human Services, under contract HHSN272200800060C (M. G. K.) and
contract HHSN266200700005C (J.A.R.). We thank the staff of the Rocky
Mountain Veterinary Branch (Division of Intramural Research (DIR),
NIAID, NIH) for their assistance with the nonhuman primate work. In
addition, we thank Friederike Feldmann (DIR, NIAID, NIH) for technical
assistance in biocontainment. The study was partially funded by the
Intramural research Program of the NIAID, NIH. We thank Deborah Clouser,
Darlene Sheffer, Xi Li, Qinfang Liu, and Chuanling Qiao of Kansas State
University for their assistance with the pig work.
NR 50
TC 20
Z9 21
U1 0
U2 9
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 15
PY 2012
VL 13
AR 627
DI 10.1186/1471-2164-13-627
PG 15
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 061UJ
UT WOS:000312873600001
PM 23153050
ER
PT J
AU Alonso, WJ
McCormick, BJJ
AF Alonso, Wladimir J.
McCormick, Benjamin J. J.
TI EPIPOI: A user-friendly analytical tool for the extraction and
visualization of temporal parameters from epidemiological time series
SO BMC PUBLIC HEALTH
LA English
DT Article
DE Epidemiology; Time series; Trends; Seasonality; Anomalies; Data
visualization
ID SPATIAL HIERARCHIES; INFLUENZA EPIDEMICS; TRAVELING-WAVES; MORTALITY;
THAILAND; PATTERNS; VECTORS; IMAGERY; MODELS; IMPACT
AB Background: There is an increasing need for processing and understanding relevant information generated by the systematic collection of public health data over time. However, the analysis of those time series usually requires advanced modeling techniques, which are not necessarily mastered by staff, technicians and researchers working on public health and epidemiology. Here a user-friendly tool, EPIPOI, is presented that facilitates the exploration and extraction of parameters describing trends, seasonality and anomalies that characterize epidemiological processes. It also enables the inspection of those parameters across geographic regions. Although the visual exploration and extraction of relevant parameters from time series data is crucial in epidemiological research, until now it had been largely restricted to specialists.
Methods: EPIPOI is freely available software developed in Matlab (The Mathworks Inc) that runs both on PC and Mac computers. Its friendly interface guides users intuitively through useful comparative analyses including the comparison of spatial patterns in temporal parameters.
Results: EPIPOI is able to handle complex analyses in an accessible way. A prototype has already been used to assist researchers in a variety of contexts from didactic use in public health workshops to the main analytical tool in published research.
Conclusions: EPIPOI can assist public health officials and students to explore time series data using a broad range of sophisticated analytical and visualization tools. It also provides an analytical environment where even advanced users can benefit by enabling a higher degree of control over model assumptions, such as those associated with detecting disease outbreaks and pandemics.
C1 [Alonso, Wladimir J.; McCormick, Benjamin J. J.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Alonso, WJ (reprint author), NIH, Fogarty Int Ctr, Bldg 10, Bethesda, MD 20892 USA.
EM alonsow@mail.nih.gov
FU MISMS project, MAL-ED; Bill and Melinda Gates Foundation; Premio
Santander Universidades
FX EPIPOI is available at http://www.epipoi.info. The authors are grateful
to the Department of Vital Statistics from the Brazilian Ministry of
Health for providing the mortality data used as an example dataset. We
thank Cynthia Schuck-Paim, Jennifer Weisent and Camille Pelat for their
valuable comments on manuscript. The development of this tool has been
possible using the support of MISMS project, MAL-ED funded by the Bill
and Melinda Gates Foundation, and the Premio Santander Universidades.
Torrence and Compo (Torrence and Compo 1998) graciously made codes which
have been integrated in EPIPOI to perform wavelet analyses freely
available. This tool has certainly benefited from comments from users.
We are grateful for this and hope to keep receiving such feedback in the
future (for this, please go to www.epipoi.info).
NR 29
TC 9
Z9 9
U1 0
U2 11
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2458
J9 BMC PUBLIC HEALTH
JI BMC Public Health
PD NOV 15
PY 2012
VL 12
AR 982
DI 10.1186/1471-2458-12-982
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 060QU
UT WOS:000312793900001
PM 23153033
ER
PT J
AU Gozzelino, R
Andrade, BB
Larsen, R
Luz, NF
Vanoaica, L
Seixas, E
Coutinho, A
Cardoso, S
Rebelo, S
Poli, M
Barral-Netto, M
Darshan, D
Kuhn, LC
Soares, MP
AF Gozzelino, Raffaella
Andrade, Bruno Bezerril
Larsen, Rasmus
Luz, Nivea F.
Vanoaica, Liviu
Seixas, Elsa
Coutinho, Antonio
Cardoso, Silvia
Rebelo, Sofia
Poli, Maura
Barral-Netto, Manoel
Darshan, Deepak
Kuehn, Lukas C.
Soares, Miguel P.
TI Metabolic Adaptation to Tissue Iron Overload Confers Tolerance to
Malaria
SO CELL HOST & MICROBE
LA English
DT Article
ID NF-KAPPA-B; ALPHA-INDUCED APOPTOSIS; NECROSIS-FACTOR-ALPHA; FERRITIN
HEAVY-CHAIN; INDUCED CELL-DEATH; HEME OXYGENASE-1; IN-VITRO;
INFECTIOUS-DISEASES; BRAZILIAN AMAZON; OXIDATIVE STRESS
AB Disease tolerance is a defense strategy that limits the fitness costs of infection irrespectively of pathogen burden. While restricting iron (Fe) availability to pathogens is perceived as a host defense strategy, the resulting tissue Fe overload can be cytotoxic and promote tissue damage to exacerbate disease severity. Examining this interplay during malaria, the disease caused by Plasmodium infection, we find that expression of the Fe sequestering protein ferritin H chain (FtH) in mice, and ferritin in humans, is associated with reduced tissue damage irrespectively of pathogen burden. FtH protection relies on its ferroxidase activity, which prevents labile Fe from sustaining proapoptotic c-Jun N-terminal kinase (JNK) activation. FtH expression is inhibited by JNK activation, promoting tissue Fe overload, tissue damage, and malaria severity. Mimicking FtH's antioxidant effect or inhibiting JNK activation pharmacologically confers therapeutic tolerance to malaria in mice. Thus, FtH provides metabolic adaptation to tissue Fe overload, conferring tolerance to malaria.
C1 [Gozzelino, Raffaella; Larsen, Rasmus; Seixas, Elsa; Coutinho, Antonio; Cardoso, Silvia; Rebelo, Sofia; Soares, Miguel P.] Inst Gulbenkian Ciencias, P-2780156 Oeiras, Portugal.
[Andrade, Bruno Bezerril] NIAID, Immunobiol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Luz, Nivea F.; Barral-Netto, Manoel] Fdn Oswaldo Cruz FIOCRUZ, Ctr Pesquisas Goncalo Moniz, BR-40296710 Salvador, BA, Brazil.
[Luz, Nivea F.; Barral-Netto, Manoel] Univ Fed Bahia, Fac Med, BR-40110100 Salvador, BA, Brazil.
[Vanoaica, Liviu; Darshan, Deepak; Kuehn, Lukas C.] Ecole Polytech Fed Lausanne, Swiss Inst Expt Canc Res ISREC, CH-1015 Lausanne, Switzerland.
[Poli, Maura] Univ Brescia, Dipartimento Materno Infantile & Tecnol Biomed, I-25123 Brescia, Italy.
RP Soares, MP (reprint author), Inst Gulbenkian Ciencias, P-2780156 Oeiras, Portugal.
EM mpsoares@igc.gulbenkian.pt
RI Darshan, Deepak/B-8259-2013; Barral Netto, Manoel/B-3904-2009;
Imunologia, Inct/I-2124-2013; Gozzelino, Raffaella/J-4524-2013; Andrade,
Bruno/J-9111-2012; Gozzelino, Raffaella/E-8147-2017
OI Coutinho, Antonio/0000-0002-0857-9227; Darshan,
Deepak/0000-0001-9719-5980; Barral Netto, Manoel/0000-0002-5823-7903;
Gozzelino, Raffaella/0000-0002-1195-8527; Farias Luz,
Nivea/0000-0003-1958-7043; Soares, Miguel/0000-0002-9314-4833; Andrade,
Bruno/0000-0001-6833-3811; Gozzelino, Raffaella/0000-0002-1195-8527
FU Fundacao pars a Ciencia e Tecnologia (Portugal)
[PTDC/BIA-BCM/101311/2008, PTDC/SAU-FCF/100762/2008,
PTDC/SAU-TOX/116627/2010]; European Community [LSH-2005-1.2.5-1,
ERC-2011-AdG. 294709]; Financiadora de Estudos e Projetos/Fundo Nacional
de Desenvolvimento Cientifico e Tecnologico Amazonia, Brazil
[010409605]; Conselho Nacional de Pesquisa e Tecnologia (Brazil);
intramural research program of the National Institute of Allergy and
Infectious Diseases, NIH
FX We thank John Eaton (University of Louisville) and Luis Teixeira and
Thiago Carvalho (Instituto Gulbenkian de Ciencia) for critical review of
the manuscript; Viktoria Jeney (University of Debrecen, Hungary) for
help in heme measurement; Emanuela Tolosano and Francesca Vinchi
(University of Turin) for help in Fe measurements; and Aldina Barral,
Antonio Reis-Filho, Sebastiao Souza-Neto, Jorge Tolentino, and Elze
Leite (Centro de Pesquisas Goncalo Moniz, Fundacao Oswaldo Cruz, Brazil)
and Marcelo Camargo (Faculdades Sao Lucas and University of Sao Paulo,
Brazil) for critical help in logistics of the clinical study. Funding
was provided by Fundacao pars a Ciencia e Tecnologia (Portugal) grants
to R.G., R.L., E.S., and M.P.S. (PTDC/BIA-BCM/101311/2008,
PTDC/SAU-FCF/100762/2008, and PTDC/SAU-TOX/116627/2010) and European
Community 6th Framework Grant LSH-2005-1.2.5-1 and 7th Framework Grant
ERC-2011-AdG. 294709 DAMAGECONTROL to M.P.S. The clinical study was
funded by Financiadora de Estudos e Projetos (Grant 010409605)/Fundo
Nacional de Desenvolvimento Cientifico e Tecnologico Amazonia, Brazil.
N.F.L. receives a fellowship from Conselho Nacional de Pesquisa e
Tecnologia (Brazil). M.B.-N. is a senior investigator from the Conselho
Nacional de Ciencia e Tecnologia (CNPq), Brazil. B.B.A. is supported by
the intramural research program of the National Institute of Allergy and
Infectious Diseases, NIH. R.G. performed all the experimental work, with
help from R.L., E.S., and S.C., and contributed to the study design.
L.V., D.D., and L.C.K. generated Fthlox/lox mice. M.P.
generated reagents/protocols. S.R. and S.C. established
Fthlox/lox and FthDelta/Delta mouse colony. B.B.A.
and M.B.-N. designed and implemented the clinical protocol. B.B.A.
coordinated the clinical evaluation of the patients and the experiments
to estimate hepatic damage. N.F.L. analyzed ferritin and free heme
plasma concentrations with the help of R.G. M.P.S. formulated the
hypothesis that FtH confers tolerance to Plasmodium infection,
supervised the study design and execution, and wrote the manuscript with
R.G. All authors read and approved the manuscript.
NR 52
TC 32
Z9 33
U1 0
U2 16
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1931-3128
J9 CELL HOST MICROBE
JI Cell Host Microbe
PD NOV 15
PY 2012
VL 12
IS 5
BP 693
EP 704
DI 10.1016/j.chom.2012.10.011
PG 12
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 046KY
UT WOS:000311765100011
PM 23159058
ER
PT J
AU Fiskus, W
Rao, R
Balusu, R
Ganguly, S
Tao, JG
Sotomayor, E
Mudunuru, U
Smith, JE
Hembruff, SL
Atadja, P
Marquez, VE
Bhalla, K
AF Fiskus, Warren
Rao, Rekha
Balusu, Ramesh
Ganguly, Siddhartha
Tao, Jianguo
Sotomayor, Eduardo
Mudunuru, Uma
Smith, Jacqueline E.
Hembruff, Stacey L.
Atadja, Peter
Marquez, Victor E.
Bhalla, Kapil
TI Superior Efficacy of a Combined Epigenetic Therapy against Human Mantle
Cell Lymphoma Cells
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID GROUP PROTEIN EZH2; HISTONE DEACETYLASE INHIBITORS; POLYCOMB-GROUP
PROTEINS; ACUTE-LEUKEMIA CELLS; DNA METHYLATION; HEMATOLOGICAL
MALIGNANCIES; METHYLTRANSFERASE EZH2; GENE-EXPRESSION; CANCER;
OVEREXPRESSION
AB Purpose: A deregulated epigenome contributes to the transformed phenotype of mantle cell lymphoma (MCL). This involves activity of the polycomb repressive complex (PRC) 2, containing three core proteins, EZH2, SUZ12, and EED, in which the SET domain of EZH2 mediates the histone methyltransferase activity. We determined the effects of 3-deazaneplanocin A (DZNep), an S-adenosylhomocysteine hydrolase inhibitor, and/or pan-histone deacetylase inhibitor panobinostat (PS) on cultured and primary MCL cells.
Experimental Design: Following treatment with DZNep and/or PS, apoptosis and the levels and activity of EZH2 and PRC2 proteins in cultured and primary MCL cells were determined.
Results: Treatment with DZNep depleted EZH2, SUZ12, and 3MeK27H3 in the cultured human MCL cells. DZNep also increased expression of p21, p27, and FBXO32, whereas it depleted Cyclin D1 and Cyclin E1 levels in MCL cells. In addition, DZNep treatment induced cell-cycle arrest and apoptosis in cultured and primary MCL cells. Furthermore, as compared with treatment with each agent alone, cotreatment with DZNep and PS caused greater depletion of EZH2, SUZ12, 3MeK27H3, and Cyclin D1 levels, whereas it induced greater expression of FBXO32, p16, p21, and p27. Combined treatment with DZNep and PS synergistically induced apoptosis of cultured and primary MCL cells while relatively sparing normal CD34 + cells. Cotreatment with DZNep and PS also caused significantly greater inhibition of tumor growth of JeKo-1 xenografts in NOD/SCID mice.
Conclusions: These preclinical in vitro and in vivo findings show that cotreatment with DZNep and PS is an active combined epigenetic therapy worthy of further in vivo testing against MCL. Clin Cancer Res; 18(22); 6227-38. (C)2012 AACR.
C1 [Fiskus, Warren; Rao, Rekha; Balusu, Ramesh; Ganguly, Siddhartha; Mudunuru, Uma; Smith, Jacqueline E.; Hembruff, Stacey L.; Bhalla, Kapil] Univ Kansas, Ctr Canc, Kansas City, KS 66160 USA.
[Tao, Jianguo; Sotomayor, Eduardo] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Atadja, Peter] Novartis Inst Biomed Res Inc, Cambridge, MA USA.
[Marquez, Victor E.] NIH, Bethesda, MD 20892 USA.
RP Bhalla, K (reprint author), Univ Kansas, Ctr Canc, 3901 Rainbow Blvd,4030 Robinson,MS 1027, Kansas City, KS 66160 USA.
EM kbhalla@kumc.edu
FU Novartis Pharmaceuticals
FX K.N. Bhalla: commercial research grant and honoraria of speakers' bureau
from Novartis Pharmaceuticals. No potential conflicts of interest were
disclosed by the other authors.
NR 50
TC 28
Z9 29
U1 0
U2 5
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 2012
VL 18
IS 22
BP 6227
EP 6238
DI 10.1158/1078-0432.CCR-12-0873
PG 12
WC Oncology
SC Oncology
GA 050AC
UT WOS:000312023800017
PM 22932665
ER
PT J
AU Chahal, H
Backlund, JYC
Cleary, PA
Lachin, JM
Polak, JF
Lima, JAC
Bluemke, DA
AF Chahal, Harjit
Backlund, Jye-Yu C.
Cleary, Patricia A.
Lachin, John M.
Polak, Joseph F.
Lima, Joao A. C.
Bluemke, David A.
CA DCCT EDIC Res Grp
TI Relation Between Carotid Intima-Media Thickness and Left Ventricular
Mass in Type 1 Diabetes Mellitus (from the Epidemiology of Diabetes
Interventions and Complications [EDIC] Study)
SO AMERICAN JOURNAL OF CARDIOLOGY
LA English
DT Article
ID SECONDARY HYPERTENSION; ARTERY; GEOMETRY; TRIAL
AB Type 1 diabetes mellitus (DM) is associated with early atherosclerosis and increased cardiovascular mortality. The relation between carotid intima-media thickness (cIMT), a marker of subclinical atherosclerosis, and left ventricular (LV) mass, an independent predictor of cardiovascular morbidity, has not been previously studied in type 1 DM. The Epidemiology of Diabetes Interventions and Complications (EDIC) study is a multicenter observational study designed to follow up the Diabetes Control and Complications Trial (DCCT) cohort. LV mass was measured with cardiac magnetic resonance imaging at EDIC year 15 and common cIMT was assessed using B-mode ultrasound at EDIC year 12. Multivariable linear regression models were used to assess the relation between cIMT at year 12 and LV mass at year 15. In total 889 participants had cardiac magnetic resonance imaging and cIMT measurements available for these analyses. At EDIC year 15, mean age of the participants was 49 +/- 7 years, mean DM duration was 28 +/- 5 years, and 52% were men. Spearman correlation coefficient (r) between LV mass and cIMT was 0.33 (p <0.0001). After adjusting for basic covariates (machine, reader, age, and gender), a significant association between LV mass and cIMT (estimate 2.0 g/m(2) per 0.1-mm cIMT increment, p <0.0001) was observed. This association was decreased by the addition of systolic blood pressure, in particular 1.15 g/m(2) per 0.1-mm cIMT increment (p <0.0001), and to a lesser extent other cardiovascular disease risk factors. Furthermore, the relation observed between LV mass and cIMT was stronger in patients with shorter duration. of DM. In conclusion, cIMT was an independent predictor of larger LV mass in a well-characterized population with type 1 DM. (C) 2012 Published by Elsevier Inc. (Am J Cardiol 2012;110: 1534-1540)
C1 [Chahal, Harjit; Lima, Joao A. C.; Bluemke, David A.] Johns Hopkins Sch Med, Dept Radiol, Baltimore, MD 21205 USA.
[Chahal, Harjit; Lima, Joao A. C.; Bluemke, David A.] Johns Hopkins Sch Med, Dept Cardiol, Baltimore, MD USA.
[Backlund, Jye-Yu C.; Cleary, Patricia A.; Lachin, John M.] George Washington Univ, Ctr Biostat, Rockville, MD USA.
[Polak, Joseph F.] Tufts Univ, Sch Med, Tufts Med Ctr, Boston, MA 02111 USA.
[Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
RP Bluemke, DA (reprint author), Johns Hopkins Sch Med, Dept Radiol, Baltimore, MD 21205 USA.
EM bluemked@nih.gov
OI Lachin, John/0000-0001-9838-2841; Bluemke, David/0000-0002-8323-8086
FU Division of Diabetes Endocrinology and Metabolic Diseases of National
Institute of Diabetes and Digestive and Kidney Disease; National Eye
Institute; National Institute of Neurologic Disorders and Stroke;
Genetic Clinical Research Centers Program; Clinical Translational
Science Center Program, Bethesda, Maryland
FX Acknowledgement for The DCCT/EDIC has been supported by U01 Cooperative
Agreement grants (1983-93) and contracts (1994-present) with the
Division of Diabetes Endocrinology and Metabolic Diseases of the
National Institute of Diabetes and Digestive and Kidney Disease, and
through support by the National Eye Institute, the National Institute of
Neurologic Disorders and Stroke, the Genetic Clinical Research Centers
Program (1993-2007), and Clinical Translational Science Center Program
(2006-present), Bethesda, Maryland.
NR 17
TC 3
Z9 3
U1 0
U2 5
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 0002-9149
EI 1879-1913
J9 AM J CARDIOL
JI Am. J. Cardiol.
PD NOV 15
PY 2012
VL 110
IS 10
BP 1534
EP 1540
DI 10.1016/j.amjcard.2012.07.014
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 043DU
UT WOS:000311523900024
PM 22884107
ER
PT J
AU Mahavadi, P
Guenther, A
Gochuico, BR
AF Mahavadi, Poornima
Guenther, Andreas
Gochuico, Bernadette R.
TI Hermansky-Pudlak Syndrome Interstitial Pneumonia It's the Epithelium,
Stupid!
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Editorial Material
ID IDIOPATHIC PULMONARY-FIBROSIS; ENDOPLASMIC-RETICULUM STRESS; MOUSE
MODEL; APOPTOSIS; TYPE-2
C1 [Mahavadi, Poornima; Guenther, Andreas] Univ Giessen, Marburg Lung Ctr, Giessen, Germany.
[Guenther, Andreas] Agaples Lung Clin Waldhof Elgershausen, Greifenstein, Germany.
[Guenther, Andreas] German Ctr Lung Res, Giessen, Germany.
[Gochuico, Bernadette R.] NHGRI, NIH, Bethesda, MD 20892 USA.
RP Mahavadi, P (reprint author), Univ Giessen, Marburg Lung Ctr, Giessen, Germany.
NR 18
TC 2
Z9 2
U1 0
U2 1
PU AMER THORACIC SOC
PI NEW YORK
PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA
SN 1073-449X
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD NOV 15
PY 2012
VL 186
IS 10
BP 939
EP 940
DI 10.1164/rccm.201210-1771ED
PG 2
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 046LI
UT WOS:000311766100004
PM 23155210
ER
PT J
AU Vanden Berghe, W
Sabbe, L
Kaileh, M
Haegeman, G
Heyninck, K
AF Vanden Berghe, Wim
Sabbe, Linde
Kaileh, Mary
Haegeman, Guy
Heyninck, Karen
TI Molecular insight in the multifunctional activities of Withaferin A
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Review
DE Withaferin A; Carcinogenesis; Inflammation; Angiogenesis; Therapy
ID NF-KAPPA-B; BREAST-CANCER CELLS; FIBRILLARY ACIDIC PROTEIN; EHRLICH
ASCITES-CARCINOMA; ESTROGEN-RECEPTOR-ALPHA; HERBAL DRUG WITHAFERIN;
LIVER-X-RECEPTORS; WITHANIA-SOMNIFERA; IN-VIVO; DOWN-REGULATION
AB Herbal medicine which involves the use of plants for their medicinal value, dates as far back as the origin of mankind and demonstrates an array of applications including cardiovascular protection and anticancer activities, via antioxidant, anti-inflammatory and metabolic activities. Even today the popularity of medicinal herbs is still growing like in traditional medicines such as the Indian medicine, Ayurveda. One of the Ayurvedic medicinal plants is Withania somnifera Dunal, of which the important constituents are the withanolides. Among them, Withaferin A is one of the most bioactive compounds, exerting anti-inflammatory, pro-apoptotic but also anti-invasive and anti-angiogenic effects. In the context of modern pharmacology, a better insight in the underlying mechanism of the broad range of bioactivities exerted by Withaferin A is compulsory. Therefore, a lot of effort was made to explore the intracellular effects of Withaferin A and to characterize its target proteins. This review provides a decisive insight on the molecular basis of the health-promoting potential of Withaferin A. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Vanden Berghe, Wim; Sabbe, Linde; Haegeman, Guy; Heyninck, Karen] Univ Ghent, Dept Physiol, Lab Eukaryot Gene Express & Signal Transduct, B-9000 Ghent, Belgium.
[Vanden Berghe, Wim] Univ Antwerp, Dept Biomed Sci, Lab Prot Sci Prote & Epigenet Signalling PPES, Antwerp, Belgium.
[Kaileh, Mary] NIA, Cellular & Mol Biol Lab, NIH, Baltimore, MD 21224 USA.
RP Heyninck, K (reprint author), Univ Ghent, Dept Physiol, Lab Eukaryot Gene Express & Signal Transduct, Proeftuinstr 86, B-9000 Ghent, Belgium.
EM karen.heyninck@ugent.be
FU FLAVIOLA [FP7-KBBE-2008-2B]; Multiple Myeloma Research Foundation (MMRF)
FX This research is partially financial supported by FP7-KBBE-2008-2B grant
FLAVIOLA ("Targeted delivery of dietary flavanol for optimal human cell
function: Effects on cardiovascular health" (www.flaviola.org)) and the
Research Grant from the Multiple Myeloma Research Foundation (MMRF).
NR 116
TC 28
Z9 28
U1 2
U2 22
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 2012
VL 84
IS 10
SI SI
BP 1282
EP 1291
DI 10.1016/j.bcp.2012.08.027
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 047VV
UT WOS:000311870500008
PM 22981382
ER
PT J
AU Brenchley, JM
Vinton, C
Tabb, B
Hao, XP
Connick, E
Paiardini, M
Lifson, JD
Silvestri, G
Estes, JD
AF Brenchley, Jason M.
Vinton, Carol
Tabb, Brian
Hao, Xing Pei
Connick, Elizabeth
Paiardini, Mirko
Lifson, Jeffrey D.
Silvestri, Guido
Estes, Jacob D.
TI Differential infection patterns of CD4(+) T cells and lymphoid tissue
viral burden distinguish progressive and nonprogressive lentiviral
infections
SO BLOOD
LA English
DT Article
ID SIMIAN-IMMUNODEFICIENCY-VIRUS; AFRICAN-GREEN MONKEYS; NATURAL SIV HOSTS;
SOOTY MANGABEYS; IN-VIVO; HIV-1 INFECTION; RHESUS MACAQUES; REPLICATION;
VIREMIA; AIDS
AB Nonhuman primate natural hosts for simian immunodeficiency viruses (SIV) develop a nonresolving chronic infection but do not develop AIDS. Mechanisms to explain the nonprogressive nature of SIV infection in natural hosts that underlie maintained high levels of plasma viremia without apparent loss of target cells remain unclear. Here we used comprehensive approaches (ie, FACS sorting, quantitative RT-PCR, immunohistochemistry, and in situ hybridization) to study viral infection within subsets of peripheral blood and lymphoid tissue (LT) CD4(+) T cells in cohorts of chronically SIV-infected rhesus macaques (RMs), HIV-infected humans, and SIVsmm-infected sooty mangabeys (SMs). We find: (1) infection frequencies among CD4(+) T cells in chronically SIV-infected RMs are significantly higher than those in SIVsmm-infected SMs; (2) infected cells are found in distinct anatomic LT niches and different CD4(+) T-cell subsets in SIV-infected RMs and SMs, with infection patterns of RMs reflecting HIV infection in humans; (3) TFH cells are infected at higher frequencies in RMs and humans than in SMs; and (4) LT viral burden, including follicular dendritic cell deposition of virus, is increased in RMs and humans compared with SMs. These data provide insights into how natural hosts are able to maintain high levels of plasma viremia while avoiding development of immunodeficiency. (Blood. 2012; 120(20): 4172-4181)
C1 [Brenchley, Jason M.; Vinton, Carol] NIAID, Program Barrier Immun & Repair, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Tabb, Brian; Lifson, Jeffrey D.; Estes, Jacob D.] SAIC Frederick Inc, AIDS & Canc Virus Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Hao, Xing Pei] SAIC Frederick Inc, Pathol & Histotechnol Lab, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Connick, Elizabeth] Univ Colorado Denver, Div Infect Dis, Aurora, CO USA.
[Paiardini, Mirko; Silvestri, Guido] Emory Univ, Div Microbiol & Immunol, Yerkes Natl Primate Res Ctr, Atlanta, GA 30322 USA.
RP Brenchley, JM (reprint author), NIAID, Program Barrier Immun & Repair, Mol Microbiol Lab, NIH, 4 Ctr Dr,Rm 201,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM jbrenchl@mail.nih.gov; estesj@mail.nih.gov
FU Intramural National Institute of Allergy and Infectious Diseases,
National Institutes of Health program; National Cancer Institute,
National Institutes of Health [HHSN261200800001E, R01AI-084836]
FX This work was supported by the Intramural National Institute of Allergy
and Infectious Diseases, National Institutes of Health program, and the
National Cancer Institute, National Institutes of Health (contract
HHSN261200800001E and R01AI-084836, M.P.).
NR 54
TC 61
Z9 61
U1 3
U2 8
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 15
PY 2012
VL 120
IS 20
BP 4172
EP 4181
DI 10.1182/blood-2012-06-437608
PG 10
WC Hematology
SC Hematology
GA 044QN
UT WOS:000311637400012
PM 22990012
ER
PT J
AU Bergman, A
Ryden, A
Law, RJ
de Boer, J
Covaci, A
Alaee, M
Birnbaum, L
Petreas, M
Rose, M
Sakai, S
Van den Eede, N
van der Veen, I
AF Bergman, Ake
Ryden, Andreas
Law, Robin J.
de Boer, Jacob
Covaci, Adrian
Alaee, Mehran
Birnbaum, Linda
Petreas, Myrto
Rose, Martin
Sakai, Shinichi
Van den Eede, Nele
van der Veen, Ike
TI A novel abbreviation standard for organobromine, organochlorine and
organophosphorus flame retardants and some characteristics of the
chemicals
SO ENVIRONMENT INTERNATIONAL
LA English
DT Review
DE Brominated flame retardants; Chlorinated flame retardants; Phosphorus
flame retardants; Nomenclature; Abbreviations; Physico-chemical
properties
ID POLYCHLORINATED-BIPHENYLS; ENVIRONMENT; TRENDS; DIPHENYLETHERS;
METABOLITES
AB Ever since the interest in organic environmental contaminants first emerged 50 years ago, there has been a need to present discussion of such chemicals and their transformation products using simple abbreviations so as to avoid the repetitive use of long chemical names. As the number of chemicals of concern has increased, the number of abbreviations has also increased dramatically, sometimes resulting in the use of different abbreviations for the same chemical. In this article, we propose abbreviations for flame retardants (FRs) substituted with bromine or chlorine atoms or including a functional group containing phosphorus, i.e. BFRs, CFRs and PFRs, respectively. Due to the large number of halogenated and organophosphorus FRs, it has become increasingly important to develop a strategy for abbreviating the chemical names of FRs. In this paper, a two step procedure is proposed for deriving practical abbreviations (PRABs) for the chemicals discussed. In the first step, structural abbreviations (STABs) are developed using specific STAB criteria based on the FR structure. However, since several of the derived STABs are complicated and long, we propose instead the use of PRABs. These are, commonly, an extract of the most essential part of the STAB, while also considering abbreviations previously used in the literature. We indicate how these can be used to develop an abbreviation that can be generally accepted by scientists and other professionals involved in FR related work. Tables with PRABs and STABs for BFRs, CFRs and PERs are presented, including CAS (Chemical Abstract Service) numbers, notes of abbreviations that have been used previously, CA (Chemical Abstract) name, common names and trade names, as well as some fundamental physicochemical constants. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Bergman, Ake; Ryden, Andreas] Stockholm Univ, Dept Mat & Environm Chem, Environm Chem Unit, SE-10691 Stockholm, Sweden.
[Law, Robin J.] Cefas Lowestoft Lab, Ctr Environm Fisheries & Aquaculture Sci, Lowestoft NR33 OHT, Suffolk, England.
[de Boer, Jacob; van der Veen, Ike] Vrije Univ Amsterdam, Inst Environm Studies, NL-1081 HV Amsterdam, Netherlands.
[Covaci, Adrian; Van den Eede, Nele] Univ Antwerp, Toxicol Ctr, B-2610 Antwerp, Belgium.
[Alaee, Mehran] Environm Canada, Canada Ctr Inland Waters, Natl Water Res Inst, Burlington, ON L7R 4A6, Canada.
[Birnbaum, Linda] NIEHS, Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
[Petreas, Myrto] Calif Dept Tox Subst Control, Environm Chem Lab, Berkeley, CA 94710 USA.
[Rose, Martin] Food & Environm Res Agcy, York YO41 1LZ, N Yorkshire, England.
[Sakai, Shinichi] Kyoto Univ, Environm Preservat Res Ctr, Kyoto, Japan.
RP Bergman, A (reprint author), Stockholm Univ, Dept Mat & Environm Chem, Environm Chem Unit, SE-10691 Stockholm, Sweden.
EM ake.bergman@mmk.su.se
RI Covaci, Adrian/A-9058-2008; van der veen, ike/B-7228-2014; de Boer,
Jacob/L-5094-2013;
OI Covaci, Adrian/0000-0003-0527-1136; de Boer, Jacob/0000-0001-6949-4828;
van der Veen, ike/0000-0003-0237-093X; Van den Eede,
Nele/0000-0002-0198-6591; Rose, Martin/0000-0001-7071-180X
FU Flanders Research Foundation (FWO); Stockholm University; Stockholm
University's Strategic Marine Environmental Research Funds through the
Baltic Ecosystem Adaptive Management (BEAM)
FX NVDE and AC acknowledge PhD and post-doctoral fellowships from the
Flanders Research Foundation (FWO). AR acknowledges faculty funding from
Stockholm University and Stockholm University's Strategic Marine
Environmental Research Funds through the Baltic Ecosystem Adaptive
Management (BEAM). The opinions expressed here are those of the authors
and do not necessarily reflect the views of the California Department of
Toxic Substances Control, or of NIEHS, NIH, or the U.S. Government.
NR 45
TC 110
Z9 114
U1 26
U2 191
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0160-4120
J9 ENVIRON INT
JI Environ. Int.
PD NOV 15
PY 2012
VL 49
BP 57
EP 82
DI 10.1016/j.envint.2012.08.003
PG 26
WC Environmental Sciences
SC Environmental Sciences & Ecology
GA 044DV
UT WOS:000311600500008
PM 22982223
ER
PT J
AU Mason, RP
Ganini, D
Ranguelova, K
Bonini, MG
AF Mason, Ronald P.
Ganini, Douglas
Ranguelova, Kalina
Bonini, Marcelo G.
TI Two hypotheses for the oxidation of SOD1-Cu(I)
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Letter
ID CU,ZN-SUPEROXIDE DISMUTASE; HYDROGEN-PEROXIDE; PEROXYMONOCARBONATE;
MECHANISM; KINETICS
C1 [Mason, Ronald P.; Ganini, Douglas; Ranguelova, Kalina] NIEHS, Lab Pharmacol & Toxicol, NIH, Res Triangle Pk, NC 27709 USA.
[Bonini, Marcelo G.] Univ Illinois, Dept Med, Cardiol Sect, Chicago, IL USA.
[Bonini, Marcelo G.] Univ Illinois, Dept Pharmacol, Chicago, IL USA.
RP Mason, RP (reprint author), NIEHS, Lab Pharmacol & Toxicol, NIH, MD F0-02,POB 12233, Res Triangle Pk, NC 27709 USA.
EM mason4@niehs.nih.gov
NR 7
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 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD NOV 15
PY 2012
VL 53
IS 10
BP 1991
EP 1992
DI 10.1016/j.freeradbiomed.2012.10.524
PG 2
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 040MZ
UT WOS:000311328300019
PM 23137624
ER
PT J
AU Jeang, KT
AF Jeang, Kuan-Teh
TI Highlights, predictions, and changes
SO RETROVIROLOGY
LA English
DT Editorial Material
ID HIV-1; RESTRICTION
AB Recent literature highlights at Retrovirology are described. Predictions are made regarding "hot" retrovirology research trends for the coming year based on recent journal access statistics. Changes in Retrovirology editor and the frequency of the Retrovirology Prize are announced.
C1 NIH, Bethesda, MD 20892 USA.
RP Jeang, KT (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
EM kjeang@nih.gov
FU Intramural NIH HHS
NR 13
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PD NOV 15
PY 2012
VL 9
AR 96
DI 10.1186/1742-4690-9-96
PG 2
WC Virology
SC Virology
GA 046DH
UT WOS:000311745200001
PM 23153244
ER
PT J
AU Morgan, HP
Walsh, MJ
Blackburn, EA
Wear, MA
Boxer, MB
Shen, M
Veith, H
McNae, IW
Nowicki, MW
Michels, PAM
Auld, DS
Fothergill-Gilmore, LA
Walkinshaw, MD
AF Morgan, Hugh P.
Walsh, Martin J.
Blackburn, Elizabeth A.
Wear, Martin A.
Boxer, Matthew B.
Shen, Min
Veith, Henrike
McNae, Iain W.
Nowicki, Matthew W.
Michels, Paul A. M.
Auld, Douglas S.
Fothergill-Gilmore, Linda A.
Walkinshaw, Malcolm D.
TI A new family of covalent inhibitors block nucleotide binding to the
active site of pyruvate kinase
SO BIOCHEMICAL JOURNAL
LA English
DT Article
DE covalent inhibitor; Leishmania mexicana; lysine covalent modification;
nucleotide binding; pyruvate kinase; saccharin analogue
ID FORM TRYPANOSOMA-BRUCEI; GLYCOLYTIC-ENZYMES; DEFICIENCY; ADENOSINE;
DESIGN; TARGET; TERMS; DRUGS
AB PYK (pyruvate kinase) plays a central role in the metabolism of many organisms and cell types, but the elucidation of the details of its function in a systems biology context has been hampered by the lack of specific high-affinity small-molecule inhibitors. High-throughput screening has been used to identify a family of saccharin derivatives which inhibit LmPYK (Leishmania mexicana PYK) activity in a time- (and dose-) dependent manner, a characteristic of irreversible inhibition. The crystal structure of DBS {4-[(1,1-dioxo-1,2-benzothiazol-3-yl)sulfanyl]benzoic acid} complexed with LmPYK shows that the saccharin moiety reacts with an active-site lysine residue (Lys(335)), forming a covalent bond and sterically hindering the binding of ADP/ATP. Mutation of the lysine residue to an arginine residue eliminated the effect of the inhibitor molecule, providing confirmation of the proposed inhibitor mechanism. This lysine residue is conserved in the active sites of the four human PYK isoenzymes, which were also found to be irreversibly inhibited by DBS. X-ray structures of PYK isoforms show structural differences at the DBS-binding pocket, and this covalent inhibitor of PYK provides a chemical scaffold for the design of new families of potentially isoform-specific irreversible inhibitors.
C1 [Morgan, Hugh P.; Blackburn, Elizabeth A.; Wear, Martin A.; McNae, Iain W.; Nowicki, Matthew W.; Fothergill-Gilmore, Linda A.; Walkinshaw, Malcolm D.] Univ Edinburgh, Sch Biol Sci, Ctr Translat & Chem Biol, Edinburgh EH9 3JR, Midlothian, Scotland.
[Walsh, Martin J.; Boxer, Matthew B.; Shen, Min; Veith, Henrike; Auld, Douglas S.] NHGRI, Chem Genom Ctr, Ctr Translat Therapeut, NIH, Rockville, MD 20850 USA.
[Michels, Paul A. M.] Catholic Univ Louvain, Biochem Lab, B-1200 Brussels, Belgium.
[Michels, Paul A. M.] Catholic Univ Louvain, Res Unit Trop Dis, de Duve Inst, B-1200 Brussels, Belgium.
RP Walkinshaw, MD (reprint author), Univ Edinburgh, Sch Biol Sci, Ctr Translat & Chem Biol, Michael Swann Bldg,Kings Bldg,Mayfield Rd, Edinburgh EH9 3JR, Midlothian, Scotland.
EM m.walkinshaw@ed.ac.uk
RI Michels, Paul/A-5637-2009;
OI walkinshaw, malcolm/0000-0001-5955-9325
FU Molecular Libraries Initiative of the National Institutes of Health
Roadmap for Medical Research; National Human Genome Research Institute,
National Institutes of Health; Medical Research Council; European
Commission through its INCO-DEV programme; Wellcome Trust; Biotechnology
and Biological Sciences Research Council
FX This work was supported, in part, by the Molecular Libraries Initiative
of the National Institutes of Health Roadmap for Medical Research and
the Intramural Research Program of the National Human Genome Research
Institute, National Institutes of Health. Additional funding was from
the Medical Research Council, and the European Commission through its
INCO-DEV programme. The Centre for Translational and Chemical Biology
and the Edinburgh Protein Production Facility are funded by the Wellcome
Trust and the Biotechnology and Biological Sciences Research Council.
NR 25
TC 8
Z9 8
U1 0
U2 18
PU PORTLAND PRESS LTD
PI LONDON
PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND
SN 0264-6021
J9 BIOCHEM J
JI Biochem. J.
PD NOV 15
PY 2012
VL 448
BP 67
EP 72
DI 10.1042/BJ20121014
PN 1
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 042HP
UT WOS:000311462600007
PM 22906073
ER
PT J
AU Triquigneaux, MM
Ehrenshaft, M
Roth, E
Silman, I
Ashani, Y
Mason, RP
Weiner, L
Deterding, LJ
AF Triquigneaux, Mathilde M.
Ehrenshaft, Marilyn
Roth, Esther
Silman, Israel
Ashani, Yakov
Mason, Ronald P.
Weiner, Lev
Deterding, Leesa J.
TI Targeted oxidation of Torpedo californica acetylcholinesterase by
singlet oxygen: identification of N-formylkynurenine tryptophan
derivatives within the active-site gorge of its complex with the
photosensitizer Methylene Blue
SO BIOCHEMICAL JOURNAL
LA English
DT Article
DE acetylcholinesterase (AChE); active-site gorge; mass spectrometry;
N-formylkynurenine; singlet oxygen; site-specific photo-oxidation
ID TANDEM MASS-SPECTROMETRY; IMMUNOLOGICAL DETECTION; PEPTIDES; BINDING;
RESIDUES; MS/MS
AB The principal role of AChE (acetylcholinesterase) is termination of impulse transmission at cholinergic synapses by rapid hydrolysis of the neurotransmitter acetylcholine. The active site of AChE is near the bottom of a long and narrow gorge lined with aromatic residues. It contains a CAS (catalytic 'anionic' subsite) and a second PAS (peripheral 'anionic' site), the gorge mouth, both of which bind acetylcholine via pi-cation interactions, primarily with two conserved tryptophan residues. It was shown previously that generation of O-1(2) by illumination of MB (Methylene Blue) causes irreversible inactivation of TcAChE (Torpedo californica AChE), and suggested that photo-oxidation of tryptophan residues might be responsible. In the present study, structural modification of the TcAChE tryptophan residues induced by MB-sensitized oxidation was investigated using anti-N-formylkynurenine antibodies and MS. From these analyses, we determined that N-formylkynurenine derivatives were specifically produced from Trp(84) and Trp(279), present at the CAS and PAS respectively. Peptides containing these two oxidized tryptophan residues were not detected when the competitive inhibitors, edrophonium and propidium (which should displace MB from the gorge) were present during illumination, in agreement with their efficient protection against the MB-induced photo-inactivation. Thus the bound MB elicited selective action of O-1(2), on the tryptophan residues facing on to the water-filled active-site gorge. The findings of the present study thus demonstrate the localized action and high specificity of MB-sensitized photo-oxidation of TcAChE, as well as the value of this enzyme as a model system for studying the mechanism of action and specificity of photosensitizing agents.
C1 [Triquigneaux, Mathilde M.; Ehrenshaft, Marilyn; Mason, Ronald P.] NIEHS, Lab Toxicol & Pharmacol, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
[Roth, Esther; Silman, Israel; Ashani, Yakov] Weizmann Inst Sci, Dept Neurobiol, IL-76100 Rehovot, Israel.
[Weiner, Lev] Weizmann Inst Sci, Dept Chem Res Support, IL-76100 Rehovot, Israel.
[Deterding, Leesa J.] NIEHS, Struct Biol Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
RP Triquigneaux, MM (reprint author), NIEHS, Lab Toxicol & Pharmacol, NIH, DHHS, POB 12233,MD F0-03, Res Triangle Pk, NC 27709 USA.
EM triquigneauxm@mail.nih.gov
FU NIH (National Institutes of Health), National Institutes of
Environmental Health Sciences [ES050139, ES050171]
FX This work was supported by the Intramural Research Program of the NIH
(National Institutes of Health), National Institutes of Environmental
Health Sciences [projects ES050139 and ES050171].
NR 28
TC 6
Z9 6
U1 5
U2 24
PU PORTLAND PRESS LTD
PI LONDON
PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND
SN 0264-6021
J9 BIOCHEM J
JI Biochem. J.
PD NOV 15
PY 2012
VL 448
BP 83
EP 91
DI 10.1042/BJ20120992
PN 1
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 042HP
UT WOS:000311462600009
PM 22888904
ER
PT J
AU Cunningham, MD
Gause, M
Cheng, YZ
Noyes, A
Dorsett, D
Kennison, JA
Kassis, JA
AF Cunningham, Melissa D.
Gause, Maria
Cheng, Yuzhong
Noyes, Amanda
Dorsett, Dale
Kennison, James A.
Kassis, Judith A.
TI Wapl antagonizes cohesin binding and promotes Polycomb-group silencing
in Drosophila
SO DEVELOPMENT
LA English
DT Article
DE Cohesin; Polycomb; Gene expression
ID TRITHORAX GROUP PROTEINS; RESPONSE ELEMENTS; ENGRAILED GENE; HOMEOTIC
GENE; NIPPED-B; MELANOGASTER; CHROMOSOME; ASSOCIATION; MECHANISMS;
REGULATORS
AB Wapl protein regulates binding of the cohesin complex to chromosomes during interphase and helps remove cohesin from chromosomes at mitosis. We isolated a dominant mutation in wapl (wapl(AG)) in a screen for mutations that counteract silencing mediated by an engrailed Polycomb-group response element. wapl(AG) hemizygotes die as pharate adults and have an extra sex combs phenotype characteristic of males with mutations in Polycomb-group (PcG) genes. The wapl gene encodes two proteins, a long form and a short form. wapl(AG) introduces a stop codon at amino acid 271 of the long form and produces a truncated protein. The expression of a transgene encoding the truncated Wapl-AG protein causes an extra-sex-comb phenotype similar to that seen in the wapl(AG) mutant. Mutations in the cohesin-associated genes Nipped-B and pds5 suppress and enhance wapl(AG) phenotypes, respectively. A Pds5-Wapl complex (releasin) removes cohesin from DNA, while Nipped-B loads cohesin. This suggests that Wapl-AG might exert its effects through changes in cohesin binding. Consistent with this model, Wapl-AG was found to increase the stability of cohesin binding to polytene chromosomes. Our data suggest that increasing cohesin stability interferes with PcG silencing at genes that are co-regulated by cohesin and PcG proteins.
C1 [Cunningham, Melissa D.; Cheng, Yuzhong; Noyes, Amanda; Kennison, James A.; Kassis, Judith A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
[Gause, Maria; Dorsett, Dale] St Louis Univ, Sch Med, Edward A Doisy Dept Biochem & Mol Biol, St Louis, MO 63104 USA.
RP Kassis, JA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
EM jk14p@nih.gov
OI Kassis, Judith/0000-0001-9268-3213; Dorsett, Dale/0000-0002-0507-2762
FU National Institutes of Health (NIH) [R01 GM055683]; National Institute
of Child Health and Human Development, NIH
FX This research was supported by the National Institutes of Health (NIH)
[R01 GM055683 to D. D. and M. G.] and by the Intramural Research Program
of the National Institute of Child Health and Human Development, NIH.
Deposited in PMC for release after 12 months.
NR 31
TC 14
Z9 14
U1 0
U2 8
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 2012
VL 139
IS 22
BP 4172
EP 4179
DI 10.1242/dev.084566
PG 8
WC Developmental Biology
SC Developmental Biology
GA 028OZ
UT WOS:000310433200010
PM 23034634
ER
PT J
AU Okamura, D
Maeda, I
Taniguchi, H
Tokitake, Y
Ikeda, M
Ozato, K
Mise, N
Abe, K
Noce, T
Belmonte, JCI
Matsui, Y
AF Okamura, Daiji
Maeda, Ikuma
Taniguchi, Hirofumi
Tokitake, Yuko
Ikeda, Makiko
Ozato, Keiko
Mise, Nathan
Abe, Kuniya
Noce, Toshiaki
Izpisua Belmonte, Juan Carlos
Matsui, Yasuhisa
TI Cell cycle gene-specific control of transcription has a critical role in
proliferation of primordial germ cells
SO GENES & DEVELOPMENT
LA English
DT Article
DE primordial germ cell; CDK inhibitor; transcription; P-TEFb; 7SK snRNP;
Larp7
ID BROMODOMAIN PROTEIN BRD4; P-TEFB; MOUSE EMBRYOS; ELONGATION; MICE;
EXPRESSION; PROGRESSION; REGULATORS; COMPONENT; CHROMATIN
AB Transcription elongation is stimulated by positive transcription elongation factor b (P-TEFb), for which activity is repressed in the 7SK small nuclear ribonucleoprotein (7SK snRNP) complex. We show here a critical role of 7SK snRNP in growth control of primordial germ cells (PGCs). The expression of p15(INK4b), a cyclin-dependent kinase inhibitor (CDKI) gene, in PGCs is selectively activated by P-TEFb and its recruiting molecule, Brd4, when the amount of active P-TEFb is increased due to reduction of the 7SK snRNP, and PGCs consequently undergo growth arrest. These results indicate that CDKI gene-specific control of transcription by 7SK snRNP plays a pivotal role in the maintenance of PGC proliferation.
C1 [Okamura, Daiji; Izpisua Belmonte, Juan Carlos] Salk Inst Biol Studies, Gene Express Lab, La Jolla, CA 92037 USA.
[Okamura, Daiji; Maeda, Ikuma; Taniguchi, Hirofumi; Tokitake, Yuko; Ikeda, Makiko; Matsui, Yasuhisa] Tohoku Univ, Cell Resource Ctr Biomed Res, Inst Dev Aging & Canc, Sendai, Miyagi 9808575, Japan.
[Ozato, Keiko] NICHHD, NIH, Lab Mol Growth Regulat, Bethesda, MD 20892 USA.
[Mise, Nathan; Abe, Kuniya] RIKEN, BioResource Ctr, Tsukuba, Ibaraki 3050074, Japan.
[Noce, Toshiaki] Keio Univ, Sch Med, Dept Physiol, Tokyo 1130021, Japan.
[Izpisua Belmonte, Juan Carlos] Ctr Regenerat Med Barcelona, Barcelona 08003, Spain.
RP Belmonte, JCI (reprint author), Salk Inst Biol Studies, Gene Express Lab, 10010 N Torrey Pines Rd, La Jolla, CA 92037 USA.
EM belmonte@salk.edu; ymatsui@idac.tohoku.ac.jp
RI noce, toshiaki/L-1739-2013
FU Ministry of Education, Culture, Sports, Science, and Technology of Japan
FX We are grateful to Dr. Anup Dey for the antibody recognizing Brd4, Dr.
Shin-ichiro Chuma for the antibodies recognizing Scp3 and TDRD1, Dr.
Shinya Yamanaka for the antibody recognizing Dnmt3L, and Dr. Takeshi
Egawa for helpful advice on the experiments. Y.M. was supported by
Grants-in-Aid for Scientific Research from the Ministry of Education,
Culture, Sports, Science, and Technology of Japan.
NR 34
TC 9
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U1 2
U2 12
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 0890-9369
J9 GENE DEV
JI Genes Dev.
PD NOV 15
PY 2012
VL 26
IS 22
BP 2477
EP 2482
DI 10.1101/gad.202242.112
PG 6
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA 039VS
UT WOS:000311275800005
PM 23154982
ER
PT J
AU Liu, SY
Chow, HM
Xu, YS
Erkkinen, MG
Swett, KE
Eagle, MW
Rizik-Baer, DA
Braun, AR
AF Liu, Siyuan
Chow, Ho Ming
Xu, Yisheng
Erkkinen, Michael G.
Swett, Katherine E.
Eagle, Michael W.
Rizik-Baer, Daniel A.
Braun, Allen R.
TI Neural Correlates of Lyrical Improvisation: An fMRI Study of Freestyle
Rap
SO SCIENTIFIC REPORTS
LA English
DT Article
ID MEDIAL FRONTAL-CORTEX; PREFRONTAL CORTEX; COGNITIVE CONTROL; MACAQUE
MONKEY; MOTOR AREAS; GENERATION; BRAIN; ORGANIZATION; PERFORMANCE;
DECISIONS
AB The neural correlates of creativity are poorly understood. Freestyle rap provides a unique opportunity to study spontaneous lyrical improvisation, a multidimensional form of creativity at the interface of music and language. Here we use functional magnetic resonance imaging to characterize this process. Task contrast analyses indicate that improvised performance is characterized by dissociated activity in medial and dorsolateral prefrontal cortices, providing a context in which stimulus-independent behaviors may unfold in the absence of conscious monitoring and volitional control. Connectivity analyses reveal widespread improvisation-related correlations between medial prefrontal, cingulate motor, perisylvian cortices and amygdala, suggesting the emergence of a network linking motivation, language, affect and movement. Lyrical improvisation appears to be characterized by altered relationships between regions coupling intention and action, in which conventional executive control may be bypassed and motor control directed by cingulate motor mechanisms. These functional reorganizations may facilitate the initial improvisatory phase of creative behavior.
C1 [Liu, Siyuan; Chow, Ho Ming; Xu, Yisheng; Erkkinen, Michael G.; Swett, Katherine E.; Braun, Allen R.] Nat Inst Deafness & Other Commun Disorders, NIH, Bethesda, MD USA.
RP Liu, SY (reprint author), Nat Inst Deafness & Other Commun Disorders, NIH, Bethesda, MD USA.
EM siyuan.liu@nih.gov
RI Liu, Siyuan/D-2227-2012
FU NIH intramural program
FX This study was funded by NIH intramural program. The authors thank
Steven Wise for critical discussions and comments on the manuscript. We
also thank the rap musicians who participated in the study.
NR 47
TC 38
Z9 38
U1 4
U2 40
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 15
PY 2012
VL 2
AR 834
DI 10.1038/srep00834
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 040RM
UT WOS:000311340600001
PM 23155479
ER
PT J
AU Portal-Nunez, S
Shankavaram, UT
Rao, M
Datrice, N
Atay, S
Aparicio, M
Camphausen, KA
Fernandez-Salguero, PM
Chang, H
Lin, PP
Schrump, DS
Garantziotis, S
Cuttitta, F
Zudaire, E
AF Portal-Nunez, Sergio
Shankavaram, Uma T.
Rao, Mahadev
Datrice, Nicole
Atay, Scott
Aparicio, Marta
Camphausen, Kevin A.
Fernandez-Salguero, Pedro M.
Chang, Han
Lin, Pinpin
Schrump, David S.
Garantziotis, Stavros
Cuttitta, Frank
Zudaire, Enrique
TI Aryl Hydrocarbon Receptor-Induced Adrenomedullin Mediates Cigarette
Smoke Carcinogenicity in Humans and Mice
SO CANCER RESEARCH
LA English
DT Article
ID POSSIBLE PROMOTION MECHANISM; LUNG-CANCER; AH-RECEPTOR; IN-VIVO;
ENDOMETRIAL CANCER; TUMOR ANGIOGENESIS; DIOXIN RECEPTOR;
GENE-EXPRESSION; UP-REGULATION; CELL-LINES
AB Cigarette smoking (CS) is a leading cause of death worldwide. The aryl hydrocarbon receptor (AHR) is partially responsible for tobacco-induced carcinogenesis although the underlying mechanisms involving early effector genes have yet to be determined. Here, we report that adrenomedullin (ADM) significantly contributes to the carcinogenicity of tobacco-activated AHR. CS and AHR activating ligands induced ADM in vitro and in vivo but not in AHR-deficient fibroblasts and mice. Ectopic transfection of AHR rescued ADM expression in AHR(-/-) fibroblasts whereas AHR blockage with siRNA in wild type cells significantly decreased ADM expression. AHR regulates ADM expression through two intronic xenobiotic response elements located close to the start codon in the ADM gene. Using tissue microarrays we showed that ADM and AHR were coupregulated in lung tumor biopsies from smoker patients. Microarray meta-analysis of 304 independent microarray experiments showed that ADM is elevated in smokers and smokers with cancer. In addition, ADM coassociated with a subset of AHR responsive genes and efficiently differentiated patients with lung cancer from nonsmokers. In a novel preclinical model of CS-induced tumor progression, host exposure to CS extracts significantly elevated tumor ADM although systemic treatment with the ADM antagonist NSC16311 efficiently blocked tobacco-induced tumor growth. In conclusion, ADM significantly contributes the carcinogenic effect of AHR and tobacco combustion products. We suggest that therapeutics targeting the AHR/ADM axis may be of clinical relevance in the treatment of tobacco-induced pulmonary malignancies. Cancer Res; 72(22); 5790-800. (C) 2012 AACR.
C1 [Zudaire, Enrique] NCI, Tumor Angiogenesis Sect, Mouse Canc Genet Program, NIH, Frederick, MD 21702 USA.
[Portal-Nunez, Sergio; Aparicio, Marta; Cuttitta, Frank; Zudaire, Enrique] NCI, Angiogenesis Core Facil, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Rao, Mahadev; Datrice, Nicole; Atay, Scott; Schrump, David S.] NCI, Sect Thorac Oncol, Surg Branch, NIH, Bethesda, MD 20892 USA.
[Fernandez-Salguero, Pedro M.] Univ Extremadura, Dept Bioquim & Biol Mol, Badajoz, Spain.
[Chang, Han] China Med Univ, China Med Univ Hosp, Dept Pathol, Shenyang, Peoples R China.
[Chang, Han] China Med Univ, Sch Med, Shenyang, Peoples R China.
[Lin, Pinpin] Natl Hlth Res Inst, Div Environm Hlth & Occupat Med, Miaoli, Taiwan.
[Garantziotis, Stavros] NIEHS, Lab Resp Biol, Res Triangle Pk, NC 27709 USA.
RP Zudaire, E (reprint author), NCI, Tumor Angiogenesis Sect, Mouse Canc Genet Program, NIH, POB B,Bldg 560,1050 Boyles St, Frederick, MD 21702 USA.
EM zudairee@mail.nih.gov
RI Lin, Pinpin/B-2668-2010; Portal-Nunez, Sergio/L-7391-2014; Cuttitta,
Frank/B-4758-2016; Garantziotis, Stavros/A-6903-2009;
OI Portal-Nunez, Sergio/0000-0003-0659-1545; Garantziotis,
Stavros/0000-0003-4007-375X; Fernandez-Salguero, Pedro
M./0000-0003-2839-5027
FU Intramural NIH HHS [ZIA ES102605-02, ZIA ES102605-03, ZIA ES102605-04,
Z99 CA999999, ZIA ES102605-05, ZIA ES102605-06, Z01 ES102605-01, ZIA
ES102605-07]
NR 51
TC 17
Z9 17
U1 1
U2 5
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 2012
VL 72
IS 22
BP 5790
EP 5800
DI 10.1158/0008-5472.CAN-12-0818
PG 11
WC Oncology
SC Oncology
GA 037YB
UT WOS:000311141300016
PM 22993405
ER
PT J
AU Wan, XL
Yeung, C
Kim, SY
Dolan, JG
Ngo, VN
Burkett, S
Khan, J
Staudt, LM
Helman, LJ
AF Wan, Xiaolin
Yeung, Choh
Kim, Su Young
Dolan, Joseph G.
Ngo, Vu N.
Burkett, Sandra
Khan, Javed
Staudt, Louis M.
Helman, Lee J.
TI Identification of FoxM1/Bub1b Signaling Pathway as a Required Component
for Growth and Survival of Rhabdomyosarcoma
SO CANCER RESEARCH
LA English
DT Article
ID PREMATURE CHROMATID SEPARATION; ONCOGENIC TRANSCRIPTION FACTOR; MOSAIC
VARIEGATED ANEUPLOIDY; MITOTIC-SPINDLE CHECKPOINT; BUBR1 INSUFFICIENCY;
CANCER; CELLS; ENDOREDUPLICATION; INSTABILITY; PROTEIN
AB We identified Bub1b as an essential element for the growth and survival of rhabdomyosarcoma (RMS) cells using a bar-coded, tetracycline-inducible short hairpin RNA (shRNA) library screen. Knockdown of Bub1b resulted in suppression of tumor growth in vivo, including the regression of established tumors. The mechanism by which this occurs is via postmitotic endoreduplication checkpoint and mitotic catastrophe. Furthermore, using a chromatin immunoprecipitation assay, we found that Bub1b is a direct transcriptional target of Forkhead Box M1 (FoxM1). Suppression of FoxM1 either by shRNA or the inhibitor siomycin A resulted in reduction of Bub1b expression and inhibition of cell growth and survival. These results show the important role of the Bub1b/FoxM1 pathway in RMS and provide potential therapeutic targets. Cancer Res; 72(22); 5889-99. (C) 2012 AACR.
C1 [Wan, Xiaolin; Helman, Lee J.] NCI, Mol Oncol Sect, Pediat Oncol Branch, CCR,CRC,NIH, Bethesda, MD 20892 USA.
[Burkett, Sandra] NCI, Oncogen Sect, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Ngo, Vu N.; Staudt, Louis M.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Khan, Javed] NCI, Comparat Mol Cytogenet Core Facil, NIH, Bethesda, MD 20892 USA.
RP Wan, XL (reprint author), NCI, Mol Oncol Sect, Pediat Oncol Branch, CCR,CRC,NIH, 1-3860,10 Ctr Dr, Bethesda, MD 20892 USA.
EM xiaolinw@mail.nih.gov; helmanl@nih.gov
RI Khan, Javed/P-9157-2014
OI Khan, Javed/0000-0002-5858-0488
FU Intramural NIH HHS [Z99 CA999999]
NR 44
TC 17
Z9 17
U1 0
U2 3
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 2012
VL 72
IS 22
BP 5889
EP 5899
DI 10.1158/0008-5472.CAN-12-1991
PG 11
WC Oncology
SC Oncology
GA 037YB
UT WOS:000311141300025
PM 23002205
ER
PT J
AU Qian, XL
Durkin, ME
Wang, DR
Tripathi, BK
Olson, L
Yang, XY
Vass, WC
Popescu, NC
Lowy, DR
AF Qian, Xiaolan
Durkin, Marian E.
Wang, Dunrui
Tripathi, Brajendra K.
Olson, Lyra
Yang, Xu-Yu
Vass, William C.
Popescu, Nicholas C.
Lowy, Douglas R.
TI Inactivation of the Dlc1 Gene Cooperates with Downregulation of
p15(INK4b) and p16(Ink4a), Leading to Neoplastic Transformation and Poor
Prognosis in Human Cancer
SO CANCER RESEARCH
LA English
DT Article
ID GTPASE-ACTIVATING PROTEIN; TUMOR-SUPPRESSOR; HEPATOCELLULAR-CARCINOMA;
EMBRYONIC-DEVELOPMENT; RAS TRANSFORMATION; CELL CARCINOMA; SH2 DOMAIN;
RHO; IDENTIFICATION; METASTASIS
AB The tumor suppressor gene deleted in liver cancer-1 (DLC1), which encodes a protein with strong RhoGAP (GTPase activating protein) activity and weak Cdc42GAP activity, is inactivated in various human malignancies. Following Dlc1 inactivation, mouse embryo fibroblasts (MEF) with a conditional Dlc1 knockout allele reproducibly underwent neoplastic transformation. In addition to inactivation of Dlc1 and increased activity of Rho and Cdc42, transformation depended on the subsequent decreased expression of the Cdk4/6 inhibitors p15(Ink4b) and p16(Ink4a) together with increased expression and activation of Cdk4/6. The level of expression of these cell-cycle regulatory genes was relevant to human tumors with low DLC1 expression. Analysis of publicly available annotated datasets of lung and colon cancer with gene expression microarray profiles indicated that, in pairwise comparisons, low DLC1 expression occurred frequently together (P < 0.01) with downregulation of p15(Ink4b) or p16(Ink4a) or upregulation of CDK4 or CDK6. In addition, an unfavorable prognosis (P < 0.05) was associated with low DLC1 and low p15(Ink4b) in lung cancer and colon cancer, low DLC1 and low p16(Ink4a) in lung cancer, low DLC1 and high CDK4 in lung cancer, and low DLC1 and high CDK6 in colon cancer. Thus, several genes and biochemical activities collaborate with the inactivation of DLC1 to give rise to cell transformation in MEFs, and the identified genes are relevant to human tumors with low DLC1 expression. Cancer Res; 72(22); 5900-11. (C) 2012 AACR.
C1 [Qian, Xiaolan; Tripathi, Brajendra K.; Olson, Lyra; Vass, William C.; Lowy, Douglas R.] NCI, Cellular Oncol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Durkin, Marian E.; Yang, Xu-Yu; Popescu, Nicholas C.] NCI, Expt Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Wang, Dunrui] W2MOTIF LLC, San Diego, CA USA.
RP Lowy, DR (reprint author), NCI, Cellular Oncol Lab, Ctr Canc Res, NIH, Bldg 37,Room 4106, Bethesda, MD 20892 USA.
EM Lowyd@mail.nih.gov
FU Intramural Research Program, NIH, National Cancer Institute; Center for
Cancer Research
FX This research was supported by the Intramural Research Program, NIH,
National Cancer Institute, and Center for Cancer Research.
NR 36
TC 12
Z9 14
U1 1
U2 7
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 2012
VL 72
IS 22
BP 5900
EP 5911
DI 10.1158/0008-5472.CAN-12-2368
PG 12
WC Oncology
SC Oncology
GA 037YB
UT WOS:000311141300026
PM 23010077
ER
PT J
AU Weaver, Z
Difilippantonio, S
Carretero, J
Martin, PL
El Meskini, R
Iacovelli, AJ
Gumprecht, M
Kulaga, A
Guerin, T
Schlomer, J
Baran, M
Kozlov, S
McCann, T
Mena, S
Al-Shahrour, F
Alexander, D
Wong, KK
Van Dyke, T
AF Weaver, Zoe
Difilippantonio, Simone
Carretero, Julian
Martin, Philip L.
El Meskini, Rajaa
Iacovelli, Anthony J.
Gumprecht, Michelle
Kulaga, Alan
Guerin, Theresa
Schlomer, Jerome
Baran, Maureen
Kozlov, Serguei
McCann, Thomas
Mena, Salvador
Al-Shahrour, Fatima
Alexander, Danny
Wong, Kwok-Kin
Van Dyke, Terry
TI Temporal Molecular and Biological Assessment of an Erlotinib-Resistant
Lung Adenocarcinoma Model Reveals Markers of Tumor Progression and
Treatment Response
SO CANCER RESEARCH
LA English
DT Article
ID OVARIAN-CANCER; CELL-GROWTH; THERAPY; PERTURBATION; GLUTATHIONE;
DISCOVERY; ONCOGENES; GLUTAMINE; PLASMA; MTOR
AB Patients with lung cancer with activating mutations in the EGF receptor (EGFR) kinase, who are treated long-term with tyrosine kinase inhibitors (TKI), often develop secondary mutations in EGFR associated with resistance. Mice engineered to develop lung adenocarcinomas driven by the human EGFR T790M resistance mutation are similarly resistant to the EGFR TKI erlotinib. By tumor volume endpoint analysis, these mouse tumors respond to BIBW 2992 (an irreversible EGFR/HER2 TKI) and rapamycin combination therapy. To correlate EGFR-driven changes in the lung with response to drug treatment, we conducted an integrative analysis of global transcriptome and metabolite profiling compared with quantitative imaging and histopathology at several time points during tumor progression and treatment. Responses to single-drug treatments were temporary, whereas combination therapy elicited a sustained response. During tumor development, metabolomic signatures indicated a shift to high anabolic activity and suppression of antitumor programs with 11 metabolites consistently present in both lung tissue and blood. Combination drug treatment reversed many of the molecular changes found in tumored lung. Data integration linking cancer signaling networks with metabolic activity identified key pathways such as glutamine and glutathione metabolism that signified response to single or dual treatments. Results from combination drug treatment suggest that metabolic transcriptional control through C-MYC and SREBP, as well as ELK1, NRF1, and NRF2, depends on both EGFR and mTORC1 signaling. Our findings establish the importance of kinetic therapeutic studies in preclinical assessment and provide in vivo evidence that TKI-mediated antiproliferative effects also manifest in specific metabolic regulation. Cancer Res; 72(22); 5921-33. (C) 2012 AACR.
C1 [Van Dyke, Terry] NCI, Mouse Canc Genet Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Weaver, Zoe; Difilippantonio, Simone; Martin, Philip L.; El Meskini, Rajaa; Iacovelli, Anthony J.; Gumprecht, Michelle; Kulaga, Alan; Guerin, Theresa; Schlomer, Jerome; Baran, Maureen; Kozlov, Serguei; Van Dyke, Terry] SAIC Frederick Inc, Ctr Adv Preclin Res, Frederick Natl Lab Canc Res, NCI, Frederick, MD USA.
[Carretero, Julian; Wong, Kwok-Kin] Harvard Univ, Brigham & Womens Hosp, Div Genet, Sch Med,Dept Med, Boston, MA 02115 USA.
[Al-Shahrour, Fatima] Harvard Univ, Brigham & Womens Hosp, Div Hematol, Sch Med,Dept Med, Boston, MA 02115 USA.
[Carretero, Julian; Wong, Kwok-Kin] Harvard Canc Ctr, Ludwig Ctr Dana Farber, Boston, MA USA.
[Mena, Salvador] Univ Valencia, Dept Physiol, E-46100 Burjassot, Spain.
[McCann, Thomas] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Al-Shahrour, Fatima] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Alexander, Danny] Metabolon Inc, Durham, NC USA.
RP Van Dyke, T (reprint author), NCI, Mouse Canc Genet Program, Frederick Natl Lab Canc Res, 1050 Boyles St, Frederick, MD 21702 USA.
EM vandyket@mail.nih.gov
RI Mena, Salvador/L-8780-2014; Carretero, Julian/N-5214-2014; Mena,
Salvador/F-6696-2016;
OI Mena, Salvador/0000-0002-6423-4741; Carretero,
Julian/0000-0001-7269-8506; wong, kwok kin/0000-0001-6323-235X
FU National Cancer Institute, Intramural Research Program, NIH
FX This research was supported with federal funds from the National Cancer
Institute, Intramural Research Program, NIH.
NR 35
TC 16
Z9 16
U1 1
U2 20
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 2012
VL 72
IS 22
BP 5921
EP 5933
DI 10.1158/0008-5472.CAN-12-0736
PG 13
WC Oncology
SC Oncology
GA 037YB
UT WOS:000311141300028
PM 22969147
ER
PT J
AU Pouliot, LM
Chen, YC
Bai, J
Guha, R
Martin, SE
Gottesman, MM
Hall, MD
AF Pouliot, Lynn M.
Chen, Yu-Chi
Bai, Jennifer
Guha, Rajarshi
Martin, Scott E.
Gottesman, Michael M.
Hall, Matthew D.
TI Cisplatin Sensitivity Mediated by WEE1 and CHK1 Is Mediated by miR-155
and the miR-15 Family
SO CANCER RESEARCH
LA English
DT Article
ID DNA-DAMAGING AGENTS; RESISTANT CELL-LINES; CANCER-CELLS;
MULTIDRUG-RESISTANCE; CHECKPOINT KINASE-1; REDUCED EXPRESSION;
BINDING-PROTEINS; DRUG-RESISTANCE; TARGETING BCL2; OVARIAN-CANCER
AB Resistance to platinum-based therapies arises by multiple mechanisms, including by alterations to cell-cycle kinases that mediate G(2)-M phase arrest. In this study, we conducted parallel high-throughput screens for microRNAs (miRNA) that could restore sensitivity to cisplatin-resistant cells, and we screened for kinases targeted by miRNAs that mediated cisplatin resistance. Overexpression of the cell-cycle kinases WEE1 and CHK1 occurred commonly in cisplatin-resistant cells. miRNAs in the miR-15/16/195/424/497 family were found to sensitize cisplatin-resistant cells to apoptosis by targeting WEE1 and CHK1. Loss-of-function and gain-of-function studies showed that miR-15 family members controlled the expression of WEE1 and CHK1. Supporting these results, we found that in the presence of cisplatin altering expression of miR-16 or related genes altered cell cycle distribution. Our findings reveal critical regulation of miRNAs and their cell-cycle-associated kinase targets in mediating resistance to cisplatin. Cancer Res; 72(22); 5945-55. (C) 2012 AACR.
C1 [Pouliot, Lynn M.; Bai, Jennifer; Gottesman, Michael M.; Hall, Matthew D.] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Pouliot, Lynn M.] Georgetown Univ, Dept Microbiol & Immunol, Washington, DC USA.
[Chen, Yu-Chi; Guha, Rajarshi; Martin, Scott E.] NIH, RNAi Screening Facil, Natl Ctr Adv Translat Sci, Rockville, MD USA.
RP Gottesman, MM (reprint author), NCI, Cell Biol Lab, Ctr Canc Res, NIH, 37 Convent Dr,Rm 2108, Bethesda, MD 20892 USA.
EM gottesmm@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute.
NR 43
TC 44
Z9 51
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 2012
VL 72
IS 22
BP 5945
EP 5955
DI 10.1158/0008-5472.CAN-12-1400
PG 11
WC Oncology
SC Oncology
GA 037YB
UT WOS:000311141300030
PM 22942255
ER
PT J
AU Chow, HY
Jubb, AM
Koch, JN
Jaffer, ZM
Stepanova, D
Campbell, DA
Duron, SG
O'Farrell, M
Cai, KQ
Klein-Szanto, AJP
Gutkind, JS
Hoeflich, KP
Chernoff, J
AF Chow, Hoi Yee
Jubb, Adrian M.
Koch, Jennifer N.
Jaffer, Zahara M.
Stepanova, Dina
Campbell, David A.
Duron, Sergio G.
O'Farrell, Marie
Cai, Kathy Q.
Klein-Szanto, Andres J. P.
Gutkind, J. Silvio
Hoeflich, Klaus P.
Chernoff, Jonathan
TI p21-Activated Kinase 1 Is Required for Efficient Tumor Formation and
Progression in a Ras-Mediated Skin Cancer Model
SO CANCER RESEARCH
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMAS; MEK INHIBITOR PD0325901; PAK PROTEIN-KINASES;
CONDITIONAL EXPRESSION; BREAST-CANCER; PD 0325901; IN-VITRO; K-RAS;
GROWTH; MUTATIONS
AB The RAS genes are the most commonly mutated oncogenes in human cancer and present a particular therapeutic dilemma, as direct targeting of Ras proteins by small molecules has proved difficult. Signaling pathways downstream of Ras, in particular Raf/Mek/Erk and PI3K/Akt/mTOR, are dominated by lipid and protein kinases that provide attractive alternate targets in Ras-driven tumors. As p21-activated kinase 1 (Pak1) has been shown to regulate both these signaling pathways and is itself upregulated in many human cancers, we assessed the role of Pak1 in Ras-driven skin cancer. In human squamous cell carcinoma (SCC), we found a strong positive correlation between advanced stage and grade and PAK1 expression. Using a mouse model of Kras-driven SCC, we showed that deletion of the mouse Pak1 gene led to markedly decreased tumorigenesis and progression, accompanied by near total loss of Erk and Akt activity. Treatment of Kras(G12D) mice with either of two distinct small molecule Pak inhibitors (PF3758309 and FRAX597) caused tumor regression and loss of Erk and Akt activity. Tumor regression was also seen in mice treated with a specific Mek inhibitor, but not with an Akt inhibitor. These findings establish Pak1 as a new target in KRAS-driven tumors and suggest a mechanism of action through the Erk, but not the Akt, signaling pathway. Cancer Res; 72(22); 5966-75. (C) 2012 AACR.
C1 [Chow, Hoi Yee; Koch, Jennifer N.; Jaffer, Zahara M.; Stepanova, Dina; Cai, Kathy Q.; Klein-Szanto, Andres J. P.; Chernoff, Jonathan] Fox Chase Canc Ctr, Canc Biol Program, Philadelphia, PA 19111 USA.
[Jubb, Adrian M.] Univ Oxford, Weatherall Inst Mol Med, Oxford, England.
[Hoeflich, Klaus P.] Genentech Inc, Dept Translat Oncol, San Francisco, CA 94080 USA.
[Campbell, David A.; Duron, Sergio G.; O'Farrell, Marie] Afraxis, La Jolla, CA USA.
[Gutkind, J. Silvio] Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD USA.
RP Chernoff, J (reprint author), Fox Chase Canc Ctr, Canc Biol Program, 333 Cottman Ave, Philadelphia, PA 19111 USA.
EM Jonathan.Chernoff@fccc.edu
RI Chernoff, Jonathan/I-7631-2014
OI Chernoff, Jonathan/0000-0002-4803-7836
FU NIH [R01 CA142928, R01 CA117884]; Fox Chase Cancer Center [P30
CA006927]; state of Pennsylvania
FX This work was supported by grants from the NIH to J. Chernoff (R01
CA142928 and R01 CA117884) and to the Fox Chase Cancer Center (P30
CA006927), as well as by an appropriation from the state of
Pennsylvania.
NR 43
TC 52
Z9 53
U1 1
U2 13
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD NOV 15
PY 2012
VL 72
IS 22
BP 5966
EP 5975
DI 10.1158/0008-5472.CAN-12-2246
PG 10
WC Oncology
SC Oncology
GA 037YB
UT WOS:000311141300032
PM 22983922
ER
PT J
AU Kim, HS
Woolard, K
Lai, C
Bauer, PO
Maric, D
Song, H
Li, AG
Kotliarova, S
Zhang, W
Fine, HA
AF Kim, Hong Sug
Woolard, Kevin
Lai, Chen
Bauer, Peter O.
Maric, Dragan
Song, Hua
Li, Aiguo
Kotliarova, Svetlana
Zhang, Wei
Fine, Howard A.
TI Gliomagenesis Arising from Pten- and Ink4a/Arf-Deficient Neural
Progenitor Cells Is Mediated by the p53-Fbxw7/Cdc4 Pathway, Which
Controls c-Myc
SO CANCER RESEARCH
LA English
DT Article
ID TUMOR-SUPPRESSOR GENE; CANCER STEM-CELLS; MALIGNANT ASTROCYTOMA;
INITIATING CELLS; IN-VIVO; DIFFERENTIATION; GLIOBLASTOMA; GLIOMA;
PROLIFERATION; PROTEIN
AB Glioblastoma multiforme is the most common type of primary malignant brain tumor and may arise from a cell with neural stem-like properties. Deregulation of the retinoblastoma, phosphoinositide-3 kinase (PI3K), and p53 pathways are molecular hallmarks of this disease. Recent work has shown that p53(-/-)Pten(-/-) mice form gliomas in a c-Myc-dependent manner. To explore the role of the INK4A/ARF locus and Pten deletions in gliomagenesis, we generated Pten(-/-)Ink4a/Arf(-/-) mouse neural stem cells (mNSC) and such cells were highly proliferative, self-renewing, relatively refractory to differentiation, and induced both low-and high-grade glioma formation in vivo. In contrast to p53(-/-)Pten(-/-) mNSCs, however, Pten(-/-)Ink4a/Arf(-/-) mNSCs do not express appreciable levels of c-Myc in vitro, although glioma stem cells derived from thesecells did. Sequencing of Pten(-/-)Ink4a/Arf(-/-) mNSC-derived tumors revealed spontaneous mutations in Tp53 in vivo with subsequent downregulation of Fbxw7. Expression of p53 mutants in Pten(-/-)Ink4a/Arf(-/-) mNSC or knockdown of Fbxw7 resulted in reexpression of c-Myc with enhanced Pten(-/-)Ink4a/Arf(-/-) mNSC tumorigenecity. We propose that p53 mutations contribute to gliomagenesis by both allowing the overexpression of c-Myc through downregulation of Fbxw7 and by protecting against c-Myc-induced apoptosis. Cancer Res; 72(22); 6065-75. (C) 2012 AACR.
C1 [Kim, Hong Sug; Woolard, Kevin; Lai, Chen; Bauer, Peter O.; Maric, Dragan; Song, Hua; Li, Aiguo; Kotliarova, Svetlana; Zhang, Wei; Fine, Howard A.] Natl Inst Neurol Disorders & Stroke, Neurooncol Branch, NCI, NIH, Bethesda, MD USA.
RP Fine, HA (reprint author), NYU, Langone Med Ctr, 522 1st Ave,Smilow 1101, New York, NY 10016 USA.
EM Howard.Fine@nyumc.org
FU Intramural Research Program of the NIH, National Cancer Institute;
Center for Cancer Research
FX This research was supported by grants from the Intramural Research
Program of the NIH, National Cancer Institute, and Center for Cancer
Research.
NR 35
TC 13
Z9 17
U1 0
U2 1
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 2012
VL 72
IS 22
BP 6065
EP 6075
DI 10.1158/0008-5472.CAN-12-2594
PG 11
WC Oncology
SC Oncology
GA 037YB
UT WOS:000311141300040
PM 22986743
ER
PT J
AU Popuri, V
Croteau, DL
Brosh, RM
Bohr, VA
AF Popuri, Venkateswarlu
Croteau, Deborah L.
Brosh, Robert M., Jr.
Bohr, Vilhelm A.
TI RECQ1 is required for cellular resistance to replication stress and
catalyzes strand exchange on stalled replication fork structures
SO CELL CYCLE
LA English
DT Article
DE strand exchange; RecQ helicases; DNA replication; chromosomal
condensation; RECQ1; RPA phosphorylation
ID INTERSTRAND CROSS-LINKS; DNA-REPLICATION; SUBSTRATE-SPECIFICITY;
ANNEALING ACTIVITIES; HOLLIDAY JUNCTIONS; HELICASE ACTIVITY;
ESCHERICHIA-COLI; BRANCH MIGRATION; HUMAN RECQ5-BETA; PROTEIN
AB RECQ1 is the most abundant of the five human RecQ helicases, but little is known about its biological significance. Recent studies indicate that RECQ1 is associated with origins of replication, suggesting a possible role in DNA replication. However, the functional role of RECQ1 at damaged or stalled replication forks is still unknown. Here, for the first time, we show that RECQ1 promotes strand exchange on synthetic stalled replication fork-mimicking structures and comparatively analyze RECQ1 with the other human RecQ helicases. RECQ1 actively unwinds the leading strand of the fork, similar to WRN, while RECQ4 and RECQ5 beta can only unwind the lagging strand of the replication fork. Human replication protein A modulates the strand exchange activity of RECQ1 and shifts the equilibrium more to the unwinding mode, an effect also observed for WRN. Stable depletion of RECQ1 affects cell proliferation and renders human cells sensitive to various DNA damaging agents that directly or indirectly block DNA replication fork progression. Consequently, loss of RECQ1 activates DNA damage response signaling, leads to hyper-phosphorylation of RPA32 and activation of CHK1, indicating replication stress. Furthermore, depletion of RECQ1 leads to chromosomal condensation defects and accumulation of undercondensed chromosomes. Collectively, our observations provide a new insight into the role of RECQ1 in replication fork stabilization and its role in the DNA damage response to maintain genomic stability.
C1 [Popuri, Venkateswarlu; Croteau, Deborah L.; Brosh, Robert M., Jr.; Bohr, Vilhelm A.] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
RP Bohr, VA (reprint author), NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
EM vbohr@nih.gov
FU Intramural Research Program of the National Institute on Aging, NIH
[AG000726-20]
FX We thank Drs. Chandrika Cangovi and Takashi Tadokoro for critical
reading of the manuscript. We thank Dr. Mahesh Ramamoorthy for his
technical expertise in the preparation of lentivirus. We thank Dr.
Sommers Joshua for the expression and purification of recombinant RECQ1.
This work was supported by funds from the Intramural Research Program of
the National Institute on Aging, NIH, AG000726-20.
NR 61
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Z9 18
U1 0
U2 5
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 2012
VL 11
IS 22
BP 4252
EP 4265
DI 10.4161/cc.22581
PG 14
WC Cell Biology
SC Cell Biology
GA 038FT
UT WOS:000311161300027
PM 23095637
ER
PT J
AU Braunschweig, D
Golub, MS
Koenig, CM
Qi, LH
Pessah, IN
Van de Water, J
Berman, RF
AF Braunschweig, Daniel
Golub, Mari S.
Koenig, Claire M.
Qi, Lihong
Pessah, Isaac N.
Van de Water, Judy
Berman, Robert F.
TI Maternal autism-associated IgG antibodies delay development and produce
anxiety in a mouse gestational transfer model
SO JOURNAL OF NEUROIMMUNOLOGY
LA English
DT Article
DE Autism; Maternal antibodies; Passive transfer; Immune; Mouse behavior
ID FETAL-BRAIN; MICE; DISORDERS; CHILDREN; BEHAVIOR; MOTHERS; SYSTEM;
IMPAIRMENT; TRANSPORT; LUPUS
AB A murine passive transfer model system was employed to ascertain the effects of gestational exposure to a single, intravenous dose of purified, brain-reactive IgG antibodies from individual mothers of children with autism (MAU) or mothers with typically developing children (MTD). Growth and behavioral outcomes in offspring were measured from postnatal days 8 to 65 in each group. Comparisons revealed alterations in early growth trajectories, significantly impaired motor and sensory development, and increased anxiety. This report demonstrates for the first time the effects of a single, low dose gestational exposure of IgG derived from individual MAU on their offspring's physical and social development. Published by Elsevier BM.
C1 [Braunschweig, Daniel; Pessah, Isaac N.; Van de Water, Judy] Univ Calif Davis, MIND Inst, Davis, CA 95616 USA.
[Braunschweig, Daniel; Van de Water, Judy] Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
[Braunschweig, Daniel; Koenig, Claire M.; Qi, Lihong; Pessah, Isaac N.; Van de Water, Judy; Berman, Robert F.] Univ Calif Davis, NIEHS Ctr Childrens Environm Hlth, Davis, CA 95616 USA.
[Qi, Lihong] Univ Calif Davis, Sch Med, Div Biostat, Dept Publ Hlth Sci, Davis, CA 95616 USA.
[Golub, Mari S.] Univ Calif Davis, Dept Environm Toxicol, Davis, CA 95616 USA.
[Pessah, Isaac N.] Univ Calif Davis, Dept Vet Mol Biosci, Davis, CA 95616 USA.
[Koenig, Claire M.; Berman, Robert F.] Univ Calif Davis, Sch Med, Dept Neurol Surg, Davis, CA 95616 USA.
RP Braunschweig, D (reprint author), Univ Calif Davis, MIND Inst, Davis, CA 95616 USA.
EM dnau@ucdavis.edu
FU NIEHS [1P01ES11269-0]; U.S. EPA [R829388]; Autism Speaks; JB Johnson
Foundation
FX This work was supported in part by NIEHS 1P01ES11269-0 and U.S. EPA
Grant R829388, a Targeted Research Grant from Autism Speaks and an
unrestricted research grant from the JB Johnson Foundation.
NR 36
TC 23
Z9 23
U1 1
U2 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-5728
J9 J NEUROIMMUNOL
JI J. Neuroimmunol.
PD NOV 15
PY 2012
VL 252
IS 1-2
BP 56
EP 65
DI 10.1016/j.jneuroim.2012.08.002
PG 10
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA 037UR
UT WOS:000311132500007
PM 22951357
ER
PT J
AU Kucka, M
Pogrmic-Majkic, K
Fa, S
Stojilkovic, SS
Kovacevic, R
AF Kucka, Marek
Pogrmic-Majkic, Kristina
Fa, Svetlana
Stojilkovic, Stanko S.
Kovacevic, Radmila
TI Atrazine acts as an endocrine disrupter by inhibiting cAMP-specific
phosphodiesterase-4
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE Endocrine disrupters; Atrazine; Pituitary cells; Leydig cells;
cAMP-specific phosphodiesterases
ID CYCLIC-NUCLEOTIDE PHOSPHODIESTERASES; LEYDIG-CELL STEROIDOGENESIS;
PERIPUBERTAL MALE RATS; ESTROGEN-RECEPTOR; IN-VITRO; AROMATASE
EXPRESSION; PROLACTIN-RELEASE; GENE-EXPRESSION; EXPOSURE; LACTOTROPHS
AB Atrazine, one of the most commonly used herbicides worldwide, acts as an endocrine disruptor, but the mechanism of its action has not been characterized. In this study, we show that atrazine rapidly increases cAMP levels in cultured rat pituitary and testicular Leydig cells in a concentration-dependent manner, but less effectively than 3-isobutyl-1-methylxanthine, a competitive non-specific inhibitor of phosphodiesterases (PDEs). In forskolin (an activator of adenylyl cyclase)- and probenecid (an inhibitor of cyclic nucleotide transporters)-treated cells, but not in 3-isobutyl-1-methylxanthine-treated cells, atrazine further increased cAMP levels, indicating that inhibition of PDEs accounts for accumulation of CAMP. In contrast to cAMP, atrazine did not alter cGMP levels, further indicating that it inhibits cAMP-specific PDEs. Atrazine-induced changes in cAMP levels were sufficient to stimulate prolactin release in pituitary cells and androgen production in Leydig cells, indicating that it acts as an endocrine disrupter both in cells that secrete by exocytosis of prestored hormones and in cells that secrete by de novo hormone synthesis. Rolipram abolished the stimulatory effect of atrazine on CAMP release in both cell types, suggesting that it acts as an inhibitor of PDE4s, isoforms whose mRNA transcripts dominate in pituitary and Leydig cells together with mRNA for PDE8A. In contrast, immortalized lacto-somatotrophs showed low expression of these mRNA transcripts and several fold higher cAMP levels compared to normal pituitary cells, and atrazine was unable to further increase cAMP levels. These results indicate that atrazine acts as a general endocrine disrupter by inhibiting cAMP-specific PDE4s. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Pogrmic-Majkic, Kristina; Fa, Svetlana; Kovacevic, Radmila] Univ Novi Sad, Fac Sci, Dept Biol & Ecol, Lab Ecotoxicol, Novi Sad 21000, Serbia.
[Kucka, Marek; Stojilkovic, Stanko S.] NICHD, Sect Cellular Signaling, Program Dev Neurosci, NIH, Bethesda, MD USA.
RP Kovacevic, R (reprint author), Univ Novi Sad, Fac Sci, Dept Biol & Ecol, Lab Ecotoxicol, Dositej Obradov Sq 2, Novi Sad 21000, Serbia.
EM radmila.kovacevic@dbe.uns.ac.rs
FU Ministry of Science, Republic of Serbia [173037]; Eunce Kennedy Shiver
National Institute of Health and Human Development Intramural Grant
FX We are grateful to Dr. G. D. Niswender for the supply of testosterone
antiserum. This work is supported by the Ministry of Science, Republic
of Serbia (grant no. 173037), and a Eunce Kennedy Shiver National
Institute of Health and Human Development Intramural Grant.
NR 38
TC 26
Z9 27
U1 5
U2 39
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 2012
VL 265
IS 1
BP 19
EP 26
DI 10.1016/j.taap.2012.09.019
PG 8
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 037WD
UT WOS:000311136300003
PM 23022511
ER
PT J
AU Chouker, A
Ohta, A
Martignoni, A
Lukashev, D
Zacharia, LC
Jackson, EK
Schnermann, J
Ward, JM
Kaufmann, I
Klaunberg, B
Sitkovsky, MV
Thiel, M
AF Chouker, Alexander
Ohta, Akio
Martignoni, Andre
Lukashev, Dmitriy
Zacharia, Lefteris C.
Jackson, Edwin K.
Schnermann, Juergen
Ward, Jerrold M.
Kaufmann, Ines
Klaunberg, Brenda
Sitkovsky, Michail V.
Thiel, Manfred
TI In Vivo Hypoxic Preconditioning Protects From Warm Liver
Ischemia-Reperfusion Injury Through the Adenosine A2B Receptor
SO TRANSPLANTATION
LA English
DT Article
DE Hypoxia; Murine liver ischemia; Preconditioning; Hepatoprotection
ID ADENYLATE ENERGY-CHARGE; ISCHEMIA/REPERFUSION INJURY; CYTOSOL
5'-NUCLEOTIDASE; A(2A) RECEPTORS; PATHWAY; A(1); TRANSPLANTATION;
INFLAMMATION; ANTAGONIST; ACTIVATION
AB Background. Liver ischemia-reperfusion injury (IRI) is a known risk factor for the postoperative outcome of patients undergoing liver surgery/transplantation. Attempts to protect from organ damage require multidisciplinary strategies and are of emerging interest in view of patients with higher age and American Society of Anesthesiology status. Ischemic preconditioning has been successfully applied to prevent from IRI during liver resection/transplantation. Because even short periods of ischemia during preconditioning inevitably lead to hypoxia and formation of anti-inflammatory/cytoprotective acting adenosine, we reasoned that short nonischemic hypoxia also protects against hepatic IRI.
Methods. Mice underwent hypoxic preconditioning (HPC) by breathing 10% oxygen for 10 min followed by 10 min of 21% oxygen before left liver lobe ischemia (45 min) and reperfusion (4 hr). The interactions of hypoxia -> adenosine -> adenosine receptors were tested by pharmacologic antagonism at adenosine receptor (AR) sites in wild-type mice and in mice with genetic deletions at the A1, A2A, A2B, and A3 ARs. Hepatocellular damage, inflammation, and metabolic effects were quantified by enzyme activities, cytokines, liver myeloperoxidase, blood adenosine, and tissue AMP, respectively.
Results. Hepatoprotection by HPC was significant in wild-type and A1, A2A, and A3 AR knockout mice as quantified by lower alanine aminotransferase serum activities, cytokine levels, histologic damage scores, tissue myeloperoxidase concentrations, and preserved AMP concentrations. Protection by HPC was blunted in mice pretreated with the A2B AR antagonist MRS1754 or in A2B AR knockout mice.
Conclusions. Because liver protective effects of HPC are negated when the A2B receptor is nonfunctional, the hypoxia -> adenosine -> A2B receptor pathway plays a critical role in the prevention of warm IRI in vivo. Hypoxic activation of this pathway warrants use of selective A2B AR agonists or even intermittent hypoxia (e. g., in deceased organ donors) to protect from liver IRI.
C1 [Chouker, Alexander; Martignoni, Andre; Kaufmann, Ines] Univ Munich, Dept Anesthesiol, D-81377 Munich, Germany.
[Chouker, Alexander; Ohta, Akio; Lukashev, Dmitriy; Ward, Jerrold M.; Sitkovsky, Michail V.] NIAID, NIH, Bethesda, MD 20892 USA.
[Ohta, Akio; Lukashev, Dmitriy; Sitkovsky, Michail V.] Northeastern Univ, New England Inflammat & Tissue Protect Inst Conso, Boston, MA 02115 USA.
[Zacharia, Lefteris C.] Ctr Res & Technol Thessaly, Dept Biomed Res & Technol, Larisa, Greece.
[Jackson, Edwin K.] Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Pittsburgh, PA USA.
[Schnermann, Juergen] NIDDKD, NIH, Bethesda, MD 20892 USA.
[Klaunberg, Brenda] NINDS, MIF, NIH, Bethesda, MD 20892 USA.
[Thiel, Manfred] Univ Heidelberg, Dept Anaesthesiol & Intens Care, Med Fac Mannheim, D-6800 Mannheim, Germany.
RP Chouker, A (reprint author), Univ Munich, Dept Anesthesiol, Marchioninistr 15, D-81377 Munich, Germany.
EM achouker@med.uni-muenchen.de
OI Zacharia, Lefteris/0000-0002-0327-2373
FU National Institutes of Health, National Institute of Allergy and
Infectious Diseases; John E. Fogarty research grant; Department of
Anesthesiology of the LMU-Munich; National Institutes of Health
[DK079307, HL109002, DK068575]
FX This research work was supported in part by the Intramural Research
Program of the National Institutes of Health, National Institute of
Allergy and Infectious Diseases, John E. Fogarty research grant (awarded
to A.C.); Department of Anesthesiology of the LMU-Munich; and National
Institutes of Health grants DK079307, HL109002, and DK068575 (awarded to
E.K.J.).
NR 46
TC 16
Z9 17
U1 1
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0041-1337
J9 TRANSPLANTATION
JI Transplantation
PD NOV 15
PY 2012
VL 94
IS 9
BP 894
EP 902
DI 10.1097/TP.0b013e31826a9a46
PG 9
WC Immunology; Surgery; Transplantation
SC Immunology; Surgery; Transplantation
GA 033JN
UT WOS:000310791500005
PM 23073466
ER
PT J
AU Sam, WJ
Chamberlain, CE
Lee, SJ
Goldstein, JA
Hale, DA
Mannon, RB
Kirk, AD
Hon, YY
AF Sam, Wai-Johnn
Chamberlain, Christine E.
Lee, Su-Jun
Goldstein, Joyce A.
Hale, Douglas A.
Mannon, Roslyn B.
Kirk, Allan D.
Hon, Yuen Yi
TI Associations of ABCB1 and IL-10 Genetic Polymorphisms With
Sirolimus-Induced Dyslipidemia in Renal Transplant Recipients
SO TRANSPLANTATION
LA English
DT Article
DE Sirolimus; ABCB1; Total and LDL cholesterol; Triglyceride;
Pharmacogenetics
ID RESISTANCE P-GLYCOPROTEINS; APOLIPOPROTEIN-E GENOTYPES;
CORONARY-HEART-DISEASE; FRAMINGHAM RISK SCORE; IMMUNOSUPPRESSIVE
REGIMENS; MYOCARDIAL-INFARCTION; CARDIOVASCULAR RISK; COMMON VARIANTS;
ATORVASTATIN; HYPERLIPIDEMIA
AB Background. Hyperlipidemia is a common adverse effect of sirolimus (SRL). We previously showed significant associations of ABCB1 3435C>T and IL-10 -1082G>A with log-transformed SRL dose-adjusted weighted-normalized trough. We further examined to see whether these polymorphisms were also associated with SRL-induced dyslipidemia.
Methods. Genotyping was performed for ABCB1 1236C>T, 2677 G>T/A, and 3435C>T; CYP3A4 -392A>G; CYP3A5 6986A>G and 14690G>A; IL-10 -1082G>A; TNF -308G>A; and ApoE epsilon 2, epsilon 3, and epsilon 4 alleles. The longitudinal changes of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglyceride (TG) levels after SRL treatment before statin therapy were analyzed by a linear mixed-effects model, with adjustments for selected covariates for each lipid.
Results. Under the dominant genetic model, ABCB1 3435C>T was associated with TC (P=0.0001) and LDL-C (P<0.0001) values after SRL administration. Mean TC and LDL-C levels were 26.9 and 24.9 mg/dL higher, respectively, in ABCB1 3435T carriers than 3435CC homozygotes at an average SRL trough concentration of 4 ng/mL without concomitant medication. ABCB1 1236C>T under the recessive model and IL-10 -1082G>A under the dominant model were associated with log-transformed TG values (P=0.0051 and 0.0436, respectively). Mean TG value was 25.1% higher in ABCB1 1236TT homozygotes compared with ABCB1 1236C carriers and was 12.4% higher in IL-10 -1082AA homozygotes than -1082G carriers.
Conclusions. ABCB1 polymorphisms were found to be associated with lipid responses to SRL treatment, confirming the role of ABCB1 gene in SRL pharmacokinetics and pharmacodynamics. Further studies are necessary to define the role of ABCB1 and IL-10 polymorphisms on SRL-induced dyslipidemia in renal transplantation.
C1 [Sam, Wai-Johnn; Chamberlain, Christine E.; Hon, Yuen Yi] NIH, Ctr Clin, Dept Pharm, Bethesda, MD 20892 USA.
[Lee, Su-Jun; Goldstein, Joyce A.] Natl Inst Environm Hlth Sci, Lab Toxicol & Pharmacol, Res Triangle Pk, NC USA.
[Hale, Douglas A.; Mannon, Roslyn B.; Kirk, Allan D.] NIDDKD, Transplantat Branch, Bethesda, MD 20892 USA.
[Lee, Su-Jun] Inje Univ, Dept Pharmacol, Coll Med, Pusan, South Korea.
[Hale, Douglas A.] Vanderbilt Univ, Div Kidney Pancreas Transplantat, Nashville, TN USA.
[Mannon, Roslyn B.] Univ Alabama Birmingham, Dept Med, Div Nephrol, Birmingham, AL 35294 USA.
[Kirk, Allan D.] Emory Univ, Sch Med, Dept Surg, Atlanta, GA 30322 USA.
[Kirk, Allan D.] Emory Univ, Sch Med, Dept Pediat, Atlanta, GA USA.
RP Hon, YY (reprint author), NIH, Ctr Clin, Dept Pharm, Bldg 10,Rm 1C240,10 Ctr Dr, Bethesda, MD 20892 USA.
EM chon@cc.nih.gov
FU National Institutes of Health Clinical Center Pharmacy Department,
National Institute of Diabetes and Digestive and Kidney Diseases
Transplantation Branch; National Institute of Environmental Health
Sciences [Z01ES02124]
FX This work was supported by the Intramural Research Program of the
National Institutes of Health Clinical Center Pharmacy Department,
National Institute of Diabetes and Digestive and Kidney Diseases
Transplantation Branch, and National Institute of Environmental Health
Sciences (Z01ES02124). There was no commercial sponsorship.
NR 48
TC 2
Z9 4
U1 0
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0041-1337
J9 TRANSPLANTATION
JI Transplantation
PD NOV 15
PY 2012
VL 94
IS 9
BP 971
EP 977
DI 10.1097/TP.0b013e31826b55e2
PG 7
WC Immunology; Surgery; Transplantation
SC Immunology; Surgery; Transplantation
GA 033JN
UT WOS:000310791500016
PM 23073467
ER
PT J
AU Yang, G
Shu, XO
Chow, WH
Zhang, XL
Li, HL
Ji, BT
Cai, H
Wu, SH
Gao, YT
Zheng, W
AF Yang, Gong
Shu, Xiao Ou
Chow, Wong-Ho
Zhang, Xianglan
Li, Hong-Lan
Ji, Bu-Tian
Cai, Hui
Wu, Shenghui
Gao, Yu-Tang
Zheng, Wei
TI Soy Food Intake and Risk of Lung Cancer: Evidence From the Shanghai
Womens Health Study and a Meta-Analysis
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Review
DE cohort studies; lung neoplasms; meta-analysis; risk; soy foods; women
ID ESTROGEN-RECEPTOR-BETA; BREAST-CANCER; POSTMENOPAUSAL WOMEN; PROSPECTIVE
COHORT; ISOFLAVONE INTAKE; NORTHEAST CHINA; IN-VITRO; CELLS; GENISTEIN;
MECHANISMS
AB The authors prospectively evaluated the association of soy food intake with lung cancer risk, overall and by tumor aggressiveness, and performed a meta-analysis of published data. Included in the analysis were 71,550 women recruited into the Shanghai Womens Health Study (Shanghai, China) in 19972000. Usual soy food intake was assessed at baseline and reassessed during follow-up through in-person interviews. During a mean follow-up period of 9.1 years, 370 incident lung cancer cases were identified; 340 patients were lifetime never smokers. After adjustment for potential confounders, soy food intake was inversely associated with subsequent risk of lung cancer (P-trend 0.004); the hazard ratio for the highest quintile of intake compared with the lowest was 0.63 (95 confidence interval: 0.44, 0.90). This inverse association appeared predominately among women with later age at menopause (P-interaction 0.01) and for aggressive lung cancer as defined by length of survival (12 months vs. epsilon 12 months; P-heterogeneity 0.057). Meta-analysis of 7 studies conducted among nonsmokers found a summary relative risk of 0.59 (95 confidence interval: 0.49, 0.71) for the highest categories of soy or isoflavone intake versus the lowest. This study suggests that soy food consumption may reduce lung cancer risk in nonsmoking women, particularly for aggressive tumors, and its effect may be modified by endogenous estrogens.
C1 [Yang, Gong; Shu, Xiao Ou; Zhang, Xianglan; Cai, Hui; Wu, Shenghui; Zheng, Wei] Vanderbilt Univ, Div Epidemiol, Dept Med, Sch Med, Nashville, TN 37203 USA.
[Yang, Gong; Shu, Xiao Ou; Zhang, Xianglan; Cai, Hui; Wu, Shenghui; Zheng, Wei] Vanderbilt Univ, Vanderbilt Ingram Canc Ctr, Med Ctr, Nashville, TN 37203 USA.
[Chow, Wong-Ho; Ji, Bu-Tian] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Li, Hong-Lan; Gao, Yu-Tang] Shanghai Canc Inst, Dept Epidemiol, Shanghai, Peoples R China.
RP Yang, G (reprint author), Vanderbilt Univ, Div Epidemiol, Dept Med, Sch Med, 2525 W End Ave,Suite 600, Nashville, TN 37203 USA.
EM gong.yang@vanderbilt.edu
FU US National Cancer Institute, National Institutes of Health
[R37CA070867, RFP N02 CP1101066]
FX This work was supported by the US National Cancer Institute, National
Institutes of Health (grants R37CA070867 to W. Z. and RFP N02 CP1101066
to X. O. S.).
NR 54
TC 10
Z9 12
U1 0
U2 16
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 2012
VL 176
IS 10
BP 846
EP 855
DI 10.1093/aje/kws168
PG 10
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 034SH
UT WOS:000310892700002
PM 23097255
ER
PT J
AU Schmader, KE
Oxman, MN
Levin, MJ
Johnson, G
Zhang, JH
Betts, R
Morrison, VA
Gelb, L
Guatelli, JC
Harbecke, R
Pachucki, C
Keay, S
Menzies, B
Griffin, MR
Kauffman, C
Marques, A
Toney, J
Keller, PM
Li, X
Chan, ISF
Annunziato, P
AF Schmader, K. E.
Oxman, M. N.
Levin, M. J.
Johnson, G.
Zhang, J. H.
Betts, R.
Morrison, V. A.
Gelb, L.
Guatelli, J. C.
Harbecke, R.
Pachucki, C.
Keay, S.
Menzies, B.
Griffin, M. R.
Kauffman, C.
Marques, A.
Toney, J.
Keller, P. M.
Li, X.
Chan, I. S. F.
Annunziato, P.
CA Shingles Prevention Study Grp
TI Persistence of the Efficacy of Zoster Vaccine in the Shingles Prevention
Study and the Short-Term Persistence Substudy
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID HERPES-ZOSTER; POSTHERPETIC NEURALGIA; OLDER-ADULTS; TRIALS; BURDEN;
PAIN
AB Background. The Shingles Prevention Study (SPS; Department of Veterans Affairs Cooperative Study 403) demonstrated that zoster vaccine was efficacious through 4 years after vaccination. The Short-Term Persistence Substudy (STPS) was initiated after the SPS to further assess the persistence of vaccine efficacy.
Methods. The STPS re-enrolled 7320 vaccine and 6950 placebo recipients from the 38 546-subject SPS population. Methods of surveillance, case determination, and follow-up were analogous to those in the SPS. Vaccine efficacy for herpes zoster (HZ) burden of illness, incidence of postherpetic neuralgia (PHN), and incidence of HZ were assessed for the STPS population, for the combined SPS and STPS populations, and for each year through year 7 after vaccination.
Results. In the STPS as compared to the SPS, vaccine efficacy for HZ burden of illness decreased from 61.1% to 50.1%, vaccine efficacy for the incidence of PHN decreased from 66.5% to 60.1%, and vaccine efficacy for the incidence of HZ decreased from 51.3% to 39.6%, although the differences were not statistically significant. Analysis of vaccine efficacy in each year after vaccination for all 3 outcomes showed a decrease in vaccine efficacy after year 1, with a further decline thereafter. Vaccine efficacy was statistically significant for the incidence of HZ and the HZ burden of illness through year 5.
Conclusions. Vaccine efficacy for each study outcome was lower in the STPS than in the SPS. There is evidence of the persistence of vaccine efficacy through year 5 after vaccination but, vaccine efficacy is uncertain beyond that point.
C1 [Schmader, K. E.] Durham Dept Vet Affairs VA Med Ctr MC, GRECC, Durham, NC USA.
[Schmader, K. E.] Duke Univ, Durham, NC USA.
[Oxman, M. N.; Guatelli, J. C.; Harbecke, R.] VA San Diego Healthcare Syst, San Diego, CA USA.
[Oxman, M. N.; Guatelli, J. C.; Harbecke, R.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Levin, M. J.] Univ Colorado Denver, Aurora, CO USA.
[Levin, M. J.] Hlth Sci Ctr, Aurora, CO USA.
[Johnson, G.; Zhang, J. H.] VA Cooperat Studies Program Coordinating Ctr, West Haven, CT USA.
[Betts, R.] Univ Rochester, New York, NY USA.
[Morrison, V. A.] VAMC, Minneapolis, MN USA.
[Morrison, V. A.] Univ Minnesota, Minneapolis, MN USA.
[Gelb, L.] VAMC, St Louis, MO USA.
[Pachucki, C.] Hines VAMC, Chicago, IL USA.
[Keay, S.] Baltimore VAMC, Baltimore, MD USA.
[Keay, S.] Univ Maryland, Baltimore, MD 21201 USA.
[Marques, A.] NIAID, Bethesda, MD 20892 USA.
[Menzies, B.] VAMC, Seattle, WA USA.
[Griffin, M. R.] Vanderbilt Univ, GRECC, Nashville, TN USA.
[Griffin, M. R.] VA Tennessee Valley Hlth Care Syst, Nashville, TN USA.
[Kauffman, C.] VA Ann Arbor Hlth Care Syst, Ann Arbor, MI USA.
[Kauffman, C.] Univ Michigan, Sch Med, Ann Arbor, MI USA.
[Toney, J.] VAMC, Tampa, FL USA.
[Keller, P. M.; Li, X.; Chan, I. S. F.; Annunziato, P.] Merck Sharp & Dhome Corp, Whitehouse Stn, NJ USA.
RP Schmader, KE (reprint author), Durham VA Med Ctr, 182 GRECC,508 Fulton St, Durham, NC 27705 USA.
EM kenneth.schmader@dm.duke.edu
RI Irwin, Michael/H-4870-2013
OI Irwin, Michael/0000-0002-1502-8431
FU VA CSP [403]; Merck
FX This work was supported by funding from VA CSP 403 and a grant from
Merck to the VA Cooperative Studies Program and, subsequently, to the
Veterans Medical Research Foundation and the VA Connecticut Research and
Education Foundation.
NR 13
TC 60
Z9 61
U1 0
U2 19
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 2012
VL 55
IS 10
BP 1320
EP 1328
DI 10.1093/cid/cis638
PG 9
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 027SV
UT WOS:000310374600013
PM 22828595
ER
PT J
AU Gamaletsou, MN
Kontoyiannis, DP
Sipsas, NV
Moriyama, B
Alexander, E
Roilides, E
Brause, B
Walsh, TJ
AF Gamaletsou, Maria N.
Kontoyiannis, Dimitrios P.
Sipsas, Nikolaos V.
Moriyama, Brad
Alexander, Elizabeth
Roilides, Emmanuel
Brause, Barry
Walsh, Thomas J.
TI Candida Osteomyelitis: Analysis of 207 Pediatric and Adult Cases
(1970-2011)
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; TROPICALIS VERTEBRAL OSTEOMYELITIS;
TORULOPSIS-GLABRATA OSTEOMYELITIS; LIPOSOMAL AMPHOTERICIN-B;
OF-THE-LITERATURE; CHRONIC-RENAL-FAILURE; ALBICANS OSTEOMYELITIS; SPINAL
OSTEOMYELITIS; STERNAL OSTEOMYELITIS; DIABETIC FOOT
AB Background. The epidemiology, pathogenesis, clinical manifestations, management, and outcome of Candida osteomyelitis are not well understood.
Methods. Cases of Candida osteomyelitis from 1970 through 2011 were reviewed. Underlying conditions, microbiology, mechanisms of infection, clinical manifestations, antifungal therapy, and outcome were studied in 207 evaluable cases.
Results. Median age was 30 years (range, <= 1 month to 88 years) with a >2:1 male: female ratio. Most patients (90%) were not neutropenic. Localizing pain, tenderness, and/or edema were present in 90% of patients. Mechanisms of bone infection followed a pattern of hematogenous dissemination (67%), direct inoculation (25%), and contiguous infection (9%). Coinciding with hematogenous infection, most patients had >= 2 infected bones. When analyzed by age, the most common distribution of infected sites for adults was vertebra (odds ratio [OR], 0.09; 95% confidence interval [CI], .04-.25), rib, and sternum; for pediatric patients (<= 18 years) the pattern was femur (OR, 20.6; 95% CI, 8.4-48.1), humerus, then vertebra/ribs. Non-albicans Candida species caused 35% of cases. Bacteria were recovered concomitantly from 12% of cases, underscoring the need for biopsy and/or culture. Candida septic arthritis occurred concomitantly in 21%. Combined surgery and antifungal therapy were used in 48% of cases. The overall complete response rate of Candida osteomyelitis of 32% reflects the difficulty in treating this infection. Relapsed infection, possibly related to inadequate duration of therapy, occurred among 32% who ultimately achieved complete response.
Conclusions. Candida osteomyelitis is being reported with increasing frequency. Localizing symptoms are usually present. Vertebrae are the most common sites in adults vs femora in children. Timely diagnosis of Candida osteomyelitis with extended courses of 6-12 months of antifungal therapy, and surgical intervention, when indicated, may improve outcome.
C1 [Walsh, Thomas J.] Cornell Univ, Weill Cornell Med Ctr, Transplantat Oncol Infect Dis Program, Div Infect Dis, New York, NY 10065 USA.
[Gamaletsou, Maria N.; Sipsas, Nikolaos V.] Univ Athens, Sch Med, Dept Pathophysiol, Athens, Greece.
[Gamaletsou, Maria N.; Sipsas, Nikolaos V.; Roilides, Emmanuel; Brause, Barry; Walsh, Thomas J.] Hosp Special Surg, Ctr Osteoarticular Mycoses, New York, NY 10021 USA.
[Kontoyiannis, Dimitrios P.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Moriyama, Brad] NIH, Dept Pharm, Ctr Clin, Bethesda, MD 20892 USA.
[Roilides, Emmanuel] Aristotle Univ Thessaloniki, Sch Med, Hippokrat Hosp, Dept Pediat 3, GR-54006 Thessaloniki, Greece.
RP Walsh, TJ (reprint author), Cornell Univ, Weill Cornell Med Ctr, Transplantat Oncol Infect Dis Program, Div Infect Dis, 1300 York Ave,Rm A-421, New York, NY 10065 USA.
EM thw2003@med.cornell.edu
FU Special Account for Research Funds of the National and Kapodistrian
University of Athens; National Institutes of Health through an MD
Anderson Cancer Center Support Grant [CA016672]; Save Our Sick Children
Foundation; Weill Cornell Clinical and Translational Science Center;
Postdoctoral Scientist Award [KL2RR024997]
FX This work was supported by the Special Account for Research Funds (to M.
N. G., N. V. S.) of the National and Kapodistrian University of Athens;
National Institutes of Health through an MD Anderson Cancer Center
Support Grant (CA016672); Save Our Sick Children Foundation (T. J. W.);
Weill Cornell Clinical and Translational Science Center; and
Postdoctoral Scientist Award (KL2RR024997 to E. A.).
NR 145
TC 24
Z9 26
U1 1
U2 5
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 2012
VL 55
IS 10
BP 1338
EP 1351
DI 10.1093/cid/cis660
PG 14
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 027SV
UT WOS:000310374600015
PM 22911646
ER
PT J
AU Shiels, MS
Landgren, O
Costello, R
Zingone, A
Goedert, JJ
Engels, EA
AF Shiels, Meredith S.
Landgren, Ola
Costello, Rene
Zingone, Adriana
Goedert, James J.
Engels, Eric A.
TI Free Light Chains and the Risk of AIDS-Defining Opportunistic Infections
in HIV-Infected Individuals
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; SOLUBLE CD30; UNDETERMINED SIGNIFICANCE;
MONOCLONAL GAMMOPATHY; PROGRESSION; HEMOPHILIA; PREVALENCE; LYMPHOMA;
DISEASE
AB Background. The relevance of B-cell dysfunction for progression to AIDS among human immunodeficiency virus (HIV)-infected individuals has not been clearly defined. We evaluated the association between circulating kappa and. free light chains (FLCs), which are markers of B-cell dysfunction, and risk of developing an AIDS-defining opportunistic infection in HIV-infected men.
Methods. The study included 252 case patients with clinical AIDS and 252 HIV-infected controls from the Multicenter Hemophilia Cohort Study I. Case patients were matched to controls on birth date, specimen type, blood sample collection date, and CD4 cell count. Levels of kappa and lambda FLCs were measured in serum or plasma collected 0-2.5 years before selection. Elevated FLC levels (kappa or lambda, above the upper limit of normal) were classified as polyclonal (normal kappa-lambda ratio) or monoclonal (abnormally skewed kappa-lambda ratio). We used conditional logistic regression to estimate odds ratios (ORs) for AIDS.
Results. FLC levels were higher in case patients than in controls, for kappa (median, 4.03 vs 2.98 mg/dL) and lambda (3.77 vs 2.42 mg/dL) FLCs. Compared with normal levels, above-normal FLC levels were associated with AIDS (OR, 3.13 [95% confidence interval (CI), 1.78-5.49] for kappa and 3.47 [2.31-5.20] for lambda FLCs), and the association with AIDS was strengthened with increasing kappa and lambda FLC levels (P trends < .0001). Polyclonal FLC elevation was associated with a 4-fold increase in the risk of AIDS (OR, 3.85; 95% CI, 1.97-7.54), but monoclonal FLC elevation was not associated with AIDS.
Conclusions. Circulating FLCs are associated with elevated risk of AIDS in HIV-infected individuals. Polyclonal B-cell dysfunction may contribute to HIV-related immune suppression and predispose to clinical AIDS events.
C1 [Shiels, Meredith S.] NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20892 USA.
[Landgren, Ola; Costello, Rene; Zingone, Adriana] NCI, Multiple Myeloma Sect, Ctr Canc Res, Rockville, MD 20892 USA.
RP Shiels, MS (reprint author), NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,EPS 7059, Rockville, MD 20892 USA.
EM shielsms@mail.nih.gov
FU Intramural Research Program of the National Cancer Institute
FX This work was supported by the Intramural Research Program of the
National Cancer Institute.
NR 21
TC 4
Z9 4
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 2012
VL 55
IS 10
BP E103
EP E108
DI 10.1093/cid/cis692
PG 6
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 027SV
UT WOS:000310374600006
PM 22893577
ER
PT J
AU Martin, LK
Grecula, J
Jia, G
Wei, L
Yang, XY
Otterson, GA
Wu, X
Harper, E
Kefauver, C
Zhou, BS
Yen, Y
Bloomston, M
Knopp, M
Ivy, SP
Grever, M
Bekaii-Saab, T
AF Martin, Ludmila Katherine
Grecula, John
Jia, Guang
Wei, Lai
Yang, Xiangyu
Otterson, Gregory A.
Wu, Xin
Harper, Erica
Kefauver, Cheryl
Zhou, Bing-Sen
Yen, Yun
Bloomston, Mark
Knopp, Michael
Ivy, S. Percy
Grever, Michael
Bekaii-Saab, Tanios
TI A Dose Escalation and Pharmacodynamic Study of Triapine and Radiation in
Patients With Locally Advanced Pancreas Cancer
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
ID RIBONUCLEOTIDE REDUCTASE INHIBITOR; 3-AMINOPYRIDINE-2-CARBOXALDEHYDE
THIOSEMICARBAZONE 3-AP; PHASE-I; SOLID TUMORS; ADENOCARCINOMA; SCHEDULE;
SUBUNIT
AB Purpose: Triapine, a novel inhibitor of the M2 subunit of ribonucleotide reductase (RR), is a potent radiosensitizer. This phase 1 study, sponsored by the National Cancer Institute Cancer Therapy Evaluation Program, assessed the safety and tolerability of triapine in combination with radiation (RT) in patients with locally advanced pancreas cancer (LAPCA).
Methods and Materials: We evaluated 3 dosage levels of triapine (24 mg/m(2), 48 mg/m(2), 72 mg/m(2)) administered with 50.4 Gy of RT in 28 fractions. Patients with LAPCA received triapine thrice weekly, every other week during the course of RT. Dose-limiting toxicity (DLT) was assessed during RT and for 4 weeks after its completion. Dynamic contrast-enhanced magnetic resonance imaging and serum RR levels were evaluated as potential predictors for early response.
Results: Twelve patients were treated. Four patients (1 nonevaluable) were enrolled at dosage level 1 (DL1), 3 patients at DL2, and 5 patients (2 nonevaluable) at DL3. No DLTs were observed, and the maximum tolerated dose was not reached. Two patients (17%) achieved partial response, and 6 patients (50%) had stable disease. One patient underwent R0 resection after therapy. Ninety-two percent of patients (100% at DL3) experienced freedom from local tumor progression. In 75% of patients who eventually experienced progression, metastases developed without local progression. RR levels did not seem to predict outcome. In 4 patients with available data, dynamic contrast-enhanced magnetic resonance imaging may predict early response or resistance to therapy.
Conclusion: The combination of triapine at 72 mg/m(2) 3 times weekly every other week and standard RT is tolerable with interesting activity in patients with LAPCA. (C) 2012 Elsevier Inc.
C1 [Martin, Ludmila Katherine; Otterson, Gregory A.; Grever, Michael; Bekaii-Saab, Tanios] Ohio State Univ, Dept Internal Med, Div Surg Oncol, Columbus, OH 43210 USA.
[Grecula, John] Ohio State Univ, Dept Radiat Oncol, Div Surg Oncol, Columbus, OH 43210 USA.
[Jia, Guang; Yang, Xiangyu; Knopp, Michael] Ohio State Univ, Dept Radiol, Div Surg Oncol, Columbus, OH 43210 USA.
[Bloomston, Mark] Ohio State Univ, Dept Surg, Div Surg Oncol, Columbus, OH 43210 USA.
[Wei, Lai] Ohio State Univ, Ctr Biostat, Columbus, OH 43210 USA.
[Wu, Xin; Harper, Erica; Kefauver, Cheryl] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
[Zhou, Bing-Sen; Yen, Yun] City Hope Comprehens Canc Ctr, Duarte, CA USA.
[Ivy, S. Percy] NCI, Canc Therapeut Evaluat Program, Rockville, MD USA.
RP Bekaii-Saab, T (reprint author), A454 Starling Loving Hall,320 W 10th Ave, Columbus, OH 43210 USA.
EM Tanios.Saab@osumc.edu
RI Jia, Guang/E-3312-2011; Bloomston, Mark/E-2767-2011; Bekaii-Saab,
Tanios/E-2733-2011; Grecula, John/E-3149-2011; Mendez, Pedro
/J-8955-2016; Yang, Xiangyu/E-4342-2011; Jia, Guang/A-1275-2016
OI Mendez, Pedro /0000-0001-6713-7907; Yang, Xiangyu/0000-0002-1541-667X;
FU National Cancer Institute-Cancer Therapy Evaluation Program [U01CA
76576-03]
FX Supported by the National Cancer Institute-Cancer Therapy Evaluation
Program U01CA 76576-03.
NR 20
TC 6
Z9 6
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD NOV 15
PY 2012
VL 84
IS 4
BP E475
EP E481
DI 10.1016/j.ijrobp.2012.06.003
PG 7
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 030IV
UT WOS:000310565300005
PM 22818416
ER
PT J
AU Ota, T
Doyle-Cooper, C
Cooper, AB
Huber, M
Falkowska, E
Doores, KJ
Hangartner, L
Le, K
Sok, D
Jardine, J
Lifson, J
Wu, XL
Mascola, JR
Poignard, P
Binley, JM
Chakrabarti, BK
Schief, WR
Wyatt, RT
Burton, DR
Nemazee, D
AF Ota, Takayuki
Doyle-Cooper, Colleen
Cooper, Anthony B.
Huber, Michael
Falkowska, Emilia
Doores, Katherine J.
Hangartner, Lars
Le, Khoa
Sok, Devin
Jardine, Joseph
Lifson, Jeffrey
Wu, Xueling
Mascola, John R.
Poignard, Pascal
Binley, James M.
Chakrabarti, Bimal K.
Schief, William R.
Wyatt, Richard T.
Burton, Dennis R.
Nemazee, David
TI Anti-HIV B Cell Lines as Candidate Vaccine Biosensors
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; HUMAN MONOCLONAL-ANTIBODY; BROADLY
NEUTRALIZING ANTIBODIES; PBL-SCID MICE; IN-VITRO; POTENT NEUTRALIZATION;
PASSIVE-IMMUNIZATION; CRYSTAL-STRUCTURE; CD4-BINDING SITE; DOMAIN
EXCHANGE
AB Challenge studies following passive immunization with neutralizing Abs suggest that an HIV vaccine could be efficacious were it able to elicit broadly neutralizing Abs (bNAbs). To better understand the requirements for activation of B cells producing bNAbs, we generated cell lines expressing bNAbs or their germline-reverted versions (gl-bNAbs) as BCRs. We then tested the abilities of the bNAb-expressing cells to recognize HIV pseudovirions and vaccine candidate proteins by binding and activation assays. The results suggest that HIV envelope (Env) Ag-expressing, infection-competent virions are poorly recognized by high-affinity bNAb-expressing cells, as measured by the inability of Ags to induce rapid increases in intracellular calcium levels. Other Ag forms appear to be highly stimulatory, in particular, soluble gp140 trimers and a multimerized, scaffolded epitope protein. Virions failed to efficiently activate bNAb-expressing B cells owing to delayed or inefficient BCR recognition, most likely caused by the low density of Env spikes. Importantly, B cells carrying gl-bNAb BCRs were not stimulated by any of the tested vaccine candidates. These data provide insight into why many HIV immunogens, as well as natural HIV infections, fail to rapidly stimulate bNAb responses and suggest that bNAb-expressing cell lines might be useful tools in evaluation of vaccine Ags for infectious diseases. Because soluble Env trimers or multimerized scaffolded epitopes are best at activating B cell-expressing bNAbs, these antigenic forms should be considered as preferred vaccine components, although they should be modified to better target naive gl-bNAb B cells. The Journal of Immunology, 2012, 189: 4816-4824.
C1 [Ota, Takayuki; Doyle-Cooper, Colleen; Cooper, Anthony B.; Huber, Michael; Falkowska, Emilia; Doores, Katherine J.; Hangartner, Lars; Le, Khoa; Sok, Devin; Jardine, Joseph; Poignard, Pascal; Chakrabarti, Bimal K.; Schief, William R.; Wyatt, Richard T.; Burton, Dennis R.; Nemazee, David] Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
[Huber, Michael; Hangartner, Lars] Univ Zurich, Inst Med Virol, CH-8057 Zurich, Switzerland.
[Jardine, Joseph; Poignard, Pascal; Chakrabarti, Bimal K.; Schief, William R.; Wyatt, Richard T.; Burton, Dennis R.] Scripps Res Inst, Int AIDS Vaccine Initiat Neutralizing Antibody Ct, La Jolla, CA 92037 USA.
[Lifson, Jeffrey] Frederick Natl Lab Canc Res, Frederick, MD 21701 USA.
[Wu, Xueling; Mascola, John R.] NIAID, Vaccine Res Ctr, Nihon Univ, Bethesda, MD 20892 USA.
[Binley, James M.] Torrey Pines Inst Mol Studies, San Diego, CA 92121 USA.
[Burton, Dennis R.] Ragon Inst MGH MIT & Harvard, Boston, MA 02129 USA.
RP Nemazee, D (reprint author), Scripps Res Inst, 10550 N Torrey Pines Rd,Mail Drop IM29, La Jolla, CA 92130 USA.
EM nemazee@scripps.edu
RI poignard, pascal/N-6678-2013; Huber, Michael/B-8509-2015; Hangartner,
Lars/H-3503-2011;
OI Doores, Katie/0000-0002-5507-1725
FU National Institutes of Health Research [R01 AI073148, U01 AI078224, UM1
AI100663]; International AIDS Vaccine Initiative Neutralizing Antibody
Center; Ragon Institute of MGH; Ragon Institute of MIT; Ragon Institute
of Harvard; Creative and Novel Ideas in HIV Research award
FX This work was supported by National Institutes of Health Research Grants
R01 AI073148, U01 AI078224, and UM1 AI100663, as well as by the
International AIDS Vaccine Initiative Neutralizing Antibody Center and
the Ragon Institute of MGH, MIT and Harvard. T.O. is a recipient of a
Creative and Novel Ideas in HIV Research award.
NR 60
TC 27
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U1 0
U2 12
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 2012
VL 189
IS 10
BP 4816
EP 4824
DI 10.4049/jimmunol.1202165
PG 9
WC Immunology
SC Immunology
GA 032IU
UT WOS:000310710600015
PM 23066156
ER
PT J
AU Peters, NC
Bertholet, S
Lawyer, PG
Charmoy, M
Romano, A
Ribeiro-Gomes, FL
Stamper, LW
Sacks, DL
AF Peters, Nathan C.
Bertholet, Sylvie
Lawyer, Phillip G.
Charmoy, Melanie
Romano, Audrey
Ribeiro-Gomes, Flavia L.
Stamper, Lisa W.
Sacks, David L.
TI Evaluation of Recombinant Leishmania Polyprotein Plus Glucopyranosyl
Lipid A Stable Emulsion Vaccines against Sand Fly-Transmitted Leishmania
major in C57BL/6 Mice
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID CANINE VISCERAL LEISHMANIASIS; CUTANEOUS LEISHMANIASIS; LEISH-F1+MPL-SE
VACCINE; MEGLUMINE ANTIMONIATE; CLINICAL-TRIAL; T-CELLS; PROTECTIVE
IMMUNITY; VIRULENT CHALLENGE; SUSCEPTIBLE MICE; INFECTION
AB Numerous experimental Leishmania vaccines have been developed to prevent the visceral and cutaneous forms of Leishmaniasis, which occur after exposure to the bite of an infected sand fly, yet only one is under evaluation in humans. KSAC and L110f, recombinant Leishmania polyproteins delivered in a stable emulsion (SE) with the TLR4 agonists monophosphoryl lipid A or glucopyranosyl lipid A (GLA) have shown protection in animal models. KSAC+GLA-SE protected against cutaneous disease following sand fly transmission of Leishmania major in susceptible BALB/c mice. Similar polyprotein adjuvant combinations are the vaccine candidates most likely to see clinical evaluation. We assessed immunity generated by KSAC or L110f vaccination with GLA-SE following challenge with L. major by needle or infected sand fly bite in resistant C57BL/6 mice. Polyprotein-vaccinated mice had a 60-fold increase in CD4(+)IFN-gamma T+ cell numbers versus control animals at 2 wk post-needle inoculation of L. major, and this correlated with a 100-fold reduction in parasite load. Immunity did not, however, reach levels observed in mice with a healed primary infection. Following challenge by infected sand fly bite, polyprotein-vaccinated animals had comparable parasite loads, greater numbers of neutrophils at the challenge site, and reduced CD4(+)IFN-gamma(+)/IL-17(+) ratios versus nonvaccinated controls. In contrast, healed animals had significantly reduced parasite loads and higher CD4(+) IFN-gamma(+)/IL-17(+) ratios. These observations demonstrate that vaccine-induced protection against needle challenge does not necessarily translate to protection following challenge by infected sand fly bite. The Journal of Immunology, 2012, 189: 4832-4841.
C1 [Peters, Nathan C.; Lawyer, Phillip G.; Charmoy, Melanie; Romano, Audrey; Ribeiro-Gomes, Flavia L.; Stamper, Lisa W.; Sacks, David L.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Bertholet, Sylvie] Infect Dis Res Inst, Seattle, WA 98104 USA.
RP Peters, NC (reprint author), NIAID, Parasit Dis Lab, NIH, 4 Ctr Dr,MSC 0425, Bethesda, MD 20892 USA.
EM NPeters@niaid.nih.gov
RI Ribeiro-Gomes, Flavia/F-7609-2015
FU National Institutes of Health, National Institute of Allergy and
Infectious Diseases
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Allergy and
Infectious Diseases.
NR 49
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U1 0
U2 1
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 2012
VL 189
IS 10
BP 4832
EP 4841
DI 10.4049/jimmunol.1201676
PG 10
WC Immunology
SC Immunology
GA 032IU
UT WOS:000310710600017
PM 23045616
ER
PT J
AU White, KL
Roth, BL
AF White, Kate L.
Roth, Bryan L.
TI Psychotomimetic Effects of Kappa Opioid Receptor Agonists
SO BIOLOGICAL PSYCHIATRY
LA English
DT Editorial Material
ID SALVINORIN-A; PATHWAYS; BEHAVIOR; RATS
C1 [White, Kate L.; Roth, Bryan L.] Univ N Carolina, Sch Med, Dept Pharmacol, Chapel Hill, NC 27599 USA.
[Roth, Bryan L.] Univ N Carolina, Sch Med, Dept Psychiat, Chapel Hill, NC 27599 USA.
[Roth, Bryan L.] Univ N Carolina, Program Neurosci, Sch Med, Chapel Hill, NC 27599 USA.
[Roth, Bryan L.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Sch Med, Chapel Hill, NC 27599 USA.
[Roth, Bryan L.] Univ N Carolina, Neurodev Disorders Res Ctr, Sch Med, Chapel Hill, NC 27599 USA.
[Roth, Bryan L.] Univ N Carolina, Div Chem Biol & Med Chem, Sch Med, Chapel Hill, NC 27599 USA.
[Roth, Bryan L.] NIMH, Psychoact Drug Screening Program, Chapel Hill, NC USA.
RP Roth, BL (reprint author), Univ N Carolina, Sch Med, Dept Pharmacol, CB 7365, Chapel Hill, NC 27599 USA.
EM bryan_roth@med.unc.edu
RI Roth, Bryan/F-3928-2010
FU NIDA NIH HHS [R01 DA017204]; NIGMS NIH HHS [T32 GM007040]
NR 10
TC 3
Z9 3
U1 0
U2 14
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 NOV 15
PY 2012
VL 72
IS 10
BP 797
EP 798
DI 10.1016/j.biopsych.2012.08.014
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 027KT
UT WOS:000310351800004
PM 23083945
ER
PT J
AU Fucito, LM
Park, A
Gulliver, SB
Mattson, ME
Gueorguieva, RV
O'Malley, SS
AF Fucito, Lisa M.
Park, Aesoon
Gulliver, Suzy Bird
Mattson, Margaret E.
Gueorguieva, Ralitza V.
O'Malley, Stephanie S.
TI Cigarette Smoking Predicts Differential Benefit from Naltrexone for
Alcohol Dependence
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Acamprosate; alcohol dependence; behavioral treatment; cigarette
smoking; naltrexone; pharmacotherapy
ID LOW-DOSE NALTREXONE; RANDOMIZED CONTROLLED-TRIAL; CLINICAL PREDICTORS;
DRINKING RATES; HEAVY DRINKING; NICOTINE; CESSATION; SMOKERS;
INTERVENTIONS; REINFORCEMENT
AB Background: Identifying factors that modify responsiveness to pharmacotherapies for alcohol dependence is important for treatment planning. Cigarette smoking predicts more severe alcohol dependence and poorer treatment response in general. Nevertheless, there is limited research on cigarette smoking as a potential predictor of differential response to pharmacological treatment of alcoholism.
Methods: We examined the association between cigarette smoking and drinking outcomes in the COMBINE (Combined Pharmacotherapies and Behavioral Interventions for Alcohol Dependence) study, a randomized, double-blind placebo-controlled 16-week trial comparing combinations of medications (i.e., acamprosate and naltrexone) and behavioral interventions (i.e., medical management, combined behavioral therapy) in 1383 alcohol-dependent individuals.
Results: Smokers (i.e., more than one half the sample) significantly differed from nonsmokers on several demographic and drinking-related variables at baseline and generally had poorer treatment outcomes than nonsmokers. However, smokers who received naltrexone had better drinking outcomes than smokers who received placebo, whereas alcohol use among nonsmokers did not vary by naltrexone assignment. This pattern of findings occurred independent of whether patients received combined behavioral intervention or medical management and remained after controlling for alcoholism typology and baseline demographic differences. Approximately 9% of smokers quit smoking, and an additional 10% reduced their cigarette intake during treatment. Reductions in smoking did not vary by treatment assignment.
Conclusions: These results suggest that naltrexone might be particularly beneficial for improving alcohol use outcomes in alcohol-dependent smokers.
C1 [Fucito, Lisa M.] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT 06511 USA.
[O'Malley, Stephanie S.] Yale Canc Ctr, New Haven, CT USA.
[Gueorguieva, Ralitza V.] Yale Univ, Sch Publ Hlth, New Haven, CT USA.
[Park, Aesoon] Syracuse Univ, Dept Psychol, Syracuse, NY USA.
[Gulliver, Suzy Bird] VA VISN 17 Ctr Excellence Res Returning War Vet, Waco, TX USA.
[Gulliver, Suzy Bird] Cent Texas Vet Hlth Care Syst, Temple, TX USA.
[Mattson, Margaret E.] Natl Inst Alcohol Abuse & Alcoholism, Div Treatment Res, Bethesda, MD USA.
[Mattson, Margaret E.] Subst Abuse & Mental Hlth Serv Adm, Ctr Behav Hlth Stat & Qual, Rockville, MD USA.
RP Fucito, LM (reprint author), Yale Univ, Sch Med, Dept Psychiat, 1 Long Wharf Dr,Box 18, New Haven, CT 06511 USA.
EM lisa.fucito@yale.edu
OI Gueorguieva, Ralitza/0000-0003-0944-5973
FU National Institute on Alcohol Abuse and Alcoholism [K05-AA014715,
R01-AA016621, K23-AA02000, T32-AA015496]; National Institute on Alcohol
Abuse and Alcoholism, National Institutes of Health, Department of
Health and Human Services; Eli Lilly; Janssen; Johnson Johnson; Schering
Plough; Lundbeck; GlaxoSmithKline; Alkermes
FX This research was supported in part by grants from the National
Institute on Alcohol Abuse and Alcoholism: K05-AA014715 (SSO),
R01-AA016621 (SSO, RG), K23-AA02000 (LMF), and T32-AA015496 (LMF).We
acknowledge that the reported results are, in whole or in part, based on
analyses of the COMBINE Data Set. These data were collected as part of a
multisite clinical trial of alcoholism treatments supported by a series
of grants from the National Institute on Alcohol Abuse and Alcoholism,
National Institutes of Health, Department of Health and Human Services.
This report has not been reviewed or endorsed by National Institute on
Alcohol Abuse and Alcoholism or the COMBINE Research Group and does not
necessarily represent the opinions of its members or National Institute
on Alcohol Abuse and Alcoholism, who are not responsible for the
contents.; Dr. Stephanie O'Malley is a member American College of
Neuropsychopharmacogy workgroup, the Alcohol Clinical Trial Initiative,
sponsored by Eli Lilly, Janssen, Johnson & Johnson, Schering Plough,
Lundbeck, GlaxoSmithKline, and Alkermes; has served as partner with
Applied Behavioral Research; has been under contract with Nabi
Biopharmaceuticals; has received medication supplies from Pfizer; has
served on the Advisory Board of Gilead Pharmaceuticals; has served as
consultant to GlaxoSmithKline, Lundbeck, Brown University; and has
served on the Scientific Panel of Advisors of Hazelden. All other
authors report no biomedical financial interests or potential conflicts
of interest.
NR 51
TC 16
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U1 1
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD NOV 15
PY 2012
VL 72
IS 10
BP 832
EP 838
DI 10.1016/j.biopsych.2012.03.023
PG 7
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 027KT
UT WOS:000310351800011
PM 22541040
ER
PT J
AU Martin, DJ
FitzMorris, PE
Li, B
Ayestas, M
Sally, EJ
Dersch, CM
Rothman, RB
Deveau, AM
AF Martin, David J.
FitzMorris, Paul E.
Li, Bo
Ayestas, Mario
Sally, Ellicott J.
Dersch, Christina M.
Rothman, Richard B.
Deveau, Amy M.
TI An efficient synthesis of 3-OBn-6 beta,14-epoxy-bridged opiates from
naltrexone and identification of a related dual MOR inverse agonist/KOR
agonist
SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
LA English
DT Article
DE Naltrexone; Naltrexol; Antagonist; Inverse Agonist; Opiate; 6
beta,14-Epoxymorphinan; Conformation; Rigid analog
ID MU-OPIOID RECEPTOR; CONFORMATIONAL RESTRICTION; FUNCTIONAL SELECTIVITY;
NARCOTIC DEPENDENCE; NALOXONE; 6-BETA-NALTREXOL; DERIVATIVES;
ANTAGONISTS; AFFINITY; PHARMACOLOGY
AB In an effort to better understand the conformational preferences that inform the biological activity of naltrexone and related naltrexol derivatives, a new synthesis of the restricted analog 3-OBn-6 beta,14-epoxymorphinan 4 is described. 4 was synthesized starting from naltrexone in 50% overall yield, proceeding through the OBn-6 alpha-triflate intermediate 8. Key steps to the synthesis include benzylation (96% yield), reduction (90% yield, alpha:beta:3:2), followed by a one-pot triflation/displacement sequence (96% yield) to yield the desired bridged epoxy derivative 4. X-ray crystallographic analysis of intermediate 3-OBn-6 alpha-naltrexol 7a supports population of the key boat conformation required for the epoxy ring closure. We also report that the 6 beta-mesylate 10-a high affinity opioid receptor ligand, the epimeric derivative of 11, and an analog of 12-functions as an inverse agonist at the mu opioid receptor using herkinorin pre-conditioned cells and an agonist at the kappa opioid receptor when evaluated in independent in vitro [S-35]-GTP-gamma-S assays. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Martin, David J.; FitzMorris, Paul E.; Deveau, Amy M.] Univ New England, Coll Arts & Sci, Dept Chem & Phys, Biddeford, ME 04005 USA.
[Martin, David J.] Univ New England, Coll Osteopath Med, Biddeford, ME 04005 USA.
[Li, Bo] Boston Coll, Xray Crystallog Ctr, Dept Chem, Chestnut Hill, MA 02467 USA.
[Ayestas, Mario; Sally, Ellicott J.; Dersch, Christina M.; Rothman, Richard B.] NIDA, NIH, Addict Res Ctr, Baltimore, MD 21224 USA.
RP Deveau, AM (reprint author), Univ New England, Coll Arts & Sci, Dept Chem & Phys, Biddeford, ME 04005 USA.
EM adeveau@une.edu
FU University of New England; Research Mini-Grants; Chemistry & Physics
Department; Carman Pettapiece Student Research Fund of the College of
Osteophatic Medicine (COM) at UNE; CAS; COM Dean's Offices; Provost's
office; Intramural Research Program, National Institute on Drug Abuse,
National Institutes of Health
FX This Letter is dedicated to Professor Timothy Macdonald for his many
contributions to the field of Organic and Medicinal Chemistry. The
authors are indebted to Dr. Kenner C. Rice and Kejun Chung of the Drug
Design and Synthesis Section, National Institute on Drug Abuse, National
Institutes of Health, Bethesda, MD, for providing a sample of KC-2-009
for use in functional binding assays. The authors are also grateful to
Mallinckrodt, Inc. for generously donating naltrexone free base. We
thank Dr. Rebecca Conry (Colby College, Waterville, ME) for valuable
advice and assistance in preparing X-ray quality crystals of 7a. We
gratefully acknowledge the support of the University of New England
(UNE) for College of Arts & Sciences (CAS) Research Mini-Grants and the
Chemistry & Physics Department for monies to support research &
conference travel (awarded to A. M. D.). We thank the Carman Pettapiece
Student Research Fund of the College of Osteophatic Medicine (COM) at
UNE as well as the CAS and COM Dean's Offices and the Provost's office
for research support (awarded to D.J.M./A.M.D.). Portions of this work
were supported by the Intramural Research Program, National Institute on
Drug Abuse, National Institutes of Health.
NR 45
TC 0
Z9 0
U1 1
U2 7
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-894X
J9 BIOORG MED CHEM LETT
JI Bioorg. Med. Chem. Lett.
PD NOV 15
PY 2012
VL 22
IS 22
BP 6801
EP 6805
DI 10.1016/j.bmcl.2012.06.056
PG 5
WC Chemistry, Medicinal; Chemistry, Organic
SC Pharmacology & Pharmacy; Chemistry
GA 027LL
UT WOS:000310353700003
PM 22771010
ER
PT J
AU Gildersleeve, JC
Wang, BM
Achilefu, S
Tu, Z
Xu, M
AF Gildersleeve, Jeffrey C.
Wang, Baomei
Achilefu, Samuel
Tu, Zhude
Xu, Mai
TI Glycan array analysis of the antigen repertoire targeted by
tumor-binding antibodies
SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
LA English
DT Article
DE Glycan array; Antibody; Carbohydrate; Tumor antigen; Cancer vaccine
ID BLOOD GROUP ANTIGENS; MONOCLONAL-ANTIBODIES; COLON-CANCER; VACCINES;
IMMUNOTHERAPY; MICROARRAY; CELLS; SPECIFICITY; MELANOMA; EPITOPES
AB Immunization with whole cells has been used extensively to generate monoclonal antibodies, produce protective immune responses, and discover new disease antigens. While glycans are abundant on cell surfaces, anti-glycan immune responses have not been well-characterized. We used glycan microarrays to profile 49 tumor-binding monoclonal antibodies generated by immunizing mice with whole cancer cells. A substantial proportion (41%) of the tumor binding antibodies bound carbohydrate antigens. The antibodies primarily recognize a group of 5 glycan antigens: Sialyl Lewis A (SLeA), Lewis A (LeA), Lewis X (LeX), blood group A (BG-A), and blood group H on a type 2 chain (BG-H2). The results have important implications for monoclonal antibody production and cancer vaccine development. Published by Elsevier Ltd.
C1 [Gildersleeve, Jeffrey C.] NCI, Biol Chem Lab, Frederick, MD 21702 USA.
[Wang, Baomei] Univ Louisville, James Graham Brown Canc Ctr, Dept Microbiol & Immunol, Louisville, KY 40202 USA.
[Achilefu, Samuel; Tu, Zhude; Xu, Mai] Washington Univ, Sch Med, Dept Radiol, St Louis, MO 63110 USA.
RP Gildersleeve, JC (reprint author), NCI, Biol Chem Lab, Frederick, MD 21702 USA.
EM gildersj@mail.nih.gov; xum@mir.wustl.edu
RI Gildersleeve, Jeffrey/N-3392-2014;
OI Achilefu, Samuel/0000-0002-3133-6717
FU Intramural Research Program of the NIH, NCI
FX We thank Jack Simpson (Protein Chemistry Laboratory, SAIC/NCI-Frederick)
for MALDI-MS analysis of BSA conjugates. This research was supported in
part by the Intramural Research Program of the NIH, NCI.
NR 45
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Z9 8
U1 2
U2 22
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-894X
J9 BIOORG MED CHEM LETT
JI Bioorg. Med. Chem. Lett.
PD NOV 15
PY 2012
VL 22
IS 22
BP 6839
EP 6843
DI 10.1016/j.bmcl.2012.09.055
PG 5
WC Chemistry, Medicinal; Chemistry, Organic
SC Pharmacology & Pharmacy; Chemistry
GA 027LL
UT WOS:000310353700011
PM 23063402
ER
PT J
AU Scott, JG
Bauchet, L
Fraum, TJ
Nayak, L
Cooper, AR
Chao, ST
Suh, JH
Vogelbaum, MA
Peereboom, DM
Zouaoui, S
Mathieu-Daude, H
Fabbro-Peray, P
Rigau, V
Taillandier, L
Abrey, LE
DeAngelis, LM
Shih, JH
Iwamoto, FM
AF Scott, Jacob G.
Bauchet, Luc
Fraum, Tyler J.
Nayak, Lakshmi
Cooper, Anna R.
Chao, Samuel T.
Suh, John H.
Vogelbaum, Michael A.
Peereboom, David M.
Zouaoui, Sonia
Mathieu-Daude, Helene
Fabbro-Peray, Pascale
Rigau, Valerie
Taillandier, Luc
Abrey, Lauren E.
DeAngelis, Lisa M.
Shih, Joanna H.
Iwamoto, Fabio M.
TI Recursive Partitioning Analysis of Prognostic Factors for Glioblastoma
Patients Aged 70 Years or Older
SO CANCER
LA English
DT Article
DE glioblastoma; elderly; surgery; prognosis; aging
ID MALIGNANT GLIOMAS; ELDERLY-PATIENTS; BRAIN-TUMORS; PATTERNS; CARE;
EPIDEMIOLOGY; RADIOTHERAPY; SURVIVAL
AB BACKGROUND: The most-used prognostic scheme for malignant gliomas included only patients aged 18 to 70 years. The purpose of this study was to develop a prognostic model for patients >= 70 years of age with newly diagnosed glioblastoma. METHODS: A total of 437 patients >= 70 years of age with newly diagnosed glioblastoma, pooled from 2 tertiary academic institutions, was identified for recursive partitioning analysis (RPA). The resulting prognostic model, based on the final pruned RPA tree, was validated using 265 glioblastoma patients >= 70 years of age from a data set independently compiled by a French consortium. RESULTS: RPA produced 9 terminal nodes, which were pruned to 4 prognostic subgroups with markedly different median survivals: subgroup I = patients <75.5 years of age who underwent surgical resection (9.3 months); subgroup II = patients >= 75.5 years of age who underwent surgical resection (6.4 months); subgroup III = patients with Karnofsky performance status of 70 to 100 who underwent biopsy only (4.6 months); and subgroup IV = patients with Karnofsky performance status <70 who underwent biopsy only (2.3 months). Application of this prognostic model to the French cohort also resulted in significantly different (P < .0001) median survivals for subgroups I (8.5 months), II (7.7 months), III (4.3 months), and IV (3.1 months). CONCLUSIONS: This model divides elderly glioblastoma patients into prognostic subgroups that can be easily implemented in both the patient care and the clinical trial settings. This purely clinical prognostic model serves as a backbone for the future incorporation of the increasing number of potential molecular prognostic markers. Cancer 2012. (c) 2012 American Cancer Society.
C1 [Fraum, Tyler J.; Iwamoto, Fabio M.] NCI, Neurooncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Scott, Jacob G.] Univ S Florida, H Lee Moffitt Canc Ctr, Dept Radiat Oncol, Tampa, FL 33682 USA.
[Bauchet, Luc; Zouaoui, Sonia] CHU Montpellier, Hop St Eloi Gui de Chauliac, Dept Neurosurg, Montpellier, France.
[Bauchet, Luc; Zouaoui, Sonia] CHU Montpellier, Hop St Eloi Gui de Chauliac, INSERM, U1051, Montpellier, France.
[Fraum, Tyler J.] Duke Univ, Sch Med, Durham, NC USA.
[Nayak, Lakshmi; Abrey, Lauren E.; DeAngelis, Lisa M.] Mem Sloan Kettering Canc Ctr, Brain Tumor Ctr, New York, NY 10021 USA.
[Nayak, Lakshmi; Abrey, Lauren E.; DeAngelis, Lisa M.] Mem Sloan Kettering Canc Ctr, Dept Neurol, New York, NY 10021 USA.
[Cooper, Anna R.] Univ Rochester, Med Ctr, Dept Orthoped, Rochester, NY 14642 USA.
[Chao, Samuel T.; Suh, John H.; Vogelbaum, Michael A.; Peereboom, David M.] Cleveland Clin, Brain Tumor Inst, Cleveland, OH 44106 USA.
[Mathieu-Daude, Helene] Ctr Lutte Canc Val dAurelle, Registre Tumeurs Herault, Neurooncol Grp Languedoc Roussillon, Dept Epidemiol, Montpellier, France.
[Fabbro-Peray, Pascale] Inst Univ Rech Clin, Dept Biostat, Montpellier, France.
[Fabbro-Peray, Pascale] Ctr Hosp Univ, Nimes, France.
[Rigau, Valerie] CHU Montpellier, Hop Gui de Chauliac, Dept Pathol, Montpellier, France.
[Taillandier, Luc] Hop Neurol, Dept Neurooncol, Nancy, France.
[Shih, Joanna H.] NCI, Biometr Res Branch, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
RP Iwamoto, FM (reprint author), NCI, Neurooncol Branch, Ctr Canc Res, NIH, 9030 Old Georgetown Rd,Room 221, Bethesda, MD 20892 USA.
EM fi2146@columbia.edu
OI ZOUAOUI, Sonia/0000-0003-0467-3280
FU US National Institutes of Health (NIH) Intramural Research Program
[1ZIDBC011098-02]; NIH; Pfizer Inc.; National Cancer Institute Clinical
Investigator Development Program; NIH Intramural Program
[1ZIABC011347-01, 1ZIABC011348-01]; French government (INCa);
Association des Neuro-Oncologues d'Expression Francaise (ANOCEF);
Societe Francaise de NeuroChirurgie (SFNC); Societe Francaise de
Neuropathologie (SFNP)
FX This study has been supported by the US National Institutes of Health
(NIH) Intramural Research Program (1ZIDBC011098-02). Dr. Fraum is a
Fellow in the Clinical Research Training Program, a public-private
partnership supported jointly by NIH and Pfizer Inc. (via a grant to the
Foundation for NIH from Pfizer Inc.). Dr. Iwamoto is supported by the
National Cancer Institute Clinical Investigator Development Program and
the NIH Intramural Program (1ZIABC011347-01 and 1ZIABC011348-01). Drs.
Zouaoui, Mathieu-Daude, Fabbro-Peray, Rigau, Taillandier, and Bauchet
acknowledge the support of the French government (INCa), Association des
Neuro-Oncologues d'Expression Francaise (ANOCEF), Societe Francaise de
NeuroChirurgie (SFNC), and Societe Francaise de Neuropathologie (SFNP).
NR 21
TC 28
Z9 28
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
J9 CANCER-AM CANCER SOC
JI Cancer
PD NOV 15
PY 2012
VL 118
IS 22
BP 5595
EP 5600
DI 10.1002/cncr.27570
PG 6
WC Oncology
SC Oncology
GA 029GW
UT WOS:000310483800017
PM 22517216
ER
PT J
AU Shiels, MS
Engels, EA
Shi, JX
Landi, MT
Albanes, D
Chatterjee, N
Chanock, SJ
Caporaso, NE
Chaturvedi, AK
AF Shiels, Meredith S.
Engels, Eric A.
Shi, Jianxin
Landi, Maria Teresa
Albanes, Demetrius
Chatterjee, Nilanjan
Chanock, Stephen J.
Caporaso, Neil E.
Chaturvedi, Anil K.
TI Genetic Variation in Innate Immunity and Inflammation Pathways
Associated With Lung Cancer Risk
SO CANCER
LA English
DT Article
DE lung cancer; genetics; inflammation; immunity; epidemiology
ID SUSCEPTIBILITY LOCUS; POLYMORPHISMS; PREVENTION; LYMPHOMA; SMOKING;
NFKB1
AB BACKGROUND: Pulmonary inflammation may contribute to lung cancer etiology. The authors conducted a broad evaluation of the association of single nucleotide polymorphisms (SNPs) in innate immunity and inflammation pathways with lung cancer risk and conducted comparisons with a lung cancer genome-wide association study (GWAS). METHODS: In total, 378 patients with lung cancer (cases) and a group of 450 controls from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial were included. A proprietary oligonucleotide pool assay was used to genotype 1429 SNPs. Odds ratios and 95% confidence intervals were estimated for each SNP, and P values for trend (P-trend) were calculated. For statistically significant SNPs (P-trend < .05), the results were replicated with genotyped or imputed SNPs in the GWAS, and P values were adjusted for multiple testing. RESULTS: In the PLCO analysis, a significant association was observed between lung cancer and 81 SNPs located in 44 genes (P-trend < .05). Of these 81 SNPS, there was evidence for confirmation in the GWAS for 10 SNPs. However, after adjusting for multiple comparisons, the only SNP that retained a significant association with lung cancer in the replication phase was reference SNP rs4648127 (nuclear factor of kappa light polypeptide gene enhancer of B-cells 1 [NFKB1]) (multiple testing-adjusted P-trend = .02). The cytosine-thymine (CT)/TT genotype of NFKB1 was associated with reduced odds of lung cancer in the PLCO study (odds ratio, 0.56; 95% confidence interval, 0.37-0.86) and the in the GWAS (odds ratio, 0.79; 95% confidence interval, 0.69-0.90). CONCLUSIONS: A significant association was observed between a variant in the NFKB1 gene and the risk of lung cancer. The current findings add to evidence implicating inflammation and immunity in lung cancer etiology. Cancer 2012. Published 2012 by the American Cancer Society.
C1 [Shiels, Meredith S.; Engels, Eric A.; Chaturvedi, Anil K.] NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20892 USA.
[Shi, Jianxin; Chatterjee, Nilanjan] NCI, Biostat Branch, Div Canc Epidemiol & Genet, Rockville, MD 20892 USA.
[Landi, Maria Teresa; Caporaso, Neil E.] NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20892 USA.
[Albanes, Demetrius] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20892 USA.
[Chanock, Stephen J.] NCI, Lab Translat Genom, Div Canc Epidemiol & Genet, Rockville, MD 20892 USA.
RP Shiels, MS (reprint author), NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,EPS 7059, Rockville, MD 20892 USA.
EM shielsms@mail.nih.gov
RI Albanes, Demetrius/B-9749-2015; Chaturvedi, Anil/J-2024-2015
OI Chaturvedi, Anil/0000-0003-2696-8899
FU National Cancer Institute; National Institutes of Health, National
Cancer Institute (NCI), Division of Cancer Epidemiology and Genetics;
NCI [NO1-CN-25,514, NO1-CN-25,522, NO1-CN-25,515, NO1-CN-25,512,
NO1-CN-25,513, NO1-CN-25,516, NO1-CN-25,511, NO1-CN-25,524,
NO1-CN-75,022, NO1-CN-25,476, NO1-CN-25,404]; US. Public Health Service
from the NCI [N01-CN-45,165, N01-RC-45,035, N01-RC-37,004]; American
Cancer Society
FX This study was supported by the Intramural Research Program of the
National Cancer Institute. The Environment and Genetics in Lung Cancer
Etiology (EAGLE), Prostate, Lung, Colon, Ovary Screening Trial (PLCO),
and Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) studies
were supported by the Intramural Research Program of the National
Institutes of Health, National Cancer Institute (NCI), Division of
Cancer Epidemiology and Genetics. PLCO also was supported by individual
contracts from the NCI to the University of Colorado Denver
(NO1-CN-25,514), Georgetown University (NO1-CN-25,522), the Pacific
Health Research Institute (NO1-CN-25,515), the Henry Ford Health System
(NO1-CN-25,512), the University of Minnesota, (NO1-CN-25,513),
Washington University (NO1-CN-25,516), the University of Pittsburgh
(NO1-CN-25,511), the University of Utah (NO1-CN-25,524), the Marshfield
Clinic Research Foundation (NO1-CN-25,518), the University of Alabama at
Birmingham (NO1-CN-75,022), Westat, Inc. (NO1-CN-25,476), and the
University of California, Los Angeles (NO1-CN-25,404). ATBC also was
supported by US. Public Health Service contracts (N01-CN-45,165,
N01-RC-45,035, and N01-RC-37,004) from the NCI. The Cancer Prevention
Study-II (CPS-II) Nutrition Cohort was supported by the American Cancer
Society.
NR 26
TC 14
Z9 14
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
J9 CANCER-AM CANCER SOC
JI Cancer
PD NOV 15
PY 2012
VL 118
IS 22
BP 5630
EP 5636
DI 10.1002/cncr.27605
PG 7
WC Oncology
SC Oncology
GA 029GW
UT WOS:000310483800022
PM 23044494
ER
PT J
AU Feuer, EJ
Lee, M
Mariotto, AB
Cronin, KA
Scoppa, S
Penson, DF
Hachey, M
Cynkin, L
Carter, GA
Campbell, D
Percy-Laurry, A
Zou, ZH
Schrag, D
Hankey, BF
AF Feuer, Eric J.
Lee, Minjung
Mariotto, Angela B.
Cronin, Kathy A.
Scoppa, Steve
Penson, David F.
Hachey, Mark
Cynkin, Laurie
Carter, Ginger A.
Campbell, David
Percy-Laurry, Antoinette
Zou, Zhaohui
Schrag, Deborah
Hankey, Benjamin F.
TI The Cancer Survival Query System: Making Survival Estimates From the
Surveillance, Epidemiology, and End Results Program More Timely and
Relevant for Recently Diagnosed Patients
SO CANCER
LA English
DT Article
DE competing risk analysis; survival analysis; proportional hazards;
prostate cancer; nomograms; prognosis; shared decision-making
ID BREAST
AB BACKGROUND: Population-based cancer registries that include patient follow-up generally provide information regarding net survival (ie, survival associated with the risk of dying of cancer in the absence of competing risks). However, registry data also can be used to calculate survival from cancer in the presence of competing risks, which is more clinically relevant. METHODS: Statistical methods were developed to predict the risk of death from cancer and other causes, as well as natural life expectancy if the patient did not have cancer based on a profile of prognostic factors including characteristics of the cancer, demographic factors, and comorbid conditions. The Surveillance, Epidemiology, and End Results (SEER) Program database was used to calculate the risk of dying of cancer. Because the risks of dying of cancer versus other causes are assumed to be independent conditional on the prognostic factors, a wide variety of independent data sources can be used to calculate the risk of death from other causes. Herein, the risk of death from other causes was estimated using SEER and Medicare claims data, and was matched to the closest fitting portion of the US life table to obtain a health status-adjusted age. RESULTS: A nomogram was developed for prostate cancer as part of a Web-based Cancer Survival Query System that is targeted for use by physicians and patients to obtain information on a patient's prognosis. More nomograms currently are being developed. CONCLUSIONS: Nomograms of this type can be used as one tool to assist cancer physicians and their patients to better understand their prognosis and to weigh alternative treatment and palliative strategies. Cancer 2012. (c) 2012 American Cancer Society.
C1 [Hankey, Benjamin F.] CANSTAT, Plano, TX 75024 USA.
[Feuer, Eric J.; Lee, Minjung; Mariotto, Angela B.; Cronin, Kathy A.; Cynkin, Laurie; Percy-Laurry, Antoinette] NCI, Surveillance Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Scoppa, Steve; Hachey, Mark; Carter, Ginger A.; Campbell, David; Zou, Zhaohui] Informat Management Serv Inc, Silver Spring, MD USA.
[Penson, David F.] Vanderbilt Univ, Med Ctr, Ctr Surg Qual & Outcomes Res, Nashville, TN USA.
[Penson, David F.] Tennessee Valley Geriatr Res Educ & Clin Ctr GREC, Vet Adm, Nashville, TN USA.
[Schrag, Deborah] Dana Farber Canc Inst, Dept Med, Boston, MA 02115 USA.
RP Hankey, BF (reprint author), CANSTAT, 6805 Colonnade Dr, Plano, TX 75024 USA.
EM bhankey0411@aol.com
FU National Cancer Institute
FX Supported by the National Cancer Institute.
NR 24
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U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
J9 CANCER-AM CANCER SOC
JI Cancer
PD NOV 15
PY 2012
VL 118
IS 22
BP 5652
EP 5662
DI 10.1002/cncr.27615
PG 11
WC Oncology
SC Oncology
GA 029GW
UT WOS:000310483800025
PM 22569947
ER
PT J
AU Reeve, BB
Stover, AM
Jensen, RE
Chen, RC
Taylor, KL
Clauser, SB
Collins, SP
Potosky, AL
AF Reeve, Bryce B.
Stover, Angela M.
Jensen, Roxanne E.
Chen, Ronald C.
Taylor, Kathryn L.
Clauser, Steven B.
Collins, Sean P.
Potosky, Arnold L.
TI Impact of Diagnosis and Treatment of Clinically Localized Prostate
Cancer on Health-Related Quality of Life for Older Americans A
Population-Based Study
SO CANCER
LA English
DT Article
DE prostate cancer; health-related quality of life; population-based;
prospective; older Americans
ID ANDROGEN DEPRIVATION THERAPY; RANDOMIZED DOSE-ESCALATION; 5-YEAR
FOLLOW-UP; PROPENSITY-SCORE; SEXUAL FUNCTION; MANAGED CARE;
RADIOTHERAPY; OUTCOMES; CARCINOMA; SURVEILLANCE
AB BACKGROUND: Few studies have measured longitudinal changes in health-related quality of life (HRQOL) among patients with prostate cancer starting before their cancer diagnosis or have provided simultaneous comparisons with a matched noncancer cohort. In the current study, the authors addressed these gaps by providing unique estimates of the effects of a cancer diagnosis on HRQOL accounting for the confounding effects of ageing and comorbidity. METHODS: Data from the Surveillance, Epidemiology, and End Results registry were linked with Medicare Health Outcomes Survey (MHOS) data. Eligible patients (n = 445) were Medicare beneficiaries aged >= 65 years from 1998 to 2003 whose first prostate cancer diagnosis occurred between their baseline and follow-up MHOS. By using propensity score matching, 2225 participants without cancer were identified from the MHOS data. Analysis of covariance models were used to estimate changes in HRQOL as assessed with the Medical Outcomes Study Short Form-36 survey and the activities of daily living scale. RESULTS: Before diagnosis, patients with prostate cancer reported HRQOL similar to that of men without cancer. After diagnosis, men with prostate cancer experienced significant decrements in physical, mental, and social aspects of their lives relative to controls, especially within the first 6 months after diagnosis. For men who were surveyed beyond 1 year after diagnosis, HRQOL was similar to that for controls. However, an increased risk for major depressive disorder was observed among men who received either conservative management or external beam radiation. CONCLUSIONS: The current findings illustrated the time-sensitive nature of decline in HRQOL after a cancer diagnosis and enhanced understanding of the impact of prostate cancer diagnosis and treatment on physical, mental, and social well being among older men. Cancer 2012;118;5679-87. (C) 2012 American Cancer Society.
C1 [Reeve, Bryce B.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Gillings Sch Global Publ Hlth, Dept Hlth Policy & Management, Chapel Hill, NC 27599 USA.
[Stover, Angela M.] Univ N Carolina, Dept Hlth Behav & Hlth Educ, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
[Jensen, Roxanne E.; Taylor, Kathryn L.; Potosky, Arnold L.] Georgetown Univ, Dept Oncol, Canc Control Program, Lombardi Comprehens Canc Ctr, Washington, DC USA.
[Chen, Ronald C.] Univ N Carolina, Dept Radiat Oncol, Chapel Hill, NC USA.
[Clauser, Steven B.] NCI, Outcomes Res Branch, Appl Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Collins, Sean P.] Georgetown Univ Hosp, Dept Radiat Oncol, Washington, DC 20007 USA.
RP Reeve, BB (reprint author), 135 Dauer Dr,1101-D McGavran Greenberg Bldg, Chapel Hill, NC 27599 USA.
EM bbreeve@email.unc.edu
FU National Cancer Institute [HHSN261201000642P]
FX Dr. Reeve's work was supported under a National Cancer Institute
contract to the University of North Carolina at Chapel Hill
(HHSN261201000642P).
NR 54
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U1 1
U2 17
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
J9 CANCER-AM CANCER SOC
JI Cancer
PD NOV 15
PY 2012
VL 118
IS 22
BP 5679
EP 5687
DI 10.1002/cncr.27578
PG 9
WC Oncology
SC Oncology
GA 029GW
UT WOS:000310483800028
PM 22544633
ER
PT J
AU Jain, M
Zhang, LS
He, M
Patterson, EE
Nilubol, N
Fojo, AT
Joshi, B
Puri, R
Kebebew, E
AF Jain, Meenu
Zhang, Lisa
He, Mei
Patterson, Erin E.
Nilubol, Naris
Fojo, Antonio T.
Joshi, Bharat
Puri, Raj
Kebebew, Electron
TI Interleukin-13 Receptor Alpha2 Is a Novel Therapeutic Target for Human
Adrenocortical Carcinoma
SO CANCER
LA English
DT Article
DE interleukin-13 receptor alpha2; interleuken-13-Pseudomonas exotoxin;
adrenocortical carcinoma; invasion
ID CHIMERIC FUSION PROTEINS; SQUAMOUS-CELL CARCINOMA; PSEUDOMONAS EXOTOXIN;
SIGNAL-TRANSDUCTION; MALIGNANT GLIOMAS; CANCER THERAPY; EXPRESSION;
CHAIN; TUMORS; HEAD
AB BACKGROUND. Adrenocortical carcinoma (ACC) is a relatively rare but aggressive malignancy with limited therapeutic options. Previous genome-wide expression studies have demonstrated the overexpression of interleukin-13 receptor alpha2 (IL13R alpha 2) in some human malignancies. METHODS. The authors evaluated IL13R alpha 2 mRNA and protein expression in 21 normal samples, 78 benign samples, 10 primary malignant samples, and 25 metastatic/recurrent samples and performed functional analyses with IL13 ligand and IL13 R alpha 2 knockdown in vitro. The sensitivity of 2 ACC cell lines (NCI-H295R [high IL13R alpha 2 expression] and SW13 [low IL13R alpha 2 expression]) to a highly specific IL-13 conjugated with Pseudomonas exotoxin (IL-13-PE) also was evaluated in both in vitro and in vivo models. RESULTS. IL13R alpha 2 was overexpressed in malignant tumors compared with benign and normal samples (15-fold higher; P < .05). Immunohistochemistry also confirmed higher protein expression in malignant and benign tumors than in normal adrenocortical tissues (P < .05). The half-maximal inhibitory concentration for IL-13-PE was 1.3 ng/mL in the NCI-H295R cell line and 1000 ng/mL in the SW13 cell line. Mice that received intratumoral or intraperitoneal IL-13-PE injection had a significant reduction in tumor size and increased tumor necrosis compared with control groups (P < .05) and also had prolonged survival (P < .05). IL13R alpha 2 protein expression increased in cells that were treated with IL-13 ligand along with cell invasion (P < .05). Direct IL13R alpha 2 knockdown decreased cellular proliferation and invasion (P < .05). CONCLUSIONS. The current results indicated that IL13R alpha 2 is overexpressed in ACC and regulates cell invasion and proliferation. IL13R alpha 2 is a novel therapeutic target for the treatment of human ACC. Cancer 2012;118;5698-708 (C) 2012 American Cancer Society.
C1 [Kebebew, Electron] NCI, Endocrine Oncol Branch, CRC Hatfield Clin Res Ctr 10, NIH, Bethesda, MD 20892 USA.
[Joshi, Bharat; Puri, Raj] US FDA, Tumor Vaccines & Biotechnol Branch, Div Cellular & Gene Therapies, Ctr Biol Evaluat & Res, Bethesda, MD 20014 USA.
[Fojo, Antonio T.] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Kebebew, E (reprint author), NCI, Endocrine Oncol Branch, CRC Hatfield Clin Res Ctr 10, NIH, Bethesda, MD 20892 USA.
EM electron.kebebew@nih.gov
FU Center for Cancer Research, National Cancer Institute, National
Institutes of Health [1ZIABC011286-01, 1ZIABC011275-01]
FX This study was supported by the Intramural Research Program of the
Center for Cancer Research, National Cancer Institute, National
Institutes of Health (grants 1ZIABC011286-01 and 1ZIABC011275-01).
NR 41
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U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
J9 CANCER-AM CANCER SOC
JI Cancer
PD NOV 15
PY 2012
VL 118
IS 22
BP 5698
EP 5708
DI 10.1002/cncr.27629
PG 11
WC Oncology
SC Oncology
GA 029GW
UT WOS:000310483800030
PM 22570059
ER
PT J
AU Mollersen, L
Rowe, AD
Illuzzi, JL
Hildrestrand, GA
Gerhold, KJ
Tveteras, L
Bjolgerud, A
Wilson, DM
Bjoras, M
Klungland, A
AF Mollersen, Linda
Rowe, Alexander D.
Illuzzi, Jennifer L.
Hildrestrand, Gunn A.
Gerhold, Katharina J.
Tveteras, Linda
Bjolgerud, Anja
Wilson, David M., III
Bjoras, Magnar
Klungland, Arne
TI Neil1 is a genetic modifier of somatic and germline CAG trinucleotide
repeat instability in R6/1 mice
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID OXIDATIVELY DAMAGED DNA; HUNTINGTONS-DISEASE; TRANSGENIC MICE;
GLYCOSYLASES NEIL1; OXIDIZED BASES; IN-VIVO; REPAIR; EXCISION; MUTATION;
EXPANSION
AB Huntingtons disease (HD) is a progressive neurodegenerative disorder caused by trinucleotide repeat (TNR) expansions. We show here that somatic TNR expansions are significantly reduced in several organs of R6/1 mice lacking exon 2 of Nei-like 1 (Neil1) (R6/1/Neil1(/)), when compared with R6/1/Neil1(/) mice. Somatic TNR expansion is measured by two different methods, namely mean repeat change and instability index. Reduced somatic expansions are more pronounced in male R6/1/Neil1(/) mice, although expansions are also significantly reduced in brain regions of female R6/1/Neil1(/) mice. In addition, we show that the lack of functional Neil1 significantly reduces germline expansion in R6/1 male mice. In vitro, purified human NEIL1 protein binds and excises 5-hydroxycytosine in duplex DNA more efficiently than in hairpin substrates. NEIL1 excision of cytosine-derived oxidative lesions could therefore be involved in initiating the process of TNR expansion, although other DNA modifications might also contribute. Altogether, these results imply that Neil1 contributes to germline and somatic HD CAG repeat expansion.
C1 [Mollersen, Linda; Rowe, Alexander D.; Hildrestrand, Gunn A.; Tveteras, Linda; Bjoras, Magnar; Klungland, Arne] Natl Hosp Norway, Oslo Univ Hosp, Inst Med Microbiol, NO-0027 Oslo, Norway.
[Illuzzi, Jennifer L.; Wilson, David M., III] NIA, Lab Mol Gerontol, NIH, IRP,Biomed Res Ctr, Baltimore, MD 21224 USA.
RP Klungland, A (reprint author), Natl Hosp Norway, Oslo Univ Hosp, Inst Med Microbiol, Sognsvannsveien 20, NO-0027 Oslo, Norway.
EM arne.klungland@rr-research.no
FU Norwegian Research Council; Norwegian Cancer Society; Centre for
Molecular Biology and Neuroscience; Health Region South-East of Norway;
Oslo University Hospital; National Institute on Aging, NIH
FX This work was supported by the Norwegian Research Council (L. M.,
K.J.G., A. B.), the Norwegian Cancer Society (G. A. H., L. T.), the
Centre for Molecular Biology and Neuroscience (A. D. R.), the Health
Region South-East of Norway (A. D. R.), Oslo University Hospital (M. B.,
A. K.) and the Intramural Research Program of the National Institute on
Aging, NIH (J.L.I. and D. M. W.). Funding to pay the Open Access
publication charges for this article was provided by the Health Region
South-East of Norway.
NR 39
TC 23
Z9 23
U1 0
U2 3
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 2012
VL 21
IS 22
BP 4939
EP 4947
DI 10.1093/hmg/dds337
PG 9
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 027QV
UT WOS:000310369000012
PM 22914735
ER
PT J
AU Timofeeva, MN
Hung, RJ
Rafnar, T
Christiani, DC
Field, JK
Bickeboller, H
Risch, A
McKay, JD
Wang, YF
Dai, JC
Gaborieau, V
McLaughlin, J
Brenner, D
Narod, SA
Caporaso, NE
Albanes, D
Thun, M
Eisen, T
Wichmann, HE
Rosenberger, A
Han, YH
Chen, W
Zhu, DK
Spitz, M
Wu, XF
Pande, M
Zhao, Y
Zaridze, D
Szeszenia-Dabrowska, N
Lissowska, J
Rudnai, P
Fabianova, E
Mates, D
Bencko, V
Foretova, L
Janout, V
Krokan, HE
Gabrielsen, ME
Skorpen, F
Vatten, L
Njolstad, I
Chen, C
Goodman, G
Lathrop, M
Benhamou, S
Vooder, T
Valk, K
Nelis, M
Metspalu, A
Raji, O
Chen, Y
Gosney, J
Liloglou, T
Muley, T
Dienemann, H
Thorleifsson, G
Shen, HB
Stefansson, K
Brennan, P
Amos, CI
Houlston, R
Landi, MT
AF Timofeeva, Maria N.
Hung, Rayjean J.
Rafnar, Thorunn
Christiani, David C.
Field, John K.
Bickeboeller, Heike
Risch, Angela
McKay, James D.
Wang, Yufei
Dai, Juncheng
Gaborieau, Valerie
McLaughlin, John
Brenner, Darren
Narod, Steven A.
Caporaso, Neil E.
Albanes, Demetrius
Thun, Michael
Eisen, Timothy
Wichmann, H. -Erich
Rosenberger, Albert
Han, Younghun
Chen, Wei
Zhu, Dakai
Spitz, Margaret
Wu, Xifeng
Pande, Mala
Zhao, Yang
Zaridze, David
Szeszenia-Dabrowska, Neonilia
Lissowska, Jolanta
Rudnai, Peter
Fabianova, Eleonora
Mates, Dana
Bencko, Vladimir
Foretova, Lenka
Janout, Vladimir
Krokan, Hans E.
Gabrielsen, Maiken Elvestad
Skorpen, Frank
Vatten, Lars
Njolstad, Inger
Chen, Chu
Goodman, Gary
Lathrop, Mark
Benhamou, Simone
Vooder, Tonu
Vaelk, Kristjan
Nelis, Mari
Metspalu, Andres
Raji, Olaide
Chen, Ying
Gosney, John
Liloglou, Triantafillos
Muley, Thomas
Dienemann, Hendrik
Thorleifsson, Gudmar
Shen, Hongbing
Stefansson, Kari
Brennan, Paul
Amos, Christopher I.
Houlston, Richard
Landi, Maria Teresa
CA TRICL Res Team
TI Influence of common genetic variation on lung cancer risk: meta-analysis
of 14 900 cases and 29 485 controls
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; CORONARY-ARTERY-DISEASE; DNA DOUBLE-STRAND;
SUSCEPTIBILITY LOCI; LARGE-SCALE; JAPANESE POPULATION; GENOTYPE
IMPUTATION; NICOTINE DEPENDENCE; IN-VIVO; VARIANTS
AB Recent genome-wide association studies (GWASs) have identified common genetic variants at 5p15.33, 6p216p22 and 15q25.1 associated with lung cancer risk. Several other genetic regions including variants of CHEK2 (22q12), TP53BP1 (15q15) and RAD52 (12p13) have been demonstrated to influence lung cancer risk in candidate- or pathway-based analyses. To identify novel risk variants for lung cancer, we performed a meta-analysis of 16 GWASs, totaling 14 900 cases and 29 485 controls of European descent. Our data provided increased support for previously identified risk loci at 5p15 (P 7.2 10(16)), 6p21 (P 2.3 10(14)) and 15q25 (P 2.2 10(63)). Furthermore, we demonstrated histology-specific effects for 5p15, 6p21 and 12p13 loci but not for the 15q25 region. Subgroup analysis also identified a novel disease locus for squamous cell carcinoma at 9p21 (CDKN2A/p16(INK4A)/p14(ARF)/CDKN2B/p15(INK4B)/ANRIL; rs1333040, P 3.0 10(7)) which was replicated in a series of 5415 Han Chinese (P 0.03; combined analysis, P 2.3 10(8)). This large analysis provides additional evidence for the role of inherited genetic susceptibility to lung cancer and insight into biological differences in the development of the different histological types of lung cancer.
C1 [Wu, Xifeng; Pande, Mala] Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
[Spitz, Margaret] Baylor Coll Med, Houston, TX 77030 USA.
[Wichmann, H. -Erich] Univ Munich, Inst Med Informat Biometry & Epidemiol, Chair Epidemiol, D-81377 Munich, Germany.
[Wichmann, H. -Erich] Helmholtz Ctr Munich, Inst Epidemiol 1, D-85764 Neuherberg, Germany.
[Eisen, Timothy] Cambridge Univ Hosp NHS Fdn Trust, Dept Oncol, Cambridge, England.
[Thun, Michael] Amer Canc Soc Epidemiol & Surveillance Res, Atlanta, GA 30301 USA.
[Narod, Steven A.] Womens Coll Res Inst, Toronto, ON, Canada.
[Caporaso, Neil E.; Albanes, Demetrius; Landi, Maria Teresa] NCI, Div Canc Epidemiol & Genet, NIH, US Publ Hlth Serv, Bethesda, MD 20892 USA.
[Dai, Juncheng; Shen, Hongbing] Nanjing Med Univ, Sch Publ Hlth, Dept Epidemiol & Biostat, Nanjing, Jiangsu, Peoples R China.
[Wang, Yufei; Houlston, Richard] Inst Canc Res, Div Genet & Epidemiol, Sutton SM2 5NG, Surrey, England.
[Risch, Angela] DKFZ German Canc Res Ctr, Translat Lung Res Ctr Heidelberg TLRC H, D-69120 Heidelberg, Germany.
[Bickeboeller, Heike; Rosenberger, Albert] Univ Gottingen, Dept Genet Epidemiol, Univ Med Ctr, D-37073 Gottingen, Germany.
[Field, John K.; Raji, Olaide; Chen, Ying; Gosney, John; Liloglou, Triantafillos] Univ Liverpool, Roy Castle Lung Canc Res Programme, Dept Mol & Clin Canc Med, Canc Res Ctr,Inst Translat Med, Liverpool L69 3BX, Merseyside, England.
[Christiani, David C.; Zhao, Yang] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Rafnar, Thorunn; Thorleifsson, Gudmar; Stefansson, Kari] DeCODE Genet, Reykjavik, Iceland.
[Hung, Rayjean J.; McLaughlin, John; Brenner, Darren] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Toronto, ON M5G 1X5, Canada.
[Timofeeva, Maria N.; McKay, James D.; Gaborieau, Valerie; Brennan, Paul] Int Agcy Res Canc, F-69008 Lyon, France.
[Zaridze, David] Russian NN Blokhin Canc Res Ctr, Inst Carcinogenesis, Moscow 115478, Russia.
[Szeszenia-Dabrowska, Neonilia] Inst Occupat Med, Dept Epidemiol, PL-91348 Lodz, Poland.
[Lissowska, Jolanta] M Sklodowska Curie Mem Canc Ctr, PL-02781 Warsaw, Poland.
[Lissowska, Jolanta] Inst Oncol, PL-02781 Warsaw, Poland.
[Fabianova, Eleonora] Reg Author Publ Hlth, Banska Bystrica 97556, Slovakia.
[Rudnai, Peter] Natl Inst Environm Hlth, H-1097 Budapest, Hungary.
[Mates, Dana] Natl Inst Publ Hlth, Bucharest 050463, Romania.
[Bencko, Vladimir] Charles Univ Prague, Inst Hyg & Epidemiol, Fac Med 1, Prague 12800 2, Czech Republic.
[Foretova, Lenka] Masaryk Mem Canc Inst, Dept Canc Epidemiol & Genet, Brno 65653, Czech Republic.
[Janout, Vladimir] Palacky Univ, Olomouc 77515, Czech Republic.
[Krokan, Hans E.; Gabrielsen, Maiken Elvestad] Norwegian Univ Sci & Technol, Fac Med, Dept Canc Res & Mol Med, N-7489 Trondheim, Norway.
[Skorpen, Frank] Norwegian Univ Sci & Technol, Dept Lab Med Childrens & Womens Hlth, Fac Med, N-7489 Trondheim, Norway.
[Vatten, Lars] Norwegian Univ Sci & Technol, Dept Publ Hlth & Gen Practice, Fac Med, N-7489 Trondheim, Norway.
[Njolstad, Inger] Univ Tromso, Dept Community Med, N-9037 Tromso, Norway.
[Chen, Chu; Goodman, Gary] Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA.
[Lathrop, Mark] Ctr Etud Polymorphisme Humain, F-75010 Paris, France.
[Benhamou, Simone] INSERM, U946, F-75010 Paris, France.
[Vooder, Tonu] Univ Tartu, Inst Mol & Cell Biol, EE-51010 Tartu, Estonia.
[Vaelk, Kristjan] Competence Ctr Reprod Med & Biol, EE-50410 Tartu, Estonia.
[Nelis, Mari; Metspalu, Andres] Estonian Genome Ctr, Inst Mol & Cell Biol, EE-51010 Tartu, Estonia.
[Nelis, Mari] Univ Geneva, Sch Med, Dept Genet Med & Dev, CH-1211 Geneva, Switzerland.
[Muley, Thomas] Univ Klinikum Heidelberg, Translat Res Unit, Heidelberg, Germany.
[Dienemann, Hendrik] Univ Klinikum Heidelberg, Dept Thorac Surg, Thoraxklin, Heidelberg, Germany.
[Amos, Christopher I.] Dartmouth Coll, Dept Community & Family Med, Geisel Sch Med, Hanover, NH 03750 USA.
[Han, Younghun; Chen, Wei; Zhu, Dakai; Amos, Christopher I.] Univ Texas MD Anderson Canc Ctr, Dept Genet, Houston, TX 77030 USA.
RP Amos, CI (reprint author), Dartmouth Coll, Geisel Sch Med, Dept Community & Family Med, 46 Centerra Pkwy,Suite 330, Lebanon, NH 03766 USA.
EM Christopher.I.Amos@Dartmouth.edu
RI Hung, Rayjean/A-7439-2013; McLaughlin, John/E-4577-2013; Zaridze,
David/K-5605-2013; Janout, Vladimir/M-5133-2014; Albanes,
Demetrius/B-9749-2015; Szeszenia-Dabrowska, Neonila/F-7190-2010;
Benhamou, Simone/K-6554-2015; Risch, Angela/H-2669-2013; Chen,
Ying/I-4349-2013;
OI Houlston, Richard/0000-0002-5268-0242; Risch,
Angela/0000-0002-8026-5505; mates, dana/0000-0002-6219-9807; Lissowska,
Jolanta/0000-0003-2695-5799; Field, John/0000-0003-3951-6365
FU National Institute of Health (NIH) [U19CA148127, 5R01CA055769,
5R01CA127219, 5R01CA133996, 5R01CA121197, P50 CA70907, R01CA121197, RO1
CA127219, U19 CA148127, RO1 CA55769, HHSN268200782096C, CA074386,
CA092824, CA090578]; Canadian Cancer Society Research Institute
[020214]; Ontario Institute of Cancer; Cancer Care Ontario Chair Award;
Cancer Research UK [C1298/A8780, C1298/A8362]; NCRN, HEAL;
Sanofi-Aventis; Roy Castle Lung Cancer Foundation, UK; Deutsche
Krebshilfe [70-2919]; Helmholtz-DAAD fellowship [A/07/97379]; National
Institute of Health (USA) [U19CA148127]; GSF; German Federal Ministry of
Education, Science, Research and Technology; State of Bavaria; National
Genome Research Network (NGFN); DFG [BI 576/2-1, BI 576/2-2];
Helmholtzgemeinschaft (HGF); Federal office for Radiation Protection
[BfS: STSch4454]; Institut National du Cancer, France; European
Community [LSHG-CT-2005-512113]; Norwegian Cancer Association and the
Functional Genomics Programme of Research Council of Norway; European
Regional Development Fund; State Budget of the Czech Republic (RECAMO)
[CZ.1.05/2.1.00/03.0101]; National Cancer Institute of the U.S. National
Institutes of Health [R01 CA111703, UO1 CA63673]; Fred Hutchinson Cancer
Research Center; US National Cancer Institute [R01 CA092039]; FP7 grant
[REGPOT 245536]; Estonian Government [SF0180142s08]; EU RDF; IARC; NCI,
Division of Cancer Epidemiology and Genetics; U.S. Public Health Service
from the NCI [N01-CN-45165, N01-RC-45035, N01-RC-37004]; NCI
[NO1-CN-25514]; Georgetown University [NO1-CN-25522]; Pacific Health
Research Institute [NO1-CN-25515]; Henry Ford Health System
[NO1-CN-25512]; University of Minnesota [NO1-CN-25513]; Washington
University [NO1-CN-25516]; University of Pittsburgh [NO1-CN-25511];
University of Utah [NO1-CN-25524]; Marshfield Clinic Research Foundation
[NO1-CN-25518]; University of Alabama at Birmingham [NO1-CN-75022];
University of Alabama at Birmingham, Westat, Inc. [NO1-CN-25476];
University of California, Los Angeles [NO1-CN-25404]; American Cancer
Society; NIH Genes, Environment and Health Initiative (GEI)
[HG-06-033-NCI-01, RO1HL091172-01]; CPRIT grant [RP100443]; China
National High-Tech Research and Development Program Grant
[2009AA022705]; National Key Basic Research Program Grant
[2011CB503805]; National Natural Science Foundation of China [30730080,
30972541, 30901233, 30872178]
FX This study was supported by the grant from the National Institute of
Health (NIH) (U19CA148127). The SLRI study was supported by Canadian
Cancer Society Research Institute (020214), Ontario Institute of Cancer
and Cancer Care Ontario Chair Award to R. H. The ICR study was supported
by Cancer Research UK (C1298/A8780 and C1298/A8362-Bobby Moore Fund for
Cancer Research UK) and NCRN, HEAL and Sanofi-Aventis. Additional
funding was obtained from NIH grants (5R01CA055769, 5R01CA127219,
5R01CA133996, and 5R01CA121197). The Liverpool Lung Project (LLP) was
supported by The Roy Castle Lung Cancer Foundation, UK. The ICR and LLP
studies made use of genotyping data from the Wellcome Trust Case Control
Consortium 2 (WTCCC2); a full list of the investigators who contributed
to the generation of the data is available from www.wtccc.org.uk. Sample
collection for the Heidelberg lung cancer study was in part supported by
a grant (70-2919) from the Deutsche Krebshilfe. The work was
additionally supported by a Helmholtz-DAAD fellowship (A/07/97379 to
M.N.T.) and by the National Institute of Health (USA) (U19CA148127). The
KORA Surveys were financed by the GSF, which is funded by the German
Federal Ministry of Education, Science, Research and Technology and the
State of Bavaria. The LUng Cancer in the Young study (LUCY) was funded
in part by the National Genome Research Network (NGFN), the DFG (BI
576/2-1; BI 576/2-2), the Helmholtzgemeinschaft (HGF) and the Federal
office for Radiation Protection (BfS: STSch4454). Genotyping was
performed in the Genome Analysis Center (GAC) of the Helmholtz Zentrum
Muenchen. Support for the Central Europe, HUNT2/Tromso and CARET
genome-wide studies was provided by Institut National du Cancer, France.
Support for the HUNT2/Tromso genome-wide study was also provided by the
European Community (Integrated Project DNA repair, LSHG-CT-2005-512113),
the Norwegian Cancer Association and the Functional Genomics Programme
of Research Council of Norway. Support for the Central Europe study,
Czech Republic, was also provided by the European Regional Development
Fund and the State Budget of the Czech Republic (RECAMO,
CZ.1.05/2.1.00/03.0101). Support for the CARET genome-wide study was
also provided by grants from the National Cancer Institute of the U.S.
National Institutes of Health (R01 CA111703 and UO1 CA63673) and by
funds from the Fred Hutchinson Cancer Research Center. Additional
funding for study coordination, genotyping of replication studies and
statistical analysis was provided by the US National Cancer Institute
(R01 CA092039). The lung cancer GWAS from Estonia was partly supported
by a FP7 grant (REGPOT 245536), by the Estonian Government
(SF0180142s08), by EU RDF in the frame of Centre of Excellence in
Genomics and Estoinian Research Infrastructure's Roadmap and by
University of Tartu (SP1GVARENG). The work reported in this paper was
partly undertaken during the tenure of a Postdoctoral Fellowship from
the IARC (for MNT). The Environment and Genetics in Lung Cancer Etiology
(EAGLE), the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study
(ATBC) and the Prostate, Lung, Colon, Ovary Screening Trial (PLCO)
studies and the genotyping of ATBC, the Cancer Prevention Study II
Nutrition Cohort (CPS-II) and part of PLCO were supported by the
Intramural Research Program of NIH, NCI, Division of Cancer Epidemiology
and Genetics. ATBC was also supported by U.S. Public Health Service
contracts (N01-CN-45165, N01-RC-45035 and N01-RC-37004) from the NCI.;
PLCO was also supported by individual contracts from the NCI to the
University of Colorado Denver (NO1-CN-25514), Georgetown University
(NO1-CN-25522), Pacific Health Research Institute (NO1-CN-25515), Henry
Ford Health System (NO1-CN-25512), University of Minnesota
(NO1-CN-25513), Washington University (NO1-CN-25516), University of
Pittsburgh (NO1-CN-25511), University of Utah (NO1-CN-25524), Marshfield
Clinic Research Foundation (NO1-CN-25518), University of Alabama at
Birmingham (NO1-CN-75022, Westat, Inc. NO1-CN-25476), University of
California, Los Angeles (NO1-CN-25404). The Cancer Prevention Study II
Nutrition Cohort was supported by the American Cancer Society. The NIH
Genes, Environment and Health Initiative (GEI) partly funded DNA
extraction and statistical analyses (HG-06-033-NCI-01 and
RO1HL091172-01), genotyping at the Johns Hopkins University Center for
Inherited Disease Research (U01HG004438 and NIH HHSN268200782096C) and
study coordination at the GENEVA Coordination Center (U01 HG004446) for
EAGLE and part of PLCO studies. Funding for the MD Anderson Cancer Study
was provided by NIH grants (P50 CA70907, R01CA121197, RO1 CA127219, U19
CA148127, RO1 CA55769) and CPRIT grant (RP100443). Genotyping services
were provided by the Center for Inherited Disease Research (CIDR). CIDR
is funded through a federal contract from the National Institutes of
Health to The Johns Hopkins University (HHSN268200782096C). The Harvard
Lung Cancer Study was funded by Funded by National Institutes of Health
(CA074386, CA092824, CA090578). The Nanjing study and Beijing studies
were funded by the China National High-Tech Research and Development
Program Grant (2009AA022705), the National Key Basic Research Program
Grant (2011CB503805) and the National Natural Science Foundation of
China (30730080, 30972541, 30901233 and 30872178). Funding to pay the
Open Access publication charges for this article was provided by the
grant from the National Institute of Health (NIH) (U19CA148127).
NR 92
TC 68
Z9 70
U1 0
U2 33
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 2012
VL 21
IS 22
BP 4980
EP 4995
DI 10.1093/hmg/dds334
PG 16
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 027QV
UT WOS:000310369000016
PM 22899653
ER
PT J
AU Keller, MF
Saad, M
Bras, J
Bettella, F
Nicolaou, N
Simon-Sanchez, J
Mittag, F
Buchel, F
Sharma, M
Gibbs, JR
Schulte, C
Moskvina, V
Durr, A
Holmans, P
Kilarski, LL
Guerreiro, R
Hernandez, DG
Brice, A
Ylikotila, P
Stefansson, H
Majamaa, K
Morris, HR
Williams, N
Gasser, T
Heutink, P
Wood, NW
Hardy, J
Martinez, M
Singleton, AB
Nalls, MA
AF Keller, Margaux F.
Saad, Mohamad
Bras, Jose
Bettella, Francesco
Nicolaou, Nayia
Simon-Sanchez, Javier
Mittag, Florian
Buechel, Finja
Sharma, Manu
Gibbs, J. Raphael
Schulte, Claudia
Moskvina, Valentina
Durr, Alexandra
Holmans, Peter
Kilarski, Laura L.
Guerreiro, Rita
Hernandez, Dena G.
Brice, Alexis
Ylikotila, Pauli
Stefansson, Hreinn
Majamaa, Kari
Morris, Huw R.
Williams, Nigel
Gasser, Thomas
Heutink, Peter
Wood, Nicholas W.
Hardy, John
Martinez, Maria
Singleton, Andrew B.
Nalls, Michael A.
CA IPDGC
WTCCC2
TI Using genome-wide complex trait analysis to quantify 'missing
heritability' in Parkinson's disease
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID FAMILIAL AGGREGATION; GLUCOCEREBROSIDASE MUTATIONS; RARE VARIANTS;
COMMON SNPS; EARLY-ONSET; ASSOCIATION; METAANALYSIS; GENETICS; TWINS;
SUSCEPTIBILITY
AB Genome-wide association studies (GWASs) have been successful at identifying single-nucleotide polymorphisms (SNPs) highly associated with common traits; however, a great deal of the heritable variation associated with common traits remains unaccounted for within the genome. Genome-wide complex trait analysis (GCTA) is a statistical method that applies a linear mixed model to estimate phenotypic variance of complex traits explained by genome-wide SNPs, including those not associated with the trait in a GWAS. We applied GCTA to 8 cohorts containing 7096 case and 19 455 control individuals of European ancestry in order to examine the missing heritability present in Parkinsons disease (PD). We meta-analyzed our initial results to produce robust heritability estimates for PD types across cohorts. Our results identify 27 (95 CI 1738, P 8.08E 08) phenotypic variance associated with all types of PD, 15 (95 CI 0.2 to 33, P 0.09) phenotypic variance associated with early-onset PD and 31 (95 CI 1744, P 1.34E 05) phenotypic variance associated with late-onset PD. This is a substantial increase from the genetic variance identified by top GWAS hits alone (between 3 and 5) and indicates there are substantially more risk loci to be identified. Our results suggest that although GWASs are a useful tool in identifying the most common variants associated with complex disease, a great deal of common variants of small effect remain to be discovered.
C1 [Nalls, Michael A.] NIA, Mol Genet Sect, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Keller, Margaux F.] Temple Univ, Dept Biol Anthropol, Philadelphia, PA 19122 USA.
[Saad, Mohamad; Mittag, Florian; Buechel, Finja; Martinez, Maria] Ctr Physiopathol Toulouse Purpan, INSERM, UMR 1043, F-31073 Toulouse, France.
[Saad, Mohamad; Martinez, Maria] Univ Toulouse 3, F-31062 Toulouse, France.
[Bras, Jose; Gibbs, J. Raphael; Guerreiro, Rita; Hernandez, Dena G.; Wood, Nicholas W.; Hardy, John] UCL, Dept Mol Neurosci, Inst Neurol, London, England.
[Wood, Nicholas W.] UCL, UCL Genet Inst, London, England.
[Bettella, Francesco; Stefansson, Hreinn; Heutink, Peter] DeCODE Genet, Sci Serv, IS-101 Reykjavik, Iceland.
[Nicolaou, Nayia; Simon-Sanchez, Javier] Vrije Univ Amsterdam Med Ctr, Dept Clin Genet, Sect Med Gen, Amsterdam, Netherlands.
[Sharma, Manu; Schulte, Claudia; Gasser, Thomas] Univ Tubingen, Dept Neurodegenerat Dis, Hertie Inst Clin Brain Res, Tubingen, Germany.
[Sharma, Manu; Schulte, Claudia; Gasser, Thomas] German Ctr Neurodegenerat Dis, Tubingen, Germany.
[Moskvina, Valentina; Holmans, Peter; Kilarski, Laura L.; Morris, Huw R.; Williams, Nigel] Cardiff Univ, MRC, Ctr Neuropsychiat Genet & Genom, Sch Med, Cardiff, S Glam, Wales.
[Moskvina, Valentina; Holmans, Peter; Kilarski, Laura L.; Morris, Huw R.; Williams, Nigel] Cardiff Univ, Inst Psychol Med & Clin Neurosci, Cardiff, S Glam, Wales.
[Durr, Alexandra; Brice, Alexis] Univ Paris 06, Ctr Rech, Inst Cerveau & Moelle Epiniere, UMR S975, Paris, France.
[Durr, Alexandra; Brice, Alexis] Hop La Pitie Salpetriere, AP HP, Dept Genet, Paris, France.
[Durr, Alexandra; Brice, Alexis] INSERM, UMR S975, Paris, France.
[Durr, Alexandra; Brice, Alexis] CNRS, UMR 7225, Paris, France.
[Ylikotila, Pauli] Turku Univ Hosp, Dept Neurol, Turku, Finland.
[Ylikotila, Pauli] Univ Turku, SF-20500 Turku, Finland.
[Majamaa, Kari] Univ Oulu, Dept Clin Med, Oulu, Finland.
RP Nalls, MA (reprint author), NIA, Mol Genet Sect, Neurogenet Lab, NIH, Bldg 35,35 Convent Dr, Bethesda, MD 20892 USA.
EM nallsm@mail.nih.gov
RI Blackwell, Jenefer/H-3015-2015; Trabzuni, Daniah/C-4034-2012; Mathew,
Christopher/G-3434-2015; Martinez, Maria/B-3111-2013; Guerreiro,
Rita/A-1327-2011; corvol, jean-christophe/I-6387-2012; Revesz,
Tamas/A-8732-2010; Deuschl, Gunther/A-7986-2010; Morris,
Huw/B-8527-2008; Hardy, John/C-2451-2009; Scheffer, Hans/E-4644-2012;
lambert, jean-charles/F-8787-2013; Wood, Nicholas/C-2505-2009; LICEND,
CEMND/F-1296-2015; Traynor, Bryan/G-5690-2010; Bloem,
Bastiaan/E-3812-2010; Bras, Jose/A-1428-2011; Charlesworth,
Gavin/B-5895-2011; Singleton, Andrew/C-3010-2009; O'Sullivan,
Sean/C-9333-2012; Jankowski, Janusz/H-2706-2012
OI Chen, Honglei/0000-0003-3446-7779; Pirinen, Matti/0000-0002-1664-1350;
Kilarski, Laura/0000-0003-0645-3134; Gillman,
Matthew/0000-0002-2340-6930; Holmans, Peter/0000-0003-0870-9412; Plomin,
Robert/0000-0002-0756-3629; Stefansson, Hreinn/0000-0002-9331-6666;
Escott-Price, Valentina/0000-0003-1784-5483; Rivadeneira,
Fernando/0000-0001-9435-9441; Palmer, Colin/0000-0002-6415-6560; Bhatia,
Kailash/0000-0001-8185-286X; Trabzuni, Daniah/0000-0003-4826-9570;
Mathew, Christopher/0000-0003-4178-1838; Martinez,
Maria/0000-0003-2180-4537; corvol, jean-christophe/0000-0001-7325-0199;
Revesz, Tamas/0000-0003-2501-0259; Bras, Jose/0000-0001-8186-0333;
Corvin, Aiden/0000-0001-6717-4089; Morris, Huw/0000-0002-5473-3774;
Scheffer, Hans/0000-0002-2986-0915; Wood, Nicholas/0000-0002-9500-3348;
O'Sullivan, Sean/0000-0002-0583-7956; Jankowski,
Janusz/0000-0003-2130-9181
FU National Institute on Aging, National Institute of Neurological
Disorders and Stroke, NIEHS; NHGRI of the National Institutes of Health,
Department of Health and Human Services [Z01-AG000949-02, Z01-ES101986];
US Department of Defense [W81XWH-09-2-0128]; National Institutes of
Health [NS057105, RR024992]; American Parkinson Disease Association
(APDA); Barnes Jewish Hospital Foundation; Greater St Louis Chapter of
the APDA; Hersenstichting Nederland; Neuroscience Campus Amsterdam;
Prinses Beatrix Fonds; section of medical genomics; Forschungszentrum
fur Umwelt und Gesundheit; German Federal Ministry of Education,
Science, Research, and Technology; State of Bavaria; German National
Genome Network (NGFNplus) [01GS08134]; German Ministry for Education and
Research; German Federal Ministry of Education and Research [NGFN
01GR0468, PopGen]; ERA-NET NEURON [01EW0908]; Helmholtz Alliance Mental
Health in an Ageing Society [HA-215]; Helmholtz Association; French
National Agency of Research [ANR-08-MNP-012]; Michael J. Fox Foundation;
Landspitali University Hospital; Icelandic Research Council; European
Community [PIAP-GA-2008-230596]; Wellcome Trust [083948/Z/07/Z]; Medical
Research Council; Wellcome Trust disease centre [WT089698/Z/09/Z];
Parkinson's UK [8047, J-0804]; Medical Research Council [G0700943];
Department of Health's National Institute for Health Research Biomedical
Research Centres; Wellcome Trust/Medical Research Council Joint Call in
Neurodegeneration award [WT089698]; France Parkinson Association
FX This work was supported by the Intramural Research Programs of the
National Institute on Aging, National Institute of Neurological
Disorders and Stroke, NIEHS and NHGRI of the National Institutes of
Health, Department of Health and Human Services (project numbers
Z01-AG000949-02 and Z01-ES101986), human subjects protocol 2003-077.
This work was also supported by the US Department of Defense (award
number W81XWH-09-2-0128); National Institutes of Health (grants NS057105
and RR024992); American Parkinson Disease Association (APDA); Barnes
Jewish Hospital Foundation; Greater St Louis Chapter of the APDA;
Hersenstichting Nederland; Neuroscience Campus Amsterdam; and the
section of medical genomics, the Prinses Beatrix Fonds. The KORA
(Cooperative Research in the Region of Augsburg) research platform was
started and financed by the Forschungszentrum fur Umwelt und Gesundheit,
which is funded by the German Federal Ministry of Education, Science,
Research, and Technology and by the State of Bavaria. This study was
also funded by the German National Genome Network (NGFNplus number
01GS08134, German Ministry for Education and Research); by the German
Federal Ministry of Education and Research (NGFN 01GR0468, PopGen); and
01EW0908 in the frame of ERA-NET NEURON and Helmholtz Alliance Mental
Health in an Ageing Society (HA-215), which was funded by the Initiative
and Networking Fund of the Helmholtz Association. The French GWAS work
was supported by the French National Agency of Research
(ANR-08-MNP-012). This study was also funded by the Michael J. Fox
Foundation (MS), and sponsored by the Landspitali University Hospital
Research Fund (grant to S.Sv.); Icelandic Research Council (grant to
S.Sv.); and European Community Framework Programme 7, People Programme
and IAPP on novel genetic and phenotypic markers of Parkinson's disease
and Essential Tremor (MarkMD), contract number PIAP-GA-2008-230596
MarkMD (to H. P. and J.Hu.). Genotyping of UK replication cases on
ImmunoChip was part of the WTCCC2 project, which was funded by the
Wellcome Trust (083948/Z/07/Z). This study was supported by the Medical
Research Council and Wellcome Trust disease centre (grant
WT089698/Z/09/Z to N.W.W., J. Ha. and A.Sc.). This study was also
supported by Parkinson's UK (grants 8047 and J-0804) and the Medical
Research Council (G0700943). DNA extraction work that was done in the UK
was undertaken at University College London Hospitals, University
College London, which received a proportion of funding from the
Department of Health's National Institute for Health Research Biomedical
Research Centres funding. This study was supported in part by the
Wellcome Trust/Medical Research Council Joint Call in Neurodegeneration
award (WT089698) to the Parkinson's Disease Consortium (UKPDC), whose
members are from the UCL Institute of Neurology, University of Sheffield
and the Medical Research Council Protein Phosphorylation Unit at the
University of Dundee. Mohamad Saad was funded by the France Parkinson
Association.
NR 48
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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 2012
VL 21
IS 22
BP 4996
EP 5009
DI 10.1093/hmg/dds335
PG 14
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 027QV
UT WOS:000310369000017
PM 22892372
ER
PT J
AU Song, YQ
Yeung, E
Liu, AY
VanderWeele, TJ
Chen, LW
Lu, C
Liu, CL
Schisterman, EF
Ning, Y
Zhang, CL
AF Song, Yiqing
Yeung, Edwina
Liu, Aiyi
VanderWeele, Tyler J.
Chen, Liwei
Lu, Chen
Liu, Chunling
Schisterman, Enrique F.
Ning, Yi
Zhang, Cuilin
TI Pancreatic beta-cell function and type 2 diabetes risk: quantify the
causal effect using a Mendelian randomization approach based on
meta-analyses
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; SUSCEPTIBILITY LOCI; CLINICAL-TRIALS; TCF7L2;
GENETICS; GLUCOSE; EPIDEMIOLOGY; MECHANISMS; MELLITUS; ISLETS
AB The objective of the study is to quantify the causal effect of -cell function on type 2 diabetes by minimizing residual confounding and reverse causation. We employed a Mendelian randomization (MR) approach using TCF7L2 variant rs7903146 as an instrument for lifelong levels of -cell function. We first conducted two sets of meta-analyses to quantify the association of the TCF7L2 variant with the risk of type 2 diabetes among 55 436 cases and 106 020 controls from 66 studies by calculating pooled odds ratio (OR) and to quantify the associations with multiple direct or indirect measures of -cell function among 35 052 non-diabetic individuals from 31 studies by calculating pooled mean difference. We further applied the method of MR to obtain the causal estimates for the effect of -cell function on type 2 diabetes risk based on findings from the meta-analyses. The OR [95 confidence interval (CI)] was 0.87 (0.810.93) for each five unit increment in homeostasis model assessment of insulin secretion (HOMA-B) (P 3.0 10(5)). In addition, for measures based on intravenous glucose tolerance test, ORs (95 CI) associated with type 2 diabetes risk were 0.24 (0.080.74) (P 0.01) and 0.14 (0.040.48) (P 0.002) for per 1 standard deviation increment in insulin sensitivity index and disposition index, respectively. Findings from the present study lend support to a causal role of pancreatic -cell function itself in the etiology of type 2 diabetes.
C1 [Yeung, Edwina; Schisterman, Enrique F.; Zhang, Cuilin] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Rockville, MD USA.
[Liu, Aiyi] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Biostat & Bioinfomat Branch, Div Epidemiol Stat & Prevent Res, Rockville, MD USA.
[Song, Yiqing] Peking Univ, Inst Vasc Med, Hosp 3, Beijing 100191, Peoples R China.
[Song, Yiqing] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Prevent Med, Boston, MA 02115 USA.
[VanderWeele, Tyler J.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[VanderWeele, Tyler J.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Chen, Liwei] Louisiana State Univ, Hlth Sci Ctr, Sch Publ Hlth, Program Epidemiol, New Orleans, LA USA.
[Lu, Chen] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Liu, Chunling] Hong Kong Polytech Univ, Dept Appl Math, Hong Kong, Hong Kong, Peoples R China.
[Ning, Yi] Virginia Commonwealth Univ, Sch Med, Dept Epidemiol & Community Med, Richmond, VA USA.
RP Zhang, CL (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Rockville, MD USA.
EM zhangcu@mail.nih.gov
RI Lu, Chen/D-8514-2015; Yeung, Edwina/F-5992-2015; Liu,
Chunling/A-4827-2015;
OI Yeung, Edwina/0000-0002-3851-2613; Liu, Chunling/0000-0003-3410-445X;
Liu, Aiyi/0000-0002-6618-5082; Schisterman, Enrique/0000-0003-3757-641X
FU Eunice Kennedy Shriver National Institute of Child Health & Human
Development, National Institutes of Health; National Institutes of
Health [ES017876, HD060696]
FX C.Z., E.Y., C. L. and E. F. S. are supported by the Intramural Research
Program of the Eunice Kennedy Shriver National Institute of Child Health
& Human Development, National Institutes of Health. T.J.V. is supported
by grants from the National Institutes of Health (ES017876 and
HD060696).
NR 38
TC 8
Z9 8
U1 0
U2 12
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 2012
VL 21
IS 22
BP 5010
EP 5018
DI 10.1093/hmg/dds339
PG 9
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 027QV
UT WOS:000310369000018
PM 22936689
ER
PT J
AU Ghedin, E
Holmes, EC
DePasse, JV
Pinilla, LT
Fitch, A
Hamelin, ME
Papenburg, J
Boivin, G
AF Ghedin, Elodie
Holmes, Edward C.
DePasse, Jay V.
Pinilla, Lady Tatiana
Fitch, Adam
Hamelin, Marie-Eve
Papenburg, Jesse
Boivin, Guy
TI Presence of Oseltamivir-Resistant Pandemic A/H1N1 Minor Variants Before
Drug Therapy With Subsequent Selection and Transmission
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID NEURAMINIDASE INHIBITORS; MIXED INFECTION; HIV-1 INFECTION;
INFLUENZA-VIRUS; H1N1 VIRUS; EMERGENCE; GENOME
AB A small proportion (1%-1.5%) of 2009 pandemic influenza A/H1N1 virus strains (A[H1N1]pdm09) are oseltamivir resistant, almost exclusively because of a H275Y mutation in the neuraminidase protein. However, many individuals infected with resistant strains had not received antivirals. Whether drug-resistant viruses are initially present as minor variants in untreated individuals before they emerge as the dominant strain in a virus population is of great importance for predicting the speed at which resistance will arise. To address this issue, we used ultra-deep sequencing of viral populations from serial nasopharyngeal specimens from an immunocompromised child and from 2 individuals in a household outbreak. We observed that the Y275 mutation was present as a minor variant in infected hosts before the onset of therapy. We also found evidence for the transmission of this drug-resistant variant with drug-susceptible viruses. These observations provide important information on the relative fitness of the Y275 mutation in the absence of oseltamivir treatment.
C1 [Ghedin, Elodie; DePasse, Jay V.; Fitch, Adam] Univ Pittsburgh, Ctr Vaccine Res, Sch Med, Dept Computat & Syst Biol, Pittsburgh, PA 15261 USA.
[Holmes, Edward C.] Penn State Univ, Dept Biol, Ctr Infect Dis Dynam, University Pk, PA 16802 USA.
[Holmes, Edward C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Pinilla, Lady Tatiana; Hamelin, Marie-Eve; Boivin, Guy] Ctr Hosp Univ Quebec, Ctr Rech, Quebec City, PQ, Canada.
[Pinilla, Lady Tatiana; Hamelin, Marie-Eve; Boivin, Guy] Univ Laval, Quebec City, PQ, Canada.
[Papenburg, Jesse] McGill Univ, Ctr Hlth, Montreal, PQ, Canada.
RP Ghedin, E (reprint author), Univ Pittsburgh, Ctr Vaccine Res, Sch Med, Dept Computat & Syst Biol, 3501 5th Ave,BST3 Rm 9043B, Pittsburgh, PA 15261 USA.
EM elg21@pitt.edu; guy.boivin@crchul.ulaval.ca
OI Holmes, Edward/0000-0001-9596-3552
FU National Institute of Allergy and Infectious Diseases at the National
Institutes of Health [U54 GM088491]; National Institute of General
Medical Sciences at the National Institutes of Health [2R01
GM080533-06]; Canadian Institutes of Health Research; GlaxoSmithKline
FX This work was supported in part by National Institute of Allergy and
Infectious Diseases at the National Institutes of Health (U54 GM088491),
National Institute of General Medical Sciences at the National
Institutes of Health (2R01 GM080533-06 to E. C. H.), and the Canadian
Institutes of Health Research (to G. B.).; G. B. has received a research
grant from GlaxoSmithKline. All other authors: No conflicts.
NR 26
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Z9 30
U1 0
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
EI 1537-6613
J9 J INFECT DIS
JI J. Infect. Dis.
PD NOV 15
PY 2012
VL 206
IS 10
BP 1504
EP 1511
DI 10.1093/infdis/jis571
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 025UI
UT WOS:000310220000006
PM 22966122
ER
PT J
AU Fowkes, FJI
McGready, R
Cross, NJ
Hommel, M
Simpson, JA
Elliott, SR
Richards, JS
Lackovic, K
Viladpai-Nguen, J
Narum, D
Tsuboi, T
Anders, RF
Nosten, F
Beeson, JG
AF Fowkes, Freya J. I.
McGready, Rose
Cross, Nadia J.
Hommel, Mirja
Simpson, Julie A.
Elliott, Salenna R.
Richards, Jack S.
Lackovic, Kurt
Viladpai-Nguen, Jacher
Narum, David
Tsuboi, Takafumi
Anders, Robin F.
Nosten, Francois
Beeson, James G.
TI New Insights into Acquisition, Boosting, and Longevity of Immunity to
Malaria in Pregnant Women
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID FALCIPARUM-INFECTED ERYTHROCYTES; PLASMODIUM-FALCIPARUM; MEROZOITE
ANTIGENS; ANTIBODY-RESPONSES; VIVAX MALARIA; CHILDREN; PARASITEMIA;
PROTECTION; DURATION; VAR2CSA
AB Background. How antimalarial antibodies are acquired and maintained during pregnancy and boosted after reinfection with Plasmodium falciparum and Plasmodium vivax is unknown.
Methods. A nested case-control study of 467 pregnant women (136 Plasmodium-infected cases and 331 uninfected control subjects) in northwestern Thailand was conducted. Antibody levels to P. falciparum and P. vivax merozoite antigens and the pregnancy-specific PfVAR2CSA antigen were determined at enrollment (median 10 weeks gestation) and throughout pregnancy until delivery.
Results. Antibodies to P. falciparum and P. vivax were highly variable over time, and maintenance of high levels of antimalarial antibodies involved highly dynamic responses resulting from intermittent exposure to infection. There was evidence of boosting with each successive infection for P. falciparum responses, suggesting the presence of immunological memory. However, the half-lives of Plasmodium antibody responses were relatively short, compared with measles (457 years), and much shorter for merozoite responses (0.8-7.6 years), compared with PfVAR2CSA responses (36-157 years). The longer half-life of antibodies to PfVAR2CSA suggests that antibodies acquired in one pregnancy may be maintained to protect subsequent pregnancies.
Conclusions. These findings may have important practical implications for predicting the duration of vaccine-induced responses by candidate antigens and supports the development of malaria vaccines to protect pregnant women.
C1 [Fowkes, Freya J. I.; Cross, Nadia J.; Hommel, Mirja; Richards, Jack S.; Beeson, James G.] Macfarlane Burnet Inst Med Res, Melbourne, Vic 3004, Australia.
[Fowkes, Freya J. I.; Simpson, Julie A.] Melbourne Sch Populat Hlth, Ctr Mol Environm Genet & Analyt Epidemiol, Melbourne, Vic, Australia.
[Richards, Jack S.] Univ Melbourne, Dept Med Biol, Melbourne, Vic 3010, Australia.
[Fowkes, Freya J. I.; Cross, Nadia J.; Hommel, Mirja; Elliott, Salenna R.; Richards, Jack S.; Lackovic, Kurt; Beeson, James G.] Royal Melbourne Hosp, Walter & Eliza Hall Inst Med Res, Parkville, Vic 3050, Australia.
[Anders, Robin F.] La Trobe Univ, Dept Biochem, Bundoora, Vic 3086, Australia.
[McGready, Rose; Viladpai-Nguen, Jacher; Nosten, Francois] Mae Sot, Shoklo Malaria Res Unit, Bangkok, Thailand.
[McGready, Rose; Nosten, Francois] Mahidol Univ, Fac Trop Med, Bangkok, Thailand.
[McGready, Rose; Nosten, Francois] Univ Oxford, Ctr Trop Med, Nuffield Dept Clin Med, CCVTM, Oxford OX1 2JD, England.
[Narum, David] NIAID, Malaria Vaccine Dev Branch, NIH, Rockville, MD USA.
[Tsuboi, Takafumi] Ehime Univ, Cell Free Sci & Technol Res Ctr, Matsuyama, Ehime 790, Japan.
RP Fowkes, FJI (reprint author), Macfarlane Burnet Inst Med Res, 85 Commercial Rd, Melbourne, Vic 3004, Australia.
EM fowkes@burnet.edu.au; beeson@burnet.edu.au
OI Fowkes, Freya/0000-0001-5832-9464; Simpson, Julie/0000-0002-2660-2013;
Nosten, Francois/0000-0002-7951-0745; McGready, Rose/0000-0003-1621-3257
FU National Health and Medical Research Council of Australia; Australian
Research Council; Victorian State Government; Wellcome Trust of Great
Britain
FX This work was supported by the National Health and Medical Research
Council of Australia (to J.B., F. F., and J. R.), Infrastructure for
Research Institutes Support Scheme Grant, Australian Research Council
(to J. B.), and Victorian State Government Operational Infrastructure
Support. SMRU is part of the Mahidol Oxford University Tropical Medicine
Research Unit supported by the Wellcome Trust of Great Britain. 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 6
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 2012
VL 206
IS 10
BP 1612
EP 1621
DI 10.1093/infdis/jis566
PG 10
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 025UI
UT WOS:000310220000018
PM 22966126
ER
PT J
AU Huang, JH
Ofek, G
Laub, L
Louder, MK
Doria-Rose, NA
Longo, NS
Imamichi, H
Bailer, RT
Chakrabarti, B
Sharma, SK
Alam, SM
Wang, T
Yang, YP
Zhang, BS
Migueles, SA
Wyatt, R
Haynes, BF
Kwong, PD
Mascola, JR
Connors, M
AF Huang, Jinghe
Ofek, Gilad
Laub, Leo
Louder, Mark K.
Doria-Rose, Nicole A.
Longo, Nancy S.
Imamichi, Hiromi
Bailer, Robert T.
Chakrabarti, Bimal
Sharma, Shailendra K.
Alam, S. Munir
Wang, Tao
Yang, Yongping
Zhang, Baoshan
Migueles, Stephen A.
Wyatt, Richard
Haynes, Barton F.
Kwong, Peter D.
Mascola, John R.
Connors, Mark
TI Broad and potent neutralization of HIV-1 by a gp41-specific human
antibody
SO NATURE
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; PROXIMAL EXTERNAL REGION;
MONOCLONAL-ANTIBODIES; GLYCOPROTEIN GP41; T-CELLS; EPITOPE; MEMBRANE;
BINDING; 4E10; SPECIFICITIES
AB Characterization of human monoclonal antibodies is providing considerable insight into mechanisms of broad HIV-1 neutralization. Here we report an HIV-1 gp41 membrane-proximal external region (MPER)-specific antibody, named 10E8, which neutralizes similar to 98% of tested viruses. An analysis of sera from 78 healthy HIV-1-infected donors demonstrated that 27% contained MPER-specific antibodies and 8% contained 10E8-like specificities. In contrast to other neutralizing MPER antibodies, 10E8 did not bind phospholipids, was not autoreactive, and bound cell-surface envelope. The structure of 10E8 in complex with the complete MPER revealed a site of vulnerability comprising a narrow stretch of highly conserved gp41-hydrophobic residues and a critical arginine or lysine just before the transmembrane region. Analysis of resistant HIV-1 variants confirmed the importance of these residues for neutralization. The highly conserved MPER is a target of potent, non-self-reactive neutralizing antibodies, suggesting that HIV-1 vaccines should aim to induce antibodies to this region of HIV-1 envelope glycoprotein.
C1 [Huang, Jinghe; Laub, Leo; Imamichi, Hiromi; Migueles, Stephen A.; Connors, Mark] NIAID, HIV Specif Immun Sect, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Ofek, Gilad; Louder, Mark K.; Doria-Rose, Nicole A.; Longo, Nancy S.; Bailer, Robert T.; Wang, Tao; Yang, Yongping; Zhang, Baoshan; Kwong, Peter D.; Mascola, John R.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Chakrabarti, Bimal; Sharma, Shailendra K.; Wyatt, Richard] Scripps Res Inst, Dept Immunol & Microbial Sci, IAVI Neutralizing Antibody Ctr, La Jolla, CA 92037 USA.
[Alam, S. Munir; Haynes, Barton F.] Duke Univ, Duke Human Vaccine Inst, Durham, NC 27710 USA.
RP Connors, M (reprint author), NIAID, HIV Specif Immun Sect, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
EM mconnors@nih.gov
RI Huang, Jinghe/O-1986-2015
FU NIAID; National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; US Department of Energy, Basic Energy Sciences,
Office of Science [W-31-109-Eng-38]
FX We thank C. W. Hallahan for statistical analyses. We thank K. Lloyd. R.
Parks, J. Eudailey and J. Blinn for performing autoantibody assays. We
also thank M. Zwick for providing us with the HIV-1 JR2 MPER alanine
mutant pseudovirus plasmids. HIV-2/HIV-1 chimaeras were provided by G.
Shaw and L. Morris. We thank J. Stuckey for assistance with figures, and
members of the Structural Biology Section and Structural Bioinformatics
Core, Vaccine Research Center, for discussions and comments on the
manuscript. This project has been funded in part with federal funds from
the Intramural Research Programs of NIAID and the National Cancer
Institute, National Institutes of Health, under Contract no.
HHSN261200800001E. Use of sector 22 (Southeast Region Collaborative
Access team) at the Advanced Photon Source was supported by the US
Department of Energy, Basic Energy Sciences, Office of Science, under
contract number W-31-109-Eng-38. The content of this publication does
not necessarily reflect the views or policies of the Department of
Health and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the US Government.
NR 56
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U1 6
U2 92
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 15
PY 2012
VL 491
IS 7424
BP 406
EP +
DI 10.1038/nature11544
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 036MY
UT WOS:000311031600038
PM 23151583
ER
PT J
AU Liu, ZM
de Zwart, JA
Yao, B
van Gelderen, P
Kuo, LW
Duyn, JH
AF Liu, Zhongming
de Zwart, Jacco A.
Yao, Bing
van Gelderen, Peter
Kuo, Li-Wei
Duyn, Jeff H.
TI Finding thalamic BOLD correlates to posterior alpha EEG
SO NEUROIMAGE
LA English
DT Article
DE EEG-fMRI; Alpha; Thalamus; Pulvinar; Lateral geniculate nucleus
ID CHOLINERGIC RETICULAR SYSTEM; VISUOSPATIAL ATTENTION; RESPONSE FUNCTION;
VISUAL-ATTENTION; HUMAN PULVINAR; METABOLIC-RATE; RHYTHM; CORTEX; FMRI;
BRAIN
AB Oscillatory electrical brain activity in the alpha (8-13 Hz) band is a prominent feature of human electroencephalography (EEG) during alert wakefulness, and is commonly thought to arise primarily from the occipital and parietal parts of the cortex. While the thalamus is considered to play a supportive role in the generation and modulation of cortical alpha rhythms, its precise function remains controversial and incompletely understood. To address this, we evaluated the correlation between the blood oxygenation level dependent (BOLD) functional magnetic resonance imaging (fMRI) signals in the thalamus and the spontaneous modulation of posterior alpha rhythms based on EEG fMRI data acquired concurrently during an eyes-closed task-free condition. We observed both negative and positive correlations in the thalamus. The negative correlations were mostly seen within the visual thalamus, with a preference for the pulvinar over lateral geniculate nuclei. The positive correlations were found at the anterior and medial dorsal nuclei. Through functional connectivity analysis of the fMRI data, the pulvinar was found to be functionally associated with the same widespread cortical visual areas where the fMRI signals were negatively correlated with the posterior alpha modulation. In contrast, the dorsal nuclei were part of a distinct functional network that included brain stem, cingulate cortex and cerebellum. These observations are consistent with previous animal electrophysiology studies and the notion that the visual thalamus, and the pulvinar in particular, is intimately involved in the generation and spontaneous modulation of posterior alpha rhythms, facilitated by its reciprocal and widespread interaction with the cortical visual areas. We further postulate that the anterior and medial dorsal nuclei, being part of the ascending neuromodulatory system, may indirectly modulate cortical alpha rhythms by affecting vigilance and arousal levels. Published by Elsevier Inc.
C1 [Liu, Zhongming; de Zwart, Jacco A.; Yao, Bing; van Gelderen, Peter; Kuo, Li-Wei; Duyn, Jeff H.] NINDS, Adv MRI Sect, LEMI, NIH,Lab Funct & Mol Imaging, Bethesda, MD 20982 USA.
RP Liu, ZM (reprint author), NINDS, Adv MRI Sect, LEMI, NIH,Lab Funct & Mol Imaging, Bldg 10,Room B1D-723,9000 Rockville Pike,MSC 106, Bethesda, MD 20982 USA.
EM liuz5@mail.nih.gov
RI Kuo, Li-Wei/G-4007-2011
FU National Institute of Neurological Disorders and Stroke, National
Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Institute of Neurological Disorders and Stroke, National
Institutes of Health.
NR 66
TC 20
Z9 20
U1 2
U2 18
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
EI 1095-9572
J9 NEUROIMAGE
JI Neuroimage
PD NOV 15
PY 2012
VL 63
IS 3
BP 1060
EP 1069
DI 10.1016/j.neuroimage.2012.08.025
PG 10
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 027UK
UT WOS:000310379100007
PM 22986355
ER
PT J
AU Zanotti-Fregonara, P
Hines, CS
Zoghbi, SS
Liow, JS
Zhang, Y
Pike, VW
Drevets, WC
Mallinger, AG
Zarate, CA
Fujita, M
Innis, RB
AF Zanotti-Fregonara, Paolo
Hines, Christina S.
Zoghbi, Sami S.
Liow, Jeih-San
Zhang, Yi
Pike, Victor W.
Drevets, Wayne C.
Mallinger, Alan G.
Zarate, Carlos A., Jr.
Fujita, Masahiro
Innis, Robert B.
TI Population-based input function and image-derived input function for
[C-11](R)-rolipram PET imaging: Methodology, validation and application
to the study of major depressive disorder
SO NEUROIMAGE
LA English
DT Article
DE Population-based input function; Image-derived input function;
[C-11](R)-rolipram; Major depressive disorder
ID BODY-SURFACE-AREA; INDEPENDENT COMPONENT ANALYSIS;
POSITRON-EMISSION-TOMOGRAPHY; CEREBRAL METABOLIC-RATE; BLOOD-SAMPLING
SITE; BRAIN PET; DRUG CONCENTRATION; MARKED DEPENDENCE; FDG PET;
QUANTIFICATION
AB Quantitative PET studies of neuroreceptor tracers typically require that arterial input function be measured. The aim of this study was to explore the use of a population-based input function (PBIF) and an image-derived input function (IDIF) for [C-11](R)-rolipram kinetic analysis, with the goal of reducing - and possibly eliminating - the number of arterial blood samples needed to measure parent radioligand concentrations.
Methods: A PBIF was first generated using [C-11](R)-rolipram parent time-activity curves from 12 healthy volunteers (Group 1). Both invasive (blood samples) and non-invasive (body weight, body surface area, and lean body mass) scaling methods for PBIF were tested. The scaling method that gave the best estimate of the Logan-V-T values was then used to determine the test-retest variability of PBIF in Group 1 and then prospectively applied to another population of 25 healthy subjects (Group 2), as well as to a population of 26 patients with major depressive disorder (Group 3). Results were also compared to those obtained with an image-derived input function (IDIF) from the internal carotid artery. In some subjects, we measured arteriovenous differences in [C-11](R)-rolipram concentration to see whether venous samples could be used instead of arterial samples. Finally, we assessed the ability of IDIF and PBIF to discriminate depressed patients (MDD) and healthy subjects.
Results: Arterial blood-scaled PBIF gave better results than any non-invasive scaling technique. Excellent results were obtained when the blood-scaled PBIF was prospectively applied to the subjects in Group 2 (V-T ratio 1.02 +/- 0.05; mean +/- SD) and Group 3 (V-T ratio 1.03 +/- 0.04). Equally accurate results were obtained for two subpopulations of subjects drawn from Groups 2 and 3 who had very differently shaped (i.e. "flatter" or "steeper") input functions compared to PBIF (V-T ratio 1.07 +/- 0.04 and 0.99 +/- 0.04, respectively).
Results obtained via PBIF were equivalent to those obtained via IDIF (V-T ratio 0.99 +/- 0.05 and 1.00 +/- 0.04 for healthy subjects and MDD patients, respectively). Retest variability of PBIF was equivalent to that obtained with full input function and IDIF (14.5%, 15.2%, and 14.1%, respectively). Due to [C-11](R)-rolipram arteriovenous differences, venous samples could not be substituted for arterial samples. With both IDIF and PBIF, depressed patients had a 20% reduction in [C-11](R)-rolipram binding as compared to control (two-way ANOVA: p = 0.008 and 0.005, respectively). These results were almost equivalent to those obtained using 23 arterial samples.
Conclusion: Although some arterial samples are still necessary, both PBIF and IDIF are accurate and precise alternatives to full arterial input function for [C-11](R)-rolipram PET studies. Both techniques give accurate results with low variability, even for clinically different groups of subjects and those with very differently shaped input functions. Published by Elsevier Inc.
C1 [Zanotti-Fregonara, Paolo; Hines, Christina S.; Zoghbi, Sami S.; Liow, Jeih-San; Zhang, Yi; Pike, Victor W.; Fujita, Masahiro; Innis, Robert B.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Drevets, Wayne C.] Univ Oklahoma, Hlth Sci Ctr, Sch Community Med, Dept Psychiat, Tulsa, OK USA.
[Mallinger, Alan G.; Zarate, Carlos A., Jr.] NIMH, Expt Therapeut & Pathophysiol Branch, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
RP Innis, RB (reprint author), NIMH, Mol Imaging Branch, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM robert.innis@nih.gov
FU National Institute of Mental Health, National Institutes of Health
(IRP-NIMH-NIH)
FX Dr. Zarate is listed as a co-inventor on a patent application for the
use of ketamine and its metabolites in major depression. Dr. Zarate has
assigned his rights in the patent to the U.S. government but will share
a percentage of any royalties that may be received by the government.
This study was supported by the Intramural Research Program of the
National Institute of Mental Health, National Institutes of Health
(IRP-NIMH-NIH).
NR 54
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Z9 15
U1 0
U2 6
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD NOV 15
PY 2012
VL 63
IS 3
BP 1532
EP 1541
DI 10.1016/j.neuroimage.2012.08.007
PG 10
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 027UK
UT WOS:000310379100054
PM 22906792
ER
PT J
AU Handwerker, DA
Roopchansingh, V
Gonzalez-Castillo, J
Bandettini, PA
AF Handwerker, Daniel A.
Roopchansingh, Vinai
Gonzalez-Castillo, Javier
Bandettini, Peter A.
TI Periodic changes in fMRI connectivity
SO NEUROIMAGE
LA English
DT Article
DE BOLD; fMRI; Posterior cingulate; Default mode; Spontaneous fluctuations;
Resting-state
ID FUNCTIONAL CONNECTIVITY; BRAIN ACTIVITY; RESTING BRAIN; FLUCTUATIONS;
REGRESSION; NETWORKS; SIGNAL
AB The first two decades of brain research using fMRI have been dominated by studies that measure signal changes in response to a presented task. A rapidly increasing number of studies are showing that consistent activation maps appear by assessment of signal correlations during time periods in which the subjects were not directed to perform any specific task (i.e. "resting state correlations"). Even though neural interactions can happen on much shorter time scales, most "resting state" studies assess these temporal correlations over a period of about 5 to 10 min. Here we investigate how these temporal correlations change on a shorter time scale. We examine changes in brain correlations to the posterior cingulate cortex (PCC) across a 10-minute scan. We show: (1) fMRI correlations fluctuate over time, (2) these fluctuations can be periodic, and (3) correlations between the PCC and other brain regions fluctuate at distinct frequencies. While the precise frequencies of correlation fluctuations vary across subjects and runs, it is still possible to parse brain regions and combinations of brain regions based on fluctuation frequency differences. To evaluate the potential biological significance of these empirical observations, we then use synthetic time series data with identical amplitude spectra, but randomized phase to show that similar effects can still appear even if the timing relationships between voxels are randomized. This implies that observed correlation fluctuations could occur between regions with distinct amplitude spectra, whether or not there are dynamic changes in neural connectivity between such regions. As more studies of brain connectivity dynamics appear, particularly studies using correlation as a key metric, it is vital to better distinguish true neural connectivity dynamics from connectivity fluctuations that are inherently part of this method. Our results also highlight the rich information in the power spectra of fMRI data that can be used to parse brain regions. Published by Elsevier Inc.
C1 [Handwerker, Daniel A.; Gonzalez-Castillo, Javier; Bandettini, Peter A.] NIMH, Sect Funct Imaging Methods, Lab Brain & Cognit, Bethesda, MD 20892 USA.
[Roopchansingh, Vinai; Bandettini, Peter A.] NIMH, Funct MRI Facil, Bethesda, MD 20892 USA.
RP Handwerker, DA (reprint author), NIMH, Sect Funct Imaging Methods, Lab Brain & Cognit, Bldg 10,Rm 1D80,10 Ctr Dr,MSC 1148, Bethesda, MD 20892 USA.
EM handwerkerd@mail.nih.gov
OI Gonzalez-Castillo, Javier/0000-0002-6520-5125
FU NIMH Intramural Research Program at NIH
FX Some of these data were collected by K. Murphy and R.M. Birn. Comments
from the handling editor, Stephen Smith, and anonymous reviewers
significantly altered and improved this manuscript. Catie Chang gave
advice and suggested useful references. This research was supported by
the NIMH Intramural Research Program at NIH.
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PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD NOV 15
PY 2012
VL 63
IS 3
BP 1712
EP 1719
DI 10.1016/j.neuroimage.2012.06.078
PG 8
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 027UK
UT WOS:000310379100069
PM 22796990
ER
PT J
AU Nasr, S
Tootell, RBH
AF Nasr, Shahin
Tootell, Roger B. H.
TI Role of fusiform and anterior temporal cortical areas in facial
recognition
SO NEUROIMAGE
LA English
DT Article
DE fMRI; Face recognition; Face inversion; Contrast reversal; FFA; Anterior
temporal face patch
ID SURFACE-BASED ANALYSIS; FACE RECOGNITION; CONGENITAL PROSOPAGNOSIA;
OBJECT RECOGNITION; CEREBRAL-CORTEX; OCCIPITAL FACE; NEURAL BASIS;
PERCEPTION; FMRI; INVERSION
AB Recent fMRI studies suggest that cortical face processing extends well beyond the fusiform face area (FFA), including unspecified portions of the anterior temporal lobe. However, the exact location of such anterior temporal region(s), and their role during active face recognition, remain unclear. Here we demonstrate that (in addition to FFA) a small bilateral site in the anterior tip of the collateral sulcus ('AT: the anterior temporal face patch) is selectively activated during recognition of faces but not houses (a non-face object). In contrast to the psychophysical prediction that inverted and contrast reversed faces are processed like other non-face objects, both FFA and AT (but not other visual areas) were also activated during recognition of inverted and contrast reversed faces. However, response accuracy was better correlated to recognition-driven activity in AT, compared to FFA. These data support a segregated, hierarchical model of face recognition processing, extending to the anterior temporal cortex. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Nasr, Shahin; Tootell, Roger B. H.] Massachusetts Gen Hosp, Athinioula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Tootell, Roger B. H.] Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02115 USA.
[Tootell, Roger B. H.] NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA.
[Tootell, Roger B. H.] MIT, Dept Hlth Sci & Technol, Cambridge, MA 02139 USA.
RP Nasr, S (reprint author), Massachusetts Gen Hosp, Athinioula A Martinos Ctr Biomed Imaging, 149 13th St, Charlestown, MA 02129 USA.
EM shahin@nmr.mgh.harvard.edu
FU National Institutes of Health (NIH) [R01 MH67529, R01 EY017081];
Martinos Center for Biomedical Imaging; NCRR; MIND Institute
FX We thank Xiaomin Yue, Garth Coombs and Ellen Lau for help with data
collection, and Jon Polimini for help with imaging protocols. We thank
Daphne Holt for review and suggestions on the manuscript. This study was
supported by the National Institutes of Health (NIH grants R01 MH67529
and R01 EY017081 to RBHT), the Martinos Center for Biomedical Imaging,
the NCRR, the MIND Institute.
NR 64
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U2 27
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD NOV 15
PY 2012
VL 63
IS 3
BP 1743
EP 1753
DI 10.1016/j.neuroimage.2012.08.031
PG 11
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 027UK
UT WOS:000310379100072
PM 23034518
ER
PT J
AU Svoboda, MD
Christie, JM
Eroglu, Y
Freeman, KA
Steiner, RD
AF Svoboda, Melissa D.
Christie, Jill M.
Eroglu, Yasemen
Freeman, Kurt A.
Steiner, Robert D.
TI Treatment of Smith-Lemli-Opitz Syndrome and Other Sterol Disorders
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS
LA English
DT Article
DE Smith-Lemli-Opitz syndrome; sterol disorders; cholesterol
supplementation; simvastatin; behavior
ID ABNORMAL CHOLESTEROL-METABOLISM; MULTIPLE CONGENITAL-ANOMALIES; AUTISM
SPECTRUM DISORDERS; PLASMA CHOLESTANOL LEVELS; CEREBROTENDINOUS
XANTHOMATOSIS; CHENODEOXYCHOLIC ACID; 7-DEHYDROCHOLESTEROL-DERIVED
OXYSTEROLS; SIMVASTATIN TREATMENT; RETINAL DEGENERATION;
DIETARY-CHOLESTEROL
AB Smith-Lemli-Opitz syndrome (SLOS) is an autosomal recessive genetic condition with a broad phenotype that results from deficiency of the final enzyme of the cholesterol synthesis pathway. This defect causes low or low-normal plasma cholesterol levels and increased 7- and 8-dehydrocholesterol (DHC) levels. Many therapies for SLOS and other disorders of sterol metabolism have been proposed, and a few of them have been undertaken in selected patients, but robust prospective clinical trials with validated outcome measures are lacking. We review the current literature and expert opinion on treatments for SLOS and other selected sterol disorders, including dietary cholesterol therapy, statin treatment, bile acid supplementation, medical therapies, and surgical interventions, as well as directions for future therapies and treatment research. (C) 2012 Wiley Periodicals, Inc.
C1 [Steiner, Robert D.] Oregon Hlth & Sci Univ, Dept Pediat, Fac Pediat Mol & Med Genet, Portland, OR 97239 USA.
[Eroglu, Yasemen] Oregon Hlth & Sci Univ, Div Pediat Gastroenterol, Portland, OR 97239 USA.
[Steiner, Robert D.] Oregon Hlth & Sci Univ, Program Mol & Cellular Biosci, Portland, OR 97239 USA.
[Steiner, Robert D.] NIH, Sterol & Isoprenoid Res Consortium, STAIR, Rare Dis Clin Res Consortium RDCRC, Bethesda, MD 20892 USA.
RP Steiner, RD (reprint author), Oregon Hlth & Sci Univ, Dept Pediat, Fac Pediat Mol & Med Genet, 707 SW Gaines St CDRC P, Portland, OR 97239 USA.
EM steinerr@ohsu.edu
OI Steiner, Robert/0000-0003-4177-4590
FU NIH Rare Diseases Clinical Research Network (RDCRN) via the Sterol and
Isoprenoid Research (STAIR) consortium; HHS [U54 HD 061939, R01 HL
073980]; [HHS U54 HD061939]; [HHS R01 HL 073980]
FX Grant sponsor: HHS U54 HD061939.; Grant sponsor: HHS R01 HL 073980.; The
authors thank Mary Lou Oster-Granite for her review of the manuscript.
R. D. S. is supported by the NIH Rare Diseases Clinical Research Network
(RDCRN) via the Sterol and Isoprenoid Research (STAIR) consortium, HHS
grant U54 HD 061939, and by HHS grant R01 HL 073980. The authors thank
Jean-Baptiste Roullet for creation of the figure.
NR 87
TC 10
Z9 10
U1 2
U2 15
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4868
EI 1552-4876
J9 AM J MED GENET C
JI Am. J. Med. Genet. C
PD NOV 15
PY 2012
VL 160C
IS 4
SI SI
BP 285
EP 294
DI 10.1002/ajmg.c.31347
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 023YB
UT WOS:000310072700005
PM 23042642
ER
PT J
AU Wolfe, LA
Morava, E
He, M
Vockley, J
Gibson, KM
AF Wolfe, Lynne A.
Morava, Eva
He, Miao
Vockley, Jerry
Gibson, K. Michael
TI Heritable disorders in the metabolism of the dolichols: A bridge from
sterol biosynthesis to molecular glycosylation
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS
LA English
DT Article
DE ichthyosis; retinitis pigmentosa; muscular dystrophy; dolichol;
glycosylation; mannosylation; isoprene; isoprenoids; cholesterol
ID PHOSPHATE-MANNOSE SYNTHASE; CONGENITAL DISORDER; DPM1; DEFICIENCY;
MUTATION; IE
AB Dolichols, polyisoprene alcohols derived from the mevalonate pathway of cholesterol synthesis, serve as carriers of glycan precursors for the formation of oligosaccharides important in protein glycosylation. Seven autosomal-recessively inherited disorders in the metabolism (synthesis, utilization, recycling) of the dolichols have recently been described, and all are associated with decreased lipid-linked oligosaccharides leading to underglycosylated proteins or lipids which facilitate their detection in the diagnostic laboratory. Multisystem pathology encompasses developmental delays and eye, heart, skin and muscle abnormalities; outcomes range from death in infancy to mild, late-onset diseasdisease. (C) 2012 Wiley Periodicals, Inc.
C1 [Wolfe, Lynne A.] NIH, Undiagnosed Dis Program, Bethesda, MD 20892 USA.
[Morava, Eva] Tulane Univ, Hayward Genet Ctr, New Orleans, LA 70118 USA.
[Morava, Eva] Radboud Univ Nijmegen, Med Ctr, Nijmegen Ctr Disorders Glycosylat, IGMD, Nijmegen, Netherlands.
[He, Miao] Emory Univ, Dept Human Genet, Atlanta, GA 30322 USA.
[He, Miao] Emory Univ, Emory Biochem Genet Lab, Atlanta, GA 30322 USA.
[Vockley, Jerry; Gibson, K. Michael] Emory Univ, Emory Biochem Genet Lab, Atlanta, GA 30322 USA.
[Vockley, Jerry] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA 15260 USA.
[Vockley, Jerry] Childrens Hosp Pittsburgh, Pittsburgh, PA USA.
[Gibson, K. Michael] Washington State Univ, Coll Pharm, Pullman, WA 99164 USA.
[Gibson, K. Michael] Oregon Hlth & Sci Univ, Biochem Genet Labs, Portland, OR 97201 USA.
RP Wolfe, LA (reprint author), NIH, Undiagnosed Dis Program, 10 Ctr DR,MSC 1205,RM 3-2551, Bethesda, MD 20892 USA.
EM lynne.wolfe@nih.gov
RI Morava, E./L-4529-2015;
OI Vockley, Jerry/0000-0002-8180-6457
FU Sterol and Isoprenoid Diseases (STAIR), a component of the NIH Rare
Diseases Clinical Research Network (RDCRN) [U54HD61939]; NIH Office of
Rare Diseases Research (ORDR)
FX The authors are indebted to Drs. F. D. Porter and W. A. Gahl for their
assistance in manuscript preparation. Partial support from the Sterol
and Isoprenoid Diseases (STAIR) consortium (U54HD61939), a component of
the NIH Rare Diseases Clinical Research Network (RDCRN), and the NIH
Office of Rare Diseases Research (ORDR) is gratefully acknowledged (MH,
JV, and KMG). The views expressed in written materials or publications
do not necessarily reflect the official policies of the Department of
Health and Human Services; nor does mention by trade names, commercial
practices, or organizations imply endorsement by the U.S. Government.
NR 31
TC 2
Z9 2
U1 1
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4868
J9 AM J MED GENET C
JI Am. J. Med. Genet. C
PD NOV 15
PY 2012
VL 160C
IS 4
SI SI
BP 322
EP 328
DI 10.1002/ajmg.c.31345
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA 023YB
UT WOS:000310072700008
PM 23059969
ER
PT J
AU Hooth, MJ
Nyska, A
Fomby, LM
Vasconcelos, DY
Vallant, M
DeVito, MJ
Walker, NJ
AF Hooth, Michelle J.
Nyska, Abraham
Fomby, Laurene M.
Vasconcelos, Daphne Y.
Vallant, Molly
DeVito, Michael J.
Walker, Nigel J.
TI Repeated dose toxicity and relative potency of
1,2,3,4,6,7-hexachloronaphthalene (PCN 66)
1,2,3,5,6,7-hexachloronaphthalene (PCN 67) compared to
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for induction of CYP1A1,
CYP1A2 and thymic atrophy in female Harlan Sprague-Dawley rats
SO TOXICOLOGY
LA English
DT Article
DE 1,2,3,4,6,7-hexachloronaphthalene (PCN 66);
1,2,3,5,6,7-hexachloronaphthalene (PCN 67);
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD); Toxic equivalency factor;
Relative potency; TEF
ID DIOXIN-LIKE COMPOUNDS; DIBENZO-P-DIOXINS; POLYCHLORINATED NAPHTHALENES;
ORGANOCHLORINE CONTAMINANTS; AROMATIC-HYDROCARBONS; EQUIVALENCY FACTORS;
ADIPOSE-TISSUE; LESIONS; BIPHENYLS; EXPOSURE
AB In this study we assessed the relative toxicity and potency of the chlorinated naphthalenes 1,2,3,4,6,7-hexachloronaphthalene (PCN 66) and 1,2,3,5,6,7-hexachloronaphthalene (PCN 67) relative to that of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Chemicals were administered in corn oil:acetone (99:1) by gavage to female Harlan Sprague-Dawley rats at dosages of 0 (vehicle), 500, 1500, 5000, 50,000 and 500,000 ng/kg (PCN 66 and PCN 67) and 1, 3, 10, 100, and 300 ng/kg (TCDD) for 2 weeks. Histopathologic changes were observed in the thymus, liver and lung of TCDD treated animals and in the liver and thymus of PCN treated animals. Significant increases in CYP1A1 and CYP1A2 associated enzyme activity were observed in all animals exposed to TCDD, PCN 66 and PCN 67. Dose response modeling of CYP1A1, CYP1A2 and thymic atrophy gave ranges of estimated relative potencies, as compared to TCDD, of 0.0015-0.0072, for PCN 66 and 0.00029-0.00067 for PCN 67. Given that PCN 66 and PCN 67 exposure resulted in biochemical and histopathologic changes similar to that seen with TCDD, this suggests that they should be included in the WHO toxic equivalency factor (TEF) scheme, although the estimated relative potencies indicate that these hexachlorinated naphthalenes should not contribute greatly to the overall human body burden of dioxin-like activity. (c) 2012 Published by Elsevier Ireland Ltd.
C1 [Hooth, Michelle J.; Vallant, Molly; DeVito, Michael J.; Walker, Nigel J.] NIEHS, Div Natl Toxicol Program, NIH, Res Triangle Pk, NC 27709 USA.
[Nyska, Abraham] Tel Aviv Univ, IL-69978 Tel Aviv, Israel.
[Nyska, Abraham] Tel Aviv Univ, Timrat, Israel.
[Fomby, Laurene M.; Vasconcelos, Daphne Y.] Battelle Mem Inst, Columbus, OH 43201 USA.
RP Walker, NJ (reprint author), NIEHS, Div Natl Toxicol Program, NIH, 111 Alexander Dr,POB 12233,K2-02, Res Triangle Pk, NC 27709 USA.
EM hooth@niehs.nih.gov; anyska@bezeqint.net; fombyl@battelle.org;
vasconcelosd@columbus.rr.com; vallant@niehs.nih.gov;
devitom@niehs.nih.gov; walker3@niehs.nih.gov
RI Walker, Nigel/D-6583-2012
OI Walker, Nigel/0000-0002-9111-6855
FU NIEHS; Intramural Research Program of the NIH
FX This research was supported by NIEHS and by the Intramural Research
Program of the NIH. This article is the work product of group which
includes employees of the National Institute of Environmental Health
Sciences (NIEHS), National Institutes of Health (NIH), however, the
statements, opinions or conclusions contained therein do not necessarily
represent the statements, opinions or conclusions of NIEHS, NIH or the
United States government. The authors would like to thank Drs Angelique
Braen, Alexander Fucarelli, Raj Chhabra, Hiroyoshi Toyoshiba and
colleagues at NIEHS for their help in the conduct of this project. We
would also like to thank Drs Susan Elmore and Kembra Howdeshell at NIEHS
for critical review of this manuscript.
NR 32
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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 15
PY 2012
VL 301
IS 1-3
BP 85
EP 93
DI 10.1016/j.tox.2012.07.005
PG 9
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 003RN
UT WOS:000308629100011
PM 22813907
ER
PT J
AU Balduino, A
Mello-Coelho, V
Wang, Z
Taichman, RS
Krebsbach, PH
Weeraratna, AT
Becker, KG
de Mello, W
Taub, DD
Borojevic, R
AF Balduino, Alex
Mello-Coelho, Valeria
Wang, Zhou
Taichman, Russell S.
Krebsbach, Paul H.
Weeraratna, Ashani T.
Becker, Kevin G.
de Mello, Wallace
Taub, Dennis D.
Borojevic, Radovan
TI Molecular signature and in vivo behavior of bone marrow endosteal and
subendosteal stromal cell populations and their relevance to
hematopoiesis
SO EXPERIMENTAL CELL RESEARCH
LA English
DT Article
DE Bone marrow; Trabecular bone; Microenvironment; Osteoblast; Niche
ID COLONY-STIMULATING FACTOR; STEM-CELLS; PROGENITOR CELLS; SELF-RENEWAL;
NICHE; OSTEOBLASTS; MOBILIZATION; MAINTENANCE; EXPANSION; SUPPORT
AB In the bone marrow cavity, hematopoietic stem cells (HSC) have been shown to reside in the endosteal and subendosteal perivascular niches, which play specific roles on HSC maintenance. Although cells with long-term ability to reconstitute full hematopoietic system can be isolated from both niches, several data support a heterogenous distribution regarding the cycling behavior of HSC. Whether this distinct behavior depends upon the role played by the stromal populations which distinctly create these two niches is a question that remains open. In the present report, we used our previously described in vivo assay to demonstrate that endosteal and subendosteal stromal populations are very distinct regarding skeletal lineage differentiation potential. This was further supported by a microarray-based analysis, which also demonstrated that these two stromal populations play distinct, albeit complementary, roles in HSC niche. Both stromal populations were preferentially isolated from the trabecular region and behave distinctly in vitro, as previously reported. Even though these two niches are organized in a very close range, in vivo assays and molecular analyses allowed us to identify endosteal stroma (F-OST) cells as fully committed osteoblasts and subendosteal stroma (F-RET) cells as uncommitted mesenchymal cells mainly represented by perivascular reticular cells expressing high levels of chemokine ligand, CXCL12. Interestingly, a number of cytokines and growth factors including interleukin-6 (IL-6), IL-7, IL-15, Hepatocyte growth factor (HGF) and stem cell factor (SCF) matrix metalloproteases (MMPs) were also found to be differentially expressed by F-OST and F-RET cells. Further microarray analyses indicated important mechanisms used by the two stromal compartments in order to create and coordinate the "quiescent" and "proliferative" niches in which hematopoietic stem cells and progenitors reside. Published by Elsevier Inc.
C1 [Balduino, Alex] Univ Veiga de Almeida, Ctr Pesquisa Inovacao & Tecnol, Sch Dent, BR-20271020 Rio De Janeiro, RJ, Brazil.
[Mello-Coelho, Valeria; Borojevic, Radovan] Univ Fed Rio de Janeiro, Inst Biomed Sci, Rio De Janeiro, RJ, Brazil.
[Mello-Coelho, Valeria; Weeraratna, Ashani T.; Becker, Kevin G.; Taub, Dennis D.] NIA, NIH, Baltimore, MD 21224 USA.
[Wang, Zhou; Taichman, Russell S.; Krebsbach, Paul H.] Univ Michigan, Sch Dent, Dept Periodont Prevent & Geriatr, Ann Arbor, MI 48109 USA.
[de Mello, Wallace] Inst Oswaldo Cruz, BR-20001 Rio De Janeiro, RJ, Brazil.
RP Balduino, A (reprint author), Univ Veiga de Almeida, Ctr Pesquisa Inovacao & Tecnol, Sch Dent, Rua Ibituruna,108 Maracana, BR-20271020 Rio De Janeiro, RJ, Brazil.
EM balduino@uva.edu.br
OI Taichman, Russell S./0000-0002-7890-0020; Borojevic,
Radovan/0000-0002-2393-7280; Becker, Kevin/0000-0002-6794-6656
FU CNPq; FAPERJ; National Institute on Aging, National Institutes of
Health; NIH [CA-93900, DK082481]; National Counsel of Technological and
Scientific Development
FX This research was, in part, supported by CNPq, FAPERJ, and the
Intramural Research Program of the National Institute on Aging, National
Institutes of Health, and by NIH awards CA-93900 and DK082481.; National
Counsel of Technological and Scientific Development and NIH awards
CA-93900 and DK082481. This work has also been supported, in part, by
the National Institute on Aging, NIH.
NR 45
TC 13
Z9 14
U1 0
U2 5
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4827
J9 EXP CELL RES
JI Exp. Cell Res.
PD NOV 15
PY 2012
VL 318
IS 19
BP 2427
EP 2437
DI 10.1016/j.yexcr.2012.07.009
PG 11
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 013KB
UT WOS:000309303200002
PM 22841688
ER
PT J
AU Ambs, S
AF Ambs, Stefan
TI Analysis of stromal gene expression for the identification of prognostic
and predictive molecular markers in cancer therapy
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Editorial Material
ID BREAST-CANCER; TUMOR STROMA; FIBROBLASTS; METASTASES; SIGNATURE; CD99
C1 NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Ambs, S (reprint author), NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 15
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD NOV 15
PY 2012
VL 131
IS 10
BP 2213
EP 2214
DI 10.1002/ijc.27568
PG 2
WC Oncology
SC Oncology
GA 011SM
UT WOS:000309185300001
PM 22528763
ER
PT J
AU Subbaiah, VK
Narayan, N
Massimi, P
Banks, L
AF Subbaiah, Vanitha Krishna
Narayan, Nisha
Massimi, Paola
Banks, Lawrence
TI Regulation of the DLG tumor suppressor by beta-catenin
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE DLG; ss-catenin; proteasome
ID PROTEASOME-MEDIATED DEGRADATION; CELL-ADHESION; HUMAN HOMOLOG;
COLORECTAL-CANCER; E6 PROTEINS; WNT PATHWAY; APC GENE; NE-DLG; PDZ;
EXPRESSION
AB The discs-large (DLG) tumor suppressor plays essential roles in regulating cell polarity and proliferation. It localizes at sites of cellcell contact where it acts as a scaffold for multiple protein interactions, including with the adenomatous polyposis coli (APC) tumor suppressor, which in turn regulates beta-catenin. Furthermore, many tumor types including breast and colon have increased levels of beta-catenin activity with correspondingly low levels of DLG expression. Here we provide evidence of a direct functional link between these apparently separate phenomena. We show that overexpressed beta-catenin can enhance the turnover of DLG in a proteosome dependent manner. This effect is specific to DLG and is not seen with two other PDZ domain-containing targets of beta-catenin, MAGI-1 and Scribble. Furthermore, siRNA-mediated ablation of endogenous beta-catenin expression also enhances DLG stability. beta-catenin-induced degradation of DLG appears to be a consequence of a direct association between the two proteins and requires beta-catenin PDZ binding potential. In contrast, the enhanced turnover of DLG requires the unique N-terminal sequences and its PDZ domains. Finally, we also show that the capacity of DLG to inhibit transformed cell growth in an oncogene cooperation assay is inhibited by beta-catenin. Taken together these studies suggest that one mechanism by which deregulated beta-catenin can contribute to tumorigenesis is through enhancing DLG degradation.
C1 [Subbaiah, Vanitha Krishna; Massimi, Paola; Banks, Lawrence] ICGEB, I-34012 Trieste, Italy.
[Narayan, Nisha] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Banks, L (reprint author), ICGEB, Padriciano 99, I-34012 Trieste, Italy.
EM banks@icgeb.org
FU Associazione Italiana per la Ricerca sul Cancro; Wellcome Trust
FX Grant sponsors: Associazione Italiana per la Ricerca sul Cancro,
Wellcome Trust
NR 49
TC 12
Z9 12
U1 1
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD NOV 15
PY 2012
VL 131
IS 10
BP 2223
EP 2233
DI 10.1002/ijc.27519
PG 11
WC Oncology
SC Oncology
GA 011SM
UT WOS:000309185300003
PM 22392736
ER
PT J
AU Xi, LF
Schiffman, M
Koutsky, LA
Hulbert, A
Lee, SK
DeFilippis, V
Shen, ZP
Kiviat, NB
AF Xi, Long Fu
Schiffman, Mark
Koutsky, Laura A.
Hulbert, Ayaka
Lee, Shu-Kuang
DeFilippis, Victor
Shen, Zhenping
Kiviat, Nancy B.
TI Association of human papillomavirus type 31 variants with risk of
cervical intraepithelial neoplasia grades 2-3
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE human papillomavirus; variants; cervical intraepithelial neoplasia
ID NATURAL VARIANTS; CANCER; E6; HUMAN-PAPILLOMAVIRUS-16; WOMEN;
POLYMORPHISM; BRAZIL; VIRUS
AB Although the lineages of human papillomavirus type 31 (HPV31) variants are recognized, their clinical relevance is unknown. The purpose of our study was to examine risk of cervical intraepithelial neoplasia Grades 23 (CIN2/3) by HPV31 variants. Study subjects were women who participated in the atypical squamous cells of undetermined significance and low-grade squamous intraepithelial lesion Triage Study and who had HPV31 infections detected at one or more visits. They were followed semi-annually over 2 years for detection of HPV DNA and cervical lesion. HPV31 isolates were characterized by DNA sequencing and assigned into 1 of 3 variant lineages. CIN2/3 was histologically confirmed in 127 (27.0%) of the 470 HPV31-positive women, 83 diagnosed at the first HPV31-positive visit and 44 thereafter. The odds ratio for the association of 2-year cumulative risk of CIN2/3 was 1.7 (95% CI: 1.02.9) for infections with A variants and 2.2 (95% CI: 1.23.9) for infections with B variants as compared to those with C variants. Among women without CIN2/3 at the first HPV31-positive visit, the risk of subsequent CIN2/3 was 2.2-fold greater for those with A variants (95% CI: 1.04.8) and 2.0-fold greater for those with B variants (95% CI: 0.94.9) as compared to those with C variants. Similar associations were observed when CIN3 was used as the endpoint. The findings from our study help to tag HPV31 variants that differ in risk of CIN2/3 and to explain in part why some HPV31 infections regress spontaneously and others lead to disease progression.
C1 [Xi, Long Fu] Univ Washington, Harborview Med Ctr, Dept Pathol, Sch Med, Seattle, WA 98104 USA.
[Xi, Long Fu; Koutsky, Laura A.; Lee, Shu-Kuang] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98104 USA.
[Schiffman, Mark] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[DeFilippis, Victor] Oregon Hlth & Sci Univ, Vaccine & Gene Therapy Inst, Portland, OR 97201 USA.
RP Xi, LF (reprint author), Univ Washington, Harborview Med Ctr, Dept Pathol, Sch Med, NJB Ste 1187,325 9th Ave, Seattle, WA 98104 USA.
EM longfu@u.washington.edu
FU Public Health Service [CA133569]
FX Grant sponsor: Public Health Service; Grant number: CA133569
NR 33
TC 17
Z9 17
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD NOV 15
PY 2012
VL 131
IS 10
BP 2300
EP 2307
DI 10.1002/ijc.27520
PG 8
WC Oncology
SC Oncology
GA 011SM
UT WOS:000309185300011
PM 22396129
ER
PT J
AU Becker, N
Falster, MO
Vajdic, CM
de Sanjose, S
Martinez-Maza, O
Bracci, PM
Melbye, M
Smedby, KE
Engels, EA
Turner, J
Vineis, P
Costantini, AS
Holly, EA
Spinelli, JJ
La Vecchia, C
Zheng, TZ
Chiu, BCH
Montella, M
Cocco, P
Maynadie, M
Foretova, L
Staines, A
Brennan, P
Davis, S
Severson, R
Cerhan, JR
Breen, EC
Birmann, B
Cozen, W
Grulich, AE
Newton, R
AF Becker, Nikolaus
Falster, Michael O.
Vajdic, Claire M.
de Sanjose, Silvia
Martinez-Maza, Otoniel
Bracci, Paige M.
Melbye, Mads
Smedby, Karin Ekstrom
Engels, Eric A.
Turner, Jennifer
Vineis, Paolo
Costantini, Adele Seniori
Holly, Elizabeth A.
Spinelli, John J.
La Vecchia, Carlo
Zheng, Tongzhang
Chiu, Brian C. -H.
Montella, Maurizio
Cocco, Pierluigi
Maynadie, Marc
Foretova, Lenka
Staines, Anthony
Brennan, Paul
Davis, Scott
Severson, Richard
Cerhan, James R.
Breen, Elizabeth C.
Birmann, Brenda
Cozen, Wendy
Grulich, Andrew E.
Newton, Robert
TI Self-reported history of infections and the risk of non-Hodgkin
lymphoma: An InterLymph pooled analysis
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE Non-Hodgkin lymphoma; Infection; pooled analysis
ID MEDICAL HISTORY; EPIDEMIOLOGY; IMMUNE; ATOPY
AB We performed a pooled analysis of data on self-reported history of infections in relation to the risk of non-Hodgkin lymphoma (NHL) from 17 casecontrol studies that included 12,585 cases and 15,416 controls aged 1696 years at recruitment. Pooled odds ratios (OR) and 95% confidence intervals (95% CI) were estimated in two-stage random-effect or joint fixed-effect models, adjusting for age, sex and study centre. Data from the 2 years before diagnosis (or date of interview for controls) were excluded. A self-reported history of infectious mononucleosis was associated with an excess risk of NHL (OR = 1.26, 95% CI = 1.011.57 based on data from 16 studies); study-specific results indicate significant (I2 = 51%, p = 0.01) heterogeneity. A self-reported history of measles or whooping cough was associated with an approximate 15% reduction in risk. History of other infection was not associated with NHL. We find little clear evidence of an association between NHL risk and infection although the limitations of data based on self-reported medical history (particularly of childhood illness reported by older people) are well recognized.
C1 [Newton, Robert] Univ York, Dept Hlth Sci, Epidemiol & Genet Unit, York YO10 5DD, N Yorkshire, England.
[Newton, Robert] Univ York, Hull York Med Sch, York YO10 5DD, N Yorkshire, England.
[Cozen, Wendy] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Birmann, Brenda] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Birmann, Brenda] Harvard Univ, Sch Med, Boston, MA USA.
[Breen, Elizabeth C.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA.
[Cerhan, James R.] Mayo Clin, Coll Med, Dept Hlth Sci Res, Rochester, MN USA.
[Severson, Richard] Wayne State Univ, Dept Family Med, Detroit, MI USA.
[Severson, Richard] Wayne State Univ, Sch Med, Karmanos Canc Inst, Detroit, MI USA.
[Davis, Scott] Univ Washington, Fred Hutchinson Canc Res Ctr, Seattle, WA 98195 USA.
[Davis, Scott] Univ Washington, Sch Publ Hlth & Community Med, Seattle, WA 98195 USA.
[Brennan, Paul] Int Agcy Res Canc, F-69372 Lyon, France.
[Staines, Anthony] Dublin City Univ, Sch Nursing, Dublin 9, Ireland.
[Foretova, Lenka] Masaryk Mem Canc Inst, Dept Canc Epidemiol & Genet, Brno, Czech Republic.
[Maynadie, Marc] Registry Hematol Malignancies Cote dOr, Dijon, France.
[Cocco, Pierluigi] Univ Cagliari, Dept Publ Hlth, Occupat Hlth Sect, Cagliari, Italy.
[Montella, Maurizio] Fdn G Pascale, Ist Nazl Tumori, Serv Epidemiol, Naples, Italy.
[Chiu, Brian C. -H.] Univ Chicago, Dept Hlth Studies, Chicago, IL 60637 USA.
[Zheng, Tongzhang] Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA.
[La Vecchia, Carlo] Ist Ric Farmacol Mario Negri, Milan, Italy.
[Spinelli, John J.] BC Canc Agcy, Canc Control Res Program, Vancouver, BC, Canada.
[Costantini, Adele Seniori] Inst Study & Prevent Canc, Occupat & Environm Epidemiol Unit, Florence, Italy.
[Vineis, Paolo] Univ London Imperial Coll Sci Technol & Med, London, England.
[Turner, Jennifer] Douglass Hanly Moir Pathol, Dept Histopathol, Sydney, NSW, Australia.
[Engels, Eric A.] NCI, Div Canc Epidemiol & Genet, Infect & Immunoepidemiol Branch, NIH, Rockville, MD USA.
[Smedby, Karin Ekstrom] Karolinska Inst, Dept Med, Clin Epidemiol Unit, Stockholm, Sweden.
[Melbye, Mads] Statens Serum Inst, Dept Epidemiol Res, DK-2300 Copenhagen, Denmark.
[Bracci, Paige M.; Holly, Elizabeth A.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Martinez-Maza, Otoniel] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90024 USA.
[Martinez-Maza, Otoniel] Univ Calif Los Angeles, Dept Epidemiol, Los Angeles, CA USA.
[Martinez-Maza, Otoniel] Univ Calif Los Angeles, Dept Microbiol Immunol & Mol Genet, Los Angeles, CA USA.
[Martinez-Maza, Otoniel] Univ Calif Los Angeles, Dept Obstet & Gynaecol, Los Angeles, CA USA.
[de Sanjose, Silvia] Inst Catala Oncol, Unit Infect & Canc, Barcelona, Spain.
[Falster, Michael O.; Grulich, Andrew E.] Univ New S Wales, Natl Ctr HIV Epidemiol & Clin Res, Sydney, NSW, Australia.
[Falster, Michael O.; Vajdic, Claire M.] Univ New S Wales, Prince Wales Clin Sch, Integrated Canc Res Grp, UNSW Canc Res Ctr, Sydney, NSW, Australia.
[Becker, Nikolaus] German Canc Res Ctr, Div Canc Epidemiol, D-6900 Heidelberg, Germany.
RP Newton, R (reprint author), Univ York, Dept Hlth Sci, Epidemiol & Genet Unit, Seebohm Rowntree Bldg,Area 3, York YO10 5DD, N Yorkshire, England.
EM Robert.Newton@york.ac.uk
RI Spinelli, John/B-6210-2013; Martinez-Maza, Otoniel/B-2667-2009; de
Sanjose Llongueras, Silvia/H-6339-2014;
OI Martinez-Maza, Otoniel/0000-0003-1364-0675; Vajdic,
Claire/0000-0002-3612-8298; Cerhan, James/0000-0002-7482-178X; Staines,
Anthony/0000-0001-9161-1357; La Vecchia, Carlo/0000-0003-1441-897X;
Falster, Michael/0000-0001-6444-7272
FU Leukemia Foundation of Australia [LFA GIA 24]; Italian Association for
Cancer Research; Italian League Against Cancer (Avi-N, Northern Italy);
Canadian Cancer Society; Canadian Institutes for Health Research
(British Columbia); National Cancer Institute, Connecticut [CA62006];
European Commission, EpiLymph [QLK4-CT-2000-00422]; Association pour la
Recherche contre le Cancer [5111]; Fondation de France; EpiLymph, France
[1999 008471]; Compagnia di San Paolo di Torino; Programma Oncologia
2001; EpiLymph, Italy; Health Research Board; EpiLymph, Ireland; Spanish
Ministry of Health FISS [PI040091]; CIBERESP; EpiLymph, Spain
[06/06/0073]; German Federal Office for Radiation Protection; EpiLymph,
Germany [StSch4261, StSch4420]; National Institutes of Health [CA51086,
CA69269-02]; European Community; Italian League against Cancer, Italy;
National Cancer Institute, Mayo [CA92153]; National Cancer Institute
(NCI-SEER) [PC65064, PC67008, PC67009, PC67010, PC71105]; American
Institute for Cancer Research, Nebraska [99B083]; National Health and
Medical Research Council of Australia (NSW) [990920]; Swedish Cancer
Society (SCALE) [04 0458]; National Institutes of Health (UCSF)
[CA45614, CA89745, CA87014, CA104682]; Leukemia Research Fund of Great
Britain (UK)
FX Grant sponsor: Leukemia Foundation of Australia; Grant number: LFA GIA
24; Grant sponsor: Italian Association for Cancer Research and the
Italian League Against Cancer (Avi-N, Northern Italy), The Canadian
Cancer Society and the Canadian Institutes for Health Research (British
Columbia); Grant sponsor: National Cancer Institute, Connecticut; Grant
number: CA62006; Grant sponsor: European Commission, EpiLymph; Grant
number: QLK4-CT-2000-00422; Grant sponsor: Association pour la Recherche
contre le Cancer; Grant number: 5111; Grant sponsor: Fondation de
France, EpiLymph, France; Grant number: 1999 008471; Grant sponsors:
Compagnia di San Paolo di Torino, Programma Oncologia 2001, EpiLymph,
Italy, Health Research Board, EpiLymph, Ireland; Grant sponsor: Spanish
Ministry of Health FISS; Grant number: PI040091; Grant sponsor:
CIBERESP, EpiLymph, Spain; Grant number: 06/06/0073; Grant sponsor:
German Federal Office for Radiation Protection, EpiLymph, Germany; Grant
numbers: StSch4261, StSch4420; Grant sponsor: National Institutes of
Health; Grant number: CA51086; Grant sponsor: European Community and the
Italian League against Cancer, Italy, National Cancer Institute, Mayo;
Grant number: CA92153; Grant sponsor: National Cancer Institute
(NCI-SEER); Grant numbers: PC65064, PC67008, PC67009, PC67010, PC71105;
Grant sponsor: American Institute for Cancer Research, Nebraska; Grant
number: 99B083; Grant sponsor: National Health and Medical Research
Council of Australia (NSW); Grant number: 990920; Grant sponsor:
National Institutes of Health; Grant number: CA69269-02; Grant sponsor:
The Swedish Cancer Society (SCALE); Grant number: 04 0458; Grant
sponsor: National Institutes of Health (UCSF); Grant numbers: CA45614,
CA89745, CA87014, CA104682; Grant sponsor: The Leukemia Research Fund of
Great Britain (UK)
NR 23
TC 10
Z9 10
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD NOV 15
PY 2012
VL 131
IS 10
BP 2342
EP 2348
DI 10.1002/ijc.27438
PG 7
WC Oncology
SC Oncology
GA 011SM
UT WOS:000309185300015
PM 22266776
ER
PT J
AU Sultana, R
McNeill, DR
Abbotts, R
Mohammed, MZ
Zdzienicka, MZ
Qutob, H
Seedhouse, C
Laughton, CA
Fischer, PM
Patel, PM
Wilson, DM
Madhusudan, S
AF Sultana, Rebeka
McNeill, Daniel R.
Abbotts, Rachel
Mohammed, Mohammed Z.
Zdzienicka, Malgorzata Z.
Qutob, Haitham
Seedhouse, Claire
Laughton, Charles A.
Fischer, Peter M.
Patel, Poulam M.
Wilson, David M., III
Madhusudan, Srinivasan
TI Synthetic lethal targeting of DNA double-strand break repair deficient
cells by human apurinic/apyrimidinic endonuclease inhibitors
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE base excision repair (BER); BRCA deficiency; human apurinic;
apyrimidinic endonuclease 1 (APE1); synthetic lethal targeting; DNA
repair; small molecule inhibitors
ID HUMAN ABASIC ENDONUCLEASE; SMALL-MOLECULE INHIBITOR; BASE
EXCISION-REPAIR; PARP INHIBITORS; POLY(ADP-RIBOSE) POLYMERASE;
DEOXYRIBONUCLEIC-ACID; GENE-EXPRESSION; APE1; INSTABILITY; HYPOXIA
AB An apurinic/apyrimidinic (AP) site is an obligatory cytotoxic intermediate in DNA Base Excision Repair (BER) that is processed by human AP endonuclease 1 (APE1). APE1 is essential for BER and an emerging drug target in cancer. We have isolated novel small molecule inhibitors of APE1. In this study, we have investigated the ability of APE1 inhibitors to induce synthetic lethality (SL) in a panel of DNA double-strand break (DSB) repair deficient and proficient cells; i) Chinese hamster (CH) cells: BRCA2 deficient (V-C8), ATM deficient (V-E5), wild type (V79) and BRCA2 revertant [V-C8(Rev1)]. ii) Human cancer cells: BRCA1 deficient (MDA-MB-436), BRCA1 proficient (MCF-7), BRCA2 deficient (CAPAN-1 and HeLa SilenciX cells), BRCA2 proficient (PANC1 and control SilenciX cells). We also tested SL in CH ovary cells expressing a dominant-negative form of APE1 (E8 cells) using ATM inhibitors and DNA-PKcs inhibitors (DSB inhibitors). APE1 inhibitors are synthetically lethal in BRCA and ATM deficient cells. APE1 inhibition resulted in accumulation of DNA DSBs and G2/M cell cycle arrest. SL was also demonstrated in CH cells expressing a dominant-negative form of APE1 treated with ATM or DNA-PKcs inhibitors. We conclude that APE1 is a promising SL target in cancer.
C1 [Madhusudan, Srinivasan] Univ Nottingham, Translat DNA Repair Grp, Univ Nottingham Hosp, Lab Mol Oncol,Acad Unit Oncol,Sch Mol Med Sci, Nottingham NG5 1PB, England.
[McNeill, Daniel R.; Wilson, David M., III] NIA, Lab Mol Gerontol, Biomed Res Ctr, NIH, Baltimore, MD 21224 USA.
[Zdzienicka, Malgorzata Z.] Nicolaus Copernicus Univ Torun, Dept Mol Cell Genet, Coll Med Bydgoszcz, PL-85094 Bydgoszcz, Poland.
[Qutob, Haitham; Seedhouse, Claire] Univ Nottingham, Dept Acad Haematol, Univ Nottingham Hosp, Sch Mol Med Sci, Nottingham NG5 1PB, England.
[Laughton, Charles A.; Fischer, Peter M.] Univ Nottingham, Sch Pharm, Nottingham NG7 2RD, England.
[Laughton, Charles A.; Fischer, Peter M.] Univ Nottingham, Ctr Biomol Sci, Nottingham NG7 2RD, England.
RP Madhusudan, S (reprint author), Univ Nottingham, Translat DNA Repair Grp, Univ Nottingham Hosp, Lab Mol Oncol,Acad Unit Oncol,Sch Mol Med Sci, Nottingham NG5 1PB, England.
EM srinivasan.madhusudan@nottingham.ac.uk
RI SEEDHOUSE, CLAIRE/B-3570-2009; Laughton, Charles/E-5667-2010; Fischer,
Peter/E-5657-2010
OI Laughton, Charles/0000-0003-4090-3960; Madhusudan,
Srinivasan/0000-0002-5354-5480; Seedhouse, Claire/0000-0003-2280-4045;
Fischer, Peter/0000-0002-5866-9271
FU Breast Cancer Campaign, UK; Intramural Research Program of NIH, National
Institute on Aging, USA; University of Nottingham, UK; Medical Research
Council, UK
FX Grant sponsors: Breast Cancer Campaign, UK, Intramural Research Program
of NIH, National Institute on Aging, USA, University of Nottingham, UK
(M.Z. Mohammed, R Sultana and S Madhusudan), Medical Research Council,
UK (R. Abbotts)
NR 44
TC 36
Z9 36
U1 1
U2 19
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD NOV 15
PY 2012
VL 131
IS 10
BP 2433
EP 2444
DI 10.1002/ijc.27512
PG 12
WC Oncology
SC Oncology
GA 011SM
UT WOS:000309185300025
PM 22377908
ER
PT J
AU Pacak, K
Sirova, M
Giubellino, A
Lencesova, L
Csaderova, L
Laukova, M
Hudecova, S
Krizanova, O
AF Pacak, Karel
Sirova, Marta
Giubellino, Alessio
Lencesova, Lubomira
Csaderova, Lucia
Laukova, Marcela
Hudecova, Sona
Krizanova, Olga
TI NF-kappa B inhibition significantly upregulates the norepinephrine
transporter system, causes apoptosis in pheochromocytoma cell lines and
prevents metastasis in an animal model
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE NF-?B inhibition; pheochromocytoma; apoptosis; norepinephrine
transporter
ID NECROSIS-FACTOR-ALPHA; MALIGNANT PHEOCHROMOCYTOMA; B ACTIVITY;
I-131-METAIODOBENZYLGUANIDINE THERAPY; TRIPTERYGIUM-WILFORDII;
EPITHELIAL-CELLS; PC12 CELLS; TRIPTOLIDE; ACTIVATION; NEUROBLASTOMA
AB Pheochromocytomas (PHEOs) and paragangliomas (PGLs) are specific types of neuroendocrine tumors that originate in the adrenal medulla or sympathetic/parasympathetic paraganglia, respectively. Although these tumors are intensively studied, a very effective treatment for metastatic PHEO or PGL has not yet been established. Preclinical evaluations of novel therapies for these tumors are very much required. Therefore, in this study we tested the effect of triptolide (TTL), a potent nuclear factor-kappaB (NF-?B) inhibitor, on the cell membrane norepinephrine transporter (NET) system, considered to be the gatekeeper for the radiotherapeutic agent 131I-metaiodobenzylguanidine (131I-MIBG). We measured changes in the mRNA and protein levels of NET and correlated them with proapoptotic factors and metastasis inhibition. The study was performed on three different stable PHEO cell lines. We found that blocking NF-?B with TTL or capsaicin increased both NET mRNA and protein levels. Involvement of NF-?B in the upregulation of NET was verified by mRNA silencing of this site and also by using NF-?B antipeptide. Moreover, in vivo treatment with TTL significantly reduced metastatic burden in an animal model of metastatic PHEO. The present study for the first time shows how NF-?B inhibitors could be successfully used in the treatment of metastatic PHEO/PGL by a significant upregulation of NET to increase the efficacy of 131I-MIBG and by the induction of apoptosis.
C1 [Sirova, Marta; Lencesova, Lubomira; Laukova, Marcela; Hudecova, Sona; Krizanova, Olga] Slovak Acad Sci, Inst Mol Physiol & Genet, Ctr Excellence Studying Metab Aspects Dev Diagnos, Bratislava 83334, Slovakia.
[Pacak, Karel; Giubellino, Alessio] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
[Csaderova, Lucia] Slovak Acad Sci, Mol Med Ctr, Bratislava 83334, Slovakia.
RP Krizanova, O (reprint author), Slovak Acad Sci, Inst Mol Physiol & Genet, Ctr Excellence Studying Metab Aspects Dev Diagnos, Vlarska 5, Bratislava 83334, Slovakia.
FU Intramural Research Program of the NICHD, NIH [VEGA/0049/10, APVV
51/0397]
FX Grant sponsor: Intramural Research Program of the NICHD, NIH; Grant
numbers: VEGA/0049/10, APVV 51/0397
NR 43
TC 16
Z9 16
U1 1
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD NOV 15
PY 2012
VL 131
IS 10
BP 2445
EP 2455
DI 10.1002/ijc.27524
PG 11
WC Oncology
SC Oncology
GA 011SM
UT WOS:000309185300026
PM 22407736
ER
PT J
AU Bussard, KM
Smith, GH
AF Bussard, Karen M.
Smith, Gilbert H.
TI Human Breast Cancer Cells Are Redirected to Mammary Epithelial Cells
upon Interaction with the Regenerating Mammary Gland Microenvironment
In-Vivo
SO PLOS ONE
LA English
DT Article
ID TUMOR STEM-CELLS; TERATOCARCINOMA CELLS; DIFFERENTIATION; METASTASIS;
SUPPRESSOR; EXPRESSION; PROLACTIN; PREGNANCY; TISSUES; BRMS1
AB Breast cancer is the second leading cause of cancer deaths in the United States. At present, the etiology of breast cancer is unknown; however the possibility of a distinct cell of origin, i.e. a cancer stem cell, is a heavily investigated area of research. Influencing signals from the tissue niche are known to affect stem cells. Literature has shown that cancer cells lose their tumorigenic potential and display 'normal' behavior when placed into 'normal' ontogenic environments. Therefore, it may be the case that the tissue microenvironment is able to generate signals to redirect cancer cell fate. Previously, we showed that pluripotent human embryonal carcinoma cells could be redirected by the regenerating mammary gland microenvironment to contribute epithelial progeny for 'normal' gland development in-vivo. Here, we show that that human metastatic, non-metastatic, and metastasis-suppressed breast cancer cells proliferate and contribute to normal mammary gland development in-vivo without tumor formation. Immunochemistry for human-specific mitochondria, keratin 8 and 14, as well as human-specific milk proteins (alpha-lactalbumin, impregnated transplant hosts) confirmed the presence of human cell progeny. Features consistent with normal mammary gland development as seen in intact hosts (duct, lumen formation, development of secretory acini) were recapitulated in both primary and secondary outgrowths from chimeric implants. These results suggest the dominance of the tissue microenvironment over cancer cell fate. This work demonstrates that cultured human breast cancer cells (metastatic and non-metastatic) respond developmentally to signals generated by the mouse mammary gland microenvironment during gland regeneration in-vivo.
C1 [Bussard, Karen M.; Smith, Gilbert H.] NCI, Mammary Biol & Tumorigenesis Lab, NIH, Bethesda, MD 20892 USA.
RP Bussard, KM (reprint author), NCI, Mammary Biol & Tumorigenesis Lab, NIH, Bethesda, MD 20892 USA.
EM gs4d@nih.gov
FU Intramural NIH HHS
NR 38
TC 11
Z9 12
U1 1
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 14
PY 2012
VL 7
IS 11
AR e49221
DI 10.1371/journal.pone.0049221
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 038CD
UT WOS:000311151900103
PM 23155468
ER
PT J
AU Chiang, YJ
Difilippantonio, MJ
Tessarollo, L
Morse, HC
Hodes, RJ
AF Chiang, Y. Jeffrey
Difilippantonio, Michael J.
Tessarollo, Lino
Morse, Herbert C.
Hodes, Richard J.
TI Exon 1 Disruption Alters Tissue-Specific Expression of Mouse p53 and
Results in Selective Development of B Cell Lymphomas
SO PLOS ONE
LA English
DT Article
ID P53-DEFICIENT MICE; SUPPRESSION; INSTABILITY; CROSSROADS; ACTIVATION;
LEUKEMIA; SPECTRUM; DELETION; MODELS; REPAIR
AB p53 is a tumor suppressor gene mutated in >50% of human cancers, while p53 deficiency in mice results in cancers and accelerated mortality. Thymic T cell lymphoma is the most common malignancy in p53-deficient mice, making it difficult to study the role of p53 in other malignancies. To overcome this limitation, we attempted to generate mice with a reversible p53 knockout (p53(rev/rev)) by inserting a floxed transcriptional stop into the first exon of p53, anticipating that this would allow tissue-specific Cre-mediated expression of p53. Contrary to expectations, functional p53 protein was expressed in the thymus and multiple other tissues of p53(rev/rev) mice in the absence of Cre, whereas B cells expressed p53 protein only in the presence of B cell-specific CD19-Cre. In the absence of Cre, 76% of p53(rev/rev) mice developed splenic marginal zone B cell lymphomas, indicating sensitivity of this B cell subset to transformation caused by p53 deficiency. 5'-RACE identified p53 mRNA transcribed from a novel start site utilized in thymocytes but not normal B cells or B cell lymphomas from p53(rev/rev) mice. The p53(rev/rev) mouse thus demonstrates an effect of p53 deficiency in development of splenic marginal zone lymphomas and provides a model for study of p53-deficient human B cell lymphomas.
RP Chiang, YJ (reprint author), NCI, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
EM chiangj@mail.nih.gov
OI Morse, Herbert/0000-0002-9331-3705
FU Intramural NIH HHS [Z99 CA999999]
NR 34
TC 3
Z9 3
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 14
PY 2012
VL 7
IS 11
AR e49305
DI 10.1371/journal.pone.0049305
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 038CD
UT WOS:000311151900119
PM 23166633
ER
PT J
AU Makarova, KS
Anantharaman, V
Aravind, L
Koonin, EV
AF Makarova, Kira S.
Anantharaman, Vivek
Aravind, L.
Koonin, Eugene V.
TI Live virus-free or die: coupling of antivirus immunity and programmed
suicide or dormancy in prokaryotes
SO BIOLOGY DIRECT
LA English
DT Article
ID ADAPTIVE BACTERIAL IMMUNITY; TOXIN-ANTITOXIN SYSTEMS; CRISPR-CAS
SYSTEMS; ESCHERICHIA-COLI; RESTRICTION ENDONUCLEASES; COMPARATIVE
GENOMICS; PHAGE RESISTANCE; S-MODIFICATION; SEED SEQUENCE; RNA DECAY
AB Background: The virus-host arms race is a major theater for evolutionary innovation. Archaea and bacteria have evolved diverse, elaborate antivirus defense systems that function on two general principles: i) immune systems that discriminate self DNA from nonself DNA and specifically destroy the foreign, in particular viral, genomes, whereas the host genome is protected, or ii) programmed cell suicide or dormancy induced by infection.
Presentation of the hypothesis: Almost all genomic loci encoding immunity systems such as CRISPR-Cas, restriction-modification and DNA phosphorothioation also encompass suicide genes, in particular those encoding known and predicted toxin nucleases, which do not appear to be directly involved in immunity. In contrast, the immunity systems do not appear to encode antitoxins found in typical toxin-antitoxin systems. This raises the possibility that components of the immunity system themselves act as reversible inhibitors of the associated toxin proteins or domains as has been demonstrated for the Escherichia coli anticodon nuclease PrrC that interacts with the PrrI restriction-modification system. We hypothesize that coupling of diverse immunity and suicide/dormancy systems in prokaryotes evolved under selective pressure to provide robustness to the antivirus response. We further propose that the involvement of suicide/dormancy systems in the coupled antivirus response could take two distinct forms: 1) induction of a dormancy-like state in the infected cell to 'buy time' for activation of adaptive immunity; 2) suicide or dormancy as the final recourse to prevent viral spread triggered by the failure of immunity.
Testing the hypothesis: This hypothesis entails many experimentally testable predictions. Specifically, we predict that Cas2 protein present in all cas operons is a mRNA-cleaving nuclease (interferase) that might be activated at an early stage of virus infection to enable incorporation of virus-specific spacers into the CRISPR locus or to trigger cell suicide when the immune function of CRISPR-Cas systems fails. Similarly, toxin-like activity is predicted for components of numerous other defense loci.
Implications of the hypothesis: The hypothesis implies that antivirus response in prokaryotes involves key decision-making steps at which the cell chooses the path to follow by sensing the course of virus infection.
Reviewers: This article was reviewed by Arcady Mushegian, Etienne Joly and Nick Grishin. For complete reviews, go to the Reviewers' reports section.
C1 [Makarova, Kira S.; Anantharaman, Vivek; Aravind, L.; Koonin, Eugene V.] Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
RP Koonin, EV (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
EM koonin@ncbi.nlm.nih.gov
OI Anantharaman, Vivek/0000-0001-8395-0009
FU US Department of Health and Human Services intramural funds
FX We thank Yuri Wolf and Tatiana Senkevich for critical reading of the
manuscript and useful discussions. The authors' research is supported by
the US Department of Health and Human Services intramural funds (to
National Library of Medicine).
NR 63
TC 25
Z9 25
U1 2
U2 25
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1745-6150
J9 BIOL DIRECT
JI Biol. Direct
PD NOV 14
PY 2012
VL 7
AR 40
DI 10.1186/1745-6150-7-40
PG 10
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA 042PK
UT WOS:000311483100001
PM 23151069
ER
PT J
AU Henderson, LJ
Sharma, A
Monaco, MCG
Major, EO
Al-Harthi, L
AF Henderson, Lisa J.
Sharma, Amit
Monaco, Maria Chiara G.
Major, Eugene O.
Al-Harthi, Lena
TI Human Immunodeficiency Virus Type 1 (HIV-1) Transactivator of
Transcription through Its Intact Core and Cysteine-Rich Domains Inhibits
Wnt/beta-Catenin Signaling in Astrocytes: Relevance to HIV
Neuropathogenesis
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID GLYCOGEN-SYNTHASE KINASE-3-BETA; TAT-MEDIATED NEUROTOXICITY; LONG
TERMINAL REPEAT; BETA-CATENIN; NEUROCOGNITIVE DISORDERS; ANTIRETROVIRAL
THERAPY; REV FUNCTION; PROTEIN; REPLICATION; PATHWAY
AB Wnt/beta-catenin is a neuroprotective pathway regulating cell fate commitment in the CNS and many vital functions of neurons and glia. Its dysregulation is linked to a number of neurodegenerative diseases. Wnt/beta-catenin is also a repressor of HIV transcription in multiple cell types, including astrocytes, which are dysregulated in HIV-associated neurocognitive disorder. Given that HIV proteins can overcome host restriction factors and that perturbations of Wnt/beta-catenin signaling can compromise astrocyte function, we evaluated the impact of HIV transactivator of transcription (Tat) on Wnt/beta-catenin signaling in astrocytes. HIV clade B Tat, in primary progenitor-derived astrocytes and U87MG cells, inhibited Wnt/beta-catenin signaling as demonstrated by its inhibition of active beta-catenin, TOPflash reporter activity, and Axin-2 (a downstream target of Wnt/beta-catenin signaling). Point mutations in either the core region (K41A) or the cysteine-rich region (C30G) of Tat abrogated its ability to inhibit beta-catenin signaling. Clade C Tat, which lacks the dicysteine motif, did not alter beta-catenin signaling, confirming that the dicysteine motif is critical for Tat inhibition of beta-catenin signaling. Tat coprecipitated with TCF-4 (a transcription factor that partners with beta-catenin), suggesting a physical interaction between these two proteins. Furthermore, knockdown of beta-catenin or TCF-4 enhanced docking of Tat at the TAR region of the HIV long terminal repeat. These findings highlight a bidirectional interference between Tat and Wnt/beta-catenin that negatively impacts their cognate target genes. The consequences of this interaction include alleviation of Wnt/beta-catenin-mediated suppression of HIV and possible astrocyte dysregulation contributing to HIV neuropathogenesis.
C1 [Henderson, Lisa J.; Sharma, Amit; Al-Harthi, Lena] Rush Univ, Med Ctr, Dept Immunol Microbiol, Chicago, IL 60612 USA.
[Monaco, Maria Chiara G.; Major, Eugene O.] NINDS, NIH, Bethesda, MD 20892 USA.
RP Al-Harthi, L (reprint author), Rush Univ, Med Ctr, Dept Immunol & Microbiol, 1735 W Harrison St,614 Cohn, Chicago, IL 60612 USA.
EM lena_al-harthi@rush.edu
FU National Institutes of Health [R01 NS060632, F31 NS071999]; Chicago
Developmental Center for AIDS Research [P30 AI 082151]; National
Institute of Allergy and Infectious Diseases; National Cancer Institute;
National Institute of Mental Health; National Institute on Drug Abuse;
National Institute of Child Health and Human Development; National
Heart, Lung, and Blood Institute; National Center for Complementary and
Alternative Medicine
FX This work was supported by National Institutes of Health Grants R01
NS060632 (L.A.-H.) and F31 NS071999 (L.J.H.), and the Chicago
Developmental Center for AIDS Research (Grant P30 AI 082151) supported
by National Institute of Allergy and Infectious Diseases, National
Cancer Institute, National Institute of Mental Health, National
Institute on Drug Abuse, National Institute of Child Health and Human
Development, National Heart, Lung, and Blood Institute, and National
Center for Complementary and Alternative Medicine.
NR 39
TC 20
Z9 20
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 14
PY 2012
VL 32
IS 46
BP 16306
EP 16313
DI 10.1523/JNEUROSCI.3145-12.2012
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 037GU
UT WOS:000311091000024
PM 23152614
ER
PT J
AU Ko, SJ
Isozaki, K
Kim, I
Lee, JH
Cho, HJ
Sohn, SY
Oh, SR
Park, S
Kim, DG
Kim, CH
Roche, KW
AF Ko, Suk Jin
Isozaki, Kaname
Kim, Insook
Lee, Jeong Ho
Cho, Ho Jin
Sohn, Sun Young
Oh, So Ra
Park, Steven
Kim, Dong Goo
Kim, Chul Hoon
Roche, Katherine W.
TI PKC Phosphorylation Regulates mGluR5 Trafficking by Enhancing Binding of
Siah-1A
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID METABOTROPIC GLUTAMATE RECEPTORS; PROTEIN-KINASE-C; FRAGILE-X-SYNDROME;
UBIQUITIN LIGASE; CALMODULIN; DEGRADATION; ENDOCYTOSIS;
MONOUBIQUITYLATION; DISEASE; CELLS
AB Glutamate is the major excitatory neurotransmitter in the mammalian CNS and acts on both ionotropic and metabotropic glutamate receptors (mGluRs). The mGluRs are widely distributed in the CNS and modulate a variety of neuronal processes, including neurotransmitter release and ion channel function. In hippocampus and cortex, mGluR5 is highly expressed and plays an important role in the regulation of synaptic plasticity. Calmodulin (CaM) binding dynamically regulates mGluR5 surface expression; however, the mechanisms linking CaM to mGluR5 trafficking are not clear. Recent studies showed that CaM binding to mGluR7 regulates its trafficking in a phosphorylation-dependent manner by disrupting the binding of protein interacting with C kinase 1. The E3 ligase seven in absentia homolog (Siah)-1A binds to mGluR5 and competes with CaM binding, making it an intriguing molecule to regulate phosphorylation-dependent trafficking of mGluR5. In the present study, we find that CaM competes with Siah-1A for mGluR5 binding in a phosphorylation-dependent manner in rat hippocampal neurons. Specifically, phosphorylation of mGluR5 S901 favors Siah-1A binding by displacing CaM. We identified critical residues regulating Siah-1A binding to mGluR5 and showed that binding is essential for the Siah-1A effects on mGluR5 trafficking. Siah-1A binding decreases mGluR5 surface expression and increases endosomal trafficking and lysosomal degradation of mGluR5. Thus CaM-regulated Siah-1A binding to mGluR5 dynamically regulates mGluR5 trafficking. These findings support a conserved role for CaM in regulating mGluR trafficking by PKC-dependent regulation of receptor-binding proteins.
C1 [Ko, Suk Jin; Lee, Jeong Ho; Cho, Ho Jin; Sohn, Sun Young; Oh, So Ra; Park, Steven; Kim, Dong Goo; Kim, Chul Hoon] Yonsei Univ, Coll Med, Dept Pharmacol, Seoul 120752, South Korea.
[Ko, Suk Jin; Lee, Jeong Ho; Cho, Ho Jin; Kim, Dong Goo; Kim, Chul Hoon] Yonsei Univ, Coll Med, Brain Korea Project Med Sci 21, Seoul 120752, South Korea.
[Isozaki, Kaname; Roche, Katherine W.] NINDS, NIH, Bethesda, MD 20892 USA.
[Kim, Insook] Natl Inst Hlth, Dept Biomed Sci, Div Metab Dis, Osong 363951, South Korea.
[Kim, Chul Hoon] Yonsei Univ, Coll Med, Severance Biomed Sci Inst, Seoul 120752, South Korea.
RP Kim, CH (reprint author), 134 Shinchon Dong, Seoul 120752, South Korea.
EM kimhoon@yuhs.ac
RI Lee, Jeong Ho/G-7361-2012;
OI Roche, Katherine/0000-0001-7282-6539
FU Basic Science Research Program through the National Research Foundation
of Korea; Ministry of Education, Science, and Technology [2011-0003351,
2011-0001174]; Japan Society for the Promotion of Science Research
Fellowship for Japanese Biomedical and Behavioral Researchers at the
National Institutes of Health; National Institute of Neurological
Disorders and Stroke Intramural Research Program; National Institute of
Child Health and Human Development
FX This work was supported by Basic Science Research Program through the
National Research Foundation of Korea funded by the Ministry of
Education, Science, and Technology (No. 2011-0003351 and 2011-0001174)
(to C. H. K.), by the Japan Society for the Promotion of Science
Research Fellowship for Japanese Biomedical and Behavioral Researchers
at the National Institutes of Health (to K. I.) and by the National
Institute of Neurological Disorders and Stroke Intramural Research
Program (to K. W. R.). We thank the Yonsei-Carl Zeiss Advanced Imaging
Center at Yonsei University College of Medicine and Dr. Carolyn Smith at
National Institute of Neurological Disorders and Stroke Light Imaging
Facility for technical assistance. The alpha-tubulin monoclonal antibody
developed by J. Frankel and E. M. Nelsen was obtained from the
Developmental Studies Hybridoma Bank developed under the auspices of the
National Institute of Child Health and Human Development and maintained
by the University of Iowa, Department of Biology, Iowa City, Iowa.
NR 32
TC 14
Z9 14
U1 0
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 14
PY 2012
VL 32
IS 46
BP 16391
EP 16401
DI 10.1523/JNEUROSCI.1964-12.2012
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 037GU
UT WOS:000311091000031
PM 23152621
ER
PT J
AU Palm-Meinders, IH
Koppen, H
Terwindt, GM
Launer, LJ
Konishi, J
Moonen, JME
Bakkers, JTN
Hofman, PAM
van Lew, B
Middelkoop, HAM
van Buchem, MA
Ferrari, MD
Kruit, MC
AF Palm-Meinders, Inge H.
Koppen, Hille
Terwindt, Gisela M.
Launer, Lenore J.
Konishi, Junya
Moonen, Juliette M. E.
Bakkers, Jacobus T. N.
Hofman, Paul A. M.
van Lew, Baldur
Middelkoop, Huub A. M.
van Buchem, Mark A.
Ferrari, Michel D.
Kruit, Mark C.
TI Structural Brain Changes in Migraine
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID WHITE-MATTER HYPERINTENSITIES; SMALL-VESSEL DISEASE;
CARDIOVASCULAR-DISEASE; COGNITIVE FUNCTION; VERBAL FLUENCY; POPULATION;
LESIONS; MRI; METAANALYSIS; HEADACHE
AB Context A previous cross-sectional study showed an association of migraine with a higher prevalence of magnetic resonance imaging (MRI)-measured ischemic lesions in the brain.
Objective To determine whether women or men with migraine (with and without aura) have a higher incidence of brain lesions 9 years after initial MRI, whether migraine frequency was associated with progression of brain lesions, and whether progression of brain lesions was associated with cognitive decline.
Design, Setting, and Participants In a follow-up of the 2000 Cerebral Abnormalities in Migraine, an Epidemiological Risk Analysis cohort, a prospective population-based observational study of Dutch participants with migraine and an age-and sex-matched control group, 203 of the 295 baseline participants in the migraine group and 83 of 140 in the control group underwent MRI scan in 2009 to identify progression of MRI-measured brain lesions. Comparisons were adjusted for age, sex, hypertension, diabetes, and educational level. The participants in the migraine group were a mean 57 years (range, 43-72 years), and 71% were women. Those in the control group were a mean 55 years (range, 44-71 years), and 69% were women.
Main Outcome Measures Progression of MRI-measured cerebral deep white matter hyperintensities, infratentorial hyperintensities, and posterior circulation territory infarctlike lesions. Change in cognition was also measured.
Results Of the 145 women in the migraine group, 112 (77%) vs 33 of 55 women (60%) in the control group had progression of deep white matter hyperintensities (adjusted odds ratio [OR], 2.1; 95% CI, 1.0-4.1; P = .04). There were no significant associations of migraine with progression of infratentorial hyperintensities: 21 participants (15%) in the migraine group and 1 of 57 participants (2%) in the control group showed progression (adjusted OR, 7.7; 95% CI, 1.0-59.5; P = .05) or new posterior circulation territory infarctlike lesions: 10 of 203 participants (5%) in the migraine group but none of 83 in the control group (P = .07). There was no association of number or frequency of migraine headaches with progression of lesions. There was no significant association of high vs nonhigh deep white matter hyperintensity load with change in cognitive scores (-3.7 in the migraine group vs 1.4 in the control group; 95% CI, -4.4 to 0.2; adjusted P = .07).
Conclusions In a community-based cohort followed up after 9 years, women with migraine had a higher incidence of deep white matter hyperintensities but did not have significantly higher progression of other MRI-measured brain changes. There was no association of migraine with progression of any MRI-measured brain lesions in men. JAMA. 2012;308(18):1889-1897 www.jama.com
C1 [Palm-Meinders, Inge H.; Konishi, Junya; Moonen, Juliette M. E.; van Buchem, Mark A.; Kruit, Mark C.] Leiden Univ, Med Ctr, Dept Radiol, NL-2300 RC Leiden, Netherlands.
[van Lew, Baldur] Leiden Univ, Med Ctr, Div Image Proc, NL-2300 RC Leiden, Netherlands.
[Koppen, Hille; Terwindt, Gisela M.; Ferrari, Michel D.] Leiden Univ, Med Ctr, Dept Neurol, NL-2300 RC Leiden, Netherlands.
[Middelkoop, Huub A. M.] Leiden Univ, Med Ctr, Dept Neuropsychol, NL-2300 RC Leiden, Netherlands.
[Koppen, Hille] Haga Hosp, Dept Neurol, The Hague, Netherlands.
[Launer, Lenore J.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Bakkers, Jacobus T. N.] Slingeland Hosp, Dept Radiol, Doetinchem, Netherlands.
[Hofman, Paul A. M.] Acad Hosp Maastricht, Dept Radiol, Maastricht, Netherlands.
RP Kruit, MC (reprint author), Leiden Univ, Med Ctr, Dept Radiol, POB 9600, NL-2300 RC Leiden, Netherlands.
EM m.c.kruit@lumc.nl
RI Kruit, Mark/K-2431-2012
OI Kruit, Mark/0000-0002-4319-834X
FU Almirall; Coherex; Colucid; Eisai; GlaxoSmithKline; Linde; MAP;
Medtronic; Menarini; Merck; Minster; Pfizer; St Jude; National
Institutes of Health [1R01NS061382-01]; Netherlands Heart Foundation
[2007B016]; Netherlands Organisation for Scientific Research
[903-52-291, VICI 918-56-602]; National Institute on Aging [907-00-217,
Vidi 917-11-319]
FX All authors have completed and submitted the ICMJE Form for Disclosure
of Potential Conflicts of Interest. Dr Ferrari reported receiving grants
and consultancy or industry support from Almirall, Coherex, Colucid,
Eisai, GlaxoSmithKline, Linde, MAP, Medtronic, Menarini, Merck, Minster,
Pfizer, and St Jude, and independent support from the Netherlands
Organisation for Scientific Research (NOW). Dr Terwindt reported
receiving consultancy support from Merck, Janssen-Cilag, Almirall, and
Menarini. Dr Koppen reported consultancy or industry support from
Allergan, Benecke congres, Pfizer, and In circulation website. The other
authors reported no financial disclosures.; This work was supported by
grants 1R01NS061382-01 from the National Institutes of Health, 2007B016
from the Netherlands Heart Foundation, and 903-52-291, VICI 918-56-602,
and Spinoza 2009 from the Netherlands Organisation for Scientific
Research, and 907-00-217 and Vidi 917-11-319 from the Intramural
Research Program at the National Institute on Aging.
NR 35
TC 56
Z9 60
U1 1
U2 23
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 14
PY 2012
VL 308
IS 18
BP 1889
EP 1897
DI 10.1001/jama.2012.14276
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 035NA
UT WOS:000310952700025
PM 23150008
ER
PT J
AU Levin, GP
Robinson-Cohen, C
de Boer, IH
Houston, DK
Lohman, K
Liu, YM
Kritchevsky, SB
Cauley, JA
Tanaka, T
Ferrucci, L
Bandinelli, S
Patel, KV
Hagstrom, E
Michaelsson, K
Melhus, H
Wang, T
Wolf, M
Psaty, BM
Siscovick, D
Kestenbaum, B
AF Levin, Gregory P.
Robinson-Cohen, Cassianne
de Boer, Ian H.
Houston, Denise K.
Lohman, Kurt
Liu, Yongmei
Kritchevsky, Stephen B.
Cauley, Jane A.
Tanaka, Toshiko
Ferrucci, Luigi
Bandinelli, Stefania
Patel, Kushang V.
Hagstrom, Emil
Michaelsson, Karl
Melhus, Hakan
Wang, Thomas
Wolf, Myles
Psaty, Bruce M.
Siscovick, David
Kestenbaum, Bryan
TI Genetic Variants and Associations of 25-Hydroxyvitamin D Concentrations
With Major Clinical Outcomes
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID D-RECEPTOR GENE; FALSE DISCOVERY RATE; VITAMIN-D DEFICIENCY; SERUM
25-HYDROXYVITAMIN-D; OLDER-ADULTS; CANCER-RISK; 1,25-DIHYDROXYVITAMIN
D-3; CARDIOVASCULAR-DISEASE; SEASONAL-VARIATION; FRACTURE RISK
AB Context Lower serum 25-hydroxyvitamin D concentrations are associated with greater risks of many chronic diseases across large, prospective community-based studies. Substrate 25-hydroxyvitamin D must be converted to 1,25-dihydroxyvitamin D for full biological activity, and complex metabolic pathways suggest that interindividual variability in vitamin D metabolism may alter the clinical consequences of measured serum 25-hydroxyvitamin D.
Objective To investigate whether common variation within genes encoding the vitamin D-binding protein, megalin, cubilin, CYP27B1, CYP24A1, and the vitamin D receptor (VDR) modify associations of low 25-hydroxyvitamin D with major clinical outcomes.
Design, Setting, and Participants Examination of 141 single-nucleotide polymorphisms in a discovery cohort of 1514 white participants (who were recruited from 4 US regions) from the community-based Cardiovascular Health Study. Participants had serum 25-hydroxyvitamin D measurements in 1992-1993 and were followed up for a median of 11 years (through 2006). Replication meta-analyses were conducted across the independent, community-based US Health, Aging, and Body Composition (n=922; follow-up: 1998-1999 through 2005), Italian Invecchiare in Chianti (n=835; follow-up: 1998-2000 through 2006), and Swedish Uppsala Longitudinal Study of Adult Men (n=970; follow-up: 1991-1995 through 2008) cohort studies.
Main Outcome Measure Composite outcome of incident hip facture, myocardial infarction, cancer, and mortality over long-term follow-up.
Results Interactions between 5 single-nucleotide polymorphisms and low 25-hydroxyvitamin D concentration were identified in the discovery phase and 1 involving a variant in the VDR gene replicated in independent meta-analysis. Among Cardiovascular Health Study participants, low 25-hydroxyvitamin D concentration was associated with hazard ratios for risk of the composite outcome of 1.40 (95% CI, 1.12-1.74) for those who had 1 minor allele at rs7968585 and 1.82 (95% CI, 1.31-2.54) for those with 2 minor alleles at rs7968585. In contrast, there was no evidence of an association (estimated hazard ratio, 0.93 [95% CI, 0.70-1.24]) among participants who had 0 minor alleles at this single-nucleotide polymorphism.
Conclusion Known associations of low 25-hydroxyvitamin D with major health outcomes may vary according to common genetic differences in the vitamin D receptor. JAMA. 2012;308(18):1898-1905 www.jama.com
C1 [Levin, Gregory P.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Robinson-Cohen, Cassianne; de Boer, Ian H.; Psaty, Bruce M.; Siscovick, David; Kestenbaum, Bryan] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[de Boer, Ian H.; Psaty, Bruce M.; Siscovick, David; Kestenbaum, Bryan] Univ Washington, Dept Med, Seattle, WA 98195 USA.
[Patel, Kushang V.] Univ Washington, Dept Anasthesiol & Pain Med, Seattle, WA 98195 USA.
[de Boer, Ian H.; Kestenbaum, Bryan] Univ Washington, Div Nephrol, Seattle, WA 98195 USA.
[de Boer, Ian H.; Kestenbaum, Bryan] Univ Washington, Kidney Res Inst, Seattle, WA 98195 USA.
[Patel, Kushang V.] Univ Washington, Ctr Pain Res Impact Measurement & Effectiveness, Seattle, WA 98195 USA.
[Psaty, Bruce M.; Siscovick, David] Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Psaty, Bruce M.] Univ Washington, Grp Hlth Res Inst & Cooperat, Seattle, WA 98195 USA.
[Houston, Denise K.; Kritchevsky, Stephen B.] Wake Forest Univ, Dept Internal Med, Winston Salem, NC 27109 USA.
[Lohman, Kurt] Wake Forest Univ, Dept Biostat Sci, Winston Salem, NC 27109 USA.
[Liu, Yongmei] Wake Forest Univ, Dept Epidemiol & Prevent, Winston Salem, NC 27109 USA.
[Lohman, Kurt; Liu, Yongmei] Wake Forest Univ, Div Publ Hlth Sci, Winston Salem, NC 27109 USA.
[Houston, Denise K.; Lohman, Kurt; Kritchevsky, Stephen B.] Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA.
[Cauley, Jane A.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
[Tanaka, Toshiko; Ferrucci, Luigi] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
[Bandinelli, Stefania] Azienda Sanit Firenze, Geriatr Unit, Florence, Italy.
[Hagstrom, Emil; Melhus, Hakan] Uppsala Univ, Dept Med Sci, Uppsala, Sweden.
[Michaelsson, Karl] Uppsala Univ, Dept Surg Sci, Uppsala, Sweden.
[Wang, Thomas] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol,Dept Med, Boston, MA USA.
[Wolf, Myles] Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
RP Levin, GP (reprint author), Univ Washington, Dept Biostat, Box 357232, Seattle, WA 98195 USA.
EM glevin11@uw.edu
OI Kritchevsky, Stephen/0000-0003-3336-6781; Robinson-Cohen,
Cassianne/0000-0003-4783-7046; Cauley, Jane A/0000-0003-0752-4408
FU Abbott Laboratories; National Institute on Aging, National Institutes of
Health; American Society for Nutrition; Department of Veteran Affairs;
Abbott Nutrition Health Institute; National Institutes of Health; Shire;
Amgen; Abbott; Genzyme; Medtronic
FX The authors have completed and submitted the ICMJE Form for Disclosure
of Potential Conflicts of Interest. Dr de Boer reported receiving
research grant funding from Abbott Laboratories. Dr Houston reported
pending institutional grant support from the National Institute on
Aging, National Institutes of Health; and receiving payment for lectures
from the American Society for Nutrition, the Department of Veteran
Affairs, and Abbott Nutrition Health Institute. Dr Wang reported serving
as a consultant to Diasorin; receiving an investigatorinitiated grant
from Diasorin; and receiving payment for lectures from Diasorin. Dr Wolf
reported serving as a consultant to Abbott, Genzyme, Luitpold,
Mitsubishi, Cytochroma, Astellas, and Kai; receiving institutional
grants from the National Institutes of Health, Shire, and Amgen;
receiving payment for lectures from Abbott, Genzyme, and Shire; and
having a pending patent. Dr Psaty reported serving on a data and safety
monitoring board for a clinical trial of a device funded by Zoll
ZifeCor; and serving on a steering committee for the Yale Open Data
Access Project funded by Medtronic. Dr Kestenbaum reported receiving
institutional grant support from Amgen. No other authors reported
disclosures.
NR 46
TC 79
Z9 83
U1 0
U2 19
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 14
PY 2012
VL 308
IS 18
BP 1898
EP 1905
DI 10.1001/jama.2012.17304
PG 8
WC Medicine, General & Internal
SC General & Internal Medicine
GA 035NA
UT WOS:000310952700026
PM 23150009
ER
PT J
AU Wang, YJ
Abu-Asab, MS
Li, W
Aronow, ME
Singh, AD
Chan, CC
AF Wang, Yujuan
Abu-Asab, Mones S.
Li, Wei
Aronow, Mary E.
Singh, Arun D.
Chan, Chi-Chao
TI Autoantibody against transient receptor potential M1 cation channels of
retinal ON bipolar cells in paraneoplastic vitelliform retinopathy
SO BMC OPHTHALMOLOGY
LA English
DT Article
DE Paraneoplastic vitelliform retinopathy; Autoimmune retinopathy;
Transient receptor potential channel; Bipolar cell; Melanoma-associated
retinopathy; Autoantibody
ID MELANOMA-ASSOCIATED RETINOPATHY; CUTANEOUS MALIGNANT-MELANOMA;
GLUTAMATE-RECEPTOR; GENE-EXPRESSION; MESSENGER-RNA; TRPM1; PATIENT;
LOCALIZATION; MACULOPATHY; CARCINOMA
AB Background: Paraneoplastic retinopathy is caused by the cross-reaction of neoplasm-directed autoantibodies against retinal antigens and results in retinal damage. Paraneoplastic vitelliform retinopathy, a presumed paraneoplastic retinopathy with features of atypical melanoma-associated retinopathy, has recently been reported in patients with metastatic melanoma. Ocular ultrastructure and its autoantibody localization of paraneoplastic vitelliform retinopathy are still indefinable. This is the first report of anti-transient receptor potential M1 antibody directly against human retinal bipolar dendritic tips in a melanoma patient with paraneoplastic vitelliform retinopathy.
Case presentation: We present a pair of postmortem eyes of an 80-year-old male with metastatic cutaneous melanoma, who developed paraneoplastic vitelliform retinopathy. The autopsied eyes were examined with light microscopy, immunohistochemistry, and transmission electron microscopy. Microscopically, the inner nuclear layer and outer plexiform layer were the most affected retinal structures, with local thinning. The lesions extended to the outer nuclear layer, resulting in focal retinal degeneration, edema, and atrophy. No active inflammation or melanoma cells were observed. Immunohistochemistry showed tightly compact bipolar cell nuclei (protein kinase C alpha/calbindin positive) with blur/loss of ON bipolar cell dendritic tips (transient receptor potential M1 positive) in diffusely condensed outer plexiform layer. The metastatic melanoma cells in his lung also showed immunoreactivity against transient receptor potential M1 antibody. Transmission electron microscopy illustrated degenerated inner nuclear layer with disintegration of cells and loss of cytoplasmic organelles. These cells contained many lysosomal and autophagous bodies and damaged mitochondria. Their nuclei appeared pyknotic and fragmentary. The synapses in the outer plexiform layer were extensively degenerated and replaced with empty vacuoles and disintegrated organelles.
Conclusion: This case provides a convincing histological evidence of melanoma-associated autoantibodies directly against transient receptor potential M1 channels that target the ON bipolar cell structures in the inner nuclear and outer plexiform layers in paraneoplastic vitelliform retinopathy.
C1 [Wang, Yujuan; Abu-Asab, Mones S.; Chan, Chi-Chao] NEI, Sect Immunopathol, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Wang, Yujuan] Sun Yat Sen Univ, Zhongshan Ophthalm Ctr, Guangzhou 510275, Guangdong, Peoples R China.
[Li, Wei] NEI, Unit Retinal Neurophysiol, NIH, Bethesda, MD 20892 USA.
[Aronow, Mary E.; Singh, Arun D.] Cleveland Clin, Dept Ophthalm Oncol, Cole Eye Inst, Cleveland, OH 44106 USA.
RP Chan, CC (reprint author), NEI, Sect Immunopathol, Immunol Lab, NIH, 10 Ctr Dr,10-10N103, Bethesda, MD 20892 USA.
EM chanc@nei.nih.gov
RI wang, yujuan/C-8428-2016;
OI Abu-Asab, Mones/0000-0002-4047-1232
FU National Eye Institute Intramural Research Program
FX The National Eye Institute Intramural Research Program supported the
study.
NR 39
TC 7
Z9 7
U1 0
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2415
J9 BMC OPHTHALMOL
JI BMC Ophthalmol.
PD NOV 13
PY 2012
VL 12
AR 56
DI 10.1186/1471-2415-12-56
PG 6
WC Ophthalmology
SC Ophthalmology
GA 048CG
UT WOS:000311887200001
PM 23148706
ER
PT J
AU Chowell, G
Towers, S
Viboud, C
Fuentes, R
Sotomayor, V
Simonsen, L
Miller, MA
Lima, M
Villarroel, C
Chiu, M
Villarroel, JE
Olea, A
AF Chowell, Gerardo
Towers, Sherry
Viboud, Cecile
Fuentes, Rodrigo
Sotomayor, Viviana
Simonsen, Lone
Miller, Mark A.
Lima, Mauricio
Villarroel, Claudia
Chiu, Monica
Villarroel, Jose E.
Olea, Andrea
TI The influence of climatic conditions on the transmission dynamics of the
2009 A/H1N1 influenza pandemic in Chile
SO BMC INFECTIOUS DISEASES
LA English
DT Article
DE A/H1N1 influenza pandemic; Acute respiratory infection;
Influenza-like-illness; Reproduction number; Spatial heterogeneity;
School cycles; Climatological variables; Specific humidity; Temperature;
Chile
ID A H1N1 VIRUS; REPRODUCTION NUMBER; UNITED-STATES; ABSOLUTE-HUMIDITY;
EPIDEMIC; SEASONALITY; INFECTION; IMPACT; SCHOOL; WINTER
AB Background: The role of demographic factors, climatic conditions, school cycles, and connectivity patterns in shaping the spatio-temporal dynamics of pandemic influenza is not clearly understood. Here we analyzed the spatial, age and temporal evolution of the 2009 A/H1N1 influenza pandemic in Chile, a southern hemisphere country covering a long and narrow strip comprising latitudes 17 S to 56 S.
Methods: We analyzed the dissemination patterns of the 2009 A/H1N1 pandemic across 15 regions of Chile based on daily hospitalizations for severe acute respiratory disease and laboratory confirmed A/H1N1 influenza infection from 01-May to 31-December, 2009. We explored the association between timing of pandemic onset and peak pandemic activity and several geographical and demographic indicators, school vacations, climatic factors, and international passengers. We also estimated the reproduction number (R) based on the growth rate of the exponential pandemic phase by date of symptoms onset, estimated using maximum likelihood methods.
Results: While earlier pandemic onset was associated with larger population size, there was no association with connectivity, demographic, school or climatic factors. In contrast, there was a latitudinal gradient in peak pandemic timing, representing a 16-39-day lag in disease activity from the southern regions relative to the northernmost region (P < 0.001). Geographical differences in latitude of Chilean regions, maximum temperature and specific humidity explained 68.5% of the variability in peak timing (P = 0.01). In addition, there was a decreasing gradient in reproduction number from south to north Chile (P < 0.0001). The regional mean R estimates were 1.6-2.0, 1.3-1.5, and 1.2-1.3 for southern, central and northern regions, respectively, which were not affected by the winter vacation period.
Conclusions: There was a lag in the period of most intense 2009 pandemic influenza activity following a South to North traveling pattern across regions of Chile, significantly associated with geographical differences in minimum temperature and specific humidity. The latitudinal gradient in timing of pandemic activity was accompanied by a gradient in reproduction number (P < 0.0001). Intensified surveillance strategies in colder and drier southern regions could lead to earlier detection of pandemic influenza viruses and improved control outcomes.
C1 [Chowell, Gerardo; Towers, Sherry] Arizona State Univ, Math Computat & Modeling Sci Ctr, Sch Human Evolut & Social Change, Tempe, AZ 85069 USA.
[Chowell, Gerardo; Viboud, Cecile; Simonsen, Lone; Miller, Mark A.] NIH, Div Epidemiol & Populat Studies, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Towers, Sherry] Purdue Univ, Dept Math, W Lafayette, IN 47907 USA.
[Fuentes, Rodrigo; Sotomayor, Viviana; Chiu, Monica; Villarroel, Jose E.; Olea, Andrea] Minist Salud, Dept Epidemiol, Santiago, Chile.
[Simonsen, Lone] George Washington Univ, Sch Publ Hlth & Hlth Serv, Dept Global Hlth, Washington, DC USA.
[Lima, Mauricio] Pontificia Univ Catolica Chile, Ctr Adv Studies Ecol & Biodivers, Santiago, Chile.
[Villarroel, Jose E.] Direcc Meteorol Chile, Santiago, Chile.
RP Chowell, G (reprint author), Arizona State Univ, Math Computat & Modeling Sci Ctr, Sch Human Evolut & Social Change, Tempe, AZ 85069 USA.
EM gchowell@asu.edu
RI Lima, Mauricio/F-2722-2013; Chowell, Gerardo/F-5038-2012;
OI Lima, Mauricio/0000-0002-3700-2945; Chowell,
Gerardo/0000-0003-2194-2251; Simonsen, Lone/0000-0003-1535-8526
FU International Influenza Unit, Office of Global Health Affairs,
Department of Health and Human Services; RAPIDD (Research and Policy for
Infectious Disease Dynamics) program of the Science and Technology
Directorate, Department of Homeland Security; Fogarty International
Center; NSF grant [DMS-1022758]
FX This research was conducted in the context of the MISMS (Multinational
Influenza Seasonal Mortality Study), an ongoing international
collaborative effort to understand influenza epidemiological and
evolutionary patterns, led by the Fogarty International Center, National
Institutes of Health (http://www.origem.info/misms/index.php). The MISMS
study is funded by the International Influenza Unit, Office of Global
Health Affairs, Department of Health and Human Services. LS acknowledges
support from the RAPIDD (Research and Policy for Infectious Disease
Dynamics) program of the Science and Technology Directorate, Department
of Homeland Security, and the Fogarty International Center. ST
acknowledges support of NSF grant DMS-1022758.
NR 68
TC 17
Z9 17
U1 3
U2 11
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2334
J9 BMC INFECT DIS
JI BMC Infect. Dis.
PD NOV 13
PY 2012
VL 12
AR 298
DI 10.1186/1471-2334-12-298
PG 12
WC Infectious Diseases
SC Infectious Diseases
GA 054WH
UT WOS:000312375400001
PM 23148597
ER
PT J
AU Vogel, SS
Nguyen, TA
van der Meer, BW
Blank, PS
AF Vogel, Steven S.
Nguyen, Tuan A.
van der Meer, B. Wieb
Blank, Paul S.
TI The Impact of Heterogeneity and Dark Acceptor States on FRET:
Implications for Using Fluorescent Protein Donors and Acceptors
SO PLOS ONE
LA English
DT Article
ID RESONANCE ENERGY-TRANSFER; LIVING CELLS; MOLECULAR-SPECTROSCOPY;
ORIENTATION FACTOR; HOMO-FRET; MICROSCOPY; DYNAMICS; GFP; STOICHIOMETRY;
ACTIVATION
AB Forster resonance energy transfer (FRET) microscopy is widely used to study protein interactions in living cells. Typically, spectral variants of the Green Fluorescent Protein (FPs) are incorporated into proteins expressed in cells, and FRET between donor and acceptor FPs is assayed. As appreciable FRET occurs only when donors and acceptors are within 10 nm of each other, the presence of FRET can be indicative of aggregation that may denote association of interacting species. By monitoring the excited-state (fluorescence) decay of the donor in the presence and absence of acceptors, dual-component decay analysis has been used to reveal the fraction of donors that are FRET positive (i.e., in aggregates). However, control experiments using constructs containing both a donor and an acceptor FP on the same protein repeatedly indicate that a large fraction of these donors are FRET negative, thus rendering the interpretation of dual-component analysis for aggregates between separately donor-containing and acceptor-containing proteins problematic. Using Monte-Carlo simulations and analytical expressions, two possible sources for such anomalous behavior are explored: 1) conformational heterogeneity of the proteins, such that variations in the distance separating donor and acceptor FPs and/or their relative orientations persist on time-scales long in comparison with the excited-state lifetime, and 2) FP dark states.
C1 [Vogel, Steven S.; Nguyen, Tuan A.] NIAAA, Lab Mol Physiol, NIH, Bethesda, MD USA.
[van der Meer, B. Wieb] Western Kentucky Univ, Dept Phys & Astron, Bowling Green, KY 42101 USA.
[Blank, Paul S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
RP Vogel, SS (reprint author), NIAAA, Lab Mol Physiol, NIH, Bethesda, MD USA.
EM stevevog@mail.nih.gov
OI Vogel, Steven/0000-0002-3005-2667
FU National Institutes of Health, National Institute on Alcohol Abuse and
Alcoholism, Eunice Kennedy Shriver National Institute of Child Health
and Human Development, Bethesda [MD 20892]
FX This work was supported by the intramural programs of the National
Institutes of Health, National Institute on Alcohol Abuse and
Alcoholism, Eunice Kennedy Shriver National Institute of Child Health
and Human Development, Bethesda, MD 20892. The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 54
TC 15
Z9 15
U1 0
U2 30
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 13
PY 2012
VL 7
IS 11
AR e49593
DI 10.1371/journal.pone.0049593
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 039HF
UT WOS:000311234600048
PM 23152925
ER
PT J
AU Ketkar, A
Zafar, MK
Banerjee, S
Marquez, VE
Egli, M
Eoff, RL
AF Ketkar, Amit
Zafar, Maroof K.
Banerjee, Surajit
Marquez, Victor E.
Egli, Martin
Eoff, Robert L.
TI Differential Furanose Selection in the Active Sites of Archaeal DNA
Polymerases Probed by Fixed-Conformation Nucleotide Analogues
SO BIOCHEMISTRY
LA English
DT Article
ID NUCLEIC-ACID STRUCTURES; SULFOLOBUS-SOLFATARICUS; NUCLEOSIDE ANALOGS;
SUGAR PUCKER; Y-FAMILY; FIDELITY; DPO4; RIBONUCLEOTIDES; VISUALIZATION;
SUBSTITUTION
AB DNA polymerases select for the incorporation of deoxyribonucleotide triphosphates (dNTPs) using amino acid side chains that act as a "steric-gate" to bar improper incorporation of rNTPs. An additional factor in the selection of nucleotide substrates resides in the preferred geometry for the furanose moiety of the incoming nucleotide triphosphate. We have probed the role of sugar geometry during nucleotide selection by model DNA polymerases from Sulfolobus solfataricus using fixed conformation nucleotide analogues. North-methanocarba-dATP (N-MC-dATP) locks the central ring into a RNA type (C2'-exo, North) conformation near a C3'-endo Pucker, and South-methariocarba-dATP (S-MC-dATP) locks the central ring system into a (C3'-exo, South) conformation near a C2'-endo pucker. Dpo4 Preferentially inserts N-MC-dATP and in the crystal structure of Dpo4 in complex with N-MC-dAMP the nucleotide analogue superimposes almost perfectly with Dpo4 bound to unmodified dATP. Biochemical assays indicate that the S. solfataricus B-family DNA polymerase Dpo1 can insert and extend from both N-MC-dATP and S-MC-dATP. In this respect, Dpo1 is unexpectedly more tolerant of substrate conformation than Dpo4. The crystal structure of Dpo4 bound to S-MC-dADP shows that poor incorporation of the Southern pucker by the Y-family polymerase results from a hydrogen bond between the 3'-OH group of the nucleotide analogue and the OH group of the steric gate residue, Tyr12, shifting the S-MC-dADP molecule away from the dNTP binding pocket and distorting the base pair at the primer-template junction. These results provide insights into substrate specificity of DNA polymerases, as well as molecular mechanisms that act as a barrier against insertion of rNTPs.
C1 [Ketkar, Amit; Zafar, Maroof K.; Eoff, Robert L.] Univ Arkansas Med Sci, Dept Biochem & Mol Biol, Little Rock, AR 72205 USA.
[Banerjee, Surajit] Cornell Univ, NE Collaborat Access Team, Argonne, IL 60439 USA.
[Banerjee, Surajit] Cornell Univ, Dept Chem & Chem Biol, Argonne, IL 60439 USA.
[Marquez, Victor E.] NCI, Biol Chem Lab, Ctr Canc Res, Frederick, MD 21702 USA.
[Egli, Martin] Vanderbilt Univ, Dept Biochem, Sch Med, Nashville, TN 37232 USA.
RP Eoff, RL (reprint author), Univ Arkansas Med Sci, Dept Biochem & Mol Biol, Little Rock, AR 72205 USA.
EM rleoff@uams.edu
OI Banerjee, Surajit/0000-0002-9414-7163
FU U.S.P.H. Service Grants [R00 GM084460, R01 GM055237]; Intramural
Research Program of the NIH, National Cancer Institute, Center for
Cancer Research; National Center for Research Resources
[5P41RR015301-10]; National Institute of General Medical Sciences from
the National Institutes of Health [8 P41 GM103403-10]; U.S. DOE
[DE-AC02-06CH11357]
FX This work was supported in part by U.S.P.H. Service Grants R00 GM084460
(R.L.E.) and R01 GM055237 (M.E.). Supported in part by the Intramural
Research Program of the NIH, National Cancer Institute, Center for
Cancer Research. This work is based upon research conducted at the
Advanced Photon Source on the Northeastern Collaborative Access Team
beamlines, which are supported by grants from the National Center for
Research Resources (5P41RR015301-10) and the National Institute of
General Medical Sciences (8 P41 GM103403-10) from the National
Institutes of Health. Use of the Advanced Photon Source, an Office of
Science User Facility operated for the U.S. Department of Energy (DOE)
Office of Science by Argonne National Laboratory, was supported by the
U.S. DOE under Contract No. DE-AC02-06CH11357.
NR 38
TC 1
Z9 1
U1 0
U2 11
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 13
PY 2012
VL 51
IS 45
BP 9234
EP 9244
DI 10.1021/bi301043k
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 038QT
UT WOS:000311189900021
PM 23050956
ER
PT J
AU Gurnev, PA
Bezrukov, SM
AF Gurnev, Philip A.
Bezrukov, Sergey M.
TI Inversion of Membrane Surface Charge by Trivalent Cations Probed with a
Cation-Selective Channel
SO LANGMUIR
LA English
DT Article
ID LIPID BILAYER MEMBRANES; GRAMICIDIN-A CHANNELS; ION-CHANNEL; NANOFLUIDIC
DIODE; MULTIVALENT IONS; CONDUCTANCE; ADSORPTION; PHOSPHOLIPIDS;
RECTIFICATION; CONDENSATION
AB We demonstrate that the cation-selective channel formed by gramicidin A can be used as a reliable sensor for studying. the Multivalent ion accumulation at the surfaces. of charged lipid membranes and the ''charge inversion phenomenon. In asymmetrically charged membranes with the individual leaflets formed from pure negative and positive lipids bathed by 0.1 M CsCl solutions the Channel exhibits.. current rectification, which is comparable to that of a typical n/p semiconductor diode. We show that even at these highly "asymmetrical conditions the channel conductance can be satisfactorily described by the electrodiffusion equation in the constant field approximation but, due to predictable limitations, only when the applied voltages do not exceed SO mV. Analysis of the changes in the voltage dependent channel conductance upon addition of trivalent cations allows us to gauge their interactions with the membrane surface. The inversion of the sign of the effective surface charge takes place at the concentrations, which correlate with the cation size. Specifically, these concentrations are close to 0.05 mM for lanthanum, 0.25 mM for hexaamminecobalt, and 4 mM for spermidine.
C1 [Gurnev, Philip A.; Bezrukov, Sergey M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
RP Gurnev, PA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
EM gurnevp@mail.nih.gov
FU NIH, Eunice Kennedy Shriver National Institute of Child Health and Human
Development
FX This study was supported by the Intramural Research Program of the NIH,
Eunice Kennedy Shriver National Institute of Child Health and Human
Development.
NR 66
TC 14
Z9 14
U1 1
U2 28
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0743-7463
J9 LANGMUIR
JI Langmuir
PD NOV 13
PY 2012
VL 28
IS 45
BP 15824
EP 15830
DI 10.1021/la302676t
PG 7
WC Chemistry, Multidisciplinary; Chemistry, Physical; Materials Science,
Multidisciplinary
SC Chemistry; Materials Science
GA 038RH
UT WOS:000311191300010
PM 23088396
ER
PT J
AU Wentzensen, N
Follansbee, S
Borgonovo, S
Tokugawa, D
Schwartz, L
Lorey, TS
Sahasrabuddhe, VV
Lamere, B
Gage, JC
Fetterman, B
Darragh, TM
Castle, PE
AF Wentzensen, Nicolas
Follansbee, Stephen
Borgonovo, Sylvia
Tokugawa, Diane
Schwartz, Lauren
Lorey, Thomas S.
Sahasrabuddhe, Vikrant V.
Lamere, Brandon
Gage, Julia C.
Fetterman, Barbara
Darragh, Teresa M.
Castle, Philip E.
TI Human papillomavirus genotyping, human papillomavirus mRNA expression,
and p16/Ki-67 cytology to detect anal cancer precursors in HIV-infected
MSM
SO AIDS
LA English
DT Article
DE anal cancer screening; HIV; human papillomavirus; human papillomavirus
mRNA; MSM; p16
ID HIGH-RESOLUTION ANOSCOPY; CERVICAL-CANCER; INTRAEPITHELIAL NEOPLASIA;
METAANALYSIS; PERFORMANCE; PREVENTION; RISK; MEN; SEX
AB Objective: Anal cancer incidence is high in HIV-infected MSM. Screening for anal intraepithelial lesions and cancers is performed at specialized clinics and relies on high-resolution anoscopy (HRA) and anal cytology. Both approaches have limited reproducibility and sensitivity for detecting anal cancer precursors. We evaluated biomarkers for human papillomavirus (HPV)-related disease in a population of HIV-infected MSM.
Methods: A cross-sectional screening study with passive follow-up included 363 MSM followed at a HIV/AIDS clinic. All men had anal cytology samples taken and were evaluated using HRA and anal biopsies. Using a composite endpoint of biopsy results and cytology, we compared the performance of HPV16/18 genotyping, HPVE6/E7 mRNA expression, and p16/Ki-67 cytology to detect high-grade anal intraepithelial neoplasias (AINs).
Results: For all biomarkers analyzed, there was a significant trend of increasing percentage of men testing positive with increasing severity of disease (P < 0.001). HPV DNA testing had the highest sensitivity for anal intraepithelial neoplasia grade 2 and anal intraepithelial neoplasia grade 3 (AIN3), followed by p16/Ki-67, HPVE6/E7 mRNA testing, and HPV16/18 genotyping. The highest Youden's index was observed for HPVE6/E7 mRNA testing, followed by HPV16/18 genotyping, p16/Ki-67 cytology, and HPV DNA testing. Increasing the threshold for positivity of p16/Ki-67 to five or more positive cells led to significantly higher specificity, but unchanged sensitivity for detecting AIN3.
Conclusion: Molecular features of anal disease categories are similar to those of corresponding cervical lesions. Biomarkers evaluated for cervical cancer screening may be used for primary anal cancer screening or to decide who should require immediate treatment vs. expectant management. (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins
C1 [Wentzensen, Nicolas; Schwartz, Lauren; Sahasrabuddhe, Vikrant V.; Gage, Julia C.] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20852 USA.
[Follansbee, Stephen; Borgonovo, Sylvia] Kaiser Permanente Med Ctr, San Francisco, CA USA.
[Tokugawa, Diane; Lorey, Thomas S.; Fetterman, Barbara] Kaiser Permanente, TPMG Reg Lab, Berkeley, CA USA.
[Lamere, Brandon] Kaiser Permanente, Div Res, Womens Hlth Res Inst, Oakland, CA USA.
[Darragh, Teresa M.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Castle, Philip E.] Amer Soc Clin Pathologists, Washington, DC USA.
RP Wentzensen, N (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,Room 5024, Rockville, MD 20852 USA.
EM wentzenn@mail.nih.gov
FU NIH/National Cancer Institute
FX The study was supported by the Intramural Research Program of
NIH/National Cancer Institute. Roche and NorChip provided free testing
for HPV DNA, p16, and HPV mRNA for this study.
NR 22
TC 21
Z9 22
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 13
PY 2012
VL 26
IS 17
BP 2185
EP 2192
DI 10.1097/QAD.0b013e328359f255
PG 8
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 032WQ
UT WOS:000310750800007
PM 23018436
ER
PT J
AU Iyer, LM
Aravind, L
AF Iyer, Lakshminarayan M.
Aravind, L.
TI ALOG domains: provenance of plant homeotic and developmental regulators
from the DNA-binding domain of a novel class of DIRS1-type retroposons
SO BIOLOGY DIRECT
LA English
DT Article
DE DIRS1; Tyrosine recombinase; Plant development; DNA-binding; Retroposon;
Transcription factor; Chromatin protein; Plant defense
ID TRANSCRIPTION FACTORS; STRUCTURE PREDICTION; STRUCTURAL BASIS;
NATURAL-HISTORY; GENE FAMILY; PROTEIN; RETROTRANSPOSONS; RECOMBINATION;
TRANSPOSONS; ALIGNMENT
AB Members of the Arabidopsis LSH1 and Oryza G1 (ALOG) family of proteins have been shown to function as key developmental regulators in land plants. However, their precise mode of action remains unclear. Using sensitive sequence and structure analysis, we show that the ALOG domains are a distinct version of the N-terminal DNA-binding domain shared by the XerC/D-like, protelomerase, topoisomerase-IA, and Flp tyrosine recombinases. ALOG domains are distinguished by the insertion of an additional zinc ribbon into this DNA-binding domain. In particular, we show that the ALOG domain is derived from the XerC/D-like recombinases of a novel class of DIRS-1-like retroposons. Copies of this element, which have been recently inactivated, are present in several marine metazoan lineages, whereas the stramenopile Ectocarpus, retains an active copy of the same. Thus, we predict that ALOG domains help establish organ identity and differentiation by binding specific DNA sequences and acting as transcription factors or recruiters of repressive chromatin. They are also found in certain plant defense proteins, where they are predicted to function as DNA sensors. The evolutionary history of the ALOG domain represents a unique instance of a domain, otherwise exclusively found in retroelements, being recruited as a specific transcription factor in the streptophyte lineage of plants. Hence, they add to the growing evidence for derivation of DNA-binding domains of eukaryotic specific TFs from mobile and selfish elements.
C1 [Iyer, Lakshminarayan M.; Aravind, L.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Aravind, L (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
EM aravind@ncbi.nlm.nih.gov
FU US Department of Health and Human Services (National Library of
Medicine, NIH)
FX The authors' research is supported by the intramural funds of the US
Department of Health and Human Services (National Library of Medicine,
NIH). We thank Dr. R. F. de Souza for writing a script that was useful
for this analysis. This article was reviewed by Valerian Dolja and
Gaspar Jekely. Additional file 1 can also be accessed from
ftp://ftp.ncbi.nih.gov/pub/aravind/ALOG/ALOG.html
NR 39
TC 7
Z9 26
U1 1
U2 7
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1745-6150
J9 BIOL DIRECT
JI Biol. Direct
PD NOV 12
PY 2012
VL 7
AR 39
DI 10.1186/1745-6150-7-39
PG 8
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA 100TO
UT WOS:000315726700001
PM 23146749
ER
PT J
AU Kuhn, A
Kumar, A
Beilina, A
Dillman, A
Cookson, MR
Singleton, AB
AF Kuhn, Alexandre
Kumar, Azad
Beilina, Alexandra
Dillman, Allissa
Cookson, Mark R.
Singleton, Andrew B.
TI Cell population-specific expression analysis of human cerebellum
SO BMC GENOMICS
LA English
DT Article
DE Genomics; Computational biology; Cerebellum; Gene expression; Aging;
Astrocyte
ID GENE-EXPRESSION; MICROARRAY DATA; ALZHEIMERS-DISEASE; COMPLEX TISSUES;
RAT CEREBELLUM; GLIAL-CELLS; BRAIN; PROTEIN; CANCER; DECONVOLUTION
AB Background: Interpreting gene expression profiles obtained from heterogeneous samples can be difficult because bulk gene expression measures are not resolved to individual cell populations. We have recently devised Population-Specific Expression Analysis (PSEA), a statistical method that identifies individual cell types expressing genes of interest and achieves quantitative estimates of cell type-specific expression levels. This procedure makes use of marker gene expression and circumvents the need for additional experimental information like tissue composition.
Results: To systematically assess the performance of statistical deconvolution, we applied PSEA to gene expression profiles from cerebellum tissue samples and compared with parallel, experimental separation methods. Owing to the particular histological organization of the cerebellum, we could obtain cellular expression data from in situ hybridization and laser-capture microdissection experiments and successfully validated computational predictions made with PSEA. Upon statistical deconvolution of whole tissue samples, we identified a set of transcripts showing age-related expression changes in the astrocyte population.
Conclusions: PSEA can predict cell-type specific expression levels from tissues homogenates on a genome-wide scale. It thus represents a computational alternative to experimental separation methods and allowed us to identify age-related expression changes in the astrocytes of the cerebellum. These molecular changes might underlie important physiological modifications previously observed in the aging brain.
C1 [Kuhn, Alexandre; Kumar, Azad; Beilina, Alexandra; Dillman, Allissa; Cookson, Mark R.; Singleton, Andrew B.] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
RP Kuhn, A (reprint author), ASTAR, Inst Mat Res & Engn, 3 Res Link, Singapore 117602, Singapore.
EM alexandre.m.kuhn@gmail.com
FU Swiss National Science Foundation; Intramural Research Program of the
National Institutes of Health (NIH); National Institute on Aging
FX This work was supported by the Swiss National Science Foundation and in
part by the Intramural Research Program of the National Institutes of
Health (NIH), National Institute on Aging. We are grateful to Jean-Marc
Taymans for helpful discussions and Xavier Le Guezennec for comments on
the manuscript. We would like to thank the LCM Core Facility at the
National Cancer Institute for help with microdissection and the Helix
Systems group (NIH) for providing high-performance computing
infrastructure.
NR 55
TC 7
Z9 7
U1 0
U2 9
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 12
PY 2012
VL 13
AR 610
DI 10.1186/1471-2164-13-610
PG 15
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 085XN
UT WOS:000314647700001
PM 23145530
ER
PT J
AU Tobias, DK
Hu, FB
Chavarro, J
Rosner, B
Mozaffarian, D
Zhang, CL
AF Tobias, Deirdre K.
Hu, Frank B.
Chavarro, Jorge
Rosner, Bernard
Mozaffarian, Dariush
Zhang, Cuilin
TI Healthful Dietary Patterns and Type 2 Diabetes Mellitus Risk Among Women
With a History of Gestational Diabetes Mellitus
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Article
ID FOOD FREQUENCY QUESTIONNAIRE; CORONARY-HEART-DISEASE; BETA-CELL
FUNCTION; INSULIN-RESISTANCE; PHYSICAL-ACTIVITY; HISPANIC WOMEN;
PREVENTION; QUALITY; METAANALYSIS; VALIDATION
AB Background: Type 2 diabetes mellitus (T2DM) has reached epidemic proportions. Women with gestational diabetes mellitus (GDM) are at high risk for T2DM after pregnancy. Adherence to healthful dietary patterns has been inversely associated with T2DM in the general population; however, whether these dietary patterns are associated with progression to T2DM among a susceptible population is unknown.
Methods: Four thousand four hundred thirteen participants from the Nurses' Health Study II cohort with prior GDM were followed up from 1991 to 2005. We derived the alternate Mediterranean diet (aMED), Dietary Approaches to Stop Hypertension (DASH), and alternate Healthy Eating Index (aHEI) dietary pattern adherence scores from a post-GDM validated food-frequency questionnaire, with cumulative average updating every 4 years. Multivariable Cox proportional hazards models estimated the relative risk (hazard ratios) and 95% confidence intervals.
Results: We observed 491 cases of incident T2DM during 52 743 person-years. All 3 patterns were inversely associated with T2DM risk with adjustment for age, total calorie intake, age at first birth, parity, ethnicity, parental diabetes, oral contraceptive use, menopause, and smoking. When we compared participants with the highest adherence (quartile 4) vs lowest (quartile 1), the aMED pattern was associated with 40% lower risk of T2DM (hazard ratio, 0.60 [95% CI, 0.44-0.82; P = .002]); the DASH pattern, with 46% lower risk (0.54 [0.39-0.73; P < .001]); and the aHEI pattern, with 57% lower risk (0.43 [0.31-0.59; P < .001]). Adjustment for body mass index moderately attenuated these findings.
Conclusions: Adherence to healthful dietary patterns is associated with lower T2DM risk among women with a history of GDM. The inverse associations are partly mediated by body mass index.
C1 [Tobias, Deirdre K.; Hu, Frank B.; Chavarro, Jorge; Mozaffarian, Dariush] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Tobias, Deirdre K.; Hu, Frank B.; Chavarro, Jorge; Mozaffarian, Dariush] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Rosner, Bernard] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Hu, Frank B.; Chavarro, Jorge; Rosner, Bernard; Mozaffarian, Dariush] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Hu, Frank B.; Chavarro, Jorge; Rosner, Bernard; Mozaffarian, Dariush] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Zhang, Cuilin] Eunice Kennedy Shriver Natl Inst Child Hlth & Dev, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, Rockville, MD 20852 USA.
RP Tobias, DK (reprint author), Harvard Univ, Sch Publ Hlth, Dept Nutr, 665 Huntington Ave, Boston, MA 02115 USA.
EM dbanel@hsph.harvard.edu; zhangcu@mail.nih.gov
FU GlaxoSmithKline; Sigma Tau; Pronova; National Institutes of Health;
Foodminds; McKinsey Health Systems Institute; National Institute of
Diabetes and Digestive and Kidney Diseases [DK58845, P30 DK46200-18];
National Cancer Institute [CA50385]; Eunice Kennedy Shriver National
Institute of Child Health and Human Development, National Institutes of
Health
FX Dr Mozaffarian has received research grants from GlaxoSmithKline, Sigma
Tau, Pronova, and the National Institutes of Health for an
investigator-initiated, not-for-profit clinical trial of fish oil
supplements and postsurgical complications; ad hoc travel reimbursement
and/or honoraria for research presentations on diet and cardiometabolic
diseases from the International Life Sciences Institute, Aramark,
Unilever, Bunge, SPRIM, and Nutrition Impact; ad hoc consulting fees
from Foodminds and McKinsey Health Systems Institute; and royalties from
UpToDate for an online chapter on fish oil. In addition, Harvard
University has filed a provisional patent application that has been
assigned to Harvard University, listing Dr Mozaffarian as a coinventor,
to the US Patent and Trademark Office for use of trans-palmitoleic acid
to prevent and treat insulin resistance, T2DM, and related conditions.;
This study was supported by grants DK58845 and P30 DK46200-18 from the
National Institute of Diabetes and Digestive and Kidney Diseases; by
grant CA50385 from the National Cancer Institute; and by the Intramural
Research Program of the Eunice Kennedy Shriver National Institute of
Child Health and Human Development, National Institutes of Health (Dr
Zhang).
NR 36
TC 53
Z9 54
U1 0
U2 27
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 12
PY 2012
VL 172
IS 20
BP 1566
EP 1572
DI 10.1001/archinternmed.2012.3747
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 035XR
UT WOS:000310987300007
PM 22987062
ER
PT J
AU Hellmich, KA
Levinsohn, JL
Fattah, R
Newman, ZL
Maier, N
Sastalla, I
Liu, SH
Leppla, SH
Moayeri, M
AF Hellmich, Kristina A.
Levinsohn, Jonathan L.
Fattah, Rasem
Newman, Zachary L.
Maier, Nolan
Sastalla, Inka
Liu, Shihui
Leppla, Stephen H.
Moayeri, Mahtab
TI Anthrax Lethal Factor Cleaves Mouse Nlrp1b in Both Toxin-Sensitive and
Toxin-Resistant Macrophages
SO PLOS ONE
LA English
DT Article
ID SUSCEPTIBILITY; PROTEOLYSIS; KINASE
AB Anthrax lethal factor (LF) is the protease component of anthrax lethal toxin (LT). LT induces pyroptosis in macrophages of certain inbred mouse and rat strains, while macrophages from other inbred strains are resistant to the toxin. In rats, the sensitivity of macrophages to toxin-induced cell death is determined by the presence of an LF cleavage sequence in the inflammasome sensor Nlrp1. LF cleaves rat Nlrp1 of toxin-sensitive macrophages, activating caspase-1 and inducing cell death. Toxin-resistant macrophages, however, express Nlrp1 proteins which do not harbor the LF cleavage site. We report here that mouse Nlrp1b proteins are also cleaved by LF. In contrast to the situation in rats, sensitivity and resistance of Balb/cJ and NOD/LtJ macrophages does not correlate to the susceptibility of their Nlrp1b proteins to cleavage by LF, as both proteins are cleaved. Two LF cleavage sites, at residues 38 and 44, were identified in mouse Nlrp1b. Our results suggest that the resistance of NOD/LtJ macrophages to LT, and the inability of the Nlrp1b protein expressed in these cells to be activated by the toxin are likely due to polymorphisms other than those at the LF cleavage sites.
C1 [Hellmich, Kristina A.; Levinsohn, Jonathan L.; Fattah, Rasem; Newman, Zachary L.; Maier, Nolan; Sastalla, Inka; Liu, Shihui; Leppla, Stephen H.; Moayeri, Mahtab] NIAID, Microbial Pathogenesis Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Moayeri, M (reprint author), NIAID, Microbial Pathogenesis Sect, Parasit Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM mmoayeri@niaid.nih.gov
OI , /0000-0001-6103-6726
FU Intramural Research Program of the NIH, National Institute of Allergy
and Infectious Diseases
FX This research was supported by the Intramural Research Program of the
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 13
TC 37
Z9 37
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 12
PY 2012
VL 7
IS 11
AR e49741
DI 10.1371/journal.pone.0049741
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 039HA
UT WOS:000311234000075
PM 23152930
ER
PT J
AU Bleyer, A
Siegel, SE
Coccia, PF
Stock, W
Seibel, NL
AF Bleyer, Archie
Siegel, Stuart E.
Coccia, Peter F.
Stock, Wendy
Seibel, Nita L.
TI Children, Adolescents, and Young Adults With Leukemia: The Empty Half of
the Glass Is Growing
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Letter
ID ONCOLOGY GROUP; SURVIVAL
C1 [Bleyer, Archie] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Bleyer, Archie] St Charles Hlth Care Syst, Portland, OR USA.
[Siegel, Stuart E.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Siegel, Stuart E.] Univ So Calif, Los Angeles, CA USA.
[Coccia, Peter F.] Univ Nebraska Med Ctr, Omaha, NE USA.
[Stock, Wendy] Univ Chicago, Chicago, IL 60637 USA.
[Seibel, Nita L.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Bleyer, A (reprint author), Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
NR 11
TC 10
Z9 10
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 2012
VL 30
IS 32
BP 4037
EP 4038
DI 10.1200/JCO.2012.44.7466
PG 2
WC Oncology
SC Oncology
GA 035AU
UT WOS:000310914800031
PM 23032621
ER
PT J
AU Fox, CS
Matsushita, K
Woodward, M
Bilo, HJG
Chalmers, J
Lambers Heerspink, HJ
Lee, BJ
Perkins, RM
Rossing, P
Sairenchi, T
Tonelli, M
Vassalotti, JA
Yamagishi, K
Coresh, J
de Jong, PE
Wen, CP
Nelson, RG
AF Fox, Caroline S.
Matsushita, Kunihiro
Woodward, Mark
Bilo, Henk J. G.
Chalmers, John
Lambers Heerspink, Hiddo J.
Lee, Brian J.
Perkins, Robert M.
Rossing, Peter
Sairenchi, Toshimi
Tonelli, Marcello
Vassalotti, Joseph A.
Yamagishi, Kazumasa
Coresh, Josef
de Jong, Paul E.
Wen, Chi-Pang
Nelson, Robert G.
CA Chronic Kidney Dis Prognosis Conso
TI Associations of kidney disease measures with mortality and end-stage
renal disease in individuals with and without diabetes: a meta-analysis
SO LANCET
LA English
DT Article
ID GLOMERULAR-FILTRATION-RATE; RISK POPULATION COHORTS; COLLABORATIVE
METAANALYSIS; HIGHER ALBUMINURIA; ALL-CAUSE; UNITED-STATES; ESTIMATED
GFR; PREVALENCE; OUTCOMES; PROTEINURIA
AB Background Chronic kidney disease is characterised by low estimated glomerular fi ltration rate (eGFR) and high albuminuria, and is associated with adverse outcomes. Whether these risks are modifi ed by diabetes is unknown.
Methods We did a meta-analysis of studies selected according to Chronic Kidney Disease Prognosis Consortium criteria. Data transfer and analyses were done between March, 2011, and June, 2012. We used Cox proportional hazards models to estimate the hazard ratios (HR) of mortality and end-stage renal disease (ESRD) associated with eGFR and albuminuria in individuals with and without diabetes.
Findings We analysed data for 1 024 977 participants (128 505 with diabetes) from 30 general population and highrisk cardiovascular cohorts and 13 chronic kidney disease cohorts. In the combined general population and highrisk cohorts with data for all-cause mortality, 75 306 deaths occurred during a mean follow-up of 8.5 years (SD 5.0). In the 23 studies with data for cardiovascular mortality, 21 237 deaths occurred from cardiovascular disease during a mean follow-up of 9.2 years (SD 4.9). In the general and high-risk cohorts, mortality risks were 1.2-1.9 times higher for participants with diabetes than for those without diabetes across the ranges of eGFR and albumin-tocreatinine ratio (ACR). With fi xed eGFR and ACR reference points in the diabetes and no diabetes groups, HR of mortality outcomes according to lower eGFR and higher ACR were much the same in participants with and without diabetes (eg, for all-cause mortality at eGFR 45 mL/min per 1.73 m y [vs 95 mL/min per 1.73 m y], HR 1.35; 95% CI 1.18-1.55; vs 1.33; 1.19-1.48 and at ACR 30 mg/g [vs 5 mg/g], 1.50; 1.35-1.65 vs 1.52; 1.38-1.67). The overall interactions were not signifi cant. We identifi ed much the same fi ndings for ESRD in the chronic kidney disease cohorts.
Interpretation Despite higher risks for mortality and ESRD in diabetes, the relative risks of these outcomes by eGFR and ACR are much the same irrespective of the presence or absence of diabetes, emphasising the importance of kidney disease as a predictor of clinical outcomes.
C1 [Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Fox, Caroline S.] Ctr Populat Studies, Framingham, MA USA.
[Fox, Caroline S.] Brigham & Womens Hosp, Div Endocrinol, Boston, MA 02115 USA.
[Fox, Caroline S.] Harvard Univ, Sch Med, Boston, MA USA.
[Matsushita, Kunihiro; Woodward, Mark; Coresh, Josef] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Woodward, Mark; Chalmers, John] Univ Sydney, George Inst Glocal Hlth, Sydney, NSW 2006, Australia.
[Bilo, Henk J. G.] Isala Clin, Dept Internal Med, Zwolle, Netherlands.
[Lambers Heerspink, Hiddo J.] Univ Groningen, Univ Med Ctr Groningen, Dept Clin Pharmacol, Groningen, Netherlands.
[de Jong, Paul E.] Univ Groningen, Univ Med Ctr Groningen, Dept Nephrol, Groningen, Netherlands.
[Lee, Brian J.] Moanalua Med Ctr, Honolulu, HI USA.
[Perkins, Robert M.] Geisinger Med Ctr, Dept Nephrol, Danville, PA 17822 USA.
[Rossing, Peter] Steno Diabet Ctr, DK-2820 Gentofte, Denmark.
[Rossing, Peter] Univ Aarhus, HEALTH, Aarhus, Denmark.
[Sairenchi, Toshimi] Dokkyo Med Univ, Sch Med, Dept Publ Hlth, Mibu, Tochigi, Japan.
[Sairenchi, Toshimi; Yamagishi, Kazumasa] Ibaraki Hlth Serv Assoc, Mito, Ibaraki, Japan.
[Tonelli, Marcello] Univ Alberta, Dept Med, Edmonton, AB, Canada.
[Vassalotti, Joseph A.] Natl Kidney Fdn, New York, NY USA.
[Yamagishi, Kazumasa] Univ Tsukuba, Fac Med, Dept Publ Hlth Med, Tsukuba, Ibaraki, Japan.
[Yamagishi, Kazumasa] Osaka Med Ctr Hlth Sci & Promot, Osaka, Japan.
[Wen, Chi-Pang] China Med Univ Hosp, Taichung, Taiwan.
[Wen, Chi-Pang] Natl Hlth Res Inst, Inst Populat Hlth Sci, Zhunan, Taiwan.
[Nelson, Robert G.] NIDDKD, NIH, Phoenix, AZ USA.
RP Coresh, J (reprint author), Chron Kidney Dis Prognosis Consortium Data Coordi, Baltimore, MD 21205 USA.
EM ckdpc@jhmi.edu
RI Schottker, Ben/F-8183-2014; Lambers Heerspink, Hiddo/K-3358-2014;
Wetzels, Jack/A-1720-2014; Tonelli, Marcello/B-3028-2009; Stengel,
Benedicte/G-5730-2015; Brenner, Hermann/B-4627-2017; Kronenberg,
Florian/B-1736-2008; Woodward, Mark/D-8492-2015; de Zeeuw,
Dick/E-9080-2014; Bakker, Stephan/J-4023-2015;
OI Schottker, Ben/0000-0002-1217-4521; Lambers Heerspink,
Hiddo/0000-0002-3126-3730; Brenner, Hermann/0000-0002-6129-1572;
Townend, Jonathan/0000-0002-5881-5806; Kronenberg,
Florian/0000-0003-2229-1120; de Zeeuw, Dick/0000-0003-3434-7777; Bakker,
Stephan/0000-0003-3356-6791; rossing, peter/0000-0002-1531-4294;
yamagishi, kazumasa/0000-0003-3301-5519
FU US National Kidney Foundation; Amgen; US National Institutes of Health;
Servier; Roche; Sanofi; Abbott; Kidney Disease; AstraZeneca;
Bristol-Myers Squibb; Boehringer Ingelheim; Lilly; Novo Nordisk;
Novartis; Pfizer; CTI Clinical Trial Services; Litholink Chronic Kidney
Disease Advisory Board; US National Institutes of Health, and Amgen;
Merck; Dutch Kidney Foundation
FX KM's institution has received grants from the US National Kidney
Foundation, Amgen, and US National Institutes of Health. MW's
institution has received a grant from Servier; he has received
consultancy fees from Roche and speaker's fees from Sanofi and Servier.
JCh's institution has received grants from Servier; and he has received
speaker's fees from them. HJLH has served as a consultant for Abbott,
Reata, Johnson & Johnson, and Vitae; and he has received speaker's fees
from Abbott. BJL has received travel expenses from Kidney Disease:
Improving Global Outcomes. RMP has received grants from the US National
Kidney Foundation. PR's institution has received consultancy fees from
Abbott, AstraZeneca, Bristol-Myers Squibb, Boehringer Ingelheim, Lilly,
and Novo Nordisk, and has received grants from Abbott, Novartis, Pfizer,
and speaker's fees from Abbott, AstraZeneca, Bristol-Myers Squibb,
Boehringer Ingelheim, Lilly, and Novo Nordisk; he holds stock in Novo
Nordisk. JAV has received consultancy fees from CTI Clinical Trial
Services and Litholink Chronic Kidney Disease Advisory Board; his
institution has received grants from the US National Institutes of
Health; and he has received speaker's fees from Gore Creative
Technologies and Elsevier. JCo's institution has received grants from
the US National Kidney Foundation, US National Institutes of Health, and
Amgen, and has received consultancy fees from Amgen and Merck. PEdJ's
institution has received a grant from the Dutch Kidney Foundation. CSF,
HJGB, TS, MT, KY, C-PW and RGN declare that they have no conflicts of
interest.
NR 34
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U1 3
U2 42
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0140-6736
J9 LANCET
JI Lancet
PD NOV 10
PY 2012
VL 380
IS 9854
BP 1662
EP 1673
DI 10.1016/S0140-6736(12)61350-6
PG 12
WC Medicine, General & Internal
SC General & Internal Medicine
GA 035MN
UT WOS:000310951400028
PM 23013602
ER
PT J
AU Waclawiw, MA
Wu, CO
Yang, S
AF Waclawiw, Myron A.
Wu, Colin O.
Yang, Song
TI Special Issue: Papers from the 2010 National Heart, Lung and Blood
Institute Clinical Trial Workshop Preface
SO STATISTICS IN MEDICINE
LA English
DT Editorial Material
C1 [Waclawiw, Myron A.; Wu, Colin O.; Yang, Song] NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
RP Waclawiw, MA (reprint author), NHLBI, Off Biostat Res, 6701 Rockledge Dr,Room 9216, Bethesda, MD 20892 USA.
EM Myron.Waclawiw@nih.hhs.gov
NR 0
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD NOV 10
PY 2012
VL 31
IS 25
SI SI
BP 2937
EP 2937
DI 10.1002/sim.5407
PG 1
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 019MY
UT WOS:000309745200001
PM 23055179
ER
PT J
AU Zheng, G
Wu, CO
Yang, S
Waclawiw, MA
DeMets, DL
Geller, NL
AF Zheng, Gang
Wu, Colin O.
Yang, Song
Waclawiw, Myron A.
DeMets, David L.
Geller, Nancy L.
TI NHLBI clinical trials workshop: an executive summary
SO STATISTICS IN MEDICINE
LA English
DT Article
DE Adaptive design; Bayesian clinical trials; comparative effectiveness
research; genomic trials; missing data; personalized medicine; reporting
clinical trials; surrogate endpoints
ID ADAPTIVE SIGNATURE DESIGN; CHOLESTEROL
AB On September 1314, 2010, the National Heart, Lung and Blood Institute (NHLBI) organized a workshop: Clinical Trials: Past, Present and Future. The workshop covered many areas in clinical trials, including the history of clinical trials at NHLBI, Bayesian clinical trials, surrogate endpoints, reporting clinical trials, handling missing data, flexible designs and adaptive trials, personalized medicine and genomic clinical trials, and comparative effectiveness research. In this report, we summarize the main discussions and conclusions based on the presentations of the invited speakers at the workshop. Copyright (c) 2012 John Wiley & Sons, Ltd.
C1 [Zheng, Gang; Wu, Colin O.; Yang, Song; Waclawiw, Myron A.; Geller, Nancy L.] NHLBI, Off Biostat Res, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
[DeMets, David L.] Univ Wisconsin, Dept Biostat & Med Informat, Madison, WI 53792 USA.
RP Zheng, G (reprint author), NHLBI, Off Biostat Res, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
EM zhengg@nhlbi.nih.gov
NR 17
TC 1
Z9 1
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD NOV 10
PY 2012
VL 31
IS 25
SI SI
BP 2938
EP 2943
DI 10.1002/sim.5406
PG 6
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 019MY
UT WOS:000309745200002
PM 22733431
ER
PT J
AU Fleming, TR
Powers, JH
AF Fleming, Thomas R.
Powers, John H.
TI Biomarkers and surrogate endpoints in clinical trials
SO STATISTICS IN MEDICINE
LA English
DT Article
DE validation; accelerated approval; correlate; indirect measure;
clinically meaningful endpoint; replacement endpoint; clinical efficacy
measure; effect modifiers
ID CHRONIC KIDNEY-DISEASE; ACUTE MYOCARDIAL-INFARCTION; VENOUS
THROMBOEMBOLISM; PREVENTION; XIMELAGATRAN; ALTEPLASE; RETEPLASE;
WARFARIN; EPOETIN; EVENTS
AB One of the most important considerations in designing clinical trials is the choice of outcome measures. These outcome measures could be clinically meaningful endpoints that are direct measures of how patients feel, function, and survive. Alternatively, indirect measures, such as biomarkers that include physical signs of disease, laboratory measures, and radiological tests, often are considered as replacement endpoints or surrogates for clinically meaningful endpoints. We discuss the definitions of clinically meaningful endpoints and surrogate endpoints, and provide examples from recent clinical trials. We provide insight into why indirect measures such as biomarkers may fail to provide reliable evidence about the benefit-to-risk profile of interventions. We also discuss the nature of evidence that is important in assessing whether treatment effects on a biomarker reliably predict effects on a clinically meaningful endpoint, and provide insights into why this reliability is specific to the context of use of the biomarker. Copyright (c) 2012 John Wiley & Sons, Ltd.
C1 [Fleming, Thomas R.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Powers, John H.] Sci Applicat Int Corp, Frederick, MD USA.
[Powers, John H.] NIH, Bethesda, MD 20892 USA.
[Powers, John H.] George Washington Univ, Sch Med, Washington, DC USA.
RP Fleming, TR (reprint author), Univ Washington, Dept Biostat, Box 357232, Seattle, WA 98195 USA.
EM tfleming@u.washington.edu
FU NIH/NIAID [R37 AI 29168]; National Cancer Institute, National Institutes
of Health [N01-CO-12400]; National Institute of Allergy and Infectious
Disease
FX For T. Fleming, the source of financial support for research described
in this article is an NIH/NIAID grant entitled 'Statistical Issues in
AIDS Research' (R37 AI 29168). For JH Powers, this project was funded in
whole or in part with federal funds from the National Cancer Institute,
National Institutes of Health, under contract N01-CO-12400. The content
of this publication does not necessarily reflect the views or policies
of the Department of Health and Human Services, nor does mention of
trade names, commercial products, or organizations imply endorsement by
the U. S. Government. This research was supported in part by the
National Institute of Allergy and Infectious Disease. Collaborative
Clinical Research Branch, John H Powers, MD, SAIC-Frederick, Inc.,
NCI-Frederick, Frederick, Maryland 21702.
NR 30
TC 93
Z9 93
U1 2
U2 19
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
EI 1097-0258
J9 STAT MED
JI Stat. Med.
PD NOV 10
PY 2012
VL 31
IS 25
SI SI
BP 2973
EP 2984
DI 10.1002/sim.5403
PG 12
WC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Medicine, Research &
Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Research & Experimental
Medicine; Mathematics
GA 019MY
UT WOS:000309745200005
PM 22711298
ER
PT J
AU Proschan, MA
Lan, KKG
AF Proschan, Michael A.
Lan, K. K. Gordon
TI Spending functions and continuous-monitoring boundaries
SO STATISTICS IN MEDICINE
LA English
DT Article
DE boundaries; Brownian motion; B-value; group-sequential monitoring;
information fraction; interim analyses; power; spending functions
ID CLINICAL-TRIALS; BROWNIAN-MOTION
AB Clinical trials are monitored periodically for safety, efficacy, and futility. The spending function is a popular tool for efficacy monitoring because it does not require pre-specification of the number or timing of interim analyses. But there are infinitely many spending functions, so some guidance on how to choose one is helpful. We consider spending functions that are generated from different continuous-monitoring boundaries for Brownian motion. We use properties of the continuous-monitoring boundaries to derive properties of the associated spending function. Copyright (c) 2012 John Wiley & Sons, Ltd.
C1 [Proschan, Michael A.] NIAID, Biostat Res Branch, Bethesda, MD 20892 USA.
[Lan, K. K. Gordon] Johnson & Johnson, Raritan, NJ USA.
RP Proschan, MA (reprint author), NIAID, Biostat Res Branch, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM proscham@niaid.nih.gov
NR 14
TC 0
Z9 0
U1 0
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD NOV 10
PY 2012
VL 31
IS 25
SI SI
BP 3024
EP 3030
DI 10.1002/sim.5481
PG 7
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 019MY
UT WOS:000309745200009
PM 22807204
ER
PT J
AU Simon, R
AF Simon, Richard
TI Clinical trials for predictive medicine
SO STATISTICS IN MEDICINE
LA English
DT Article
DE clinical trials; predictive medicine; predictive biomarkers; re-sampling
methods
ID REQUIRING PROLONGED OBSERVATION; ADAPTIVE SIGNATURE DESIGN; SUBSET;
EFFICIENCY; PATIENT; CANCER
AB Developments in biotechnology and genomics are providing a biological basis for the heterogeneity of clinical course and response to treatment that have long been apparent to clinicians. The ability to molecularly characterize human diseases presents new opportunities to develop more effective treatments and new challenges for the design and analysis of clinical trials. In oncology, treatment of broad populations with regimens that benefit a minority of patients is less economically sustainable with expensive molecularly targeted therapeutics. The established molecular heterogeneity of human diseases requires the development of new paradigms for the design and analysis of randomized clinical trials as a reliable basis for predictive medicine. We review prospective designs for the development of new therapeutics and predictive biomarkers to inform their use. We cover designs for a wide range of settings. At one extreme is the development of a new drug with a single candidate biomarker and strong biological evidence that marker negative patients are unlikely to benefit from the new drug. At the other extreme are Phase III clinical trials involving both genome-wide discovery of a predictive classifier and internal validation of that classifier. We have outlined a prediction-based approach to the analysis of randomized clinical trials that both preserves the Type I error and provides a reliable internally validated basis for predicting which patients are most likely or unlikely to benefit from the new regimen. Copyright (c) 2012 John Wiley & Sons, Ltd.
C1 NCI, Biometr Res Branch, Bethesda, MD 20892 USA.
RP Simon, R (reprint author), NCI, Biometr Res Branch, 9000 Rockville Pike,MSC7434, Bethesda, MD 20892 USA.
EM rsimon@nih.gov
NR 19
TC 22
Z9 22
U1 2
U2 18
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD NOV 10
PY 2012
VL 31
IS 25
SI SI
BP 3031
EP 3040
DI 10.1002/sim.5401
PG 10
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 019MY
UT WOS:000309745200010
PM 22714719
ER
PT J
AU Lauer, MS
AF Lauer, Michael S.
TI Commentary: How the debate about comparative effectiveness research
should impact the future of clinical trials
SO STATISTICS IN MEDICINE
LA English
DT Article
DE comparative effectiveness; randomized trials; observational studies
ID POLICY; GISSI; STORY
AB Comparative effectiveness research represents the kind of research that arguably more directly affects clinical practice and policy. It includes observational studies, clinical trials, and systematic syntheses of existing literature. In this commentary, I argue for the ongoing and critical role of randomization in comparative effectiveness, noting the key differences between practical and explanatory trials. Copyright (c) 2012 John Wiley & Sons, Ltd.
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 15
TC 2
Z9 2
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD NOV 10
PY 2012
VL 31
IS 25
SI SI
BP 3051
EP 3053
DI 10.1002/sim.5400
PG 3
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 019MY
UT WOS:000309745200012
PM 23055180
ER
PT J
AU Lauer, MS
AF Lauer, Michael S.
TI Responses to commentaries
SO STATISTICS IN MEDICINE
LA English
DT Article
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 6
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD NOV 10
PY 2012
VL 31
IS 25
SI SI
BP 3066
EP 3067
DI 10.1002/sim.5396
PG 2
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 019MY
UT WOS:000309745200017
ER
PT J
AU D'Agostino, R
DeMets, D
Friedewald, W
Goodman, S
Witte, J
Geller, NL
AF D'Agostino, Ralph, Sr.
DeMets, David
Friedewald, William
Goodman, Steven
Witte, John
Geller, Nancy L.
TI The future of clinical trials: A panel discussion
SO STATISTICS IN MEDICINE
LA English
DT Article
C1 [D'Agostino, Ralph, Sr.; DeMets, David; Friedewald, William; Goodman, Steven; Witte, John; Geller, Nancy L.] NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
RP Geller, NL (reprint author), NHLBI, Off Biostat Res, Bldg 10, Bethesda, MD 20892 USA.
EM ng@helix.nih.gov
FU Intramural NIH HHS [Z99 HL999999]
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD NOV 10
PY 2012
VL 31
IS 25
SI SI
BP 3068
EP 3072
DI 10.1002/sim.5484
PG 5
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 019MY
UT WOS:000309745200018
PM 22806631
ER
PT J
AU Ferrarone, J
Knoper, RC
Li, R
Kozak, CA
AF Ferrarone, John
Knoper, Ryan C.
Li, Randolph
Kozak, Christine A.
TI Second site mutation in the virus envelope expands the host range of a
cytopathic variant of Moloney murine leukemia virus
SO VIROLOGY
LA English
DT Article
DE Mouse ecotropic gammaretrovirus; Retrovirus host range; Cat-1 retrovirus
receptor; Retrovirus entry; Virus-induced syncytia; Receptor binding
domain
ID ENDOTHELIAL-CELL TROPISM; SYNCYTIUM FORMATION; RECEPTOR-BINDING;
PROTEIN; ENTRY; IDENTIFICATION; GLYCOSYLATION; RETROVIRUSES; PVC-211;
LINES
AB Spl574 MLV (murine leukemia virus) is a variant of Moloney ecotropic MLV (MoMLV) that is cytopathic in Mus dunni cells and restricted by other mouse cells. Its host range and cytopathicity are due to a mutation, S82F, at a site critical for binding to the CAT-1 receptor. To identify residues that affect affinity for receptor variants, virus with S82F was passed in restrictive cells. The env genes of the adapted viruses contained 18 novel mutations, including one, E114G, present in 6 of 30 sequenced envs. MoMLV-E114G efficiently infected all mouse cells as well as ecotropic MLV resistant Chinese hamster cells. Virus with E114G and S82F induced large multinucleated syncytia in NIH 3T3 and SC-1 cells as well as M. dunni cells. Inoculation of Mo-S82F,E114G into mice produced lymphomas typical of MoMLV. Residues at env position 114 are thus important determinants of host range, and E114G suppresses host range restriction due to S82F, but does not affect S82F-governed cytopathicity. Published by Elsevier Inc.
C1 [Kozak, Christine A.] NIAID, NIH, LMM, Bethesda, MD 20892 USA.
RP Kozak, CA (reprint author), NIAID, NIH, LMM, Bldg 4,Room 329,4 Ctr Dr,MSC 0460, Bethesda, MD 20892 USA.
EM john.ferrarone@gmail.com; knoperr@gmail.com; bludragen88@gmail.com;
ckozak@niaid.nih.gov
FU Intramural Research Program of the NIAID, NIH
FX This research was supported by the Intramural Research Program of the
NIAID, NIH. We thank Esther Shaffer and Qingping Liu for expert
technical assistance, Alicia Buckler-White and Ronald Plishka for
sequencing, Michael A. Dolan of the Bioinformatics and Computational
Biosciences Branch, Office of Cyber Infrastructure and Computational
Biology, NIAID for assistance with figure preparation, and the following
members of the Division of Veterinary Resources, Office of Research
Services, NIH, for pathological evaluation: Lauren Brinster, Mark
Bryant, Michael Eckhaus, Randy Elkins, Victoria Hoffmann, and Matthew
Starost.
NR 31
TC 3
Z9 3
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD NOV 10
PY 2012
VL 433
IS 1
BP 7
EP 11
DI 10.1016/j.virol.2012.06.031
PG 5
WC Virology
SC Virology
GA 020GS
UT WOS:000309797600002
PM 22835818
ER
PT J
AU Escalera-Zamudio, M
Cobian-Guemes, G
Soto-del Rio, MD
Isa, P
Sanchez-Betancourt, I
Parissi-Crivelli, A
Martinez-Cazares, MT
Romero, P
Velazquez-Salinas, L
Huerta-Lozano, B
Nelson, M
Montero, H
Vinuesa, P
Lopez, S
Arias, CF
AF Escalera-Zamudio, Marina
Cobian-Gueemes, Georgina
de los Dolores Soto-del Rio, Maria
Isa, Pavel
Sanchez-Betancourt, Ivan
Parissi-Crivelli, Aurora
Teresa Martinez-Cazares, Maria
Romero, Pedro
Velazquez-Salinas, Lauro
Huerta-Lozano, Belem
Nelson, Martha
Montero, Hilda
Vinuesa, Pablo
Lopez, Susana
Arias, Carlos F.
TI Characterization of an influenza A virus in Mexican swine that is
related to the A/H1N1/2009 pandemic clade
SO VIROLOGY
LA English
DT Article
DE Influenza; Pandemics; Swine; Genetic diversity; Evolution; La Gloria;
Mexico
ID RECEPTOR-BINDING PROPERTIES; H1N1 VIRUS; ALIGNMENT; INFECTION; EMERGENCE
AB In the spring of 2009, swine-origin influenza H1N1pdm09 viruses caused the first influenza pandemic of this century. We characterized the influenza viruses that circulated early during the outbreak in Mexico, including one newly sequenced swine H1N1pdm09 virus and three newly sequenced human H1N1pdm09 viruses that circulated in the outbreak of respiratory disease in La Gloria, Veracruz. Phylogenetic analysis revealed that the swine isolate (A/swine/Mexico/4/2009) collected in April 2009 is positioned in a branch that is basal to the rest of the H1N1pdm09 clade in two (NP and PA) of the eight single-gene trees. In addition, the concatenated HA-NA and the complete whole-genome trees also showed a basal position for A/swine/Mexico/4/2009. Furthermore, this swine virus was found to share molecular traits with non-HIN1pdm09 H1N1 viral lineages. These results suggest that this isolate could potentially be the first one detected from a sister lineage closely related to the H1N1pdm09 viruses. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Escalera-Zamudio, Marina; Cobian-Gueemes, Georgina; de los Dolores Soto-del Rio, Maria; Isa, Pavel; Romero, Pedro; Lopez, Susana; Arias, Carlos F.] Univ Nacl Autonoma Mexico, Inst Biotecnol, Cuernavaca 62210, Morelos, Mexico.
[Sanchez-Betancourt, Ivan] Univ Nacl Autonoma Mexico, Fac Med Vet & Zootecnia, Cuernavaca 62210, Morelos, Mexico.
[Parissi-Crivelli, Aurora; Teresa Martinez-Cazares, Maria] Serv Salud Veracruz, Lab Estatal Salud Publ, Orizaba, Veracruz, Mexico.
[Velazquez-Salinas, Lauro; Huerta-Lozano, Belem] Comis Mexico Estados Unidos Prevenc Fiebre Aftosa, Mexico City, DF, Mexico.
[Nelson, Martha] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Montero, Hilda] Univ Veracruzana, Inst Salud Publ, Xalapa 91000, Veracruz, Mexico.
[Vinuesa, Pablo] Univ Nacl Autonoma Mexico, Ctr Ciencias Genom, Cuernavaca 62210, Morelos, Mexico.
RP Arias, CF (reprint author), Univ Nacl Autonoma Mexico, Inst Biotecnol, Av Univ 2001, Cuernavaca 62210, Morelos, Mexico.
EM arias@ibt.unam.mx
FU National Council for Science and Technology (Conacyt)-Mexico [5549,
10110/184/09]; Instituto de Ciencia y Tecnologia del Distrito Federal,
Mexico [PICOSI09-209]; CONACYT-Mexico
FX We thank Ricardo Grande and Veronica Jimenez, of the next-generation
sequencing core facility of the National University of Mexico for their
technical support. We are grateful to all personnel from the molecular
biology and virus isolation units of CPA for their work in the diagnosis
of the Queretaro swine pandemic influenza virus. This work was supported
by Grants 5549 and 10110/184/09 from the National Council for Science
and Technology (Conacyt)-Mexico, and Grant PICOSI09-209 from the
Instituto de Ciencia y Tecnologia del Distrito Federal, Mexico. Marina
Escalera-Zamudio, Maria de los Dolores Soto del Rio y Georgina
Cobian-Guemes were supported by a scholarship from CONACYT-Mexico.
NR 26
TC 6
Z9 6
U1 0
U2 8
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD NOV 10
PY 2012
VL 433
IS 1
BP 176
EP 182
DI 10.1016/j.virol.2012.08.003
PG 7
WC Virology
SC Virology
GA 020GS
UT WOS:000309797600020
PM 22921315
ER
PT J
AU Hanyu, O
Nakae, H
Miida, T
Higashi, Y
Fuda, H
Endo, M
Kohjitani, A
Sone, H
Strott, CA
AF Hanyu, Osamu
Nakae, Hanako
Miida, Takashi
Higashi, Yuko
Fuda, Hirotoshi
Endo, Motohiro
Kohjitani, Atsushi
Sone, Hirohito
Strott, Charles A.
TI Cholesterol sulfate induces expression of the skin barrier protein
filaggrin in normal human epidermal keratinocytes through induction of
ROR alpha
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Cholesterol sulfate; ROR alpha; Filaggrin; SULT2B1b; NHEKs
ID ORPHAN RECEPTOR-ALPHA; TRANSCRIPTIONAL REGULATION; GENE-EXPRESSION;
RETINOIC ACID; DIFFERENTIATION; PROMOTER; ENVELOPE; ANGSTROM; LIGAND;
AP-1
AB Cholesterol sulfate is abundant in the human epidermis and is a putative natural ligand for retinoic acid receptor-related orphan receptor alpha (ROR alpha). Although direct binding of cholesterol sulfate is expected to activate ROR alpha, cholesterol sulfate can also induce ROR alpha expression and increase ROR alpha target gene expression. The purpose of this study was to determine whether cholesterol sulfate induces profilaggrin expression, a precursor of the barrier protein filaggrin in the epidermis, through activation of ROR alpha by directly binding to ROR alpha, or through increased ROR alpha expression. Immunohistochemical and polymerase chain reaction (PCR) analyses showed that ROR alpha was expressed in normal human epidermal keratinocytes (NHEKs) and that its expression increased during keratinocyte differentiation in parallel with that of profilaggrin and cholesterol sulfotransferase, which catalyzes the synthesis of cholesterol sulfate. Exogenous cholesterol sulfate significantly increased both ROR alpha and profilaggrin expression in NHEKs, whereas no effect on profilaggrin expression was observed in cells in which ROR alpha was knocked down with small interfering RNA (siRNA). Additionally, a luciferase reporter gene assay revealed that exogenous ROR alpha dose-dependently increased the activity of the profilaggrin gene promoter even in the absence of cholesterol sulfate, and that this response involves activator protein-1. In conclusion, the results of this study indicate that cholesterol sulfate induces filaggrin expression through increased ROR alpha expression. Further studies are required to fully elucidate the mechanisms involved. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Hanyu, Osamu; Sone, Hirohito] Niigata Univ, Grad Sch Med & Dent Sci, Div Endocrinol & Metab, Chuo Ku, Niigata 9518510, Japan.
[Hanyu, Osamu; Nakae, Hanako; Higashi, Yuko; Fuda, Hirotoshi; Endo, Motohiro; Kohjitani, Atsushi; Strott, Charles A.] NICHHD, Sect Steroid Regulat, Endocrinol & Reprod Res Branch, NIH, Bethesda, MD 20892 USA.
[Miida, Takashi] Juntendo Univ, Sch Med, Dept Clin Lab Med, Bunkyo Ku, Tokyo 1138421, Japan.
RP Hanyu, O (reprint author), Niigata Univ, Grad Sch Med & Dent Sci, Div Endocrinol & Metab, Chuo Ku, 1-757 Asahimachi, Niigata 9518510, Japan.
EM hanyuo@med.niigata-u.ac.jp; tmiida@juntendo.ac.jp
RI Miida, Takashi/A-5589-2012
OI Miida, Takashi/0000-0002-4294-8030
NR 24
TC 10
Z9 10
U1 0
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD NOV 9
PY 2012
VL 428
IS 1
BP 99
EP 104
DI 10.1016/j.bbrc.2012.10.013
PG 6
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 043DN
UT WOS:000311523200017
PM 23063684
ER
PT J
AU Bond, LM
Arden, SD
Kendrick-Jones, J
Buss, F
Sellers, JR
AF Bond, Lisa M.
Arden, Susan D.
Kendrick-Jones, John
Buss, Folma
Sellers, James R.
TI Dynamic Exchange of Myosin VI on Endocytic Structures
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID CLATHRIN-MEDIATED ENDOCYTOSIS; SNELLS-WALTZER MICE; LARGE STEP-SIZE;
CELLULAR FUNCTIONS; ACTIN-FILAMENTS; MOTOR; DEAFNESS; BINDING; DOMAIN;
MYO6
AB The actin-based molecular motor myosin VI functions in the endocytic uptake pathway, both during the early stages of clathrin-mediated uptake and in later transport to/from early endosomes. This study uses fluorescence recovery after photobleaching (FRAP) to examine the turnover rate of myosin VI during endocytosis. The results demonstrate that myosin VI turns over dynamically on endocytic structures with a characteristic half-life common to both the large insert isoform of myosin VI on clathrin-coated structures and the no-insert isoform on early endosomes. This half-life is shared by the myosin VI-binding partner Dab2 and is identical for full-length myosin VI and the cargo-binding tail region. The 4-fold slower half-life of an artificially dimerized construct of myosin VI on clathrin-coated structures suggests that wild type myosin VI does not function as a stable dimer, but either as a monomer or in a monomer/dimer equilibrium. Taken together, these FRAP results offer insight into both the basic turnover dynamics and the monomer/dimer nature of myosin VI.
C1 [Bond, Lisa M.; Arden, Susan D.; Buss, Folma] Univ Cambridge, Cambridge Inst Med Res, Cambridge CB2 0XY, England.
[Bond, Lisa M.; Sellers, James R.] NHLBI, Lab Mol Physiol, NIH, Bethesda, MD 20892 USA.
[Kendrick-Jones, John] MRC, Mol Biol Lab, Cambridge CB2 2QH, England.
RP Buss, F (reprint author), Univ Cambridge, Cambridge Inst Med Res, Wellcome Trust Med Res Council Bldg,Hills Rd, Cambridge CB2 0XY, England.
EM fb1@mole.bio.cam.ac.uk; sellersj@nhlbi.nih.gov
FU NHLBI, National Institutes of Health, Intramural Program; Wellcome
Trust; Winston Churchill Foundation of the United States; National
Institutes of Health-Oxford-Cambridge Ph.D. studentship; Medical
Research Council
FX This work was supported, in whole or in part, by the NHLBI, National
Institutes of Health, Intramural Program (to J. R. S.). This work was
also supported by the Wellcome Trust (to F. B.), a scholarship from the
Winston Churchill Foundation of the United States (to L. M. B.), a
National Institutes of Health-Oxford-Cambridge Ph.D. studentship (to L.
M. B.), and the Medical Research Council (to J. K-J.). The Cambridge
Institute for Medical Research received a strategic award from the
Wellcome Trust.
NR 48
TC 5
Z9 6
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 9
PY 2012
VL 287
IS 46
BP 38637
EP 38646
DI 10.1074/jbc.M112.373969
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 035WJ
UT WOS:000310982800023
PM 22992744
ER
PT J
AU Devaiah, BN
Singer, DS
AF Devaiah, Ballachanda N.
Singer, Dinah S.
TI Cross-talk Among RNA Polymerase II Kinases Modulates C-terminal Domain
Phosphorylation
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID BROMODOMAIN PROTEIN BRD4; ELONGATION-FACTOR-B; P-TEFB; TRANSCRIPTION
ELONGATION; ACTIVATING KINASE; CTD KINASE; CHROMATIN; TFIIH; TAF7;
REGULATOR
AB The RNA polymerase II (Pol II) C-terminal domain (CTD) serves as a docking site for numerous proteins, bridging various nuclear processes to transcription. The recruitment of these proteins is mediated by CTD phospho-epitopes generated during transcription. The mechanisms regulating the kinases that establish these phosphorylation patterns on the CTD are not known. We report that three CTD kinases, CDK7, CDK9, and BRD4, engage in cross-talk, modulating their subsequent CTD phosphorylation. BRD4 phosphorylates PTEFb/CDK9 at either Thr-29 or Thr-186, depending on its relative abundance, which represses or activates CDK9 CTD kinase activity, respectively. Conversely, CDK9 phosphorylates BRD4 enhancing its CTD kinase activity. The CTD Ser-5 kinase CDK7 also interacts with and phosphorylates BRD4, potently inhibiting BRD4 kinase activity. Additionally, the three kinases regulate each other indirectly through the general transcription factor TAF7. An inhibitor of CDK9 and CDK7 CTD kinase activities, TAF7 also binds to BRD4 and inhibits its kinase activity. Each of these kinases phosphorylates TAF7, affecting its subsequent ability to inhibit the other two. Thus, a complex regulatory network governs Pol II CTD kinases.
C1 [Devaiah, Ballachanda N.; Singer, Dinah S.] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
RP Singer, DS (reprint author), NCI, Expt Immunol Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM dinah.singer@nih.gov
FU NCI, Center for Cancer Research, National Institutes of Health
FX This work was supported, by the Intramural Research Program of the NCI,
Center for Cancer Research, National Institutes of Health.
NR 27
TC 18
Z9 18
U1 0
U2 10
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 9
PY 2012
VL 287
IS 46
BP 38755
EP 38766
DI 10.1074/jbc.M112.412015
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 035WJ
UT WOS:000310982800033
PM 23027873
ER
PT J
AU Ghosh, A
Corbett, GT
Gonzalez, FJ
Pahan, K
AF Ghosh, Arunava
Corbett, Grant T.
Gonzalez, Frank J.
Pahan, Kalipada
TI Gemfibrozil and Fenofibrate, Food and Drug Administration-approved
Lipid-lowering Drugs, Up-regulate Tripeptidyl-peptidase 1 in Brain Cells
via Peroxisome Proliferator-activated Receptor alpha IMPLICATIONS FOR
LATE INFANTILE BATTEN DISEASE THERAPY
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID NEURONAL CEROID-LIPOFUSCINOSIS; RETINOID-X-RECEPTOR;
DENSITY-LIPOPROTEIN-CHOLESTEROL; LYSOSOMAL STORAGE DISORDERS; KAPPA-B;
MOUSE MODEL; ADOPTIVE TRANSFER; HUMAN ASTROCYTES; GENE-EXPRESSION;
MESSENGER-RNAS
AB The classical late infantile neuronal ceroid lipofuscinosis (LINCLs) is an autosomal recessive disease, where the defective gene is Cln2, encoding tripeptidyl-peptidase I (TPP1). At the molecular level, LINCL is caused by accumulation of autofluorescent storage materials in neurons and other cell types. Currently, there is no established treatment for this fatal disease. This study reveals a novel use of gemfibrozil and fenofibrate, Food and Drug Administration-approved lipid-lowering drugs, in up-regulating TPP1 in brain cells. Both gemfibrozil and fenofibrate up-regulated mRNA, protein, and enzymatic activity of TPP1 in primary mouse neurons and astrocytes as well as human astrocytes and neuronal cells. Because gemfibrozil and fenofibrate are known to activate peroxisome proliferator-activated receptor-alpha (PPAR alpha), the role of PPAR alpha in gemfibrozil-and fenofibrate-mediated up-regulation of TPP1 was investigated revealing that both drugs up-regulated TPP1 mRNA, protein, and enzymatic activity both in vitro and in vivo in wild type (WT) and PPAR alpha(-/-), but not PPAR alpha(-/-), mice. In an attempt to delineate the mechanism of TPP1 up-regulation, it was found that the effects of the fibrate drugs were abrogated in the absence of retinoid X receptor-alpha (RXR alpha), a molecule known to form a heterodimer with PPAR alpha. Accordingly, all-trans-retinoic acid, alone or together with gemfibrozil, up-regulated TPP1. Co-immuno-precipitation and ChIP studies revealed the formation of a PPAR alpha/RXR alpha heterodimer and binding of the heterodimer to an RXR-binding site on the Cln2 promoter. Together, this study demonstrates a unique mechanism for the up-regulation of TPP1 by fibrate drugs via PPAR alpha /RXR alpha pathway.
C1 [Ghosh, Arunava; Corbett, Grant T.; Pahan, Kalipada] Rush Univ, Med Ctr, Dept Neurol Sci, Chicago, IL 60612 USA.
[Gonzalez, Frank J.] NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Pahan, K (reprint author), Rush Univ, Med Ctr, Dept Neurol Sci, 1735 W Harrison St,Ste Cohn 320, Chicago, IL 60612 USA.
EM Kalipada_Pahan@rush.edu
FU National Institutes of Health [AT6681, NS64564, NS71479]; Noah's Hope
Foundation
FX This work was supported, in whole or in part, by National Institutes of
Health Grants AT6681, NS64564, and NS71479. This work was also supported
by a generous donation from Noah's Hope Foundation.
NR 48
TC 15
Z9 15
U1 1
U2 6
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 9
PY 2012
VL 287
IS 46
BP 38922
EP 38935
DI 10.1074/jbc.M112.365148
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 035WJ
UT WOS:000310982800048
PM 22989886
ER
PT J
AU Della-Maria, J
Hegde, ML
McNeill, DR
Matsumoto, Y
Tsai, MS
Ellenberger, T
Wilson, DM
Mitra, S
Tomkinson, AE
AF Della-Maria, Julie
Hegde, Muralidhar L.
McNeill, Daniel R.
Matsumoto, Yoshihiro
Tsai, Miaw-Sheue
Ellenberger, Tom
Wilson, David M., III
Mitra, Sankar
Tomkinson, Alan E.
TI The Interaction between Polynucleotide Kinase Phosphatase and the DNA
Repair Protein XRCC1 Is Critical for Repair of DNA Alkylation Damage and
Stable Association at DNA Damage Sites
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID BASE EXCISION-REPAIR; STRAND BREAK REPAIR; N-TERMINAL DOMAIN; LIGASE
III-ALPHA; POLYMERASE-BETA; AP ENDONUCLEASE; HUMAN-CELLS;
POLY(ADP-RIBOSE) POLYMERASE; BRCT DOMAIN; IN-VITRO
AB XRCC1 plays a key role in the repair of DNA base damage and single-strand breaks. Although it has no known enzymatic activity, XRCC1 interacts with multiple DNA repair proteins and is a subunit of distinct DNA repair protein complexes. Here we used the yeast two-hybrid genetic assay to identify mutant versions of XRCC1 that are selectively defective in interacting with a single protein partner. One XRCC1 mutant, A482T, that was defective in binding to polynucleotide kinase phosphatase (PNKP) not only retained the ability to interact with partner proteins that bind to different regions of XRCC1 but also with aprataxin and aprataxin-like factor whose binding sites overlap with that of PNKP. Disruption of the interaction between PNKP and XRCC1 did not impact their initial recruitment to localized DNA damage sites but dramatically reduced their retention there. Furthermore, the interaction between PNKP and the DNA ligase III alpha-XRCC1 complex significantly increased the efficiency of reconstituted repair reactions and was required for complementation of the DNA damage sensitivity to DNA alkylation agents of xrcc1 mutant cells. Together our results reveal novel roles for the interaction between PNKP and XRCC1 in the retention of XRCC1 at DNA damage sites and in DNA alkylation damage repair.
C1 [Della-Maria, Julie] Univ Maryland, Sch Med, Radiat Oncol Res Lab, Dept Radiat Oncol, Baltimore, MD 21201 USA.
[Della-Maria, Julie] Univ Maryland, Sch Med, Marlene & Stewart Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
[Hegde, Muralidhar L.; Mitra, Sankar] Univ Texas Med Branch, Dept Biochem & Mol Biol, Galveston, TX 77555 USA.
[McNeill, Daniel R.; Wilson, David M., III] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
[Matsumoto, Yoshihiro; Tomkinson, Alan E.] Univ New Mexico, Dept Internal Med, Albuquerque, NM 87131 USA.
[Matsumoto, Yoshihiro; Tomkinson, Alan E.] Univ New Mexico, Ctr Canc, Albuquerque, NM 87131 USA.
[Tsai, Miaw-Sheue] Univ Calif Berkeley, Ernest Lawrence Berkeley Natl Lab, Berkeley, CA 94720 USA.
[Ellenberger, Tom] Washington Univ, Sch Med, Div Oncol, Dept Med, St Louis, MO 63110 USA.
RP Tomkinson, AE (reprint author), 1 Univ New Mexico, Canc Res Facil, 915 Camino Salud, Albuquerque, NM 87131 USA.
EM atomkinson@salud.unm.edu
OI Hegde, Muralidhar/0000-0001-7333-8123
FU National Institutes of Health [R01 ES 012512, R01 CA81063, R01 GM052504,
P01 CA 92584]; Intramural Research Program of the NIA, National
Institutes of Health
FX This work was supported, in whole or in part, by National Institutes of
Health Grants R01 ES 012512 (to A. E. T.), R01 CA81063 (to S. M.), R01
GM052504 (to T. E.), and P01 CA 92584 (to A. E. T., S. M., and T. E.)
and by the Intramural Research Program of the NIA, National Institutes
of Health.
NR 49
TC 9
Z9 9
U1 2
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 9
PY 2012
VL 287
IS 46
BP 39233
EP 39244
DI 10.1074/jbc.M112.369975
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 035WJ
UT WOS:000310982800078
PM 22992732
ER
PT J
AU Bintu, L
Ishibashi, T
Dangkulwanich, M
Wu, YY
Lubkowska, L
Kashlev, M
Bustamante, C
AF Bintu, Lacramioara
Ishibashi, Toyotaka
Dangkulwanich, Manchuta
Wu, Yueh-Yi
Lubkowska, Lucyna
Kashlev, Mikhail
Bustamante, Carlos
TI Nucleosomal Elements that Control the Topography of the Barrier to
Transcription
SO CELL
LA English
DT Article
ID RNA-POLYMERASE-II; HISTONE TAIL DOMAINS; DNA TRANSLOCATION;
KINETIC-MODEL; ELONGATION; CHROMATIN; ACETYLATION; STABILITY; DYNAMICS;
ARREST
AB The nucleosome represents a mechanical barrier to transcription that operates as a general regulator of gene expression. We investigate how each nucleosomal component-the histone tails, the specific histone-DNA contacts, and the DNA sequence-contributes to the strength of the barrier. Removal of the tails favors progression of RNA polymerase II into the entry region of the nucleosome by locally increasing the wrapping-unwrapping rates of the DNA around histones. In contrast, point mutations that affect histone-DNA contacts at the dyad abolish the barrier to transcription in the central region by decreasing the local wrapping rate. Moreover, we show that the nucleosome amplifies sequence-dependent transcriptional pausing, an effect mediated through the structure of the nascent RNA. Each of these nucleosomal elements controls transcription elongation by affecting distinctly the density and duration of polymerase pauses, thus providing multiple and alternative mechanisms for control of gene expression by chromatin remodeling and transcription factors.
C1 [Bintu, Lacramioara; Bustamante, Carlos] Univ Calif Berkeley, Jason L Choy Lab Single Mol Biophys, Berkeley, CA 94720 USA.
[Bintu, Lacramioara; Bustamante, Carlos] Univ Calif Berkeley, Dept Phys, Berkeley, CA 94720 USA.
[Ishibashi, Toyotaka; Bustamante, Carlos] Univ Calif Berkeley, Inst QB3, Berkeley, CA 94720 USA.
[Dangkulwanich, Manchuta; Bustamante, Carlos] Univ Calif Berkeley, Dept Chem, Berkeley, CA 94720 USA.
[Wu, Yueh-Yi; Bustamante, Carlos] Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA.
[Bustamante, Carlos] Univ Calif Berkeley, Howard Hughes Med Inst, Berkeley, CA 94720 USA.
[Lubkowska, Lucyna; Kashlev, Mikhail] NCI Ctr Canc Res, Frederick, MD 21702 USA.
RP Bustamante, C (reprint author), Univ Calif Berkeley, Jason L Choy Lab Single Mol Biophys, Berkeley, CA 94720 USA.
EM carlos@alice.berkeley.edu
OI Ishibashi, Toyotaka/0000-0001-8015-2319
FU NIH [R01-GM032543-31]; U.S. Department of Energy, Office of Basic Energy
Sciences, Division of Materials Sciences and Engineering
[DE-AC02-05CH11231]; JSPS
FX We thank C. Hodges, S. Kassube, S. Sternberg, B. Zamft, and members of
the Bustamante laboratory for assistance and discussions. T. I. is
supported by a fellowship from JSPS. This work was supported by NIH
grant R01-GM032543-31 (C. B.) and by the U.S. Department of Energy,
Office of Basic Energy Sciences, Division of Materials Sciences and
Engineering under Contract No. DE-AC02-05CH11231 (C.B.).
NR 41
TC 59
Z9 62
U1 1
U2 60
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD NOV 9
PY 2012
VL 151
IS 4
BP 738
EP 749
DI 10.1016/j.cell.2012.10.009
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 035CV
UT WOS:000310921200007
PM 23141536
ER
PT J
AU Zhu, XW
Westcott, MM
Bi, X
Liu, MX
Gowdy, KM
Seo, J
Cao, Q
Gebre, AK
Fessler, MB
Hitbold, EM
Parks, JS
AF Zhu, Xuewei
Westcott, Marlena M.
Bi, Xin
Liu, Mingxia
Gowdy, Kymberly M.
Seo, Jeongmin
Cao, Qiang
Gebre, Abraham K.
Fessler, Michael B.
Hitbold, Elizabeth M.
Parks, John S.
TI Myeloid Cell-Specific ABCA1 Deletion Protects Mice From Bacterial
Infection
SO CIRCULATION RESEARCH
LA English
DT Article
DE ATP-binding cassette transporter A1; bacterial killing; chemotaxis;
macrophage
ID CASSETTE TRANSPORTER 1; LISTERIA-MONOCYTOGENES; TANGIER-DISEASE;
CHEMOKINE RECEPTOR; FREE-CHOLESTEROL; GENE-EXPRESSION; BONE-MARROW;
APOA-I; MACROPHAGES; ATHEROSCLEROSIS
AB Rationale: ATP-binding cassette transporter A1 (ABCA1) plays a critical role in eliminating excess free cholesterol from tissues by effluxing cellular free cholesterol and phospholipids to lipid-poor apolipoprotein AI. Macrophage ABCA1 also dampens proinflammatory myeloid differentiation primary-response protein 88-dependent toll-like receptor signaling by reducing cellular membrane free cholesterol and lipid raft content, indicating a role of ABCA1 in innate immunity. However, whether ABCA1 expression has a role in regulating macrophage function in vivo is unknown.
Objective: We investigated whether macrophage ABCA1 expression impacts host defense function, including microbial killing and chemotaxis.
Methods and Results: Myeloid cell-specific ABCA1 knockout (MSKO) vs wild-type mice were infected with Listeria monocytogenes (Lm) for 36 hours or 72 hours before euthanasia. Lm-induced monocytosis was similar for wild-type and MSKO mice; however, MSKO mice were more resistant to Lm infection, with significantly less body weight loss, less Lm burden in liver and spleen, and less hepatic damage 3 days postinfection. In addition, Lminfected MSKO mouse livers had: (1) greater monocyte chemoattractant protein-1 and macrophage inflammatory protein-2 expression; (2) more monocyte/macrophage infiltration; (3) less neutral lipid accumulation; and (4) diminished expression of lipogenic genes. MSKO macrophages showed enhanced chemotaxis toward chemokines in vitro and increased migration from peritoneum in response to lipopolysaccharide in vivo. Lm infection of wildtype macrophages markedly reduced expression of ABCA1 protein, as well as other cholesterol export proteins (such as ATP-binding cassette transporter G1 and apolipoprotein E).
Conclusions: Myeloid-specific ABCA1 deletion favors host response to and clearance of Lm. Macrophage Lm infection reduces expression of cholesterol export proteins, suggesting that diminished cholesterol efflux enhances innate immune function of macrophages. (Circ Res. 2012;111:1398-1409.)
C1 [Zhu, Xuewei; Bi, Xin; Liu, Mingxia; Seo, Jeongmin; Gebre, Abraham K.; Parks, John S.] Wake Forest Sch Med, Dept Pathol Lipid Sci, Winston Salem, NC 27157 USA.
[Gowdy, Kymberly M.; Fessler, Michael B.] NIEHS, Lab Resp Biol, Res Triangle Pk, NC 27709 USA.
RP Parks, JS (reprint author), Wake Forest Sch Med, Dept Pathol, Sect Lipid Sci, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM jparks@wakehealth.edu
FU Mass Spectroscopy Facility of the Comprehensive Cancer Center
[5P30CA12197]; North Carolina Biotechnology Center of Wake Forest School
of Medicine [2007-IDG-1021]; National Institutes of Health [HL49373,
HL94525]; American Heart Association fellowship [09POST2250225]
FX The authors gratefully acknowledge Karen Klein (Research Support Core,
Wake Forest School of Medicine) for editing the manuscript, and Dr
Michael J. Thomas (Department of Biochemistry, Wake Forest School of
Medicine) and the Mass Spectroscopy Facility of the Comprehensive Cancer
Center (5P30CA12197 and North Carolina Biotechnology Center
2007-IDG-1021) of Wake Forest School of Medicine for the macrophage
oxysterol measurements.; This study was supported by National Institutes
of Health Grants HL49373, HL94525 (J.S. Parks) and by American Heart
Association fellowship 09POST2250225 (X. Zhu).
NR 35
TC 15
Z9 17
U1 1
U2 5
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 9
PY 2012
VL 111
IS 11
BP 1398
EP U108
DI 10.1161/CIRCRESAHA.112.269043
PG 22
WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Hematology
GA 035AM
UT WOS:000310914000006
PM 22955730
ER
PT J
AU Xu, ZX
Felsenfeld, G
AF Xu, Zhixiong
Felsenfeld, Gary
TI Order from Chaos in the Nucleus
SO MOLECULAR CELL
LA English
DT Editorial Material
ID CHROMOSOME CONFORMATION; GENOME; ORGANIZATION; PRINCIPLES
C1 [Xu, Zhixiong; Felsenfeld, Gary] NIDDKD, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Felsenfeld, G (reprint author), NIDDKD, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM gary.felsenfeld@nih.gov
FU Intramural NIH HHS [ZIA DK036148-06]
NR 10
TC 1
Z9 1
U1 1
U2 10
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 9
PY 2012
VL 48
IS 3
BP 327
EP 328
DI 10.1016/j.molcel.2012.10.021
PG 2
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 039QF
UT WOS:000311260900002
PM 23141201
ER
PT J
AU Jo, HJ
Saad, ZS
Gotts, SJ
Martin, A
Cox, RW
AF Jo, Hang Joon
Saad, Ziad S.
Gotts, Stephen J.
Martin, Alex
Cox, Robert W.
TI Quantifying Agreement between Anatomical and Functional Interhemispheric
Correspondences in the Resting Brain
SO PLOS ONE
LA English
DT Article
ID HUMAN CEREBRAL-CORTEX; SPONTANEOUS FLUCTUATIONS; VISUAL-CORTEX; STATE
FMRI; CALLOSAL PROJECTIONS; CORTICAL NETWORK; CORPUS-CALLOSUM; MACAQUE
MONKEY; NEURAL BASIS; CONNECTIVITY
AB The human brain is composed of two broadly symmetric cerebral hemispheres, with an abundance of reciprocal anatomical connections between homotopic locations. However, to date, studies of hemispheric symmetries have not identified correspondency precisely due to variable cortical folding patterns. Here we present a method to establish accurate correspondency using position on the unfolded cortical surface relative to gyral and sulcal landmarks. The landmark method is shown to outperform the method of reversing standard volume coordinates, and it is used to quantify the functional symmetry in resting fMRI data throughout the cortex. Resting brain activity was found to be maximally correlated with locations less than 1 cm away on the cortical surface from the corresponding anatomical location in nearly half of the cortex. While select locations exhibited asymmetric patterns, precise symmetric relationships were found to be the norm, with fine-grained symmetric functional maps demonstrated in motor, occipital, and inferior frontal cortex. Citation: Jo HJ, Saad ZS, Gotts SJ, Martin A, Cox RW (2012) Quantifying Agreement between Anatomical and Functional Interhemispheric Correspondences in the Resting Brain. PLoS ONE 7(11): e48847. doi: 10.1371/journal.pone.0048847
C1 [Jo, Hang Joon; Saad, Ziad S.; Cox, Robert W.] NIMH, Sci & Stat Comp Core, NIH, Bethesda, MD 20892 USA.
[Gotts, Stephen J.; Martin, Alex] NIMH, Cognit Neuropsychol Sect, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
RP Jo, HJ (reprint author), NIMH, Sci & Stat Comp Core, NIH, Bethesda, MD 20892 USA.
EM hangjoon.jo@nih.gov
RI JO, HANG JOON/D-1775-2011; Gotts, Stephen/J-4842-2012
OI JO, HANG JOON/0000-0002-9180-3831;
FU Intramural NIH HHS
NR 69
TC 11
Z9 11
U1 0
U2 12
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 8
PY 2012
VL 7
IS 11
AR e48847
DI 10.1371/journal.pone.0048847
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 053KE
UT WOS:000312269500038
PM 23144995
ER
PT J
AU Roeseler, DA
Sachdev, S
Buckley, DM
Joshi, T
Wu, DK
Xu, D
Hannink, M
Waters, ST
AF Roeseler, David A.
Sachdev, Shrikesh
Buckley, Desire M.
Joshi, Trupti
Wu, Doris K.
Xu, Dong
Hannink, Mark
Waters, Samuel T.
TI Elongation Factor 1 alpha1 and Genes Associated with Usher Syndromes Are
Downstream Targets of GBX2
SO PLOS ONE
LA English
DT Article
ID TRANSCRIPTION FACTOR-BINDING; IN-VITRO TRANSCRIPTION; CREST
CELL-MIGRATION; INNER-EAR; HOMEOBOX GENE; ISTHMIC ORGANIZER; TATA BOX;
MID/HINDBRAIN ORGANIZER; INTRON ENHANCER; ZEBRAFISH GBX1
AB Gbx2 encodes a DNA-binding transcription factor that plays pivotal roles during embryogenesis. Gain-and loss-of-function studies in several vertebrate species have demonstrated a requirement for Gbx2 in development of the anterior hindbrain, spinal cord, inner ear, heart, and neural crest cells. However, the target genes through which GBX2 exerts its effects remain obscure. Using chromatin immunoprecipitation coupled with direct sequencing (ChIP-Seq) analysis in a human prostate cancer cell line, we identified cis-regulatory elements bound by GBX2 to provide insight into its direct downstream targets. The analysis revealed more than 286 highly significant candidate target genes, falling into various functional groups, of which 51% are expressed in the nervous system. Several of the top candidate genes include EEF1A1, ROBO1, PLXNA4, SLIT3, NRP1, and NOTCH2, as well as genes associated with the Usher syndrome, PCDH15 and USH2A, and are plausible candidates contributing to the developmental defects in Gbx2(-/-) mice. We show through gel shift analyses that sequences within the promoter or introns of EEF1A1, ROBO1, PCDH15, USH2A and NOTCH2, are directly bound by GBX2. Consistent with these in vitro results, analyses of Gbx2(-/-) embryos indicate that Gbx2 function is required for migration of Robo1-expressing neural crest cells out of the hindbrain. Furthermore, we show that GBX2 activates transcriptional activity through the promoter of EEF1A1, suggesting that GBX2 could also regulate gene expression indirectly via EEF1A. Taken together, our studies show that GBX2 plays a dynamic role in development and diseases. Citation: Roeseler DA, Sachdev S, Buckley DM, Joshi T, Wu DK, et al. (2012) Elongation Factor 1 alpha1 and Genes Associated with Usher Syndromes Are Downstream Targets of GBX2. PLoS ONE 7(11): e47366. doi:10.1371/journal.pone.0047366
C1 [Roeseler, David A.; Buckley, Desire M.; Waters, Samuel T.] Univ Missouri, Div Biol Sci, Columbia, MO 65211 USA.
[Roeseler, David A.; Sachdev, Shrikesh; Buckley, Desire M.; Joshi, Trupti; Xu, Dong; Hannink, Mark; Waters, Samuel T.] Univ Missouri, Christopher S Bond Life Sci Ctr, Columbia, MO 65211 USA.
[Sachdev, Shrikesh; Hannink, Mark] Univ Missouri, Dept Biochem, Columbia, MO 65211 USA.
[Joshi, Trupti; Xu, Dong] Univ Missouri, Dept Comp Sci, Columbia, MO 65211 USA.
[Wu, Doris K.] NIDCD, Mol Biol Lab, NIH, Bethesda, MD USA.
[Joshi, Trupti; Xu, Dong] Univ Missouri, Inst Informat, Columbia, MO 65211 USA.
RP Waters, ST (reprint author), Univ Missouri, Div Biol Sci, Columbia, MO 65211 USA.
EM waterssa@missouri.edu
FU National Science Foundation [NSF 1021288]
FX This work has been funded by the National Science Foundation, NSF
1021288. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 83
TC 5
Z9 7
U1 3
U2 10
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 8
PY 2012
VL 7
IS 11
AR e47366
DI 10.1371/journal.pone.0047366
PG 15
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 053KE
UT WOS:000312269500008
PM 23144817
ER
PT J
AU Micci, L
Cervasi, B
Ende, ZS
Iriele, RI
Reyes-Aviles, E
Vinton, C
Else, J
Silvestri, G
Ansari, AA
Villinger, F
Pahwa, S
Estes, JD
Brenchley, JM
Paiardini, M
AF Micci, Luca
Cervasi, Barbara
Ende, Zachary S.
Iriele, Robin I.
Reyes-Aviles, Elane
Vinton, Carol
Else, James
Silvestri, Guido
Ansari, Aftab A.
Villinger, Francois
Pahwa, Savita
Estes, Jacob D.
Brenchley, Jason M.
Paiardini, Mirko
TI Paucity of IL-21-producing CD4(+) T cells is associated with Th17 cell
depletion in SIV infection of rhesus macaques
SO BLOOD
LA English
DT Article
ID CHRONIC VIRAL-INFECTION; PROGRESSIVE HIV-INFECTION; IMMUNE ACTIVATION;
SOOTY MANGABEYS; T(H)17 CELLS; IL-21; VIRUS; AIDS; DIFFERENTIATION;
INTERLEUKIN-21
AB IL-21 regulates Th17 cell homeostasis, enhances the differentiation of memory B cells and antibody-secreting plasma cells, and promotes the maintenance of CD8(+) T-cell responses. In this study, we investigated the phenotype, function, and frequency of blood and intestinal IL-21-producing cells in nonhuman primates that are hosts of progressive (rhesus macaques [RMs]) and nonprogressive (sooty mangabeys [SMs]) SIV infection. We found that, in both species, memory CD4(+)CD95(+)CCR6(-) T cells are the main IL-21 producers, and that only a small fraction of CD4(+)IL-21(+) T cells produce IL-17. During chronic SIV infection of RMs, CD4(+)IL-21(+) T cells were significantly depleted in both blood and rectal mucosa, with the extent of this depletion correlating with the loss of Th17 cells. Furthermore, treatment with IL-21 increased the in vivo levels of Th17 cells in SIV-infected RMs. In contrast, normal levels of CD4(+)IL-21(+) T cells were found in SIV-infected SMs. Collectively, these data indicate that depletion of IL-21-producing CD4(+) T cells distinguishes progressive from nonprogressive SIV infection of RMs and SMs, and suggest that depletion of CD4(+)IL-21(+) T cells is involved in the preferential loss of Th17 cells that is associated with SIV disease progression. Further preclinical studies of IL-21 as a potential immunotherapeutic agent for HIV infection may be warranted. (Blood. 2012;120(19):3925-3935)
C1 [Paiardini, Mirko] Emory Univ, Sch Med, Yerkes Natl Primate Res Ctr, Div Microbiol & Immunol, Atlanta, GA 30329 USA.
[Reyes-Aviles, Elane] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Vinton, Carol; Brenchley, Jason M.] NIAID, Program Barrier Immun & Repair, NIH, Bethesda, MD 20892 USA.
[Vinton, Carol; Brenchley, Jason M.] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Else, James; Silvestri, Guido; Ansari, Aftab A.; Villinger, Francois; Paiardini, Mirko] Emory Univ, Sch Med, Dept Pathol & Lab Med, Atlanta, GA 30329 USA.
[Villinger, Francois] Emory Univ, Div Pathol, Yerkes Natl Primate Res Ctr, Atlanta, GA 30329 USA.
[Pahwa, Savita] Univ Miami, Miller Sch Med, Dept Microbiol & Immunol, Miami, FL 33136 USA.
[Estes, Jacob D.] NCI Frederick, AIDS Canc Virus Program, Frederick, MD USA.
RP Paiardini, M (reprint author), Emory Univ, Sch Med, Yerkes Natl Primate Res Ctr, Div Microbiol & Immunol, 954 Gatewood Rd, Atlanta, GA 30329 USA.
EM mirko.paiardini@emory.edu
FU National Institutes of Health (NIH) [R01-AI084836, R56-AI087186,
R37-AI66998, P01-AI 76174]; National Cancer Institute, NIH
[HHSN261200800001E]; National Center for Research Resources [P51RR165];
Office of Research Infrastructure Programs/OD [P51OD11132]
FX This work was supported by the National Institutes of Health (NIH;
grants R01-AI084836 and R56-AI087186, M. P.; grants R37-AI66998 and
P01-AI 76174, G. S.), and in part by the National Cancer Institute, NIH
(contract HHSN261200800001E), and the National Center for Research
Resources P51RR165 (currently supported by the Office of Research
Infrastructure Programs/OD P51OD11132).
NR 52
TC 33
Z9 33
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 8
PY 2012
VL 120
IS 19
BP 3925
EP 3935
DI 10.1182/blood-2012-04-420240
PG 11
WC Hematology
SC Hematology
GA 044OL
UT WOS:000311629600014
PM 22990011
ER
PT J
AU Segarra, M
Ohnuki, H
Maric, D
Salvucci, O
Hou, X
Kumar, A
Li, XR
Tosato, G
AF Segarra, Marta
Ohnuki, Hidetaka
Maric, Dragan
Salvucci, Ombretta
Hou, Xu
Kumar, Anil
Li, Xuri
Tosato, Giovanna
TI Semaphorin 6A regulates angiogenesis by modulating VEGF signaling
SO BLOOD
LA English
DT Article
ID LAMINA-RESTRICTED PROJECTION; HIPPOCAMPAL MOSSY FIBERS;
VASCULAR-PERMEABILITY; NEUROPILIN-1 INTERNALIZATION; RETINAL
VASCULATURE; TUMOR ANGIOGENESIS; CELLS; MICE; PLEXIN-A4; GROWTH
AB Formation of new vessels during development and in the mature mammal generally proceeds through angiogenesis. Although a variety of molecules and signaling pathways are known to underlie endothelial cell sprouting and remodeling during angiogenesis, many aspects of this complex process remain unexplained. Here we show that the transmembrane semaphorin6A (Sema6A) is expressed in endothelial cells, and regulates endothelial cell survival and growth by modulating the expression and signaling of VEGFR2, which is known to maintain endothelial cell viability by autocrine VEGFR signaling. The silencing of Sema6A in primary endothelial cells promotes cell death that is not rescued by exogenous VEGF-A or FGF2, attributable to the loss of prosurvival signaling from endogenous VEGF. Analyses of mouse tissues demonstrate that Sema6A is expressed in angiogenic and remodeling vessels. Mice with null mutations of Sema6A exhibit significant defects in hyaloid vessels complexity associated with increased endothelial cell death, and in retinal vessels development that is abnormally reduced. Adult Sema6A-null mice exhibit reduced tumor, matrigel, and choroidal angiogenesis compared with controls. Sema6A plays important roles in development of the nervous system. Here we show that it also regulates vascular development and adult angiogenesis. (Blood. 2012; 120(19): 4104-4115)
C1 [Segarra, Marta; Ohnuki, Hidetaka; Salvucci, Ombretta; Tosato, Giovanna] NCI, Cellular Oncol Lab, CCR, NIH, Bethesda, MD 20892 USA.
[Maric, Dragan] NINDS, Lab Neurophysiol, NIH, Bethesda, MD 20892 USA.
[Hou, Xu; Kumar, Anil; Li, Xuri] NEI, NIH, Rockville, MD USA.
RP Ohnuki, H (reprint author), NCI, Cellular Oncol Lab, CCR, NIH, Bldg 37,Rm 4124, Bethesda, MD 20892 USA.
EM ohnukih@mail.nih.gov
RI Kumar, Anil/K-8504-2012
FU Intramural Research Program at NIH; CCR; NCI; Fulbright/Ministerio
Educacion y Ciencia postdoctoral grant; Strategic Young Researcher
Overseas Visiting Program for accelerating Brain Research Circulation;
JSPS (Japan Society for the Promotion of Science); [S2207]
FX This research was supported by the Intramural Research Program at NIH,
CCR, NCI. M.S. was supported in part by a Fulbright/Ministerio Educacion
y Ciencia postdoctoral grant; and H.O. was supported in part by
Grant-in-Aid for Scientific Research (S2207 S. Higashiyama); and
Strategic Young Researcher Overseas Visiting Program for accelerating
Brain Research Circulation, JSPS (Japan Society for the Promotion of
Science).
NR 50
TC 26
Z9 28
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 8
PY 2012
VL 120
IS 19
BP 4104
EP 4115
DI 10.1182/blood-2012-02-410076
PG 12
WC Hematology
SC Hematology
GA 044OL
UT WOS:000311629600033
PM 23007403
ER
PT J
AU Ndebele, PM
Wassenaar, D
Munalula, E
Masiye, F
AF Ndebele, Paul M.
Wassenaar, Douglas
Munalula, Esther
Masiye, Francis
TI Improving understanding of clinical trial procedures among low literacy
populations: an intervention within a microbicide trial in Malawi
SO BMC MEDICAL ETHICS
LA English
DT Article
DE Assessment; Comprehension; Double-blinding; Informed consent;
Intervention; Randomisation; Placebo; Malawi; Understanding
ID INFORMED-CONSENT PROCESS; PSYCHOTIC DISORDERS; PARTICIPATION;
PREVENTION; CANCER
AB Background: The intervention reported in this paper was a follow up to an empirical study conducted in Malawi with the aim of assessing trial participants' understanding of randomisation, double-blinding and placebo use. In the empirical study, the majority of respondents (61.1%; n=124) obtained low scores (lower than 75%) on understanding of all three concepts under study. Based on these findings, an intervention based on a narrative which included all three concepts and their personal implications was designed. The narrative used daily examples from the field of Agriculture because Malawi has an agro-based economy.
Methods: The intervention was tested using a sample of 36 women who had been identified as low scorers during the empirical study. The 36 low scorers were randomly assigned to control (n=18) and intervention arms (n=18). The control arm went through a session in which they were provided with standard informed consent information for the microbicide trial. The intervention arm went through a session in which they were provided with a narrative in ChiChewa, the local language, with the assistance of a power point presentation which included pictures as well as discussions on justification and personal implications of the concepts under study.
Results: The findings on the efficacy of the intervention suggest that the 3 scientific concepts and their personal implications can be understood by low literacy populations using simple language and everyday local examples. The findings also suggest that the intervention positively impacted on understanding of trial procedures under study, as 13 of the 18 women in the intervention arm, obtained high scores (above 75%) during the post intervention assessment and none of the 18 in the control arm obtained a high score. Using Fischer's exact test, it was confirmed that the effect of the intervention on understanding of the three procedures was statistically significant (p=0.0001).
Conclusions: Potential trial participants can be assisted to understand key clinical trial procedures, their justification and personal implications by using innovative tailored local narratives.
C1 [Ndebele, Paul M.] NIAID, HJF DAIDS, NIH, Bethesda, MD 20817 USA.
[Wassenaar, Douglas] Univ KwaZulu Natal, Pietermaritzburg, South Africa.
[Munalula, Esther] Univ Zambia, Lusaka, Zambia.
[Masiye, Francis] Univ Malawi, Coll Med, Blantyre, Malawi.
RP Ndebele, PM (reprint author), NIAID, HJF DAIDS, NIH, 6700A Rockledge Dr,Room 42A193,2nd Floor, Bethesda, MD 20817 USA.
EM pndexas@yahoo.com
RI Wassenaar, Douglas/N-5301-2013
OI Wassenaar, Douglas/0000-0003-0839-9231
FU South African Research Ethics Training Initiative (SARETI) (National
Institutes of Health Fogarty International Center [5 R25 TW001599-09];
Scholars Rescue Fund (SRF)
FX The authors are very grateful to all the microbicide trial participants
who volunteered to participate in this study, and to the Principal
Investigators and study staff at the two sites. The work was partly
supported by the South African Research Ethics Training Initiative
(SARETI) (National Institutes of Health Fogarty International Center
grant number 5 R25 TW001599-09 and Scholars Rescue Fund (SRF). The
authors are also grateful to all colleagues that participated in the
various components of the project including design of tools, statistical
support and data collection.
NR 42
TC 4
Z9 4
U1 1
U2 7
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1472-6939
J9 BMC MED ETHICS
JI BMC Med. Ethics
PD NOV 8
PY 2012
VL 13
AR 29
DI 10.1186/1472-6939-13-29
PG 14
WC Ethics; Medical Ethics; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Biomedical Social
Sciences
GA 044HY
UT WOS:000311611400001
PM 23136958
ER
PT J
AU Bandettini, PA
AF Bandettini, Peter A.
TI The BOLD Plot Thickens: Sign- and Layer-Dependent Hemodynamic Changes
with Activation
SO NEURON
LA English
DT Editorial Material
ID HUMAN BRAIN
AB In this issue of Neuron, Goense et al. (2012) report on high-resolution, layer-specific measurements of BOLD, cerebral blood volume, and cerebral blood flow in regions of positive and negative BOLD associated with a simple visual stimulus. The findings strongly suggest that the hemodynamic mechanisms behind negative signal changes are quite different from those behind positive signal changes.
C1 NIMH, Sect Funct Imaging Methods, Lab Brain & Cognit, Bethesda, MD 20892 USA.
RP Bandettini, PA (reprint author), NIMH, Sect Funct Imaging Methods, Lab Brain & Cognit, Bethesda, MD 20892 USA.
EM bandettp@mail.nih.gov
NR 10
TC 3
Z9 3
U1 0
U2 12
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
J9 NEURON
JI Neuron
PD NOV 8
PY 2012
VL 76
IS 3
BP 468
EP 469
DI 10.1016/j.neuron.2012.10.026
PG 2
WC Neurosciences
SC Neurosciences & Neurology
GA 036WT
UT WOS:000311063700003
PM 23141059
ER
PT J
AU Veran, J
Kumar, J
Pinheiro, PS
Athane, A
Mayer, ML
Perrais, D
Mulle, C
AF Veran, Julien
Kumar, Janesh
Pinheiro, Paulo S.
Athane, Axel
Mayer, Mark L.
Perrais, David
Mulle, Christophe
TI Zinc Potentiates GluK3 Glutamate Receptor Function by Stabilizing the
Ligand Binding Domain Dimer Interface
SO NEURON
LA English
DT Article
ID MOSSY-FIBER SYNAPSES; GLUK3-CONTAINING KAINATE RECEPTORS; NMDA RECEPTOR;
CRYSTAL-STRUCTURE; SUBUNIT; DESENSITIZATION; INHIBITION; MODULATION;
MECHANISM; GLUR7
AB Kainate receptors (KARs) play a key role in the regulation of synaptic networks. Here, we show that zinc, a cation released at a subset of glutamatergic synapses, potentiates glutamate currents mediated by homomeric and heteromeric KARs containing GluK3 at 10-100 mu M concentrations, whereas it inhibits other KAR subtypes. Potentiation of GluK3 currents is mainly due to reduced desensitization, as shown by kinetic analysis and desensitization mutants. Crystallographic and mutation analyses revealed that a specific zinc binding site is formed at the base of the ligand binding domain (LBD) dimer interface by a GluK3-specific aspartate (Asp759), together with two conserved residues, His762 and Asp730, the latter located on the partner subunit. In addition, we propose that tetrameric GluK2/GluK3 receptors are likely assembled as pairs of heterodimeric LBDs. Therefore, zinc binding stabilizes the labile GluK3 dimer interface, slows desensitization, and potentiates currents, providing a mechanism for KAR potentiation at glutamatergic synapses.
C1 [Veran, Julien; Pinheiro, Paulo S.; Athane, Axel; Perrais, David; Mulle, Christophe] Univ Bordeaux, F-33000 Bordeaux, France.
[Veran, Julien; Pinheiro, Paulo S.; Athane, Axel; Perrais, David; Mulle, Christophe] CNRS, Interdisciplinary Inst Neurosci, UMR 5297, F-33000 Bordeaux, France.
[Kumar, Janesh; Mayer, Mark L.] NICHHD, Lab Cellular & Mol Neurophysiol, Porter Neurosci Res Ctr, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Mulle, C (reprint author), Univ Bordeaux, F-33000 Bordeaux, France.
EM mulle@u-bordeaux2.fr
RI Mayer, Mark/H-5500-2013;
OI Perrais, David/0000-0002-5878-5408; Pinheiro, Paulo/0000-0002-9024-1021;
Mulle, Christophe/0000-0003-2709-6615
FU Centre National de la Recherche Scientifique; Fondation pour la
Recherche Medicale; Conseil Regional d'Aquitaine; Agence Nationale de la
Recherche (contract SynapticZinc); NICHD, NIH; U.S. Department of
Energy, Office of Science, Office of Basic Energy Sciences
[DE-AC02-06CH11357]
FX This work was supported by the Centre National de la Recherche
Scientifique, the Fondation pour la Recherche Medicale, the Conseil
Regional d'Aquitaine, the Agence Nationale de la Recherche (contract
SynapticZinc), and the intramural research program of NICHD, NIH.
Synchrotron diffraction data were collected at SER-CAT beamline 22 ID.
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. We thank Remi Sterling for cell culture
maintenance, and Francoise Coussen, Severine Desforges, and Carla
Glasser for help with molecular biology. Pierre Paoletti provided
insightful suggestions along the course of this study. We are also
grateful for members of the C.M. laboratory for helpful discussions.
NR 55
TC 21
Z9 21
U1 2
U2 11
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
EI 1097-4199
J9 NEURON
JI Neuron
PD NOV 8
PY 2012
VL 76
IS 3
BP 565
EP 578
DI 10.1016/j.neuron.2012.08.027
PG 14
WC Neurosciences
SC Neurosciences & Neurology
GA 036WT
UT WOS:000311063700012
PM 23141068
ER
PT J
AU Goense, J
Merkle, H
Logothetis, NK
AF Goense, Jozien
Merkle, Hellmut
Logothetis, Nikos K.
TI High-Resolution fMRI Reveals Laminar Differences in Neurovascular
Coupling between Positive and Negative BOLD Responses
SO NEURON
LA English
DT Article
ID CEREBRAL-BLOOD-FLOW; CLASSICAL RECEPTIVE-FIELD; PRIMARY SOMATOSENSORY
CORTEX; VASCULAR SPACE OCCUPANCY; MACAQUE STRIATE CORTEX; PRIMARY
VISUAL-CORTEX; NEURONAL-ACTIVITY; FUNCTIONAL MRI; HUMAN-BRAIN;
HEMODYNAMIC-RESPONSE
AB The six cortical layers have distinct anatomical and physiological properties, like different energy use and different feedforward and feedback connectivity. It is not known if and how layer-specific neural processes are reflected in the fMRI signal. To address this question we used high-resolution fMRI to measure BOLD, CBV, and CBF responses to stimuli that elicit positive and negative BOLD signals in macaque primary visual cortex. We found that regions with positive BOLD responses had parallel increases in CBV and CBF, whereas areas with negative BOLD responses showed a decrease in CBF but an increase in CBV. For positive BOLD responses, CBF and CBV increased in the center of the cortex, but for negative BOLD responses, CBF decreased superficially while CBV increased in the center. Our findings suggest different mechanisms for neurovascular coupling for BOLD increases and decreases, as well as laminar differences in neurovascular coupling.
C1 [Goense, Jozien; Logothetis, Nikos K.] Max Planck Inst Biol Cybernet, Dept Physiol Cognit Proc, D-72076 Tubingen, Germany.
[Merkle, Hellmut] NINDS, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20814 USA.
[Logothetis, Nikos K.] Univ Manchester, Div Imaging Sci & Biomed Engn, Manchester M13 9PT, Lancs, England.
RP Goense, J (reprint author), Max Planck Inst Biol Cybernet, Dept Physiol Cognit Proc, D-72076 Tubingen, Germany.
EM jozien.goense@tuebingen.mpg.de
FU Max-Planck Society; National Institutes of Health, National Institute of
Neurological Disorders and Stroke, Bethesda, MD, USA
FX We are grateful to Dr. Daniel Gembris and Dr. Franek Hennel from Bruker
BioSpin GmbH for the sequence to simultaneously measure the BOLD, CBF,
and VASO signals and Dr. Mark Augath for technical support. Dr. Kevin
Whittingstall provided comments on earlier versions of the manuscript.
We also thank the reviewers for their suggestions. The research was
supported by the Max-Planck Society and in part by the Intramural
Program of the National Institutes of Health, National Institute of
Neurological Disorders and Stroke, Bethesda, MD, USA (to H.M.).
NR 81
TC 83
Z9 83
U1 2
U2 44
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
EI 1097-4199
J9 NEURON
JI Neuron
PD NOV 8
PY 2012
VL 76
IS 3
BP 629
EP 639
DI 10.1016/j.neuron.2012.09.019
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 036WT
UT WOS:000311063700017
PM 23141073
ER
PT J
AU Visco, AG
Brubaker, L
Richter, HE
Nygaard, I
Paraiso, MFR
Menefee, SA
Schaffer, J
Lowder, J
Khandwala, S
Sirls, L
Spino, C
Nolen, TL
Wallace, D
Meikle, SF
AF Visco, Anthony G.
Brubaker, Linda
Richter, Holly E.
Nygaard, Ingrid
Paraiso, Marie Fidela R.
Menefee, Shawn A.
Schaffer, Joseph
Lowder, Jerry
Khandwala, Salil
Sirls, Larry
Spino, Cathie
Nolen, Tracy L.
Wallace, Dennis
Meikle, Susan F.
CA Pelvic Floor Disorders Network
TI Anticholinergic Therapy vs. OnabotulinumtoxinA for Urgency Urinary
Incontinence
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID OVERACTIVE BLADDER QUESTIONNAIRE; TOXIN TYPE-A; DETRUSOR OVERACTIVITY;
OAB-Q; PERSISTENCE; TRIAL; WOMEN; EFFICACY
AB Background
Anticholinergic medications and onabotulinumtoxinA are used to treat urgency urinary incontinence, but data directly comparing the two types of therapy are needed.
Methods
We performed a double-blind, double-placebo-controlled, randomized trial involving women with idiopathic urgency urinary incontinence who had five or more episodes of urgency urinary incontinence per 3-day period, as recorded in a diary. For a 6-month period, participants were randomly assigned to daily oral anticholinergic medication (solifenacin, 5 mg initially, with possible escalation to 10 mg and, if necessary, subsequent switch to trospium XR, 60 mg) plus one intradetrusor injection of saline or one intradetrusor injection of 100 U of onabotulinumtoxinA plus daily oral placebo. The primary outcome was the reduction from baseline in mean episodes of urgency urinary incontinence per day over the 6-month period, as recorded in 3-day diaries submitted monthly. Secondary outcomes included complete resolution of urgency urinary incontinence, quality of life, use of catheters, and adverse events.
Results
Of 249 women who underwent randomization, 247 were treated, and 241 had data available for the primary outcome analyses. The mean reduction in episodes of urgency urinary incontinence per day over the course of 6 months, from a baseline average of 5.0 per day, was 3.4 in the anticholinergic group and 3.3 in the onabotulinumtoxinA group (P = 0.81). Complete resolution of urgency urinary incontinence was reported by 13% and 27% of the women, respectively (P = 0.003). Quality of life improved in both groups, without significant between-group differences. The anticholinergic group had a higher rate of dry mouth (46% vs. 31%, P = 0.02) but lower rates of catheter use at 2 months (0% vs. 5%, P = 0.01) and urinary tract infections (13% vs. 33%, P<0.001).
Conclusions
Oral anticholinergic therapy and onabotulinumtoxinA by injection were associated with similar reductions in the frequency of daily episodes of urgency urinary incontinence. The group receiving onabotulinumtoxinA was less likely to have dry mouth and more likely to have complete resolution of urgency urinary incontinence but had higher rates of transient urinary retention and urinary tract infections. (Funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the National Institutes of Health Office of Research on Women's Health; ClinicalTrials.gov number, NCT01166438.)
C1 [Visco, Anthony G.] Duke Univ, Dept Obstet & Gynecol, Med Ctr, Durham, NC 27707 USA.
[Nolen, Tracy L.; Wallace, Dennis] RTI Int, Res Triangle Pk, NC USA.
[Brubaker, Linda] Loyola Univ, Stritch Sch Med, Dept Obstet & Gynecol, Chicago, IL 60611 USA.
[Brubaker, Linda] Loyola Univ, Stritch Sch Med, Dept Urol, Chicago, IL 60611 USA.
[Richter, Holly E.] Univ Alabama Birmingham, Dept Obstet & Gynecol, Birmingham, AL USA.
[Nygaard, Ingrid] Univ Utah, Dept Obstet & Gynecol, Salt Lake City, UT USA.
[Paraiso, Marie Fidela R.] Cleveland Clin, Dept Obstet & Gynecol, Cleveland, OH USA.
[Menefee, Shawn A.] Kaiser Permanente San Diego, Dept Obstet & Gynecol, San Diego, CA USA.
[Schaffer, Joseph] Univ Texas SW Med Ctr Dallas, Dept Obstet & Gynecol, Dallas, TX 75390 USA.
[Lowder, Jerry] Univ Pittsburgh, Pittsburgh, PA USA.
[Khandwala, Salil] Oakwood Hosp & Med Ctr, Dearborn, MI USA.
[Sirls, Larry] Oakland Univ, William Beaumont Sch Med, Dept Urol, Beaumont Hlth Syst, Royal Oak, MI USA.
[Spino, Cathie] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Meikle, Susan F.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Contracept & Reprod Hlth Branch, Populat Res Ctr, NIH, Rockville, MD USA.
RP Visco, AG (reprint author), Duke Univ, Dept Obstet & Gynecol, Med Ctr, 5324 McFarland Dr,Suite 310, Durham, NC 27707 USA.
EM anthony.visco@duke.edu
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development; National Institutes of Health Office of Research on Women's
Health; Eunice Kennedy Shriver National Institute of Child Health and
Human Development [2-U10-HD04267-12, U10-HD054136, 2-U10-HD041261-11,
U10-HD041250, 2-U10-HD054215-06, 2-U10-HD054214-06, 1-U10-HD069006-01,
2-U10-HD054241-06, U01-HD41249, 1-U01-HD069010-01]; Astellas Pharma;
GlaxoSmithKline; Uromedica; IDEO; Pfizer; Xanodyne Pharmaceuticals;
Pelvalon; Warner Chilcott; Ethicon; Ferring Pharmaceuticals; Cadence
FX Funded by the Eunice Kennedy Shriver National Institute of Child Health
and Human Development and the National Institutes of Health Office of
Research on Women's Health; ClinicalTrials.gov number, NCT01166438.;
Supported by grants from the Eunice Kennedy Shriver National Institute
of Child Health and Human Development (2-U10-HD04267-12, to Duke
University Medical Center; U10-HD054136, to Loyola University;
2-U10-HD041261-11, to the University of Alabama at Birmingham;
U10-HD041250, to the University of Utah; 2-U10-HD054215-06, to the
Cleveland Clinic; 2-U10-HD054214-06, to the University of California,
San Diego; 1-U10-HD069006-01, to the University of Pittsburgh;
2-U10-HD054241-06, to the University of Texas Southwestern Medical
Center; U01-HD41249, to the University of Michigan; and
1-U01-HD069010-01, to RTI International) and the National Institutes of
Health Office of Research on Women's Health.; Dr. Richter reports
receiving consulting fees from Astellas Pharma, GlaxoSmithKline,
Uromedica, IDEO, Pfizer, and Xanodyne Pharmaceuticals and grant support
on behalf of her institution from Pelvalon, Astellas Pharma, Warner
Chilcott, and Pfizer; Dr. Paraiso, receiving consulting fees from
Ethicon; and Dr. Shaffer, receiving consulting fees from Astellas
Pharma, Ferring Pharmaceuticals, and Cadence, lecture fees from Astellas
Pharma and Cadence, and royalties from McGraw-Hill Companies. No other
potential conflict of interest relevant to this article was reported.
NR 22
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U1 1
U2 13
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 8
PY 2012
VL 367
IS 19
BP 1803
EP 1813
DI 10.1056/NEJMoa1208872
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 033DG
UT WOS:000310773200007
PM 23036134
ER
PT J
AU Teicher, BA
Doroshow, JH
AF Teicher, Beverly A.
Doroshow, James H.
TI The Promise of Antibody-Drug Conjugates
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
ID GROWTH-FACTOR RECEPTOR; CANCER
C1 [Teicher, Beverly A.; Doroshow, James H.] NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
RP Teicher, BA (reprint author), NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
NR 7
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Z9 27
U1 0
U2 12
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 8
PY 2012
VL 367
IS 19
BP 1847
EP 1848
DI 10.1056/NEJMe1211736
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 033DG
UT WOS:000310773200015
PM 23134386
ER
PT J
AU Caporaso, NE
AF Caporaso, Neil E.
TI Statins and Cancer-Related Mortality - Let's Work Together
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
ID THERAPY; RISK
C1 NCI, Genet Epidemiol Branch, NIH, Bethesda, MD 20892 USA.
RP Caporaso, NE (reprint author), NCI, Genet Epidemiol Branch, NIH, Bethesda, MD 20892 USA.
NR 7
TC 8
Z9 8
U1 0
U2 4
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 8
PY 2012
VL 367
IS 19
BP 1848
EP 1850
DI 10.1056/NEJMe1210002
PG 4
WC Medicine, General & Internal
SC General & Internal Medicine
GA 033DG
UT WOS:000310773200016
PM 23134387
ER
PT J
AU Liu, MY
Chen, KQ
Yoshimura, T
Liu, Y
Gong, WH
Wang, AM
Gao, JL
Murphy, PM
Wang, JM
AF Liu, Mingyong
Chen, Keqiang
Yoshimura, Teizo
Liu, Ying
Gong, Wanghua
Wang, Aimin
Gao, Ji-Liang
Murphy, Philip M.
Wang, Ji Ming
TI Formylpeptide receptors are critical for rapid neutrophil mobilization
in host defense against Listeria monocytogenes
SO SCIENTIFIC REPORTS
LA English
DT Article
ID FORMYL-PEPTIDE RECEPTORS; IMMUNE-RESPONSES; MICE LACKING; INFECTION;
EPIDEMIOLOGY; INFLAMMATION; MACROPHAGE; INTERNALIN; MIGRATION; CXCR1/2
AB Listeria monocytogenes ( Listeria) causes opportunistic infection in immunocompromised hosts with high mortality. Resistance to Listeria depends on immune responses and recruitment of neutrophils of the immune system into infected sites is an early and critical step. Mouse neutrophils express two G protein-coupled formylpeptide receptor subtypes Fpr1 and Fpr2 that recognize bacterial and host-derived chemotactic molecules including Listeria peptides for cell migration and activation. Here we report deficiency in Fprs exacerbated the severity of the infection and increased the mortality of infected mice. The mechanism involved impaired early neutrophil recruitment to the liver with Fpr1 and Fpr2 being sole receptors for neutrophils to sense Listeria chemoattractant signals and for production of bactericidal superoxide. Thus, Fprs are essential sentinels to guide the first wave of neutrophil infiltration in the liver of Listeria-infected mice for effective elimination of the invading pathogen.
C1 [Liu, Mingyong] Third Mil Med Univ, Daping Hosp, Dept Spine Surg, Chongqing 400042, Peoples R China.
[Liu, Mingyong; Chen, Keqiang; Yoshimura, Teizo; Liu, Ying; Wang, Ji Ming] Frederick Natl Lab Canc Res, Lab Mol Immunoregulat, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21702 USA.
[Gong, Wanghua] SAIC Frederick, Basic Res Program, Frederick, MD 21702 USA.
[Wang, Aimin] Third Mil Med Univ, Daping Hosp, Ctr Orthoped, Chongqing 400042, Peoples R China.
[Gao, Ji-Liang; Murphy, Philip M.] NIAID, Lab Mol Immunol, Bethesda, MD 20892 USA.
RP Liu, MY (reprint author), Third Mil Med Univ, Daping Hosp, Dept Spine Surg, Chongqing 400042, Peoples R China.
EM liu_mingyong@yahoo.com.cn; wangji@mail.nih.gov
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]
FX We thank Drs. J.J. Oppenheim and G. Trinchieri for critically reviewing
the manuscript; C. Lamb for secretarial assistance. This project was
funded in part by federal funds from the National Cancer Institute,
National Institutes of Health, under Contract No. HHSN261200800001E and
was supported in part by the Intramural Research Program of the NCI,
NIH.
NR 37
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PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD NOV 8
PY 2012
VL 2
AR 786
DI 10.1038/srep00786
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 034MM
UT WOS:000310877600002
PM 23139859
ER
PT J
AU Grivennikov, SI
Wang, KP
Mucida, D
Stewart, CA
Schnabl, B
Jauch, D
Taniguchi, K
Yu, GY
Osterreicher, CH
Hung, KE
Datz, C
Feng, Y
Fearon, ER
Oukka, M
Tessarollo, L
Coppola, V
Yarovinsky, F
Cheroutre, H
Eckmann, L
Trinchieri, G
Karin, M
AF Grivennikov, Sergei I.
Wang, Kepeng
Mucida, Daniel
Stewart, C. Andrew
Schnabl, Bernd
Jauch, Dominik
Taniguchi, Koji
Yu, Guann-Yi
Oesterreicher, Christoph H.
Hung, Kenneth E.
Datz, Christian
Feng, Ying
Fearon, Eric R.
Oukka, Mohamed
Tessarollo, Lino
Coppola, Vincenzo
Yarovinsky, Felix
Cheroutre, Hilde
Eckmann, Lars
Trinchieri, Giorgio
Karin, Michael
TI Adenoma-linked barrier defects and microbial products drive
IL-23/IL-17-mediated tumour growth
SO NATURE
LA English
DT Article
ID PROMOTES COLON TUMORIGENESIS; COLORECTAL-CANCER; APC(MIN/+) MICE;
CUTTING EDGE; HELPER-CELLS; MOUSE MODEL; INFLAMMATION; RECEPTOR;
COLITIS; DIFFERENTIATION
AB Approximately 2% of colorectal cancer is linked to pre-existing inflammation known as colitis-associated cancer, but most develops in patients without underlying inflammatory bowel disease. Colorectal cancer often follows a genetic pathway whereby loss of the adenomatous polyposis coli (APC) tumour suppressor and activation of beta-catenin are followed by mutations in K-Ras, PIK3CA and TP53, as the tumour emerges and progresses(1,2). Curiously, however, 'inflammatory signature' genes characteristic of colitis-associated cancer are also upregulated in colorectal cancer(3,4). Further, like most solid tumours, colorectal cancer exhibits immune/inflammatory infiltrates(5), referred to as 'tumour-elicited inflammation'(6). Although infiltrating CD4(+) T(H)1 cells and CD8(+) cytotoxic T cells constitute a positive prognostic sign in colorectal cancer(7,8), myeloid cells and T-helper interleukin (IL)-17-producing (T(H)17) cells promote tumorigenesis(5,6), and a 'T(H)17 expression signature' in stage I/II colorectal cancer is associated with a drastic decrease in disease-free survival(9). Despite its pathogenic importance, the mechanisms responsible for the appearance of tumour-elicited inflammation are poorly understood. Many epithelial cancers develop proximally to microbial communities, which are physically separated from immune cells by an epithelial barrier(10). We investigated mechanisms responsible for tumour-elicited inflammation in a mouse model of colorectal tumorigenesis, which, like human colorectal cancer, exhibits upregulation of IL-23 and IL-17. Here we show that IL-23 signalling promotes tumour growth and progression, and development of a tumoural IL-17 response. IL-23 is mainly produced by tumour-associated myeloid cells that are likely to be activated by microbial products, which penetrate the tumours but not adjacent tissue. Both early and late colorectal neoplasms exhibit defective expression of several barrier proteins. We propose that barrier deterioration induced by colorectal-cancer-initiating genetic lesions results in adenoma invasion by microbial products that trigger tumour-elicited inflammation, which in turn drives tumour growth.
C1 [Grivennikov, Sergei I.; Wang, Kepeng; Jauch, Dominik; Taniguchi, Koji; Yu, Guann-Yi; Karin, Michael] Univ Calif San Diego, Lab Gene Regulat & Signal Transduct, Dept Pharmacol, La Jolla, CA 92093 USA.
[Grivennikov, Sergei I.; Wang, Kepeng; Jauch, Dominik; Taniguchi, Koji; Yu, Guann-Yi; Karin, Michael] Univ Calif San Diego, Dept Pathol, Sch Med, La Jolla, CA 92093 USA.
[Wang, Kepeng] Shenzhen PKU HKUST Med Ctr, Biomed Res Inst, Shenzhen, Guangdong, Peoples R China.
[Mucida, Daniel; Cheroutre, Hilde] La Jolla Inst Allergy & Immunol, La Jolla, CA 92093 USA.
[Mucida, Daniel] Rockefeller Univ, Lab Mucosal Immunol, New York, NY 10065 USA.
[Stewart, C. Andrew; Trinchieri, Giorgio] NCI, Canc & Inflammat Program, Expt Immunol Lab, Ctr Canc Res,NIH, Frederick, MD 21702 USA.
[Schnabl, Bernd; Oesterreicher, Christoph H.; Eckmann, Lars] Univ Calif San Diego, Sch Med, Dept Med, La Jolla, CA 92093 USA.
[Taniguchi, Koji] Keio Univ, Sch Med, Dept Microbiol & Immunol, Tokyo 1608582, Japan.
[Oesterreicher, Christoph H.] Med Univ Vienna, Ctr Physiol & Pharmacol, Inst Pharmacol, Vienna, Austria.
[Hung, Kenneth E.] Tufts Med Ctr, Dept Med, Boston, MA 02111 USA.
[Datz, Christian] Paracelsus Med Univ, Oberndorf Hosp, Dept Internal Med, Salzburg, Austria.
[Feng, Ying; Fearon, Eric R.] Univ Michigan, Sch Med, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Feng, Ying; Fearon, Eric R.] Univ Michigan, Sch Med, Dept Human Genet, Ann Arbor, MI 48109 USA.
[Feng, Ying; Fearon, Eric R.] Univ Michigan, Sch Med, Dept Pathol, Ann Arbor, MI 48109 USA.
[Oukka, Mohamed] Seattle Childrens Res Inst, Seattle, WA 98105 USA.
[Tessarollo, Lino] NCI, Mouse Canc Genet Program, NIH, Frederick, MD 21702 USA.
[Coppola, Vincenzo] Ohio State Univ, Ctr Comprehens Canc, Wexner Med Ctr, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA.
[Yarovinsky, Felix] Univ Texas SW Med Ctr Dallas, Dept Immunol, Dallas, TX 75390 USA.
RP Karin, M (reprint author), Univ Calif San Diego, Lab Gene Regulat & Signal Transduct, Dept Pharmacol, 9500 Gilman Dr, La Jolla, CA 92093 USA.
EM karinoffice@ucsd.edu
RI Coppola, Vincenzo/E-2917-2011; Stewart, Charles/G-2470-2012; Wang,
Kepeng/F-8363-2014;
OI Coppola, Vincenzo/0000-0001-6163-1779; Wang, Kepeng/0000-0001-6428-4709;
Mucida, Daniel/0000-0002-0000-0452
FU Crohn's and Colitis Foundation of America [2693]; NIH/National Institute
of Diabetes and Digestive and Kidney Diseases [K99-DK088589]; University
of California, San Diego, Digestive Disease Research Development Center
Pilot Grant [DK080506]; Croucher Foundation; China Postdoctoral Science
Foundation [20110490919]; Strategic Young Researcher Overseas Visits
Program for Accelerating Brain Circulation; SPAR Austria; NIH
[R01CA082223, AI043477, DK035108]; American Association for Cancer
Research [07-60-21-KARI]
FX We thank eBioscience, GeneTex, Santa Cruz, BioLegend and Cell Signaling
for antibodies; Genentech and Amgen for Il23-/- and
Il17ra-/- mice, respectively, and S. Reid and E. Southon for
the help in generating Il23rF/F mice. This work was supported
by Crohn's and Colitis Foundation of America (Career Development Award
number 2693), NIH/National Institute of Diabetes and Digestive and
Kidney Diseases (K99-DK088589) and a University of California, San
Diego, Digestive Disease Research Development Center Pilot Grant
(DK080506) to S. I. G.; Croucher Foundation and China Postdoctoral
Science Foundation (20110490919) to K. W.; Strategic Young Researcher
Overseas Visits Program for Accelerating Brain Circulation to K. T.;
SPAR Austria to C. D.; NIH (R01CA082223) to E. R. F.; and NIH (AI043477;
DK035108) and American Association for Cancer Research (07-60-21-KARI)
grants to M. K., who is an American Cancer Society Research Professor.
The content is solely the responsibility of the authors and does not
necessarily represent the official views of the NIH.
NR 44
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PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 8
PY 2012
VL 491
IS 7423
BP 254
EP +
DI 10.1038/nature11465
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 033DP
UT WOS:000310774300044
PM 23034650
ER
PT J
AU Yoshizaki, A
Miyagaki, T
DiLillo, DJ
Matsushita, T
Horikawa, M
Kountikov, EI
Spolski, R
Poe, JC
Leonard, WJ
Tedder, TF
AF Yoshizaki, Ayumi
Miyagaki, Tomomitsu
DiLillo, David J.
Matsushita, Takashi
Horikawa, Mayuka
Kountikov, Evgueni I.
Spolski, Rosanne
Poe, Jonathan C.
Leonard, Warren J.
Tedder, Thomas F.
TI Regulatory B cells control T-cell autoimmunity through IL-21-dependent
cognate interactions
SO NATURE
LA English
DT Article
ID B10 CELLS; TRANSGENIC MICE; LYMPHOCYTE DEVELOPMENT; CUTTING EDGE;
PLASMA-CELLS; HUMAN CD19; MEMORY B; IN-VIVO; IL-21; IL-10
AB B cells regulate immune responses by producing antigen-specific antibodies(1). However, specific B-cell subsets can also negatively regulate T-cell immune responses, and have been termed regulatory B cells(2-4). Human and mouse regulatory B cells (B10 cells) with the ability to express the inhibitory cytokine interleukin-10 (IL-10) have been identified(2-5). Although rare, B10 cells are potent negative regulators of antigen-specific inflammation and T-cell-dependent autoimmune diseases in mice(5-7). How B10-cell IL-10 production and regulation of antigen-specific immune responses are controlled in vivo without inducing systemic immunosuppression is unknown. Using a mouse model for multiple sclerosis, here we show that B10-cell maturation into functional IL-10-secreting effector cells that inhibit in vivo autoimmune disease requires IL-21 and CD40-dependent cognate interactions with T cells. Moreover, the ex vivo provision of CD40 and IL-21 receptor signals can drive B10-cell development and expansion by four-million-fold, and generate B10 effector cells producing IL-10 that markedly inhibit disease symptoms when transferred into mice with established autoimmune disease. The ex vivo expansion and reinfusion of autologous B10 cells may provide a novel and effective in vivo treatment for severe autoimmune diseases that are resistant to current therapies.
C1 [Yoshizaki, Ayumi; Miyagaki, Tomomitsu; DiLillo, David J.; Matsushita, Takashi; Horikawa, Mayuka; Kountikov, Evgueni I.; Poe, Jonathan C.; Tedder, Thomas F.] Duke Univ, Med Ctr, Dept Immunol, Durham, NC 27710 USA.
[Spolski, Rosanne; Leonard, Warren J.] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
RP Tedder, TF (reprint author), Duke Univ, Med Ctr, Dept Immunol, Durham, NC 27710 USA.
EM thomas.tedder@duke.edu
RI Matsushita, Takashi /C-4750-2015
OI Matsushita, Takashi /0000-0002-1617-086X
FU National Institutes of Health (NIH) [AI56363, AI057157]; Lymphoma
Research Foundation; Division of Intramural Research, National Heart,
Lung, and Blood Institute, NIH
FX We thank D. Maseda, E. Weimer, J. Bryant, K. Candando and G. Venturi for
help and comments. These studies were supported by grants from the
National Institutes of Health (NIH; AI56363 and AI057157), the Lymphoma
Research Foundation, and the Division of Intramural Research, National
Heart, Lung, and Blood Institute, NIH.
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PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 8
PY 2012
VL 491
IS 7423
BP 264
EP +
DI 10.1038/nature11501
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 033DP
UT WOS:000310774300046
PM 23064231
ER
PT J
AU Kim, S
Bolton, EE
Bryant, SH
AF Kim, Sunghwan
Bolton, Evan E.
Bryant, Stephen H.
TI Effects of multiple conformers per compound upon 3-D similarity search
and bioassay data analysis
SO JOURNAL OF CHEMINFORMATICS
LA English
DT Article
ID DATA FUSION; BIOLOGICAL-ACTIVITIES; MOLECULAR SHAPE; PUBCHEM3D;
CONFORMATIONS; COEFFICIENTS; PERFORMANCE; DESIGN; VALIDATION; CATALYST
AB Background: To improve the utility of PubChem, a public repository containing biological activities of small molecules, the PubChem3D project adds computationally-derived three-dimensional (3-D) descriptions to the small-molecule records contained in the PubChem Compound database and provides various search and analysis tools that exploit 3-D molecular similarity. Therefore, the efficient use of PubChem3D resources requires an understanding of the statistical and biological meaning of computed 3-D molecular similarity scores between molecules.
Results: The present study investigated effects of employing multiple conformers per compound upon the 3-D similarity scores between ten thousand randomly selected biologically-tested compounds (10-K set) and between non-inactive compounds in a given biological assay (156-K set). When the "best-conformer-pair" approach, in which a 3-D similarity score between two compounds is represented by the greatest similarity score among all possible conformer pairs arising from a compound pair, was employed with ten diverse conformers per compound, the average 3-D similarity scores for the 10-K set increased by 0.11, 0.09, 0.15, 0.16, 0.07, and 0.18 for STST-opt, CTST-opt, ComboT(ST-opt), STCT-opt, CTCT-opt, and ComboT(CT-opt), respectively, relative to the corresponding averages computed using a single conformer per compound. Interestingly, the best-conformer-pair approach also increased the average 3-D similarity scores for the non-inactive-non-inactive (NN) pairs for a given assay, by comparable amounts to those for the random compound pairs, although some assays showed a pronounced increase in the per-assay NN-pair 3-D similarity scores, compared to the average increase for the random compound pairs.
Conclusion: These results suggest that the use of ten diverse conformers per compound in PubChem bioassay data analysis using 3-D molecular similarity is not expected to increase the separation of non-inactive from random and inactive spaces "on average", although some assays show a noticeable separation between the non-inactive and random spaces when multiple conformers are used for each compound. The present study is a critical next step to understand effects of conformational diversity of the molecules upon the 3-D molecular similarity and its application to biological activity data analysis in PubChem. The results of this study may be helpful to build search and analysis tools that exploit 3-D molecular similarity between compounds archived in PubChem and other molecular libraries in a more efficient way.
C1 [Kim, Sunghwan; Bolton, Evan E.; Bryant, Stephen H.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, US Dept HHS, Bethesda, MD 20894 USA.
RP Bolton, EE (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, US Dept HHS, 8600 Rockville Pike, Bethesda, MD 20894 USA.
EM bolton@ncbi.nlm.nih.gov
RI Kim, Sunghwan/A-6738-2008
OI Kim, Sunghwan/0000-0001-9828-2074
FU Intramural Research Program of the National Library of Medicine,
National Institutes of Health, U.S. Department of Health and Human
Services
FX We are grateful to the NCBI Systems staff, especially Ron Patterson,
Charlie Cook, and Don Preuss, whose efforts helped to make the PubChem3D
project possible. We are also thankful to the reviewers for their
insightful suggestions and comments. SK thanks to Volker Hahnke for
fruitful discussion on this study. This research was supported in part
by the Intramural Research Program of the National Library of Medicine,
National Institutes of Health, U.S. Department of Health and Human
Services.
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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 7
PY 2012
VL 4
AR 28
DI 10.1186/1758-2946-4-28
PG 30
WC Chemistry, Multidisciplinary; Computer Science, Information Systems;
Computer Science, Interdisciplinary Applications
SC Chemistry; Computer Science
GA 067ED
UT WOS:000313275800001
PM 23134593
ER
PT J
AU Gassman, NR
Stefanick, DF
Kedar, PS
Horton, JK
Wilson, SH
AF Gassman, Natalie R.
Stefanick, Donna F.
Kedar, Padmini S.
Horton, Julie K.
Wilson, Samuel H.
TI Hyperactivation of PARP Triggers Nonhomologous End-Joining in
Repair-Deficient Mouse Fibroblasts
SO PLOS ONE
LA English
DT Article
ID DOUBLE-STRAND BREAKS; DNA-POLYMERASE-BETA; DEPENDENT PROTEIN-KINASE;
CELL-DEATH PARTHANATOS; POLY(ADP-RIBOSE) POLYMERASE; MAMMALIAN-CELLS;
DAMAGE; KU; IDENTIFICATION; PATHWAY
AB Regulation of poly(ADP-ribose) (PAR) synthesis and turnover is critical to determining cell fate after genotoxic stress. Hyperactivation of PAR synthesis by poly(ADP-ribose) polymerase-1 (PARP-1) occurs when cells deficient in DNA repair are exposed to genotoxic agents; however, the function of this hyperactivation has not been adequately explained. Here, we examine PAR synthesis in mouse fibroblasts deficient in the base excision repair enzyme DNA polymerase beta (pol beta). The extent and duration of PARP-1 activation was measured after exposure to either the DNA alkylating agent, methyl methanesulfonate (MMS), or to low energy laser-induced DNA damage. There was strong DNA damage-induced hyperactivation of PARP-1 in pol beta null cells, but not in wild-type cells. In the case of MMS treatment, PAR synthesis did not lead to cell death in the pol b null cells, but instead resulted in increased PARylation of the nonhomologous end-joining (NHEJ) protein Ku70 and increased association of Ku70 with PARP-1. Inhibition of the NHEJ factor DNA-PK, under conditions of MMS-induced PARP-1 hyperactivation, enhanced necrotic cell death. These data suggest that PARP-1 hyperactivation is a protective mechanism triggering the classical-NHEJ DNA repair pathway when the primary alkylated base damage repair pathway is compromised.
C1 [Gassman, Natalie R.; Stefanick, Donna F.; Kedar, Padmini S.; Horton, Julie K.; Wilson, Samuel H.] NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA.
RP Wilson, SH (reprint author), NIEHS, Struct Biol Lab, POB 12233, Res Triangle Pk, NC 27709 USA.
EM wilson5@niehs.nih.gov
OI Gassman, Natalie/0000-0002-8488-2332
FU Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences [Z01-ES050158,
Z01-ES050159]
FX This research was supported by Research Project Numbers Z01-ES050158 and
Z01-ES050159 in the Intramural Research Program of the National
Institutes of Health, National Institute of Environmental Health
Sciences. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 58
TC 10
Z9 10
U1 0
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 7
PY 2012
VL 7
IS 11
AR e49301
DI 10.1371/journal.pone.0049301
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 048TK
UT WOS:000311935800242
PM 23145148
ER
PT J
AU Golkar, A
Lonsdorf, TB
Olsson, A
Lindstrom, KM
Berrebi, J
Fransson, P
Schalling, M
Ingvar, M
Ohman, A
AF Golkar, Armita
Lonsdorf, Tina B.
Olsson, Andreas
Lindstrom, Kara M.
Berrebi, Jonathan
Fransson, Peter
Schalling, Martin
Ingvar, Martin
Ohman, Arne
TI Distinct Contributions of the Dorsolateral Prefrontal and Orbitofrontal
Cortex during Emotion Regulation
SO PLOS ONE
LA English
DT Article
ID THREAT-RELATED STIMULI; COGNITIVE CONTROL; NEGATIVE EMOTION; VOLUNTARY
SUPPRESSION; WORKING-MEMORY; AMYGDALA; FMRI; RESPONSES; ANXIETY;
NEUROSCIENCE
AB The lateral prefrontal and orbitofrontal cortices have both been implicated in emotion regulation, but their distinct roles in regulation of negative emotion remain poorly understood. To address this issue we enrolled 58 participants in an fMRI study in which participants were instructed to reappraise both negative and neutral stimuli. This design allowed us to separately study activations reflecting cognitive processes associated with reappraisal in general and activations specifically related to reappraisal of negative emotion. Our results confirmed that both the dorsolateral prefrontal cortex (DLPFC) and the lateral orbitofrontal cortex (OFC) contribute to emotion regulation through reappraisal. However, activity in the DLPFC was related to reappraisal independently of whether negative or neutral stimuli were reappraised, whereas the lateral OFC was uniquely related to reappraisal of negative stimuli. We suggest that relative to the lateral OFC, the DLPFC serves a more general role in emotion regulation, perhaps by reflecting the cognitive demand that is inherent to the regulation task.
C1 [Golkar, Armita; Lonsdorf, Tina B.; Olsson, Andreas; Lindstrom, Kara M.; Berrebi, Jonathan; Fransson, Peter; Ingvar, Martin; Ohman, Arne] Karolinska Inst, Stockholm Brain Inst, Dept Clin Neurosci, Solna, Sweden.
[Golkar, Armita; Lonsdorf, Tina B.; Olsson, Andreas; Ingvar, Martin; Ohman, Arne] Nord Ctr Excellence Cognit Control, Stockholm, Sweden.
[Lonsdorf, Tina B.] Univ Hosp Hamburg Eppendorf, Inst Syst Neurosci, Hamburg, Germany.
[Lindstrom, Kara M.] NIMH, Mood & Anxiety Program, Bethesda, MD 20892 USA.
[Schalling, Martin] Karolinska Inst, Ctr Mol Med & Surg, Solna, Sweden.
[Ingvar, Martin] Osher Ctr Integrat Med, Stockholm, Sweden.
[Ohman, Arne] NIH, Ctr Study Emot & Attent, Gainesville, FL USA.
RP Golkar, A (reprint author), Karolinska Inst, Stockholm Brain Inst, Dept Clin Neurosci, Solna, Sweden.
EM armita.golkar@ki.se
RI Fransson, Peter/M-5679-2014;
OI Fransson, Peter/0000-0002-1305-9875; Ingvar, Martin/0000-0002-9041-5714;
Golkar, Armita/0000-0003-3077-0391
FU Swedish Research Council; Nordic Research Council for the Humanities and
Social Sciences (NOS-HS); National Institute of Mental Health, Center
for the Study of Emotion and Attention; Barbro and Bernard Osher
Foundation; Swedish Governmental Agency for Innovation Systems
(VINNOVA); Swedish Foundation for Strategic Research
FX This work was supported by grants from the Swedish Research Council (to
A.O., M.S., M.I.), the Nordic Research Council for the Humanities and
Social Sciences (NOS-HS, to A.O.), the National Institute of Mental
Health, Center for the Study of Emotion and Attention (to A.O.), the
Barbro and Bernard Osher Foundation (M.I.), The Swedish Governmental
Agency for Innovation Systems (VINNOVA) and The Swedish Foundation for
Strategic Research (A.O., M.I.). The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 46
TC 36
Z9 36
U1 5
U2 36
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 7
PY 2012
VL 7
IS 11
AR e48107
DI 10.1371/journal.pone.0048107
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 048TK
UT WOS:000311935800035
PM 23144849
ER
PT J
AU Hajnal, A
Zharikov, A
Polston, JE
Fields, MR
Tomasko, J
Rogers, AM
Volkow, ND
Thanos, PK
AF Hajnal, Andras
Zharikov, Alevtina
Polston, James E.
Fields, Maxine R.
Tomasko, Jonathan
Rogers, Ann M.
Volkow, Nora D.
Thanos, Panayotis K.
TI Alcohol Reward Is Increased after Roux-en-Y Gastric Bypass in Dietary
Obese Rats with Differential Effects following Ghrelin Antagonism
SO PLOS ONE
LA English
DT Article
ID STIMULATES LOCOMOTOR-ACTIVITY; BARIATRIC SURGERY; NUCLEUS-ACCUMBENS; GUT
HORMONE; GASTROINTESTINAL HORMONES; INSULIN SENSITIVITY; RECEPTOR
ANTAGONISM; DEFICIENT MICE; FOOD REWARD; SWEET TASTE
AB Roux-en-Y gastric bypass (RYGB) is one of the most successful treatments for severe obesity and associated comorbidities. One potential adverse outcome, however, is increased risk for alcohol use. As such, we tested whether RYGB alters motivation to self-administer alcohol in outbred dietary obese rats, and investigated the involvement of the ghrelin system as a potential underlying mechanism. High fat (60% kcal from fat) diet-induced obese, non-diabetic male Sprague Dawley rats underwent RYGB (n = 9) or sham operation (Sham, n = 9) and were tested 4 months after surgery on a progressive ratio-10 (PR10) schedule of reinforcement operant task for 2, 4, and 8% ethanol. In addition, the effects of the ghrelin-1a-receptor antagonist D-[Lys3]-GHRP-6 (50, 100 nmol/kg, IP) were tested on PR10 responding for 4% ethanol. Compared to Sham, RYGB rats made significantly more active spout responses to earn reward, more consummatory licks on the ethanol spout, and achieved higher breakpoints. Pretreatment with a single peripheral injection of D-[Lys3]-GHRP-6 at either dose was ineffective in altering appetitive or consummatory responses to 4% ethanol in the Sham group. In contrast, RYGB rats demonstrated reduced operant performance to earn alcohol reward on the test day and reduced consummatory responses for two subsequent days following the drug. Sensitivity to threshold doses of D-[LYS3]-GHRP-6 suggests that an augmented ghrelin system may contribute to increased alcohol reward in RYGB. Further research is warranted to confirm applicability of these findings to humans and to explore ghrelin-receptor targets for treatment of alcohol-related disorders in RYGB patients.
C1 [Hajnal, Andras; Zharikov, Alevtina; Polston, James E.; Fields, Maxine R.] Penn State Univ, Coll Med, Dept Neural & Behav Sci, Hershey, PA 17033 USA.
[Hajnal, Andras; Tomasko, Jonathan; Rogers, Ann M.] Penn State Univ, Coll Med, Dept Surg, Hershey, PA USA.
[Volkow, Nora D.; Thanos, Panayotis K.] NIAAA, Lab Neuroimaging, Intramural Program, NIH, Bethesda, MD 90034 USA.
[Thanos, Panayotis K.] Brookhaven Natl Lab, Behav Neuropharmacol & Neuroimaging Lab, Upton, NY 11973 USA.
RP Hajnal, A (reprint author), Penn State Univ, Coll Med, Dept Neural & Behav Sci, Hershey, PA 17033 USA.
EM ahajnal@psu.edu
OI Hajnal, Andras/0000-0001-7297-7134
FU National Institute of Diabetes and Digestive and Kidney Diseases Grant
[DK080899]
FX This research was supported by National Institute of Diabetes and
Digestive and Kidney Diseases Grant DK080899 (to AH). The funders had no
role in study design, data collection and analysis, decision to publish,
or preparation of the manuscript.
NR 73
TC 18
Z9 18
U1 0
U2 13
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 7
PY 2012
VL 7
IS 11
AR e49121
DI 10.1371/journal.pone.0049121
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 048TK
UT WOS:000311935800211
PM 23145091
ER
PT J
AU Huang, SH
Wu, CH
Chang, YC
Kwon-Chung, KJ
Brown, RJ
Jong, A
AF Huang, Sheng-He
Wu, Chun-Hua
Chang, Yun C.
Kwon-Chung, Kyung J.
Brown, Robert J.
Jong, Ambrose
TI Cryptococcus neoformans-Derived Microvesicles Enhance the Pathogenesis
of Fungal Brain Infection
SO PLOS ONE
LA English
DT Article
ID MICROVASCULAR ENDOTHELIAL-CELLS; CAPSULE-ASSOCIATED GENE; EXTRACELLULAR
VESICLES; MEMBRANE-VESICLES; EXOSOMES; VIRULENCE; INVASION;
POLYSACCHARIDE; MACROPHAGES; LEISHMANIA
AB Cryptococcal meningoencephalitis is the most common fungal disease in the central nervous system. The mechanisms by which Cryptococcus neoformans invades the brain are largely unknown. In this study, we found that C. neoformans-derived microvesicles (CnMVs) can enhance the traversal of the blood-brain barrier (BBB) by C. neoformans in vitro. The immunofluorescence imaging demonstrates that CnMVs can fuse with human brain microvascular endothelial cells (HBMECs), the constituents of the BBB. This activity is presumably due to the ability of the CnMVs to activate HBMEC membrane rafts and induce cell fusogenic activity. CnMVs also enhanced C. neoformans infection of the brain, found in both infected brains and cerebrospinal fluid. In infected mouse brains, CnMVs are distributed inside and around C. neoformans-induced cystic lesions. GFAP (glial fibrillary acidic protein)-positive astrocytes were found surrounding the cystic lesions, overlapping with the 14-3-3-GFP (14-3-3-green fluorescence protein fusion) signals. Substantial changes could be observed in areas that have a high density of CnMV staining. This is the first demonstration that C. neoformans-derived microvesicles can facilitate cryptococcal traversal across the BBB and accumulate at lesion sites of C. neoformans-infected brains. Results of this study suggested that CnMVs play an important role in the pathogenesis of cryptococcal meningoencephalitis.
C1 [Wu, Chun-Hua; Brown, Robert J.; Jong, Ambrose] Univ So Calif, Keck Sch Med, Div Hematol Oncol, Saban Res Inst,Childrens Hosp Los Angeles,Dept Pe, Los Angeles, CA 90033 USA.
[Huang, Sheng-He] Univ So Calif, Keck Sch Med, Div Infect Dis, Saban Res Inst,Childrens Hosp Los Angeles,Dept Pe, Los Angeles, CA 90033 USA.
[Chang, Yun C.; Kwon-Chung, Kyung J.] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
RP Jong, A (reprint author), Univ So Calif, Keck Sch Med, Div Hematol Oncol, Saban Res Inst,Childrens Hosp Los Angeles,Dept Pe, Los Angeles, CA 90033 USA.
EM ajong@chla.usc.edu
FU Public Health Service grants from National Institutes of Health
[R01-NS047599, R01-AI40635]; intramural program of the National
Institute of Allergy and Infectious Diseases, National Institutes of
Health
FX This project was financially supported by Public Health Service grants
R01-NS047599 (A.J.) and R01-AI40635 (S. H. H.) from the National
Institutes of Health. The work of Kyung J. Kwon-Chung and Yun C. Chang
was supported by funds from the intramural program of the National
Institute of Allergy and Infectious Diseases, National Institutes of
Health. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 32
TC 23
Z9 25
U1 0
U2 8
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 7
PY 2012
VL 7
IS 11
AR e48570
DI 10.1371/journal.pone.0048570
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 048TK
UT WOS:000311935800077
PM 23144903
ER
PT J
AU Martin-Manso, G
Navarathna, DHMLP
Galli, S
Soto-Pantoja, DR
Kuznetsova, SA
Tsokos, M
Roberts, DD
AF Martin-Manso, Gema
Navarathna, Dhammika H. M. L. P.
Galli, Susana
Soto-Pantoja, David R.
Kuznetsova, Svetlana A.
Tsokos, Maria
Roberts, David D.
TI Endogenous Thrombospondin-1 Regulates Leukocyte Recruitment and
Activation and Accelerates Death from Systemic Candidiasis
SO PLOS ONE
LA English
DT Article
ID HUMAN-NEUTROPHILS; MACROPHAGE ACTIVATION; EXTRACELLULAR-MATRIX;
IMMUNE-RESPONSE; IN-VIVO; EXPRESSION; CELL; CHEMOKINE; ALBICANS;
PROMOTES
AB Disseminated Candida albicans infection results in high morbidity and mortality despite treatment with existing antifungal drugs. Recent studies suggest that modulating the host immune response can improve survival, but specific host targets for accomplishing this goal remain to be identified. The extracellular matrix protein thrombospondin-1 is released at sites of tissue injury and modulates several immune functions, but its role in C. albicans pathogenesis has not been investigated. Here, we show that mice lacking thrombospondin-1 have an advantage in surviving disseminated candidiasis and more efficiently clear the initial colonization from kidneys despite exhibiting fewer infiltrating leukocytes. By examining local and systemic cytokine responses to C. albicans and other standard inflammatory stimuli, we identify a crucial function of phagocytes in this enhanced resistance. Subcutaneous air pouch and systemic candidiasis models demonstrated that endogenous thrombospondin-1 enhances the early innate immune response against C. albicans and promotes activation of inflammatory macrophages (inducible nitric oxide synthase(+), IL-6(high), TNF-alpha(high), IL-10(low)), release of the chemokines MIP-2, JE, MIP-1 alpha, and RANTES, and CXCR2-driven polymorphonuclear leukocytes recruitment. However, thrombospondin-1 inhibited the phagocytic capacity of inflammatory leukocytes in vivo and in vitro, resulting in increased fungal burden in the kidney and increased mortality in wild type mice. Thus, thrombospondin-1 enhances the pathogenesis of disseminated candidiasis by creating an imbalance in the host immune response that ultimately leads to reduced phagocytic function, impaired fungal clearance, and increased mortality. Conversely, inhibitors of thrombospondin-1 may be useful drugs to improve patient recovery from disseminated candidiasis.
C1 [Martin-Manso, Gema; Navarathna, Dhammika H. M. L. P.; Galli, Susana; Soto-Pantoja, David R.; Kuznetsova, Svetlana A.; Tsokos, Maria; Roberts, David D.] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Roberts, DD (reprint author), NCI, Pathol Lab, Ctr Canc Res, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM droberts@helix.nih.gov
RI Roberts, David/A-9699-2008; Martin Manso, Maria Gema/D-4612-2013
OI Roberts, David/0000-0002-2481-2981;
FU Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research; grant BEFI from Instituto de Salud Carlos
III
FX Grant support: This research was supported by the Intramural Research
Program of the NIH, National Cancer Institute, Center for Cancer
Research (DDR, MT). GMM was recipient of a grant BEFI from Instituto de
Salud Carlos III (www.isciii.es). The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 64
TC 10
Z9 10
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 7
PY 2012
VL 7
IS 11
AR e48775
DI 10.1371/journal.pone.0048775
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 048TK
UT WOS:000311935800128
PM 23144964
ER
PT J
AU Minamimoto, T
Hori, Y
Richmond, BJ
AF Minamimoto, Takafumi
Hori, Yukiko
Richmond, Barry J.
TI Is Working More Costly than Waiting in Monkeys?
SO PLOS ONE
LA English
DT Article
ID PREFRONTAL CORTEX; DECISION-MAKING; REWARD; DELAY; MOTIVATION; PIGEONS;
HUMANS
AB We studied how value for instrumental action is discounted by predicted effort and delay. The monkeys were trained to perform instrumental trials that required a bar release when a visual target changed from red-to-green. There were two trial conditions. In delay trials, after the monkeys performed one instrumental trial correctly a reward was delivered 0-7 seconds later. In work trials, the monkeys had to perform 0, 1, or 2 additional instrumental trials to obtain a reward. The lengths of trials in delay matched the time it took to complete work trials. The length of delay or number of trials was indicated by a visual cue presented throughout the trial. Our hypothesis was that the monkeys would all show temporal discounting of reward in the delay trials, and that in the work trials the monkeys' performance might reflect an additional cost due to working. The error rate increased linearly as remaining cost increased for all 8 monkeys. For 4 monkeys the error rate was significantly larger in work trials than in delay trials (effort sensitive monkeys). For the other 4 monkeys there was no significant difference in error rate (effort insensitive monkeys). Since the error rate has an inverse relation with value for action, these results suggest that value is discounted hyperbolically by effort as well as by delay. Error rates generally increased as the testing sessions progressed and the total reward accumulated (i.e., effect of reward devaluation). The relative impact of delay and effort on error rates was reasonably stable within subjects. Thus, within the monkey population there seems to be a significant dichotomy in the sensitivity governing whether working is more costly than waiting, possibly arising from a constitutional or genetic trait.
C1 [Minamimoto, Takafumi; Hori, Yukiko] Natl Inst Radiol Sci, Mol Imaging Ctr, Dept Mol Neuroimaging, Chiba 260, Japan.
[Minamimoto, Takafumi; Richmond, Barry J.] NIMH, Neuropsychol Lab, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Minamimoto, Takafumi] Japan Sci & Technol Agcy JST, PRESTO, Saitama, Japan.
RP Minamimoto, T (reprint author), Natl Inst Radiol Sci, Mol Imaging Ctr, Dept Mol Neuroimaging, Chiba 260, Japan.
EM minamoto@nirs.go.jp
RI Minamimoto, Takafumi/D-6610-2012
OI Minamimoto, Takafumi/0000-0003-4305-0174
FU Ministry of Education, Culture, Sports, Science and Technology, MEXT
Japan [KAKENHI 21012005, 23011006]; PRESTO/JST; National Institute of
Mental Health; JSPS
FX This research was supported by a Grant-in-Aid for Scientific Research on
Priority Areas, from the Ministry of Education, Culture, Sports, Science
and Technology, MEXT Japan (KAKENHI 21012005, 23011006 to TM),
PRESTO/JST (to TM), and Intramural Research Program of the National
Institute of Mental Health (to BJR). TM was partly supported by JSPS
Research Fellowship for Japanese Biomedical and Behavioral Researchers
at 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 20
TC 1
Z9 1
U1 1
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 7
PY 2012
VL 7
IS 11
AR e48434
DI 10.1371/journal.pone.0048434
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 048TK
UT WOS:000311935800061
PM 23144881
ER
PT J
AU Ryan, PE
Kales, SC
Yadavalli, R
Nau, MM
Zhang, H
Lipkowitz, S
AF Ryan, Philip E.
Kales, Stephen C.
Yadavalli, Rajgopal
Nau, Marion M.
Zhang, Han
Lipkowitz, Stanley
TI Cbl-c Ubiquitin Ligase Activity Is Increased via the Interaction of Its
RING Finger Domain with a LIM Domain of the Paxillin Homolog, Hic 5
SO PLOS ONE
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; CONFORMATIONAL-CHANGE; POSSIBLE INVOLVEMENT;
CONJUGATING ENZYME; ADHESION KINASE; FOCAL ADHESIONS; PROTEIN HIC-5;
ACTIVATION; SENESCENCE; COMPLEX
AB Cbl proteins (Cbl, Cbl-b and Cbl-c) are ubiquitin ligases that are critical regulators of tyrosine kinase signaling. In this study we identify a new Cbl-c interacting protein, Hydrogen peroxide Induced Construct 5 (Hic-5). The two proteins interact through a novel interaction mediated by the RING finger of Cbl-c and the LIM2 domain of Hic-5. Further, this interaction is mediated and dependent on specific zinc coordinating complexes within the RING finger and LIM domain. Binding of Hic-5 to Cbl-c leads to an increase in the ubiquitin ligase activity of Cbl-c once Cbl-c has been activated by Src phosphorylation or through an activating phosphomimetic mutation. In addition, co-transfection of Hic-5 with Cbl-c leads to an increase in Cblc mediated ubiquitination of the EGFR. These data suggest that Hic-5 enhances Cbl-c ubiquitin ligase activity once Cbl-c has been phosphorylated and activated. Interactions between heterologous RING fingers have been shown to activate E3s. This is the first demonstration of enhancement of ubiquitin ligase activity of a RING finger ubiquitin ligase by the direct interaction of a LIM zinc coordinating domain.
C1 [Ryan, Philip E.; Kales, Stephen C.; Yadavalli, Rajgopal; Nau, Marion M.; Zhang, Han; Lipkowitz, Stanley] NCI, Lab Cellular & Mol Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Ryan, Philip E.] George Washington Univ, Inst Biomed Sci, Washington, DC USA.
RP Lipkowitz, S (reprint author), NCI, Lab Cellular & Mol Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM lipkowis@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 48
TC 5
Z9 8
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 7
PY 2012
VL 7
IS 11
AR e49428
DI 10.1371/journal.pone.0049428
PG 13
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 048TK
UT WOS:000311935800258
PM 23145173
ER
PT J
AU Snyder, JS
Ferrante, SC
Cameron, HA
AF Snyder, Jason S.
Ferrante, Sarah C.
Cameron, Heather A.
TI Late Maturation of Adult-Born Neurons in the Temporal Dentate Gyrus
SO PLOS ONE
LA English
DT Article
ID GENERATED GRANULE CELLS; HIPPOCAMPAL NEUROGENESIS; VENTRAL HIPPOCAMPUS;
ENTORHINAL CORTEX; RAT HIPPOCAMPUS; FOS EXPRESSION; SPATIAL MEMORY;
TOTAL NUMBER; WATER MAZE; BEHAVIOR
AB Hippocampal function varies along its septotemporal axis, with the septal (dorsal) pole more frequently involved in spatial learning and memory and the temporal (ventral) pole playing a greater role in emotional behaviors. One feature that varies across these subregions is adult neurogenesis. New neurons are more numerous in the septal hippocampus but are more active in the temporal hippocampus during water maze training. However, many other aspects of adult neurogenesis remain unexplored in the context of septal versus temporal subregions. In addition, the dentate gyrus contains another functionally important anatomical division along the transverse axis, with the suprapyramidal blade showing greater experience-related activity than the infrapyramidal blade. Here we ask whether new neurons differ in their rates of survival and maturation along the septotemporal and transverse axes. We found that neurogenesis is initially higher in the infrapyramidal than suprapyramidal blade, but these cells are less likely to survive, resulting in similar densities of neurons in the two blades by four weeks. Across the septotemporal axis, neurogenesis was higher in septal than temporal pole, while the survival rate of new neurons did not differ. Maturation was assessed by immunostaining for the neuronal marker, NeuN, which increases in expression level with maturation, and for the immediate-early gene, Arc, which suggests a neuron is capable of undergoing activity-dependent synaptic plasticity. Maturation occurred approximately 1-2 weeks earlier in the septal pole than in the temporal pole. This suggests that septal neurons may contribute to function sooner; however, the prolonged maturation of new temporal neurons may endow them with a longer window of plasticity during which their functions could be distinct from those of the mature granule cell population. These data point to subregional differences in new neuron maturation and suggest that changes in neurogenesis could alter different hippocampus-dependent behaviors with different time courses.
C1 [Snyder, Jason S.; Ferrante, Sarah C.; Cameron, Heather A.] NIMH, Unit Neuroplast, NIH, Bethesda, MD 20892 USA.
RP Snyder, JS (reprint author), Univ British Columbia, Dept Psychol, Vancouver, BC, Canada.
EM jasonscottsnyder@psych.ubc.ca
RI Cameron, Heather/E-6221-2011;
OI Cameron, Heather/0000-0002-3245-5777; Snyder, Jason/0000-0002-5509-0272
FU National Institutes of Health, National Institute of Mental Health
[1ZIAMH002784]
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Mental Health,
1ZIAMH002784. The funders had no role in study design, data collection
and analysis, decision to publish, or preparation of the manuscript.
NR 66
TC 36
Z9 37
U1 0
U2 8
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 7
PY 2012
VL 7
IS 11
AR e48757
DI 10.1371/journal.pone.0048757
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 048TK
UT WOS:000311935800122
PM 23144957
ER
PT J
AU Matsubara, T
Tanaka, N
Krausz, KW
Manna, SK
Kang, DW
Anderson, ER
Luecke, H
Patterson, AD
Shah, YM
Gonzalez, FJ
AF Matsubara, Tsutomu
Tanaka, Naoki
Krausz, Kristopher W.
Manna, Soumen K.
Kang, Dong Wook
Anderson, Erik R.
Luecke, Hans
Patterson, Andrew D.
Shah, Yatrik M.
Gonzalez, Frank J.
TI Metabolomics Identifies an Inflammatory Cascade Involved in Dioxin- and
Diet-Induced Steatohepatitis
SO CELL METABOLISM
LA English
DT Article
ID ARYL-HYDROCARBON RECEPTOR; 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN TCDD;
DEFICIENT MICE; DBA/2J MICE; INDUCTION; TOXICITY; TERATOGENESIS;
DISRUPTION; MICROARRAY; EXPRESSION
AB 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is among the most potent environmentally toxic compounds. Serum metabolomics identified azelaic acid monoesters as significantly increased metabolites after TCDD treatment, due to downregulation of hepatic carboxylesterase 3 (CES3, also known as triglyceride hydrolase) expression in an arylhydrocarbon receptor (AhR)-dependent manner in mice. The decreased CES3 expression was accomplished by TODD-stimulated TGF beta-SMAD3 and IL6-STAT3 signaling, but not by direct AhR signaling. Methionine- and choline-deficient (MCD) diet-treated mice also showed enhanced serum azelaic acid monoester levels after attenuation of hepatic CES3 expression, while db/db mice did not, thus suggesting an association with steatohepatitis. Forced expression of CES3 reversed serum azelaic acid monoester/azelaic acid ratios and hepatic TGF beta mRNA levels in TCDD- and MCD diet-treated mice and ameliorated steatohepatitis induced by MCD diet. These results support the view that azelaic acid monoesters are possible indicators of TCDD exposure and steatohepatitis and suggest a link between CES3, TGF beta, and steatohepatitis.
C1 [Matsubara, Tsutomu; Tanaka, Naoki; Krausz, Kristopher W.; Manna, Soumen K.; Patterson, Andrew D.; Gonzalez, Frank J.] NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Kang, Dong Wook; Luecke, Hans] NIDDKD, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Anderson, Erik R.; Shah, Yatrik M.] Univ Michigan, Dept Mol & Integrat Physiol & Internal Med, Div Gastroenterol, Sch Med, Ann Arbor, MI 48109 USA.
RP Gonzalez, FJ (reprint author), NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM gonzalef@mail.nih.gov
RI Patterson, Andrew/G-3852-2012
OI Patterson, Andrew/0000-0003-2073-0070
FU National Cancer Institute Intramural Research Program, Center for Cancer
Research; Japanese Society for the Promotion of Science
FX This study was supported by the National Cancer Institute Intramural
Research Program, Center for Cancer Research. We thank John Buckley and
Linda Byrd for technical assistance (National Cancer Institute, NIH).
Lalage Wakefield (National Cancer Institute, NIH) provided the SMAD3
expression vector and the SMAD3-binding luciferase vector, Arthur
Hurwitz (National Cancer Institute, NIH) provided the STAT3 expression
vector and the STAT3-binding luciferase vector, and Shioko Kimura
(National Cancer Institute, NIH) furnished the CEBP alpha expression
vector. T.M. was supported by a fellowship from the Japanese Society for
the Promotion of Science.
NR 24
TC 32
Z9 32
U1 3
U2 32
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 7
PY 2012
VL 16
IS 5
BP 634
EP 644
DI 10.1016/j.cmet.2012.10.006
PG 11
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 046LE
UT WOS:000311765700012
PM 23140643
ER
PT J
AU Bayeva, M
Khechaduri, A
Puig, S
Chang, HC
Patial, S
Blackshear, PJ
Ardehali, H
AF Bayeva, Marina
Khechaduri, Arineh
Puig, Sergi
Chang, Hsiang-Chun
Patial, Sonika
Blackshear, Perry J.
Ardehali, Hossein
TI mTOR Regulates Cellular Iron Homeostasis through Tristetraprolin
SO CELL METABOLISM
LA English
DT Article
ID MESSENGER-RNA DEGRADATION; SIGNALING PATHWAY; MAMMALIAN TARGET;
DEFICIENCY; METABOLISM; PROTEIN; CELLS; SIROLIMUS; DISEASE; ALPHA
AB Iron is an essential cofactor with unique redox properties. Iron-regulatory proteins 1 and 2 (IRP1/2) have been established as important regulators of cellular iron homeostasis, but little is known about the role of other pathways in this process. Here we report that the mammalian target of rapamycin (mTOR) regulates iron homeostasis by modulating transferrin receptor 1 (TfR1) stability and altering cellular iron flux. Mechanistic studies identify tristetraprolin (TTP), a protein involved in anti-inflammatory response, as the downstream target of mTOR that binds to and enhances degradation of TfR1 mRNA. We also show that TTP is strongly induced by iron chelation, promotes downregulation of iron-requiring genes in both mammalian and yeast cells, and modulates survival in low-iron states. Taken together, our data uncover a link between metabolic, inflammatory, and iron-regulatory pathways, and point toward the existence of a yeast-like TTP-mediated iron conservation program in mammals.
C1 [Bayeva, Marina; Khechaduri, Arineh; Chang, Hsiang-Chun; Ardehali, Hossein] Northwestern Univ, Sch Med, Feinberg Cardiovasc Res Inst, Chicago, IL 60611 USA.
[Puig, Sergi] CSIC, Inst Agroquim & Tecnol Alimentos, Dept Biotecnol, Valencia 46100, Spain.
[Patial, Sonika; Blackshear, Perry J.] NIEHS, Lab Signal Transduct, Res Triangle Pk, NC 27709 USA.
RP Ardehali, H (reprint author), Northwestern Univ, Sch Med, Feinberg Cardiovasc Res Inst, Chicago, IL 60611 USA.
EM h-ardehali@northwestern.edu
RI Puig, Sergi/E-4788-2010
OI Puig, Sergi/0000-0002-1856-490X
FU Northwestern University Flow Cytometry Facility; Cancer Center Support
Grant [NCI CA060553]; American Heart Association [10PRE4430021]; NIH
[K02 HL107448, R01 HL104181, P01 HL108795, R01 HL087149]
FX We thank Dr. Seth A. Brooks for help with TTP RNA coIP experiments, Drs.
Sarah Rice, Navdeep Chandel, and Elizabeth Leibold for the critical
review of the manuscript, and Drs. William F.C. Rigby, M. Celeste Simon,
and Tracey A. Rouault for their generous gifts of the human TTP
antibody, ARNT KO MEFs, and IRP1 and 2 KO MEFs, respectively. This work
was supported by the Northwestern University Flow Cytometry Facility and
a Cancer Center Support Grant (NCI CA060553). M.B. and H.A. designed the
research. M.B., A.K., and S.P. performed the experiments and data
analysis. P.J.B and S.P. provided tools and reagents. M.B. wrote the
manuscript, which all authors commented on. H.A. supervised the project.
M.B. is supported by the American Heart Association 10PRE4430021. H.A.
is supported by NIH grants K02 HL107448, R01 HL104181, P01 HL108795, and
R01 HL087149.
NR 39
TC 23
Z9 23
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 7
PY 2012
VL 16
IS 5
BP 645
EP 657
DI 10.1016/j.cmet.2012.10.001
PG 13
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 046LE
UT WOS:000311765700013
PM 23102618
ER
PT J
AU Low, LA
Millecamps, M
Seminowicz, DA
Naso, L
Thompson, SJ
Stone, LS
Bushnell, MC
AF Low, Lucie A.
Millecamps, Magali
Seminowicz, David A.
Naso, Lina
Thompson, Scott J.
Stone, Laura S.
Bushnell, M. Catherine
TI Nerve injury causes long-term attentional deficits in rats
SO NEUROSCIENCE LETTERS
LA English
DT Article
DE Neuropathic pain; Cognition; Rat; Chronic pain; Attention; Longitudinal
study
ID CHRONIC BACK-PAIN; PERIPHERAL NEUROPATHIC PAIN; CHRONIC INFLAMMATORY
PAIN; TACTILE ALLODYNIA; BRAIN; MODEL; ANXIETY; AMYGDALA; BEHAVIOR;
MORPHINE
AB Human chronic pain sufferers frequently report problems with attention and concentration that affect daily functioning and quality of life. Chronic pain is also commonly associated with anxiety and depression. It is currently not known if the pain causes these co-morbidities, or if they are pre-disposing risk factors for the development of chronic pain. Animal studies suggest a possible causative effect of pain on cognition, but usually tests are conducted during acute ongoing pain when the pain may act as a distracter to normal cognitive and emotional processing. Here we examine long-term effects of nerve injury on cognitive functioning in a rat model, which contributes to better understanding of the relationship between cognitive impairment and chronic pain experience in human populations. This study investigated attentional capability, anxiety-like behavior and sensory functioning 6 months after spared nerve injury (SNI) surgery a time-point well beyond the acute pain phase and akin to decades of pain experience in humans. Male Long Evans rats subjected to nerve injury remained hypersensitive to sensory stimuli from the time of injury to the 6-month post-injury assessment. At 6 months they were impaired on a visual non-selective, non-sustained attention task and displayed anxiety-like behaviors in the elevated plus maze. These findings show that cognitive disturbances observed during acute pain persist for months in a rodent chronic pain model and suggest that cognitive alterations in chronic pain patients are at least partially caused by the chronic pain state. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
C1 [Low, Lucie A.; Millecamps, Magali; Naso, Lina; Thompson, Scott J.; Stone, Laura S.; Bushnell, M. Catherine] McGill Univ, Alan Edwards Ctr Res Pain, Montreal, PQ, Canada.
[Low, Lucie A.; Millecamps, Magali; Thompson, Scott J.; Stone, Laura S.; Bushnell, M. Catherine] McGill Univ, Fac Dent, Montreal, PQ, Canada.
[Stone, Laura S.; Bushnell, M. Catherine] McGill Univ, Dept Anesthesia, Montreal, PQ, Canada.
[Millecamps, Magali; Naso, Lina; Stone, Laura S.] McGill Univ, Montreal, PQ H3G 0G1, Canada.
[Seminowicz, David A.] Univ Maryland, Sch Dent, Dept Neural & Pain Sci, Baltimore, MD 21201 USA.
[Low, Lucie A.; Thompson, Scott J.; Bushnell, M. Catherine] McGill Univ, Montreal, PQ H3A 0C7, Canada.
RP Low, LA (reprint author), NIH, NCCAM, 10-CRC 4-1743,10 Ctr Dr, Bethesda, MD 20892 USA.
EM lucie.low@mail.mcgill.ca
RI Seminowicz, David/F-8732-2015;
OI Seminowicz, David/0000-0003-3111-3756; Low, Lucie/0000-0001-6082-8625
FU Pfizer Canada
FX This work was supported by a Neuropathic Pain Research grant from Pfizer
Canada.
NR 30
TC 19
Z9 19
U1 0
U2 13
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0304-3940
J9 NEUROSCI LETT
JI Neurosci. Lett.
PD NOV 7
PY 2012
VL 529
IS 2
BP 103
EP 107
DI 10.1016/j.neulet.2012.09.027
PG 5
WC Neurosciences
SC Neurosciences & Neurology
GA 039RK
UT WOS:000311264000001
PM 22999928
ER
PT J
AU Pitcher, D
Goldhaber, T
Duchaine, B
Walsh, V
Kanwisher, N
AF Pitcher, David
Goldhaber, Tanya
Duchaine, Bradley
Walsh, Vincent
Kanwisher, Nancy
TI Two Critical and Functionally Distinct Stages of Face and Body
Perception
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID HUMAN VISUAL-CORTEX; HUMAN EXTRASTRIATE CORTEX; SURFACE-BASED ANALYSIS;
OCCIPITOTEMPORAL CORTEX; MAGNETIC STIMULATION; DIRECTED ATTENTION;
OCCIPITAL FACE; NEURAL BASIS; AREA; TIME
AB Cortical regions that respond preferentially to particular object categories, such as faces and bodies, are essential for visual perception of these object categories. However, precisely when these regions play a causal role in recognition of their preferred categories is unclear. Here we addressed this question using transcranial magnetic stimulation (TMS). Across a series of experiments, TMS was delivered over the functionally localized right occipital face area (rOFA) or right extrastriate body area (rEBA) at different latencies, up to 150 ms, after stimulus onset while adult human participants performed delayed match-to-sample tasks on face and body stimuli. Results showed that TMS disrupted task performance during two temporally distinct time periods after stimulus onset, the first at 40/50 ms and the second at 100/110 ms. These two time periods exhibited functionally distinct patterns of impairment: TMS delivered during the early time period (at 40/50 ms) disrupted task performance for both preferred (faces at rOFA and bodies at rEBA) and nonpreferred (bodies at rOFA and faces at rEBA) categories. In contrast, TMS delivered during the later time period (at 100/110 ms) disrupted task performance for the preferred category only of each area (faces at rOFA and bodies at rEBA). These results indicate that category-selective cortical regions are critical for two functionally distinct stages of visual object recognition: an early, presumably preparatory stage that is not category selective occurring almost immediately after stimulus onset, followed by a later stage of category-specific perceptual processing.
C1 [Pitcher, David; Goldhaber, Tanya; Kanwisher, Nancy] MIT, McGovern Inst Brain Res, Cambridge, MA 02139 USA.
[Pitcher, David; Walsh, Vincent] UCL, Inst Cognit Neurosci, London WC1N 3AR, England.
[Duchaine, Bradley] Dartmouth Coll, Dept Psychol & Brain Sci, Hanover, NH 03755 USA.
RP Pitcher, D (reprint author), NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA.
EM david.pitcher@nih.gov
FU National Institutes of Health [EY13455]; Biotechnology and Biological
Sciences Research Council [BB/F022875/1]
FX This work was supported by National Institutes of Health Grant EY13455
(N.K.) and Biotechnology and Biological Sciences Research Council Grant
BB/F022875/1 (B. D. and V. W.). Thanks to Rebecca Lawson, Danny Dilks,
Julie Golomb, and Ed Vul.
NR 46
TC 27
Z9 27
U1 1
U2 15
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 7
PY 2012
VL 32
IS 45
BP 15877
EP 15885
DI 10.1523/JNEUROSCI.2624-12.2012
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 034AH
UT WOS:000310842000022
PM 23136426
ER
PT J
AU Furl, N
Hadj-Bouziane, F
Liu, N
Averbeck, BB
Ungerleider, LG
AF Furl, Nicholas
Hadj-Bouziane, Fadila
Liu, Ning
Averbeck, Bruno B.
Ungerleider, Leslie G.
TI Dynamic and Static Facial Expressions Decoded from Motion-Sensitive
Areas in the Macaque Monkey
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID SUPERIOR TEMPORAL SULCUS; FACE-PROCESSING NETWORK; POLYSENSORY AREA;
CONTRAST AGENT; IMPLIED MOTION; CORTEX; RECOGNITION; PERCEPTION;
IDENTITY; FMRI
AB Humans adeptly use visual motion to recognize socially relevant facial information. The macaque provides a model visual system for studying neural coding of expression movements, as its superior temporal sulcus (STS) possesses brain areas selective for faces and areas sensitive to visual motion. We used functional magnetic resonance imaging and facial stimuli to localize motion-sensitive areas [motion in faces (Mf) areas], which responded more to dynamic faces compared with static faces, and face-selective areas, which responded selectively to faces compared with objects and places. Using multivariate analysis, we found that information about both dynamic and static facial expressions could be robustly decoded from Mf areas. By contrast, face-selective areas exhibited relatively less facial expression information. Classifiers trained with expressions from one motion type (dynamic or static) showed poor generalization to the other motion type, suggesting that Mf areas employ separate and nonconfusable neural codes for dynamic and static presentations of the same expressions. We also show that some of the motion sensitivity elicited by facial stimuli was not specific to faces but could also be elicited by moving dots, particularly in fundus of the superior temporal and middle superior temporal polysensory/lower superior temporal areas, confirming their already well established low-level motion sensitivity. A different pattern was found in anterior STS, which responded more to dynamic than to static faces but was not sensitive to dot motion. Overall, we show that emotional expressions are mostly represented outside of face-selective cortex, in areas sensitive to motion. These regions may play a fundamental role in enhancing recognition of facial expression despite the complex stimulus changes associated with motion.
C1 [Furl, Nicholas; Averbeck, Bruno B.] NIMH, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA.
[Hadj-Bouziane, Fadila; Liu, Ning; Ungerleider, Leslie G.] NIMH, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
RP Furl, N (reprint author), Med Res Council Cognit & Brain Sci Unit, 15 Chaucer Rd, Cambridge CB2 7EF, England.
EM nick.furl@mrc-cbu.cam.ac.uk
RI Hadj-Bouziane, Fadila/A-1180-2013;
OI furl, nicholas/0000-0003-2488-1343
FU National Institute of Mental Health; United Kingdom Economic and Social
Research Council [RES-062-23-2925]
FX This work was supported by funding from the National Institute of Mental
Health Intramural Research Program to N.F., B. A., F. H-B., N.L., and L.
G. U and funding from the United Kingdom Economic and Social Research
Council (RES-062-23-2925) to N.F. We are grateful to our colleagues at
the National Institute of Mental Health: Fern Baldwin and Lucas Glover
for their help in training the animals; Jennifer Frihauf and Kathleen
Hansen for their help with stimulus preparation; Ziad Saad and Maria
Barsky for their help with data analysis; Frank Ye, Charles Zhu, Neal
Phelps, and Wenming Luh for their assistance during scanning, and George
Dold, David Ide, and Tom Talbot for technical assistance. Editorial
assistance for the article was provided by the National Institutes of
Health Fellows Editorial Board.
NR 56
TC 15
Z9 15
U1 3
U2 30
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 7
PY 2012
VL 32
IS 45
BP 15952
EP 15962
DI 10.1523/JNEUROSCI.1992-12.2012
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 034AH
UT WOS:000310842000029
PM 23136433
ER
PT J
AU Li, M
Craigie, R
AF Li, Min
Craigie, Robert
TI Retroviral Intasomes: Progress and Questions
SO STRUCTURE
LA English
DT Editorial Material
ID DNA STRAND TRANSFER; INTEGRATION; MECHANISM
C1 [Li, Min; Craigie, Robert] NIDDKD, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Craigie, R (reprint author), NIDDKD, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM bobc@helix.nih.gov
FU Intramural NIH HHS [ZIA DK036169-07]
NR 9
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0969-2126
J9 STRUCTURE
JI Structure
PD NOV 7
PY 2012
VL 20
IS 11
BP 1804
EP 1805
DI 10.1016/j.str.2012.10.004
PG 2
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 034GR
UT WOS:000310861400004
PM 23141692
ER
PT J
AU Freudenthal, BD
Beard, WA
Wilson, SH
AF Freudenthal, Bret D.
Beard, William A.
Wilson, Samuel H.
TI Structures of dNTP Intermediate States during DNA Polymerase Active Site
Assembly
SO STRUCTURE
LA English
DT Article
ID BASE EXCISION-REPAIR; METAL-IONS; GASTRIC-CANCER; BETA STRUCTURE;
MECHANISM; FIDELITY; DISCRIMINATION; CONFORMATION; COMPLEXES; EXTENSION
AB DNA polymerase and substrate conformational changes are essential for high-fidelity DNA synthesis. Structures of DNA polymerase (pol) beta in complex with DNA show the enzyme in an "open" conformation. Subsequent to binding the nucleotide, the polymerase "closes" around the nascent base pair with two metals positioned for chemistry. However, structures of substrate/active site intermediates prior to closure are lacking. By destabilizing the closed complex, we determined unique ternary complex structures of pol beta with correct and incorrect incoming nucleotides bound to the open conformation. These structures reveal that Watson-Crick hydrogen bonding is assessed upon initial complex formation. Importantly, nucleotide-bound states representing intermediate metal coordination states occur with active site assembly. The correct, but not incorrect, nucleotide maintains Watson-Crick hydrogen bonds during interconversion of these states. These structures indicate that the triphosphate of the incoming nucleotide undergoes rearrangement prior to closure, providing an opportunity to deter misinsertion and increase fidelity.
C1 [Freudenthal, Bret D.; Beard, William A.; Wilson, Samuel H.] NIEHS, Lab Struct Biol, NIH, Res Triangle Pk, NC 27709 USA.
RP Wilson, SH (reprint author), NIEHS, Lab Struct Biol, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM wilson5@niehs.nih.gov
FU National Institutes of Health, National Institute of Environmental
Health Sciences [Z01-ES050158, Z01-ES050161]; National Institutes of
Health [1U19CA105010]
FX We thank Drs. R.E. London, L.C. Pedersen, and V.K. Batra for critical
reading of the manuscript and Dr. C.E. McKenna for the
alpha,beta-difluoromethylene dCTP analog. This research was supported by
Research Project Numbers Z01-ES050158 and Z01-ES050161 to S.H.W. in the
Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences and was in
association with the National Institutes of Health Grant 1U19CA105010.
B.D.F., W.A.B., and S.H.W. designed the research; B.D.F., W.A.B., and
S.H.W. analyzed data; B.D.F. performed research; and B.D.F., W.A.B., and
S.H.W. wrote the paper.
NR 37
TC 18
Z9 18
U1 0
U2 9
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0969-2126
EI 1878-4186
J9 STRUCTURE
JI Structure
PD NOV 7
PY 2012
VL 20
IS 11
BP 1829
EP 1837
DI 10.1016/j.str.2012.08.008
PG 9
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 034GR
UT WOS:000310861400008
PM 22959623
ER
PT J
AU Daviglus, ML
Talavera, GA
Aviles-Santa, ML
Allison, M
Cai, J
Criqui, MH
Gellman, M
Giachello, AL
Gouskova, N
Kaplan, RC
LaVange, L
Penedo, F
Perreira, K
Pirzada, A
Schneiderman, N
Wassertheil-Smoller, S
Sorlie, PD
Stamler, J
AF Daviglus, Martha L.
Talavera, Gregory A.
Aviles-Santa, M. Larissa
Allison, Matthew
Cai, Jianwen
Criqui, Michael H.
Gellman, Marc
Giachello, Aida L.
Gouskova, Natalia
Kaplan, Robert C.
LaVange, Lisa
Penedo, Frank
Perreira, Krista
Pirzada, Amber
Schneiderman, Neil
Wassertheil-Smoller, Sylvia
Sorlie, Paul D.
Stamler, Jeremiah
TI Prevalence of Major Cardiovascular Risk Factors and Cardiovascular
Diseases Among Hispanic/Latino Individuals of Diverse Backgrounds in the
United States
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID NUTRITION EXAMINATION SURVEY; CORONARY HEART-DISEASE; MEXICAN-AMERICANS;
MYOCARDIAL-INFARCTION; NATIONAL-HEALTH; LATIN-AMERICAN; PUERTO-RICANS;
ACCULTURATION; ADULTS; HYPERTENSION
AB Context Major cardiovascular diseases (CVDs) are leading causes of mortality among US Hispanic and Latino individuals. Comprehensive data are limited regarding the prevalence of CVD risk factors in this population and relations of these traits to socioeconomic status (SES) and acculturation.
Objectives To describe prevalence of major CVD risk factors and CVD (coronary heart disease [CHD] and stroke) among US Hispanic/Latino individuals of different backgrounds, examine relationships of SES and acculturation with CVD risk profiles and CVD, and assess cross-sectional associations of CVD risk factors with CVD.
Design, Setting, and Participants Multicenter, prospective, population-based Hispanic Community Health Study/Study of Latinos including individuals of Cuban(n=2201), Dominican (n=1400), Mexican (n=6232), Puerto Rican (n=2590), Central American (n=1634), and South American backgrounds(n=1022) aged 18 to 74 years. Analyses involved 15 079 participants with complete data enrolled between March 2008 and June 2011.
Main Outcome Measures Adverse CVD risk factors defined using national guidelines for hypercholesterolemia, hypertension, obesity, diabetes, and smoking. Prevalence of CHD and stroke were ascertained from self-reported data.
Results Age-standardized prevalence of CVD risk factors varied by Hispanic/Latino background; obesity and current smoking rates were highest among Puerto Rican participants (for men, 40.9% and 34.7%; for women, 51.4% and 31.7%, respectively); hypercholesterolemia prevalence was highest among Central American men (54.9%) and Puerto Rican women (41.0%). Large proportions of participants (80% of men, 71% of women) had at least 1 risk factor. Age-and sex-adjusted prevalence of 3 or more risk factors was highest in Puerto Rican participants (25.0%) and significantly higher (P<.001) among participants with less education (16.1%), those who were US-born (18.5%), those who had lived in the United States 10 years or longer (15.7%), and those who preferred English (17.9%). Overall, self-reported CHD and stroke prevalence were low (4.2% and 2.0% in men; 2.4% and 1.2% in women, respectively). In multivariate-adjusted models, hypertension and smoking were directly associated with CHD in both sexes as were hypercholesterolemia and obesity in women and diabetes in men (odds ratios [ORs], 1.5-2.2). For stroke, associations were positive with hypertension in both sexes, diabetes in men, and smoking in women (ORs, 1.7-2.6).
Conclusion Among US Hispanic/Latino adults of diverse backgrounds, a sizeable proportion of men and women had adverse major risk factors; prevalence of adverse CVD risk profiles was higher among participants with Puerto Rican background, lower SES, and higher levels of acculturation.
C1 [Daviglus, Martha L.] Univ Illinois, Inst Minor Hlth Res, Dept Med, Gen Internal Med Sect, Chicago, IL 60612 USA.
[Talavera, Gregory A.] San Diego State Univ, Grad Sch Publ Hlth, San Diego, CA 92182 USA.
[Aviles-Santa, M. Larissa; Sorlie, Paul D.] NHLBI, Div Cardiovasc Sci, NIH, Bethesda, MD 20892 USA.
[Allison, Matthew; Criqui, Michael H.] Univ Calif San Diego, Dept Family & Prevent Med, La Jolla, CA 92093 USA.
[Cai, Jianwen; Gouskova, Natalia; LaVange, Lisa; Perreira, Krista] Univ N Carolina, Collaborat Studies Coordinating Ctr, Chapel Hill, NC USA.
[Gellman, Marc; Schneiderman, Neil] Univ Miami, Dept Psychol, Behav Med Res Ctr, Miami, FL USA.
[Daviglus, Martha L.; Giachello, Aida L.; Pirzada, Amber; Stamler, Jeremiah] Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
[Penedo, Frank] Northwestern Univ, Feinberg Sch Med, Dept Med Social Sci, Chicago, IL 60611 USA.
[Kaplan, Robert C.; Wassertheil-Smoller, Sylvia] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA.
RP Daviglus, ML (reprint author), Univ Illinois, Inst Minor Hlth Res, Dept Med, Gen Internal Med Sect, 1819 W Polk St,Ste 246, Chicago, IL 60612 USA.
EM daviglus@uic.edu
OI Gouskova, Natalia/0000-0001-7488-5014; Allison,
Matthew/0000-0003-0777-8272
FU National Heart, Lung, and Blood Institute (NHLBI) [N01-HC65233,
N01-HC65234, N01-HC65235, N01-HC65236, N01-HC65237]; National Center on
Minority Health and Health Disparities; National Institute on Deafness
and Other Communications Disorders; National Institute of Dental and
Craniofacial Research; National Institute of Diabetes and Digestive and
Kidney Diseases; National Institute of Neurological Disorders and
Stroke; Office of Dietary Supplements
FX The Hispanic Community Health Study/Study of Latinos was carried out as
a collaborative study supported by contracts from the National Heart,
Lung, and Blood Institute (NHLBI) to the University of North Carolina
(N01-HC65233), University of Miami (N01-HC65234), Albert Einstein
College of Medicine (N01-HC65235), Northwestern University
(N01-HC65236), and San Diego State University (N01-HC65237). The
following institutes, centers, or offices contribute to the HCHS/SOL
through a transfer of funds to the NHLBI: National Center on Minority
Health and Health Disparities, the National Institute on Deafness and
Other Communications Disorders, the National Institute of Dental and
Craniofacial Research, the National Institute of Diabetes and Digestive
and Kidney Diseases, the National Institute of Neurological Disorders
and Stroke, and the Office of Dietary Supplements.
NR 35
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U2 32
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 7
PY 2012
VL 308
IS 17
BP 1775
EP 1784
DI 10.1001/jama.2012.14517
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 032NR
UT WOS:000310726500024
PM 23117778
ER
PT J
AU Lauer, MS
AF Lauer, Michael S.
TI Time for a Creative Transformation of Epidemiology in the United States
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
ID BLOOD INSTITUTE; NATIONAL HEART; LUNG
C1 NHLBI, Off Director, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
RP Lauer, MS (reprint author), NHLBI, Off Director, 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 16
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Z9 30
U1 0
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 7
PY 2012
VL 308
IS 17
BP 1804
EP 1805
DI 10.1001/jama.2012.14838
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 032NR
UT WOS:000310726500028
PM 23117782
ER
PT J
AU Towers, S
Chowell, G
AF Towers, S.
Chowell, G.
TI Impact of weekday social contact patterns on the modeling of influenza
transmission, and determination of the influenza latent period
SO JOURNAL OF THEORETICAL BIOLOGY
LA English
DT Article
DE Epidemic model; Weekday contact patterns; Influenza latent period;
Influenza incubation period; Pandemic influenza model
ID PANDEMIC INFLUENZA; A H1N1; INFECTIOUS-DISEASES; UNITED-STATES; SIR
MODEL; SCHOOL; SEASONALITY; OUTBREAK; PREDICT; CLOSURE
AB Human social contact patterns show marked day-of-week variations, with a higher frequency of contacts occurring during weekdays when children are in school, and adults are in contact with co-workers, than typically occur on weekends. Using epidemic modeling, we show that using the average of social contacts during the week in the model yields virtually identical predictions of epidemic final size and the timing of the epidemic incidence peak as a model that incorporates weekday social contact patterns. This is true of models with a constant weekly average contact rate throughout the year, and also of models that assume seasonality of transmission.
Our modeling studies reveal, however, that weekday social contact patterns can produce substantial weekday variations in an influenza incidence curve, and the pattern of variation is sensitive to the influenza latent period. The possible observability of weekday patterns in daily influenza incidence data opens up an interesting avenue of further inquiry that can shed light on the latent period of pandemic influenza. The duration of the latent period must be known with precision in order to design effective disease intervention strategies, such as use of antivirals. For a hypothetical influenza pandemic, we thus perform a simulation study to determine the number of cases needed to observe the weekday variation pattern in influenza epidemic incidence data. Our studies suggest that these patterns should be observable at 95% confidence in daily influenza hospitalization data from large cities over 75% of the time.
Using 2009 A(H1N1) daily case data recorded by a large hospital in Santiago, Chile, we show that significant weekday incidence patterns are evident. From these weekday incidence patterns, we estimate the latent period of influenza to be [0.04, 0.60] days (95% CI). This method for determination of the influenza latent period in a community setting is novel, and unique in its approach. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Towers, S.] Purdue Univ, W Lafayette, IN 47907 USA.
[Towers, S.; Chowell, G.] Arizona State Univ, Tempe, AZ USA.
[Chowell, G.] NIH, Div Epidemiol & Populat Studies, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Towers, S (reprint author), Purdue Univ, W Lafayette, IN 47907 USA.
EM stowers@purdue.edu
RI Chowell, Gerardo/F-5038-2012
OI Chowell, Gerardo/0000-0003-2194-2251
FU NSF [DMS-1022758]; Fogarty International Center, NIH
FX This research is partially supported by NSF grant DMS-1022758 (ST) and
by the Fogarty International Center, NIH (GC).
NR 46
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U1 3
U2 17
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0022-5193
EI 1095-8541
J9 J THEOR BIOL
JI J. Theor. Biol.
PD NOV 7
PY 2012
VL 312
BP 87
EP 95
DI 10.1016/j.jtbi.2012.07.023
PG 9
WC Biology; Mathematical & Computational Biology
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
Biology
GA 014KB
UT WOS:000309373400009
PM 22871362
ER
PT J
AU Abdeladhim, M
Jochim, RC
Ben Ahmed, M
Zhioua, E
Chelbi, I
Cherni, S
Louzir, H
Ribeiro, JMC
Valenzuela, JG
AF Abdeladhim, Maha
Jochim, Ryan C.
Ben Ahmed, Melika
Zhioua, Elyes
Chelbi, Ifhem
Cherni, Saifedine
Louzir, Hechmi
Ribeiro, Jose M. C.
Valenzuela, Jesus G.
TI Updating the Salivary Gland Transcriptome of Phlebotomus papatasi
(Tunisian Strain): The Search for Sand Fly-Secreted Immunogenic Proteins
for Humans
SO PLOS ONE
LA English
DT Article
ID GLOSSINA-MORSITANS-MORSITANS; DELAYED-TYPE HYPERSENSITIVITY;
LUTZOMYIA-LONGIPALPIS; CUTANEOUS LEISHMANIASIS; VISCERAL LEISHMANIASIS;
CIMEX-LECTULARIUS; ANTIBODY-RESPONSE; IMMUNE-RESPONSE; TSETSE-FLY; BED
BUG
AB Introduction: Sand fly saliva plays an important role in both blood feeding and outcome of Leishmania infection. A cellular immune response against a Phlebotomus papatasi salivary protein was shown to protect rodents against Leishmania major infection. In humans, P. papatasi salivary proteins induce a systemic cellular immune response as well as a specific antisaliva humoral immune response, making these salivary proteins attractive targets as markers of exposure for this Leishmania vector. Surprisingly, the repertoire of salivary proteins reported for P. papatasi-a model sand fly for Leishmania-vector-host molecular interactions-is very limited compared with other sand fly species. We hypothesize that a more comprehensive study of the transcripts present in the salivary glands of P. papatasi will provide better knowledge of the repertoire of proteins of this important vector and will aid in selection of potential immunogenic proteins for humans and of those proteins that are highly conserved between different sand fly strains.
Methods and Findings: A cDNA library from P. papatasi (Tunisian strain) salivary glands was constructed, and randomly selected transcripts were sequenced and analyzed. The most abundant transcripts encoding secreted proteins were identified and compared with previously reported sequences. Importantly, we identified salivary proteins not described before in this sand fly species.
Conclusions: Comparative analysis between the salivary proteins of P. papatasi from Tunisia and Israel strains shows a high level of identity, suggesting these proteins as potential common targets for markers of vector exposure or inducers of cellular immune responses in humans for different geographic areas.
C1 [Jochim, Ryan C.; Valenzuela, Jesus G.] NIAID, Vector Mol Biol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
[Abdeladhim, Maha; Ben Ahmed, Melika; Louzir, Hechmi] Pasteur Inst Tunis, Lab Transmiss Control & Immunobiol Infect Dis, Tunis, Tunisia.
[Ben Ahmed, Melika; Louzir, Hechmi] Tunis El Manar Univ, Fac Med Tunis, Tunis, Tunisia.
[Zhioua, Elyes; Chelbi, Ifhem; Cherni, Saifedine] Pasteur Inst Tunis, Lab Vector Ecol, Tunis, Tunisia.
[Ribeiro, Jose M. C.] NIAID, Vector Biol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
RP Valenzuela, JG (reprint author), NIAID, Vector Mol Biol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
EM jvalenzuela@niaid.nih.gov
RI Jochim, Ryan/C-6756-2013; Ribeiro, Jose/J-7011-2015
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases (NIAID)
FX The study was funded by the Division of Intramural Research, National
Institute of Allergy and Infectious Diseases (NIAID). The funders had no
role in study design, data collection and analysis, decision to publish,
or preparation of the manuscript.
NR 48
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U1 0
U2 14
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 6
PY 2012
VL 7
IS 11
AR e47347
DI 10.1371/journal.pone.0047347
PG 16
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 040IE
UT WOS:000311315300007
PM 23139741
ER
PT J
AU Baysan, M
Bozdag, S
Cam, MC
Kotliarova, S
Ahn, S
Walling, J
Killian, JK
Stevenson, H
Meltzer, P
Fine, HA
AF Baysan, Mehmet
Bozdag, Serdar
Cam, Margaret C.
Kotliarova, Svetlana
Ahn, Susie
Walling, Jennifer
Killian, Jonathan K.
Stevenson, Holly
Meltzer, Paul
Fine, Howard A.
TI G-Cimp Status Prediction Of Glioblastoma Samples Using mRNA Expression
Data
SO PLOS ONE
LA English
DT Article
ID VALIDATION; MICROARRAY; SUBTYPES
AB Glioblastoma Multiforme (GBM) is a tumor with high mortality and no known cure. The dramatic molecular and clinical heterogeneity seen in this tumor has led to attempts to define genetically similar subgroups of GBM with the hope of developing tumor specific therapies targeted to the unique biology within each of these subgroups. Recently, a subset of relatively favorable prognosis GBMs has been identified. These glioma CpG island methylator phenotype, or G-CIMP tumors, have distinct genomic copy number aberrations, DNA methylation patterns, and (mRNA) expression profiles compared to other GBMs. While the standard method for identifying G-CIMP tumors is based on genome-wide DNA methylation data, such data is often not available compared to the more widely available gene expression data. In this study, we have developed and evaluated a method to predict the G-CIMP status of GBM samples based solely on gene expression data.
C1 [Baysan, Mehmet; Cam, Margaret C.; Kotliarova, Svetlana; Ahn, Susie; Walling, Jennifer; Fine, Howard A.] NCI, Neurooncol Branch, NIH, Bethesda, MD 20892 USA.
[Bozdag, Serdar] Marquette Univ, Dept Math Stat & Comp Sci, Milwaukee, WI 53233 USA.
[Killian, Jonathan K.; Stevenson, Holly; Meltzer, Paul] NCI, Genet Branch, NIH, Bethesda, MD 20892 USA.
[Fine, Howard A.] NYU, Inst Canc, Langone Med Ctr, New York, NY USA.
RP Fine, HA (reprint author), NCI, Neurooncol Branch, NIH, Bethesda, MD 20892 USA.
EM Howard.Fine@nyumc.org
FU National Institutes of Health Intramural Research Program
FX This study was funded through the National Institutes of Health
Intramural Research Program. The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
NR 17
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Z9 10
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 6
PY 2012
VL 7
IS 11
AR e47839
DI 10.1371/journal.pone.0047839
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 040IE
UT WOS:000311315300013
PM 23139755
ER
PT J
AU Khaibullina, A
Kenyon, N
Guptill, V
Quezado, MM
Wang, L
Koziol, D
Wesley, R
Moya, PR
Zhang, ZJ
Saha, A
Mukherjee, AB
Quezado, ZMN
AF Khaibullina, Alfia
Kenyon, Nicholas
Guptill, Virginia
Quezado, Martha M.
Wang, Li
Koziol, Deloris
Wesley, Robert
Moya, Pablo R.
Zhang, Zhongjian
Saha, Arjun
Mukherjee, Anil B.
Quezado, Zenaide M. N.
TI In a Model of Batten Disease, Palmitoyl Protein Thioesterase-1
Deficiency Is Associated with Brown Adipose Tissue and Thermoregulation
Abnormalities
SO PLOS ONE
LA English
DT Article
ID NEURONAL CEROID-LIPOFUSCINOSIS; ENERGY-METABOLISM; NONSHIVERING
THERMOGENESIS; ACTIVATION; MICE; INCL; NEURODEGENERATION; APOPTOSIS;
UCP1; FAT
AB Infantile neuronal ceroid lipofuscinosis (INCL) is a fatal neurodegenerative disorder caused by a deficiency of palmitoyl-protein thioesterase-1 (PPT1). We have previously shown that children with INCL have increased risk of hypothermia during anesthesia and that PPT1-deficiency in mice is associated with disruption of adaptive energy metabolism, downregulation of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1 alpha), and mitochondrial dysfunction. Here we hypothesized that Ppt1-knockout mice, a well-studied model of INCL that shows many of the neurologic manifestations of the disease, would recapitulate the thermoregulation impairment observed in children with INCL. We also hypothesized that when exposed to cold, Ppt1-knockout mice would be unable to maintain body temperature as in mice thermogenesis requires upregulation of Pgc-1 alpha and uncoupling protein 1 (Ucp-1) in brown adipose tissue. We found that the Ppt1-KO mice had lower basal body temperature as they aged and developed hypothermia during cold exposure. Surprisingly, this inability to maintain body temperature during cold exposure in Ppt1-KO mice was associated with an adequate upregulation of Pgc-1 alpha and Ucp-1 but with lower levels of sympathetic neurotransmitters in brown adipose tissue. In addition, during baseline conditions, brown adipose tissue of Ppt1-KO mice had less vacuolization (lipid droplets) compared to wild-type animals. After cold stress, wild-type animals had significant decreases whereas Ppt1-KO had insignificant changes in lipid droplets compared with baseline measurements, thus suggesting that Ppt1-KO had less lipolysis in response to cold stress. These results uncover a previously unknown phenotype associated with PPT1 deficiency, that of altered thermoregulation, which is associated with impaired lipolysis and neurotransmitter release to brown adipose tissue during cold exposure. These findings suggest that INCL should be added to the list of neurodegenerative diseases that are linked to alterations in peripheral metabolic processes. In addition, extrapolating these findings clinically, impaired thermoregulation and hypothermia are potential risks in patients with INCL.
C1 [Khaibullina, Alfia; Kenyon, Nicholas; Wang, Li; Quezado, Zenaide M. N.] Childrens Natl Med Ctr, Sheikh Zayed Inst Pediat Surg Innovat, Washington, DC 20010 USA.
[Guptill, Virginia; Quezado, Zenaide M. N.] NIH, Dept Perioperat Med, Ctr Clin, Bethesda, MD 20892 USA.
[Quezado, Martha M.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Koziol, Deloris; Wesley, Robert] NIH, Biostat & Clin Epidemiol Serv, Off Director, Ctr Clin, Bethesda, MD USA.
[Moya, Pablo R.] NIMH, Clin Sci Lab, NIH, Bethesda, MD 20892 USA.
[Zhang, Zhongjian; Saha, Arjun; Mukherjee, Anil B.] NICHHD, Sect Dev Genet, Program Dev Endocrinol & Genet, NIH, Bethesda, MD 20892 USA.
RP Quezado, ZMN (reprint author), Childrens Natl Med Ctr, Sheikh Zayed Inst Pediat Surg Innovat, Washington, DC 20010 USA.
EM zquezado@cnmc.org
RI Quezado, Zenaide/O-4860-2016
OI Quezado, Zenaide/0000-0001-9793-4368
FU Intramural Research Program of the National Institutes of Health, NIH
Clinical Center; Eunice Kennedy Shriver National Institute of Child
Health and Human Development, Bethesda, MD; Sheikh Zayed Institute for
Pediatric Surgical Innovation, Children's National Medical Center,
Washington, DC
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, NIH Clinical Center, the Eunice Kennedy
Shriver National Institute of Child Health and Human Development,
Bethesda, MD, and the The Sheikh Zayed Institute for Pediatric Surgical
Innovation, Children's National Medical Center, Washington, DC. The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 41
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Z9 1
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 6
PY 2012
VL 7
IS 11
AR e48733
DI 10.1371/journal.pone.0048733
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 040IE
UT WOS:000311315300053
PM 23139814
ER
PT J
AU Langlais, KK
Brown, JL
Kassis, JA
AF Langlais, Kristofor K.
Brown, J. Lesley
Kassis, Judith A.
TI Polycomb Group Proteins Bind an engrailed PRE in Both the "ON" and "OFF"
Transcriptional States of engrailed
SO PLOS ONE
LA English
DT Article
ID DROSOPHILA BITHORAX COMPLEX; GROUP RESPONSE ELEMENTS;
CUBITUS-INTERRUPTUS; CELLULAR MEMORY; PCG PROTEINS; GENOME-WIDE;
MELANOGASTER; MECHANISMS; EXPRESSION; GENES
AB Polycomb group (PcG) and trithorax Group (trxG) proteins maintain the "OFF" and "ON" transcriptional states of HOX genes and other targets by modulation of chromatin structure. In Drosophila, PcG proteins are bound to DNA fragments called Polycomb group response elements (PREs). The prevalent model holds that PcG proteins bind PREs only in cells where the target gene is "OFF". Another model posits that transcription through PREs disrupts associated PcG complexes, contributing to the establishment of the "ON" transcriptional state. We tested these two models at the PcG target gene engrailed. engrailed exists in a gene complex with invected, which together have 4 well-characterized PREs. Our data show that these PREs are not transcribed in embryos or larvae. We also examined whether PcG proteins are bound to an engrailed PRE in cells where engrailed is transcribed. By FLAG-tagging PcG proteins and expressing them specifically where engrailed is "ON" or "OFF", we determined that components of three major PcG protein complexes are present at an engrailed PRE in both the "ON" and "OFF" transcriptional states in larval tissues. These results show that PcG binding per se does not determine the transcriptional state of engrailed.
C1 [Langlais, Kristofor K.; Brown, J. Lesley; Kassis, Judith A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
RP Kassis, JA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
EM jkassis@mail.nih.gov
FU Intramural Research Program of the NIH/NICHD
FX This research was supported by the Intramural Research Program of the
NIH/NICHD. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 40
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Z9 9
U1 0
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 6
PY 2012
VL 7
IS 11
AR e48765
DI 10.1371/journal.pone.0048765
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 040IE
UT WOS:000311315300056
PM 23139817
ER
PT J
AU Rothfuchs, AG
Roffe, E
Gibson, A
Cheever, AW
Ezekowitz, RAB
Takahashi, K
Steindel, M
Sher, A
Bafica, A
AF Rothfuchs, Antonio Gigliotti
Roffe, Ester
Gibson, Amanda
Cheever, Allen W.
Ezekowitz, R. Alan B.
Takahashi, Kazue
Steindel, Mario
Sher, Alan
Bafica, Andre
TI Mannose-Binding Lectin Regulates Host Resistance and Pathology during
Experimental Infection with Trypanosoma cruzi
SO PLOS ONE
LA English
DT Article
ID CHAGAS-DISEASE; MAMMALIAN-CELLS; DEFICIENT MICE; PROTEIN; TISSUE; SERUM;
SUSCEPTIBILITY; AMASTIGOTES; CARDIOMYOPATHY; RECOGNITION
AB Mannose-binding lectin (MBL) is a humoral pattern-recognition molecule important for host defense. Although recent genetic studies suggest an involvement of MBL/MASP2-associated pathways in Chagas' disease, it is currently unknown whether MBL plays a role in host resistance to the intracellular protozoan Trypanosoma cruzi, the causative agent of Chagas' disease. In this study we employed MBL-/- mice to assess the role of MBL in resistance to experimental infection with T. cruzi. T. cruzi infection enhanced tissue expression of MBL both at the mRNA and protein level. Similarly, symptomatic acute Chagas' disease patients displayed increased serum concentrations of MBL compared to patients with indeterminate, asymptomatic forms of the disease. Furthermore, increased parasite loads in the blood and/or tissue were observed in MBL-/- mice compared to WT controls. This was associated with reduced systemic levels of IL-12/23p40 in MBL-/- mice. Importantly, MBL-/- mice infected with a cardiotropic strain of T. cruzi displayed increased myocarditis and cardiac fibrosis compared to WT controls. The latter was accompanied by elevated hydroxyproline content and mRNA levels of collagen-1 and -6 in the heart. These observations point to a previously unappreciated role for MBL in regulating host resistance and cardiac inflammation during infection with a major human pathogen.
C1 [Rothfuchs, Antonio Gigliotti; Gibson, Amanda; Cheever, Allen W.; Sher, Alan] NIAID, Immunobiol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Roffe, Ester] NIAID, Mol Signaling Sect, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Cheever, Allen W.] Biomed Res Inst, Rockville, MD 20852 USA.
[Ezekowitz, R. Alan B.; Takahashi, Kazue] Harvard Univ, Sch Med, Dept Pediat, Lab Dev Immunol,Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Rothfuchs, Antonio Gigliotti] Karolinska Inst, Dept Microbiol Tumor & Cell Biol MTC, Stockholm, Sweden.
[Steindel, Mario; Bafica, Andre] Univ Fed Santa Catarina, Dept Microbiol Immunol & Parasitol, Florianopolis, SC, Brazil.
RP Rothfuchs, AG (reprint author), NIAID, Immunobiol Sect, Parasit Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM antonio.rothfuchs@ki.se; andre.bafica@ufsc.br
RI Rothfuchs, Antonio/F-5981-2013; Vacinas, Inct/J-9431-2013; Roffe,
Ester/H-4688-2012
OI Rothfuchs, Antonio/0000-0001-6001-7240;
FU Intramural Research Program of the NIAID; EU [FP7-MC-IRG-247684];
Swedish Society for Medicine
FX This work was supported by the Intramural Research Program of the NIAID.
AB and MS are CNPq senior research fellows. AGR is a recipient of a
Marie Curie International Reintegration grant from the EU
(FP7-MC-IRG-247684) and a project grant from the Swedish Society for
Medicine. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 54
TC 7
Z9 8
U1 1
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 6
PY 2012
VL 7
IS 11
AR e47835
DI 10.1371/journal.pone.0047835
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 040IE
UT WOS:000311315300012
PM 23139754
ER
PT J
AU Fernandes, AM
Fero, K
Arrenberg, AB
Bergeron, SA
Driever, W
Burgess, HA
AF Fernandes, Antonio M.
Fero, Kandice
Arrenberg, Aristides B.
Bergeron, Sadie A.
Driever, Wolfgang
Burgess, Harold A.
TI Deep Brain Photoreceptors Control Light-Seeking Behavior in Zebrafish
Larvae
SO CURRENT BIOLOGY
LA English
DT Article
ID EXTRARETINAL PHOTORECEPTORS; ABLATION; CELLS; HYPOTHALAMUS; PHYSIOLOGY;
VISION; MICE; RAT
AB Most vertebrates process visual information using elaborately structured photosensory tissues, including the eyes and pineal. However, there is strong evidence that other tissues can detect and respond to photic stimuli [1-3]. Many reports suggest that photosensitive elements exist within the brain itself and influence physiology and behavior; however, a long-standing puzzle has been the identity of the neurons and photoreceptor molecules involved [4, 5]. We tested whether light cues influence behavior in zebrafish larvae through deep brain photosensors. We found that larvae lacking eyes and pineal perform a simple light-seeking behavior triggered by loss of illumination ("dark photokinesis"). Neuroanatomical considerations prompted us to test orthopedia(otpa)-deficient fish, which show a profound reduction in dark photokinesis. Using targeted genetic ablations, we narrowed the photosensitive region to neurons in the preoptic area. Neurons in this region express several photoreceptive molecules, but expression of the melanopsin opn4a is selectively lost in otpa mutants, suggesting that opn4a mediates dark photokinesis. Our findings shed light on the identity and function of deep brain photoreceptors and suggest that otpa specifies an ancient population of sensory neurons that mediate behavioral responses to light.
C1 [Fero, Kandice; Bergeron, Sadie A.; Burgess, Harold A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Genom Differentiat, Bethesda, MD 20892 USA.
[Fernandes, Antonio M.; Arrenberg, Aristides B.; Driever, Wolfgang] Univ Freiburg, Dev Biol Unit, Fac Biol, BIOSS Ctr Biol Signalling Studies, D-79104 Freiburg, Germany.
[Fernandes, Antonio M.; Arrenberg, Aristides B.; Driever, Wolfgang] Univ Freiburg, FRIAS Freiburg Inst Adv Studies, D-79104 Freiburg, Germany.
RP Burgess, HA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Genom Differentiat, Bethesda, MD 20892 USA.
EM burgessha@mail.nih.gov
RI Burgess, Harold/B-8474-2015;
OI Burgess, Harold/0000-0003-1966-7801; Bergeron, Sadie/0000-0002-1238-8730
FU National Institute for Child Health and Human Development; German
Research Foundation [DFG-SFB780-B6]; European Commission (FP7 DOPAMINET)
FX We thank the Sanger Zebrafish Mutation Project for the
otpbsa0115 allele, Alida Filippi for opn4a histological
sections, Jochen Wittbrodt for chokhs399 fish, the European
Zebrafish Resource Center and J. Maier for chokht25327 fish,
Josh Bonkowsky for Tg(otpb.A:Gal4)zc67 fish, Erin Beddows and Mattanja
Sonn for excellent technical support, the zebrafish community for
sharing reagents, and H. Codore and S. Gotter for expert zebrafish care.
This work was supported by the Intramural Research Program of the
National Institute for Child Health and Human Development (to H.A.B.),
the German Research Foundation (DFG-SFB780-B6 to W.D.), and the European
Commission (FP7 DOPAMINET to W.D.).
NR 35
TC 57
Z9 57
U1 3
U2 44
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 6
PY 2012
VL 22
IS 21
BP 2042
EP 2047
DI 10.1016/j.cub.2012.08.016
PG 6
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 036VK
UT WOS:000311060200026
PM 23000151
ER
PT J
AU Zhao, HY
Schuck, P
AF Zhao, Huaying
Schuck, Peter
TI Global Multi-Method Analysis of Affinities and Cooperativity in Complex
Systems of Macromolecular Interactions
SO ANALYTICAL CHEMISTRY
LA English
DT Article
ID ISOTHERMAL TITRATION CALORIMETRY; PROTEIN INTERACTIONS; KINETIC-DATA;
BINDING; CELL
AB Cooperativity, multisite, and multicomponent interactions are hallmarks of biological systems of interacting macromolecules. Their thermodynamic characterization is often very challenging due to the notoriously low information content of binding isotherms. We introduce a strategy for the global multimethod analysis of data from multiple techniques (GMMA) that exploits enhanced information content emerging from the mutual constraints of the simultaneous modeling of orthogonal observables from calorimetric, spectroscopic, hydrodynamic, biosensing, or other thermodynamic binding experiments. We describe new approaches to address statistical problems that arise in the analysis of dissimilar data sets. The GMMA approach can significantly increase the complexity of interacting systems that can be accurately thermodynamically characterized.
C1 [Schuck, Peter] Natl Inst Biomed Imaging, Dynam Macromol Assembly Sect, Lab Cellular Imaging & Macromol Biophys, NIH, Bethesda, MD USA.
Natl Inst Bioengn, Dynam Macromol Assembly Sect, Lab Cellular Imaging & Macromol Biophys, NIH, Bethesda, MD USA.
RP Schuck, P (reprint author), Natl Inst Biomed Imaging, Dynam Macromol Assembly Sect, Lab Cellular Imaging & Macromol Biophys, NIH, Bethesda, MD USA.
EM Peter.Schuck@nih.gov
OI Schuck, Peter/0000-0002-8859-6966
FU Intramural Research Program of the National Institute of Biomedical
Imaging and Bioengineering, National Institutes of Health
FX We thank Andrea Balbo for expert technical assistance with the protein
purification. This work was supported by the Intramural Research Program
of the National Institute of Biomedical Imaging and Bioengineering,
National Institutes of Health.
NR 34
TC 17
Z9 17
U1 0
U2 16
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 6
PY 2012
VL 84
IS 21
BP 9513
EP 9519
DI 10.1021/ac302357w
PG 7
WC Chemistry, Analytical
SC Chemistry
GA 031TG
UT WOS:000310664600089
PM 23020071
ER
PT J
AU Keteyian, SJ
Leifer, ES
Houston-Miller, N
Kraus, WE
Brawner, CA
O'Connor, CM
Whellan, DJ
Cooper, LS
Fleg, JL
Kitzman, DW
Cohen-Solal, A
Blumenthal, JA
Rendall, DS
Pina, IL
AF Keteyian, Steven J.
Leifer, Eric S.
Houston-Miller, Nancy
Kraus, William E.
Brawner, Clinton A.
O'Connor, Christopher M.
Whellan, David J.
Cooper, Lawton S.
Fleg, Jerome L.
Kitzman, Dalane W.
Cohen-Solal, Alain
Blumenthal, James A.
Rendall, David S.
Pina, Ileana L.
CA HF-ACTION Investigators
TI Relation Between Volume of Exercise and Clinical Outcomes in Patients
With Heart Failure
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Article
DE cardiac rehabilitation; dose response; exercise training
ID RANDOMIZED CONTROLLED-TRIAL; LEFT-VENTRICULAR FUNCTION; CARDIAC
REHABILITATION; HF-ACTION; ENDOTHELIAL DYSFUNCTION; SKELETAL-MUSCLE;
METAANALYSIS; ACTIVATION; PREVENTION; MORBIDITY
AB Objectives This study determined whether greater volumes of exercise were associated with greater reductions in clinical events.
Background The HF-ACTION (Heart Failure: A Controlled Trial Investigating Outcomes of Exercise Training) trial showed that among patients with heart failure (HF), regular exercise confers a modest reduction in the adjusted risk for all-cause mortality or hospitalization.
Methods Patients randomized to the exercise training arm of HF-ACTION who were event-free at 3 months after randomization were included (n = 959). Median follow-up was 28.2 months. Clinical endpoints were all-cause mortality or hospitalization and cardiovascular mortality or HF hospitalization.
Results A reverse J-shaped association was observed between exercise volume and adjusted clinical risk. On the basis of Cox regression, exercise volume was not a significant linear predictor but was a logarithmic predictor (p = 0.03) for all-cause mortality or hospitalization. For cardiovascular mortality or HF hospitalization, exercise volume was a significant (p = 0.001) linear and logarithmic predictor. Moderate exercise volumes of 3 to <5 metabolic equivalent (MET)-h and 5 to <7 MET-h per week were associated with reductions in subsequent risk that exceeded 30%. Exercise volume was positively associated with the change in peak oxygen uptake at 3 months (r = 0.10; p = 0.005).
Conclusions In patients with chronic systolic HF, volume of exercise is associated with the risk for clinical events, with only moderate levels (3 to 7 MET-h per week) of exercise needed to observe a clinical benefit. Although further study is warranted to confirm the relationship between volume of exercise completed and clinical events, our findings support the use of regular exercise in the management of these patients. (Heart Failure: A Controlled Trial Investigating Outcomes of Exercise Training [HF-ACTION]; NCT00047437) (J Am Coll Cardiol 2012;60:1899-905) (C) 2012 by the American College of Cardiology Foundation
C1 [Keteyian, Steven J.] Henry Ford Hosp, Dept Cardiovasc Med, Div Cardiovasc Med, Detroit, MI 48202 USA.
[Leifer, Eric S.; Cooper, Lawton S.; Fleg, Jerome L.] NHLBI, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
[Houston-Miller, Nancy] Stanford Univ, Dept Med, Stanford, CA 94305 USA.
[Kraus, William E.; O'Connor, Christopher M.; Rendall, David S.] Duke Univ, Sch Med, Dept Med, Durham, NC 27706 USA.
[O'Connor, Christopher M.; Whellan, David J.] Duke Univ, Sch Med, Duke Clin Res Inst, Durham, NC USA.
[Whellan, David J.] Thomas Jefferson Univ, Jefferson Med Coll, Dept Med, Philadelphia, PA 19107 USA.
[Kitzman, Dalane W.] Wake Forest Univ, Bowman Gray Sch Med, Dept Internal Med, Winston Salem, NC 27103 USA.
[Cohen-Solal, Alain] Hop Lariboisiere, APHP, Sci Mixt Res Unit S942, Fac Paris Diderot, F-75475 Paris, France.
[Pina, Ileana L.] Montefiore Med Ctr, Albert Einstein Coll Med, Bronx, NY 10467 USA.
RP Keteyian, SJ (reprint author), Henry Ford Hosp, Dept Cardiovasc Med, Div Cardiovasc Med, 6525 2nd Ave, Detroit, MI 48202 USA.
EM sketeyi1@hfhs.org
OI Brawner, Clinton A./0000-0002-1705-6620; Kraus, William
E/0000-0003-1930-9684
FU National Heart, Lung and Blood Institute (NHLBI), National Institutes of
Health (NIH), Bethesda, Maryland; NIH; GE Healthcare; Amgen; Servier;
Astra Zeneca; Menarini; Takeda; IPSEN Genzyme; Novartis; Sorin
FX This work was supported by the National Heart, Lung and Blood Institute
(NHLBI), National Institutes of Health (NIH), Bethesda, Maryland. Dr.
Keteyian received grants or funding, personal income for consulting, and
honoraria from the NIH, GE Healthcare, and Amgen; and is a consultant to
Janssen Research & Development and the Duke University Medical Center.
Dr. Leifer is an employee of NHLBI. Dr. Kraus received grants or
funding, personal income for consulting, and honoraria from the NIH, GE
Healthcare, and Amgen. Dr. O'Connor received grants or funding, personal
income for consulting, and honoraria from the NIH, GE Healthcare, and
Amgen. Dr. Whellan received grants or funding, personal income for
consulting, and honoraria from the NIH, GE Healthcare, and Amgen. Drs.
Cooper and Fleg are employees of NHLBI. Dr. Kitzman received grants or
funding, personal income for consulting, and honoraria from the NIH, GE
Healthcare, and Amgen. Dr. Cohen-Solal received grants or funding from
Servier, Astra Zeneca, Menarini, Takeda, Amgen, IPSEN Genzyme, GE Health
Care, Novartis, and Sorin. Dr. Pi a received grants or funding, personal
income for consulting, and honoraria from the NIH, GE Healthcare, and
Amgen. All other authors have reported that they have no relationships
relevant to the contents of this paper to disclose.
NR 38
TC 47
Z9 47
U1 1
U2 12
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 6
PY 2012
VL 60
IS 19
BP 1899
EP 1905
DI 10.1016/j.jacc.2012.08.958
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 027LB
UT WOS:000310352600008
PM 23062530
ER
PT J
AU Nestorovich, EM
Karginov, VA
Berezhkovskii, AM
Parsegian, VA
Bezrukov, SM
AF Nestorovich, Ekaterina M.
Karginov, Vladimir A.
Berezhkovskii, Alexander M.
Parsegian, V. Adrian
Bezrukov, Sergey M.
TI Kinetics and thermodynamics of binding reactions as exemplified by
anthrax toxin channel blockage with a cationic cyclodextrin derivative
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE protein-ligand binding; molecular docking
ID DRUG DESIGN; TEMPERATURE; DEPENDENCE; STRENGTH; WATER; PORE
AB The thermodynamics of binding reactions is usually studied in the framework of the linear van't Hoff analysis of the temperature dependence of the equilibrium constant. The logarithm of the equilibrium constant is plotted versus inverse temperature to discriminate between two terms: an enthalpic contribution that is linear in the inverse temperature, and a temperature-independent entropic contribution. When we apply this approach to a particular case-blockage of the anthrax PA(63) channel by a multicharged cyclodextrin derivative-we obtain a nearly linear behavior with a slope that is characterized by enthalpy of about 1 kcal/mol. In contrast, from blocker partitioning between the channel and the bulk, we estimate the depth of the potential well for the blocker in the channel to be at least 8 kcal/mol. To understand this apparent discrepancy, we use a simple model of particle interaction with the channel and show that this significant difference between the two estimates is due to the temperature dependence of the physical forces between the blocker and the channel. In particular, we demonstrate that if the major component of blocker-channel interaction is van der Waals interactions and/or Coulomb forces in water, the van't Hoff enthalpy of the binding reaction may be close to zero or even negative, including cases of relatively strong binding. The results are quite general and, therefore, of importance for studies of enzymatic reactions, rational drug design, small-molecule binding to proteins, protein-protein interactions, and protein folding, among others.
C1 [Bezrukov, Sergey M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
[Nestorovich, Ekaterina M.] Catholic Univ Amer, Dept Biol, Washington, DC 20064 USA.
[Karginov, Vladimir A.] Innovat Biol, Herndon, VA 20171 USA.
[Berezhkovskii, Alexander M.] NIH, Math & Stat Comp Lab, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
[Parsegian, V. Adrian] Univ Massachusetts, Dept Phys, Amherst, MA 01003 USA.
RP Bezrukov, SM (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
EM bezrukos@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health, Eunice
Kennedy Shriver National Institute of Child Health and Human
Development; Center for Information Technology
FX We thank Donald Rau for fruitful discussions and reading the manuscript.
This study was supported by the Intramural Research Program of the
National Institutes of Health, Eunice Kennedy Shriver National Institute
of Child Health and Human Development, and Center for Information
Technology.
NR 27
TC 10
Z9 10
U1 0
U2 13
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 6
PY 2012
VL 109
IS 45
BP 18453
EP 18458
DI 10.1073/pnas.1208771109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 038DZ
UT WOS:000311156700051
PM 23100532
ER
PT J
AU Bartoshuk, LM
Catalanotto, F
Hoffman, H
Logan, H
Snyder, DJ
AF Bartoshuk, Linda M.
Catalanotto, Frank
Hoffman, Howard
Logan, Henrietta
Snyder, Derek J.
TI Taste damage (otitis media, tonsillectomy and head and neck cancer),
oral sensations and BMI
SO PHYSIOLOGY & BEHAVIOR
LA English
DT Article
DE Taste; Otitis media; Tonsillectomy; Head and neck cancer; Body mass
index; Pain
ID CHORDA TYMPANI NERVE; MIDDLE-EAR DISEASE; INTRAORAL SUCROSE; GUSTATORY
FUNCTION; INDUCED ANALGESIA; FAT PERCEPTION; WEIGHT-LOSS; ANESTHESIA;
PSYCHOPHYSICS; PREFERENCE
AB Otitis media and tonsillectomy are associated with enhanced palatability of energy dense foods and with weight gain. Otitis media can damage the chorda tympani nerve (CN VII); tonsillectomy and head and neck radiation treatment can damage the glossopharyngeal nerve (CN IX). Both of these nerves function prominently in taste sensation. The present study utilizes these sources of damage to study central interactions among the nerves that mediate oral sensations. Mild damage restricted to one of these nerves can actually intensify sensations evoked from undamaged nerves (i.e., whole-mouth taste, oral tactile sensations evoked by fats and irritants). These intensifications may result from disruption of central inhibitory taste circuits, as taste damage appears to disinhibit other oral sensory nerves. In addition, mild damage restricted to one taste nerve can intensify odors perceived from foods in the mouth during chewing and swallowing (i.e., retronasal olfaction); this may be a secondary consequence of the intensification of whole-mouth taste. Damage to both nerves leads to widespread oral sensory loss. At present, the link between sensory alterations and weight gain has not been established for adults (e.g., does increased fat preference occur in individuals with oral sensory intensifications, those with losses, or both?). Finally, pain in non-oral locations is also related to taste loss. When participants rated "the most intense pain of any kind they had ever experienced," those with the greatest taste loss gave the highest ratings. These effects suggest that taste loss significantly influences long-term health outcomes. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Bartoshuk, Linda M.] Univ Florida, Ctr Smell & Taste, Gainesville, FL 32608 USA.
[Catalanotto, Frank; Logan, Henrietta; Snyder, Derek J.] Univ Florida, CDBS, Gainesville, FL 32610 USA.
[Hoffman, Howard] NIDCD, Natl Inst Deafness, NIH, Bethesda, MD 20892 USA.
[Snyder, Derek J.] San Diego State Univ, San Diego, CA 92182 USA.
RP Bartoshuk, LM (reprint author), Univ Florida, Ctr Smell & Taste, 4073 SW 21st Terrace, Gainesville, FL 32608 USA.
EM lbartoshuk@dental.ufl.edu; FCatalanotto@dental.ufl.edu;
HoffmanH@ms.nidcd.nih.gov; HLogan@dental.ufl.edu; DSnyder@dental.ufl.edu
FU NIDCD [DC283, DC8613]
FX This research was supported by NIDCD grants DC283 and DC8613.
NR 98
TC 20
Z9 20
U1 1
U2 14
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0031-9384
J9 PHYSIOL BEHAV
JI Physiol. Behav.
PD NOV 5
PY 2012
VL 107
IS 4
SI SI
BP 516
EP 526
DI 10.1016/j.physbeh.2012.06.013
PG 11
WC Psychology, Biological; Behavioral Sciences
SC Psychology; Behavioral Sciences
GA 067PR
UT WOS:000313308100010
PM 22728784
ER
PT J
AU Bot, A
Ahn, M
Bosch, M
Brockstedt, D
Butterfield, LH
Cornforth, A
Harrop, R
Kast, WM
Koya, R
Marincola, F
Margolin, K
McCoy, C
Pawelec, G
Rothman, J
Ramirez-Montagut, T
Schlom, J
Srivastava, P
Wallis, S
Walter, S
Wang, E
Waslif, J
AF Bot, Adrian
Ahn, Mark
Bosch, Marnix
Brockstedt, Dirk
Butterfield, Lisa H.
Cornforth, Andrew
Harrop, Richard
Kast, W. Martin
Koya, Richard
Marincola, Francesco
Margolin, Kim
McCoy, Candice
Pawelec, Graham
Rothman, John
Ramirez-Montagut, Teresa
Schlom, Jeffrey
Srivastava, Pramod
Wallis, Sarah
Walter, Steffen
Wang, Ena
Waslif, John
TI A novel series of conferences tackling the hurdles confronting the
translation of novel cancer immunotherapies
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
ID STEM-CELLS; REGRESSION; GROWTH
AB While there has been significant progress in advancing novel immune therapies to the bedside, much more needs to be done to fully tap into the potential of the immune system. It has become increasingly clear that besides practical and operational challenges, the heterogeneity of cancer and the limited efficacy profile of current immunotherapy platforms are the two main hurdles. Nevertheless, the promising clinical data of several approaches point to a roadmap that carries the promise to significantly advance cancer immunotherapy. A new annual series sponsored by Arrowhead Publishers and Conferences aims at bringing together scientific and business leadership from academia and industry, to identify, share and discuss most current priorities in research and translation of novel immune interventions. This Editorial provides highlights of the first event held earlier this year and outlines the focus of the second meeting to be held in 2013 that will be dedicated to stem cells and immunotherapy.
C1 [Bot, Adrian] Kite Pharma Inc, Los Angeles, CA USA.
[Ahn, Mark] Galena Biopharma Inc, Lake Oswego, OR USA.
[Bosch, Marnix] Northwest Biotherapeut, Bethesda, MD USA.
[Brockstedt, Dirk] Aduro Biotech, Berkeley, CA USA.
[Butterfield, Lisa H.] Univ Pittsburgh, Dept Med Surg & Immunol, UPCI Immunol Monitoring & Cellular Prod Lab, Pittsburgh, PA USA.
[Cornforth, Andrew] Calif Stem Cell, Irvine, CA USA.
[Harrop, Richard] Oxford BioMed, Oxford, England.
[Kast, W. Martin] Univ So Calif, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
[Harrop, Richard] Univ Calif Los Angeles, Dept Surg Oncol, Los Angeles, CA USA.
[Marincola, Francesco; Wang, Ena] NIH, Dept Transfus Med, Infect Dis & Immunogenet Sect, Bethesda, MD 20892 USA.
[Margolin, Kim] Univ Washington, Div Med Oncol, Seattle, WA 98195 USA.
[McCoy, Candice] Dendreon Corp, Seattle, WA USA.
[Pawelec, Graham] Univ Tubingen, Med Res Ctr, Tubingen, Germany.
[Rothman, John; Ramirez-Montagut, Teresa] Novartis Res Fdn, Advaxis Inc, Genom Inst, Princeton, NJ USA.
[Schlom, Jeffrey] NIH, Immunotherapeut Grp, Bethesda, MD 20892 USA.
[Srivastava, Pramod] Univ Connecticut, Ctr Hlth, Dept Immunol, Farmington, CT USA.
[Wallis, Sarah; Waslif, John] Arrowhead Publishers & Conferences, Minneapolis, MN USA.
[Walter, Steffen] Immat Biotechnol GmbH, Tubingen, Germany.
RP Bot, A (reprint author), Kite Pharma Inc, Los Angeles, CA USA.
EM abot@kitepharma.com
OI Pawelec, Graham/0000-0002-3600-0163
NR 13
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 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD NOV 5
PY 2012
VL 10
AR 218
DI 10.1186/1479-5876-10-218
PG 5
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 074TV
UT WOS:000313837600001
PM 23127127
ER
PT J
AU Blanford, S
Jenkins, NE
Read, AF
Thomas, MB
AF Blanford, Simon
Jenkins, Nina E.
Read, Andrew F.
Thomas, Matthew B.
TI Evaluating the lethal and pre-lethal effects of a range of fungi against
adult Anopheles stephensi mosquitoes
SO MALARIA JOURNAL
LA English
DT Article
ID AEGYPTI DIPTERA-CULICIDAE; AFRICAN MALARIA MOSQUITOS; ANISOPLIAE IP 46;
ENTOMOPATHOGENIC FUNGUS; METARHIZIUM-ANISOPLIAE; AEDES-AEGYPTI;
BEAUVERIA-BASSIANA; INSECTICIDE RESISTANCE; CULEX-QUINQUEFASCIATUS;
VECTOR CONTROL
AB Background: Insecticide resistance is seriously undermining efforts to eliminate malaria. In response, research on alternatives to the use of chemical insecticides against adult mosquito vectors has been increasing. Fungal entomopathogens formulated as biopesticides have received much attention and have shown considerable potential. This research has necessarily focused on relatively few fungal isolates in order to 'prove concept'. Further, most attention has been paid to examining fungal virulence (lethality) and not the other properties of fungal infection that might also contribute to reducing transmission potential. Here, a range of fungal isolates were screened to examine variation in virulence and how this relates to additional pre-lethal reductions in feeding propensity.
Methods: The Asian malaria vector, Anopheles stephensi was exposed to 17 different isolates of entomopathogenic fungi belonging to species of Beauveria bassiana, Metarhizium anisopliae, Metarhizium acridum and Isaria farinosus. Each isolate was applied to a test substrate at a standard dose rate of 1x10(9) spores ml(-1) and the mosquitoes exposed for six hours. Subsequently the insects were removed to mesh cages where survival was monitored over the next 14 days. During this incubation period the mosquitoes' propensity to feed was assayed for each isolate by offering a feeding stimulant at the side of the cage and recording the number probing.
Results and conclusions: Fungal isolates showed a range of virulence to A. stephensi with some causing >80% mortality within 7 days, while others caused little increase in mortality relative to controls over the study period. Similarly, some isolates had a large impact on feeding propensity, causing >50% pre-lethal reductions in feeding rate, whereas other isolates had very little impact. There was clear correlation between fungal virulence and feeding reduction with virulence explaining nearly 70% of the variation in feeding reduction. However, there were some isolates where either feeding decline was not associated with high virulence, or virulence did not automatically prompt large declines in feeding. These results are discussed in the context of choosing optimum fungal isolates for biopesticide development.
C1 [Blanford, Simon; Read, Andrew F.] Penn State Univ, Dept Biol, Ctr Infect Dis Dynam, Mueller Lab, University Pk, PA 16802 USA.
[Blanford, Simon; Jenkins, Nina E.; Read, Andrew F.; Thomas, Matthew B.] Penn State Univ, Dept Entomol, Ctr Infect Dis Dynam, Merkle Lab, University Pk, PA 16802 USA.
[Read, Andrew F.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Blanford, S (reprint author), Penn State Univ, Dept Biol, Ctr Infect Dis Dynam, Mueller Lab, University Pk, PA 16802 USA.
EM stb13@psu.edu
FU Gates Grand Challenges Explorations [53066]; National Institutes of
Health [AI088094-01]; Innovative Vector Control Consortium; Research and
Policy for Infectious Disease Dynamics (RAPIDD) program; Pennsylvania
Department of Health
FX This research was part-funded by grants from Gates Grand Challenges
Explorations (No. 53066), the National Institutes of Health
(AI088094-01), the Innovative Vector Control Consortium and by the
Research and Policy for Infectious Disease Dynamics (RAPIDD) program.
This project was also funded, in part, under a grant with the
Pennsylvania Department of Health using Tobacco Settlement Funds. The
Department specifically disclaims responsibility for any analyses,
interpretations or conclusions. All funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
NR 77
TC 4
Z9 4
U1 3
U2 42
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1475-2875
J9 MALARIA J
JI Malar. J.
PD NOV 5
PY 2012
VL 11
AR 365
DI 10.1186/1475-2875-11-365
PG 10
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 058SS
UT WOS:000312654900001
PM 23126549
ER
PT J
AU Merritt, P
Stangl, B
Hirshman, E
Verbalis, J
AF Merritt, Paul
Stangl, Bethany
Hirshman, Elliot
Verbalis, Joseph
TI Administration of dehydroepiandrosterone (DHEA) increases serum levels
of androgens and estrogens but does not enhance short-term memory in
post-menopausal women
SO BRAIN RESEARCH
LA English
DT Article
DE Hormone replacement therapy; Aging; Short-term memory; Cognition
ID GABA-A RECEPTOR; COGNITIVE FUNCTION; WORKING-MEMORY; HORMONE
REPLACEMENT; RECOGNITION MEMORY; TOBACCO ABSTINENCE; STEROID-HORMONES;
EPISODIC MEMORY; SULFATE DHEAS; OLDER-ADULTS
AB The current study examines the effect of administering dehydroepiandrosterone (DHEA) on short-term memory. This experiment used a double-blind placebo-controlled cross-over design to explore the effects of a four week regimen of 50 mg oral DHEA on performance on the digit span, verbal span, and modified Sternberg (Oberauer) tasks. The results demonstrate that the current regimen of drug administration significantly increases serum levels of DHEA, DHEAS, testosterone and estrone and substantially alters the patterns of correlations among the serum levels of these hormones. Despite this substantial change in the hormonal milieu, DHEA administration produced no beneficial effects on cognitive performance in the digit span, verbal span, or modified Sternberg paradigm tasks. Ancillary analyses of the relation between hormone levels and cognitive performance demonstrated a strong positive correlation between DHEA levels and performance on digit span forward/backward and verbal span forward in the placebo drug condition, but not in the DHEA condition. We interpret the juxtaposition of the null results of DHEA administration and the correlation of DHEA levels and performance in the placebo condition to indicate that the referenced correlations arise because a third variable (i.e., age) is associated with both performance and DHEA levels. Additional analyses supported this hypothesis. (C) 2012 Elsevier B.V. All rights reserved.
C1 [Merritt, Paul] Clemson Univ, Dept Psychol, Clemson, SC 29634 USA.
[Stangl, Bethany] NIAAA, NIH, Bethesda, MD USA.
[Hirshman, Elliot] San Diego State Univ, Dept Psychol, San Diego, CA 92182 USA.
[Verbalis, Joseph] Georgetown Univ, Med Ctr, Dept Med, Washington, DC 20007 USA.
RP Merritt, P (reprint author), Clemson Univ, Dept Psychol, Clemson, SC 29634 USA.
EM pmerrit@clemson.edu
FU NIA NIH HHS [R01 AG020543]
NR 53
TC 6
Z9 6
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD NOV 5
PY 2012
VL 1483
BP 54
EP 62
DI 10.1016/j.brainres.2012.09.015
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 038KZ
UT WOS:000311174900006
PM 22985672
ER
PT J
AU Vascellari, S
Orru, CD
Hughson, AG
King, D
Barron, R
Wilham, JM
Baron, GS
Race, B
Pani, A
Caughey, B
AF Vascellari, Sarah
Orru, Christina D.
Hughson, Andrew G.
King, Declan
Barron, Rona
Wilham, Jason M.
Baron, Gerald S.
Race, Brent
Pani, Alessandra
Caughey, Byron
TI Prion Seeding Activities of Mouse Scrapie Strains with Divergent PrPSc
Protease Sensitivities and Amyloid Plaque Content Using RT-QuIC and
eQuIC
SO PLOS ONE
LA English
DT Article
ID MISFOLDING CYCLIC AMPLIFICATION; QUAKING-INDUCED CONVERSION;
CREUTZFELDT-JAKOB-DISEASE; TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY;
IN-VITRO; CEREBROSPINAL-FLUID; MAMMALIAN PRIONS; INFECTIOUS PRIONS;
BRAIN; TIME
AB Different transmissible spongiform encephalopathy (TSE)-associated forms of prion protein (e.g. PrPSc) can vary markedly in ultrastructure and biochemical characteristics, but each is propagated in the host. PrPSc propagation involves conversion from its normal isoform, PrPC, by a seeded or templated polymerization mechanism. Such a mechanism is also the basis of the RT-QuIC and eQuIC prion assays which use recombinant PrP (rPrP(Sen)) as a substrate. These ultrasensitive detection assays have been developed for TSE prions of several host species and sample tissues, but not for murine models which are central to TSE pathogenesis research. Here we have adapted RT-QuIC and eQuIC to various murine prions and evaluated how seeding activity depends on glycophosphatidylinositol (GPI) anchoring and the abundance of amyloid plaques and protease-resistant PrPSc (PrPRes). Scrapie brain dilutions up to 10(-8) and 10(-13) were detected by RT-QuIC and eQuIC, respectively. Comparisons of scrapie-affected wild-type mice and transgenic mice expressing GPI anchorless PrP showed that, although similar concentrations of seeding activity accumulated in brain, the heavily amyloid-laden anchorless mouse tissue seeded more rapid reactions. Next we compared seeding activities in the brains of mice with similar infectivity titers, but widely divergent PrPRes levels. For this purpose we compared the 263K and 139A scrapie strains in transgenic mice expressing P101L PrPC. Although the brains of 263K-affected mice had little immunoblot-detectable PrPRes, RT-QuIC indicated that seeding activity was comparable to that associated with a high-PrPRes strain, 139A. Thus, in this comparison, RT-QuIC seeding activity correlated more closely with infectivity than with PrPRes levels. We also found that eQuIC, which incorporates a PrPSc immunoprecipitation step, detected seeding activity in plasma from wild-type and anchorless PrP transgenic mice inoculated with 22L, 79A and/or RML scrapie strains. Overall, we conclude that these new mouse-adapted prion seeding assays detect diverse types of PrPSc.
C1 [Vascellari, Sarah; Orru, Christina D.; Hughson, Andrew G.; Wilham, Jason M.; Baron, Gerald S.; Race, Brent; Caughey, Byron] NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, NIH, Hamilton, MT USA.
[Vascellari, Sarah; Orru, Christina D.; Pani, Alessandra] Univ Cagliari, Dept Biomed Sci, Monserrato, Italy.
[King, Declan; Barron, Rona] Univ Edinburgh, Div Neurobiol, Roslin Inst, Roslin, Midlothian, Scotland.
[King, Declan; Barron, Rona] Univ Edinburgh, R D SVS, Roslin, Midlothian, Scotland.
RP Caughey, B (reprint author), NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, NIH, Hamilton, MT USA.
EM bcaughey@nih.gov
RI Barron, Rona/C-7703-2013; Pani, Alessandra/B-7831-2011;
OI Pani, Alessandra/0000-0002-0437-2499; Barron, Rona/0000-0003-4512-9177
FU National Institute for Allergy and Infectious Diseases, National
Institutes of Health; Department for Environment, Food and Rural Affairs
(Defra), UK [SE1790, SE2016]; Master and Back Program of the Regione
Sardegna (Italy)
FX This study supported by the Intramural Research Program of the National
Institute for Allergy and Infectious Diseases, National Institutes of
Health, as well as contracts SE1790 and SE2016 from the Department for
Environment, Food and Rural Affairs (Defra), UK. The funders had no role
in study design, data collection and analysis, decision to publish, or
preparation of the manuscript.; We thank Lynne Raymond for providing
bacterial expression vectors for the recombinant PrPSen used
as substrate in these studies. We also thank Anita Mora for graphic arts
assistance, and Drs. Suzette Priola, Roger Moore and Jay Carroll for
their critical evaluation of the manuscript. The 101LL knock-in
transgenic line was kindly supplied by Prof Jean Manson, Roslin
Institute. S.V. was partially supported by the Master and Back Program
of the Regione Sardegna (Italy). We thank Drs. Franziska Kuhn, Bjorn
Schroeder and Alex Raber at Prionics AG for the gift of 15B3 antibody.
NR 62
TC 27
Z9 27
U1 1
U2 11
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 5
PY 2012
VL 7
IS 11
AR e48969
DI 10.1371/journal.pone.0048969
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 032TG
UT WOS:000310741400065
PM 23139828
ER
PT J
AU Auer, PL
Johnsen, JM
Johnson, AD
Logsdon, BA
Lange, LA
Nalls, MA
Zhang, GS
Franceschini, N
Fox, K
Lange, EM
Rich, SS
O'Donnell, CJ
Jackson, RD
Wallace, RB
Chen, Z
Graubert, TA
Wilson, JG
Tang, H
Lettre, G
Reiner, AP
Ganesh, SK
Li, Y
AF Auer, Paul L.
Johnsen, Jill M.
Johnson, Andrew D.
Logsdon, Benjamin A.
Lange, Leslie A.
Nalls, Michael A.
Zhang, Guosheng
Franceschini, Nora
Fox, Keolu
Lange, Ethan M.
Rich, Stephen S.
O'Donnell, Christopher J.
Jackson, Rebecca D.
Wallace, Robert B.
Chen, Zhao
Graubert, Timothy A.
Wilson, James G.
Tang, Hua
Lettre, Guillaume
Reiner, Alex P.
Ganesh, Santhi K.
Li, Yun
CA Natl Heart Lung Blood Inst
TI Imputation of Exome Sequence Variants into Population-Based Samples and
Blood-Cell-Trait-Associated Loci in African Americans: NHLBI GO Exome
Sequencing Project
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; HUMAN GENE-EXPRESSION; GENOTYPE IMPUTATION;
POSITIVE SELECTION; GLOBIN GENE; DISEASE; THROMBOCYTOSIS; DESIGN;
DISCOVERY; MUTATION
AB Researchers have successfully applied exome sequencing to discover causal variants in selected individuals with familial, highly penetrant disorders. We demonstrate the utility of exome sequencing followed by imputation for discovering low-frequency variants associated with complex quantitative traits. We performed exome sequencing in a reference panel of 761 African Americans and then imputed newly discovered variants into a larger sample of more than 13,000 African Americans for association testing with the blood cell traits hemoglobin, hematocrit, white blood count, and platelet count. First, we illustrate the feasibility of our approach by demonstrating genome-wide-significant associations for variants that are not covered by conventional genotyping arrays; for example, one such association is that between higher platelet count and an MPL c.117G>T (p.Lys39Asn) variant encoding a p.Lys39Asn amino acid substitution of the thrombpoietin receptor gene (p = 1.5 x 10(-11)). Second, we identified an association between missense variants of LCT and higher white blood count (p = 4 x 10(-13)). Third, we identified low-frequency coding variants that might account for allelic heterogeneity at several known blood cell-associated loci: MPL c.754T>C (p.Tyr252His) was associated with higher platelet count; CD36 c.975T>G (p.Tyr325*) was associated with lower platelet count; and several missense variants at the alpha-globin gene locus were associated with lower hemoglobin. By identifying low-frequency missense variants associated with blood cell traits not previously reported by genome-wide association studies, we establish that exome sequencing followed by imputation is a powerful approach to dissecting complex, genetically heterogeneous traits in large population-based studies.
C1 [Auer, Paul L.; Logsdon, Benjamin A.; Reiner, Alex P.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA.
[Johnsen, Jill M.] Puget Sound Blood Ctr, Res Inst, Seattle, WA 98109 USA.
[Johnsen, Jill M.; Fox, Keolu] Univ Washington, Dept Med, Seattle, WA 98195 USA.
[Johnsen, Jill M.; Fox, Keolu] Univ Washington, Dept Epidemiol & Genome Sci, Seattle, WA 98195 USA.
[Johnson, Andrew D.; O'Donnell, Christopher J.] NHLBI, Ctr Populat Studies, Framingham Heart Study, Framingham, MA 01702 USA.
[Lange, Leslie A.; Zhang, Guosheng; Franceschini, Nora; Lange, Ethan M.; Li, Yun] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC 27599 USA.
[Lange, Leslie A.; Zhang, Guosheng; Franceschini, Nora; Lange, Ethan M.; Li, Yun] Univ N Carolina, Dept Genet, Chapel Hill, NC 27599 USA.
[Lange, Leslie A.; Zhang, Guosheng; Franceschini, Nora; Lange, Ethan M.; Li, Yun] Univ N Carolina, Dept Biostat Bioinformat & Computat Biol, Chapel Hill, NC 27599 USA.
[Nalls, Michael A.; Reiner, Alex P.] NIA, Mol Genet Sect, Neurogenet Lab, Bethesda, MD 20892 USA.
[Rich, Stephen S.] Univ Virginia, Dept Publ Hlth Sci, Ctr Publ Hlth Gen, Charlottesville, VA 22908 USA.
[Jackson, Rebecca D.] Ohio State Univ, Div Endocrinol Diabet & Metab, Columbus, OH 43210 USA.
[Wallace, Robert B.] Univ Iowa, Coll Publ Hlth, Dept Epidemiol, Iowa City, IA 52242 USA.
[Chen, Zhao] Univ Arizona, Mel & Enid Zuckerman Coll Publ Hlth, Div Epidemiol & Biostat, Tucson, AZ 85724 USA.
[Graubert, Timothy A.] Washington Univ, Sch Med, Dept Internal Med, St Louis, MO 63110 USA.
[Wilson, James G.] Univ Mississippi, Med Ctr, Dept Physiol & Biophys, Jackson, MS 39216 USA.
[Tang, Hua] Stanford Univ, Dept Genet, Stanford, CA 94305 USA.
[Tang, Hua] Stanford Univ, Dept Stat, Stanford, CA 94305 USA.
[Lettre, Guillaume] Montreal Heart Inst, Montreal, PQ H1T 1C8, Canada.
[Lettre, Guillaume] Univ Montreal, Dept Med, Montreal, PQ H1T 1C8, Canada.
[Ganesh, Santhi K.] Univ Michigan, Dept Internal Med, Div Cardiovasc Med, Ann Arbor, MI 48108 USA.
RP Reiner, AP (reprint author), Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA.
EM apreiner@u.washington.edu; yunli@med.unc.edu
RI Johnson, Andrew/G-6520-2013;
OI Graubert, Timothy/0000-0002-7710-1171
FU National Heart, Lung, and Blood Institute (NHLBI); NHLBI [RC2 HL-103010,
RC2 HL-102923, RC2 HL-102924, RC2 HL-102925, RC2 HL-102926,
HHSN268200960009C]; National Human Genome Research Institute
[R01HG006292, R01HG006703]; Intramural Research Program of the National
Institutes of Health, National Institute on Aging [Z01-AG000932-04]
FX The authors wish to acknowledge the support of the National Heart, Lung,
and Blood Institute (NHLBI) and the contributions of the research
institutions, study investigators, field staff, and study participants
in creating this resource for biomedical research. Funding for GO ESP
was provided by NHLBI grants RC2 HL-103010 (HeartGO), RC2 HL-102923
(LungGO), and RC2 HL-102924 (WHISP). The exome sequencing was performed
through NHLBI grants RC2 HL-102925 (BroadGO) and RC2 HL-102926
(SeattleGO). CARe was supported by a contract from NHLBI
(HHSN268200960009C) to create a phenotype and genotype database for
dissemination to the biomedical research community. Eight parent studies
contributed phenotypic data and DNA samples through the Broad Institute
(N01-HC-65226): the Atherosclerosis Risk in Communities study (ARIC),
the Cleveland Family Study (CFS), the Coronary Artery Risk Development
in Young Adults study (CARDIA), the Jackson Heart Study OHS), the
Multi-Ethnic Study of Atherosclerosis (MESA) study, the Cardiovascular
Health Study (CHS), the Framingham Heart Study (FHS), and the Sleep
Heart Health Study (SHHS). Support for CARe also came from the
individual research institutions, investigators, field staff, and study
participants. This research was supported in part by grants from the
National Human Genome Research Institute to Y.L. (R01HG006292 and
R01HG006703). This research was also supported in part by the Intramural
Research Program of the National Institutes of Health, National
Institute on Aging (Z01-AG000932-04), and this study utilized the
high-performance computational capabilities of the Biowulf Linux cluster
at the National Institutes of Health (see Web Resources).
NR 83
TC 50
Z9 50
U1 1
U2 9
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 2
PY 2012
VL 91
IS 5
BP 794
EP 808
DI 10.1016/j.ajhg.2012.08.031
PG 15
WC Genetics & Heredity
SC Genetics & Heredity
GA 036FI
UT WOS:000311011400003
PM 23103231
ER
PT J
AU Asselbergs, FW
Guo, YR
van Iperen, EPA
Sivapalaratnam, S
Tragante, V
Lanktree, MB
Lange, LA
Almoguera, B
Appelman, YE
Barnard, J
Baumert, J
Beitelshees, AL
Bhangale, TR
Chen, YDI
Gaunt, TR
Gong, Y
Hopewell, JC
Johnson, T
Kleber, ME
Langaee, TY
Li, MY
Li, YR
Liu, KA
McDonough, CW
Meijs, ME
Middelberg, RPS
Musunuru, K
Nelson, CP
O'Connell, JR
Padmanabhan, S
Pankow, JS
Pankratz, N
Rafelt, S
Rajagopalan, R
Romaine, SPR
Schork, NJ
Shaffer, J
Shen, HQ
Smith, EN
Tischfield, SE
van der Most, PJ
van Vliet-Ostaptchouk, JV
Verweij, N
Volcik, KA
Zhang, L
Bailey, KR
Bailey, KM
Bauer, F
Boer, JMA
Braund, PS
Burt, A
Burton, PR
Buxbaum, SG
Chen, W
Cooper-DeHoff, RM
Cupples, LA
deJong, JS
Delles, C
Duggan, D
Fornage, M
Furlong, CE
Glazer, N
Gums, JG
Hastie, C
Holmes, MV
Illig, T
Kirkland, SA
Kivimaki, M
Klein, R
Klein, BE
Kooperberg, C
Kottke-Marchant, K
Kumari, M
LaCroix, AZ
Mallela, L
Murugesan, G
Ordovas, J
Ouwehand, WH
Post, WS
Saxena, R
Scharnagl, H
Schreiner, PJ
Shah, T
Shields, DC
Shimbo, D
Srinivasan, SR
Stolk, RP
Swerdlow, DI
Taylor, HA
Topo, EJ
Toskala, E
van Pelt, JL
van Setten, J
Yusuf, S
Whittaker, JC
Zwinderman, AH
Anand, SS
Balmforth, AJ
Berenson, GS
Bezzina, CR
Boehm, BO
Boerwinkle, E
Casas, JP
Caulfield, MJ
Clarke, R
Connell, JM
Cruickshanks, KJ
Davidson, KW
Day, INM
de Bakker, PIW
Doevendans, PA
Dominiczak, AE
Hall, AS
Hartman, CA
Hengstenberg, C
Hillege, HL
Hofker, MH
Humphries, SE
Jarvik, GP
Johnson, JA
Kaess, BM
Kathiresan, S
Koenig, W
Lawlor, DA
Maerz, W
Melander, O
Mitchell, BD
Montgomery, GW
Munroe, PB
Murray, SS
Newhouse, SJ
Onland-Moret, NC
Poulter, N
Psaty, B
Redline, S
Rich, SS
Rotter, JI
Schunkert, H
Sever, P
Shuldiner, AR
Silverstein, RL
Stanton, A
Thorand, B
Trip, MD
Tsai, MY
van der Harst, P
van der Schoot, E
van der Schouw, YT
Verschuren, WMM
Watkins, H
Wilde, AAM
Wolffenbuttel, BHR
Whitfield, JB
Hovingh, GK
Ballantyne, CM
Wijmenga, C
Reilly, MP
Martin, NG
Wilson, JG
Rader, DJ
Samani, NJ
Reiner, AP
Hegele, RA
Kastelein, JJP
Hingorani, AD
Talmud, PJ
Hakonarson, H
Elbers, CC
Keating, BJ
Drenos, F
AF Asselbergs, Folkert W.
Guo, Yiran
van Iperen, Erik P. A.
Sivapalaratnam, Suthesh
Tragante, Vinicius
Lanktree, Matthew B.
Lange, Leslie A.
Almoguera, Berta
Appelman, Yolande E.
Barnard, John
Baumert, Jens
Beitelshees, Amber L.
Bhangale, Tushar R.
Chen, Yii-Der Ida
Gaunt, Tom R.
Gong, Yan
Hopewell, Jemma C.
Johnson, Toby
Kleber, Marcus E.
Langaee, Taimour Y.
Li, Mingyao
Li, Yun R.
Liu, Kiang
McDonough, Caitrin W.
Meijs, Matthijs El.
Middelberg, Rita P. S.
Musunuru, Kiran
Nelson, Christopher P.
O'Connell, Jeffery R.
Padmanabhan, Sandosh
Pankow, James S.
Pankratz, Nathan
Rafelt, Suzanne
Rajagopalan, Ramakrishnan
Romaine, Simon P. R.
Schork, Nicholas J.
Shaffer, Jonathan
Shen, Haiqing
Smith, Erin N.
Tischfield, Sam E.
van der Most, Peter J.
van Vliet-Ostaptchouk, Jana V.
Verweij, Niek
Volcik, Kelly A.
Zhang, Li
Bailey, Kent R.
Bailey, Kristian M.
Bauer, Florianne
Boer, Jolanda M. A.
Braund, Peter S.
Burt, Amber
Burton, Paul R.
Buxbaum, Sarah G.
Chen, Wei
Cooper-DeHoff, Rhonda M.
Cupples, L. Adrienne
deJong, Jonas S.
Delles, Christian
Duggan, David
Fornage, Myriam
Furlong, Clement E.
Glazer, Nicole
Gums, John G.
Hastie, Claire
Holmes, Michael V.
Illig, Thomas
Kirkland, Susan A.
Kivimaki, Mika
Klein, Ronald
Klein, Barbara E.
Kooperberg, Charles
Kottke-Marchant, Kandice
Kumari, Meena
LaCroix, Andrea Z.
Mallela, Laya
Murugesan, Gurunathan
Ordovas, Jose
Ouwehand, Willem H.
Post, Wendy S.
Saxena, Richa
Scharnagl, Hubert
Schreiner, Pamela J.
Shah, Tina
Shields, Denis C.
Shimbo, Daichi
Srinivasan, Sathanur R.
Stolk, Ronald P.
Swerdlow, Daniel I.
Taylor, Herman A., Jr.
Topo, Eric J.
Toskala, Elina
van Pelt, Joost L.
van Setten, Jessica
Yusuf, Salim
Whittaker, John C.
Zwinderman, A. H.
Anand, Sonia S.
Balmforth, Anthony J.
Berenson, Gerald S.
Bezzina, Connie R.
Boehm, Bernhard O.
Boerwinkle, Eric
Casas, Juan P.
Caulfield, Mark J.
Clarke, Robert
Connell, John M.
Cruickshanks, Karen J.
Davidson, Karina W.
Day, Ian N. M.
de Bakker, Paul I. W.
Doevendans, Pieter A.
Dominiczak, Anna E.
Hall, Alistair S.
Hartman, Catharina A.
Hengstenberg, Christian
Hillege, Hans L.
Hofker, Marten H.
Humphries, Steve E.
Jarvik, Gail P.
Johnson, Julie A.
Kaess, Bernhard M.
Kathiresan, Sekar
Koenig, Wolfgang
Lawlor, Debbie A.
Maerz, Winfried
Melander, Olle
Mitchell, Braxton D.
Montgomery, Grant W.
Munroe, Patricia B.
Murray, Sarah S.
Newhouse, Stephen J.
Onland-Moret, N. Charlotte
Poulter, Neil
Psaty, Bruce
Redline, Susan
Rich, Stephen S.
Rotter, Jerome I.
Schunkert, Heribert
Sever, Peter
Shuldiner, Alan R.
Silverstein, Roy L.
Stanton, Alice
Thorand, Barbara
Trip, Mieke D.
Tsai, Michael Y.
van der Harst, Pim
van der Schoot, Ellen
van der Schouw, Yvonne T.
Verschuren, W. M. Monique
Watkins, Hugh
Wilde, Arthur A. M.
Wolffenbuttel, Bruce H. R.
Whitfield, John B.
Hovingh, G. Kees
Ballantyne, Christie M.
Wijmenga, Cisca
Reilly, Muredach P.
Martin, Nicholas G.
Wilson, James G.
Rader, Daniel J.
Samani, Nilesh J.
Reiner, Alex P.
Hegele, Robert A.
Kastelein, John J. P.
Hingorani, Aroon D.
Talmud, Philippa J.
Hakonarson, Hakon
Elbers, Clara C.
Keating, Brendan J.
Drenos, Fotios
CA LifeLines Cohort Study
TI Large-Scale Gene-Centric Meta-analysis across 32 Studies Identifies
Multiple Lipid Loci
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; DENSITY-LIPOPROTEIN CHOLESTEROL;
CORONARY-HEART-DISEASE; FAMILIAL HYPERCHOLESTEROLEMIA; APOLIPOPROTEIN
B-100; MISSING HERITABILITY; PLASMA TRIGLYCERIDES; QUANTITATIVE TRAITS;
STATISTICAL-MODEL; COMPLEX TRAITS
AB Genome-wide association studies (GWASs) have identified many SNPs underlying variations in plasma-lipid levels. We explore whether additional loci associated with plasma-lipid phenotypes, such as high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), and triglycerides (TGs), can be identified by a dense gene-centric approach. Our meta-analysis of 32 studies in 66,240 individuals of European ancestry was based on the custom similar to 50,000 SNP genotyping array (the ITMAT-Broad-CARe array) covering similar to 2,000 candidate genes. SNP-lipid associations were replicated either in a cohort comprising an additional 24,736 samples or within the Global Lipid Genetic Consortium. We identified four, six, ten, and four unreported SNPs in established lipid genes for HDL-C, LDL-C, TC, and TGs, respectively. We also identified several lipid-related SNPs in previously unreported genes: DGAT2, HCAR2, GPIHBP1, PPARG, and FTO for HDL-C; SOCS3, APOH, SPTY2D1, BRCA2, and VLDLR for LDL-C; SOCS3, UGT1A1, BRCA2, UBE3B, FCGR2A, CHUK, and INSIG2 for TC; and SERPINF2, C4B, GCK, GATA4, INSR, and LPAL2 for TGs. The proportion of explained phenotypic variance in the subset of studies providing individual-level data was 9.9% for HDL-C, 9.5% for LDL-C, 10.3% for TC, and 8.0% for TGs. This large meta-analysis of lipid phenotypes with the use of a dense gene-centric approach identified multiple SNPs not previously described in established lipid genes and several previously unknown loci. The explained phenotypic variance from this approach was comparable to that from a meta-analysis of GWAS data, suggesting that a focused genotyping approach can further increase the understanding of heritability of plasma lipids.
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[Asselbergs, Folkert W.; Bauer, Florianne; de Bakker, Paul I. W.; Onland-Moret, N. Charlotte; van der Schouw, Yvonne T.; Elbers, Clara C.] Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, NL-3508 GA Utrecht, Netherlands.
[Asselbergs, Folkert W.; Tragante, Vinicius; van Setten, Jessica] Univ Med Ctr Utrecht, Dept Med Genet, NL-3584 CX Utrecht, Netherlands.
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[van Iperen, Erik P. A.] Durrer Ctr Cardiogenet Res, NL-1105 AZ Amsterdam, Netherlands.
[van Iperen, Erik P. A.] Univ Amsterdam, Acad Med Ctr, Dept Clin Epidemiol Biostat & Bioinformat, NL-1105 AZ Amsterdam, Netherlands.
[Sivapalaratnam, Suthesh; Hovingh, G. Kees] Univ Amsterdam, Acad Med Ctr, Dept Vasc Med, NL-1105 AZ Amsterdam, Netherlands.
[Lanktree, Matthew B.] Univ Western Ontario, Schulich Sch Med & Dent, Dept Med, London, ON N6A 3K6, Canada.
[Lanktree, Matthew B.] Univ Western Ontario, Schulich Sch Med & Dent, Dept Biochem, London, ON N6A 3K6, Canada.
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[Illig, Thomas] Hannover Med Sch, Hannover Unified Biobank, D-30625 Hannover, Germany.
[Kirkland, Susan A.] Dalhousie Univ, Dept Med, Halifax, NS B3H 1V7, Canada.
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[Whittaker, John C.] GlaxoSmithKline, Stevenage SG1 2NY, Herts, England.
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[Zwinderman, A. H.] Acad Med Ctr, Department Clin Epidemiol Biostat & Bioinformat, NL-1100 DE Amsterdam, Netherlands.
[LifeLines Cohort Study] Univ Groningen, Univ Med Ctr Groningen, LifeLines Cohort Study, NL-9700 RB Groningen, Netherlands.
[Bezzina, Connie R.] Univ Amsterdam, Acad Med Ctr, Mol & Expt Cardiol Grp, NL-1105 AZ Amsterdam, Netherlands.
[Boehm, Bernhard O.] Univ Hosp, Dept Med, Dept Internal Med, D-89069 Ulm, Germany.
[Casas, Juan P.] Univ London London Sch Hyg & Trop Med, Fac Epidemiol & Populat Hlth, London WC1E 7HT, England.
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[Humphries, Steve E.; Talmud, Philippa J.; Drenos, Fotios] UCL, Fac Populat Hlth Sci, Inst Cardiovasc Sci, Ctr Cardiovasc Genet, London WC1E 6JF, England.
[Koenig, Wolfgang] Univ Ulm, Med Ctr, Dept Internal Med Cardiol 2, D-89081 Ulm, Germany.
[Maerz, Winfried] Synlab Acad, D-68165 Mannheim, Germany.
[Melander, Olle] Malmo Univ Hosp, Clin Res Ctr, SE-20502 Malmo, Sweden.
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RP Keating, BJ (reprint author), Childrens Hosp Philadelphia, Abramson Res Ctr, Ctr Appl Genom, Philadelphia, PA 19104 USA.
EM bkeating@mail.med.upenn.edu; f.drenos@ucl.ac.uk
RI Buxbaum, Sarah/E-1970-2013; Montgomery, Grant/B-7148-2008; Hegele,
Robert/G-3301-2011; Newhouse, Stephen/C-9330-2011; Padmanabhan,
Sandosh/S-3963-2016; Verweij, Niek/A-4499-2017; Guo, Yiran/H-4120-2011;
Stolk, Ronald/B-2341-2013; Wolffenbuttel, Bruce/A-8419-2011; Stanton,
Alice/F-4697-2012; de Bakker, Paul/B-8730-2009; Wijmenga,
Cisca/D-2173-2009; van der Schouw, Yvonne/F-8327-2014; Thorand,
Barbara/B-5349-2014; Jarvik, Gail/N-6476-2014; Gaunt, Tom/O-3918-2014;
Boehm, Bernhard/F-8750-2015; Onland-Moret, N. Charlotte/G-9185-2011
OI van Iperen, Erik/0000-0001-7107-3168; Topol, Eric/0000-0002-1478-4729;
Mitchell, Braxton/0000-0003-4920-4744; Ouwehand,
Willem/0000-0002-7744-1790; Lawlor, Debbie A/0000-0002-6793-2262;
Pankow, James/0000-0001-7076-483X; Kleber, Marcus/0000-0003-0663-7275;
Martin, Nicholas/0000-0003-4069-8020; Buxbaum,
Sarah/0000-0002-4886-3564; Talmud, Philippa/0000-0002-5560-1933;
Johnson, Toby/0000-0002-5998-3270; Swerdlow, Daniel/0000-0002-7946-3459;
Padmanabhan, Sandosh/0000-0003-3869-5808; Humphries, Stephen
E/0000-0002-8221-6547; Wijmenga, Cisca/0000-0002-5635-1614; Kumari,
Meena/0000-0001-9716-1035; Verweij, Niek/0000-0002-4303-7685; Klein,
Ronald/0000-0002-4428-6237; Watkins, Hugh/0000-0002-5287-9016;
Montgomery, Grant/0000-0002-4140-8139; Newhouse,
Stephen/0000-0002-1843-9842; Shah, Tina/0000-0001-7724-7210; Franke,
Lude/0000-0002-5159-8802; Cupples, L. Adrienne/0000-0003-0273-7965;
Lanktree, Matthew/0000-0002-5750-6286; Stanton,
Alice/0000-0002-4961-165X; van Vliet-Ostaptchouk,
Jana/0000-0002-7943-3153; Kivimaki, Mika/0000-0002-4699-5627; Guo,
Yiran/0000-0002-6549-8589; Stolk, Ronald/0000-0002-0518-1205;
Wolffenbuttel, Bruce/0000-0001-9262-6921; de Bakker,
Paul/0000-0001-7735-7858; van der Schouw, Yvonne/0000-0002-4605-435X;
Thorand, Barbara/0000-0002-8416-6440; Jarvik, Gail/0000-0002-6710-8708;
Gaunt, Tom/0000-0003-0924-3247;
FU AHRQ HHS [HS06516]; British Heart Foundation [CH/03/001, CH/98001,
PG/02/128, PG/07/131/24254, PG/07/132/24256, PG/07/133/24260,
RG/07/005/23633, RG/08/008, RG/08/008/25291, RG/10/12/28456, RG/2001004,
SP/07/007/23671, SP/08/005/25115]; Department of Health; Intramural NIH
HHS; Medical Research Council [G0802432, G9521010, G9521010D,
MC_U137686857]; NCATS NIH HHS [UL1 TR000064, UL1 TR000124, UL1 TR000135,
UL1 TR000454]; NCI NIH HHS [P30 CA015704]; NCRR NIH HHS [UL1 RR025774,
UL1RR025005]; NEI NIH HHS [U10EY06594]; NHGRI NIH HHS [U01HG004402];
NHLBI NIH HHS [HL36310, K24 HL084034, N01-HC-05187, N01-HC-15103,
N01-HC-25195, N01-HC-35129, N01-HC-45134, N01-HC-45204, N01-HC-45205,
N01-HC-48047, N01-HC-48048, N01-HC-48049, N01-HC-48050, N01-HC-55015,
N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021,
N01-HC-55022, N01-HC-55222, N01-HC-75150, N01-HC-85079, N01-HC-85080,
N01-HC-85081, N01-HC-85082, N01-HC-85083, N01-HC-85084, N01-HC-85085,
N01-HC-85086, N01-HC-95095, N01-HC-95100, N01-HC-95159, N01-HC-95160,
N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165,
N01-HC-95166, N01-HC-95167, N01-HC-95168, N01-HC-95169, P01 HL088117,
P50HL81011, R01 HL088119, R01 HL091099, R01 HL105756, R01 HL67406,
R01-HL-071205, R01-HL-076784, R01-HL-092577, R01HL086694, R01HL087641,
R01HL59367, U01 HL72515, U01-HL-080295]; NIA NIH HHS [AG-16592, AG13196,
R01 AG011099, R01 AG016592, R01 AG021917, R01 AG18728, R01-AG-028321,
R01AG021917, R37 AG011099, R37AG11099]; NICHD NIH HHS [HD-061437,
HD-062783]; NIDDK NIH HHS [P30 DK063491, P30 DK072488]; NIGMS NIH HHS
[U01 GM074492, U01-GM074492]; NIMHD NIH HHS [P20 MD006899]; Wellcome
Trust [, 090532]
NR 76
TC 95
Z9 95
U1 4
U2 41
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 2
PY 2012
VL 91
IS 5
BP 823
EP 838
DI 10.1016/j.ajhg.2012.08.032
PG 16
WC Genetics & Heredity
SC Genetics & Heredity
GA 036FI
UT WOS:000311011400005
PM 23063622
ER
PT J
AU Park, KS
Kim, KK
Kim, KE
AF Park, Key Sun
Kim, Kee Kwang
Kim, Kyoon Eon
TI Histone modification-mediated Lhx2 gene expression
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Lhx2; E2F1; HDAC3; Histone deacetylation; Trichostatin A
ID HOMEODOMAIN TRANSCRIPTION FACTOR; LIM-HOMEOBOX GENE; DOMAIN PROTEINS;
DEACETYLASES; HORMONE; ACETYLATION; DIFFERENTIATION; ACTIVATION;
MECHANISMS; CHROMATIN
AB Lhx2, a member of LIM homeobox transcription factors, plays a key role in central nervous system (CNS) and embryonic tissue development. However, molecular mechanism of Lhx2 gene regulation remains largely unknown. Here, we identified and characterized a regulatory region of Lhx2 gene which mediates responses to two different signals such as inhibition of HDAC3 and stimulation by E2F1. In particular, the promoter region of -229 to -126 was responsible not only for basal expression but also for a inhibitor of histone deacetylase, trichostatin A (TSA)-mediated activation of Lhx2 gene. Intriguingly, transcription factor E2F1 also activates Lhx2 gene via direct binding to the same -229 to -126 region. Based on these observations, we could have demonstrated that E2F1 is necessary for TSA-mediated activation of Lhx2 gene and acetylation of histone 3 is involved in this event. This study provides evidence that the histone modification and E2F1 binding are integral parts of the mechanism for Lhx2 gene expression. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Park, Key Sun; Kim, Kee Kwang; Kim, Kyoon Eon] Chungnam Natl Univ, Dept Biochem, Taejon 305764, South Korea.
[Kim, Kee Kwang] NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA.
RP Kim, KE (reprint author), Chungnam Natl Univ, Dept Biochem, Taejon 305764, South Korea.
EM kyoonkim@cnu.ac.kr
RI Kim, Kee/F-8784-2011
FU Ministry of Science, Education and Technology, Korea [WCI 2009-002]
FX This work was supported by the grant "World Class Institute (WCI
2009-002)" program of the Ministry of Science, Education and Technology,
Korea.
NR 33
TC 1
Z9 1
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD NOV 2
PY 2012
VL 427
IS 4
BP 718
EP 724
DI 10.1016/j.bbrc.2012.09.123
PG 7
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 037VN
UT WOS:000311134700006
PM 23036195
ER
PT J
AU Gao, Y
Li, Z
Lin, ZY
Zhu, LJ
Tannenbaum, A
Bouix, S
Wong, CP
AF Gao, Yi
Li, Zhuo
Lin, Ziyin
Zhu, Liangjia
Tannenbaum, Allen
Bouix, Sylvain
Wong, C. P.
TI Automated dispersion and orientation analysis for carbon nanotube
reinforced polymer composites
SO NANOTECHNOLOGY
LA English
DT Article
ID NANOCOMPOSITES; FUNCTIONALIZATION; MATRIX; FILMS
AB The properties of carbon nanotube (CNT)/polymer composites are strongly dependent on the dispersion and orientation of CNTs in the host matrix. Quantification of the dispersion and orientation of CNTs by means of microstructure observation and image analysis has been demonstrated as a useful way to understand the structure-property relationship of CNT/polymer composites. However, due to the various morphologies and large amount of CNTs in one image, automatic and accurate identification of CNTs has become the bottleneck for dispersion/orientation analysis. To solve this problem, shape identification is performed for each pixel in the filler identification step, so that individual CNTs can be extracted from images automatically. The improved filler identification enables more accurate analysis of CNT dispersion and orientation. The dispersion index and orientation index obtained for both synthetic and real images from model compounds correspond well with the observations. Moreover, these indices help to explain the electrical properties of CNT/silicone composite, which is used as a model compound. This method can also be extended to other polymer composites with high-aspect-ratio fillers.
C1 [Li, Zhuo; Lin, Ziyin; Wong, C. P.] Georgia Inst Technol, Sch Mat Sci & Engn, Atlanta, GA 30332 USA.
[Gao, Yi; Bouix, Sylvain] Harvard Univ, Sch Med, Psychiat Neuroimaging Lab, Boston, MA 02115 USA.
[Zhu, Liangjia] Georgia Inst Technol, Dept Elect, Atlanta, GA 30332 USA.
[Zhu, Liangjia] Georgia Inst Technol, Dept Comp Engn, Atlanta, GA 30332 USA.
[Tannenbaum, Allen] Boston Univ, Dept Elect, Boston, MA 02115 USA.
[Tannenbaum, Allen] Boston Univ, Dept Comp Engn, Boston, MA 02115 USA.
[Tannenbaum, Allen] Univ Alabama Birmingham, Wallace Canc Ctr, Birmingham, AL 35294 USA.
[Tannenbaum, Allen] NCI, Bethesda, MD 20814 USA.
[Wong, C. P.] Chinese Univ Hong Kong, Coll Engn, Shatin, Hong Kong, Peoples R China.
RP Wong, CP (reprint author), Georgia Inst Technol, Sch Mat Sci & Engn, Atlanta, GA 30332 USA.
EM gaoyi@bwh.harvard.edu; zli33@gatech.edu; zylin@gatech.edu;
ljzhu@gatech.edu; arobertan@gmail.com; sylvain@bwh.harvard.edu;
cp.wong@mse.gatech.edu
OI Bouix, Sylvain/0000-0003-1326-6054
FU US Department of Energy [DE-SC0001967]; NSF; AFOSR; ARO; NIH through
Brigham [R01 MH82918, NAC P41 RR-13218, NAC P41-EB-015902, NA-MIC U54
EB-005149]
FX We would like to thank the anonymous reviewers for their help in
improving the manuscript. This work was supported by the US Department
of Energy through project number DE-SC0001967. This work was also
supported in part by grants from NSF, AFOSR, ARO, as well as by grants
from NIH (R01 MH82918, NAC P41 RR-13218, NAC P41-EB-015902, and NA-MIC
U54 EB-005149) through Brigham and Women's Hospital.
NR 32
TC 7
Z9 7
U1 0
U2 28
PU IOP PUBLISHING LTD
PI BRISTOL
PA TEMPLE CIRCUS, TEMPLE WAY, BRISTOL BS1 6BE, ENGLAND
SN 0957-4484
EI 1361-6528
J9 NANOTECHNOLOGY
JI Nanotechnology
PD NOV 2
PY 2012
VL 23
IS 43
AR 435706
DI 10.1088/0957-4484/23/43/435706
PG 10
WC Nanoscience & Nanotechnology; Materials Science, Multidisciplinary;
Physics, Applied
SC Science & Technology - Other Topics; Materials Science; Physics
GA 030MA
UT WOS:000310573600017
PM 23060008
ER
PT J
AU Visweswaraiah, J
Lee, SJ
Hinnebusch, AG
Sattlegger, E
AF Visweswaraiah, Jyothsna
Lee, Su Jung
Hinnebusch, Alan G.
Sattlegger, Evelyn
TI Overexpression of Eukaryotic Translation Elongation Factor 3 Impairs
Gcn2 Protein Activation
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID EIF-2-ALPHA KINASE GCN2; UNCHARGED TRANSFER-RNA; ACID-STARVED CELLS;
SACCHAROMYCES-CEREVISIAE; RIBOSOMAL ATPASE; BINDING-PROTEIN; EIF2 ALPHA;
E-SITE; YEAST; DOMAIN
AB In eukaryotes, phosphorylation of translation initiation factor 2 alpha (eIF2 alpha) by the kinase Gcn2 (general control nonderepressible 2) is a key response to amino acid starvation. Sensing starvation requires that Gcn2 directly contacts its effector protein Gcn1, and both must contact the ribosome. We have proposed that Gcn2 is activated by uncharged tRNA bound to the ribosomal decoding (A) site, in a manner facilitated by ribosome-bound Gcn1. Protein synthesis requires cyclical association of eukaryotic elongation factors (eEFs) with the ribosome. Gcn1 and Gcn2 are large proteins, raising the question of whether translation and monitoring amino acid availability can occur on the same ribosome. Part of the ribosome-binding domain in Gcn1 has homology to one of the ribosome-binding domains in eEF3, suggesting that these proteins utilize overlapping binding sites on the ribosome and consequently cannot function simultaneously on the same ribosome. Supporting this idea, we found that eEF3 overexpression in Saccharomyces cerevisiae diminished growth on amino acid starvation medium (Gcn(-) phenotype) and decreased eIF2 alpha phosphorylation, and that the growth defect associated with constitutively active Gcn2 was diminished by eEF3 overexpression. Overexpression of the eEF3 HEAT domain, or C terminus, was sufficient to confer a Gcn(-) phenotype, and both fragments have ribosome affinity. eEF3 overexpression did not significantly affect Gcn1-ribosome association, but it exacerbated the Gcn(-) phenotype of Gcn1-M7A that has reduced ribosome affinity. Together, this suggests that eEF3 blocks Gcn1 regulatory function on the ribosome. We propose that the Gcn1-Gcn2 complex only functions on ribosomes with A-site-bound uncharged tRNA, because eEF3 does not occupy these stalled complexes.
C1 [Sattlegger, Evelyn] Massey Univ, Inst Nat Sci, N Shore Mail Ctr, Auckland 0745, Albany, New Zealand.
[Hinnebusch, Alan G.; Sattlegger, Evelyn] NICHD, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA.
RP Sattlegger, E (reprint author), Massey Univ, Inst Nat Sci, N Shore Mail Ctr, POB 102 904, Auckland 0745, Albany, New Zealand.
EM e.sattlegger@massey.ac.nz
FU National Institutes of Health; Marsden Fund Council Grant [MAU0607];
Massey University
FX This work was supported in part by National Institutes of Health
Intramural Research Program (to A. G. H.). This work was also supported
by Marsden Fund Council Grant MAU0607 administered by the Royal Society
of New Zealand, a Massey University Technicians Award (to E. S. for
supporting S. J. L.), the Massey University Research Fund (to E. S.),
and a Massey University Ph.D. Scholarship (to J. V.).
NR 40
TC 5
Z9 8
U1 1
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 2
PY 2012
VL 287
IS 45
DI 10.1074/jbc.M112.368266
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 031LP
UT WOS:000310642200015
PM 22888004
ER
PT J
AU Krepkiy, D
Gawrisch, K
Swartz, KJ
AF Krepkiy, Dmitriy
Gawrisch, Klaus
Swartz, Kenton J.
TI Structural Interactions between Lipids, Water and S1-S4 Voltage-Sensing
Domains
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Article
DE NMR; S4 helix; voltage-activated ion channel; anionic lipids; DOTAP
ID SHAKER K+ CHANNEL; SOLID-STATE NMR; DEPENDENT CONFORMATIONAL-CHANGES;
INTEGRAL MEMBRANE-PROTEINS; X-RAY-STRUCTURE; POTASSIUM CHANNEL;
GATING-CHARGE; MAGNETIC-RESONANCE; ELECTROSTATIC INTERACTIONS;
BIOLOGICAL-MEMBRANES
AB Membrane proteins serve crucial signaling and transport functions, yet relatively little is known about their structures in membrane environments or how lipids interact with these proteins. For voltage-activated ion channels, X-ray structures suggest that the mobile voltage-sensing S4 helix would be exposed to the membrane, and functional studies reveal that lipid modification can profoundly alter channel activity. Here, we use solid-state NMR to investigate structural interactions of lipids and water with Si S4 voltage-sensing domains and to explore whether lipids influence the structure of the protein. Our results demonstrate that S1-S4 domains exhibit extensive interactions with lipids and that these domains are heavily hydrated when embedded in a membrane. We also find evidence for preferential interactions of anionic lipids with S1-S4 domains and that these interactions have lifetimes on the timescale of <= 10(-3) s. Arg residues within S1-S4 domains are well hydrated and are positioned in close proximity to lipids, exhibiting local interactions with both lipid headgroups and acyl chains. Comparative studies with a positively charged lipid lacking a phosphodiester group reveal that this lipid modification has only modest effects on the structure and hydration of S1-S4 domains. Taken together, our results demonstrate that Arg residues in S1-S4 voltage-sensing domains reside in close proximity to the hydrophobic interior of the membrane yet are well hydrated, a requirement for carrying charge and driving protein motions in response to changes in membrane voltage. Published by Elsevier Ltd.
C1 [Gawrisch, Klaus] NIAAA, Lab Membrane Biochem & Biophys, NIH, Bethesda, MD 20892 USA.
[Krepkiy, Dmitriy; Swartz, Kenton J.] Natl Inst Neurol Disorders & Stroke, Mol Physiol & Biophys Sect, Porter Neurosci Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Gawrisch, K (reprint author), NIAAA, Lab Membrane Biochem & Biophys, NIH, Bethesda, MD 20892 USA.
EM klausg@mail.nih.gov; swartzk@ninds.nih.gov
FU Intramural Research Program of the NINDS, National Institutes of Health;
National Institute on Alcohol Abuse and Alcoholism, National Institutes
of Health
FX We thank the National Institute of Neurological Disorders and Stroke
(NINDS) DNA sequencing facility and Howard Jaffe in the NINDS Protein
Facility for MS analysis. We thank members of the Swartz, Gawrisch,
Mindell and Mayer laboratories for discussions and critique. This work
was supported by the Intramural Research Program of the NINDS, National
Institutes of Health (to K.J.S.) and the National Institute on Alcohol
Abuse and Alcoholism, National Institutes of Health (to K.G.).
NR 97
TC 16
Z9 16
U1 3
U2 43
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 2
PY 2012
VL 423
IS 4
BP 632
EP 647
DI 10.1016/j.jmb.2012.07.015
PG 16
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 028IK
UT WOS:000310415800016
PM 22858867
ER
PT J
AU Kenney, J
Singer, R
Derby, N
Aravantinou, M
Abraham, CJ
Menon, R
Seidor, S
Zhang, SM
Gettie, A
Blanchard, J
Piatak, M
Lifson, JD
Fernandez-Romero, JA
Zydowsky, TM
Robbiani, M
AF Kenney, Jessica
Singer, Rachel
Derby, Nina
Aravantinou, Meropi
Abraham, Ciby J.
Menon, Radhika
Seidor, Samantha
Zhang, Shimin
Gettie, Agegnehu
Blanchard, James
Piatak, Michael, Jr.
Lifson, Jeffrey D.
Fernandez-Romero, Jose A.
Zydowsky, Thomas M.
Robbiani, Melissa
TI A Single Dose of a MIV-150/Zinc Acetate Gel Provides 24 h of Protection
Against Vaginal Simian Human Immunodeficiency Virus Reverse
Transcriptase Infection, with More Limited Protection Rectally 8-24 h
After Gel Use
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Article
ID HIV-1 INFECTION; VIRAL LOAD; IN-VITRO; ZINC; MICROBICIDE; MACAQUES;
EFFICACY; WOMEN; TRANSMISSION; INHIBITION
AB Previously we showed that repeated vaginal application of a MIV-150/zinc acetate carrageenan (MIV-150/ZA/CG) gel and a zinc acetate carrageenan (ZA/CG) gel significantly protected macaques from vaginal simian human immunodeficiency virus reverse transcriptase (SHIV-RT) infection. Gels were applied either daily for 2 weeks or every other day for 4 weeks, and the animals were challenged 4-24 h later. Herein, we examined the effects of a single vaginal dose administered either before or after virus challenge. Encouraged by the vaginal protection seen with MIV-150/ZA/CG, we also tested it rectally. Vaginal applications of MIV-150/ZA/CG, ZA/CG, and CG gel were performed once 8-24 h before, 1 h after, or 24 h before and 1 h after vaginal challenge. Rectal applications of MIV-150/ZA/CG and CG gel were performed once 8 or 24 h before rectal challenge. While vaginal pre-challenge and pre/post-challenge application of MIV-150/ZA/CG gel offered significant protection (88%, p < 0.002), post-challenge application alone did not significantly protect. ZA/CG gel reduced infection prechallenge, but not significantly, and the effect was completely lost post-challenge. Rectal application of MIV-150/ZA/CG gel afforded limited protection against rectal challenge when applied 8-24 h before challenge. Thus, MIV-150/ZA/CG gel is a highly effective vaginal microbicide that demonstrates 24 h of protection from vaginal infection and may demonstrate efficacy against rectal infection when given close to the time of HIV exposure.
C1 [Robbiani, Melissa] Populat Council, Ctr Biomed Res, New York, NY 10065 USA.
[Gettie, Agegnehu] Rockefeller Univ, Aaron Diamond AIDS Res Ctr, New York, NY 10021 USA.
[Blanchard, James] Tulane Univ, Tulane Natl Primate Res Ctr, Covington, LA USA.
[Piatak, Michael, Jr.; Lifson, Jeffrey D.] NCI, AIDS & Canc Virus Program, SAIC Frederick Inc, Frederick, MD 21701 USA.
RP Robbiani, M (reprint author), Populat Council, Ctr Biomed Res, 1230 York Ave, New York, NY 10065 USA.
EM mrobbiani@popcouncil.org
FU United States Agency for International Development (USAID)
[GPO-A-00-04-00019-00]; Swedish Ministry of Foreign Affairs; Swedish
International Development Cooperation Agency; NIH [RR00164]; National
Cancer Institute, NIH [HHSN261200800001E]
FX We thank the veterinary staff at the TNPRC for continued support and
Laiju (John) Zhang for statistical assistance. This work was supported
by the United States Agency for International Development (USAID)
Cooperative Agreement GPO-A-00-04-00019-00, the Swedish Ministry of
Foreign Affairs, the Swedish International Development Cooperation
Agency, the NIH base grant RR00164, and with federal funds from the
National Cancer Institute, NIH, under contract HHSN261200800001E. This
research is made possible by the generous support of the American people
through the USAID.
NR 29
TC 30
Z9 31
U1 0
U2 3
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2012
VL 28
IS 11
BP 1476
EP 1484
DI 10.1089/aid.2012.0087
PG 9
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 032XP
UT WOS:000310754100012
PM 22737981
ER
PT J
AU Aravantinou, M
Singer, R
Derby, N
Calenda, G
Mawson, P
Abraham, CJ
Menon, R
Seidor, S
Goldman, D
Kenney, J
Villegas, G
Gettie, A
Blanchard, J
Lifson, JD
Piatak, M
Fernandez-Romero, JA
Zydowsky, TM
Teleshova, N
Robbiani, M
AF Aravantinou, Meropi
Singer, Rachel
Derby, Nina
Calenda, Giulia
Mawson, Paul
Abraham, Ciby J.
Menon, Radhika
Seidor, Samantha
Goldman, Daniel
Kenney, Jessica
Villegas, Guillermo
Gettie, Agegnehu
Blanchard, James
Lifson, Jeffrey D.
Piatak, Michael, Jr.
Fernandez-Romero, Jose A.
Zydowsky, Thomas M.
Teleshova, Natalia
Robbiani, Melissa
TI The Nonnucleoside Reverse Transcription Inhibitor MIV-160 Delivered from
an Intravaginal Ring, But Not from a Carrageenan Gel, Protects Against
Simian/Human Immunodeficiency Virus-RT Infection
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Article
ID HIV-NEGATIVE WOMEN; VAGINAL MICROBICIDE GEL; IN-VITRO; TOPICAL
MICROBICIDES; CONTROLLED-TRIAL; TENOFOVIR GEL; RECTAL TRANSMISSION;
RHESUS MACAQUE; DAPIVIRINE; PREVENTION
AB We previously showed that a carrageenan (CG) gel containing 50 mu M MIV-150 (MIV-150/CG) reduced vaginal simian/human immunodeficiency virus (SHIV)-RT infection of macaques (56%, p > 0.05) when administered daily for 2 weeks with the last dose given 8 h before challenge. Additionally, when 100 mg of MIV-150 was loaded into an intravaginal ring (IVR) inserted 24 h before challenge and removed 2 weeks after challenge, > 80% protection was observed (p < 0.03). MIV-160 is a related NNRTI with a similar IC50, greater aqueous solubility, and a shorter synthesis. To objectively compare MIV-160 with MIV-150, herein we evaluated the antiviral effects of unformulated MIV-160 in vitro as well as the in vivo protection afforded by MIV-160 delivered in CG (MIV-160/CG gel) and in an IVR under regimens used with MIV-150 in earlier studies. Like MIV-150, MIV-160 exhibited potent antiviral activity against SHIV-RT in macaque vaginal explants. However, formulated MIV-160 exhibited divergent effects in vivo. The MIV-160/CG gel offered no protection compared to CG alone, whereas the MIV-160 IVRs protected significantly. Importantly, the results of in vitro release studies of the MIV-160/CG gel and the MIV-160 IVR suggested that in vivo efficacy paralleled the amount of MIV-160 released in vitro. Hundreds of micrograms of MIV-160 were released daily from IVRs while undetectable amounts of MIV-160 were released from the CG gel. Our findings highlight the importance of testing different modalities of microbicide delivery to identify the optimal formulation for efficacy in vivo.
C1 [Robbiani, Melissa] Populat Council, Ctr Biomed Res, New York, NY 10065 USA.
[Gettie, Agegnehu] Rockefeller Univ, Aaron Diamond AIDS Res Ctr, New York, NY 10021 USA.
[Blanchard, James] Tulane Univ, Tulane Natl Primate Res Ctr, Covington, LA USA.
[Lifson, Jeffrey D.; Piatak, Michael, Jr.] NCI, AIDS & Canc Virus Program, SAIC Frederick Inc, Frederick, MD 21701 USA.
RP Robbiani, M (reprint author), Populat Council, Ctr Biomed Res, 1230 York Ave, New York, NY 10065 USA.
EM mrobbiani@popcouncil.org
FU United States Agency for International Development (USAID)
[GPO-A-00-04-00019-00]; NIH [RR00164]; National Cancer Institute, NIH
[HHSN261200800001E]
FX We thank the veterinary staff at the TNPRC for continued support. This
work was supported by the United States Agency for International
Development (USAID) Cooperative Agreement GPO-A-00-04-00019-00, the NIH
base grant RR00164, and with federal funds from the National Cancer
Institute, NIH, under contract HHSN261200800001E. This research is made
possible by the generous support of the American people through the
USAID.
NR 57
TC 19
Z9 19
U1 0
U2 4
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2012
VL 28
IS 11
BP 1467
EP 1475
DI 10.1089/aid.2012.0080
PG 9
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 032XP
UT WOS:000310754100011
PM 22816564
ER
PT J
AU Lo Surdo, J
Bauer, SR
AF Lo Surdo, Jessica
Bauer, Steven R.
TI Quantitative Approaches to Detect Donor and Passage Differences in
Adipogenic Potential and Clonogenicity in Human Bone Marrow-Derived
Mesenchymal Stem Cells
SO TISSUE ENGINEERING PART C-METHODS
LA English
DT Article
ID MULTIPOTENT STROMAL CELLS; LIMITING DILUTION ASSAYS; OSTEOGENIC
DIFFERENTIATION; ADIPOSE-TISSUE; PROGENITOR CELLS; EXPRESSION;
POPULATIONS; EXPANSION; CULTURES; PROLIFERATION
AB Bone marrow-derived multipotent stromal cells (MSCs), also known as mesenchymal stem cells, have great promise due to their capacity for tri-lineage differentiation and immunosuppressive properties, which allows for their allogeneic use and ultimately may allow for treatment of many diseases. MSCs will require extensive expansion and passaging to obtain cells in sufficient numbers necessary for cell therapies. MSCs from many donors could potentially be used. Because of this, there is a need to understand the role of passaging and donor differences on differentiation capacity using quantitative approaches. Here, we evaluated MSCs from two donors (noted as PCBM1632 and PCBM1641 by the manufacturer) at tissue culture passages 3, 5, and 7. We used a colony forming unit (CFU) assay and limiting dilution to quantify clonogenicity and precursor frequency during adipogenesis, and quantitative real-time-polymerase chain reaction for adipogenic markers to evaluate changes on a gene expression level. Further, we observed changes in cell size, and we sorted small and large populations to evaluate size-related adipogenic potential. While the adipogenic precursor frequency of similar to 1 in 76 cells remained similar through passages for cells from PCBM1641, we found a large decrease in the adipogenic potential of MSCs from PCBM1632, with 1 in 2035 cells being capable of differentiating into an adipocyte at passage 7. MSCs from both donors showed an increase in cell diameter with increasing passage, which correlates with a decrease in clonogenicity by CFU analysis. We also measured adipose lineage gene expression following induction of adipocyte differentiation. Expression of these genes decreased with passage number for MSCs from PCBM1632 and correlated with the decrease in adipogenic potential by passage 7. In contrast, MSCs from PCBM1641 showed increased expression of these genes with increasing passage. We have shown that several quantitative assays can detect differences in MSC differentiation capacity, clonogenicity, and cell size between donors and passages. These quantitative methods are useful to assess the quality of MSCs.
C1 [Lo Surdo, Jessica; Bauer, Steven R.] US FDA, Cellular & Tissue Therapies Branch, Div Cellular & Gene Therapies, Off Cellular Tissue & Gene Therapies,Ctr Biol Eva, Bethesda, MD 20892 USA.
RP Bauer, SR (reprint author), US FDA, Cellular & Tissue Therapies Branch, Div Cellular & Gene Therapies, Off Cellular Tissue & Gene Therapies,Ctr Biol Eva, NIH Bldg,29B 2NN10 HFM-740,8800 Rockville Pike, Bethesda, MD 20892 USA.
EM steven.bauer@fda.hhs.gov
OI Bauer, Steven/0000-0003-2831-846X
FU FDA Modernizing Science grant program; BARDA grant; Division of Cell and
Gene Therapies; FDA's Office of the Chief Scientist; BARDA; Division of
Cellular and Gene Therapies
FX This project was supported in part by Jessica Lo Surdo's appointment to
the Research Participation Program at CBER administered by the Oak Ridge
Institute for Science and Education through US DOE and US FDA. This work
was also supported in part by the FDA Modernizing Science grant program,
a BARDA grant, and Division of Cell and Gene Therapies. The authors
would like to acknowledge Drs. Cheng-Hong Wei and Jeffry Smith for
reviewing this article and Howard Mostowski for his assistance in
sorting MSC samples. Research support came from FDA's Office of the
Chief Scientist, BARDA, and operating funds from the Division of
Cellular and Gene Therapies.
NR 65
TC 32
Z9 32
U1 0
U2 5
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1937-3384
J9 TISSUE ENG PART C-ME
JI Tissue Eng. Part C-Methods
PD NOV
PY 2012
VL 18
IS 11
BP 877
EP 889
DI 10.1089/ten.tec.2011.0736
PG 13
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell
Biology
SC Cell Biology; Biotechnology & Applied Microbiology
GA 030MN
UT WOS:000310574900006
PM 22563812
ER
PT J
AU Peltzer, K
Ramlagan, S
Jones, D
Weiss, SM
Fomundam, H
Chanetsa, L
AF Peltzer, Karl
Ramlagan, Shandir
Jones, Deborah
Weiss, Stephen M.
Fomundam, Henry
Chanetsa, Lucia
TI Efficacy of a lay health worker led group antiretroviral medication
adherence training among non-adherent HIV-positive patients in
KwaZulu-Natal, South Africa: Results from a randomized trial
SO SAHARA J-JOURNAL OF SOCIAL ASPECTS OF HIV-AIDS
LA English
DT Article
DE medication adherence intervention (MAI); lay health worker; adherence;
antiretroviral therapy; HIV/AIDS; South Africa
ID SMART/EST WOMENS PROJECT; SUB-SAHARAN AFRICA; THERAPY ADHERENCE;
INFECTED INDIVIDUALS; VIRAL LOAD; INTERVENTIONS; DEPRESSION; IMPACT;
METAANALYSIS; DISTRESS
AB There is a lack of theory-based randomized controlled trials to examine the effect of antiretroviral adherence in sub-Saharan Africa. We assessed the effectiveness of a lay health worker lead structured group intervention to improve adherence to antiretroviral therapy (ART) in a cohort of HIV-infected adults. This two-arm randomized controlled trial was undertaken at an HIV clinic in a district hospital in South Africa. A total of 152 adult patients on ART and with adherence problems were randomized 1: 1 to one of two conditions, a standard adherence intervention package plus a structured three session group intervention or to a standard adherence intervention package alone. Self-reported adherence was measured using the Adult AIDS Clinical Trials Group adherence instrument prior to, post intervention and at follow-up. Baseline characteristics were similar for both conditions. At post-intervention, adherence information knowledge increased significantly in the intervention condition in comparison to the standard of care, while adherence motivation and skills did not significantly change among the conditions over time. There was a significant improvement in ART adherence and CD4 count and a significant reduction of depression scores over time in both conditions, however, no significant intervention effect between conditions was found. Lay health workers may be a useful adjunct to treatment to enhance the adherence information component of the medication adherence intervention, but knowledge may be necessary but not sufficient to increase adherence in this sample. Psychosocial informational interventions may require more advanced skill training in lay health workers to achieve superior adherence outcomes in comparison standard care in this resource-constrained setting.
C1 [Peltzer, Karl] Human Sci Res Council, Res Programme HIV AIDS STI & TB HAST, Pretoria, South Africa.
[Peltzer, Karl] Free State Univ, Bloemfontein, South Africa.
[Jones, Deborah] Univ Miami, Miller Sch Med, Dept Psychiat & Behav Sci, Maimi, FL USA.
[Weiss, Stephen M.] Univ Miami, Sch Med, Coral Gables, FL 33124 USA.
[Weiss, Stephen M.] NHLBI, NIH, Behav Med Branch, Bethesda, MD USA.
[Fomundam, Henry; Chanetsa, Lucia] Howard Univ, HIV AIDS Pharmaceut Care Program, Pretoria, South Africa.
RP Peltzer, K (reprint author), Human Sci Res Council, Res Programme HIV AIDS STI & TB HAST, Pretoria, South Africa.
EM kpeltzer@hsrc.ac.za
NR 41
TC 12
Z9 12
U1 1
U2 5
PU SA MEDICAL ASSOC HEALTH & MEDICAL PUBL GROUP
PI CLAREMONT
PA 21 DREYER ST, 4TH FLOOR, SANCLARE BLDG, CLAREMONT, 7700, SOUTH AFRICA
SN 1729-0376
J9 SAHARA J-J SOC ASP H
JI Sahara J-J. Soc. Asp. HIV/AIDS
PD NOV
PY 2012
VL 9
IS 4
BP 218
EP 226
DI 10.1080/17290376.2012.745640
PG 9
WC Health Policy & Services; Public, Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 181ZB
UT WOS:000321708400005
PM 23234350
ER
PT J
AU Drews, E
Zimmer, A
AF Drews, Eva
Zimmer, Andreas
TI The endogenous cannabinoid system
SO NEUROFORUM
LA German
DT Article
DE endocannabinoids; chronic pain; inflammation; beta-caryophyllene
ID PAIN; RECEPTORS
AB The hemp plant Cannabis saliva has been cultivated since thousands of years and is used as a medical plant and intoxicant. Scientific research on the psychoactive substances of Cannabis sativa and their effects on the brain has started around 50 years ago and led to the discovery of the endogenous cannabinoid system. Today we know that this system represent an important feedback mechanism that modulates the communication between neurons. However, this system is not only active in the brain, but is known to be activated in different tissues and organs during specific disease states. Consequently, there is an increasing interest in this system as a possible target for the development of new drugs. The currently commercially available drugs are based on cannabis extracts or synthetic compounds of the plant's active components and are mainly used to treat chronic pain. In this review we will elucidate the mechanisms of the endogenous cannabinoid system in pain perception and present a new herbal (phyto)cannabinoid which is a constituent of our daily food.
C1 [Zimmer, Andreas] Max Planck Inst Biophys Chem, D-37077 Gottingen, Germany.
[Zimmer, Andreas] Zentrum Mol Biol, Heidelberg, Germany.
[Zimmer, Andreas] NIMH, Bethesda, MD USA.
[Drews, Eva] Univ Bonn, D-53127 Bonn, Germany.
[Drews, Eva; Zimmer, Andreas] Univ Bonn, Inst Mol Psychiat, D-53127 Bonn, Germany.
RP Drews, E (reprint author), Univ Bonn, Inst Mol Psychiat, Sigmund Freud Str 25, D-53127 Bonn, Germany.
EM edrews@uni-bonn.ce; neuro@uni-bonn.de
NR 11
TC 0
Z9 0
U1 0
U2 6
PU SPEKTRUM AKADEMISCHER VERLAG-SPRINGER-VERLAG GMBH
PI HEILDEBERG
PA TIERGARTENSTRASSE 17, HEILDEBERG, 69121, GERMANY
SN 0947-0875
EI 1868-856X
J9 NEUROFORUM
JI Neuroforum
PD NOV
PY 2012
VL 18
IS 4
BP 290
EP +
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA 182FA
UT WOS:000321725900002
ER
PT J
AU Williams, AR
Douglas, AD
Miura, K
Illingworth, JJ
Choudhary, P
Murungi, LM
Furze, JM
Diouf, A
Miotto, O
Crosnier, C
Wright, GJ
Kwiatkowski, DP
Fairhurst, RM
Long, CA
Draper, SJ
AF Williams, Andrew R.
Douglas, Alexander D.
Miura, Kazutoyo
Illingworth, Joseph J.
Choudhary, Prateek
Murungi, Linda M.
Furze, Julie M.
Diouf, Ababacar
Miotto, Olivo
Crosnier, Cecile
Wright, Gavin J.
Kwiatkowski, Dominic P.
Fairhurst, Rick M.
Long, Carole A.
Draper, Simon J.
TI Enhancing Blockade of Plasmodium falciparum Erythrocyte Invasion:
Assessing Combinations of Antibodies against PfRH5 and Other Merozoite
Antigens
SO PLOS PATHOGENS
LA English
DT Article
ID APICAL MEMBRANE ANTIGEN-1; MALARIA VACCINE CANDIDATE; RECEPTOR-BINDING
DOMAIN; SURFACE PROTEIN-1; ADJUVANT VACCINES; PROTECTION; DIVERSITY;
PATHWAYS; IMMUNOGENICITY; CHALLENGES
AB No vaccine has yet proven effective against the blood-stages of Plasmodium falciparum, which cause the symptoms and severe manifestations of malaria. We recently found that PfRH5, a P. falciparum-specific protein expressed in merozoites, is efficiently targeted by broadly-neutralizing, vaccine-induced antibodies. Here we show that antibodies against PfRH5 efficiently inhibit the in vitro growth of short-term-adapted parasite isolates from Cambodia, and that the EC50 values of antigen-specific antibodies against PfRH5 are lower than those against PfAMA1. Since antibody responses elicited by multiple antigens are speculated to improve the efficacy of blood-stage vaccines, we conducted detailed assessments of parasite growth inhibition by antibodies against PfRH5 in combination with antibodies against seven other merozoite antigens. We found that antibodies against PfRH5 act synergistically with antibodies against certain other merozoite antigens, most notably with antibodies against other erythrocyte-binding antigens such as PfRH4, to inhibit the growth of a homologous P. falciparum clone. A combination of antibodies against PfRH4 and basigin, the erythrocyte receptor for PfRH5, also potently inhibited parasite growth. This methodology provides the first quantitative evidence that polyclonal vaccine-induced antibodies can act synergistically against P. falciparum antigens and should help to guide the rational development of future multi-antigen vaccines.
C1 [Williams, Andrew R.; Douglas, Alexander D.; Illingworth, Joseph J.; Choudhary, Prateek; Murungi, Linda M.; Furze, Julie M.; Draper, Simon J.] Univ Oxford, Jenner Inst, Oxford, England.
[Miura, Kazutoyo; Diouf, Ababacar; Fairhurst, Rick M.; Long, Carole A.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
[Murungi, Linda M.] KEMRI Ctr Geog Med Res, Kilifi, Kenya.
[Miotto, Olivo; Kwiatkowski, Dominic P.] Univ Oxford, MRC Ctr Genom & Global Hlth, Oxford, England.
[Miotto, Olivo] Mahidol Univ, Mahidol Oxford Trop Med Res Unit, Bangkok 10700, Thailand.
[Crosnier, Cecile; Wright, Gavin J.; Kwiatkowski, Dominic P.] Wellcome Trust Sanger Inst, Cambridge, England.
[Kwiatkowski, Dominic P.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
RP Williams, AR (reprint author), Univ Oxford, Jenner Inst, Oxford, England.
EM arwilliams@graduate.uwa.edu.au
RI Draper, Simon/F-1758-2011; Douglas, Alexander/E-7040-2012;
OI Draper, Simon/0000-0002-9415-1357; Douglas,
Alexander/0000-0002-5410-7562; Miotto, Olivo/0000-0001-8060-6771;
Williams, Andrew/0000-0002-8231-282X; Kwiatkowski,
Dominic/0000-0002-5023-0176
FU Wellcome Trust [089455/2/09/z]; PhD studentship in the Infection,
Immunology and Translational Medicine PhD Programme [092873/z/10/z];
Sanger Institute Core Funding [09805]; GJW [077108]; UK Medical Research
Council; Career Development Fellowship [G1000527]; EU FP7 through
EVIMalaR [242095]; NIAID, NIH; PATH Malaria Vaccine Initiative;
[G0600718]
FX This research was supported by the Wellcome Trust
(www.wellcome.ac.uk-Training fellowship for Clinicians in Basic Sciences
[grant number 089455/2/09/z] to ADD; PhD studentship in the Infection,
Immunology and Translational Medicine PhD Programme [grant number
092873/z/10/z] to JJI; Sanger Institute Core Funding to DPK [grant
number 09805] and GJW [grant number 077108]); the UK Medical Research
Council (www.mrc.ac.uk, MRC Centre for Genomics and Global Health [grant
number G0600718] to DPK and OM; Career Development Fellowship [grant
number G1000527] to SJD); EU FP7 through EVIMalaR (www.evimalar.org,
grant number 242095]) and the Intramural Research Program of the NIAID,
NIH (www.niaid.nih.gov). The international GIA reference laboratory is
supported by the PATH Malaria Vaccine Initiative
(www.malariavaccine.org). SJD is a Jenner Investigator. The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 53
TC 49
Z9 49
U1 0
U2 10
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD NOV
PY 2012
VL 8
IS 11
AR e1002991
DI 10.1371/journal.ppat.1002991
PG 15
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 049PY
UT WOS:000311997100014
PM 23144611
ER
PT J
AU Revell, A
Wang, D
Alvarez-Uria, G
Streinu-Cercel, A
Ene, L
Wensing, A
Hamers, R
Morrow, C
Wood, R
Tempelman, H
Dewolf, F
Nelson, M
Montaner, J
Lane, H
Larder, B
AF Revell, A.
Wang, D.
Alvarez-Uria, G.
Streinu-Cercel, A.
Ene, L.
Wensing, A.
Hamers, R.
Morrow, C.
Wood, R.
Tempelman, H.
Dewolf, F.
Nelson, M.
Montaner, J.
Lane, H.
Larder, B.
CA RDI Study Grp
TI Computational models that predict response to HIV therapy can reduce
virological failure and therapy costs in resource-limited settings
SO JOURNAL OF THE INTERNATIONAL AIDS SOCIETY
LA English
DT Meeting Abstract
C1 [Revell, A.; Wang, D.; Larder, B.] HIV Resistance Response Database Initiat RDI, London, England.
[Alvarez-Uria, G.] Rural Dev Trust Hosp, Bathalapalli, India.
[Streinu-Cercel, A.] Natl Inst Infect Dis Prof Dr Matei Bals, Bucharest, Romania.
[Ene, L.] Dr Victor Babes Hosp Infect & Trop Dis, Bucharest, Romania.
[Wensing, A.] Univ Med Ctr, Dept Virol & Med Microbiol, Utrecht, Netherlands.
[Hamers, R.] Univ Amsterdam, Acad Med Ctr, Dept Global Hlth, PharmAccess Fdn, NL-1105 AZ Amsterdam, Netherlands.
[Morrow, C.; Wood, R.] Desmond Tutu HIV Ctr, Cape Town, South Africa.
[Tempelman, H.] Ndlovu Care Grp, Elandsdoorn, South Africa.
[Dewolf, F.] Netherlands HIV Monitoring Fdn, Amsterdam, Netherlands.
[Nelson, M.] Chelsea & Westminster Hosp, London, England.
[Montaner, J.] BC Ctr Excellence HIV AIDS, Vancouver, BC, Canada.
[Lane, H.] NIAID, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU INT AIDS SOCIETY
PI GENEVA
PA AVENUE DE FRANCE 23, GENEVA, 1202, SWITZERLAND
SN 1758-2652
J9 J INT AIDS SOC
JI J. Int. AIDS Soc.
PD NOV
PY 2012
VL 15
SU 4
BP 9
EP 9
DI 10.7448/IAS.15.6.18114
PG 1
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 167SH
UT WOS:000320654200025
ER
PT J
AU Hochhalter, AK
Bryant, LL
Hunter, R
Liu, R
Friedman, DB
Price, AE
Sharkey, J
Reddy, S
Caprio, AJ
McCrystle, S
AF Hochhalter, Angela K.
Bryant, Lucinda L.
Hunter, Rebecca
Liu, Rui
Friedman, Daniela B.
Price, Anna E.
Sharkey, Joseph
Reddy, Swarna
Caprio, Anthony J.
McCrystle, Sindy
TI Multisite Qualitative Study of Primary Care Physicians' and Midlevel
Providers' Self-Reported Practices and Perceptions About Maintaining
Cognitive Health
SO PREVENTING CHRONIC DISEASE
LA English
DT Article
ID OLDER-ADULTS; BRAIN
AB Introduction
To facilitate national efforts to maintain cognitive health through public health practice, the Healthy Brain Initiative recommended examining diverse groups to identify stakeholder perspectives on cognitive health. In response, the Healthy Aging Research Network (HAN), funded by the Centers for Disease Control and Prevention (CDC), coordinated projects to document the perspectives of older adults, caregivers of people with dementia, and primary care providers (PCPs) on maintaining cognitive health. Our objective was to describe PCPs' perceptions and practices regarding cognitive health.
Methods
HAN researchers conducted 10 focus groups and 3 interviews with physicians (N = 28) and advanced practice providers (N = 21) in Colorado, Texas, and North Carolina from June 2007 to November 2008. Data were transcribed and coded axially.
Results
PCPs reported addressing cognitive health with patients only indirectly in the context of physical health or in response to observed functional changes and patient or family requests. Some providers felt evidence on the efficacy of preventive strategies for cognitive health was insufficient, but many reported suggesting activities such as games and social interaction when queried by patients. PCPs identified barriers to talking with patients about cognitive health such as lack of time and patient reactions to recommendations.
Conclusion
Communicating new evidence on cognitive health and engaging older adults in making lasting lifestyle changes recommended by PCPs and others may be practical ways in which public health practitioners can partner with PCPs to address cognitive health in health care settings.
C1 [Hochhalter, Angela K.] Scott & White Healthcare, Temple, TX 76508 USA.
[Hochhalter, Angela K.] Texas A& M Hlth Sci Ctr, Coll Med, Temple, TX 76508 USA.
[Bryant, Lucinda L.] Univ Colorado, Colorado Sch Publ Hlth, Aurora, CO USA.
[Hunter, Rebecca; Caprio, Anthony J.] Univ N Carolina, Chapel Hill, NC USA.
[Liu, Rui] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
[Friedman, Daniela B.] Univ S Carolina, Columbia, SC 29208 USA.
[Price, Anna E.] Univ Cattolica Sacro Cuore, Fairfield, CT USA.
[Sharkey, Joseph] Texas A&M Univ, Sch Rural Publ Hlth, College Stn, TX USA.
[Reddy, Swarna] North Carolina Div Aging & Adult Serv, Raleigh, NC USA.
[McCrystle, Sindy] Carolinas Med Ctr, Charlotte, NC 28203 USA.
RP Hochhalter, AK (reprint author), Scott & White Healthcare, 2401 S 31st St,MS-09-C633A, Temple, TX 76508 USA.
EM ahochhalter@sw.org
FU CDC HAN [13-04, 8-06, 1-U48-DP-000025, 1-U48-DP-000033, 1-U48-DP-000045,
1-U48-DP-000048, 1-U48-DP-000050, 1-U48-DP-000051, 1-U48-DP-000052,
1-U48-DP-000054, 1-U48-DP-000059]
FX This work was supported by cooperative agreements from the CDC HAN,
Special Interest Project nos. 13-04 and 8-06, and by cooperative
agreement nos. 1-U48-DP-000025, 1-U48-DP-000033, 1-U48-DP-000045,
1-U48-DP-000048, 1-U48-DP-000050, 1-U48-DP-000051, 1-U48-DP-000052,
1-U48-DP-000054, and 1-U48-DP-000059.
NR 14
TC 0
Z9 0
U1 0
U2 6
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1545-1151
J9 PREV CHRONIC DIS
JI Prev. Chronic Dis.
PD NOV
PY 2012
VL 9
AR UNSP 120050
DI 10.5888/pcd9.120050
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 173AV
UT WOS:000321051300010
ER
PT J
AU Piknova, B
Todd, SE
Park, JW
Swanson, KM
Schechter, AN
AF Piknova, Barbora
Todd, Sarah E.
Park, Ji Won
Swanson, Kathryn M.
Schechter, Alan N.
TI Does Dietary Ascorbic Acid Affects Nitric Oxide Metabolism and Related
Physiological Pathways? Study on Osteogenic Disorder Shionogi Rats
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 19th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine
(SFRBM)
CY NOV 14-18, 2012
CL San Diego, CA
SP Soc Free Rad Biol & Med (SFRBM)
C1 [Piknova, Barbora; Todd, Sarah E.; Park, Ji Won; Swanson, Kathryn M.; Schechter, Alan N.] NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD NOV 1
PY 2012
VL 53
SU 2
BP S185
EP S185
DI 10.1016/j.freeradbiomed.2012.10.511
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 031RS
UT WOS:000310660600491
ER
PT J
AU Lai, JP
Rosenberg, AZ
Miettinen, MM
Lee, CCR
AF Lai, Jin-Ping
Rosenberg, Avi Z.
Miettinen, Markku M.
Lee, Chyi-Chia R.
TI NY-ESO-1 expression in sarcomas A diagnostic marker and immunotherapy
target
SO ONCOIMMUNOLOGY
LA English
DT Article
DE NY-ESO-1; immunotherapy; sarcomas; synovial sarcoma; melanoma;
cancer-testis antigen; diagnostic marker; clinical trial; therapeutic
target; T-cell receptor
ID CELL
AB NY-ESO-1 (CTAG 1B) is highly expressed in the majority of synovial sarcomas and myxoid/round cell liposarcomas as well as in a subset of melanomas, but only rarely in other mesenchymal tumors. This points to a potential for using NY-ESO-1 in the differential diagnosis of these lesions. Furthermore, promising results have been obtained in clinical trials testing NY-ESO-1-targeted immunotherapy in subsets of melanoma and synovial sarcoma patients.
C1 [Lai, Jin-Ping; Rosenberg, Avi Z.; Miettinen, Markku M.; Lee, Chyi-Chia R.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
RP Lee, CCR (reprint author), NCI, Pathol Lab, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM leechy@mail.nih.gov
RI Lee, Chyi-Chia/I-1938-2013;
OI Lee, Chyi-Chia/0000-0002-5306-7781; Rosenberg, Avi/0000-0003-2356-950X
NR 9
TC 12
Z9 15
U1 0
U2 3
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 2162-4011
J9 ONCOIMMUNOLOGY
JI OncoImmunology
PD NOV
PY 2012
VL 1
IS 8
BP 1409
EP 1410
DI 10.4161/onci.21059
PG 2
WC Oncology; Immunology
SC Oncology; Immunology
GA 108GR
UT WOS:000316280700026
ER
PT J
AU Somerville, RPT
Dudley, ME
AF Somerville, Robert P. T.
Dudley, Mark E.
TI Bioreactors get personal
SO ONCOIMMUNOLOGY
LA English
DT Article
DE adoptive cell transfer; bioreactors; immunotherapy; tumor infiltrating
lymphocytes; cancer
ID TUMOR-INFILTRATING LYMPHOCYTES; CELL; IMMUNOTHERAPY; EXPANSION;
RESPONSES
AB Adoptive cell transfer immunotherapy against melanoma is highly effective. However, this therapy has seen limited dissemination, mainly due to the complexity and costs of cell expansion protocols. Two bioreactors have recently been described that simplify and streamline the production of individualized cell therapies. Such bioreactors might increase the number of patients that get access to this promising therapeutic modality.
C1 [Somerville, Robert P. T.; Dudley, Mark E.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
RP Dudley, ME (reprint author), NCI, Surg Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM med@nih.gov
NR 9
TC 11
Z9 11
U1 0
U2 2
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 2162-4011
J9 ONCOIMMUNOLOGY
JI OncoImmunology
PD NOV
PY 2012
VL 1
IS 8
BP 1435
EP 1437
DI 10.4161/onci.21206
PG 3
WC Oncology; Immunology
SC Oncology; Immunology
GA 108GR
UT WOS:000316280700036
ER
PT J
AU Greten, TF
Zhao, F
Gamrekelashvili, J
Korangy, F
AF Greten, Tim F.
Zhao, Fei
Gamrekelashvili, Jaba
Korangy, Firouzeh
TI Human Th17 cells in patients with cancer Friends or foe?
SO ONCOIMMUNOLOGY
LA English
DT Article
DE IL-17; CCR4; CCR6; liver; cancer
ID HEPATOCELLULAR-CARCINOMA
AB The role of interleukin-17 (IL-17)-secreting CD4(+) T (Th17) cells in cancer is under intense investigation. We have demonstrated that CCR4(+) CCR6(+) Th17 cells not only are increased in the peripheral blood of patients affected by hepatocellular carcinoma, but also suppress CD8(+) T-cell functions in vitro. These results suggest that Th17 cells may exert immunosuppressive functions in hepatocellular carcinoma.
C1 [Greten, Tim F.; Zhao, Fei; Gamrekelashvili, Jaba; Korangy, Firouzeh] NCI, Gastrointestinal Malignancy Sect, Med Oncol Branch, Bethesda, MD 20892 USA.
RP Greten, TF (reprint author), NCI, Gastrointestinal Malignancy Sect, Med Oncol Branch, Bethesda, MD 20892 USA.
EM tim.greten@nih.gov
RI Greten, Tim/B-3127-2015
OI Greten, Tim/0000-0002-0806-2535
NR 9
TC 7
Z9 9
U1 0
U2 1
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 2162-4011
J9 ONCOIMMUNOLOGY
JI OncoImmunology
PD NOV
PY 2012
VL 1
IS 8
BP 1438
EP 1439
DI 10.4161/onci.21245
PG 2
WC Oncology; Immunology
SC Oncology; Immunology
GA 108GR
UT WOS:000316280700037
ER
PT J
AU Kuka, M
Munitic, I
Ashwell, JD
AF Kuka, Mirela
Munitic, Ivana
Ashwell, Jonathan D.
TI Identification and characterization of polyclonal alpha beta-T cells
with dendritic cell properties
SO NATURE COMMUNICATIONS
LA English
DT Article
ID TOLL-LIKE RECEPTORS; IN-VIVO; LINEAGE DETERMINATION; EFFECTOR FUNCTIONS;
EXPRESSION; LYMPHOCYTES; INNATE; IMMUNITY; GRANZYME; DIFFERENTIATION
AB An efficient immune response requires coordination between innate and adaptive immunity, which act through cells different in origin and function. Here we report the identification of thymus-derived alpha beta-T-cell receptor(+) cells that express CD11c and major histocompatibility complex class II, and require FLT3 ligand for development (T-DC). T-DC express genes heretofore found uniquely in T cells or dendritic cells, as well as a distinctive signature of cytotoxicity-related genes. Unlike other innate T-cell subsets, T-DC have a polyclonal T-cell receptor repertoire and respond to cognate antigens. However, they differ from conventional T cells in that they do not require help from antigen-presenting cells, respond to Toll-like receptor-mediated stimulation by producing interleukin-12 and process and present antigen. The physiological relevance of T-DC, found in mice and humans, is still under investigation, but the fact that they combine key features of T and dendritic cells suggests that they provide a bridge between the innate and adaptive immune systems.
C1 [Kuka, Mirela; Munitic, Ivana; Ashwell, Jonathan D.] NCI, Lab Immune Cell Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Ashwell, JD (reprint author), NCI, Lab Immune Cell Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM jda@pop.nci.nih.gov
OI KUKA, MIRELA/0000-0001-9418-1559
FU Center for Cancer Research, National Cancer Institute, National
Institutes of Health
FX This work was supported by the Intramural Research Program of the Center
for Cancer Research, National Cancer Institute, National Institutes of
Health. We thank Ulrich H. von Andrian for providing the B16-FLT3L
melanoma cell line, Paul R. Mittelstadt for TCR-transgenic and Remy
Bosselut for Thpok-transgenic mice, respectively, Ehydel Castro for
assistance with adoptive transfer, Susan H. Garfield for assistance with
confocal microscopy, and Xiaolin Wu and Li Jia for help with generating
and analyzing the microarray data. We also thank Rafi Ahmed for the LCMV
Armstrong strain, the NIH Tetramer facility at Emory University for
tetramers, and Atef Allam for LCMV preparation.
NR 43
TC 6
Z9 6
U1 1
U2 6
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD NOV
PY 2012
VL 3
AR 1223
DI 10.1038/ncomms2223
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 104KP
UT WOS:000315992100058
PM 23187623
ER
PT J
AU Karp, BI
AF Karp, Barbara Illowsky
TI Botulinum Toxin Physiology in Focal Hand and Cranial Dystonia
SO TOXINS
LA English
DT Review
DE dystonia; blepharospasm; Meige syndrome; writer's cramp; botulinum
toxin; physiology
ID TONIC VIBRATION REFLEX; EVENT-RELATED FMRI; WRITERS CRAMP; OROMANDIBULAR
DYSTONIA; RECIPROCAL INHIBITION; SOMATOSENSORY ACTIVATION; ASSOCIATIVE
PLASTICITY; EMBOUCHURE DYSTONIA; OROFACIAL DYSTONIA; CERVICAL DYSTONIA
AB The safety and efficacy of botulinum toxin for the treatment of focal hand and cranial dystonias are well-established. Studies of these adult-onset focal dystonias reveal both shared features, such as the dystonic phenotype of muscle hyperactivity and overflow muscle contraction and divergent features, such as task specificity in focal hand dystonia which is not a common feature of cranial dystonia. The physiologic effects of botulinum toxin in these 2 disorders also show both similarities and differences. This paper compares and contrasts the physiology of focal hand and cranial dystonias and of botulinum toxin in the management of these disorders.
C1 NINDS, NIH, Bethesda, MD 20892 USA.
RP Karp, BI (reprint author), NINDS, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM karpb@ninds.nih.gov
FU Intramural Research Program of the National Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Institutes of Health.
NR 67
TC 8
Z9 8
U1 0
U2 13
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 2072-6651
J9 TOXINS
JI Toxins
PD NOV
PY 2012
VL 4
IS 11
BP 1404
EP 1414
DI 10.3390/toxins4111404
PG 11
WC Toxicology
SC Toxicology
GA 096LV
UT WOS:000315406500023
PM 23202323
ER
PT J
AU Matzat, LH
Dale, RK
Moshkovich, N
Lei, EP
AF Matzat, Leah H.
Dale, Ryan K.
Moshkovich, Nellie
Lei, Elissa P.
TI Tissue-Specific Regulation of Chromatin Insulator Function
SO PLOS GENETICS
LA English
DT Article
ID ZINC-FINGER PROTEIN; DROSOPHILA-MELANOGASTER; NUCLEAR-ORGANIZATION;
INTERACTIONS REVEALS; GYPSY INSULATOR; GENE-EXPRESSION; HUMAN GENOME;
DNA-BINDING; CTCF; POLYCOMB
AB Chromatin insulators organize the genome into distinct transcriptional domains and contribute to cell type-specific chromatin organization. However, factors regulating tissue-specific insulator function have not yet been discovered. Here we identify the RNA recognition motif-containing protein Shep as a direct interactor of two individual components of the gypsy insulator complex in Drosophila. Mutation of shep improves gypsy-dependent enhancer blocking, indicating a role as a negative regulator of insulator activity. Unlike ubiquitously expressed core gypsy insulator proteins, Shep is highly expressed in the central nervous system (CNS) with lower expression in other tissues. We developed a novel, quantitative tissue-specific barrier assay to demonstrate that Shep functions as a negative regulator of insulator activity in the CNS but not in muscle tissue. Additionally, mutation of shep alters insulator complex nuclear localization in the CNS but has no effect in other tissues. Consistent with negative regulatory activity, ChIP-seq analysis of Shep in a CNS-derived cell line indicates substantial genome-wide colocalization with a single gypsy insulator component but limited overlap with intact insulator complexes. Taken together, these data reveal a novel, tissue-specific mode of regulation of a chromatin insulator.
C1 [Matzat, Leah H.; Dale, Ryan K.; Moshkovich, Nellie; Lei, Elissa P.] NIDDK, Lab Cellular & Dev Biol, NIH, Bethesda, MD USA.
[Moshkovich, Nellie] Univ Maryland, Grad Program Mol & Cell Biol, College Pk, MD 20742 USA.
RP Matzat, LH (reprint author), NIDDK, Lab Cellular & Dev Biol, NIH, Bethesda, MD USA.
EM leielissa@niddk.nih.gov
OI Dale, Ryan/0000-0003-2664-3744
FU National Institute of Diabetes and Digestive and Kidney Diseases
FX This work was funded by the Intramural Program of the National Institute
of Diabetes and Digestive and Kidney Diseases. The funders had no role
in study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 58
TC 20
Z9 20
U1 1
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7404
J9 PLOS GENET
JI PLoS Genet.
PD NOV
PY 2012
VL 8
IS 11
AR e1003069
DI 10.1371/journal.pgen.1003069
PG 15
WC Genetics & Heredity
SC Genetics & Heredity
GA 048DY
UT WOS:000311891600053
PM 23209434
ER
PT J
AU McDonald, JP
Vaisman, A
Kuban, W
Goodman, MF
Woodgate, R
AF McDonald, John P.
Vaisman, Alexandra
Kuban, Wojciech
Goodman, Myron F.
Woodgate, Roger
TI Mechanisms Employed by Escherichia coli to Prevent Ribonucleotide
Incorporation into Genomic DNA by Pol V
SO PLOS GENETICS
LA English
DT Article
ID SOS MUTATOR ACTIVITY; RNASE-H; POLYMERASE-V; GENETIC REQUIREMENTS; UV
MUTAGENESIS; RECA PROTEIN; ERROR-PRONE; REPAIR; REPLICATION; DEFICIENT
AB Escherichia coli pol V (UmuD'C-2), the main translesion DNA polymerase, ensures continued nascent strand extension when the cellular replicase is blocked by unrepaired DNA lesions. Pol V is characterized by low sugar selectivity, which can be further reduced by a Y11A "steric-gate" substitution in UmuC that enables pol V to preferentially incorporate rNTPs over dNTPs in vitro. Despite efficient error-prone translesion synthesis catalyzed by UmuC_Y11A in vitro, strains expressing umuC_Y11A exhibit low UV mutability and UV resistance. Here, we show that these phenotypes result from the concomitant dual actions of Ribonuclease HII (RNase HII) initiating removal of rNMPs from the nascent DNA strand and nucleotide excision repair (NER) removing UV lesions from the parental strand. In the absence of either repair pathway, UV resistance and mutagenesis conferred by umuC_Y11A is significantly enhanced, suggesting that the combined actions of RNase HII and NER lead to double-strand breaks that result in reduced cell viability. We present evidence that the Y11A-specific UV phenotype is tempered by pol IV in vivo. At physiological ratios of the two polymerases, pol IV inhibits pol V-catalyzed translesion synthesis (TLS) past UV lesions and significantly reduces the number of Y11A-incorporated rNTPs by limiting the length of the pol V-dependent TLS tract generated during lesion bypass in vitro. In a recA730 lexA(Def) Delta umuDC Delta dinB strain, plasmid-encoded wild-type pol V promotes high levels of spontaneous mutagenesis. However, umuC_Y11A-dependent spontaneous mutagenesis is only similar to 7% of that observed with wild-type pol V, but increases to similar to 39% of wildtype levels in an isogenic Delta rnhB strain and similar to 72% of wild-type levels in a Delta rnhA Delta rnhB double mutant. Our observations suggest that errant ribonucleotides incorporated by pol V can be tolerated in the E. coli genome, but at the cost of higher levels of cellular mutagenesis.
C1 [McDonald, John P.; Vaisman, Alexandra; Kuban, Wojciech; Woodgate, Roger] NICHHD, Lab Genom Integr, NIH, Bethesda, MD 20892 USA.
[Goodman, Myron F.] Univ So Calif, Dept Biol Sci, Los Angeles, CA 90089 USA.
[Goodman, Myron F.] Univ So Calif, Dept Chem, Los Angeles, CA 90089 USA.
RP McDonald, JP (reprint author), NICHHD, Lab Genom Integr, NIH, Bethesda, MD 20892 USA.
EM woodgate@nih.gov
RI Vaisman, Alexandra/C-3766-2013
OI Vaisman, Alexandra/0000-0002-2521-1467
FU National Institute of Child Health and Human Development/National
Institutes of Health Intramural Research Program; National Institutes of
Health [GM21422, ESO12259]
FX This work was supported by funding from the National Institute of Child
Health and Human Development/National Institutes of Health Intramural
Research Program to RW and National Institutes of Health grants
[GM21422, ESO12259] to MFG. The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
NR 62
TC 17
Z9 17
U1 1
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7404
J9 PLOS GENET
JI PLoS Genet.
PD NOV
PY 2012
VL 8
IS 11
AR e1003030
DI 10.1371/journal.pgen.1003030
PG 12
WC Genetics & Heredity
SC Genetics & Heredity
GA 048DY
UT WOS:000311891600018
PM 23144626
ER
PT J
AU Menezes, LF
Zhou, F
Patterson, AD
Piontek, KB
Krausz, KW
Gonzalez, FJ
Germino, GG
AF Menezes, Luis F.
Zhou, Fang
Patterson, Andrew D.
Piontek, Klaus B.
Krausz, Kristopher W.
Gonzalez, Frank J.
Germino, Gregory G.
TI Network Analysis of a Pkd1-Mouse Model of Autosomal Dominant Polycystic
Kidney Disease Identifies HNF4 alpha as a Disease Modifier
SO PLOS GENETICS
LA English
DT Article
ID ILLUMINA MICROARRAY; EPITHELIAL-CELLS; SYSTEMS BIOLOGY; GENE-EXPRESSION;
CYST FORMATION; SLOW-ONSET; ADULT MICE; RAT MODEL; METABOLISM; PATHWAYS
AB Autosomal Dominant Polycystic Kidney Disease (ADPKD; MIM ID's 173900, 601313, 613095) leads to end-stage kidney disease, caused by mutations in PKD1 or PKD2. Inactivation of Pkd1 before or after P13 in mice results in distinct early- or late-onset disease. Using a mouse model of ADPKD carrying floxed Pkd1 alleles and an inducible Cre recombinase, we intensively analyzed the relationship between renal maturation and cyst formation by applying transcriptomics and metabolomics to follow disease progression in a large number of animals induced before P10. Weighted gene co-expression network analysis suggests that Pkd1-cystogenesis does not cause developmental arrest and occurs in the context of gene networks similar to those that regulate/maintain normal kidney morphology/function. Knowledge-based Ingenuity Pathway Analysis (IPA) software identifies HNF4 alpha as a likely network node. These results are further supported by a meta-analysis of 1,114 published gene expression arrays in Pkd1 wild-type tissues. These analyses also predict that metabolic pathways are key elements in postnatal kidney maturation and early steps of cyst formation. Consistent with these findings, urinary metabolomic studies show that Pkd1 cystic mutants have a distinct profile of excreted metabolites, with pathway analysis suggesting altered activity in several metabolic pathways. To evaluate their role in disease, metabolic networks were perturbed by inactivating Hnf4 alpha and Pkd1. The Pkd1/Hnf4 alpha double mutants have significantly more cystic kidneys, thus indicating that metabolic pathways could play a role in Pkd1-cystogenesis.
C1 [Menezes, Luis F.; Zhou, Fang; Germino, Gregory G.] NIDDK, NIH, Bethesda, MD USA.
[Patterson, Andrew D.; Krausz, Kristopher W.; Gonzalez, Frank J.] NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Piontek, Klaus B.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
RP Menezes, LF (reprint author), NIDDK, NIH, Bethesda, MD USA.
EM germinogg@mail.nih.gov
RI Menezes, Luis Fernando/C-7286-2015; Patterson, Andrew/G-3852-2012
OI Patterson, Andrew/0000-0003-2073-0070
FU NIH [R37DK48006]; NIDDK [1ZIADK075042]; NCI [1ZIABC005708]; National
Kidney Foundation; Polycystic Kidney Foundation
FX This work was supported by the NIH (R37DK48006), the intramural research
programs of NIDDK (1ZIADK075042) and NCI (1ZIABC005708), a National
Kidney Foundation Fellowship grant
(http://www.kidney.org/professionals/research/research_info.cfm), and a
Polycystic Kidney Foundation Fellowship grant
(http://www.pkdcure.org/Research.aspx). The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 58
TC 16
Z9 17
U1 0
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7404
J9 PLOS GENET
JI PLoS Genet.
PD NOV
PY 2012
VL 8
IS 11
AR e1003053
DI 10.1371/journal.pgen.1003053
PG 14
WC Genetics & Heredity
SC Genetics & Heredity
GA 048DY
UT WOS:000311891600040
PM 23209428
ER
PT J
AU Ruggiero, R
Kale, A
Thomas, B
Baker, NE
AF Ruggiero, Robert
Kale, Abhijit
Thomas, Barbara
Baker, Nicholas E.
TI Mitosis in Neurons: Roughex and APC/C Maintain Cell Cycle Exit to
Prevent Cytokinetic and Axonal Defects in Drosophila Photoreceptor
Neurons
SO PLOS GENETICS
LA English
DT Article
ID ALZHEIMERS-DISEASE; PATTERN-FORMATION; MITOTIC SPINDLE; EYE DEVELOPMENT;
SPECTRIN MUTATIONS; DEPENDENT KINASES; GENE INACTIVATION;
DOWN-REGULATION; PRONEURAL GENE; GAMMA-TUBULIN
AB The mechanisms of cell cycle exit by neurons remain poorly understood. Through genetic and developmental analysis of Drosophila eye development, we found that the cyclin-dependent kinase-inhibitor Roughex maintains G1 cell cycle exit during differentiation of the R8 class of photoreceptor neurons. The roughex mutant neurons re-enter the mitotic cell cycle and progress without executing cytokinesis, unlike non-neuronal cells in the roughex mutant that perform complete cell divisions. After mitosis, the binucleated R8 neurons usually transport one daughter nucleus away from the cell body into the developing axon towards the brain in a kinesin-dependent manner resembling anterograde axonal trafficking. Similar cell cycle and photoreceptor neuron defects occurred in mutants for components of the Anaphase Promoting Complex/Cyclosome. These findings indicate a neuron-specific defect in cytokinesis and demonstrate a critical role for mitotic cyclin downregulation both to maintain cell cycle exit during neuronal differentiation and to prevent axonal defects following failed cytokinesis.
C1 [Ruggiero, Robert; Kale, Abhijit; Baker, Nicholas E.] Albert Einstein Coll Med, Dept Genet, Bronx, NY 10467 USA.
[Thomas, Barbara] NCI, Biochem Lab, NIH, Bethesda, MD 20892 USA.
[Baker, Nicholas E.] Albert Einstein Coll Med, Dept Dev & Mol Biol, Bronx, NY 10467 USA.
[Baker, Nicholas E.] Albert Einstein Coll Med, Dept Ophthalmol & Visual Sci, Bronx, NY 10467 USA.
RP Ruggiero, R (reprint author), Albert Einstein Coll Med, Dept Genet, Bronx, NY 10467 USA.
EM nbaker@einstein.yu.edu
RI Kale, Abhijit/B-4212-2015
FU NIH [R01-EY021614, T32-GM007491]; Research to Prevent Blindness
FX This work was supported by the NIH (grant #R01-EY021614 and
#T32-GM007491) and by an Unrestricted Grant from Research to Prevent
Blindness to the Department of Ophthalmology and Visual Sciences. The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 82
TC 8
Z9 8
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7404
J9 PLOS GENET
JI PLoS Genet.
PD NOV
PY 2012
VL 8
IS 11
AR e1003049
DI 10.1371/journal.pgen.1003049
PG 12
WC Genetics & Heredity
SC Genetics & Heredity
GA 048DY
UT WOS:000311891600036
PM 23209426
ER
PT J
AU Tang, MZ
Lautenberger, JA
Gao, XJ
Sezgin, E
Hendrickson, SL
Troyer, JL
David, VA
Guan, L
Mcintosh, CE
Guo, XC
Zheng, YM
Liao, J
Deng, H
Malasky, M
Kessing, B
Winkler, CA
Carrington, M
de The, G
Zeng, Y
O'Brien, SJ
AF Tang, Minzhong
Lautenberger, James A.
Gao, Xiaojiang
Sezgin, Efe
Hendrickson, Sher L.
Troyer, Jennifer L.
David, Victor A.
Guan, Li
Mcintosh, Carl E.
Guo, Xiuchan
Zheng, Yuming
Liao, Jian
Deng, Hong
Malasky, Michael
Kessing, Bailey
Winkler, Cheryl A.
Carrington, Mary
de The, Guy
Zeng, Yi
O'Brien, Stephen J.
TI The Principal Genetic Determinants for Nasopharyngeal Carcinoma in China
Involve the HLA Class I Antigen Recognition Groove
SO PLOS GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; WUZHOU-CITY; SUSCEPTIBILITY; POPULATION;
MOLECULES; LINKAGE; RISK; LOCI
AB Nasopharyngeal carcinoma (NPC) is an epithelial malignancy facilitated by Epstein-Barr Virus infection. Here we resolve the major genetic influences for NPC incidence using a genome-wide association study (GWAS), independent cohort replication, and high-resolution molecular HLA class I gene typing including 4,055 study participants from the Guangxi Zhuang Autonomous Region and Guangdong province of southern China. We detect and replicate strong association signals involving SNPs, HLA alleles, and amino acid (aa) variants across the major histocompatibility complex-HLA-A, HLA -B, and HLA -C class I genes (PHLA-A-aa-site-62 = 7.4x10(-29); P (HLA-B-aa-site-116) = 6.5x10(-19); P (HLA-C-aa-site-156) = 6.8x10(-8) respectively). Over 250 NPC-HLA associated variants within HLA were analyzed in concert to resolve separate and largely independent HLA-A, -B, and -C gene influences. Multivariate logistical regression analysis collapsed significant associations in adjacent genes spanning 500 kb (OR2H1, GABBR1, HLA-F, and HCG9) as proxies for peptide binding motifs carried by HLA-A*11:01. A similar analysis resolved an independent association signal driven by HLA-B*13:01,B*38:02, and B*55:02 alleles together. NPC resistance alleles carrying the strongly associated amino acid variants implicate specific class I peptide recognition motifs in HLA-A and -B peptide binding groove as conferring strong genetic influence on the development of NPC in China.
C1 [Tang, Minzhong; Zeng, Yi] Beijing Univ Technol, Coll Life Sci & Bioengn, Beijing, Peoples R China.
[Troyer, Jennifer L.; Guan, Li; Mcintosh, Carl E.; Guo, Xiuchan; Malasky, Michael; Winkler, Cheryl A.] NCI, Lab Genom Divers, SAIC Frederick, Frederick, MD 21701 USA.
[Tang, Minzhong; Zheng, Yuming; Deng, Hong] Wuzhou Red Cross Hosp, Wuzhou Hlth Syst Key Lab Nasopharyngeal Carcinoma, Wuzhou, Guangxi, Peoples R China.
[Lautenberger, James A.; Kessing, Bailey] Frederick Natl Lab Canc Res, BSP CCR Genet Core, Frederick, MD USA.
[Gao, Xiaojiang; Carrington, Mary] SAIC Frederick, Canc & Inflammat Program, Expt Immunol Lab, Frederick Natl Lab, Frederick, MD USA.
[Gao, Xiaojiang] MIT, Ragon Inst MGH, Boston, MA USA.
[Gao, Xiaojiang] Harvard, Boston, MA USA.
[Hendrickson, Sher L.] Shepherd Univ, Dept Biol, Shepherdstown, WV USA.
[Guo, Xiuchan; Zeng, Yi] Chinese Ctr Dis Control & Prevent, State Key Lab Infect Dis Prevent & Control, Inst Viral Dis Control & Prevent, Beijing, Peoples R China.
[de The, Guy] Inst Pasteur, Paris, France.
RP Tang, MZ (reprint author), Beijing Univ Technol, Coll Life Sci & Bioengn, Beijing, Peoples R China.
EM zengy@public.bta.net.cn; lgdchief@gmail.com
RI Sezgin, Efe/B-8418-2012;
OI Sezgin, Efe/0000-0002-8000-7485; O'Brien, Stephen J./0000-0001-7353-8301
FU Frederick National Laboratory for Cancer Research, National Institutes
of Health [HHSN261200800001E, N01-CO-12400]; Guangxi science and
technology grant, China [114003A-49]; Wuzhou science and technology
grant, China [201102062]
FX This project has been funded in whole or in part with federal funds from
the Frederick National Laboratory for Cancer Research, National
Institutes of Health, under contract HHSN261200800001E, N01-CO-12400;
Guangxi science and technology grant, China (114003A-49); and Wuzhou
science and technology grant, China (201102062). The funders had no role
in study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 33
TC 24
Z9 28
U1 0
U2 8
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7390
EI 1553-7404
J9 PLOS GENET
JI PLoS Genet.
PD NOV
PY 2012
VL 8
IS 11
AR e1003103
DI 10.1371/journal.pgen.1003103
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 048DY
UT WOS:000311891600075
PM 23209447
ER
PT J
AU Zaitlen, N
Lindstrom, S
Pasaniuc, B
Cornelis, M
Genovese, G
Pollack, S
Barton, A
Bickeboller, H
Bowden, DW
Eyre, S
Freedman, BI
Friedman, DJ
Field, JK
Groop, L
Haugen, A
Heinrich, J
Henderson, BE
Hicks, PJ
Hocking, LJ
Kolonel, LN
Landi, MT
Langefeld, CD
Le Marchand, L
Meister, M
Morgan, AW
Raji, OY
Risch, A
Rosenberger, A
Scherf, D
Steer, S
Walshaw, M
Waters, KM
Wilson, AG
Wordsworth, P
Zienolddiny, S
Tchetgen, ET
Haiman, C
Hunter, DJ
Plenge, RM
Worthington, J
Christiani, DC
Schaumberg, DA
Chasman, DI
Altshuler, D
Voight, B
Kraft, P
Patterson, N
Price, AL
AF Zaitlen, Noah
Lindstroem, Sara
Pasaniuc, Bogdan
Cornelis, Marilyn
Genovese, Giulio
Pollack, Samuela
Barton, Anne
Bickeboeller, Heike
Bowden, Donald W.
Eyre, Steve
Freedman, Barry I.
Friedman, David J.
Field, John K.
Groop, Leif
Haugen, Aage
Heinrich, Joachim
Henderson, Brian E.
Hicks, Pamela J.
Hocking, Lynne J.
Kolonel, Laurence N.
Landi, Maria Teresa
Langefeld, Carl D.
Le Marchand, Loic
Meister, Michael
Morgan, Ann W.
Raji, Olaide Y.
Risch, Angela
Rosenberger, Albert
Scherf, David
Steer, Sophia
Walshaw, Martin
Waters, Kevin M.
Wilson, Anthony G.
Wordsworth, Paul
Zienolddiny, Shanbeh
Tchetgen, Eric Tchetgen
Haiman, Christopher
Hunter, David J.
Plenge, Robert M.
Worthington, Jane
Christiani, David C.
Schaumberg, Debra A.
Chasman, Daniel I.
Altshuler, David
Voight, Benjamin
Kraft, Peter
Patterson, Nick
Price, Alkes L.
TI Informed Conditioning on Clinical Covariates Increases Power in
Case-Control Association Studies
SO PLOS GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; QUANTITATIVE-TRAIT LOCI; CANCER SUSCEPTIBILITY
LOCI; DISCORDANT SIB PAIRS; GENETIC-VARIANTS; LUNG-CANCER; MACULAR
DEGENERATION; CHINESE POPULATION; COMMON VARIANT; RISK-FACTORS
AB Genetic case-control association studies often include data on clinical covariates, such as body mass index (BMI), smoking status, or age, that may modify the underlying genetic risk of case or control samples. For example, in type 2 diabetes, odds ratios for established variants estimated from low-BMI cases are larger than those estimated from high-BMI cases. An unanswered question is how to use this information to maximize statistical power in case-control studies that ascertain individuals on the basis of phenotype (case-control ascertainment) or phenotype and clinical covariates (case-controlcovariate ascertainment). While current approaches improve power in studies with random ascertainment, they often lose power under case-control ascertainment and fail to capture available power increases under case-control-covariate ascertainment. We show that an informed conditioning approach, based on the liability threshold model with parameters informed by external epidemiological information, fully accounts for disease prevalence and non-random ascertainment of phenotype as well as covariates and provides a substantial increase in power while maintaining a properly controlled falsepositive rate. Our method outperforms standard case-control association tests with or without covariates, tests of gene x covariate interaction, and previously proposed tests for dealing with covariates in ascertained data, with especially large improvements in the case of case-control-covariate ascertainment. We investigate empirical case-control studies of type 2 diabetes, prostate cancer, lung cancer, breast cancer, rheumatoid arthritis, age-related macular degeneration, and end-stage kidney disease over a total of 89,726 samples. In these datasets, informed conditioning outperforms logistic regression for 115 of the 157 known associated variants investigated (P-value = 1x10(-9)). The improvement varied across diseases with a 16% median increase in chi(2) test statistics and a commensurate increase in power. This suggests that applying our method to existing and future association studies of these diseases may identify novel disease loci.
C1 [Zaitlen, Noah; Lindstroem, Sara; Pasaniuc, Bogdan; Pollack, Samuela; Tchetgen, Eric Tchetgen; Hunter, David J.; Christiani, David C.; Schaumberg, Debra A.; Kraft, Peter; Price, Alkes L.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Zaitlen, Noah; Pasaniuc, Bogdan; Pollack, Samuela; Tchetgen, Eric Tchetgen; Kraft, Peter; Price, Alkes L.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Zaitlen, Noah; Pasaniuc, Bogdan; Pollack, Samuela; Hunter, David J.; Plenge, Robert M.; Altshuler, David; Voight, Benjamin; Kraft, Peter; Patterson, Nick; Price, Alkes L.] Broad Inst Harvard & Massachusetts Inst Technol, Cambridge, MA USA.
[Zaitlen, Noah; Lindstroem, Sara; Pasaniuc, Bogdan; Pollack, Samuela; Hunter, David J.; Kraft, Peter; Price, Alkes L.] Harvard Univ, Sch Publ Hlth, Program Mol & Genet Epidemiol, Boston, MA 02115 USA.
[Cornelis, Marilyn; Hunter, David J.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Schaumberg, Debra A.; Chasman, Daniel I.] Harvard Univ, Sch Med, Dept Ophthalmol, Schepens Eye Res Inst, Boston, MA USA.
[Genovese, Giulio; Friedman, David J.] Beth Israel Deaconess Med Ctr, Dept Med, Div Nephrol, Boston, MA 02215 USA.
[Barton, Anne; Eyre, Steve; Worthington, Jane] Univ Manchester, Manchester Acad Hlth Sci Ctr, Arthrit Res UK Epidemiol Unit, Manchester, Lancs, England.
[Bickeboeller, Heike; Rosenberger, Albert] Univ Gottingen, Univ Med Ctr, Dept Genet Epidemiol, Gottingen, Germany.
[Bowden, Donald W.] Wake Forest Sch Med, Ctr Human Genom, Winston Salem, NC USA.
[Freedman, Barry I.] Wake Forest Sch Med, Nephrol Sect, Dept Internal Med, Winston Salem, NC USA.
[Field, John K.; Raji, Olaide Y.] Univ Liverpool, Roy Castle Lung Canc Res Programme, Liverpool L69 3BX, Merseyside, England.
[Groop, Leif] Lund Univ, Scania Univ Hosp, Diabet & Endocrinol Res Unit, Dept Clin Sci, Malmo, Sweden.
[Haugen, Aage; Zienolddiny, Shanbeh] Natl Inst Occupat Hlth, Sect Toxicol, Oslo, Norway.
[Heinrich, Joachim] German Res Ctr Environm Hlth, Inst Epidemiol, Neuherberg, Germany.
[Henderson, Brian E.; Waters, Kevin M.; Haiman, Christopher] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Hicks, Pamela J.] Wake Forest Univ, Bowman Gray Sch Med, Dept Biochem, Winston Salem, NC 27103 USA.
[Hocking, Lynne J.] Univ Aberdeen, Div Appl Med, Musculoskeletal Res Programme, Aberdeen, Scotland.
[Kolonel, Laurence N.; Le Marchand, Loic] Univ Hawaii, Canc Res Ctr, Program Epidemiol, Honolulu, HI 96813 USA.
[Landi, Maria Teresa] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Langefeld, Carl D.] Wake Forest Univ, Bowman Gray Sch Med, Div Publ Hlth Sci, Winston Salem, NC USA.
[Meister, Michael] Univ Klinikum, Thoraxklin, Heidelberg, Germany.
[Meister, Michael; Risch, Angela] German Ctr Lung Res, Translat Lung Res Ctr Heidelberg, Heidelberg, Germany.
[Morgan, Ann W.] NIHR Leeds Musculoskeletal Biomed Res Unit, Leeds, W Yorkshire, England.
[Risch, Angela; Scherf, David] DKFZ German Canc Res Ctr, Heidelberg, Germany.
[Steer, Sophia] Kings Coll Hosp, Natl Hlth Serv Fdn Trust, London, England.
[Walshaw, Martin] Liverpool Heart & Chest Hosp, Liverpool, Merseyside, England.
[Wilson, Anthony G.] Univ Sheffield, Deptartment Infect & Immun, Sheffield, S Yorkshire, England.
[Wordsworth, Paul] Nuffield Orthopaed Ctr, NIHR Oxford Musculoskeletal Biomed Res Unit, Oxford OX3 7LD, England.
[Plenge, Robert M.] Brigham & Womens Hosp, Div Genet, Boston, MA 02115 USA.
[Plenge, Robert M.] Brigham & Womens Hosp, Div Rheumatol Allergy & Immunol, Boston, MA 02115 USA.
[Christiani, David C.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Schaumberg, Debra A.] Brigham & Womens Hosp, Dept Med, Div Prevent Med, Boston, MA 02115 USA.
[Altshuler, David; Voight, Benjamin] Massachusetts Gen Hosp, Dept Mol Biol, Ctr Human Genet Res, Boston, MA 02114 USA.
[Altshuler, David; Voight, Benjamin] Massachusetts Gen Hosp, Diabet Unit, Boston, MA 02114 USA.
[Altshuler, David; Voight, Benjamin] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA.
[Altshuler, David; Voight, Benjamin] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
RP Zaitlen, N (reprint author), Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
EM nzaitlen@hsph.harvard.edu; aprice@hsph.harvard.edu
RI Altshuler, David/A-4476-2009; Worthington, Jane/M-9770-2014; Barton,
Anne/N-2053-2014; Zienolddiny, Shanbeh/O-7392-2015; Risch,
Angela/H-2669-2013;
OI Altshuler, David/0000-0002-7250-4107; Worthington,
Jane/0000-0003-0544-042X; Barton, Anne/0000-0003-3316-2527; Field,
John/0000-0003-3951-6365; Eyre, Stephen/0000-0002-1251-6974; Risch,
Angela/0000-0002-8026-5505; Hocking, Lynne J/0000-0002-2414-2826
FU National Heart, Lung, and Blood Institute [HL043851, HL69757]; National
Cancer Institute [CA 047988]; Donald W. Reynolds Foundation; Fondation
Leducq; Amgen; NIH [R01 HG006399, R21 ES020754, 5T32ES007142-27]; U.S.
National Institutes of Health, National Cancer Institute
[U01-CA98233-07, U01-CA98710-06, U01-CA98216-06, U01-CA98758-07];
Manchester Biomedical Research Centre; Arthritis Research Campaign
FX The WGHS is supported by HL043851 and HL69757 from the National Heart,
Lung, and Blood Institute and CA 047988 from the National Cancer
Institute, the Donald W. Reynolds Foundation and the Fondation Leducq,
with collaborative scientific support and funding for genotyping
provided by Amgen. This work was funded by NIH grants R01 HG006399 (B
Pasaniuc, S Pollack, N Patterson, AL Price) and R21 ES020754 (N Zaitlen,
M Cornelis, N Patterson, AL Price) and NIH fellowship 5T32ES007142-27 (N
Zaitlen). This work was supported by the U.S. National Institutes of
Health, National Cancer Institute [cooperative agreements U01-CA98233-07
to DJ Hunter, U01-CA98710-06 to S Gapstur, U01-CA98216-06 to E Riboli
and R Kaaks, and U01-CA98758-07 to BE Henderson, and Intramural Research
Program of NIH/National Cancer Institute, Division of Cancer
Epidemiology and Genetics]. A Barton, S Eyre, and J Worthington were
supported by Manchester Biomedical Research Centre and the Arthritis
Research Campaign. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 63
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Z9 33
U1 2
U2 15
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7404
J9 PLOS GENET
JI PLoS Genet.
PD NOV
PY 2012
VL 8
IS 11
AR e1003032
DI 10.1371/journal.pgen.1003032
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 048DY
UT WOS:000311891600020
PM 23144628
ER
PT J
AU Azman, AS
Luquero, FJ
Rodrigues, A
Palma, PP
Grais, RF
Banga, CN
Grenfell, BT
Lessler, J
AF Azman, Andrew S.
Luquero, Francisco J.
Rodrigues, Amabelia
Pablo Palma, Pedro
Grais, Rebecca F.
Banga, Cunhate Na
Grenfell, Bryan T.
Lessler, Justin
TI Urban Cholera Transmission Hotspots and Their Implications for Reactive
Vaccination: Evidence from Bissau City, Guinea Bissau
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID PROTECTIVE EFFICACY; FIELD TRIAL; B-SUBUNIT; OUTBREAK
AB Background: Use of cholera vaccines in response to epidemics (reactive vaccination) may provide an effective supplement to traditional control measures. In Haiti, reactive vaccination was considered but, until recently, rejected in part due to limited global supply of vaccine. Using Bissau City, Guinea-Bissau as a case study, we explore neighborhood-level transmission dynamics to understand if, with limited vaccine and likely delays, reactive vaccination can significantly change the course of a cholera epidemic.
Methods and Findings: We fit a spatially explicit meta-population model of cholera transmission within Bissau City to data from 7,551 suspected cholera cases from a 2008 epidemic. We estimated the effect reactive vaccination campaigns would have had on the epidemic under different levels of vaccine coverage and campaign start dates. We compared highly focused and diffuse strategies for distributing vaccine throughout the city. We found wide variation in the efficiency of cholera transmission both within and between areas of the city. "Hotspots", where transmission was most efficient, appear to drive the epidemic. In particular one area, Bandim, was a necessary driver of the 2008 epidemic in Bissau City. If vaccine supply were limited but could have been distributed within the first 80 days of the epidemic, targeting vaccination at Bandim would have averted the most cases both within this area and throughout the city. Regardless of the distribution strategy used, timely distribution of vaccine in response to an ongoing cholera epidemic can prevent cases and save lives.
Conclusions: Reactive vaccination can be a useful tool for controlling cholera epidemics, especially in urban areas like Bissau City. Particular neighborhoods may be responsible for driving a city's cholera epidemic; timely and targeted reactive vaccination at such neighborhoods may be the most effective way to prevent cholera cases both within that neighborhood and throughout the city.
C1 [Azman, Andrew S.; Lessler, Justin] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA.
[Luquero, Francisco J.; Grais, Rebecca F.] Epictr, Paris, France.
[Rodrigues, Amabelia; Banga, Cunhate Na] Minist Hlth, Bissau, Guinea Bissau.
[Grenfell, Bryan T.] Princeton Univ, Dept Ecol & Evolutionary Biol, Princeton, NJ 08544 USA.
[Pablo Palma, Pedro] Med Sin Fronteras, Barcelona, Spain.
[Grenfell, Bryan T.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Azman, AS (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA.
EM jlessler@jhsph.edu
OI Lessler, Justin/0000-0002-9741-8109; Azman, Andrew/0000-0001-8662-9077
FU JHSPH Sommer Scholars program; National Institutes of Health (NIAID)
[K22 AI092150-01]; Bill and Melinda Gates Foundation (Vaccine Modeling
Initiative) [705580-3]; RAPIDD program of the Science and Technology
Directorate, Department of Homeland Security; Fogarty International
Center, United States National Institutes of Health
FX AA is supported by the JHSPH Sommer Scholars program. JL is the
recipient of a Research Scholar Development Award from the National
Institutes of Health (NIAID, K22 AI092150-01). The work of JL and BTG on
this project was funded by a grant from the Bill and Melinda Gates
Foundation (Vaccine Modeling Initiative, 705580-3). BTG was also
supported by the RAPIDD program of the Science and Technology
Directorate, Department of Homeland Security, and the Fogarty
International Center, United States 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 29
TC 17
Z9 18
U1 0
U2 12
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD NOV
PY 2012
VL 6
IS 11
AR e1901
DI 10.1371/journal.pntd.0001901
PG 11
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 048CX
UT WOS:000311888900029
PM 23145204
ER
PT J
AU Dolo, H
Coulibaly, YI
Dembele, B
Konate, S
Coulibaly, SY
Doumbia, SS
Diallo, AA
Soumaoro, L
Coulibaly, ME
Diakite, SAS
Guindo, A
Fay, MP
Metenou, S
Nutman, TB
Klion, AD
AF Dolo, Housseini
Coulibaly, Yaya I.
Dembele, Benoit
Konate, Siaka
Coulibaly, Siaka Y.
Doumbia, Salif S.
Diallo, Abdallah A.
Soumaoro, Lamine
Coulibaly, Michel E.
Diakite, Seidina A. S.
Guindo, Aldiouma
Fay, Michael P.
Metenou, Simon
Nutman, Thomas B.
Klion, Amy D.
TI Filariasis Attenuates Anemia and Proinflammatory Responses Associated
with Clinical Malaria: A Matched Prospective Study in Children and Young
Adults
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID PLASMODIUM-FALCIPARUM MALARIA; SCHISTOSOMA-HAEMATOBIUM INFECTION;
TUMOR-NECROSIS-FACTOR; MALIAN CHILDREN; HELMINTH COINFECTION; LYMPHATIC
FILARIASIS; TETANUS VACCINATION; SERUM-LEVELS; CYTOKINES; SEVERITY
AB Background: Wuchereria bancrofti (Wb) and Mansonella perstans (Mp) are blood-borne filarial parasites that are endemic in many countries of Africa, including Mali. The geographic distribution of Wb and Mp overlaps considerably with that of malaria, and coinfection is common. Although chronic filarial infection has been shown to alter immune responses to malaria parasites, its effect on clinical and immunologic responses in acute malaria is unknown.
Methodology/Principal Findings: To address this question, 31 filaria-positive (FIL+) and 31 filaria-negative (FIL-) children and young adults, matched for age, gender and hemoglobin type, were followed prospectively through a malaria transmission season. Filarial infection was defined by the presence of Wb or Mp microfilariae on calibrated thick smears performed between 10 pm and 2 am and/or by the presence of circulating filarial antigen in serum. Clinical malaria was defined as axillary temperature >= 37.5 degrees C or another symptom or sign compatible with malaria infection plus the presence of asexual malaria parasites on a thick blood smear. Although the incidence of clinical malaria, time to first episode, clinical signs and symptoms, and malaria parasitemia were comparable between the two groups, geometric mean hemoglobin levels were significantly decreased in FIL- subjects at the height of the transmission season compared to FIL+ subjects (11.4 g/dL vs. 12.5 g/dL, p<0.01). Plasma levels of IL-1ra, IP-10 and IL-8 were significantly decreased in FIL+ subjects at the time of presentation with clinical malaria (99, 2145 and 49 pg/ml, respectively as compared to 474, 5522 and 247 pg/ml in FIL- subjects).
Conclusions/Significance: These data suggest that pre-existent filarial infection attenuates immune responses associated with severe malaria and protects against anemia, but has little effect on susceptibility to or severity of acute malaria infection. The apparent protective effect of filarial infection against anemia is intriguing and warrants further study in a larger cohort.
C1 [Dolo, Housseini; Coulibaly, Yaya I.; Dembele, Benoit; Konate, Siaka; Coulibaly, Siaka Y.; Doumbia, Salif S.; Diallo, Abdallah A.; Soumaoro, Lamine; Coulibaly, Michel E.; Diakite, Seidina A. S.; Guindo, Aldiouma] Univ Bamako, Fac Med Pharm & Dent, Bamako, Mali.
[Fay, Michael P.] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
[Metenou, Simon; Nutman, Thomas B.; Klion, Amy D.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Dolo, H (reprint author), Univ Bamako, Fac Med Pharm & Dent, Bamako, Mali.
EM aklion@nih.gov
RI Metenou, Simon/C-1101-2013;
OI Fay, Michael P./0000-0002-8643-9625; Klion, Amy/0000-0002-4986-5326
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health
FX This work was funded by the Division of Intramural Research, National
Institute of Allergy and Infectious Diseases, National Institutes of
Health. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 29
TC 13
Z9 14
U1 0
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD NOV
PY 2012
VL 6
IS 11
AR e1890
DI 10.1371/journal.pntd.0001890
PG 9
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 048CX
UT WOS:000311888900019
PM 23133692
ER
PT J
AU Marzouki, S
Abdeladhim, M
Ben Abdessalem, C
Oliveira, F
Ferjani, B
Gilmore, D
Louzir, H
Valenzuela, JG
Ben Ahmed, M
AF Marzouki, Soumaya
Abdeladhim, Maha
Ben Abdessalem, Chaouki
Oliveira, Fabiano
Ferjani, Beya
Gilmore, Dana
Louzir, Hechmi
Valenzuela, Jesus G.
Ben Ahmed, Melika
TI Salivary Antigen SP32 Is the Immunodominant Target of the Antibody
Response to Phlebotomus papatasi Bites in Humans
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID VISCERAL LEISHMANIASIS; LUTZOMYIA-LONGIPALPIS; IMMUNE-RESPONSE;
EPIDEMIOLOGIC MARKER; GLAND PROTEINS; ENDEMIC AREAS; EXPOSURE; VECTOR;
IDENTIFICATION; PSYCHODIDAE
AB Background: Zoonotic cutaneous leishmaniasis (ZCL) due to Leishmania major is highly prevalent in Tunisia and is transmitted by a hematophagous vector Phlebotomus papatasi (P. papatasi). While probing for a blood meal, the sand fly injects saliva into the host's skin, which contains a variety of compounds that are highly immunogenic. We recently showed that the presence of anti-saliva antibodies was associated with an enhanced risk for leishmaniasis and identified the immunodominant salivary protein of Phlebotomus papatasi as a protein of approximately 30 kDa.
Methodology/Principal Findings: We cloned and expressed in mammalian cells two salivary proteins PpSP30 and PpSP32 with predicted molecular weights close to 30 kDa from the Tunisian strain of P. papatasi. The two recombinant salivary proteins were purified by two-step HPLC (High-Performance Liquid Chromatography) and tested if these proteins correspond to the immunodominant antigen of 30 kDa previously shown to be recognized by human sera from endemic areas for ZCL and exposed naturally to P. papatasi bites. While recombinant PpSP30 (rPpSP30) was poorly recognized by human sera from endemic areas for ZCL, rPpSP32 was strongly recognized by the tested sera. The binding of human IgG antibodies to native PpSP32 was inhibited by the addition of rPpSP32. Consistently, experiments in mice showed that PpSP32 induced the highest levels of antibodies compared to other P. papatasi salivary molecules while PpSP30 did not induce any detectable levels of antibodies.
Conclusions: Our findings demonstrate that PpSP32 is the immunodominant target of the antibody response to P. papatasi saliva. They also indicate that the recombinant form of PpSP32 is similar to the native one and represents a good candidate for large scale testing of human exposure to P. papatasi bites and perhaps for assessing the risk of contracting the disease.
C1 [Marzouki, Soumaya; Abdeladhim, Maha; Ben Abdessalem, Chaouki; Ferjani, Beya; Louzir, Hechmi; Ben Ahmed, Melika] Inst Pasteur Tunis, Lab Transmiss Control & Immunobiol Infect, Tunis, Tunisia.
[Oliveira, Fabiano; Gilmore, Dana; Valenzuela, Jesus G.] NIAID, Vector Mol Biol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
[Louzir, Hechmi; Ben Ahmed, Melika] Univ Tunis El Manar, Fac Med Tunis, Tunis, Tunisia.
RP Marzouki, S (reprint author), Inst Pasteur Tunis, Lab Transmiss Control & Immunobiol Infect, LR11IPT02, Tunis, Tunisia.
EM melika.benahmed@pasteur.rns.tn
RI Oliveira, Fabiano/B-4251-2009
OI Oliveira, Fabiano/0000-0002-7924-8038
FU National Institutes of Health (NIH)/NIAID [SP50AI074178]; Division of
Intramural Research, National Institute of Allergy and Infectious
Diseases, National Institutes of Health
FX The project was supported by the National Institutes of Health
(NIH)/NIAID Grant Number SP50AI074178 and in part by the Intramural
Research Program of the Division of Intramural Research, National
Institute of Allergy and Infectious Diseases, National Institutes of
Health. The funders had no role in study design, data collection and
analysis, decision in publish, or preparation of the manuscript.
NR 32
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Z9 18
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD NOV
PY 2012
VL 6
IS 11
AR e1911
DI 10.1371/journal.pntd.0001911
PG 11
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 048CX
UT WOS:000311888900038
PM 23209854
ER
PT J
AU Schwan, TG
Anderson, JM
Lopez, JE
Fischer, RJ
Raffel, SJ
McCoy, BN
Safronetz, D
Sogoba, N
Maiga, O
Traore, SF
AF Schwan, Tom G.
Anderson, Jennifer M.
Lopez, Job E.
Fischer, Robert J.
Raffel, Sandra J.
McCoy, Brandi N.
Safronetz, David
Sogoba, Nafomon
Maiga, Ousmane
Traore, Sekou F.
TI Endemic Foci of the Tick-Borne Relapsing Fever Spirochete Borrelia
crocidurae in Mali, West Africa, and the Potential for Human Infection
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID GLYCEROPHOSPHODIESTER PHOSPHODIESTERASE GLPQ; IN-VITRO CULTIVATION;
PHYLOGENETIC ANALYSIS; LYME-DISEASE; NORTH-AMERICA; HARD-TICK; SENEGAL;
RECURRENTIS; HERMSII; BURGDORFERI
AB Background: Tick-borne relapsing fever spirochetes are maintained in endemic foci that involve a diversity of small mammals and argasid ticks in the genus Ornithodoros. Most epidemiological studies of tick-borne relapsing fever in West Africa caused by Borrelia crocidurae have been conducted in Senegal. The risk for humans to acquire relapsing fever in Mali is uncertain, as only a few human cases have been identified. Given the high incidence of malaria in Mali, and the potential to confuse the clinical diagnosis of these two diseases, we initiated studies to determine if there were endemic foci of relapsing fever spirochetes that could pose a risk for human infection.
Methodology/Principal Findings: We investigated 20 villages across southern Mali for the presence of relapsing fever spirochetes. Small mammals were captured, thin blood smears were examined microscopically for spirochetes, and serum samples were tested for antibodies to relapsing fever spirochetes. Ornithodoros sonrai ticks were collected and examined for spirochetal infection. In total, 11.0% of the 663 rodents and 14.3% of the 63 shrews tested were seropositive and 2.2% of the animals had active spirochete infections when captured. In the Bandiagara region, the prevalence of infection was higher with 35% of the animals seropositive and 10% infected. Here also Ornithodoros sonrai were abundant and 17.3% of 278 individual ticks tested were infected with Borrelia crocidurae. Fifteen isolates of B. crocidurae were established and characterized by multi-locus sequence typing.
Conclusions/Significance: The potential for human tick-borne relapsing fever exists in many areas of southern Mali.
C1 [Schwan, Tom G.; Lopez, Job E.; Fischer, Robert J.; Raffel, Sandra J.; McCoy, Brandi N.] NIAID, Lab Zoonot Pathogens, Rocky Mt Labs, Hamilton, MT USA.
[Anderson, Jennifer M.] NIAID, Lab Malaria & Vector Res, Twinbrook, MD USA.
[Safronetz, David] NIAID, Virol Lab, Rocky Mt Labs, Hamilton, MT USA.
[Sogoba, Nafomon; Maiga, Ousmane; Traore, Sekou F.] Univ Sci Tech & Technol Bamako, Malaria Res & Training Ctr, Bamako, Mali.
RP Schwan, TG (reprint author), NIAID, Lab Zoonot Pathogens, Rocky Mt Labs, Hamilton, MT USA.
EM tschwan@niaid.nih.gov
OI Fischer, Robert/0000-0002-1816-472X
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
FX This study was supported by the Division of Intramural Research,
National Institute of Allergy and Infectious Diseases, National
Institutes of Health, Bethesda, MD, USA. The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 83
TC 16
Z9 16
U1 0
U2 14
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD NOV
PY 2012
VL 6
IS 11
AR e1924
DI 10.1371/journal.pntd.0001924
PG 13
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 048CX
UT WOS:000311888900047
PM 23209863
ER
PT J
AU Ward, MM
AF Ward, Michael M.
TI Sense of control and sociodemographic differences in self-reported
health in older adults
SO QUALITY OF LIFE RESEARCH
LA English
DT Article
DE Sense of control; Self-rated health; Functional limitations; Disease
burden
ID RISK-FACTORS; SOCIOECONOMIC DIFFERENCES; PERCEIVED CONTROL;
HEART-DISEASE; AGE; MORTALITY; MASTERY; LIFE; DEPRESSION; PREDICTION
AB Purpose Stronger sense of control has been associated with improved health outcomes. This study tested whether the association between sense of control and self-reported health varied among demographic groups and whether sense of control attenuated sociodemographic differences in self-reported health.
Methods Data from 6,815 participants in the Health and Retirement Study were used to examine moderation between demographic characteristics and sense of control (measured by the personal mastery and perceived constraints scales of the Midlife Developmental Inventory) in their associations with three self-reported health measures (global rating of fair/poor health, functional limitations, and number of comorbid conditions).
Results Higher personal mastery and lower perceived constraints were associated with better self-reported health. There were no significant interactions between the sense of control measures and age, gender, education level, income, or marital status in their associations with either global self-rated health or functional limitations. Higher levels of mastery were associated with lower likelihood of functional limitations among blacks and whites, but not among those of other races. Perceived constraints were slightly more strongly associated with number of comorbid conditions among older than younger individuals.
Conclusions Sense of control measures were generally similarly associated with self-reported health across demographic groups and did not attenuate demographic differences in health.
C1 NIAMSD, NIH, Bethesda, MD 20892 USA.
RP Ward, MM (reprint author), NIAMSD, NIH, Bldg 10 CRC,Room 4-1339,10 Ctr Dr, Bethesda, MD 20892 USA.
EM wardm1@mail.nih.gov
FU National Institute of Arthritis and Musculoskeletal and Skin Diseases,
National Institutes of Health
FX This work was supported by the Intramural Research Program, National
Institute of Arthritis and Musculoskeletal and Skin Diseases, National
Institutes of Health.
NR 36
TC 6
Z9 6
U1 1
U2 13
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0962-9343
J9 QUAL LIFE RES
JI Qual. Life Res.
PD NOV
PY 2012
VL 21
IS 9
BP 1509
EP 1518
DI 10.1007/s11136-011-0068-4
PG 10
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 089MH
UT WOS:000314914200003
PM 22120892
ER
PT J
AU Heard, ME
Pabona, JMP
Clayberger, C
Krensky, AM
Simmen, FA
Simmen, RCM
AF Heard, Melissa E.
Pabona, John Mark P.
Clayberger, Carol
Krensky, Alan M.
Simmen, Frank A.
Simmen, Rosalia C. M.
TI The Reproductive Phenotype of Mice Null for Transcription Factor
Kruppel-Like Factor 13 Suggests Compensatory Function of Family Member
Kruppel-Like Factor 9 in the Peri-Implantation Uterus
SO BIOLOGY OF REPRODUCTION
LA English
DT Article
DE female reproductive tract; implantation; Kruppel-like factors;
pregnancy; progesterone/progesterone receptor; steroid hormone receptors
ID ENDOMETRIAL EPITHELIAL-CELLS; PROGESTERONE-RECEPTOR ISOFORM; BONE
MORPHOGENETIC PROTEIN-2; NUCLEAR-LOCALIZATION; MOUSE UTERUS; B-ISOFORM;
GENE-EXPRESSION; STROMAL CELLS; IN-VIVO; BINDING
AB The ovarian hormones estrogen and progesterone promote uterine receptivity and successful pregnancy through their cognate receptors functioning in concert with context-dependent nuclear coregulators. Previously, we showed that the transcription factor Kruppel-like factor (KLF) 9 is a progesterone receptor (PGR) coactivator in the uterus and that mice null for Klf9 exhibit subfertility and reduced progesterone sensitivity. The highly related family member KLF13 displays increased expression in uteri of pregnant and nonpregnant Klf9 null mice and similarly regulates PGR-mediated transactivation in endometrial stromal cells. However, a uterine phenotype with loss of Klf13 has not been reported. In the present study, we demonstrate that Klf13 deficiency in mice did not compromise female fertility and pregnancy outcome. Klf13 null females had litter sizes, numbers of implanting embryos, uterine morphology, and ovarian steroid hormone production comparable to those of wild-type (WT) counterparts. Further, pregnant WT and Klf13 null females at Day Postcoitum (DPC) 3.5 had similar uterine Pgr, estrogen receptor, and Wnt-signaling component transcript levels. Nuclear levels of KLF9 were higher in Klf13 null than in WT uteri at DPC 3.5, albeit whole-tissue KLF9 protein and transcript levels did not differ between genotypes. The lack of a similar induction of nuclear KLF9 levels in uteri of virgin Klf13((-/-)) mice relative to WT uteri was associated with lower stromal PGR expression. In differentiating human endometrial stromal cells, coincident KLF9/KLF13 knockdown by small interfering RNA targeting reduced decidualization-associated PRL expression, whereas KLF9 and KLF13 knockdowns alone reduced transcript levels of WNT4 and BMP2, respectively. Results suggest that KLF9 and KLF13 functionally compensate in peri-implantation uterus for pregnancy success.
C1 [Heard, Melissa E.; Pabona, John Mark P.; Simmen, Frank A.; Simmen, Rosalia C. M.] Univ Arkansas Med Sci, Dept Physiol & Biophys, Little Rock, AR 72205 USA.
[Pabona, John Mark P.; Simmen, Rosalia C. M.] Univ Arkansas Med Sci, Arkansas Childrens Nutr Ctr, Little Rock, AR 72205 USA.
[Simmen, Frank A.; Simmen, Rosalia C. M.] Univ Arkansas Med Sci, Winthrop Rockefeller Canc Inst, Little Rock, AR 72205 USA.
[Clayberger, Carol; Krensky, Alan M.] NCI, Lab Cellular & Mol Biol, NIH, Bethesda, MD 20892 USA.
RP Simmen, RCM (reprint author), Arkansas Childrens Nutr Ctr, 15 Childrens Way, Little Rock, AR 72211 USA.
EM simmenrosalia@uams.edu
FU National Institutes of Child Health and Human Development [HD21961];
Arkansas Biosciences Institute/Arkansas Children's Hospital Research
Institute; Arkansas Children's Hospital Research Institute Student and
Clinical Staff Intramural Program; University of Arkansas for Medical
Sciences Translational Research Institute [UL1TR000039]
FX Supported by grants from the National Institutes of Child Health and
Human Development HD21961 (R.C.M.S.), Arkansas Biosciences
Institute/Arkansas Children's Hospital Research Institute (R.C.M.S.),
Arkansas Children's Hospital Research Institute Student and Clinical
Staff Intramural Program (M.E.H.), and University of Arkansas for
Medical Sciences Translational Research Institute Grant UL1TR000039.
NR 45
TC 10
Z9 10
U1 0
U2 5
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1691 MONROE ST,SUITE # 3, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PD NOV
PY 2012
VL 87
IS 5
AR 115
DI 10.1095/biolreprod.112.102251
PG 11
WC Reproductive Biology
SC Reproductive Biology
GA 080HI
UT WOS:000314231900012
PM 22993382
ER
PT J
AU Chen, BS
Gray, JA
Sanz-Clemente, A
Wei, Z
Thomas, EV
Nicoll, RA
Roche, KW
AF Chen, Bo-Shiun
Gray, John A.
Sanz-Clemente, Antonio
Wei, Zhe
Thomas, Eleanor V.
Nicoll, Roger A.
Roche, Katherine W.
TI SAP102 Mediates Synaptic Clearance of NMDA Receptors
SO CELL REPORTS
LA English
DT Article
ID HIPPOCAMPAL SYNAPSES; DEPENDENT REGULATION; SUBUNIT COMPOSITION; NR2A
SUBUNIT; PDZ PROTEINS; TRAFFICKING; PLASTICITY; COMPLEX; PSD-95;
PHOSPHORYLATION
AB Membrane-associated guanylate kinases (MAGUKs) are the major family of scaffolding proteins at the postsynaptic density. The PSD-MAGUK subfamily, which includes PSD-95, PSD-93, SAP97, and SAP102, is well accepted to be primarily involved in the synaptic anchoring of numerous proteins, including N-methyl-D-aspartate receptors (NMDARs). Notably, the synaptic targeting of NMDARs depends on the binding of the PDZ ligand on the GluN2B subunit to MAGUK PDZ domains, as disruption of this interaction dramatically decreases NMDAR surface and synaptic expression. We recently reported a secondary interaction between SAP102 and GluN2B, in addition to the PDZ interaction. Here, we identify two critical residues on GluN2B responsible for the non-PDZ binding to SAP102. Strikingly, either mutation of these critical residues or knockdown of endogenous SAP102 can rescue the defective surface expression and synaptic localization of PDZ binding-deficient GluN2B. These data reveal an unexpected, nonscaffolding role for SAP102 in the synaptic clearance of GluN2B-containing NMDARs.
C1 [Chen, Bo-Shiun; Sanz-Clemente, Antonio; Thomas, Eleanor V.; Roche, Katherine W.] NINDS, NIH, Bethesda, MD 20892 USA.
[Chen, Bo-Shiun; Wei, Zhe] Georgia Hlth Sci Univ, Dept Neurol, Inst Mol Med & Genet, Augusta, GA 30912 USA.
[Chen, Bo-Shiun; Wei, Zhe] Georgia Hlth Sci Univ, Program Dev Neurobiol, Inst Mol Med & Genet, Augusta, GA 30912 USA.
[Gray, John A.; Nicoll, Roger A.] Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA.
[Nicoll, Roger A.] Univ Calif San Francisco, Dept Physiol, San Francisco, CA 94143 USA.
RP Chen, BS (reprint author), NINDS, NIH, Bethesda, MD 20892 USA.
EM bochen@georgiahealth.edu; rochek@ninds.nih.gov
OI Gray, John/0000-0002-7287-0748; Roche, Katherine/0000-0001-7282-6539
FU NINDS Intramural Research Program; NINDS Career Transition Award; NIMH;
NARSAD Young Investigator Award
FX We thank the NINDS sequencing facility and light imaging facility. We
also thank Kenji Sakimura (Niigata University) for the Grin2afl/fl and
Grin2bfl/fl mice. The research was supported by the NINDS Intramural
Research Program (B.-S.C., A.S.-C., E.V.T., and K.W.R.), a NINDS Career
Transition Award (E.V.T., Z.W., and B.-S.C.), grants from the NIMH
(J.A.G. and R.A.N.). J.A.G. is funded by a NARSAD Young Investigator
Award and is the NARSAD Hammerschlag Family Investigator.
NR 37
TC 15
Z9 16
U1 0
U2 5
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD NOV
PY 2012
VL 2
IS 5
BP 1120
EP 1128
DI 10.1016/j.celrep.2012.09.024
PG 9
WC Cell Biology
SC Cell Biology
GA 083IU
UT WOS:000314457700008
PM 23103165
ER
PT J
AU Zhou, ZS
Belluscio, L
AF Zhou, Zhishang
Belluscio, Leonardo
TI Coding Odorant Concentration through Activation Timing between the
Medial and Lateral Olfactory Bulb
SO CELL REPORTS
LA English
DT Article
ID AIR-FLOW; RAT; REPRESENTATIONS; DISCRIMINATION; RECEPTOR; OUTPUT;
RECOGNITION; INFORMATION; TOPOGRAPHY; INTENSITY
AB In mammals, each olfactory bulb (OB) contains a pair of mirror-symmetric glomerular maps organized to reflect odorant receptor identity. The functional implication of maintaining these symmetric medial-lateral maps within each OB remains unclear. Here, using in vivo multielectrode recordings to simultaneously detect odorant-induced activity across the entire OB, we reveal a timing difference in the odorant-evoked onset latencies between the medial and lateral halves. Interestingly, the latencies in the medial and lateral OB decreased at different rates as odorant concentration increased, causing the timing difference between them to also diminish. As a result, output neurons in the medial and lateral OB fired with greater synchrony at higher odorant concentrations. Thus, we propose that temporal differences in activity between the medial and lateral OB can dynamically code odorant concentration, which is subsequently decoded in the olfactory cortex through the integration of synchronous action potentials.
C1 [Zhou, Zhishang; Belluscio, Leonardo] NINDS, Dev Neural Plast Sect, NIH, Bethesda, MD 20892 USA.
RP Belluscio, L (reprint author), NINDS, Dev Neural Plast Sect, NIH, 35 Convent Dr, Bethesda, MD 20892 USA.
EM belluscl@ninds.nih.gov
FU National Institute of Neurological Disorders and Stroke, Intramural
Research Program, National Institutes of Health
FX We thank Haiqing Zhao and Randy Reed for providing the UBI7 mice;
Elakkat Gireesh and Dietmar Plenz for help establishing the
multielectrode recordings; and Mark Stopfer, Nick Ryba, Rory McQuiston,
and Beth Belluscio for critical comments on the manuscript. This work
was supported by the National Institute of Neurological Disorders and
Stroke, Intramural Research Program, National Institutes of Health.
NR 40
TC 13
Z9 13
U1 0
U2 7
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD NOV
PY 2012
VL 2
IS 5
BP 1143
EP 1150
DI 10.1016/j.celrep.2012.09.035
PG 8
WC Cell Biology
SC Cell Biology
GA 083IU
UT WOS:000314457700011
PM 23168258
ER
PT J
AU Wei, L
Liu, BY
Tuo, JS
Shen, DF
Chen, P
Li, ZY
Liu, XX
Ni, J
Dagur, P
Sen, HN
Jawad, S
Ling, D
Park, S
Chakrabarty, S
Meyerle, C
Agron, E
Ferris, FL
Chew, EY
McCoy, JP
Blum, E
Francis, PJ
Klein, ML
Guymer, RH
Baird, PN
Chan, CC
Nussenblatt, RB
AF Wei, Lai
Liu, Baoying
Tuo, Jingsheng
Shen, Defen
Chen, Ping
Li, Zhiyu
Liu, Xunxian
Ni, Jia
Dagur, Pradeep
Sen, H. Nida
Jawad, Shayma
Ling, Diamond
Park, Stanley
Chakrabarty, Sagarika
Meyerle, Catherine
Agron, Elvira
Ferris, Frederick L.
Chew, Emily Y.
McCoy, J. Philip
Blum, Emily
Francis, Peter J.
Klein, Michael L.
Guymer, Robyn H.
Baird, Paul N.
Chan, Chi-Chao
Nussenblatt, Robert B.
TI Hypomethylation of the IL17RC Promoter Associates with Age-Related
Macular Degeneration
SO CELL REPORTS
LA English
DT Article
ID MONOZYGOTIC TWINS; DNA METHYLATION; CELL-DIFFERENTIATION; DISEASE;
EPIGENOME; IL-17; MACULOPATHY; MECHANISMS; GENOME
AB Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in the elderly population worldwide. Although recent studies have demonstrated strong genetic associations between AMD and SNPs in a number of genes, other modes of regulation are also likely to play a role in the etiology of this disease. We identified a significantly decreased level of methylation on the IL17RC promoter in AMD patients. Furthermore, we showed that hypomethylation of the IL17RC promoter in AMD patients led to an elevated expression of its protein and messenger RNA in peripheral blood as well as in the affected retina and choroid, suggesting that the DNA methylation pattern and expression of IL17RC may potentially serve as a biomarker for the diagnosis of AMD and likely plays a role in disease pathogenesis.
C1 [Wei, Lai; Liu, Baoying; Tuo, Jingsheng; Shen, Defen; Chen, Ping; Li, Zhiyu; Ni, Jia; Sen, H. Nida; Jawad, Shayma; Ling, Diamond; Park, Stanley; Chakrabarty, Sagarika; Chan, Chi-Chao; Nussenblatt, Robert B.] NEI, Lab Immunol, NIH, Bethesda, MD 20892 USA.
[Wei, Lai; Nussenblatt, Robert B.] NIH, Ctr Human Immunol Autoimmun & Inflammat, Bethesda, MD 20892 USA.
[Wei, Lai; Liu, Xunxian; Nussenblatt, Robert B.] NIH, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
[Dagur, Pradeep] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Meyerle, Catherine; Agron, Elvira; Ferris, Frederick L.; Chew, Emily Y.] NEI, Div Epidemiol & Clin Res, NIH, Bethesda, MD 20892 USA.
[Blum, Emily; Francis, Peter J.; Klein, Michael L.] Oregon Hlth & Sci Univ, Macular Degenerat Ctr, Portland, OR 97239 USA.
[Blum, Emily; Francis, Peter J.] Oregon Hlth & Sci Univ, Leonard Christensen Eye Pathol Lab, Casey Eye Inst, Portland, OR 97239 USA.
[Guymer, Robyn H.; Baird, Paul N.] Univ Melbourne, Ctr Eye Res Australia, Royal Victorian Eye & Ear Hosp, Melbourne, Vic 3002, Australia.
RP Wei, L (reprint author), NEI, Lab Immunol, NIH, Bethesda, MD 20892 USA.
EM lai.wei@nih.gov; drbob@nei.nih.gov
RI Wei, Lai/D-1088-2014;
OI Tuo, Jingsheng/0000-0002-1372-7810; Baird, Paul/0000-0002-1305-3502
FU intramural research program of the NEI; National Center for
Complementary and Alternative Medicine; National Heart Lung and Blood
Institute; Foundation Fighting Blindness; Macular Degeneration Center
Research Fund of the CEI; Research to Prevent Blindness; National Health
and Medical Research Council Centre for Clinical Research Excellence
[529923]
FX The authors thank the ATR for access to this national resource, the
twins who volunteered for the study, and Andrea Richardson for DNA
extraction and genotyping of twin samples. We also thank Dr. Neal Young
for critically reading the manuscript. This study was supported by
grants from the intramural research program of the NEI (to R.B.N.,
C.-C.C., F.L.F., and E.Y.C.), the National Center for Complementary and
Alternative Medicine (to L.W. and R.B.N.), the National Heart Lung and
Blood Institute (to J.P.M.), the Foundation Fighting Blindness (to
P.J.F.), the Macular Degeneration Center Research Fund of the CEI (to
M.L.K. and P.J.F.), Research to Prevent Blindness (unrestricted grant to
the CEI, Career Development Award to P.J.F.), and the National Health
and Medical Research Council Centre for Clinical Research Excellence
(grant 529923, Translational Clinical Research in Major Eye Diseases and
through a Practitioner Fellowship to R.H.G.). The CERA receives
operational infrastructure support from the Victorian Government
NR 34
TC 58
Z9 62
U1 1
U2 8
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD NOV
PY 2012
VL 2
IS 5
BP 1151
EP 1158
DI 10.1016/j.celrep.2012.10.013
PG 8
WC Cell Biology
SC Cell Biology
GA 083IU
UT WOS:000314457700012
PM 23177625
ER
PT J
AU Zhang, F
Li, Y
Tang, ZS
Kumar, A
Lee, C
Zhang, LP
Zhu, CY
Klotzsche-von Ameln, A
Wang, B
Gao, ZQ
Zhang, SZ
Langer, HF
Hou, X
Jensen, L
Ma, WX
Wong, W
Chavakis, T
Liu, YZ
Cao, YH
Li, XR
AF Zhang, Fan
Li, Yang
Tang, Zhongshu
Kumar, Anil
Lee, Chunsik
Zhang, Liping
Zhu, Chaoyong
Klotzsche-von Ameln, Anne
Wang, Bin
Gao, Zhiqin
Zhang, Shizhuang
Langer, Harald F.
Hou, Xu
Jensen, Lasse
Ma, Wenxin
Wong, Wai
Chavakis, Triantafyllos
Liu, Yizhi
Cao, Yihai
Li, Xuri
TI Proliferative and Survival Effects of PUMA Promote Angiogenesis
SO CELL REPORTS
LA English
DT Article
ID PATHOLOGICAL ANGIOGENESIS; MOUSE RETINA; VEGF-B; CELLS; APOPTOSIS;
MICROGLIA; AUTOPHAGY; PATHWAY; P53; CALMODULIN
AB The p53 upregulated modulator of apoptosis (PUMA) is known as an essential apoptosis inducer. Here, we report the seemingly paradoxical finding that PUMA is a proangiogenic factor critically required for the proliferation and survival of vascular and microglia cells. Strikingly, Puma deficiency by genetic deletion or small hairpin RNA knockdown inhibited developmental and pathological angiogenesis and reduced microglia numbers in vivo, whereas Puma gene delivery increased angiogenesis and cell survival. Mechanistically, we revealed that PUMA plays a critical role in regulating autophagy by modulating Erk activation and intracellular calcium level. Our findings revealed an unexpected function of PUMA in promoting angiogenesis and warrant more careful investigations into the therapeutic potential of PUMA in treating cancer and degenerative diseases.
C1 [Zhang, Fan; Li, Yang; Tang, Zhongshu; Kumar, Anil; Lee, Chunsik; Ma, Wenxin; Wong, Wai; Li, Xuri] NEI, NIH, Rockville, MD 20852 USA.
[Tang, Zhongshu; Liu, Yizhi; Li, Xuri] Sun Yat Sen Univ, Zhongshan Ophthalm Ctr, State Key Lab Ophthalmol, Guangzhou 510060, Guangdong, Peoples R China.
[Zhang, Liping] Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD 20892 USA.
[Zhu, Chaoyong] NanTong Univ, Sch Publ Hlth, Nantong 226019, Peoples R China.
[Klotzsche-von Ameln, Anne; Chavakis, Triantafyllos] Univ Dresden, Div Vasc Inflammat Diabet & Kidney, Dept Med, D-03514630 Dresden, Germany.
[Klotzsche-von Ameln, Anne; Chavakis, Triantafyllos] Univ Dresden, Inst Physiol, D-03514630 Dresden, Germany.
[Wang, Bin] Binzhou Med Univ, Med Imaging Inst, Yantai 264003, Peoples R China.
[Gao, Zhiqin] Weifang Med Univ, Dept Cell Biol, Weifang 261053, Peoples R China.
[Zhang, Shizhuang] Weifang Med Univ, Dept Radiol, Med Imaging Ctr, Affiliated Hosp, Weifang 261053, Peoples R China.
[Langer, Harald F.] Univ Tubingen, Dept Cardiovasc Med, D-72074 Tubingen, Germany.
[Hou, Xu] Fourth Mil Med Univ, Dept Ophthalmol, Eye Inst Chinese PLA, Xijing Hosp, Xian 710032, Shaanxi, Peoples R China.
[Jensen, Lasse; Cao, Yihai] Karolinska Inst, Dept Microbiol Tumor & Cell Biol, S-17177 Stockholm, Sweden.
[Jensen, Lasse; Cao, Yihai] Linkoping Univ, Dept Med & Hlth Sci, S-58183 Linkoping, Sweden.
RP Li, XR (reprint author), NEI, NIH, Rockville, MD 20852 USA.
EM xurili18@gmail.com
RI Klotzsche - von Ameln, Anne/F-1980-2013;
OI Klotzsche - von Ameln, Anne/0000-0003-3579-1191; Jensen,
Lasse/0000-0003-2338-357X; Wong, Wai/0000-0003-0681-4016
FU ERC (ENDHOMRET); Deutsche Forschungsgemeinschaft [KFO 274]; Volkswagen
foundation (Lichtenberg program); Swedish Research Council; Swedish
Cancer Foundation; Karolinska Institute Foundation; Karolinska Institute
Distinguished Professor Award; Tianjin Natural Science Foundation
(CMM-Tianjin) [09ZCZDSF04400]; Torsten Soderbergs Foundation; European
Union Integrated Project of Metoxia [222741]; European Research Council
(ERC) ANGIOFAT [250021]; Intramural Research Program of the NIH,
National Eye Institute
FX We thank Dr. Andreas Strasser at the Walter and Eliza Hall Institute of
Medical Research, Australia, for the Puma- and Noxa-deficient mice, and
Professor Birgitta Ohberg at the Linkoping University, Sweden, for the
great help with the zebrafish work. T.C. was supported by the ERC
(ENDHOMRET) and the Deutsche Forschungsgemeinschaft. H.F.L. was
supported by the Volkswagen foundation (Lichtenberg program) and the
Deutsche Forschungsgemeinschaft (KFO 274). Y.C. is supported by the
Swedish Research Council, the Swedish Cancer Foundation, the Karolinska
Institute Foundation, the Karolinska Institute Distinguished Professor
Award, the Tianjin Natural Science Foundation (CMM-Tianjin,
09ZCZDSF04400), the Torsten Soderbergs Foundation, the European Union
Integrated Project of Metoxia (222741), and the European Research
Council (ERC) ANGIOFAT (250021). The authors declare no conflict of
interest. This research was supported by the Intramural Research Program
of the NIH, National Eye Institute.
NR 41
TC 12
Z9 14
U1 2
U2 15
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD NOV
PY 2012
VL 2
IS 5
BP 1272
EP 1285
DI 10.1016/j.celrep.2012.09.023
PG 14
WC Cell Biology
SC Cell Biology
GA 083IU
UT WOS:000314457700023
PM 23122957
ER
PT J
AU Shukla, V
Skuntz, S
Pant, HC
AF Shukla, Varsha
Skuntz, Susan
Pant, Harish C.
TI Deregulated Cdk5 Activity Is Involved in Inducing Alzheimer's Disease
SO ARCHIVES OF MEDICAL RESEARCH
LA English
DT Review
DE Cyclin-dependent kinase 5 (Cdk5); Hyperphosphorylation;
Neurodegeneration; Alzheimer's disease; Plaques; Tangles
ID CYCLIN-DEPENDENT KINASE-5; AMYLOID PRECURSOR PROTEIN; PAIRED HELICAL
FILAMENTS; NEURONAL CDC2-LIKE KINASE; NEUROFIBRILLARY TANGLES;
TAU-PROTEIN; MOUSE MODEL; ACTIVATOR P35; NEUROFILAMENT PHOSPHORYLATION;
INCREASED EXPRESSION
AB Alzheimer's disease (AD), the most devastating chronic neurodegenerative disease in adults, causes dementia and eventually, death of the affected individuals. Clinically, AD is characterized as late-onset, age-dependent cognitive decline due to loss of neurons in cortex and hippocampus. The pathologic corollary of these symptoms is the formation of senile plaques and neurofibrillary tangles. Senile plaques are formed due to accumulation of oligomeric amyloid beta (A beta) forming plaques. This occurs due to the amyloidogenic processing of the amyloid precursor protein (APP) by various secretases. On the other hand, neurofibrillary tangles are formed due to hyperphosphorylation of cytoskeleton proteins like tau and neurofilament. Both are hyperphosphorylated by cyclin-dependent kinase-5 (Cdk5) and are part of the paired helical filament (PHF), an integral part of neurofibrillary tangles. Unlike other cyclin-dependent kinases, Cdk5 plays a very important role in the neuronal development. Cdk5 gets activated by its neuronal activators p35 and p39. Upon stress, p35 and p39 are cleaved by calpain resulting in truncated products as p25 and p29. Association of Cdk5/p25 is longer and uncontrolled causing aberrant hyperphosphorylation of various substrates of Cdk5 like APP, tau and neurofilament, leading to neurodegenerative pathology like AD. Additionally recent evidence has shown increased levels of p25, A beta, hyperactivity of Cdk5, phosphorylated tau and neurofilament in human AD brains. This review briefly describes the above-mentioned aspects of involvement of Cdk5 in the pathology of AD and at the end summarizes the advances in Cdk5 as a therapeutic target. (c) 2012 IMSS. Published by Elsevier Inc.
C1 [Shukla, Varsha; Skuntz, Susan; Pant, Harish C.] NINDS, Lab Neurochem, NIH, Bethesda, MD 20892 USA.
RP Pant, HC (reprint author), NIH, Bldg 49,Room 2A35, Bethesda, MD 20892 USA.
EM panth@ninds.nih.gov
NR 96
TC 49
Z9 52
U1 2
U2 19
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0188-4409
J9 ARCH MED RES
JI Arch. Med. Res.
PD NOV
PY 2012
VL 43
IS 8
SI SI
BP 655
EP 662
DI 10.1016/j.arcmed.2012.10.015
PG 8
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 082FP
UT WOS:000314378000009
PM 23142263
ER
PT J
AU Lavine, JS
Rohani, P
AF Lavine, Jennie S.
Rohani, Pejman
TI Resolving pertussis immunity and vaccine effectiveness using incidence
time series
SO EXPERT REVIEW OF VACCINES
LA English
DT Article
DE age-stratified incidence; disease ecology; dynamical signature;
likelihood; mathematical model; reporting efficiency; statistical
inference; time-series data; transmission; whooping cough
ID BORDETELLA-PERTUSSIS; WHOOPING-COUGH; UNITED-STATES; NASOPHARYNGEAL
SAMPLES; CHANGING EPIDEMIOLOGY; SOCIAL CONTACTS; TRANSMISSION; IMPACT;
DYNAMICS; EFFICACY
AB Expert Rev. Vaccines 11(11), 1319-1329 (2012) Resolving the long-term, population-level consequence of vaccine-induced immunity to pertussis is a key challenge for control strategies and vaccine development. Controlled vaccine efficacy studies provide invaluable information; however, they are limited in scope by their sample size and follow-up duration. Long-term time series of incidence data collected by public health institutions provide insight at a broader scale, especially when the data are spatially explicit and age stratified. By using modern ecological and statistical methodolgies, which are reviewed in this paper, new insights into the duration of transmission-blocking immunity and the age-specific patterns of transmission can be gained. Recent advances in computing power and statistical software development will increasingly make these methods available to public health practitioners, vaccine developers and academics alike.
C1 [Lavine, Jennie S.; Rohani, Pejman] Univ Michigan, Dept Ecol & Evolutionary Biol, Ann Arbor, MI 48109 USA.
[Lavine, Jennie S.; Rohani, Pejman] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Rohani, Pejman] Univ Michigan, Ctr Study Complex Syst, Ann Arbor, MI 48109 USA.
RP Lavine, JS (reprint author), Univ Michigan, Dept Ecol & Evolutionary Biol, Ann Arbor, MI 48109 USA.
EM jennie.lavine@gmail.com
FU Research and Policy for Infectious Disease Dynamics program of the
Science and Technology Directorate, Department of Homeland Security;
Fogarty International Center, NIH; Vaccine Modeling Initiative of the
Bill and Melinda Gates Foundation; NIH [1R01AI101155]
FX JS Lavine and P Rohani were supported by the Research and Policy for
Infectious Disease Dynamics program of the Science and Technology
Directorate, Department of Homeland Security, and the Fogarty
International Center, NIH. P Rohani was also supported by the Vaccine
Modeling Initiative of the Bill and Melinda Gates Foundation and by a
grant from the NIH (1R01AI101155). The authors have no other relevant
affiliations or financial involvement with any organization or entity
with a financial interest in or financial conflict with the subject
matter or materials discussed in the manuscript apart from those
disclosed.
NR 63
TC 5
Z9 5
U1 0
U2 4
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1476-0584
J9 EXPERT REV VACCINES
JI Expert Rev. Vaccines
PD NOV
PY 2012
VL 11
IS 11
BP 1319
EP 1329
DI 10.1586/ERV.12.109
PG 11
WC Immunology
SC Immunology
GA 073VJ
UT WOS:000313770900012
PM 23249232
ER
PT J
AU Tadokoro, T
Ramamoorthy, M
Popuri, V
May, A
Tian, JY
Sykora, P
Rybanska, I
Wilson, DM
Croteau, DL
Bohr, VA
AF Tadokoro, Takashi
Ramamoorthy, Mahesh
Popuri, Venkateswarlu
May, Alfred
Tian, Jingyan
Sykora, Peter
Rybanska, Ivana
Wilson, David M., III
Croteau, Deborah L.
Bohr, Vilhelm A.
TI Human RECQL5 participates in the removal of endogenous DNA damage
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID BASE EXCISION-REPAIR; DOUBLE-STRAND BREAKS; RNA-POLYMERASE-II;
ROTHMUND-THOMSON-SYNDROME; WERNER-SYNDROME; SYNDROME PROTEIN; FLAP
ENDONUCLEASE-1; HELICASE ACTIVITY; GENOME STABILITY; REPLICATION FORK
AB Human RECQL5 is a member of the RecQ helicase family, which maintains genome stability via participation in many DNA metabolic processes, including DNA repair. Human cells lacking RECQL5 display chromosomal instability. We find that cells depleted of RECQL5 are sensitive to oxidative stress, accumulate endogenous DNA damage, and increase the cellular poly(ADP-ribosyl)ate response. In contrast to the RECQ helicase family members WRN, BLM, and RECQL4, RECQL5 accumulates at laser-induced single-strand breaks in normal human cells. RECQL5 depletion affects the levels of PARP-1 and XRCC1, and our collective results suggest that RECQL5 modulates and/or directly participates in base excision repair of endogenous DNA damage, thereby promoting chromosome stability in normal human cells.
C1 [Tadokoro, Takashi; Ramamoorthy, Mahesh; Popuri, Venkateswarlu; May, Alfred; Tian, Jingyan; Sykora, Peter; Rybanska, Ivana; Wilson, David M., III; Croteau, Deborah L.; Bohr, Vilhelm A.] NIA, Lab Mol Gerontol, Baltimore, MD 21224 USA.
RP Bohr, VA (reprint author), NIA, Lab Mol Gerontol, Baltimore, MD 21224 USA.
EM vbohr@nih.gov
OI Ramamoorthy, Mahesh/0000-0002-2359-5647
FU National Institutes of Health, National Institute on Aging
FX We thank Tomasz Kulikowicz for the GFP-tagged RECQL5 plasmid. We also
thank Jenq-Lin Yang, Marie Rossi, and Christopher Dunn for technical
assistance. We thank Avik K. Ghosh and Morten Scheibye-Knudsen for
critically reading the manuscript. This research was supported by funds
from the Intramural Research Program of the National Institutes of
Health, National Institute on Aging.
NR 74
TC 14
Z9 16
U1 0
U2 3
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD NOV 1
PY 2012
VL 23
IS 21
BP 4273
EP 4285
DI 10.1091/mbc.E12-02-0110
PG 13
WC Cell Biology
SC Cell Biology
GA 082PN
UT WOS:000314404500020
PM 22973052
ER
PT J
AU Snir, S
Wolf, YI
Koonin, EV
AF Snir, Sagi
Wolf, Yuri I.
Koonin, Eugene V.
TI Universal Pacemaker of Genome Evolution
SO PLOS COMPUTATIONAL BIOLOGY
LA English
DT Article
ID OVERDISPERSED MOLECULAR CLOCK; RATES; TREE; MAMMALS; LIFE; GENES; MODEL;
VARY
AB A fundamental observation of comparative genomics is that the distribution of evolution rates across the complete sets of orthologous genes in pairs of related genomes remains virtually unchanged throughout the evolution of life, from bacteria to mammals. The most straightforward explanation for the conservation of this distribution appears to be that the relative evolution rates of all genes remain nearly constant, or in other words, that evolutionary rates of different genes are strongly correlated within each evolving genome. This correlation could be explained by a model that we denoted Universal PaceMaker (UPM) of genome evolution. The UPM model posits that the rate of evolution changes synchronously across genome-wide sets of genes in all evolving lineages. Alternatively, however, the correlation between the evolutionary rates of genes could be a simple consequence of molecular clock (MC). We sought to differentiate between the MC and UPM models by fitting thousands of phylogenetic trees for bacterial and archaeal genes to supertrees that reflect the dominant trend of vertical descent in the evolution of archaea and bacteria and that were constrained according to the two models. The goodness of fit for the UPM model was better than the fit for the MC model, with overwhelming statistical significance, although similarly to the MC, the UPM is strongly overdispersed. Thus, the results of this analysis reveal a universal, genome-wide pacemaker of evolution that could have been in operation throughout the history of life.
C1 [Snir, Sagi] Univ Haifa Mt Carmel, Dept Evolutionary & Environm Biol, Haifa, Israel.
[Snir, Sagi] Univ Haifa Mt Carmel, Inst Evolut, Haifa, Israel.
[Wolf, Yuri I.; Koonin, Eugene V.] NIH, NLM, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA.
RP Snir, S (reprint author), Univ Haifa Mt Carmel, Dept Evolutionary & Environm Biol, Haifa, Israel.
EM koonin@ncbi.nlm.nih.gov
FU US Department of Health and Human Services (National Library of
Medicine); U.S.-Israel Binational Science Foundation
FX The authors are supported by intramural funds of the US Department of
Health and Human Services (National Library of Medicine) and by a grant
from the U.S.-Israel Binational Science Foundation. The funders had no
role in study design, data collection and analysis, decision to publish,
or preparation of the manuscript.
NR 40
TC 12
Z9 12
U1 0
U2 11
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7358
J9 PLOS COMPUT BIOL
JI PLoS Comput. Biol.
PD NOV
PY 2012
VL 8
IS 11
AR e1002785
DI 10.1371/journal.pcbi.1002785
PG 9
WC Biochemical Research Methods; Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology
GA 048FX
UT WOS:000311897100043
PM 23209393
ER
PT J
AU Tildesley, MJ
Ryan, SJ
AF Tildesley, Michael J.
Ryan, Sadie J.
TI Disease Prevention versus Data Privacy: Using Landcover Maps to Inform
Spatial Epidemic Models
SO PLOS COMPUTATIONAL BIOLOGY
LA English
DT Article
ID MOUTH-DISEASE; VACCINATION STRATEGIES; GREAT-BRITAIN; FOOT; UK;
DYNAMICS; IMPACT; LAND; CONSTRUCTION; TRANSMISSION
AB The availability of epidemiological data in the early stages of an outbreak of an infectious disease is vital for modelers to make accurate predictions regarding the likely spread of disease and preferred intervention strategies. However, in some countries, the necessary demographic data are only available at an aggregate scale. We investigated the ability of models of livestock infectious diseases to predict epidemic spread and obtain optimal control policies in the event of imperfect, aggregated data. Taking a geographic information approach, we used land cover data to predict UK farm locations and investigated the influence of using these synthetic location data sets upon epidemiological predictions in the event of an outbreak of foot-and-mouth disease. When broadly classified land cover data were used to create synthetic farm locations, model predictions deviated significantly from those simulated on true data. However, when more resolved subclass land use data were used, moderate to highly accurate predictions of epidemic size, duration and optimal vaccination and ring culling strategies were obtained. This suggests that a geographic information approach may be useful where individual farm-level data are not available, to allow predictive analyses to be carried out regarding the likely spread of disease. This method can also be used for contingency planning in collaboration with policy makers to determine preferred control strategies in the event of a future outbreak of infectious disease in livestock.
C1 [Tildesley, Michael J.] Univ Warwick, Ctr Complex Sci, Coventry CV4 7AL, W Midlands, England.
[Tildesley, Michael J.] US Natl Inst Hlth, Fogarty Int Ctr, Bethesda, MD USA.
[Ryan, Sadie J.] State Univ New York SUNY ESF, Coll Environm Sci & Forestry, Dept Environm & Forest Biol, Syracuse, NY USA.
RP Tildesley, MJ (reprint author), Univ Warwick, Ctr Complex Sci, Zeeman Bldg, Coventry CV4 7AL, W Midlands, England.
EM M.J.Tildesley@warwick.ac.uk
RI Ryan, Sadie/H-1595-2012;
OI Ryan, Sadie/0000-0002-4308-6321
FU National Science Foundation; U.S. Department of Homeland Security; U.S.
Department of Agriculture through NSF Award [EF-0832858]; University of
Tennessee, Knoxville; RAPIDD program of the Science & Technology
Directorate; Fogarty International Center; National Institutes of
Health; Foreign Animal Disease Modeling program of the Science and
Technology Directorate, Department of Homeland Security [ST-108-000017];
Postdoctoral Associate at the National Center for Ecological Analysis
and Synthesis; NSF [EF-0553768]; University of California, Santa
Barbara; State of California
FX This work was assisted by attendance as a Short-term Visitor at the
National Institute for Mathematical and Biological Synthesis, an
Institute sponsored by the National Science Foundation, the U.S.
Department of Homeland Security and the U.S. Department of Agriculture
through NSF Award #EF-0832858, with additional support from the
University of Tennessee, Knoxville (http://www.nimbios.org). MJT was
supported by the RAPIDD program of the Science & Technology Directorate,
the Fogarty International Center, National Institutes of Health and the
Foreign Animal Disease Modeling program of the Science and Technology
Directorate, Department of Homeland Security (grant ST-108-000017;
http://www.dhs.gov). SJR was supported as a Postdoctoral Associate at
the National Center for Ecological Analysis and Synthesis, a Center
funded by the NSF (Grant #EF-0553768; http://www.nsf.gov), the
University of California, Santa Barbara, and the State of California.
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 2
U2 13
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7358
J9 PLOS COMPUT BIOL
JI PLoS Comput. Biol.
PD NOV
PY 2012
VL 8
IS 11
AR e1002723
DI 10.1371/journal.pcbi.1002723
PG 13
WC Biochemical Research Methods; Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology
GA 048FX
UT WOS:000311897100004
PM 23133352
ER
PT J
AU Bornstein, MH
Cote, LR
Haynes, OM
Suwalsky, JTD
Bakeman, R
AF Bornstein, Marc H.
Cote, Linda R.
Haynes, O. Maurice
Suwalsky, Joan T. D.
Bakeman, Roger
TI Modalities of Infant-Mother Interaction in Japanese, Japanese American
Immigrant, and European American Dyads
SO CHILD DEVELOPMENT
LA English
DT Article
ID UNITED-STATES; MATERNAL RESPONSIVENESS; NATURALISTIC EXCHANGES;
YOUNG-CHILDREN; ATTACHMENT; AMAE; COMPETENCE; ACCULTURATION;
SIMILARITIES; SENSITIVITY
AB Cultural variation in relations and moment-to-moment contingencies of infant-mother person-oriented and object-oriented interactions were compared in 118 Japanese, Japanese American immigrant, and European American dyads with 5.5-month-olds. Infant and mother person-oriented behaviors were related in all cultural groups, but infant and mother object-oriented behaviors were related only among European Americans. Infant and mother behaviors within each modality were mutually contingent in all groups. Culture moderated lead-lag relations: Japanese infants were more likely than their mothers to respond in object-oriented interactions; European American mothers were more likely than their infants to respond in person-oriented interactions. Japanese American dyads behaved like European American dyads. Interactions, infant effects, and parent socialization findings are set in cultural and accultural models of infant-mother transactions.
C1 [Bornstein, Marc H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD 20892 USA.
[Cote, Linda R.] Marymount Univ, Los Angeles, CA USA.
[Bakeman, Roger] Georgia State Univ, Atlanta, GA 30303 USA.
RP Bornstein, MH (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Suite 8030,6705 Rockledge Dr, Bethesda, MD 20892 USA.
EM Marc_H_Bornstein@nih.gov
FU Intramural NIH HHS [Z01 HD001119-20]
NR 114
TC 6
Z9 6
U1 2
U2 20
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0009-3920
J9 CHILD DEV
JI Child Dev.
PD NOV-DEC
PY 2012
VL 83
IS 6
BP 2073
EP 2088
DI 10.1111/j.1467-8624.2012.01822.x
PG 16
WC Psychology, Educational; Psychology, Developmental
SC Psychology
GA 078PP
UT WOS:000314111900017
PM 22860874
ER
PT J
AU Ey, E
Yang, M
Katz, AM
Woldeyohannes, L
Silverman, JL
Leblond, CS
Faure, P
Torquet, N
Le Sourd, AM
Bourgeron, T
Crawley, JN
AF Ey, E.
Yang, M.
Katz, A. M.
Woldeyohannes, L.
Silverman, J. L.
Leblond, C. S.
Faure, P.
Torquet, N.
Le Sourd, A. -M.
Bourgeron, T.
Crawley, J. N.
TI Absence of deficits in social behaviors and ultrasonic vocalizations in
later generations of mice lacking neuroligin4
SO GENES BRAIN AND BEHAVIOR
LA English
DT Article
DE Adult social interaction; autism; juvenile social interaction; mouse
models; neuroligin4; resident-intruder; three-chambered social approach
task; ultrasonic vocalizations
ID AUTISM SPECTRUM DISORDERS; DE-NOVO MUTATIONS; MENTAL-RETARDATION;
TOURETTE-SYNDROME; MOUSE MODEL; NLGN4; PHENOTYPES; GENES; NETWORK
AB Mutations in NLGN4X have been identified in individuals with autism spectrum disorders and other neurodevelopmental disorders. A previous study reported that adult male mice lacking neuroligin4 (Nlgn4) displayed social approach deficits in the three-chambered test, altered aggressive behaviors and reduced ultrasonic vocalizations. To replicate and extend these findings, independent comprehensive analyses of autism-relevant behavioral phenotypes were conducted in later generations of the same line of Nlgn4 mutant mice at the National Institute of Mental Health in Bethesda, MD, USA and at the Institut Pasteur in Paris, France. Adult social approach was normal in all three genotypes of Nlgn4 mice tested at both sites. Reciprocal social interactions in juveniles were similarly normal across genotypes. No genotype differences were detected in ultrasonic vocalizations in pups separated from the nest or in adults during reciprocal social interactions. Anxiety-like behaviors, self-grooming, rotarod and open field exploration did not differ across genotypes, and measures of developmental milestones and general health were normal. Our findings indicate an absence of autism-relevant behavioral phenotypes in subsequent generations of Nlgn4 mice tested at two locations. Testing environment and methods differed from the original study in some aspects, although the presence of normal sociability was seen in all genotypes when methods taken from Jamain et al. (2008) were used. The divergent results obtained from this study indicate that phenotypes may not be replicable across breeding generations, and highlight the significant roles of environmental, generational and/or procedural factors on behavioral phenotypes.
C1 [Ey, E.; Leblond, C. S.; Torquet, N.; Le Sourd, A. -M.; Bourgeron, T.] Inst Pasteur, CNRS, URA Genes Synapses & Cognit 2182, Paris, France.
[Ey, E.; Leblond, C. S.; Torquet, N.; Le Sourd, A. -M.; Bourgeron, T.] Univ Paris Diderot, Sorbonne Paris Cite, Paris, France.
[Yang, M.; Katz, A. M.; Woldeyohannes, L.; Silverman, J. L.; Crawley, J. N.] NIMH, Lab Behav Neurosci, Bethesda, MD 20892 USA.
[Faure, P.] Univ Paris 06, CNRS, UMR 7702, Paris, France.
RP Yang, M (reprint author), Univ Calif Davis, Sch Med, Dept Psychiat & Behav Sci, Room 1001 Res 2 Bldg 96,4625 2nd Ave, Sacramento, CA 95817 USA.
EM mu.yang@ucdmc.udavis.edu
OI Torquet, Nicolas/0000-0001-9032-193X; Bourgeron,
Thomas/0000-0001-8164-9220
FU National Institute of Mental Health; Fondation de France; ANR FLEXNEURIM
[ANR09BLAN034003]; ANR [ANR-08-MNPS-037-01 - SynGen]; Neuron-ERANET
(EUHF-AUTISM); Fondation Orange; Fondation FondaMentale; Fondation
Bettencourt-Schueller
FX We are grateful to Professor Nils Brose at the Max Planck Institute for
generously contributing breeding pairs of the Nlgn4 mice which were used
to generate the mice in this study, and for encouraging our in-depth
analyses of the behavioral consequences of Nlgn4 mutations in mice. We
thank Sandrine Vandormael-Pournin (Genetique Fonctionnelle de la Souris,
Institut Pasteur) for the protocol to detect oestrus status in female
mice. M. Y., A. M. K., L. W., J. L. S. and J. N. C. were supported by
the National Institute of Mental Health Intramural Research Program. E.
E. was supported by Fondation de France, ANR FLEXNEURIM
(ANR09BLAN034003), C. S. L., N. T., A. L. S. and T. B. by ANR
(ANR-08-MNPS-037-01 - SynGen), Neuron-ERANET (EUHF-AUTISM), Fondation
Orange and the Fondation FondaMentale. P. F. was supported by the
Fondation Bettencourt-Schueller.
NR 40
TC 31
Z9 31
U1 0
U2 12
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1601-1848
J9 GENES BRAIN BEHAV
JI Genes Brain Behav.
PD NOV
PY 2012
VL 11
IS 8
BP 928
EP 941
DI 10.1111/j.1601-183X.2012.00849.x
PG 14
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 076YE
UT WOS:000313994300005
PM 22989184
ER
PT J
AU Zhang, DM
Shu, C
Chen, JJ
Sodani, K
Wang, J
Bhatnagar, J
Lan, P
Ruan, ZX
Xiao, ZJ
Ambudkar, SV
Chen, WM
Chen, ZS
Ye, WC
AF Zhang, Dong-Mei
Shu, Chang
Chen, Jun-Jiang
Sodani, Kamlesh
Wang, Jiao
Bhatnagar, Jaya
Lan, Ping
Ruan, Zhi-Xiong
Xiao, Zhi-Jie
Ambudkar, Suresh V.
Chen, Wei-Min
Chen, Zhe-Sheng
Ye, Wen-Cai
TI BBA, a Derivative of 23-Hydroxybetulinic Acid, Potently Reverses
ABCB1-Mediated Drug Resistance in Vitro and in Vivo
SO MOLECULAR PHARMACEUTICS
LA English
DT Article
DE BBA; multidrug resistance; ABCB1; ABCG2
ID MEDIATED MULTIDRUG-RESISTANCE; HEPATOCELLULAR-CARCINOMA CELLS; HUMAN
P-GLYCOPROTEIN; CANCER-CELLS; VINCRISTINE RESISTANCE; ANTICANCER DRUGS;
BINDING; TRANSPORTERS; GENE; CYTOTOXICITY
AB 23-O-(1,4'-Bipiperidine-1-carbonyl)betulinic acid (BBA), a synthetic derivative of 23-hydroxybetulinic acid (23-HBA), shows a reversal effect on multidrug resistance (MDR) in our preliminary screening. Overexpression of ATP-binding cassette (ABC) transporters such as ABCB1, ABCG2, and ABCC1 has been reported in recent studies to be a major factor contributing to MDR. Our study results showed that BBA enhanced the cytotoxicity of ABCB1 substrates and increased the accumulation of doxorubicin or rhodamine 123 in ABCB1 overexpressing cells, but had no effect on non ABCB1 substrate, such as cisplatin; what's more, BBA slightly reversed ABCG2-mediated resistance to SN-38, but did not affect the ABCC1-mediated MDR Further studies on the mechanism indicated that BBA did not alter the expression of ABCB1 at mRNA or protein levels, but affected the ABCB1 ATPase activity by stimulating the basal activity at lower concentrations and inhibiting the activity at higher concentrations. In addition, BBA inhibited the verapamil-stimulated ABCB1 ATPase activity and the photolabeling of ABCB1 with [I-125] iodoarylazidoprazosin in a concentration-dependent manner, indicating that BBA directly interacts with ABCB1. The docking study confirmed this notion that BBA could bind to the drug binding site(s) on ABCB1, but its binding position was only partially overlapping with that of verapamil or iodoarylazidoprazosin. Importantly, BBA increased the inhibitory effect of paclitaxel in ABCB1 overexpressing KB-C2 cell xenografts in nude mice. Taken together, our findings suggest that BBA can reverse ABCB1-mediated MDR by inhibiting its efflux function of ABCB1, which supports the development of BBA as a novel potential MDR reversal agent used in the clinic.
C1 [Zhang, Dong-Mei; Shu, Chang; Wang, Jiao; Lan, Ping; Ruan, Zhi-Xiong; Chen, Wei-Min; Ye, Wen-Cai] Jinan Univ, Coll Pharm, Guangzhou 510632, Guangdong, Peoples R China.
[Chen, Jun-Jiang; Sodani, Kamlesh; Ruan, Zhi-Xiong; Chen, Zhe-Sheng] St Johns Univ, Coll Pharm & Hlth Sci, Dept Pharmaceut Sci, Queens, NY USA.
[Bhatnagar, Jaya; Ambudkar, Suresh V.] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Ye, WC (reprint author), Jinan Univ, Coll Pharm, Guangzhou 510632, Guangdong, Peoples R China.
EM chenz@stjohns.edu; chywc@yahoo.com.cn
FU Technology Program of China [2009ZX09103-313, 2012ZX09103101-053];
Guangzhou City [2009A1-E011-1, 2010U1-E00531-9, 2011J2200045]; National
Science Foundation of China [30901847, 90913020]; NIH R15
[1R15CA143701]; Program for Changjiang Scholars and Innovative Research
Team in University [IRT0965]; Intramural Research Program, Center for
Cancer Research, National Cancer Institute, NIH
FX Special thanks to Prof. Kwok-Pui Fung (The Chinese University of Hong
Kong, Hong Kong) for HepG2/ADM cells, Prof. Li-Wu Fu (Sun Yat-Sen
University, China) for MCF-7/ADR cells, Prof. Michael M. Gottesman
(National Cancer Institute, NIH, USA) for KB-3-1 cells, Dr. Shin-ichi
Akiyama (Kagoshima University, Japan) for KB-C2, KB-CV60 cells, Dr.
Kazumitsu Ueda (Kyoto University, Japan) for KB-MRP1 cells, and Drs.
Susan E. Bates and Robert W. Robey (National Cancer Institute, NIH, USA)
for HEK293, ABCB1, ABCG2, and ABCC1 transfected cells. This work was
supported by Science and Technology Program of China (2009ZX09103-313
and 2012ZX09103101-053) and Guangzhou City (2009A1-E011-1,
2010U1-E00531-9, and 2011J2200045), National Science Foundation of China
(No. 30901847 and 90913020), NIH R15 (No. 1R15CA143701), and Program for
Changjiang Scholars and Innovative Research Team in University
(IRT0965). J.B. and S.V.A. were supported by the Intramural Research
Program, Center for Cancer Research, National Cancer Institute, NIH.
NR 54
TC 27
Z9 29
U1 1
U2 22
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1543-8384
J9 MOL PHARMACEUT
JI Mol. Pharm.
PD NOV
PY 2012
VL 9
IS 11
BP 3147
EP 3159
DI 10.1021/mp300249s
PG 13
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 073US
UT WOS:000313769200017
PM 23046348
ER
PT J
AU Choi, EY
Bahrami, H
Wu, CO
Greenland, P
Cushman, M
Daniels, LB
Almeida, ALC
Yoneyama, K
Opdahl, A
Jain, A
Criqui, MH
Siscovick, D
Darwin, C
Maisel, A
Bluemke, DA
Lima, JAC
AF Choi, Eui-Young
Bahrami, Hossein
Wu, Colin O.
Greenland, Philip
Cushman, Mary
Daniels, Lori B.
Almeida, Andre L. C.
Yoneyama, Kihei
Opdahl, Anders
Jain, Aditya
Criqui, Michael H.
Siscovick, David
Darwin, Christine
Maisel, Alan
Bluemke, David A.
Lima, Joao A. C.
TI N-terminal Pro-B-Type Natriuretic Peptide, Left Ventricular Mass, and
Incident Heart Failure Multi-Ethnic Study of Atherosclerosis
SO CIRCULATION-HEART FAILURE
LA English
DT Article
DE N-terminal pro-B-type natriuretic peptide; heart failure; left
ventricular mass
ID CARDIOVASCULAR EVENTS; OLDER-ADULTS; DEATH; POLYMORPHISM; ASSOCIATION;
MORTALITY; RISK; GENE
AB Background-Elevated N-terminal pro-B-type natriuretic peptide (NT-proBNP) is associated with clinically overt heart failure (HF). However, whether it provides additive prognostic information for incident HF beyond traditional risk factors and left ventricular (LV) mass index among multi-ethnic asymptomatic individuals has not yet been determined. We studied the associations of plasma NT-proBNP and magnetic resonance imaging defined LV mass index with incident HF in an asymptomatic multi-ethnic population.
Methods and Results-A total of 5597 multi-ethnic participants without clinically apparent cardiovascular disease underwent baseline measurement of NT-proBNP and were followed for 5.5 +/- 1.1 years. Among them, 4163 also underwent baseline cardiac magnetic resonance imaging. During follow-up, 111 participants experienced incident HF. Higher NT-proBNP was significantly associated with incident HF, independent of baseline age, sex, ethnicity, systolic blood pressure, diabetes mellitus, smoking, estimated glomerular filtration rate, medications (anti-hypertensive and statin), LV mass index, and interim myocardial infarction (hazard ratio: 1.95 per 1U log NT-proBNP increment, 95% CI 1.54-2.46, P<0.001). This relationship held among different ethnic groups, non-Hispanic whites, African-Americans, and Hispanics. Most importantly, NT-proBNP provided additive prognostic value beyond both traditional risk factors and LV mass index for predicting incident HF (integrated discrimination index=0.046, P<0.001; net reclassification index; 6-year risk probability categorized by <3%, 3-10%, >10% =0.175, P=0.019; category-less net reclassification index=0.561, P<0.001).
Conclusions-Plasma NT-proBNP provides incremental prognostic information beyond traditional risk factors and the magnetic resonance imaging-determined LV mass index for incident symptomatic HF in an asymptomatic multi-ethnic population.
C1 [Choi, Eui-Young; Yoneyama, Kihei; Opdahl, Anders; Jain, Aditya; Lima, Joao A. C.] Johns Hopkins Univ, Baltimore, MD USA.
[Choi, Eui-Young] Yonsei Univ, Coll Med, Seoul, South Korea.
[Bahrami, Hossein] Yale Univ, New Haven, CT USA.
[Wu, Colin O.] NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
[Greenland, Philip] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Cushman, Mary] Univ Vermont, Dept Med, Burlington, VT USA.
[Daniels, Lori B.; Criqui, Michael H.; Maisel, Alan] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Siscovick, David] Univ Washington, Dept Med & Epidemiol, Seattle, WA 98195 USA.
[Darwin, Christine] Univ Calif Los Angeles, Res Ctr, Los Angeles, CA USA.
[Bluemke, David A.] Natl Inst Biomed Imaging & Bioengn, NIH, Ctr Clin, Bethesda, MD USA.
RP Lima, JAC (reprint author), Johns Hopkins Univ Hosp, 600 N Wolfe St,Blalock 524D1, Baltimore, MD 21287 USA.
EM jlima@jhmi.edu
RI Opdahl, Anders/E-2958-2010; Opdahl, Anders/I-7580-2015
OI Opdahl, Anders/0000-0002-0599-592X; Opdahl, Anders/0000-0002-0599-592X
FU National Heart, Lung, and Blood Institute [R01-HL66075-01]; Multi-Ethnic
Study of Atherosclerosis [N01-HC-95162, N01-HC-95168, N01-HC-95169];
Roche Diagnostics
FX This study was supported by the National Heart, Lung, and Blood
Institute grant (R01-HL66075-01), the Multi-Ethnic Study of
Atherosclerosis study contracts (N01-HC-95162, N01-HC-95168, and
N01-HC-95169), and Roche Diagnostics.
NR 25
TC 25
Z9 28
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-3289
J9 CIRC-HEART FAIL
JI Circ.-Heart Fail.
PD NOV
PY 2012
VL 5
IS 6
BP 727
EP 734
DI 10.1161/CIRCHEARTFAILURE.112.968701
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 071GZ
UT WOS:000313580100019
PM 23032197
ER
PT J
AU Honorio, J
Tomasi, D
Goldstein, RZ
Leung, HC
Samaras, D
AF Honorio, Jean
Tomasi, Dardo
Goldstein, Rita Z.
Leung, Hoi-Chung
Samaras, Dimitris
TI Can a Single Brain Region Predict a Disorder?
SO IEEE TRANSACTIONS ON MEDICAL IMAGING
LA English
DT Article
DE Brain; functional magnetic resonance imaging (fMRI); pattern recognition
and classification
ID CLASSIFICATION
AB We perform prediction of diverse disorders (cocaine use, schizophrenia and Alzheimer's disease) in unseen subjects from brain functional magnetic resonance imaging. First, we show that for multisubject prediction of simple cognitive states (e.g., motor versus calculation and reading), voxels-as-features methods produce clusters that are similar for different leave-one-subject-out folds; while for group classification (e.g., cocaine addicted versus control subjects), voxels are scattered and less stable. Therefore, we chose to use a single region per experimental condition and a majority vote classifier. Interestingly, our method outperforms state-of-the-art techniques. Our method can integrate multiple experimental conditions and successfully predict disorders in unseen subjects (leave-one-subject-out generalization accuracy: 89.3% and 90.9% for cocaine use, 96.4% for schizophrenia and 81.5% for Alzheimer's disease). Our experimental results not only span diverse disorders, but also different experimental designs (block design and event related tasks), facilities, magnetic fields (1.5T, 3T, 4T) and speed of acquisition (interscan interval from 1600 to 3500 ms). We further argue that our method produces a meaningful low-dimensional representation that retains discriminability.
C1 [Honorio, Jean; Samaras, Dimitris] SUNY Stony Brook, Dept Comp Sci, Stony Brook, NY 11794 USA.
[Tomasi, Dardo] NIAAA, Bethesda, MD 20892 USA.
[Goldstein, Rita Z.] Brookhaven Natl Lab, Dept Med, Upton, NY 11973 USA.
[Leung, Hoi-Chung] SUNY Stony Brook, Dept Psychol, Stony Brook, NY 11794 USA.
RP Honorio, J (reprint author), SUNY Stony Brook, Dept Comp Sci, Stony Brook, NY 11794 USA.
EM jhonorio@cs.sunysb.edu; tomasi@bnl.gov; rgoldstein@bnl.gov;
hleung@ms.cc.sunysb.edu; samaras@cs.sunysb.edu
RI Tomasi, Dardo/J-2127-2015
FU National Institute on Drug Abuse (NIDA) [1 R01 DA020949, R21 DA02062, 1
R01 DA023579]; National Institute of Biomedical Imaging and
Bioengineering (NIBIB) [1 R01 EB007530]; National Center for Research
Resources at NIH; [U24-RR021992]
FX This work was supported in part by the National Institute on Drug Abuse
(NIDA) under Grant 1 R01 DA020949, Grant R21 DA02062, and Grant 1 R01
DA023579 and in part by the National Institute of Biomedical Imaging and
Bioengineering (NIBIB) under Grant 1 R01 EB007530.; The authors would
like to thank P. Pinel and B. Thirion for providing them with the Fast
Acquisition dataset. The schizophrenia dataset was downloaded from the
Function BIRN Data Repository, supported by grants to the Function BIRN
(U24-RR021992). Testbed funded by the National Center for Research
Resources at NIH.
NR 45
TC 10
Z9 10
U1 0
U2 8
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 0278-0062
EI 1558-254X
J9 IEEE T MED IMAGING
JI IEEE Trans. Med. Imaging
PD NOV
PY 2012
VL 31
IS 11
BP 2062
EP 2072
DI 10.1109/TMI.2012.2206047
PG 11
WC Computer Science, Interdisciplinary Applications; Engineering,
Biomedical; Engineering, Electrical & Electronic; Imaging Science &
Photographic Technology; Radiology, Nuclear Medicine & Medical Imaging
SC Computer Science; Engineering; Imaging Science & Photographic
Technology; Radiology, Nuclear Medicine & Medical Imaging
GA 072RH
UT WOS:000313689400006
PM 22752119
ER
PT J
AU Altshuler, DM
Durbin, RM
Abecasis, GR
Bentley, DR
Chakravarti, A
Clark, AG
Donnelly, P
Eichler, EE
Flicek, P
Gabriel, SB
Gibbs, RA
Green, ED
Hurles, ME
Knoppers, BM
Korbel, JO
Lander, ES
Lee, C
Lehrach, H
Mardis, ER
Marth, GT
McVean, GA
Nickerson, DA
Schmidt, JP
Sherry, ST
Wang, J
Wilson, RK
Gibbs, RA
Dinh, H
Kovar, C
Lee, S
Lewis, L
Muzny, D
Reid, J
Wang, M
Wang, J
Fang, XD
Guo, XS
Jian, M
Jiang, H
Jin, X
Li, GQ
Li, JX
Li, YR
Li, Z
Liu, X
Lu, Y
Ma, XD
Su, Z
Tai, SS
Tang, MF
Wang, B
Wang, GB
Wu, HL
Wu, RH
Yin, Y
Zhang, WW
Zhao, J
Zhao, MR
Zheng, XL
Zhou, Y
Lander, ES
Altshuler, DM
Gabriel, SB
Gupta, N
Flicek, P
Clarke, L
Leinonen, R
Smith, RE
Zheng-Bradley, X
Bentley, DR
Grocock, R
Humphray, S
James, T
Kingsbury, Z
Lehrach, H
Sudbrak, R
Albrecht, MW
Amstislavskiy, VS
Borodina, TA
Lienhard, M
Mertes, F
Sultan, M
Timmermann, B
Yaspo, ML
Sherry, ST
McVean, GA
Mardis, ER
Wilson, RK
Fulton, L
Fulton, R
Weinstock, GM
Durbin, RM
Balasubramaniam, S
Burton, J
Danecek, P
Keane, TM
Kolb-Kokocinski, A
McCarthy, S
Stalker, J
Quail, M
Schmidt, JP
Davies, CJ
Gollub, J
Webster, T
Wong, B
Zhan, YP
Auton, A
Gibbs, RA
Yu, F
Bainbridge, M
Challis, D
Evani, US
Lu, J
Muzny, D
Nagaswamy, U
Reid, J
Sabo, A
Wang, Y
Yu, J
Wang, J
Coin, LJM
Fang, L
Guo, XS
Jin, X
Li, GQ
Li, QB
Li, YR
Li, ZY
Lin, HX
Liu, BH
Luo, RB
Qin, N
Shao, HJ
Wang, BQ
Xie, YL
Ye, C
Yu, C
Zhang, F
Zheng, HC
Zhu, HM
Marth, GT
Garrison, EP
Kural, D
Lee, WP
Leong, WF
Ward, AN
Wu, JT
Zhang, MY
Lee, C
Griffin, L
Hsieh, CH
Mills, RE
Shi, XH
von Grotthuss, M
Zhang, CS
Daly, MJ
DePristo, MA
Altshuler, DM
Banks, E
Bhatia, G
Carneiro, MO
del Angel, G
Gabriel, SB
Genovese, G
Gupta, N
Handsaker, RE
Hartl, C
Lander, ES
McCarroll, SA
Nemesh, JC
Poplin, RE
Schaffner, SF
Shakir, K
Yoon, SC
Lihm, J
Makarov, V
Jin, HJ
Kim, W
Kim, KC
Korbel, JO
Rausch, T
Flicek, P
Beal, K
Clarke, L
Cunningham, F
Herrero, J
McLaren, WM
Ritchie, GRS
Smith, RE
Zheng-Bradley, X
Clark, AG
Gottipati, S
Keinan, A
Rodriguez-Flores, JL
Sabeti, PC
Grossman, SR
Tabrizi, S
Tariyal, R
Cooper, DN
Ball, EV
Stenson, PD
Bentley, DR
Barnes, B
Bauer, M
Cheetham, RK
Cox, T
Eberle, M
Humphray, S
Kahn, S
Murray, L
Peden, J
Shaw, R
Ye, K
Batzer, MA
Konkel, MK
Walker, JA
MacArthur, DG
Lek, M
Sudbrak, R
Amstislavskiy, VS
Herwig, R
Shriver, MD
Bustamante, CD
Byrnes, JK
De la Vega, FM
Gravel, S
Kenny, EE
Kidd, JM
Lacroute, P
Maples, BK
Moreno-Estrada, A
Zakharia, F
Halperin, E
Baran, Y
Craig, DW
Christoforides, A
Homer, N
Izatt, T
Kurdoglu, AA
Sinari, SA
Squire, K
Sherry, ST
Xiao, CL
Sebat, J
Bafna, V
Ye, K
Burchard, EG
Hernandez, RD
Gignoux, CR
Haussler, D
Katzman, SJ
Kent, WJ
Howie, B
Ruiz-Linares, A
Dermitzakis, ET
Lappalainen, T
Devine, SE
Liu, XY
Maroo, A
Tallon, LJ
Rosenfeld, JA
Michelson, LP
Abecasis, GR
Kang, HM
Anderson, P
Angius, A
Bigham, A
Blackwell, T
Busonero, F
Cucca, F
Fuchsberger, C
Jones, C
Jun, G
Li, Y
Lyons, R
Maschio, A
Porcu, E
Reinier, F
Sanna, S
Schlessinger, D
Sidore, C
Tan, A
Trost, MK
Awadalla, P
Hodgkinson, A
Lunter, G
McVean, GA
Marchini, JL
Myers, S
Churchhouse, C
Delaneau, O
Gupta-Hinch, A
Iqbal, Z
Mathieson, I
Rimmer, A
Xifara, DK
Oleksyk, TK
Fu, YX
Liu, XM
Xiong, MM
Jorde, L
Witherspoon, D
Xing, JC
Eichler, EE
Browning, BL
Alkan, C
Hajirasouliha, I
Hormozdiari, F
Ko, A
Sudmant, PH
Mardis, ER
Chen, K
Chinwalla, A
Ding, L
Dooling, D
Koboldt, DC
McLellan, MD
Wallis, JW
Wendl, MC
Zhang, QY
Durbin, RM
Hurles, ME
Tyler-Smith, C
Albers, CA
Ayub, Q
Balasubramaniam, S
Chen, Y
Coffey, AJ
Colonna, V
Danecek, P
Huang, N
Jostins, L
Keane, TM
Li, H
McCarthy, S
Scally, A
Stalker, J
Walter, K
Xue, YL
Zhang, YJ
Gerstein, MB
Abyzov, A
Balasubramanian, S
Chen, JM
Clarke, D
Fu, Y
Habegger, L
Harmanci, AO
Jin, MK
Khurana, E
Mu, XJ
Sisu, C
Li, YR
Luo, RB
Zhu, HM
Lee, C
Griffin, L
Hsieh, CH
Mills, RE
Shi, XH
von Grotthuss, M
Zhang, CS
Marth, GT
Garrison, EP
Kural, D
Lee, WP
Ward, AN
Wu, JT
Zhang, MY
McCarroll, SA
Altshuler, DM
Banks, E
del Angel, G
Genovese, G
Handsaker, RE
Hartl, C
Nemesh, JC
Shakir, K
Yoon, SC
Lihm, J
Makarov, V
Degenhardt, J
Flicek, P
Clarke, L
Smith, RE
Zheng-Bradley, X
Korbel, JO
Rausch, T
Stutz, AM
Bentley, DR
Barnes, B
Cheetham, RK
Eberle, M
Humphray, S
Kahn, S
Murray, L
Shaw, R
Ye, K
Batzer, MA
Konkel, MK
Walker, JA
Lacroute, P
Craig, DW
Homer, N
Church, D
Xiao, CL
Sebat, J
Bafna, V
Michaelson, JJ
Ye, K
Devine, SE
Liu, XY
Maroo, A
Tallon, LJ
Lunter, G
McVean, GA
Iqbal, Z
Witherspoon, D
Xing, JC
Eichler, EE
Alkan, C
Hajirasouliha, I
Hormozdiari, F
Ko, A
Sudmant, PH
Chen, K
Chinwalla, A
Ding, L
McLellan, MD
Wallis, JW
Hurles, ME
Ben Blackburne
Li, H
Lindsay, SJ
Ning, ZM
Scally, A
Walter, K
Zhang, YJ
Gerstein, MB
Abyzov, A
Chen, JM
Clarke, D
Khurana, E
Mu, XJ
Sisu, C
Gibbs, RA
Yu, FL
Bainbridge, M
Challis, D
Evani, US
Kovar, C
Lewis, L
Lu, J
Muzny, D
Nagaswamy, U
Reid, J
Sabo, A
Yu, J
Guo, XS
Li, YR
Wu, RH
Marth, GT
Garrison, EP
Leong, WF
Ward, AN
del Angel, G
DePristo, MA
Gabriel, SB
Gupta, N
Hartl, C
Poplin, RE
Clark, AG
Rodriguez-Flores, JL
Flicek, P
Clarke, L
Smith, RE
Zheng-Bradley, X
MacArthur, DG
Bustamante, CD
Gravel, S
Craig, DW
Christoforides, A
Homer, N
Izatt, T
Sherry, ST
Xiao, CL
Dermitzakis, ET
Abecasis, GR
Kang, HM
McVean, GA
Mardis, ER
Dooling, D
Fulton, L
Fulton, R
Koboldt, DC
Durbin, RM
Balasubramaniam, S
Keane, TM
McCarthy, S
Stalker, J
Gerstein, MB
Balasubramanian, S
Habegger, L
Garrison, EP
Gibbs, RA
Bainbridge, M
Muzny, D
Yu, FL
Yu, J
del Angel, G
Handsaker, RE
Makarov, V
Rodriguez-Flores, JL
Jin, HJ
Kim, W
Kim, KC
Flicek, P
Beal, K
Clarke, L
Cunningham, F
Herrero, J
McLaren, WM
Ritchie, GRS
Zheng-Bradley, X
Tabrizi, S
MacArthur, DG
Lek, M
Bustamante, CD
De la Vega, FM
Craig, DW
Kurdoglu, AA
Lappalainen, T
Rosenfeld, JA
Michelson, LP
Awadalla, P
Hodgkinson, A
McVean, GA
Chen, K
Tyler-Smith, C
Chen, Y
Colonna, V
Frankish, A
Harrow, J
Xue, YL
Gerstein, MB
Abyzov, A
Balasubramanian, S
Chen, JM
Clarke, D
Fu, Y
Harmanci, AO
Jin, MK
Khurana, E
Mu, XJ
Sisu, C
Gibbs, RA
Fowler, G
Hale, W
Kalra, D
Kovar, C
Muzny, D
Reid, J
Wang, J
Guo, X
Li, G
Li, Y
Zheng, X
Altshuler, DM
Flicek, P
Clarke, L
Barker, J
Kelman, G
Kulesha, E
Leinonen, R
McLaren, WM
Radhakrishnan, R
Roa, A
Smirnov, D
Smith, RE
Streeter, I
Toneva, I
Vaughan, B
Zheng-Bradley, X
Bentley, DR
Cox, T
Humphray, S
Kahn, S
Sudbrak, R
Albrecht, MW
Lienhard, M
Craig, DW
Izatt, T
Kurdoglu, AA
Sherry, ST
Ananiev, V
Belaia, Z
Beloslyudtsev, D
Bouk, N
Chen, C
Church, D
Cohen, R
Cook, C
Garner, J
Hefferon, T
Kimelman, M
Liu, C
Lopez, J
Meric, P
O'Sullivan, C
Ostapchuk, Y
Phan, L
Ponomarov, S
Schneider, V
Shekhtman, E
Sirotkin, K
Slotta, D
Xiao, CL
Zhang, H
Haussler, D
Abecasis, GR
McVean, GA
Alkan, C
Ko, A
Dooling, D
Durbin, RM
Balasubramaniam, S
Keane, TM
McCarthy, S
Stalker, J
Chakravarti, A
Knoppers, BM
Abecasis, GR
Barnes, KC
Beiswanger, C
Burchard, EG
Bustamante, CD
Cai, HY
Cao, HZ
Durbin, RM
Gharani, N
Gibbs, RA
Gignoux, CR
Gravel, S
Henn, B
Jones, D
Jorde, L
Kaye, JS
Keinan, A
Kent, A
Kerasidou, A
Li, YR
Mathias, R
McVean, GA
Moreno-Estrada, A
Ossorio, PN
Parker, M
Reich, D
Rotimi, CN
Royal, CD
Sandoval, K
Su, YY
Sudbrak, R
Tian, ZM
Timmermann, B
Tishkoff, S
Toji, LH
Tyler-Smith, C
Via, M
Wang, YH
Yang, HM
Yang, L
Zhu, JY
Bodmer, W
Bedoya, G
Ruiz-Linares, A
Ming, CZ
Yang, G
You, CJ
Peltonen, L
Garcia-Montero, A
Orfao, A
Dutil, J
Martinez-Cruzado, JC
Oleksyk, TK
Brooks, LD
Felsenfeld, AL
McEwen, JE
Clemm, NC
Duncanson, A
Dunn, M
Green, ED
Guyer, MS
Peterson, JL
Abecasis, GR
Auton, A
Brooks, LD
DePristo, MA
Durbin, RM
Handsaker, RE
Kang, HM
Marth, GT
McVean, GA
AF Altshuler, David M.
Durbin, Richard M.
Abecasis, Goncalo R.
Bentley, David R.
Chakravarti, Aravinda
Clark, Andrew G.
Donnelly, Peter
Eichler, Evan E.
Flicek, Paul
Gabriel, Stacey B.
Gibbs, Richard A.
Green, Eric D.
Hurles, Matthew E.
Knoppers, Bartha M.
Korbel, Jan O.
Lander, Eric S.
Lee, Charles
Lehrach, Hans
Mardis, Elaine R.
Marth, Gabor T.
McVean, Gil A.
Nickerson, Deborah A.
Schmidt, Jeanette P.
Sherry, Stephen T.
Wang, Jun
Wilson, Richard K.
Gibbs, Richard A.
Dinh, Huyen
Kovar, Christie
Lee, Sandra
Lewis, Lora
Muzny, Donna
Reid, Jeff
Wang, Min
Wang, Jun
Fang, Xiaodong
Guo, Xiaosen
Jian, Min
Jiang, Hui
Jin, Xin
Li, Guoqing
Li, Jingxiang
Li, Yingrui
Li, Zhuo
Liu, Xiao
Lu, Yao
Ma, Xuedi
Su, Zhe
Tai, Shuaishuai
Tang, Meifang
Wang, Bo
Wang, Guangbiao
Wu, Honglong
Wu, Renhua
Yin, Ye
Zhang, Wenwei
Zhao, Jiao
Zhao, Meiru
Zheng, Xiaole
Zhou, Yan
Lander, Eric S.
Altshuler, David M.
Gabriel, Stacey B.
Gupta, Namrata
Flicek, Paul
Clarke, Laura
Leinonen, Rasko
Smith, Richard E.
Zheng-Bradley, Xiangqun
Bentley, David R.
Grocock, Russell
Humphray, Sean
James, Terena
Kingsbury, Zoya
Lehrach, Hans
Sudbrak, Ralf
Albrecht, Marcus W.
Amstislavskiy, Vyacheslav S.
Borodina, Tatiana A.
Lienhard, Matthias
Mertes, Florian
Sultan, Marc
Timmermann, Bernd
Yaspo, Marie-Laure
Sherry, Stephen T.
McVean, Gil A.
Mardis, Elaine R.
Wilson, Richard K.
Fulton, Lucinda
Fulton, Robert
Weinstock, George M.
Durbin, Richard M.
Balasubramaniam, Senduran
Burton, John
Danecek, Petr
Keane, Thomas M.
Kolb-Kokocinski, Anja
McCarthy, Shane
Stalker, James
Quail, Michael
Schmidt, Jeanette P.
Davies, Christopher J.
Gollub, Jeremy
Webster, Teresa
Wong, Brant
Zhan, Yiping
Auton, Adam
Gibbs, Richard A.
Yu, Fuli
Bainbridge, Matthew
Challis, Danny
Evani, Uday S.
Lu, James
Muzny, Donna
Nagaswamy, Uma
Reid, Jeff
Sabo, Aniko
Wang, Yi
Yu, Jin
Wang, Jun
Coin, Lachlan J. M.
Fang, Lin
Guo, Xiaosen
Jin, Xin
Li, Guoqing
Li, Qibin
Li, Yingrui
Li, Zhenyu
Lin, Haoxiang
Liu, Binghang
Luo, Ruibang
Qin, Nan
Shao, Haojing
Wang, Bingqiang
Xie, Yinlong
Ye, Chen
Yu, Chang
Zhang, Fan
Zheng, Hancheng
Zhu, Hongmei
Marth, Gabor T.
Garrison, Erik P.
Kural, Deniz
Lee, Wan-Ping
Leong, Wen Fung
Ward, Alistair N.
Wu, Jiantao
Zhang, Mengyao
Lee, Charles
Griffin, Lauren
Hsieh, Chih-Heng
Mills, Ryan E.
Shi, Xinghua
von Grotthuss, Marcin
Zhang, Chengsheng
Daly, Mark J.
DePristo, Mark A.
Altshuler, David M.
Banks, Eric
Bhatia, Gaurav
Carneiro, Mauricio O.
del Angel, Guillermo
Gabriel, Stacey B.
Genovese, Giulio
Gupta, Namrata
Handsaker, Robert E.
Hartl, Chris
Lander, Eric S.
McCarroll, Steven A.
Nemesh, James C.
Poplin, Ryan E.
Schaffner, Stephen F.
Shakir, Khalid
Yoon, Seungtai C.
Lihm, Jayon
Makarov, Vladimir
Jin, Hanjun
Kim, Wook
Kim, Ki Cheol
Korbel, Jan O.
Rausch, Tobias
Flicek, Paul
Beal, Kathryn
Clarke, Laura
Cunningham, Fiona
Herrero, Javier
McLaren, William M.
Ritchie, Graham R. S.
Smith, Richard E.
Zheng-Bradley, Xiangqun
Clark, Andrew G.
Gottipati, Srikanth
Keinan, Alon
Rodriguez-Flores, Juan L.
Sabeti, Pardis C.
Grossman, Sharon R.
Tabrizi, Shervin
Tariyal, Ridhi
Cooper, David N.
Ball, Edward V.
Stenson, Peter D.
Bentley, David R.
Barnes, Bret
Bauer, Markus
Cheetham, R. Keira
Cox, Tony
Eberle, Michael
Humphray, Sean
Kahn, Scott
Murray, Lisa
Peden, John
Shaw, Richard
Ye, Kai
Batzer, Mark A.
Konkel, Miriam K.
Walker, Jerilyn A.
MacArthur, Daniel G.
Lek, Monkol
Sudbrak, Ralf
Amstislavskiy, Vyacheslav S.
Herwig, Ralf
Shriver, Mark D.
Bustamante, Carlos D.
Byrnes, Jake K.
De la Vega, Francisco M.
Gravel, Simon
Kenny, Eimear E.
Kidd, Jeffrey M.
Lacroute, Phil
Maples, Brian K.
Moreno-Estrada, Andres
Zakharia, Fouad
Halperin, Eran
Baran, Yael
Craig, David W.
Christoforides, Alexis
Homer, Nils
Izatt, Tyler
Kurdoglu, Ahmet A.
Sinari, Shripad A.
Squire, Kevin
Sherry, Stephen T.
Xiao, Chunlin
Sebat, Jonathan
Bafna, Vineet
Ye, Kenny
Burchard, Esteban G.
Hernandez, Ryan D.
Gignoux, Christopher R.
Haussler, David
Katzman, Sol J.
Kent, W. James
Howie, Bryan
Ruiz-Linares, Andres
Dermitzakis, Emmanouil T.
Lappalainen, Tuuli
Devine, Scott E.
Liu, Xinyue
Maroo, Ankit
Tallon, Luke J.
Rosenfeld, Jeffrey A.
Michelson, Leslie P.
Abecasis, Goncalo R.
Kang, Hyun Min
Anderson, Paul
Angius, Andrea
Bigham, Abigail
Blackwell, Tom
Busonero, Fabio
Cucca, Francesco
Fuchsberger, Christian
Jones, Chris
Jun, Goo
Li, Yun
Lyons, Robert
Maschio, Andrea
Porcu, Eleonora
Reinier, Fred
Sanna, Serena
Schlessinger, David
Sidore, Carlo
Tan, Adrian
Trost, Mary Kate
Awadalla, Philip
Hodgkinson, Alan
Lunter, Gerton
McVean, Gil A.
Marchini, Jonathan L.
Myers, Simon
Churchhouse, Claire
Delaneau, Olivier
Gupta-Hinch, Anjali
Iqbal, Zamin
Mathieson, Iain
Rimmer, Andy
Xifara, Dionysia K.
Oleksyk, Taras K.
Fu, Yunxin
Liu, Xiaoming
Xiong, Momiao
Jorde, Lynn
Witherspoon, David
Xing, Jinchuan
Eichler, Evan E.
Browning, Brian L.
Alkan, Can
Hajirasouliha, Iman
Hormozdiari, Fereydoun
Ko, Arthur
Sudmant, Peter H.
Mardis, Elaine R.
Chen, Ken
Chinwalla, Asif
Ding, Li
Dooling, David
Koboldt, Daniel C.
McLellan, Michael D.
Wallis, John W.
Wendl, Michael C.
Zhang, Qunyuan
Durbin, Richard M.
Hurles, Matthew E.
Tyler-Smith, Chris
Albers, Cornelis A.
Ayub, Qasim
Balasubramaniam, Senduran
Chen, Yuan
Coffey, Alison J.
Colonna, Vincenza
Danecek, Petr
Huang, Ni
Jostins, Luke
Keane, Thomas M.
Li, Heng
McCarthy, Shane
Scally, Aylwyn
Stalker, James
Walter, Klaudia
Xue, Yali
Zhang, Yujun
Gerstein, Mark B.
Abyzov, Alexej
Balasubramanian, Suganthi
Chen, Jieming
Clarke, Declan
Fu, Yao
Habegger, Lukas
Harmanci, Arif O.
Jin, Mike
Khurana, Ekta
Mu, Xinmeng Jasmine
Sisu, Cristina
Li, Yingrui
Luo, Ruibang
Zhu, Hongmei
Lee, Charles
Griffin, Lauren
Hsieh, Chih-Heng
Mills, Ryan E.
Shi, Xinghua
von Grotthuss, Marcin
Zhang, Chengsheng
Marth, Gabor T.
Garrison, Erik P.
Kural, Deniz
Lee, Wan-Ping
Ward, Alistair N.
Wu, Jiantao
Zhang, Mengyao
McCarroll, Steven A.
Altshuler, David M.
Banks, Eric
del Angel, Guillermo
Genovese, Giulio
Handsaker, Robert E.
Hartl, Chris
Nemesh, James C.
Shakir, Khalid
Yoon, Seungtai C.
Lihm, Jayon
Makarov, Vladimir
Degenhardt, Jeremiah
Flicek, Paul
Clarke, Laura
Smith, Richard E.
Zheng-Bradley, Xiangqun
Korbel, Jan O.
Rausch, Tobias
Stuetz, Adrian M.
Bentley, David R.
Barnes, Bret
Cheetham, R. Keira
Eberle, Michael
Humphray, Sean
Kahn, Scott
Murray, Lisa
Shaw, Richard
Ye, Kai
Batzer, Mark A.
Konkel, Miriam K.
Walker, Jerilyn A.
Lacroute, Phil
Craig, David W.
Homer, Nils
Church, Deanna
Xiao, Chunlin
Sebat, Jonathan
Bafna, Vineet
Michaelson, Jacob J.
Ye, Kenny
Devine, Scott E.
Liu, Xinyue
Maroo, Ankit
Tallon, Luke J.
Lunter, Gerton
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Oleksyk, Taras K.
Brooks, Lisa D.
Felsenfeld, Adam L.
McEwen, Jean E.
Clemm, Nicholas C.
Duncanson, Audrey
Dunn, Michael
Green, Eric D.
Guyer, Mark S.
Peterson, Jane L.
Abecasis, Goncalo R.
Auton, Adam
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DePristo, Mark A.
Durbin, Richard M.
Handsaker, Robert E.
Kang, Hyun Min
Marth, Gabor T.
McVean, Gil A.
CA 1000 Genomes Project Consortium
TI An integrated map of genetic variation from 1,092 human genomes
SO NATURE
LA English
DT Article
ID COPY NUMBER VARIATION; POPULATION-SCALE; WIDE ASSOCIATION; CODING
VARIATION; RARE; VARIANTS; DISEASE; LOCI; DISCOVERY; HISTORY
AB By characterizing the geographic and functional spectrum of human genetic variation, the 1000 Genomes Project aims to build a resource to help to understand the genetic contribution to disease. Here we describe the genomes of 1,092 individuals from 14 populations, constructed using a combination of low-coverage whole-genome and exome sequencing. By developing methods to integrate information across several algorithms and diverse data sources, we provide a validated haplotype map of 38 million single nucleotide polymorphisms, 1.4 million short insertions and deletions, and more than 14,000 larger deletions. We show that individuals from different populations carry different profiles of rare and common variants, and that low-frequency variants show substantial geographic differentiation, which is further increased by the action of purifying selection. We show that evolutionary conservation and coding consequence are key determinants of the strength of purifying selection, that rare-variant load varies substantially across biological pathways, and that each individual contains hundreds of rare non-coding variants at conserved sites, such as motif-disrupting changes in transcription-factor-binding sites. This resource, which captures up to 98% of accessible single nucleotide polymorphisms at a frequency of 1% in related populations, enables analysis of common and low-frequency variants in individuals from diverse, including admixed, populations.
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Ekta/C-4933-2013; Weinstock, George/C-6314-2013; Ning,
Zemin/D-2411-2013; Li, Heng/D-9344-2011; Abecasis, Goncalo/B-7840-2010;
Liu, Xiaoming/C-2743-2008; Xing, Jinchuan/A-2489-2012; Korbel,
Jan/G-6470-2012; Wang, Jun/B-9503-2016; Coin, Lachlan/A-9001-2014; Mu,
Xinmeng/P-2562-2016; Mills, Ryan/A-1979-2011; Shao, Haojing/C-5429-2017;
Jun, Goo/F-1941-2017; Colonna, Vincenza/H-2021-2014;
OI Via, Marc/0000-0002-9966-9921; Albers, Kees/0000-0003-4115-3727; Myers,
Simon/0000-0002-2585-9626; Angius, Andrea/0000-0003-2596-6461; Wang,
Jun/0000-0002-8540-8931; Jun, Goo/0000-0003-0891-0204; Taras,
Oleksyk/0000-0002-8148-3918; Browning, Brian/0000-0001-6454-6633;
Altshuler, David/0000-0002-7250-4107; Alkan, Can/0000-0002-5443-0706;
Weinstock, George/0000-0002-2997-4592; Li, Heng/0000-0003-4874-2874;
Liu, Xiaoming/0000-0001-8285-5528; Korbel, Jan/0000-0002-2798-3794;
Sudmant, Peter/0000-0002-9573-8248; Kidd, Jeffrey/0000-0002-9631-1465;
Sidore, Carlo/0000-0001-7504-7477; Rodriguez-Flores, Juan
L/0000-0002-0394-8062; Wang, Jun/0000-0002-2113-5874; Yu,
Jin/0000-0002-2990-6602; sanna, serena/0000-0002-3768-1749; liu,
bh/0000-0002-4948-2835; Ritchie, Graham/0000-0002-6456-9736; McVean,
Gil/0000-0002-5012-4162; Durbin, Richard/0000-0002-9130-1006; Zheng
Bradley, Xiangqun/0000-0002-9324-2708; Fuchsberger,
Christian/0000-0002-5918-8947; Sebat, Jonathan/0000-0002-9087-526X;
Lindsay, Sarah/0000-0002-0965-3070; Leinonen, Rasko/0000-0002-2639-7187;
Lunter, Gerton/0000-0002-3798-2058; Chen, Jieming/0000-0003-3767-9486;
Abyzov, Alexej/0000-0001-5405-6729; Bodmer, Walter/0000-0001-6244-9792;
Coin, Lachlan/0000-0002-4300-455X; Mu, Xinmeng/0000-0002-8079-0828;
Mills, Ryan/0000-0003-3425-6998; Shao, Haojing/0000-0002-8806-197X; Jun,
Goo/0000-0003-0891-0204; Streeter, Ian/0000-0003-4024-3552; Stuetz,
Adrian/0000-0001-7650-3470; Angius, Andrea/0000-0001-9372-1162; Kulesha,
Eugene/0000-0002-4285-6232; Radhakrishnan, Rajesh/0000-0001-7170-699X;
Sisu, Cristina/0000-0001-9371-0797; Vaughan,
Brendan/0000-0002-2199-1267; Cooper, David N./0000-0002-8943-8484;
Flicek, Paul/0000-0002-3897-7955; McLaren, William/0000-0001-6218-1116;
Walter, Klaudia/0000-0003-4448-0301; McCarthy,
Shane/0000-0002-2715-4187; Iqbal, Zamin/0000-0001-8466-7547; Keane,
Thomas/0000-0001-7532-6898; Rausch, Tobias/0000-0001-5773-5620;
Lappalainen, Tuuli/0000-0002-7746-8109; Abecasis,
Goncalo/0000-0003-1509-1825; Ayub, Qasim/0000-0003-3291-0917; Ning,
Zemin/0000-0003-4359-776X; Colonna, Vincenza/0000-0002-3966-0474;
Herrero, Javier/0000-0001-7313-717X; Clarke, Laura/0000-0002-5989-6898;
Kim, Kicheol/0000-0003-3667-9900
FU Wellcome Trust [WT098051, WT090532/Z/09/Z, WT085475/Z/08/Z,
WT095552/Z/11/Z, WT086084/Z/08/Z, WT089250/Z/09/Z, WT085532AIA]; Medical
Research Council [G0900747(91070)]; British Heart Foundation
[RG/09/12/28096]; National Basic Research Program of China (973 program)
[2011CB809201, 2011CB809202, 2011CB809203]; Chinese 863 program
[2012AA02A201]; National Natural Science Foundation of China [30890032,
31161130357]; Shenzhen Key Laboratory of Transomics Biotechnologies
[CXB201108250096A]; Shenzhen Municipal Government of China
[ZYC200903240080A, ZYC201105170397A]; Guangdong Innovative Research Team
Program [2009010016]; BMBF [01GS08201, 0315428A]; Max Planck Society;
Swiss National Science Foundation [31003A_130342]; Swiss National
Science Foundation NCCR 'Frontiers in Genetics' grant; Louis Jeantet
Foundation; Biotechnology and Biological Sciences Research Council
(BBSRC) [BB/I021213/1]; German Research Foundation [KO 4037/1-1];
Netherlands Organization for Scientific Research VENI [639.021.125];
Beatriu de Pinos Program [2006BP-A 10144, 2009BP-B 00274]; Israeli
Science Foundation [04514831]; Genome Quebec and the Ministry of
Economic Development, Innovation and Trade [PSR-SIIRI-195]; National
Institutes of Health (NIH) [UO1HG5214, RC2HG5581, RO1MH84698, R01HG4719,
R01HG3698, RC2HG5552, UO1HG6513, R01HG4960, R01HG5701, U01HG5715,
T32GM8283, U01HG5208, U01HG6569, R01HG2898, R01CA166661, UO1HG5209,
UO1HG5725, P41HG4221, P01HG4120, U01HG5728]; BAA-NIAID-DAIT-NIHAI
[2009061, T32GM7748, U54HG3079, UL1RR024131, HHSN268201100040C]
FX We thank many people who contributed to this project: A. Naranjo, M. V.
Parra and C. Duque for help with the collection of the Colombian
samples; N. Kalin and F. Laplace for discussions; A. Schlattl and T.
Zichner for assistance in managing data sets; E. Appelbaum, H. Arbery,
E. Birney, S. Bumpstead, J. Camarata, J. Carey, G. Cochrane, M. DaSilva,
S. Dokel, E. Drury, C. Duque, K. Gyaltsen, P. Jokinen, B. Lenz, S.
Lewis, D. Lu, A. Naranjo, S. Ott, I. Padioleau, M. V. Parra, N.
Patterson, A. Price, L. Sadzewicz, S. Schrinner, N. Sengamalay, J.
Sullivan, F. Ta, Y. Vaydylevich, O. Venn, K. Watkins and A. Yurovsky for
assistance, discussion and advice. We thank the people who generously
contributed their samples, from these populations: Yoruba in Ibadan,
Nigeria; the Han Chinese in Beijing, China; the Japanese in Tokyo,
Japan; the Utah CEPH community; the Luhya in Webuye, Kenya; people with
African ancestry in the Southwest United States; the Toscani in Italia;
people with Mexican ancestry in Los Angeles, California; the Southern
Han Chinese in China; the British in England and Scotland; the Finnish
in Finland; the Iberian Populations in Spain; the Colombians in
Medellin, Colombia; and the Puerto Ricans in Puerto Rico. This research
was supported in part by Wellcome Trust grants WT098051 to R. M. D., M.
E. H. and C. T. S.; WT090532/Z/09/Z, WT085475/Z/08/Z and WT095552/Z/11/Z
to P. Do.; WT086084/Z/08/Z and WT090532/Z/09/Z to G. A. M.;
WT089250/Z/09/Z to I. M.; WT085532AIA to P. F.; Medical Research Council
grant G0900747(91070) to G. A. M.; British Heart Foundation grant
RG/09/12/28096 to C. A. A.; the National Basic Research Program of China
(973 program no. 2011CB809201, 2011CB809202 and 2011CB809203); the
Chinese 863 program (2012AA02A201); the National Natural Science
Foundation of China (30890032, 31161130357); the Shenzhen Key Laboratory
of Transomics Biotechnologies (CXB201108250096A); the Shenzhen Municipal
Government of China (grants ZYC200903240080A and ZYC201105170397A);
Guangdong Innovative Research Team Program (no. 2009010016); BMBF grant
01GS08201 to H. Le.; BMBF grant 0315428A to R. H.; the Max Planck
Society; Swiss National Science Foundation 31003A_130342 to E. T. D.;
Swiss National Science Foundation NCCR 'Frontiers in Genetics' grant to
E. T. D.; Louis Jeantet Foundation grant to E. T. D.; Biotechnology and
Biological Sciences Research Council (BBSRC) grant BB/I021213/1 to A.
R.-L.; German Research Foundation (Emmy Noether Fellowship KO 4037/1-1)
to J. O. K.; Netherlands Organization for Scientific Research VENI grant
639.021.125 to K. Y.; Beatriu de Pinos Program grants 2006BP-A 10144 and
2009BP-B 00274 to M. V.; Israeli Science Foundation grant 04514831 to E.
H.; Genome Quebec and the Ministry of Economic Development, Innovation
and Trade grant PSR-SIIRI-195 to P.Aw.; National Institutes of Health
(NIH) grants UO1HG5214, RC2HG5581 and RO1MH84698 to G. R. A.; R01HG4719
and R01HG3698 to G. T. M; RC2HG5552 and UO1HG6513 to G. R. A. and G. T.
M.; R01HG4960 and R01HG5701 to B. L. B.; U01HG5715 to C. D. B. and A. G.
C.; T32GM8283 to D. Cl.; U01HG5208 to M. J. D.; U01HG6569 to M. A. D.;
R01HG2898 and R01CA166661 to S. E. D.; UO1HG5209, UO1HG5725 and
P41HG4221 to C. Le.; P01HG4120 to E. E. E.; U01HG5728 to Yu.F.;
U54HG3273 and U01HG5211 to R.A.G.; R01HL95045 to S. B. G.; U41HG4568 to
S.J.K.; P41HG2371 to W.J.K.; ES015794, AI077439, HL088133 and HL078885
to E. G. B.; RC2HL102925 to S. B. G. and D. M. A.; R01GM59290 to L.B.J.
and M. A. B.; U54HG3067 to E. S. L. and S. B. G.; T15LM7033 to B. K. M.;
T32HL94284 to J.L.R.-F.; ; DP2OD6514 and BAA-NIAID-DAIT-NIHAI 2009061 to
P. C. S.; T32GM7748 to X. S.; U54HG3079 to R. K. W.; UL1RR024131 to R.
D. H.; HHSN268201100040C to the Coriell Institute for Medical Research;
a Sandler Foundation award and an American Asthma Foundation award to E.
G. B.; an IBMOpen Collaborative Research Program award to Y.B.; an A.G.
Leventis Foundation scholarship to D. K. X.; a Wolfson Royal Society
Merit Award to P. Do.; a Howard Hughes Medical Institute International
Fellowship award to P. H. S.; a grant from T. and V. Stanley to S.C.Y.;
and a Mary Beryl Patch Turnbull Scholar Program award to K. C. B. E. H.
is a faculty fellow of the Edmond J. Safra Bioinformatics program at
Tel-Aviv University. E. E. E. and D. H. are investigators of the Howard
Hughes Medical Institute. M. V. G. is a long-term fellow of EMBO.
NR 47
TC 3036
Z9 3066
U1 71
U2 570
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 1
PY 2012
VL 491
IS 7422
BP 56
EP 65
DI 10.1038/nature11632
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 028PM
UT WOS:000310434500030
ER
PT J
AU Mudd, PA
Martins, MA
Ericsen, AJ
Tully, DC
Power, KA
Bean, AT
Piaskowski, SM
Duan, LJ
Seese, A
Gladden, AD
Weisgrau, KL
Furlott, JR
Kim, YI
de Santana, MGV
Rakasz, E
Capuano, S
Wilson, NA
Bonaldo, MC
Galler, R
Allison, DB
Piatak, M
Haase, AT
Lifson, JD
Allen, TM
Watkins, DI
AF Mudd, Philip A.
Martins, Mauricio A.
Ericsen, Adam J.
Tully, Damien C.
Power, Karen A.
Bean, Alex T.
Piaskowski, Shari M.
Duan, Lijie
Seese, Aaron
Gladden, Adrianne D.
Weisgrau, Kim L.
Furlott, Jessica R.
Kim, Young-il
Veloso de Santana, Marlon G.
Rakasz, Eva
Capuano, Saverio, III
Wilson, Nancy A.
Bonaldo, Myrna C.
Galler, Ricardo
Allison, David B.
Piatak, Michael, Jr.
Haase, Ashley T.
Lifson, Jeffrey D.
Allen, Todd M.
Watkins, David I.
TI Vaccine-induced CD8(+) T cells control AIDS virus replication
SO NATURE
LA English
DT Article
ID MAMU-B-ASTERISK-08-POSITIVE MACAQUES; RHESUS MACAQUES; IMMUNODEFICIENCY;
SIV; RESPONSES; HIV; DETERMINANTS; CHALLENGE; DISEASE; ESCAPE
AB Developing a vaccine for human immunodeficiency virus(HIV) may be aided by a complete understanding of those rare cases in which some HIV-infected individuals control replication of the virus(1-3). Most of these elite controllers express the histocompatibility alleles HLA-B*57 or HLA-B*27 (ref. 3). These alleles remain by far the most robust associations with low concentrations of plasma virus(4,5), yet the mechanism of control in these individuals is not entirely clear. Here we vaccinate Indian rhesus macaques that express Mamu-B*08, an animal model for HLA-B*27-mediated elite control(6), with three Mamu-B*08-restricted CD8(+) T-cell epitopes, and demonstrate that these vaccinated animals control replication of the highly pathogenic clonal simian immunodeficiency virus (SIV) mac239 virus. High frequencies of CD8(+) T cells against these Vif and Nef epitopes in the blood, lymph nodes and colon were associated with viral control. Moreover, the frequency of the CD8(+) T-cell response against the Nef RL10 epitope (Nef amino acids 137-146) correlated significantly with reduced acute phase viraemia. Finally, two of the eight vaccinees lost control of viral replication in the chronic phase, concomitant with escape in all three targeted epitopes, further implicating these three CD8(+) T-cell responses in the control of viral replication. Our findings indicate that narrowly targeted vaccine-induced virus-specific CD8(+) T-cell responses can control replication of the AIDS virus.
C1 [Martins, Mauricio A.; Watkins, David I.] Univ Miami, Miller Sch Med, Dept Pathol, Miami, FL 33136 USA.
[Mudd, Philip A.; Ericsen, Adam J.; Bean, Alex T.; Piaskowski, Shari M.; Weisgrau, Kim L.; Furlott, Jessica R.; Wilson, Nancy A.] Univ Wisconsin Madison, Dept Pathol & Lab Med, Madison, WI 53711 USA.
[Mudd, Philip A.] Univ Wisconsin Madison, Med Scientist Training Program, Madison, WI 53705 USA.
[Tully, Damien C.; Power, Karen A.; Seese, Aaron; Gladden, Adrianne D.; Allen, Todd M.] Ragon Inst MGH MIT & Harvard, Boston, MA 02129 USA.
[Duan, Lijie; Haase, Ashley T.] Univ Minnesota, Dept Microbiol, Minneapolis, MN 55455 USA.
[Kim, Young-il] Univ Alabama Birmingham, Dept Med, Div Prevent Med, Birmingham, AL 35294 USA.
[Veloso de Santana, Marlon G.; Bonaldo, Myrna C.] Fiocruz MS, Inst Oswaldo Cruz, Lab Biol Mol Flavivirus, BR-21045900 Rio De Janeiro, Brazil.
[Rakasz, Eva; Capuano, Saverio, III; Wilson, Nancy A.] Univ Wisconsin Madison, Wisconsin Natl Primate Res Ctr, Madison, WI 53711 USA.
[Galler, Ricardo] Fundacao Oswaldo Cruz, Inst Tecnol Imunobiol, Rio De Janeiro, Brazil.
[Allison, David B.] Univ Alabama Birmingham, Dept Biostat, Sect Stat Genet, Birmingham, AL 35294 USA.
[Piatak, Michael, Jr.; Lifson, Jeffrey D.] NCI, AIDS & Canc Virus Program, SAIC Frederick Inc, Frederick, MD 21702 USA.
RP Watkins, DI (reprint author), Univ Miami, Miller Sch Med, Dept Pathol, Miami, FL 33136 USA.
EM dwatkins@med.miami.edu
RI Bonaldo, Myrna/D-9494-2013; Vacinas, Inct/J-9431-2013; Galler,
Ricardo/B-3280-2014; Allen, Todd/F-5473-2011;
OI Martins, Mauricio/0000-0001-8336-216X; Allison,
David/0000-0003-3566-9399; Ericsen, Adam/0000-0003-4176-8270
FU National Institutes of Health (NIH) [R37 AI052056, RO1 AI076114,
RR015371, HHSN261200800001E]; FAPERJ; INCTV; CNPq; MCT; FIOCRUZ
FX We would like to thank M. Stevenson, M. Reynolds, N. Maness and J. Sacha
for discussions and suggestions. We also thank D. Evans, L. Heyer and Z.
R. Bergman for facilitating the experiments. This work was funded in
part by National Institutes of Health (NIH) grants R37 AI052056, RO1
AI076114, RR015371, contract number HHSN261200800001E and FAPERJ, INCTV,
CNPq, MCT and FIOCRUZ.
NR 24
TC 89
Z9 92
U1 2
U2 30
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 1
PY 2012
VL 491
IS 7422
BP 129
EP U152
DI 10.1038/nature11443
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 028PM
UT WOS:000310434500044
PM 23023123
ER
PT J
AU Egli, M
Koob, GF
Edwards, S
AF Egli, Mark
Koob, George F.
Edwards, Scott
TI Alcohol dependence as a chronic pain disorder
SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
LA English
DT Review
DE Alcohol dependence; Chronic pain; Nociception; Negative affect; Stress;
Anxiety; Allostasis
ID CORTICOTROPIN-RELEASING-FACTOR; CATECHOL-O-METHYLTRANSFERASE; ANTERIOR
CINGULATE CORTEX; RECEPTOR GENE POLYMORPHISM; CENTRAL AMYGDALA NEURONS;
SIGNAL-REGULATED KINASE; SUBSTANCE USE DISORDERS; CONDITIONED PLACE
PREFERENCE; OPIOID-INDUCED HYPERALGESIA; VENTRAL TEGMENTAL AREA
AB Dysregulation of pain neurocircuitry and neurochemistry has been increasingly recognized as playing a critical role in a diverse spectrum of diseases including migraine, fibromyalgia, depression, and PTSD. Evidence presented here supports the hypothesis that alcohol dependence is among the pathologies arising from aberrant neurobiological substrates of pain. In this review, we explore the possible influence of alcohol analgesia and hyperalgesia in promoting alcohol misuse and dependence. We examine evidence that neuroanatomical sites involved in the negative emotional states of alcohol dependence also play an important role in pain transmission and may be functionally altered under chronic pain conditions. We also consider possible genetic links between pain transmission and alcohol dependence. We propose an allostatic load model in which episodes of alcohol intoxication and withdrawal, traumatic stressors, and injury are each capable of dysregulating an overlapping set of neural substrates to engender sensory and affective pain states that are integral to alcohol dependence and comorbid conditions such as anxiety, depression, and chronic pain. Published by Elsevier Ltd.
C1 [Egli, Mark] NIAAA, Div Neurosci & Behav, NIH, DHHS, Bethesda, MD 20892 USA.
[Koob, George F.; Edwards, Scott] Scripps Res Inst, Comm Neurobiol Addict Disorders, La Jolla, CA 92037 USA.
RP Egli, M (reprint author), NIAAA, Div Neurosci & Behav, NIH, DHHS, 5635 Fishers Lane,Room 2059,MSC 9304, Bethesda, MD 20892 USA.
EM megli@mail.nih.gov
RI koob, george/P-8791-2016
FU National Institute on Alcohol Abuse and Alcoholism [AA008459, AA012602,
AA006420, AA007456, AA020608]; National Research Service Award
[AA018250]; Pearson Center for Alcoholism and Addiction Research at The
Scripps Research Institute
FX Preparation of this review was partially supported by funds from the
National Institute on Alcohol Abuse and Alcoholism (AA008459, AA012602,
AA006420, AA007456, and AA020608, GFK), a National Research Service
Award (AA018250, SE), and by the Pearson Center for Alcoholism and
Addiction Research at The Scripps Research Institute. We also thank
Janet Hightower and Mike Arends for graphic and editorial assistance.
This is article number 21689 from The Scripps Research Institute. The
authors declare no conflicts of interest.
NR 220
TC 51
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U1 2
U2 30
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0149-7634
J9 NEUROSCI BIOBEHAV R
JI Neurosci. Biobehav. Rev.
PD NOV
PY 2012
VL 36
IS 10
BP 2179
EP 2192
DI 10.1016/j.neubiorev.2012.07.010
PG 14
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 071SC
UT WOS:000313613500001
PM 22975446
ER
PT J
AU Nechuta, S
Shu, XO
Li, HL
Yang, G
Ji, BT
Xiang, YB
Cai, H
Chow, WH
Gao, YT
Zheng, W
AF Nechuta, Sarah
Shu, Xiao-Ou
Li, Hong-Lan
Yang, Gong
Ji, Bu-Tian
Xiang, Yong-Bing
Cai, Hui
Chow, Wong-Ho
Gao, Yu-Tang
Zheng, Wei
TI Prospective cohort study of tea consumption and risk of digestive system
cancers: results from the Shanghai Women's Health Study
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID GREEN TEA; PANCREATIC-CANCER; BLACK TEA; CIGARETTE-SMOKING; COFFEE;
CARCINOGENESIS; INHIBITION; PREVENTION; METAANALYSIS; POLYPHENOLS
AB Background: Data from in vitro and animal studies support a protective role for tea in the etiology of digestive system cancers; however, results from prospective cohort studies have been inconsistent. In addition, to our knowledge, no study has investigated the association of tea consumption with the incidence of all digestive system cancers in Chinese women.
Objective: We investigated the association of regular tea intake (>= 3 times/wk for > 6 mo) with risk of digestive system cancers.
Design: We used the Shanghai Women's Health Study, a population-based prospective cohort study of middle-aged and older Chinese women who were recruited in 1996-2000. Adjusted HRs and associated 95% CIs were derived from Cox regression models.
Results: After a mean follow-up of 11 y, 1255 digestive system cancers occurred (stomach, esophagus, colorectal, liver, pancreas, and gallbladder/bile duct cancers) in 69,310 nonsmoking and non-alcohol-drinking women. In comparison with women who never drank tea, regular tea intake (mostly green tea) was associated with reduced risk of all digestive system cancers combined (HR: 0.86; 95% CI: 0.74, 0.98), and the reduction in risk increased as the amount and years of tea consumption increased (P-trend = 0.01 and P-trend < 0.01, respectively). For example, women who consumed >= 150 g tea/mo (similar to 2-3 cups/d) had a 21% reduced risk of digestive system cancers combined (HR: 0.79; 95% CI: 0.63, 0.99). The inverse association was found primarily for colorectal and stomach/esophageal cancers.
Conclusion: In this large prospective cohort study, tea consumption was associated with reduced risk of colorectal and stomach/esophageal cancers in Chinese women. Am J Clin Nutr 2012;96:1056-63.
C1 [Zheng, Wei] Vanderbilt Univ, Sch Med, Vanderbilt Epidemiol Ctr, Div Epidemiol,Dept Med, Nashville, TN 37203 USA.
[Li, Hong-Lan; Xiang, Yong-Bing; Gao, Yu-Tang] Shanghai Canc Inst, Dept Epidemiol, Shanghai, Peoples R China.
[Ji, Bu-Tian; Chow, Wong-Ho] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
RP Zheng, W (reprint author), Vanderbilt Univ, Sch Med, Vanderbilt Epidemiol Ctr, Div Epidemiol,Dept Med, 8th Floor,Suite 800,2525 W End Ave, Nashville, TN 37203 USA.
EM wei.zheng@vanderbilt.edu
FU National Cancer Institute [R37 CA70867]
FX Supported by the National Cancer Institute (grant number R37 CA70867).
NR 45
TC 24
Z9 27
U1 3
U2 29
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD NOV
PY 2012
VL 96
IS 5
BP 1056
EP 1063
DI 10.3945/ajcn.111.031419
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 062UX
UT WOS:000312949600015
PM 23053557
ER
PT J
AU SanGiovanni, JP
Neuringer, M
AF SanGiovanni, John Paul
Neuringer, Martha
TI The putative role of lutein and zeaxanthin as protective agents against
age-related macular degeneration: promise of molecular genetics for
guiding mechanistic and translational research in the field
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article; Proceedings Paper
CT Conference on New Developments in Carotenoids Research
CY MAR 11-12, 2011
CL Tufts Univ, Jean Mayer USDA Human Nutr Res Ctr Aging, Boston, MA
SP DSM Nutrit Prod, Natl Inst Hlth, Off Dietary Supplements, Int Union Biochem & Mol Biol, Soc Free Rad Res Int
HO Tufts Univ, Jean Mayer USDA Human Nutr Res Ctr Aging
ID PIGMENT OPTICAL-DENSITY; SERUM CAROTENOID CONCENTRATIONS; OUTER-SEGMENT
MEMBRANES; APOLIPOPROTEIN-E GENE; S-TRANSFERASE M1; GROWTH IN-VITRO;
HUMAN RETINA; BETA-CAROTENE; SCAVENGER RECEPTOR; PRIMATE RETINAS
AB Age-related macular degeneration (AMD) is the primary cause of vision loss in elderly people of western European ancestry. Genetic, dietary, and environmental factors affect tissue concentrations of macular xanthophylls (MXs) within retinal cell types manifesting AMD pathology. In this article we review the history and state of science on the putative role of the MXs (lutein, zeaxanthin, and meso-zeaxanthin) in AMD and report findings on AMD-associated genes encoding enzymes, transporters, ligands, and receptors affecting or affected by MXs. We then use this context to discuss emerging research opportunities that offer promise for meaningful investigation and inference in the field. Am J Clin Nutr 2012;96(suppl):1223S-33S.
C1 [SanGiovanni, John Paul] NEI, Clin Trials Branch, Bethesda, MD 20892 USA.
[Neuringer, Martha] Oregon Hlth & Sci Univ, Oregon Natl Primate Res Ctr, Beaverton, OR USA.
[Neuringer, Martha] Oregon Hlth & Sci Univ, Casey Eye Inst, Beaverton, OR USA.
RP SanGiovanni, JP (reprint author), NEI, Clin Trials Branch, Bethesda, MD 20892 USA.
EM jpsangio@post.harvard.edu
FU NEI NIH HHS [EY021214]; NIH HHS [OD011092]
NR 184
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Z9 24
U1 0
U2 24
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
EI 1938-3207
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD NOV
PY 2012
VL 96
IS 5
BP 1223S
EP 1233S
DI 10.3945/ajcn.112.038240
PG 11
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 062UX
UT WOS:000312949600040
PM 23053548
ER
PT J
AU Staudt, LM
AF Staudt, L. M.
TI Therapeutic strategies in lymphoma based on oncogenic B receptor
signaling
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Meeting Abstract
CT 4th International Symposium on Childhood, Adolescent and Young Adult
Non-Hodgkins Lymphoma
CY NOV 01-03, 2012
CL New York, NY
C1 [Staudt, L. M.] NCI, Metab Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD NOV
PY 2012
VL 159
SU 1
SI SI
MA 2
BP 1
EP 1
PG 1
WC Hematology
SC Hematology
GA 061ZV
UT WOS:000312889800003
ER
PT J
AU Dunleavy, K
AF Dunleavy, K.
TI Diagnosis and treatment of PMBL and gray zone lymphoma in AYA patients
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Meeting Abstract
CT 4th International Symposium on Childhood, Adolescent and Young Adult
Non-Hodgkins Lymphoma
CY NOV 01-03, 2012
CL New York, NY
C1 [Dunleavy, K.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD NOV
PY 2012
VL 159
SU 1
SI SI
MA 33
BP 19
EP 19
PG 1
WC Hematology
SC Hematology
GA 061ZV
UT WOS:000312889800034
ER
PT J
AU Howard, SC
Widemann, B
Chauhan, N
Daughtery, C
King, TR
Rush, JE
AF Howard, S. C.
Widemann, B.
Chauhan, N.
Daughtery, C.
King, T. R.
Rush, J. E.
TI Pediatric clinical trial and compassionate use experience with
glucarpidase for methotrexate toxicity
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Meeting Abstract
CT 4th International Symposium on Childhood, Adolescent and Young Adult
Non-Hodgkins Lymphoma
CY NOV 01-03, 2012
CL New York, NY
C1 [Howard, S. C.] St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
[Widemann, B.] NCI, Bethesda, MD 20892 USA.
[Chauhan, N.] BTG Int, London, England.
[Daughtery, C.] BTG Int, Salt Lake City, UT USA.
[King, T. R.; Rush, J. E.] BTG Int, Philadelphia, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD NOV
PY 2012
VL 159
SU 1
SI SI
MA 115
BP 59
EP 59
PG 1
WC Hematology
SC Hematology
GA 061ZV
UT WOS:000312889800116
ER
PT J
AU Santos-Modesitt, W
Yaffe, K
Byers, AL
Simonsick, EM
Satterfield, S
Cauley, JA
Harris, TB
Barnes, DE
AF Santos-Modesitt, W.
Yaffe, K.
Byers, A. L.
Simonsick, E. M.
Satterfield, S.
Cauley, J. A.
Harris, T. B.
Barnes, D. E.
TI BRAIN-DERIVED NEUROTROPHIC FACTOR AND DEPRESSIVE SYMPTOMS IN THE HEALTH
ABC STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Santos-Modesitt, W.; Yaffe, K.; Byers, A. L.; Barnes, D. E.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Santos-Modesitt, W.; Yaffe, K.; Byers, A. L.; Barnes, D. E.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Simonsick, E. M.; Harris, T. B.] NIA, NIH, Bethesda, MD 20892 USA.
[Satterfield, S.] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA.
[Cauley, J. A.] 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 2012
VL 52
SU 1
BP 97
EP 97
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888201445
ER
PT J
AU Martin, KR
Cooper, R
Harris, TB
Guralnik, JM
Hardy, R
Kuh, D
AF Martin, K. R.
Cooper, R.
Harris, T. B.
Guralnik, J. M.
Hardy, R.
Kuh, D.
TI PATTERNS OF LEISURE-TIME PHYSICAL ACTIVITY IN A BRITISH BIRTH COHORT AT
EARLY OLD AGE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Martin, K. R.; Harris, T. B.; Guralnik, J. M.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Martin, K. R.; Cooper, R.; Hardy, R.; Kuh, D.] UCL, MRC, Unit Lifelong Hlth & Ageing, London, England.
[Guralnik, J. M.] Univ Maryland, Baltimore, MD 21201 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 2012
VL 52
SU 1
BP 195
EP 195
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202054
ER
PT J
AU Li, L
Simonsick, EM
Ferrucci, L
Lin, FR
AF Li, L.
Simonsick, E. M.
Ferrucci, L.
Lin, F. R.
TI HEARING LOSS AND GAIT SPEED AMONG OLDER ADULTS IN THE UNITED STATES
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Li, L.; Lin, F. R.] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Li, L.; Lin, F. R.] Johns Hopkins Sch Med, Baltimore, MD USA.
[Simonsick, E. M.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
[Lin, F. R.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
NR 0
TC 1
Z9 1
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 2012
VL 52
SU 1
BP 201
EP 202
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202082
ER
PT J
AU Wu, S
Hirsch, C
Durbin-Johnson, B
Buzkova, P
Patel, K
Xia, J
AF Wu, S.
Hirsch, C.
Durbin-Johnson, B.
Buzkova, P.
Patel, K.
Xia, J.
TI ASSOCIATION OF SUBCLINICAL CEREBROVASCULAR DISEASE WITH RATE OF DECLINE
IN GAIT PERFORMANCE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Wu, S.; Hirsch, C.; Durbin-Johnson, B.; Xia, J.] Univ Calif Davis Hlth Syst, Sacramento, CA USA.
[Patel, K.] NIA, Bethesda, MD 20892 USA.
[Buzkova, P.] Univ Washington, Seattle, WA 98195 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 2012
VL 52
SU 1
BP 212
EP 212
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202126
ER
PT J
AU Lo-Ciganic, W
Boudreau, R
Zgibor, JC
Donohue, JM
Gray, S
Newman, AB
Simonsick, EM
Hanlon, JT
AF Lo-Ciganic, W.
Boudreau, R.
Zgibor, J. C.
Donohue, J. M.
Gray, S.
Newman, A. B.
Simonsick, E. M.
Hanlon, J. T.
TI TIME-TREND UTILIZATION OF STATINS IN COMMUNITY-DWELLING OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Lo-Ciganic, W.; Boudreau, R.; Zgibor, J. C.; Donohue, J. M.; Newman, A. B.; Hanlon, J. T.] Univ Pittsburgh, Pittsburgh, PA USA.
[Hanlon, J. T.] VA, Pittsburgh, PA USA.
[Gray, S.] Univ Washington, Seattle, WA 98195 USA.
[Simonsick, E. M.] NIA, Intramural Res Program, 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 2012
VL 52
SU 1
BP 214
EP 214
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202133
ER
PT J
AU Shardell, M
Simonsick, EM
Hicks, G
Resnick, B
Ferrucci, L
Magaziner, J
AF Shardell, M.
Simonsick, E. M.
Hicks, G.
Resnick, B.
Ferrucci, L.
Magaziner, J.
TI ADDRESSING MISSING DATA USING PROXY REPORTS SUBJECT TO MISCLASSIFICATION
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Shardell, M.; Magaziner, J.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Simonsick, E. M.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
[Hicks, G.] Univ Delaware, Newark, DE USA.
[Resnick, B.] Univ Maryland, Sch Nursing, Baltimore, MD 21201 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 2012
VL 52
SU 1
BP 253
EP 253
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202310
ER
PT J
AU Cohen, AA
Yasar, S
Fulop, T
Bandeen-Roche, K
Xue, Q
Yong, J
Fried, LP
Ferrucci, L
AF Cohen, A. A.
Yasar, S.
Fulop, T.
Bandeen-Roche, K.
Xue, Q.
Yong, J.
Fried, L. P.
Ferrucci, L.
TI ELECTROLYTE DYSREGULATION IN AGING: A NEW TYPE OF DYSREGULATION
IDENTIFIED BY MULTIVARIATE DISTRIBUTION ANALYSIS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Cohen, A. A.; Fulop, T.] Univ Sherbrooke, Ctr Hosp, Grp Rech PRIMUS, Sherbrooke, PQ J1K 2R1, Canada.
[Yasar, S.] Johns Hopkins Univ, Baltimore, MD USA.
[Bandeen-Roche, K.; Xue, Q.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Fried, L. P.] Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA.
[Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2012
VL 52
SU 1
BP 261
EP 262
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202354
ER
PT J
AU Simonsick, EM
Schrack, JA
Moore, AZ
Ferrucci, L
AF Simonsick, E. M.
Schrack, J. A.
Moore, A. Z.
Ferrucci, L.
TI PERCEIVED AND OBSERVED BALANCE AND THE ENERGETIC COST OF AND CAPACITY
FOR WALKING
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Simonsick, E. M.; Schrack, J. A.; Moore, A. Z.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
[Simonsick, E. M.] Johns Hopkins Sch Med, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2012
VL 52
SU 1
BP 277
EP 277
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202436
ER
PT J
AU Chia, CW
Schrack, JA
Gravenstein, KS
Egan, JM
Simonsick, EM
Ferrucci, L
AF Chia, C. W.
Schrack, J. A.
Gravenstein, K. S.
Egan, J. M.
Simonsick, E. M.
Ferrucci, L.
TI LEPTIN AND ENERGETIC CAPACITY IN OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Chia, C. W.; Schrack, J. A.; Gravenstein, K. S.; Egan, J. M.; Simonsick, E. M.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2012
VL 52
SU 1
BP 278
EP 278
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202438
ER
PT J
AU Ko, S
Simonsick, EM
Schrack, JA
Ferrucci, L
AF Ko, S.
Simonsick, E. M.
Schrack, J. A.
Ferrucci, L.
TI GAIT LAB PARAMETERS, KNEE PAIN AND THE ENERGETIC COST OF NORMAL WALKING
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ko, S.] Chonnam Natl Univ, Yeosu, South Korea.
[Simonsick, E. M.; Schrack, J. A.; 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 2012
VL 52
SU 1
BP 278
EP 278
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202439
ER
PT J
AU Moore, AZ
Simonsick, EM
Schrack, JA
Metter, E
Ferrucci, L
AF Moore, A. Z.
Simonsick, E. M.
Schrack, J. A.
Metter, E.
Ferrucci, L.
TI MUSCLE STRENGTH AND THE ENERGETIC COST OF AND CAPACITY FOR WALKING IN
OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Moore, A. Z.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Simonsick, E. M.; Schrack, J. A.; Metter, E.; 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 2012
VL 52
SU 1
BP 278
EP 278
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202440
ER
PT J
AU Schrack, JA
Simonsick, EM
Moore, AZ
Gravenstein, KS
Chia, CW
Ferrucci, L
AF Schrack, J. A.
Simonsick, E. M.
Moore, A. Z.
Gravenstein, K. S.
Chia, C. W.
Ferrucci, L.
TI IMPAIRED GLUCOSE METABOLISM AS AN INDICATOR OF WALKING EFFICIENCY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Schrack, J. A.; Simonsick, E. M.; Moore, A. Z.; Gravenstein, K. S.; Chia, C. W.; 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 2012
VL 52
SU 1
BP 278
EP 278
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202437
ER
PT J
AU Glynn, NW
Santanasto, AJ
Schulz, R
Beach, S
Boudreau, R
Simonsick, EM
Newman, AB
AF Glynn, N. W.
Santanasto, A. J.
Schulz, R.
Beach, S.
Boudreau, R.
Simonsick, E. M.
Newman, A. B.
TI DEVELOPMENT OF A NOVEL SURVEY TO MEASURE PERCEIVED FATIGABILITY IN OLDER
ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Glynn, N. W.; Santanasto, A. J.; Boudreau, R.; Newman, A. B.] Univ Pittsburgh, Ctr Aging & Populat Hlth, Pittsburgh, PA USA.
[Schulz, R.; Beach, S.] Univ Pittsburgh, Ctr Social & Urban Res, Pittsburgh, PA USA.
[Simonsick, E. M.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2012
VL 52
SU 1
BP 279
EP 279
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202446
ER
PT J
AU Santanasto, AJ
Simonsick, EM
Ferrucci, L
Schrack, JA
Boudreau, R
Newman, AB
Glynn, NW
AF Santanasto, A. J.
Simonsick, E. M.
Ferrucci, L.
Schrack, J. A.
Boudreau, R.
Newman, A. B.
Glynn, N. W.
TI PERCEIVED FATIGABILITY IS ASSOCIATED WITH MOBILITY AND PERFORMANCE IN
OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Santanasto, A. J.; Boudreau, R.; Newman, A. B.; Glynn, N. W.] Univ Pittsburgh, Pittsburgh, PA USA.
[Simonsick, E. M.; Ferrucci, L.; Schrack, J. A.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2012
VL 52
SU 1
BP 279
EP 279
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202445
ER
PT J
AU McDermott, MM
Lovato, L
Guralnik, J
Newman, AB
AF McDermott, M. M.
Lovato, L.
Guralnik, J.
Newman, A. B.
TI THE ANKLE-BRACHIAL INDEX (ABI), LEG SYMPTOMS, AND PHYSICAL PERFORMANCE
IN THE LIFE STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [McDermott, M. M.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Newman, A. B.] Univ Pittsburgh, Inst Aging, Pittsburgh, PA USA.
[Guralnik, J.] NIA, Bethesda, MD 20892 USA.
[Lovato, L.] Wake Forest Sch Med, Salem, NC 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 2012
VL 52
SU 1
BP 304
EP 304
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202575
ER
PT J
AU Csiszar, A
Sosnowska, D
Lakatta, EG
Sonntag, WE
Ungvari, Z
Wang, M
AF Csiszar, A.
Sosnowska, D.
Lakatta, E. G.
Sonntag, W. E.
Ungvari, Z.
Wang, M.
TI AGE-ASSOCIATED PRO-INFLAMMATORY SECRETORY PHENOTYPE IN VASCULAR SMOOTH
MUSCLE CELLS FROM THE NON-HUMAN PRIMATE M. MULATTA: REVERSAL BY
RESVERATROL TREATMENT
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Csiszar, A.; Sosnowska, D.; Sonntag, W. E.; Ungvari, Z.] Univ Oklahoma Hlth Sci Cente, Reynolds Oklahoma Ctr Aging, Dept Geriatr Med, Oklahoma City, OK USA.
[Lakatta, E. G.; Wang, M.] NIA, Cardiovasc Sci Lab, Gerontol Res Ctr, 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 2012
VL 52
SU 1
BP 316
EP 316
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202633
ER
PT J
AU Valcarcel-Ares, MN
Gautam, T
Bailey-Downs, L
Sosnowska, D
De Cabo, R
Sonntag, WE
Ungvari, Z
Csiszar, A
AF Valcarcel-Ares, M. N.
Gautam, T.
Bailey-Downs, L.
Sosnowska, D.
De Cabo, R.
Sonntag, W. E.
Ungvari, Z.
Csiszar, A.
TI DISRUPTION OF NRF2 SIGNALING IMPAIRS ANGIOGENIC CAPACITY OF ENDOTHELIAL
CELLS: IMPLICATIONS FOR MICROVASCULAR AGING
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Valcarcel-Ares, M. N.; Gautam, T.; Bailey-Downs, L.; Sosnowska, D.; Sonntag, W. E.; Ungvari, Z.; Csiszar, A.] Univ Oklahoma, Reynolds Oklahoma Ctr Aging, Dept Geriatr Med, Hlth Sci Ctr, Oklahoma City, OK USA.
[Valcarcel-Ares, M. N.] INIBIC CHU Coruna, Aging & Inflammat Res Lab, Coruna, Spain.
[De Cabo, R.] NIH, Lab Expt Gerontol, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2012
VL 52
SU 1
BP 317
EP 318
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202638
ER
PT J
AU Rosano, C
Abebe, KZ
Aizenstein, H
Harrris, TB
Yaffe, K
Satterfield, S
Newman, AB
AF Rosano, C.
Abebe, K. Z.
Aizenstein, H.
Harrris, T. B.
Yaffe, K.
Satterfield, S.
Newman, A. B.
TI HISTORICAL BLOOD PRESSURE MEASUREMENTS IN OLDER ADULTS INDICATE
UNDERLYING SMALL VESSEL DISEASE IN THE LEFT HEMISPHERE. (CNS)
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Rosano, C.; Abebe, K. Z.; Aizenstein, H.; Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Harrris, T. B.] NIA, Bethesda, MD 20892 USA.
[Yaffe, K.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Satterfield, S.] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 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 2012
VL 52
SU 1
BP 319
EP 319
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202645
ER
PT J
AU Pilotto, A
Gallina, P
Fontana, A
Sancarlo, D
Maggi, S
Bazzano, S
Ferrucci, L
Donato, D
AF Pilotto, A.
Gallina, P.
Fontana, A.
Sancarlo, D.
Maggi, S.
Bazzano, S.
Ferrucci, L.
Donato, D.
TI DEVELOPMENT AND VALIDATION OF A MULTIDIMENSIONAL PROGNOSTIC INDEX FOR
OLDER SUBJECTS LIVING AT HOME
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Pilotto, A.; Gallina, P.; Bazzano, S.; Donato, D.] S Antonio Hosp, Azienda ULSS Padova 16, Padua, Italy.
[Pilotto, A.; Fontana, A.; Sancarlo, D.] IRCCS Casa Sollievo Sofferenza, Geriatr, San Giovanni Rotondo, Italy.
[Maggi, S.] CNR, Padua, Italy.
[Ferrucci, L.] NIA, Baltimore, MD 21224 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 2012
VL 52
SU 1
BP 335
EP 335
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888202710
ER
PT J
AU Soerensen, M
Christensen, K
Stevnsner, T
Bohr, VA
Christiansen, L
AF Soerensen, M.
Christensen, K.
Stevnsner, T.
Bohr, V. A.
Christiansen, L.
TI VARIATION IN DNA REPAIR PATHWAY GENES IS ASSOCIATED WITH HUMAN LONGEVITY
AND AGING PHENOTYPES
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Soerensen, M.; Christensen, K.; Christiansen, L.] Univ So Denmark, Inst Publ Hlth, Danish Aging Res Ctr, Odense, Denmark.
[Soerensen, M.; Christensen, K.; Christiansen, L.] Odense Univ Hosp, Dept Clin Genet, DK-5000 Odense, Denmark.
[Soerensen, M.; Christensen, K.; Christiansen, L.] Odense Univ Hosp, Dept Clin Biochem & Pharmacol, DK-5000 Odense, Denmark.
[Stevnsner, T.; Bohr, V. A.] Aarhus Univ, Danish Aging Res Ctr, Dept Mol Biol & Genet, Aarhus, Denmark.
[Bohr, V. A.] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
RI Christensen, Kaare/C-2360-2009
OI Christensen, Kaare/0000-0002-5429-5292
NR 0
TC 0
Z9 0
U1 0
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2012
VL 52
SU 1
BP 373
EP 373
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203034
ER
PT J
AU Breslau, ES
Gorin, SS
AF Breslau, E. S.
Gorin, S. Sheinfeld
TI IMPLEMENTING PERSONALIZED MEDICINE IN PRIMARY CARE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Breslau, E. S.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Gorin, S. Sheinfeld] Columbia Univ, New York, NY USA.
NR 0
TC 0
Z9 0
U1 1
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 2012
VL 52
SU 1
BP 415
EP 415
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203224
ER
PT J
AU Breslau, ES
Walter, LC
AF Breslau, E. S.
Walter, L. C.
TI FRAMEWORK FOR SCREENING DECISION MAKING
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Breslau, E. S.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Walter, L. C.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2012
VL 52
SU 1
BP 415
EP 416
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203225
ER
PT J
AU Breslau, ES
Peters, EM
AF Breslau, E. S.
Peters, E. M.
TI DECISION MAKING AMONG OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Breslau, E. S.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Peters, E. M.] Ohio State Univ, Columbus, OH 43210 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 2012
VL 52
SU 1
BP 415
EP 415
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203223
ER
PT J
AU Breslau, ES
Scheuner, MT
AF Breslau, E. S.
Scheuner, M. T.
TI APPLICATION OF GENOMIC MEDICINE IN SCREENING DECISIONS FOR OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Breslau, E. S.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Scheuner, M. T.] RAND Corp, Santa Monica, CA 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 2012
VL 52
SU 1
BP 415
EP 415
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203222
ER
PT J
AU Thorpe, R
Simonsick, EM
Zonderman, AB
Evans, MK
AF Thorpe, R.
Simonsick, E. M.
Zonderman, A. B.
Evans, M. K.
TI ASSOCIATION BETWEEN RACE, POVERTY STATUS AND GRIP STRENGTH IN MIDDLE TO
OLD AGE ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Thorpe, R.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Simonsick, E. M.; Zonderman, A. B.; Evans, M. K.] 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 2012
VL 52
SU 1
BP 419
EP 419
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203246
ER
PT J
AU Barry, L
Thorpe, R
Yaffe, K
Penninx, B
Ayonayon, HN
Satterfield, S
Newman, AB
Simonsick, EM
AF Barry, L.
Thorpe, R.
Yaffe, K.
Penninx, B.
Ayonayon, H. N.
Satterfield, S.
Newman, A. B.
Simonsick, E. M.
TI LOW HEALTH LITERACY AND BLACK-WHITE DIFFERENCES IN DEPRESSION ONSET:
FINDINGS FROM THE HEALTH, AGING, AND BODY COMPOSITION STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Barry, L.] UConn Ctr Aging, Farmington, CT USA.
[Thorpe, R.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Yaffe, K.; Ayonayon, H. N.] Univ Calif San Francisco, Sch Med, San Francisco, CA USA.
[Penninx, B.] Vrije Univ Amsterdam, Med Ctr, Amsterdam, Netherlands.
[Satterfield, S.] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA.
[Newman, A. B.] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
[Simonsick, E. M.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
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 2012
VL 52
SU 1
BP 438
EP 438
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203340
ER
PT J
AU Beavers, KM
Beavers, DP
Houston, DK
Harris, TB
Simonsick, EM
Newman, AB
Nicklas, B
Kritchevsky, SB
AF Beavers, K. M.
Beavers, D. P.
Houston, D. K.
Harris, T. B.
Simonsick, E. M.
Newman, A. B.
Nicklas, B.
Kritchevsky, S. B.
TI INCREASING THIGH INTERMUSCULAR FAT IS AN INDEPENDENT PREDICTOR OF
DECLINES IN GAIT SPEED: RESULTS FROM THE HEALTH ABC STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Beavers, K. M.; Beavers, D. P.; Houston, D. K.; Nicklas, B.; Kritchevsky, S. B.] Wake Forest Sch Med, Winston Salem, NC USA.
[Harris, T. B.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Simonsick, E. M.] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
[Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
RI Beavers, Daniel/G-5338-2016
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 2012
VL 52
SU 1
BP 447
EP 447
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203382
ER
PT J
AU Murphy, RA
Kritchevsky, SB
Houston, DK
Simonsick, EM
Newman, AB
Tylavsky, FA
Cawthon, PM
Harris, TB
AF Murphy, R. A.
Kritchevsky, S. B.
Houston, D. K.
Simonsick, E. M.
Newman, A. B.
Tylavsky, F. A.
Cawthon, P. M.
Harris, T. B.
TI BODY COMPOSITION-RELATED PROFILES OF OLDER PEOPLE WITH AND WITHOUT
FUNCTIONAL LIMITATION AND DISABILITY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Murphy, R. A.; Harris, T. B.] NIA, Bethesda, MD 20892 USA.
[Kritchevsky, S. B.; Houston, D. K.] Wake Forest Univ, Salem, NC USA.
[Simonsick, E. M.] NIA, Baltimore, MD 21224 USA.
[Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Tylavsky, F. A.] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA.
[Cawthon, P. M.] Calif Pacific Med Ctr, San Francisco, CA 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 2012
VL 52
SU 1
BP 447
EP 448
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203383
ER
PT J
AU Tseng, LA
Delmonico, M
Visser, M
Boudreau, R
Goodpaster, B
Schwartz, AV
Simonsick, EM
Newman, AB
AF Tseng, L. A.
Delmonico, M.
Visser, M.
Boudreau, R.
Goodpaster, B.
Schwartz, A. V.
Simonsick, E. M.
Newman, A. B.
TI BODY FAT AND MUSCLE ATTENUATION EXPLAIN SEX DIFFERENTIAL IN LOWER
EXTREMITY FUNCTION IN HEALTH ABC
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Tseng, L. A.; Boudreau, R.; Goodpaster, B.; Newman, A. B.] Univ Pittsburgh, Pittsburg, CA USA.
[Delmonico, M.] Univ Rhode Isl, Dept Kinesiol, Kingston, RI 02881 USA.
[Visser, M.] Vrije Univ Amsterdam, Dept Hlth Sci, Amsterdam, Netherlands.
[Visser, M.] Vrije Univ Amsterdam Med Ctr, Dept Epidemiol & Biostat, Amsterdam, Netherlands.
[Schwartz, A. V.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Simonsick, E. M.] NIA, Intramural Res Program, 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 2012
VL 52
SU 1
BP 447
EP 447
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203381
ER
PT J
AU Aizenstein, HJ
Tudorascu, DL
Harris, T
Kritchevsky, SB
Newman, AB
Yaffe, K
Rosano, C
AF Aizenstein, H. J.
Tudorascu, D. L.
Harris, T.
Kritchevsky, S. B.
Newman, A. B.
Yaffe, K.
Rosano, C.
TI MULTI-MODAL MRI MARKERS OF CNS INTEGRITY ARE ASSOCIATED WITH DEPRESSIVE
SYMPTOMS IN THE ELDERLY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Aizenstein, H. J.; Tudorascu, D. L.; Newman, A. B.; Rosano, C.] Univ Pittsburgh, Pittsburgh, PA USA.
[Harris, T.] NIH, Bethesda, MD 20892 USA.
[Kritchevsky, S. B.] Wake Forest, Winston Salem, NC USA.
[Yaffe, K.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2012
VL 52
SU 1
BP 453
EP 453
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203408
ER
PT J
AU Melzer, D
Harries, L
Llewellyn, DJ
Bandinelli, S
Guralnik, JM
Ferrucci, L
AF Melzer, D.
Harries, L.
Llewellyn, D. J.
Bandinelli, S.
Guralnik, J. M.
Ferrucci, L.
TI GENE EXPRESSION ASSOCIATIONS WITH MMSE SCORES: PHAGOCYTOSIS OF CNS BETA
AMYLIOD?
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Melzer, D.; Harries, L.; Llewellyn, D. J.] Univ Exeter, Exeter, Devon, England.
[Bandinelli, S.] Azienda Sanit, Geriatr Unit, Florence, Italy.
[Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
[Guralnik, J. M.] Univ Maryland, Baltimore, MD 21201 USA.
RI Harries, Lorna/D-2241-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2012
VL 52
SU 1
BP 453
EP 453
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203410
ER
PT J
AU Harris, T
AF Harris, T.
TI THE LIMITS OF LIMITLESS DATA
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Harris, T.] NIA, IRP, 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 2012
VL 52
SU 1
BP 481
EP 481
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203555
ER
PT J
AU von Bonsdorff, M
Muller, M
Rantanen, T
Garcia, M
Thorsdottir, I
Gudnason, V
Launer, LJ
Harris, TB
AF von Bonsdorff, M.
Muller, M.
Rantanen, T.
Garcia, M.
Thorsdottir, I.
Gudnason, V.
Launer, L. J.
Harris, T. B.
TI PERSISTENCE OF THE EFFECT OF BODY SIZE AT BIRTH ON DYSGLYCAEMIA AND TYPE
2 DIABETES IN OLD AGE: AGES-REYKJAVIK STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [von Bonsdorff, M.; Rantanen, T.] Univ Jyvaskyla, Gerontol Res Ctr, SF-40351 Jyvaskyla, Finland.
[von Bonsdorff, M.; Muller, M.; Garcia, M.; Launer, L. J.; Harris, T. B.] NIA, Lab Epidemiol Demog & Biometry, Intramural Res Program, Bethesda, MD 20892 USA.
[Muller, M.] Vrije Univ Amsterdam, Med Ctr, Dept Internal Med, Amsterdam, Netherlands.
[Gudnason, V.] Iceland Heart Assoc, Kopavogur, Iceland.
[Gudnason, V.] Univ Iceland, Fac Med, Reykjavik, Iceland.
[Thorsdottir, I.] Univ Iceland, Unit Nutr Res, Reykjavik, Iceland.
[Thorsdottir, I.] Natl Univ Hosp Iceland, Landspitali, Reykjavik, Iceland.
RI Gudnason, Vilmundur/K-6885-2015
OI Gudnason, Vilmundur/0000-0001-5696-0084
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2012
VL 52
SU 1
BP 484
EP 484
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203567
ER
PT J
AU Strotmeyer, ES
Boudreau, RM
Cauley, JA
Albert, SM
Schwartz, AV
Satterfield, S
Harris, TB
Newman, AB
AF Strotmeyer, E. S.
Boudreau, R. M.
Cauley, J. A.
Albert, S. M.
Schwartz, A. V.
Satterfield, S.
Harris, T. B.
Newman, A. B.
TI POOR SENSORIMOTOR NERVE FUNCTION INCREASES THE RISK OF INJURIOUS FALLS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Strotmeyer, E. S.; Boudreau, R. M.; Cauley, J. A.; Albert, S. M.; Newman, A. B.] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA USA.
[Schwartz, A. V.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Satterfield, S.] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA.
[Harris, T. B.] NIA, Bethesda, MD 20892 USA.
RI Strotmeyer, Elsa/F-3015-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2012
VL 52
SU 1
BP 507
EP 507
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203685
ER
PT J
AU Leishear, K
Boudreau, R
Studenski, S
Ferrucci, L
Rosano, C
Harris, TB
Newman, AB
Strotmeyer, ES
AF Leishear, K.
Boudreau, R.
Studenski, S.
Ferrucci, L.
Rosano, C.
Harris, T. B.
Newman, A. B.
Strotmeyer, E. S.
TI VITAMIN B12 AND CENTRAL AND PERIPHERAL NEUROLOGICAL FUNCTION: IS THERE A
THRESHOLD LEVEL?
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Leishear, K.; Boudreau, R.; Studenski, S.; Rosano, C.; Newman, A. B.; Strotmeyer, E. S.] Univ Pittsburgh, Pittsburgh, PA USA.
[Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
[Harris, T. B.] NIA, Bethesda, MD 20892 USA.
RI Strotmeyer, Elsa/F-3015-2014
NR 0
TC 0
Z9 0
U1 0
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2012
VL 52
SU 1
BP 508
EP 508
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203687
ER
PT J
AU Lin, FR
Yaffe, K
Xia, J
Xue, Q
Harris, TB
Purchase-Helzner, E
Ferrucci, L
Simonsick, EM
AF Lin, F. R.
Yaffe, K.
Xia, J.
Xue, Q.
Harris, T. B.
Purchase-Helzner, E.
Ferrucci, L.
Simonsick, E. M.
TI HEARING LOSS AND COGNITIVE DECLINE AMONG OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Lin, F. R.] Johns Hopkins, Otolaryngol Head & Neck Surg, Baltimore, MD USA.
[Yaffe, K.] UCSF, San Francisco, CA USA.
[Harris, T. B.; Ferrucci, L.; Simonsick, E. M.] NIA, Baltimore, MD 21224 USA.
[Purchase-Helzner, E.] SUNY Downstate, New York, NY USA.
[Lin, F. R.; Xia, J.; Xue, Q.] Johns Hopkins Ctr Aging & Hlth, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 7
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 2012
VL 52
SU 1
BP 508
EP 508
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203689
ER
PT J
AU Nocera, J
Yaffe, K
Simonsick, EM
Williamson, J
Newman, AB
Caserotti, P
Harris, T
Shorr, RI
AF Nocera, J.
Yaffe, K.
Simonsick, E. M.
Williamson, J.
Newman, A. B.
Caserotti, P.
Harris, T.
Shorr, R. I.
TI EVALUATION OF BRAIN-DERIVED NEUROTROPHIC FACTOR AND PHYSICAL FUNCTION IN
OLDER ADULTS FROM THE HEALTH ABC STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Nocera, J.; Shorr, R. I.] US Dept Vet Affairs, Gainesville, FL USA.
[Nocera, J.; Shorr, R. I.] Univ Florida, Gainesville, FL USA.
[Yaffe, K.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Simonsick, E. M.; Harris, T.] NIH, Bethesda, MD 20892 USA.
[Williamson, J.] Wake Forest Baptist Med Ctr, Winston Salem, NC USA.
[Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Caserotti, P.] Univ So Denmark, Odense, Denmark.
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 2012
VL 52
SU 1
BP 508
EP 508
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888203688
ER
EF